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060356
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Severe sepsis
amp MODS Assessment and managementDR PONGDHEP THEERAWIT MD
PULMONARY AND CRITICAL CARE
RAMATHIBODI HOSPITAL
Understanding shock state
Inadequate
tissue perfusion
Low perfusion pressure
Low CO
Low oxygen
Inadequate tissue perfusion in hypovolemic and septic shock
Hypovolemic Septic
Perfusion pressure Low Low
Cardiac output Low High
Oxygen Low Low
Stroke volume in shock
Oxygen transport
CaO2
DO2 =CO x CaO2VO2 = CO x (SaO2-SvO2)SvO2
Normal microcirculation
DO2 = 100
VO2 = 30
SvO2 = 70
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Microcirculation in sepsis
DO2 = 100
VO2 = 10
SvO2 = 90
Understanding shock state
Inadequate
tissue perfusion
Low perfusion
Pressure by
low vascular resistance
High CO
Microcirculation dysfunction
Mortality outcome of decrease vascular density in septic shock
De Backer D etal AJRCCM 2002 Sakr etal Crit Care Med 2004
Mean arterial pressure and perfused capillaries density by OPS
For all vessels and for large vessels there was NOsignificant relationship between the proportion of perfused vessels
and MAP CI pH SvO2 Hb conc
De Backer et al AJRCCM 2002
Cardiac index MAP and Microcirculation dysfunction
Characteristics of septic shock
Even high CO -gt low perfusion
Low vascular resistance -gt low perfusion pressure
Microcirculation obstruction -gt cellular
hypoxia
Even rising of MAP (higher perfusion
pressure)-gt cellular hypoxemia due
to microcirculation dysfunction
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Multiple organs dysfunction syndrome
Persistence of low
perfusion pressure
SIRS
Endothelial dysfunction
Microcirculation dysfunction
Mitochondrial dysfunction
Definition of sepsis (SSC 2012)
Severe sepsis (SSC 2012) Hemodynamic
parameters in 4 shocks
CVP PAP PCWP CO SVR
Hypovolemic Low Low Low Low High
Cardiogenic High High High Low High
Obstructive High Very high Normal Low High
Septic Not high Not high Not high High Low
Clinical signs in 4 shocks
JVP P2 CM PP DiasBP
Hypovolemic Low Soft No Narrow Low
Cardiogenic High Not loud Yes Narrow Low
Obstructive High Very loud Yes Narrow Low
Septic Not high Normal No Wide Very low
Clinical characteristics of different shocks
Clinical
Pulse pressure
Tachycardia
Extremity
Capillary refill
Bleeding
Narrow
Present
Cold
Impaired
AMI
Narrow
Present
Cold
Impaired
AMPE
Narrow
Present
Cold
Impaired
Absent
Low
Soft
Cardiomegaly
JVP
P2
Ltside
High
Loud
Rtside
High
Vloud
Sepsis
Wide
Present
Warm
Preserve
Absent
Not high
Not loud
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Assessment amp Management
Site of infection
Local
Lungs
Abdomen
Genito-urinary
Soft tissue
Systemic
Leptospirosis
Mellioidosis
Salmonellosis
Organisms
bull Gram positive
bull Gram negative
bull Community basedbull Hospital based
Gram positive bull
Gram negative bull
Primary peritonitis bullSecondary peritonitis bull
Appropriate antibiotic ASAP within 1 hr (SSC 2012)
Hemodynamic assessment
Assess cardiac output
Assess fluid responsiveness
Assess pulmonary leakage
Assess tissue perfusion
Cardiac output monitoring
Intermittent
PA catheter
ICU-US
Continuous
Thermodilution
Pulse contour analysis
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PA catheter
bull Proximal ndash cold injectate ScvO2
bull Distal ndash Draw SvO2
bull Thermistor ndash Temperature
bull Balloon inflation and deflation
Wave form
Waveform In place PA catheter
Joining Zeroing
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Others parameter calculated from PAC parameters
SVR = ( MAP - CVP CO ) x 80
PVR = ( PAP - PAOP CO ) x 80
CO = VO2 ( CaO2 - CvO2 )
DO2 = CO x Ca O2 x 10
VO2 = ( Ca O2 - Cv O2 ) x CO x10
Ca O2 = ( 139 x Hb x SaO2 ) + ( 0003 x PaO2 ) - Arterial
O2 content
Cv O2 = ( 139 x Hb x SvO2 ) + ( 0003 x PvO2 ) - Venous
O2 content
O2 extraxtion = VO2 DO2
QsQt = ( PA-a O2 ) ( PA-a O2 ) ( Ca-v O2 )
Cardiac output measurement
Fickrsquos formular
CO = VO2
CaO2-CvO2
Poor feasibility
Indicator dilution method
Indocyanine green
More accurate and reproducible
Require blood sampling
Recirculation of dye can disturb measurement
Thermodilution
More efficient
Thermo dilution method
Inject 5-10 cc of cold water
Tem
pera
ture
change (
)
Time
Stewart ndashHamilton equation
CO = ( TB ndash TI )xK
0 TB(t) dt
Hemodynamic
parameters in 4 shocks
CVP PAP PCWP CO SVR
Hypovolemic Low Low Low Low High
Cardiogenic High High High Low High
Obstructive High Very high Normal Low High
Septic Not high Not high Not high High Low
Ultrasound CO by ultrasound
A mount of blood flow going through a fixed orifice =
CSA x Flow-Velocity
SV = CSA x LVOTTVI
CSA = LVOTd2 x 078540
SV = LVOTd2 x 078540 x LVOTTVI
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LVOT diameter
LVOT VTI
good correlation between the thermodilutiontechnique and
Simpsons two-chamber method (r = 091)
Simpsons four-chamber method (r = 077)
the LVOT Doppler method (r = 094)
the LVOT Doppler method demonstrated acceptable agreement with a mean of 02
litresminute standard deviation of 082 litresminute and 95 limits of agreement of -15 to +19 litresminute
CCO-thermodilution methods Model for CCOtd
Agreement between CCO and BCO
in cardio-thoracic surgeryIntensive Care Med 199925166
Compare CCO and BCO in 20 medical ptsJ Crit Care 199813184
Conditions Number
MV 15
Vasopressor 15
Malignancy 12
Aplastic anemia
5
SLE 1
Cushing 1
CGD 1
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Good correlation between
CCO and BCO in sepsisIntensive Care Med 2002281276
Good correlation between CCO and BCO in sepsisIntensive Care Med 2002281276
Poor correlation of
CCO during hypothermia
Conclusions
Despite an excellent correlation accuracy and
precision between CCO and ICO before CPB and more than 45 minutes after hypothermic CPB a lack
of correlation in the early phase after CPB has been
found Further investigation is needed to elucidate the underlying cause of these findings and to clarify
whether ICO or CCO or both fail to represent the
real cardiac output up to 45 minutes after weaning from hypothermic CPB
19959405
Response time after sudden reduction of COAnesthesiology 199889(6)1592
Response time after sudden reduction of COCrit Care Med 1995 23 860 Advantages over IBCO
Provide continuous trend
Reduce contamination
Less time consuming
Unnecessary fluid
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Limitations
Immediate CO measurement may not be done due to average time for reduce thermal noise
Transpulmoanry thermodilution method (TPTD)
Compare TPTD and IBTDAnesthesia amp Analgesia 2010
The respiratory variation affect IBTD rather than TPTD
IBTD
TPTD
Advantages over IBTD
Less invasive
Decrease complications result from PA catheter
GEDV and EVLW can be measuredAm J Physiol Lung Cell Mol Physiol 291 L1118ndashL1131 2006
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Limitations
Canrsquot assess PA pressure and its trend
Canrsquot assess SvO2
Pulse contour analysis
Non-calibrated
Calibrated
Basic Principles
Traditional CO = HR SV
FloTrac system CO = PR x (AP )
Where = M (HR AP C(P) BSA MAP 3ap 4ap)
Validation ICOCCOAPCOCrit Care 200711R105
Validation ICOCCOAPCOCrit Care 200711R105
FloTrac amp PACCrit Care 201014R212
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FloTrac amp PACCrit Care 201014R212
FloTrac in sepsisIntensive Care 201137233
FloTrac in sepsisIntensive Care 201137233
FloTrac Vigileo G3
Advantages
Real time
Less invasive
Non-calibrated
Informative
CO CI
PPV
SvO2
SVR
Disadvantages
Algorithm-gtnot real
Accuracy
Can not assess RV
derived parameters
Require new version software
PiCCO system Need calibration
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PAC and PiCCO (AP)Crit Care 201014R212
PiCCO
Advantages
Continuos monitoring
More accurate
Informative
COCI
SVV
SVR
GEDV
EVLW
AP
Disadvantages
Require calibration q 8 hrs
Femoral site risky to
CRBSI
Early goal directed therapy
What is the CVP
CVP = Central Venous Pressure
Frank Starling amp venous return line
Stroke volume
CVP0
Frank-Starling curve
Stroke volume or EDV
JVP or CVP or PCWP
ΔSV or Δ EDV
a
b
Responders
Non-responders
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b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
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PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
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Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
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Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
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LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
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Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
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Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
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Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
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Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
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Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
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CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
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2
Microcirculation in sepsis
DO2 = 100
VO2 = 10
SvO2 = 90
Understanding shock state
Inadequate
tissue perfusion
Low perfusion
Pressure by
low vascular resistance
High CO
Microcirculation dysfunction
Mortality outcome of decrease vascular density in septic shock
De Backer D etal AJRCCM 2002 Sakr etal Crit Care Med 2004
Mean arterial pressure and perfused capillaries density by OPS
For all vessels and for large vessels there was NOsignificant relationship between the proportion of perfused vessels
and MAP CI pH SvO2 Hb conc
De Backer et al AJRCCM 2002
Cardiac index MAP and Microcirculation dysfunction
Characteristics of septic shock
Even high CO -gt low perfusion
Low vascular resistance -gt low perfusion pressure
Microcirculation obstruction -gt cellular
hypoxia
Even rising of MAP (higher perfusion
pressure)-gt cellular hypoxemia due
to microcirculation dysfunction
060356
3
Multiple organs dysfunction syndrome
Persistence of low
perfusion pressure
SIRS
Endothelial dysfunction
Microcirculation dysfunction
Mitochondrial dysfunction
Definition of sepsis (SSC 2012)
Severe sepsis (SSC 2012) Hemodynamic
parameters in 4 shocks
CVP PAP PCWP CO SVR
Hypovolemic Low Low Low Low High
Cardiogenic High High High Low High
Obstructive High Very high Normal Low High
Septic Not high Not high Not high High Low
Clinical signs in 4 shocks
JVP P2 CM PP DiasBP
Hypovolemic Low Soft No Narrow Low
Cardiogenic High Not loud Yes Narrow Low
Obstructive High Very loud Yes Narrow Low
Septic Not high Normal No Wide Very low
Clinical characteristics of different shocks
Clinical
Pulse pressure
Tachycardia
Extremity
Capillary refill
Bleeding
Narrow
Present
Cold
Impaired
AMI
Narrow
Present
Cold
Impaired
AMPE
Narrow
Present
Cold
Impaired
Absent
Low
Soft
Cardiomegaly
JVP
P2
Ltside
High
Loud
Rtside
High
Vloud
Sepsis
Wide
Present
Warm
Preserve
Absent
Not high
Not loud
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4
Assessment amp Management
Site of infection
Local
Lungs
Abdomen
Genito-urinary
Soft tissue
Systemic
Leptospirosis
Mellioidosis
Salmonellosis
Organisms
bull Gram positive
bull Gram negative
bull Community basedbull Hospital based
Gram positive bull
Gram negative bull
Primary peritonitis bullSecondary peritonitis bull
Appropriate antibiotic ASAP within 1 hr (SSC 2012)
Hemodynamic assessment
Assess cardiac output
Assess fluid responsiveness
Assess pulmonary leakage
Assess tissue perfusion
Cardiac output monitoring
Intermittent
PA catheter
ICU-US
Continuous
Thermodilution
Pulse contour analysis
060356
5
PA catheter
bull Proximal ndash cold injectate ScvO2
bull Distal ndash Draw SvO2
bull Thermistor ndash Temperature
bull Balloon inflation and deflation
Wave form
Waveform In place PA catheter
Joining Zeroing
060356
6
Others parameter calculated from PAC parameters
SVR = ( MAP - CVP CO ) x 80
PVR = ( PAP - PAOP CO ) x 80
CO = VO2 ( CaO2 - CvO2 )
DO2 = CO x Ca O2 x 10
VO2 = ( Ca O2 - Cv O2 ) x CO x10
Ca O2 = ( 139 x Hb x SaO2 ) + ( 0003 x PaO2 ) - Arterial
O2 content
Cv O2 = ( 139 x Hb x SvO2 ) + ( 0003 x PvO2 ) - Venous
O2 content
O2 extraxtion = VO2 DO2
QsQt = ( PA-a O2 ) ( PA-a O2 ) ( Ca-v O2 )
Cardiac output measurement
Fickrsquos formular
CO = VO2
CaO2-CvO2
Poor feasibility
Indicator dilution method
Indocyanine green
More accurate and reproducible
Require blood sampling
Recirculation of dye can disturb measurement
Thermodilution
More efficient
Thermo dilution method
Inject 5-10 cc of cold water
Tem
pera
ture
change (
)
Time
Stewart ndashHamilton equation
CO = ( TB ndash TI )xK
0 TB(t) dt
Hemodynamic
parameters in 4 shocks
CVP PAP PCWP CO SVR
Hypovolemic Low Low Low Low High
Cardiogenic High High High Low High
Obstructive High Very high Normal Low High
Septic Not high Not high Not high High Low
Ultrasound CO by ultrasound
A mount of blood flow going through a fixed orifice =
CSA x Flow-Velocity
SV = CSA x LVOTTVI
CSA = LVOTd2 x 078540
SV = LVOTd2 x 078540 x LVOTTVI
060356
7
LVOT diameter
LVOT VTI
good correlation between the thermodilutiontechnique and
Simpsons two-chamber method (r = 091)
Simpsons four-chamber method (r = 077)
the LVOT Doppler method (r = 094)
the LVOT Doppler method demonstrated acceptable agreement with a mean of 02
litresminute standard deviation of 082 litresminute and 95 limits of agreement of -15 to +19 litresminute
CCO-thermodilution methods Model for CCOtd
Agreement between CCO and BCO
in cardio-thoracic surgeryIntensive Care Med 199925166
Compare CCO and BCO in 20 medical ptsJ Crit Care 199813184
Conditions Number
MV 15
Vasopressor 15
Malignancy 12
Aplastic anemia
5
SLE 1
Cushing 1
CGD 1
060356
8
Good correlation between
CCO and BCO in sepsisIntensive Care Med 2002281276
Good correlation between CCO and BCO in sepsisIntensive Care Med 2002281276
Poor correlation of
CCO during hypothermia
Conclusions
Despite an excellent correlation accuracy and
precision between CCO and ICO before CPB and more than 45 minutes after hypothermic CPB a lack
of correlation in the early phase after CPB has been
found Further investigation is needed to elucidate the underlying cause of these findings and to clarify
whether ICO or CCO or both fail to represent the
real cardiac output up to 45 minutes after weaning from hypothermic CPB
19959405
Response time after sudden reduction of COAnesthesiology 199889(6)1592
Response time after sudden reduction of COCrit Care Med 1995 23 860 Advantages over IBCO
Provide continuous trend
Reduce contamination
Less time consuming
Unnecessary fluid
060356
9
Limitations
Immediate CO measurement may not be done due to average time for reduce thermal noise
Transpulmoanry thermodilution method (TPTD)
Compare TPTD and IBTDAnesthesia amp Analgesia 2010
The respiratory variation affect IBTD rather than TPTD
IBTD
TPTD
Advantages over IBTD
Less invasive
Decrease complications result from PA catheter
GEDV and EVLW can be measuredAm J Physiol Lung Cell Mol Physiol 291 L1118ndashL1131 2006
060356
10
Limitations
Canrsquot assess PA pressure and its trend
Canrsquot assess SvO2
Pulse contour analysis
Non-calibrated
Calibrated
Basic Principles
Traditional CO = HR SV
FloTrac system CO = PR x (AP )
Where = M (HR AP C(P) BSA MAP 3ap 4ap)
Validation ICOCCOAPCOCrit Care 200711R105
Validation ICOCCOAPCOCrit Care 200711R105
FloTrac amp PACCrit Care 201014R212
060356
11
FloTrac amp PACCrit Care 201014R212
FloTrac in sepsisIntensive Care 201137233
FloTrac in sepsisIntensive Care 201137233
FloTrac Vigileo G3
Advantages
Real time
Less invasive
Non-calibrated
Informative
CO CI
PPV
SvO2
SVR
Disadvantages
Algorithm-gtnot real
Accuracy
Can not assess RV
derived parameters
Require new version software
PiCCO system Need calibration
060356
12
PAC and PiCCO (AP)Crit Care 201014R212
PiCCO
Advantages
Continuos monitoring
More accurate
Informative
COCI
SVV
SVR
GEDV
EVLW
AP
Disadvantages
Require calibration q 8 hrs
Femoral site risky to
CRBSI
Early goal directed therapy
What is the CVP
CVP = Central Venous Pressure
Frank Starling amp venous return line
Stroke volume
CVP0
Frank-Starling curve
Stroke volume or EDV
JVP or CVP or PCWP
ΔSV or Δ EDV
a
b
Responders
Non-responders
060356
13
b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
3
Multiple organs dysfunction syndrome
Persistence of low
perfusion pressure
SIRS
Endothelial dysfunction
Microcirculation dysfunction
Mitochondrial dysfunction
Definition of sepsis (SSC 2012)
Severe sepsis (SSC 2012) Hemodynamic
parameters in 4 shocks
CVP PAP PCWP CO SVR
Hypovolemic Low Low Low Low High
Cardiogenic High High High Low High
Obstructive High Very high Normal Low High
Septic Not high Not high Not high High Low
Clinical signs in 4 shocks
JVP P2 CM PP DiasBP
Hypovolemic Low Soft No Narrow Low
Cardiogenic High Not loud Yes Narrow Low
Obstructive High Very loud Yes Narrow Low
Septic Not high Normal No Wide Very low
Clinical characteristics of different shocks
Clinical
Pulse pressure
Tachycardia
Extremity
Capillary refill
Bleeding
Narrow
Present
Cold
Impaired
AMI
Narrow
Present
Cold
Impaired
AMPE
Narrow
Present
Cold
Impaired
Absent
Low
Soft
Cardiomegaly
JVP
P2
Ltside
High
Loud
Rtside
High
Vloud
Sepsis
Wide
Present
Warm
Preserve
Absent
Not high
Not loud
060356
4
Assessment amp Management
Site of infection
Local
Lungs
Abdomen
Genito-urinary
Soft tissue
Systemic
Leptospirosis
Mellioidosis
Salmonellosis
Organisms
bull Gram positive
bull Gram negative
bull Community basedbull Hospital based
Gram positive bull
Gram negative bull
Primary peritonitis bullSecondary peritonitis bull
Appropriate antibiotic ASAP within 1 hr (SSC 2012)
Hemodynamic assessment
Assess cardiac output
Assess fluid responsiveness
Assess pulmonary leakage
Assess tissue perfusion
Cardiac output monitoring
Intermittent
PA catheter
ICU-US
Continuous
Thermodilution
Pulse contour analysis
060356
5
PA catheter
bull Proximal ndash cold injectate ScvO2
bull Distal ndash Draw SvO2
bull Thermistor ndash Temperature
bull Balloon inflation and deflation
Wave form
Waveform In place PA catheter
Joining Zeroing
060356
6
Others parameter calculated from PAC parameters
SVR = ( MAP - CVP CO ) x 80
PVR = ( PAP - PAOP CO ) x 80
CO = VO2 ( CaO2 - CvO2 )
DO2 = CO x Ca O2 x 10
VO2 = ( Ca O2 - Cv O2 ) x CO x10
Ca O2 = ( 139 x Hb x SaO2 ) + ( 0003 x PaO2 ) - Arterial
O2 content
Cv O2 = ( 139 x Hb x SvO2 ) + ( 0003 x PvO2 ) - Venous
O2 content
O2 extraxtion = VO2 DO2
QsQt = ( PA-a O2 ) ( PA-a O2 ) ( Ca-v O2 )
Cardiac output measurement
Fickrsquos formular
CO = VO2
CaO2-CvO2
Poor feasibility
Indicator dilution method
Indocyanine green
More accurate and reproducible
Require blood sampling
Recirculation of dye can disturb measurement
Thermodilution
More efficient
Thermo dilution method
Inject 5-10 cc of cold water
Tem
pera
ture
change (
)
Time
Stewart ndashHamilton equation
CO = ( TB ndash TI )xK
0 TB(t) dt
Hemodynamic
parameters in 4 shocks
CVP PAP PCWP CO SVR
Hypovolemic Low Low Low Low High
Cardiogenic High High High Low High
Obstructive High Very high Normal Low High
Septic Not high Not high Not high High Low
Ultrasound CO by ultrasound
A mount of blood flow going through a fixed orifice =
CSA x Flow-Velocity
SV = CSA x LVOTTVI
CSA = LVOTd2 x 078540
SV = LVOTd2 x 078540 x LVOTTVI
060356
7
LVOT diameter
LVOT VTI
good correlation between the thermodilutiontechnique and
Simpsons two-chamber method (r = 091)
Simpsons four-chamber method (r = 077)
the LVOT Doppler method (r = 094)
the LVOT Doppler method demonstrated acceptable agreement with a mean of 02
litresminute standard deviation of 082 litresminute and 95 limits of agreement of -15 to +19 litresminute
CCO-thermodilution methods Model for CCOtd
Agreement between CCO and BCO
in cardio-thoracic surgeryIntensive Care Med 199925166
Compare CCO and BCO in 20 medical ptsJ Crit Care 199813184
Conditions Number
MV 15
Vasopressor 15
Malignancy 12
Aplastic anemia
5
SLE 1
Cushing 1
CGD 1
060356
8
Good correlation between
CCO and BCO in sepsisIntensive Care Med 2002281276
Good correlation between CCO and BCO in sepsisIntensive Care Med 2002281276
Poor correlation of
CCO during hypothermia
Conclusions
Despite an excellent correlation accuracy and
precision between CCO and ICO before CPB and more than 45 minutes after hypothermic CPB a lack
of correlation in the early phase after CPB has been
found Further investigation is needed to elucidate the underlying cause of these findings and to clarify
whether ICO or CCO or both fail to represent the
real cardiac output up to 45 minutes after weaning from hypothermic CPB
19959405
Response time after sudden reduction of COAnesthesiology 199889(6)1592
Response time after sudden reduction of COCrit Care Med 1995 23 860 Advantages over IBCO
Provide continuous trend
Reduce contamination
Less time consuming
Unnecessary fluid
060356
9
Limitations
Immediate CO measurement may not be done due to average time for reduce thermal noise
Transpulmoanry thermodilution method (TPTD)
Compare TPTD and IBTDAnesthesia amp Analgesia 2010
The respiratory variation affect IBTD rather than TPTD
IBTD
TPTD
Advantages over IBTD
Less invasive
Decrease complications result from PA catheter
GEDV and EVLW can be measuredAm J Physiol Lung Cell Mol Physiol 291 L1118ndashL1131 2006
060356
10
Limitations
Canrsquot assess PA pressure and its trend
Canrsquot assess SvO2
Pulse contour analysis
Non-calibrated
Calibrated
Basic Principles
Traditional CO = HR SV
FloTrac system CO = PR x (AP )
Where = M (HR AP C(P) BSA MAP 3ap 4ap)
Validation ICOCCOAPCOCrit Care 200711R105
Validation ICOCCOAPCOCrit Care 200711R105
FloTrac amp PACCrit Care 201014R212
060356
11
FloTrac amp PACCrit Care 201014R212
FloTrac in sepsisIntensive Care 201137233
FloTrac in sepsisIntensive Care 201137233
FloTrac Vigileo G3
Advantages
Real time
Less invasive
Non-calibrated
Informative
CO CI
PPV
SvO2
SVR
Disadvantages
Algorithm-gtnot real
Accuracy
Can not assess RV
derived parameters
Require new version software
PiCCO system Need calibration
060356
12
PAC and PiCCO (AP)Crit Care 201014R212
PiCCO
Advantages
Continuos monitoring
More accurate
Informative
COCI
SVV
SVR
GEDV
EVLW
AP
Disadvantages
Require calibration q 8 hrs
Femoral site risky to
CRBSI
Early goal directed therapy
What is the CVP
CVP = Central Venous Pressure
Frank Starling amp venous return line
Stroke volume
CVP0
Frank-Starling curve
Stroke volume or EDV
JVP or CVP or PCWP
ΔSV or Δ EDV
a
b
Responders
Non-responders
060356
13
b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
4
Assessment amp Management
Site of infection
Local
Lungs
Abdomen
Genito-urinary
Soft tissue
Systemic
Leptospirosis
Mellioidosis
Salmonellosis
Organisms
bull Gram positive
bull Gram negative
bull Community basedbull Hospital based
Gram positive bull
Gram negative bull
Primary peritonitis bullSecondary peritonitis bull
Appropriate antibiotic ASAP within 1 hr (SSC 2012)
Hemodynamic assessment
Assess cardiac output
Assess fluid responsiveness
Assess pulmonary leakage
Assess tissue perfusion
Cardiac output monitoring
Intermittent
PA catheter
ICU-US
Continuous
Thermodilution
Pulse contour analysis
060356
5
PA catheter
bull Proximal ndash cold injectate ScvO2
bull Distal ndash Draw SvO2
bull Thermistor ndash Temperature
bull Balloon inflation and deflation
Wave form
Waveform In place PA catheter
Joining Zeroing
060356
6
Others parameter calculated from PAC parameters
SVR = ( MAP - CVP CO ) x 80
PVR = ( PAP - PAOP CO ) x 80
CO = VO2 ( CaO2 - CvO2 )
DO2 = CO x Ca O2 x 10
VO2 = ( Ca O2 - Cv O2 ) x CO x10
Ca O2 = ( 139 x Hb x SaO2 ) + ( 0003 x PaO2 ) - Arterial
O2 content
Cv O2 = ( 139 x Hb x SvO2 ) + ( 0003 x PvO2 ) - Venous
O2 content
O2 extraxtion = VO2 DO2
QsQt = ( PA-a O2 ) ( PA-a O2 ) ( Ca-v O2 )
Cardiac output measurement
Fickrsquos formular
CO = VO2
CaO2-CvO2
Poor feasibility
Indicator dilution method
Indocyanine green
More accurate and reproducible
Require blood sampling
Recirculation of dye can disturb measurement
Thermodilution
More efficient
Thermo dilution method
Inject 5-10 cc of cold water
Tem
pera
ture
change (
)
Time
Stewart ndashHamilton equation
CO = ( TB ndash TI )xK
0 TB(t) dt
Hemodynamic
parameters in 4 shocks
CVP PAP PCWP CO SVR
Hypovolemic Low Low Low Low High
Cardiogenic High High High Low High
Obstructive High Very high Normal Low High
Septic Not high Not high Not high High Low
Ultrasound CO by ultrasound
A mount of blood flow going through a fixed orifice =
CSA x Flow-Velocity
SV = CSA x LVOTTVI
CSA = LVOTd2 x 078540
SV = LVOTd2 x 078540 x LVOTTVI
060356
7
LVOT diameter
LVOT VTI
good correlation between the thermodilutiontechnique and
Simpsons two-chamber method (r = 091)
Simpsons four-chamber method (r = 077)
the LVOT Doppler method (r = 094)
the LVOT Doppler method demonstrated acceptable agreement with a mean of 02
litresminute standard deviation of 082 litresminute and 95 limits of agreement of -15 to +19 litresminute
CCO-thermodilution methods Model for CCOtd
Agreement between CCO and BCO
in cardio-thoracic surgeryIntensive Care Med 199925166
Compare CCO and BCO in 20 medical ptsJ Crit Care 199813184
Conditions Number
MV 15
Vasopressor 15
Malignancy 12
Aplastic anemia
5
SLE 1
Cushing 1
CGD 1
060356
8
Good correlation between
CCO and BCO in sepsisIntensive Care Med 2002281276
Good correlation between CCO and BCO in sepsisIntensive Care Med 2002281276
Poor correlation of
CCO during hypothermia
Conclusions
Despite an excellent correlation accuracy and
precision between CCO and ICO before CPB and more than 45 minutes after hypothermic CPB a lack
of correlation in the early phase after CPB has been
found Further investigation is needed to elucidate the underlying cause of these findings and to clarify
whether ICO or CCO or both fail to represent the
real cardiac output up to 45 minutes after weaning from hypothermic CPB
19959405
Response time after sudden reduction of COAnesthesiology 199889(6)1592
Response time after sudden reduction of COCrit Care Med 1995 23 860 Advantages over IBCO
Provide continuous trend
Reduce contamination
Less time consuming
Unnecessary fluid
060356
9
Limitations
Immediate CO measurement may not be done due to average time for reduce thermal noise
Transpulmoanry thermodilution method (TPTD)
Compare TPTD and IBTDAnesthesia amp Analgesia 2010
The respiratory variation affect IBTD rather than TPTD
IBTD
TPTD
Advantages over IBTD
Less invasive
Decrease complications result from PA catheter
GEDV and EVLW can be measuredAm J Physiol Lung Cell Mol Physiol 291 L1118ndashL1131 2006
060356
10
Limitations
Canrsquot assess PA pressure and its trend
Canrsquot assess SvO2
Pulse contour analysis
Non-calibrated
Calibrated
Basic Principles
Traditional CO = HR SV
FloTrac system CO = PR x (AP )
Where = M (HR AP C(P) BSA MAP 3ap 4ap)
Validation ICOCCOAPCOCrit Care 200711R105
Validation ICOCCOAPCOCrit Care 200711R105
FloTrac amp PACCrit Care 201014R212
060356
11
FloTrac amp PACCrit Care 201014R212
FloTrac in sepsisIntensive Care 201137233
FloTrac in sepsisIntensive Care 201137233
FloTrac Vigileo G3
Advantages
Real time
Less invasive
Non-calibrated
Informative
CO CI
PPV
SvO2
SVR
Disadvantages
Algorithm-gtnot real
Accuracy
Can not assess RV
derived parameters
Require new version software
PiCCO system Need calibration
060356
12
PAC and PiCCO (AP)Crit Care 201014R212
PiCCO
Advantages
Continuos monitoring
More accurate
Informative
COCI
SVV
SVR
GEDV
EVLW
AP
Disadvantages
Require calibration q 8 hrs
Femoral site risky to
CRBSI
Early goal directed therapy
What is the CVP
CVP = Central Venous Pressure
Frank Starling amp venous return line
Stroke volume
CVP0
Frank-Starling curve
Stroke volume or EDV
JVP or CVP or PCWP
ΔSV or Δ EDV
a
b
Responders
Non-responders
060356
13
b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
5
PA catheter
bull Proximal ndash cold injectate ScvO2
bull Distal ndash Draw SvO2
bull Thermistor ndash Temperature
bull Balloon inflation and deflation
Wave form
Waveform In place PA catheter
Joining Zeroing
060356
6
Others parameter calculated from PAC parameters
SVR = ( MAP - CVP CO ) x 80
PVR = ( PAP - PAOP CO ) x 80
CO = VO2 ( CaO2 - CvO2 )
DO2 = CO x Ca O2 x 10
VO2 = ( Ca O2 - Cv O2 ) x CO x10
Ca O2 = ( 139 x Hb x SaO2 ) + ( 0003 x PaO2 ) - Arterial
O2 content
Cv O2 = ( 139 x Hb x SvO2 ) + ( 0003 x PvO2 ) - Venous
O2 content
O2 extraxtion = VO2 DO2
QsQt = ( PA-a O2 ) ( PA-a O2 ) ( Ca-v O2 )
Cardiac output measurement
Fickrsquos formular
CO = VO2
CaO2-CvO2
Poor feasibility
Indicator dilution method
Indocyanine green
More accurate and reproducible
Require blood sampling
Recirculation of dye can disturb measurement
Thermodilution
More efficient
Thermo dilution method
Inject 5-10 cc of cold water
Tem
pera
ture
change (
)
Time
Stewart ndashHamilton equation
CO = ( TB ndash TI )xK
0 TB(t) dt
Hemodynamic
parameters in 4 shocks
CVP PAP PCWP CO SVR
Hypovolemic Low Low Low Low High
Cardiogenic High High High Low High
Obstructive High Very high Normal Low High
Septic Not high Not high Not high High Low
Ultrasound CO by ultrasound
A mount of blood flow going through a fixed orifice =
CSA x Flow-Velocity
SV = CSA x LVOTTVI
CSA = LVOTd2 x 078540
SV = LVOTd2 x 078540 x LVOTTVI
060356
7
LVOT diameter
LVOT VTI
good correlation between the thermodilutiontechnique and
Simpsons two-chamber method (r = 091)
Simpsons four-chamber method (r = 077)
the LVOT Doppler method (r = 094)
the LVOT Doppler method demonstrated acceptable agreement with a mean of 02
litresminute standard deviation of 082 litresminute and 95 limits of agreement of -15 to +19 litresminute
CCO-thermodilution methods Model for CCOtd
Agreement between CCO and BCO
in cardio-thoracic surgeryIntensive Care Med 199925166
Compare CCO and BCO in 20 medical ptsJ Crit Care 199813184
Conditions Number
MV 15
Vasopressor 15
Malignancy 12
Aplastic anemia
5
SLE 1
Cushing 1
CGD 1
060356
8
Good correlation between
CCO and BCO in sepsisIntensive Care Med 2002281276
Good correlation between CCO and BCO in sepsisIntensive Care Med 2002281276
Poor correlation of
CCO during hypothermia
Conclusions
Despite an excellent correlation accuracy and
precision between CCO and ICO before CPB and more than 45 minutes after hypothermic CPB a lack
of correlation in the early phase after CPB has been
found Further investigation is needed to elucidate the underlying cause of these findings and to clarify
whether ICO or CCO or both fail to represent the
real cardiac output up to 45 minutes after weaning from hypothermic CPB
19959405
Response time after sudden reduction of COAnesthesiology 199889(6)1592
Response time after sudden reduction of COCrit Care Med 1995 23 860 Advantages over IBCO
Provide continuous trend
Reduce contamination
Less time consuming
Unnecessary fluid
060356
9
Limitations
Immediate CO measurement may not be done due to average time for reduce thermal noise
Transpulmoanry thermodilution method (TPTD)
Compare TPTD and IBTDAnesthesia amp Analgesia 2010
The respiratory variation affect IBTD rather than TPTD
IBTD
TPTD
Advantages over IBTD
Less invasive
Decrease complications result from PA catheter
GEDV and EVLW can be measuredAm J Physiol Lung Cell Mol Physiol 291 L1118ndashL1131 2006
060356
10
Limitations
Canrsquot assess PA pressure and its trend
Canrsquot assess SvO2
Pulse contour analysis
Non-calibrated
Calibrated
Basic Principles
Traditional CO = HR SV
FloTrac system CO = PR x (AP )
Where = M (HR AP C(P) BSA MAP 3ap 4ap)
Validation ICOCCOAPCOCrit Care 200711R105
Validation ICOCCOAPCOCrit Care 200711R105
FloTrac amp PACCrit Care 201014R212
060356
11
FloTrac amp PACCrit Care 201014R212
FloTrac in sepsisIntensive Care 201137233
FloTrac in sepsisIntensive Care 201137233
FloTrac Vigileo G3
Advantages
Real time
Less invasive
Non-calibrated
Informative
CO CI
PPV
SvO2
SVR
Disadvantages
Algorithm-gtnot real
Accuracy
Can not assess RV
derived parameters
Require new version software
PiCCO system Need calibration
060356
12
PAC and PiCCO (AP)Crit Care 201014R212
PiCCO
Advantages
Continuos monitoring
More accurate
Informative
COCI
SVV
SVR
GEDV
EVLW
AP
Disadvantages
Require calibration q 8 hrs
Femoral site risky to
CRBSI
Early goal directed therapy
What is the CVP
CVP = Central Venous Pressure
Frank Starling amp venous return line
Stroke volume
CVP0
Frank-Starling curve
Stroke volume or EDV
JVP or CVP or PCWP
ΔSV or Δ EDV
a
b
Responders
Non-responders
060356
13
b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
6
Others parameter calculated from PAC parameters
SVR = ( MAP - CVP CO ) x 80
PVR = ( PAP - PAOP CO ) x 80
CO = VO2 ( CaO2 - CvO2 )
DO2 = CO x Ca O2 x 10
VO2 = ( Ca O2 - Cv O2 ) x CO x10
Ca O2 = ( 139 x Hb x SaO2 ) + ( 0003 x PaO2 ) - Arterial
O2 content
Cv O2 = ( 139 x Hb x SvO2 ) + ( 0003 x PvO2 ) - Venous
O2 content
O2 extraxtion = VO2 DO2
QsQt = ( PA-a O2 ) ( PA-a O2 ) ( Ca-v O2 )
Cardiac output measurement
Fickrsquos formular
CO = VO2
CaO2-CvO2
Poor feasibility
Indicator dilution method
Indocyanine green
More accurate and reproducible
Require blood sampling
Recirculation of dye can disturb measurement
Thermodilution
More efficient
Thermo dilution method
Inject 5-10 cc of cold water
Tem
pera
ture
change (
)
Time
Stewart ndashHamilton equation
CO = ( TB ndash TI )xK
0 TB(t) dt
Hemodynamic
parameters in 4 shocks
CVP PAP PCWP CO SVR
Hypovolemic Low Low Low Low High
Cardiogenic High High High Low High
Obstructive High Very high Normal Low High
Septic Not high Not high Not high High Low
Ultrasound CO by ultrasound
A mount of blood flow going through a fixed orifice =
CSA x Flow-Velocity
SV = CSA x LVOTTVI
CSA = LVOTd2 x 078540
SV = LVOTd2 x 078540 x LVOTTVI
060356
7
LVOT diameter
LVOT VTI
good correlation between the thermodilutiontechnique and
Simpsons two-chamber method (r = 091)
Simpsons four-chamber method (r = 077)
the LVOT Doppler method (r = 094)
the LVOT Doppler method demonstrated acceptable agreement with a mean of 02
litresminute standard deviation of 082 litresminute and 95 limits of agreement of -15 to +19 litresminute
CCO-thermodilution methods Model for CCOtd
Agreement between CCO and BCO
in cardio-thoracic surgeryIntensive Care Med 199925166
Compare CCO and BCO in 20 medical ptsJ Crit Care 199813184
Conditions Number
MV 15
Vasopressor 15
Malignancy 12
Aplastic anemia
5
SLE 1
Cushing 1
CGD 1
060356
8
Good correlation between
CCO and BCO in sepsisIntensive Care Med 2002281276
Good correlation between CCO and BCO in sepsisIntensive Care Med 2002281276
Poor correlation of
CCO during hypothermia
Conclusions
Despite an excellent correlation accuracy and
precision between CCO and ICO before CPB and more than 45 minutes after hypothermic CPB a lack
of correlation in the early phase after CPB has been
found Further investigation is needed to elucidate the underlying cause of these findings and to clarify
whether ICO or CCO or both fail to represent the
real cardiac output up to 45 minutes after weaning from hypothermic CPB
19959405
Response time after sudden reduction of COAnesthesiology 199889(6)1592
Response time after sudden reduction of COCrit Care Med 1995 23 860 Advantages over IBCO
Provide continuous trend
Reduce contamination
Less time consuming
Unnecessary fluid
060356
9
Limitations
Immediate CO measurement may not be done due to average time for reduce thermal noise
Transpulmoanry thermodilution method (TPTD)
Compare TPTD and IBTDAnesthesia amp Analgesia 2010
The respiratory variation affect IBTD rather than TPTD
IBTD
TPTD
Advantages over IBTD
Less invasive
Decrease complications result from PA catheter
GEDV and EVLW can be measuredAm J Physiol Lung Cell Mol Physiol 291 L1118ndashL1131 2006
060356
10
Limitations
Canrsquot assess PA pressure and its trend
Canrsquot assess SvO2
Pulse contour analysis
Non-calibrated
Calibrated
Basic Principles
Traditional CO = HR SV
FloTrac system CO = PR x (AP )
Where = M (HR AP C(P) BSA MAP 3ap 4ap)
Validation ICOCCOAPCOCrit Care 200711R105
Validation ICOCCOAPCOCrit Care 200711R105
FloTrac amp PACCrit Care 201014R212
060356
11
FloTrac amp PACCrit Care 201014R212
FloTrac in sepsisIntensive Care 201137233
FloTrac in sepsisIntensive Care 201137233
FloTrac Vigileo G3
Advantages
Real time
Less invasive
Non-calibrated
Informative
CO CI
PPV
SvO2
SVR
Disadvantages
Algorithm-gtnot real
Accuracy
Can not assess RV
derived parameters
Require new version software
PiCCO system Need calibration
060356
12
PAC and PiCCO (AP)Crit Care 201014R212
PiCCO
Advantages
Continuos monitoring
More accurate
Informative
COCI
SVV
SVR
GEDV
EVLW
AP
Disadvantages
Require calibration q 8 hrs
Femoral site risky to
CRBSI
Early goal directed therapy
What is the CVP
CVP = Central Venous Pressure
Frank Starling amp venous return line
Stroke volume
CVP0
Frank-Starling curve
Stroke volume or EDV
JVP or CVP or PCWP
ΔSV or Δ EDV
a
b
Responders
Non-responders
060356
13
b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
7
LVOT diameter
LVOT VTI
good correlation between the thermodilutiontechnique and
Simpsons two-chamber method (r = 091)
Simpsons four-chamber method (r = 077)
the LVOT Doppler method (r = 094)
the LVOT Doppler method demonstrated acceptable agreement with a mean of 02
litresminute standard deviation of 082 litresminute and 95 limits of agreement of -15 to +19 litresminute
CCO-thermodilution methods Model for CCOtd
Agreement between CCO and BCO
in cardio-thoracic surgeryIntensive Care Med 199925166
Compare CCO and BCO in 20 medical ptsJ Crit Care 199813184
Conditions Number
MV 15
Vasopressor 15
Malignancy 12
Aplastic anemia
5
SLE 1
Cushing 1
CGD 1
060356
8
Good correlation between
CCO and BCO in sepsisIntensive Care Med 2002281276
Good correlation between CCO and BCO in sepsisIntensive Care Med 2002281276
Poor correlation of
CCO during hypothermia
Conclusions
Despite an excellent correlation accuracy and
precision between CCO and ICO before CPB and more than 45 minutes after hypothermic CPB a lack
of correlation in the early phase after CPB has been
found Further investigation is needed to elucidate the underlying cause of these findings and to clarify
whether ICO or CCO or both fail to represent the
real cardiac output up to 45 minutes after weaning from hypothermic CPB
19959405
Response time after sudden reduction of COAnesthesiology 199889(6)1592
Response time after sudden reduction of COCrit Care Med 1995 23 860 Advantages over IBCO
Provide continuous trend
Reduce contamination
Less time consuming
Unnecessary fluid
060356
9
Limitations
Immediate CO measurement may not be done due to average time for reduce thermal noise
Transpulmoanry thermodilution method (TPTD)
Compare TPTD and IBTDAnesthesia amp Analgesia 2010
The respiratory variation affect IBTD rather than TPTD
IBTD
TPTD
Advantages over IBTD
Less invasive
Decrease complications result from PA catheter
GEDV and EVLW can be measuredAm J Physiol Lung Cell Mol Physiol 291 L1118ndashL1131 2006
060356
10
Limitations
Canrsquot assess PA pressure and its trend
Canrsquot assess SvO2
Pulse contour analysis
Non-calibrated
Calibrated
Basic Principles
Traditional CO = HR SV
FloTrac system CO = PR x (AP )
Where = M (HR AP C(P) BSA MAP 3ap 4ap)
Validation ICOCCOAPCOCrit Care 200711R105
Validation ICOCCOAPCOCrit Care 200711R105
FloTrac amp PACCrit Care 201014R212
060356
11
FloTrac amp PACCrit Care 201014R212
FloTrac in sepsisIntensive Care 201137233
FloTrac in sepsisIntensive Care 201137233
FloTrac Vigileo G3
Advantages
Real time
Less invasive
Non-calibrated
Informative
CO CI
PPV
SvO2
SVR
Disadvantages
Algorithm-gtnot real
Accuracy
Can not assess RV
derived parameters
Require new version software
PiCCO system Need calibration
060356
12
PAC and PiCCO (AP)Crit Care 201014R212
PiCCO
Advantages
Continuos monitoring
More accurate
Informative
COCI
SVV
SVR
GEDV
EVLW
AP
Disadvantages
Require calibration q 8 hrs
Femoral site risky to
CRBSI
Early goal directed therapy
What is the CVP
CVP = Central Venous Pressure
Frank Starling amp venous return line
Stroke volume
CVP0
Frank-Starling curve
Stroke volume or EDV
JVP or CVP or PCWP
ΔSV or Δ EDV
a
b
Responders
Non-responders
060356
13
b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
8
Good correlation between
CCO and BCO in sepsisIntensive Care Med 2002281276
Good correlation between CCO and BCO in sepsisIntensive Care Med 2002281276
Poor correlation of
CCO during hypothermia
Conclusions
Despite an excellent correlation accuracy and
precision between CCO and ICO before CPB and more than 45 minutes after hypothermic CPB a lack
of correlation in the early phase after CPB has been
found Further investigation is needed to elucidate the underlying cause of these findings and to clarify
whether ICO or CCO or both fail to represent the
real cardiac output up to 45 minutes after weaning from hypothermic CPB
19959405
Response time after sudden reduction of COAnesthesiology 199889(6)1592
Response time after sudden reduction of COCrit Care Med 1995 23 860 Advantages over IBCO
Provide continuous trend
Reduce contamination
Less time consuming
Unnecessary fluid
060356
9
Limitations
Immediate CO measurement may not be done due to average time for reduce thermal noise
Transpulmoanry thermodilution method (TPTD)
Compare TPTD and IBTDAnesthesia amp Analgesia 2010
The respiratory variation affect IBTD rather than TPTD
IBTD
TPTD
Advantages over IBTD
Less invasive
Decrease complications result from PA catheter
GEDV and EVLW can be measuredAm J Physiol Lung Cell Mol Physiol 291 L1118ndashL1131 2006
060356
10
Limitations
Canrsquot assess PA pressure and its trend
Canrsquot assess SvO2
Pulse contour analysis
Non-calibrated
Calibrated
Basic Principles
Traditional CO = HR SV
FloTrac system CO = PR x (AP )
Where = M (HR AP C(P) BSA MAP 3ap 4ap)
Validation ICOCCOAPCOCrit Care 200711R105
Validation ICOCCOAPCOCrit Care 200711R105
FloTrac amp PACCrit Care 201014R212
060356
11
FloTrac amp PACCrit Care 201014R212
FloTrac in sepsisIntensive Care 201137233
FloTrac in sepsisIntensive Care 201137233
FloTrac Vigileo G3
Advantages
Real time
Less invasive
Non-calibrated
Informative
CO CI
PPV
SvO2
SVR
Disadvantages
Algorithm-gtnot real
Accuracy
Can not assess RV
derived parameters
Require new version software
PiCCO system Need calibration
060356
12
PAC and PiCCO (AP)Crit Care 201014R212
PiCCO
Advantages
Continuos monitoring
More accurate
Informative
COCI
SVV
SVR
GEDV
EVLW
AP
Disadvantages
Require calibration q 8 hrs
Femoral site risky to
CRBSI
Early goal directed therapy
What is the CVP
CVP = Central Venous Pressure
Frank Starling amp venous return line
Stroke volume
CVP0
Frank-Starling curve
Stroke volume or EDV
JVP or CVP or PCWP
ΔSV or Δ EDV
a
b
Responders
Non-responders
060356
13
b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
9
Limitations
Immediate CO measurement may not be done due to average time for reduce thermal noise
Transpulmoanry thermodilution method (TPTD)
Compare TPTD and IBTDAnesthesia amp Analgesia 2010
The respiratory variation affect IBTD rather than TPTD
IBTD
TPTD
Advantages over IBTD
Less invasive
Decrease complications result from PA catheter
GEDV and EVLW can be measuredAm J Physiol Lung Cell Mol Physiol 291 L1118ndashL1131 2006
060356
10
Limitations
Canrsquot assess PA pressure and its trend
Canrsquot assess SvO2
Pulse contour analysis
Non-calibrated
Calibrated
Basic Principles
Traditional CO = HR SV
FloTrac system CO = PR x (AP )
Where = M (HR AP C(P) BSA MAP 3ap 4ap)
Validation ICOCCOAPCOCrit Care 200711R105
Validation ICOCCOAPCOCrit Care 200711R105
FloTrac amp PACCrit Care 201014R212
060356
11
FloTrac amp PACCrit Care 201014R212
FloTrac in sepsisIntensive Care 201137233
FloTrac in sepsisIntensive Care 201137233
FloTrac Vigileo G3
Advantages
Real time
Less invasive
Non-calibrated
Informative
CO CI
PPV
SvO2
SVR
Disadvantages
Algorithm-gtnot real
Accuracy
Can not assess RV
derived parameters
Require new version software
PiCCO system Need calibration
060356
12
PAC and PiCCO (AP)Crit Care 201014R212
PiCCO
Advantages
Continuos monitoring
More accurate
Informative
COCI
SVV
SVR
GEDV
EVLW
AP
Disadvantages
Require calibration q 8 hrs
Femoral site risky to
CRBSI
Early goal directed therapy
What is the CVP
CVP = Central Venous Pressure
Frank Starling amp venous return line
Stroke volume
CVP0
Frank-Starling curve
Stroke volume or EDV
JVP or CVP or PCWP
ΔSV or Δ EDV
a
b
Responders
Non-responders
060356
13
b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
10
Limitations
Canrsquot assess PA pressure and its trend
Canrsquot assess SvO2
Pulse contour analysis
Non-calibrated
Calibrated
Basic Principles
Traditional CO = HR SV
FloTrac system CO = PR x (AP )
Where = M (HR AP C(P) BSA MAP 3ap 4ap)
Validation ICOCCOAPCOCrit Care 200711R105
Validation ICOCCOAPCOCrit Care 200711R105
FloTrac amp PACCrit Care 201014R212
060356
11
FloTrac amp PACCrit Care 201014R212
FloTrac in sepsisIntensive Care 201137233
FloTrac in sepsisIntensive Care 201137233
FloTrac Vigileo G3
Advantages
Real time
Less invasive
Non-calibrated
Informative
CO CI
PPV
SvO2
SVR
Disadvantages
Algorithm-gtnot real
Accuracy
Can not assess RV
derived parameters
Require new version software
PiCCO system Need calibration
060356
12
PAC and PiCCO (AP)Crit Care 201014R212
PiCCO
Advantages
Continuos monitoring
More accurate
Informative
COCI
SVV
SVR
GEDV
EVLW
AP
Disadvantages
Require calibration q 8 hrs
Femoral site risky to
CRBSI
Early goal directed therapy
What is the CVP
CVP = Central Venous Pressure
Frank Starling amp venous return line
Stroke volume
CVP0
Frank-Starling curve
Stroke volume or EDV
JVP or CVP or PCWP
ΔSV or Δ EDV
a
b
Responders
Non-responders
060356
13
b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
11
FloTrac amp PACCrit Care 201014R212
FloTrac in sepsisIntensive Care 201137233
FloTrac in sepsisIntensive Care 201137233
FloTrac Vigileo G3
Advantages
Real time
Less invasive
Non-calibrated
Informative
CO CI
PPV
SvO2
SVR
Disadvantages
Algorithm-gtnot real
Accuracy
Can not assess RV
derived parameters
Require new version software
PiCCO system Need calibration
060356
12
PAC and PiCCO (AP)Crit Care 201014R212
PiCCO
Advantages
Continuos monitoring
More accurate
Informative
COCI
SVV
SVR
GEDV
EVLW
AP
Disadvantages
Require calibration q 8 hrs
Femoral site risky to
CRBSI
Early goal directed therapy
What is the CVP
CVP = Central Venous Pressure
Frank Starling amp venous return line
Stroke volume
CVP0
Frank-Starling curve
Stroke volume or EDV
JVP or CVP or PCWP
ΔSV or Δ EDV
a
b
Responders
Non-responders
060356
13
b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
12
PAC and PiCCO (AP)Crit Care 201014R212
PiCCO
Advantages
Continuos monitoring
More accurate
Informative
COCI
SVV
SVR
GEDV
EVLW
AP
Disadvantages
Require calibration q 8 hrs
Femoral site risky to
CRBSI
Early goal directed therapy
What is the CVP
CVP = Central Venous Pressure
Frank Starling amp venous return line
Stroke volume
CVP0
Frank-Starling curve
Stroke volume or EDV
JVP or CVP or PCWP
ΔSV or Δ EDV
a
b
Responders
Non-responders
060356
13
b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
13
b
CVP tells us who responders
Stroke volume or EDV
CVP or PCWP
ΔSV or Δ EDV
a
Good
Bad
CVP vs Fluid responders
Crit Care Med 20073564-8
39 cases25 cases
Does Central Venous Pressure Predict
Fluid ResponsivenessA Systematic Review of the Literature
CHEST 2008 134172ndash178
Fluid resuscitation in septic shock a positive fluid balance and elevated central venous pressure are associated with increased mortalityBoyd JH Forbes J Nakada TA Walley KR Russell JA
OBJECTIVE
To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated
with mortality
PATIENTS
The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were
receiving a minimum of 5 μg of norepinephrine per minute
MEASUREMENTS AND MAIN RESULTS
Based on net fluid balance we determined whether ones fluid balance quartile was correlated with 28-day
mortality We also analyzed whether fluid balance was predictive of central venous pressure and furthermore
whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage At
enrollment which occurred on average 12 hrs after presentation the average fluid balance was +42 L By day 4 the
cumulative average fluid balance was +11 L After correcting for age and Acute Physiology and Chronic Health
Evaluation II score a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased
mortality Central venous pressure was correlated with fluid balance at 12 hrs whereas on days 1-4 there was no
significant correlation At 12 hrs patients with central venous pressure lt8 mm Hg had the lowest mortality rate
followed by those with central venous pressure 8-12 mm Hg The highest mortality rate was observed in those with
central venous pressure gt12 mm Hg Contrary to the overall effect patients whose central venous pressure was lt8
mm Hg had improved survival with a more positive fluid balance
CONCLUSIONS
A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased
risk of mortality in septic shock Central venous pressure may be used to gauge fluid balance le 12 hrs into septic
shock but becomes an unreliable marker of fluid balance thereafter Optimal survival in the VASST study occurred
with a positive fluid balance of approximately 3 L at 12 hrs
Functional hemodynamic for predicting fluidresponsiveness
Spontaneous respiration
CVP variation gt 1 mmHg
PLR cCO gt 15 ( can be used in arrhythmia)
On mechanical ventilation
PPV gt 13
IVCd variation gt 12 ( can be used in arrhythmia)
IVC distensibility index gt 18 ( can be used in arrhythmia)
Brachail peak velocity gt 10
PLR cCO gt 15 ( can be used in arrhythmia)
PLR ET-CO2 gt 5
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
14
PP variation predict fluid responsiveness
PPV = PPmax-PPmin x 100
(PPmax+PPmin)2
PPV gt 13 indicate fluid
responsiveness
PPV 94
NPV 96
Reference Year of
publication
Clinical setting PPV threshold value()
Michard etal
Viellard-Baron etal
Kramer etal
Preisman etal
Hofer etal
Feissel etal
De Backer etal
Cannesson etal
Solus-Biguenet etal
Lafanechere etal
Monnet etal
Charron etal
Natalini etal
Feissel etal
Cannesson etal
2000
2004
2004
2005
2005
2005
2005
2006
2006
2006
2006
2006
2006
2007
2007
Medical ICU
Medical ICU
CABG
CABG
CABG
Surgical and medical ICU
Surgical and medical ICU
CABG
Hepatic resection
Medical ICU
Medical ICU
Surgical ICU
Surgical and medical ICU
Medical ICU
CABG
13
12
11
9
13
17
12
12
14
12
12
10
15
12
11
Limitations
Controlled mechanical ventilation
Tidal volume ge 8 mlkg
Sinus rhythm
How to assess lung leakage
Clinical assessment
More dyspneic
Crepitation increase
Gas exchange
Desaturation
Lower pO2
Lung mechanic
Decrease lung compliance
CXR
May be difficult to determine in ARDS
The lung compliance
Respiratory system compliance
119862119877119878 =119879119907
119875119901119897119886119905119890119886119906minus119875119864119864119875
Bedside measurement of CRS
Pressure
Time
PEEP
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
15
Bedside measurement of CRS
Pressure
Time
PEEP
Pplateau
PIP
After set Plateau time
Monitoring CRS (Volume mode)
Parameters Time 0 1 hour
PaO2 80 85
PaCO2 40 44
SaO2 96 97
PIP 35 45
Pplateau 30 36
PEEP 12 12
Exhaled TV 400 400
CRS222 167
FiO2 05 09
Fluid (ml) 0 1200
The EGDTPuzzle of formula
SvO2 Cellular oxygen
Good SvO2 means good cellular oxygenation (Low flow)
DO2 = 100
VO2 = 30
SvO2 = 70
Good SvO2 means good cellular oxygenation (heterogeneous flow)
DO2 = 100
VO2 = 10
SvO2 = 90
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
16
Correlation between perfused capillary and blood lactateDe Backer etal Crit Care Med 2006
Prognostic value of hyperlactatemia in many
different critical care conditionsBlood lactate levels are superior to oxygen-derived
variables in predicting outcome in human septic shock
J Bakker M Coffernils M Leon P Gris and J L Vincent Chest 199199956-962
plt 005
plt 0001
Lactate level after 4 hrs of resuscitationS-W Lee etal Emerg Med J 200825659-665
Prognostic value of blood lactate levels in the ED
Shapiro NI et al Serum lactate as a predictor of mortality in emergency department patients with infection Ann Emerg Med 2005 45(5) p 524-8
490
900
2840
150
450
2240
000
500
1000
1500
2000
2500
3000
0-24 25-39 gt4
28 day in hospital mortality Death
Mo
rta
lity
ra
te
Lactate
Serum lactate as a predictor of mortalityin patients with infection
S Trzeciak et alIntensive Care Med (2007) 33970ndash977
Prognostic value of blood lactate levels
in the Critical care unit at Ramathibodihospital
Survivors 27
Non-survivors
5
0
1
2
3
4
5
6
Art
eri
al la
cta
te (
mm
ol
L)
p=NS
The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and
Septic Shock (unpublished data)
Na Petvicharn C MD Theerawit P MD
Department of Internal Medicine the Faculty of Medicine Ramathibodi Hospital MahidolUniversity
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
17
LACtime the predictor of organ failureJan Bakker et alAJS 1996171221-6
Lactate
Time
Lactime
AUC
Survivors
Non-survivors
P lt 005
2 mmolL
Serial blood lactate levels can predict the
development of multiple organ failure following septic shock
MD Jan Bakker MD Philippe Gris MD Michel Coffernils MD Robert J Kahn MD PhD Jean-
Louis Vincent The American Journal of surgery Volume 171 Issue 2 Pages 221-226 February 1996
plt005
plt 001
plt005 vs initial
blood lactate
Lactate clearance and mortalityArnold RC Shock 2008
0
10
20
30
40
50
60
70
LC gt 10 LC lt 10
Mortality rate
SvO2 gt 70
P lt 0001
Odds ratio for death 49(15-159)
Early lactate clearance is associated with
improved outcome in severe sepsis and
septic shock
H Bryant Nguyen MD MS Emanuel P Rivers MD MPH Bernhard P Knoblich MD
Gordon Jacobsen MS Alexandria Muzzin BS Julie A Ressler BS Michael C Tomlanovich
MDCrit Care Med 2004 Vol 32 No 8
Lactate clearance
= (Lactate ED presentation ndash Lactate Hour 6)x100Lactate ED presentation
There was an approximately
11 decrease likelihood of mortality for each 10 increase in lactate clearance
Association between blood lactate levels Sequential Organ Failure
Assessment subscores and 28-day mortality during
early and late ICU stay A retrospective observational study
Tim C Jansen Jasper van Bommel Roger Woodward Paul G H Mulder Jan Bakker Crit Care Med 2009 Vol 37 No 8
Dynamic Lactate Indices as
Predictors of Outcome in Critically Ill Patients
Admission lactate (LACADM)
Maximum lactate (LACMAX24)
Minimum lactate (LACMIN24)
Time weighted lactate (LACTW24)
Absolute change in (delta) lactate (LACΔ24)
Percentage change in lactate (LACΔ24)
Nichol A Bailey M Egi M Pettila V French C Hart GK Stachowski E Reade MCCooper
DJ Bellomo RCrit Care 2011 15R242
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
18
Tissue perfusion
Lactate is better than SvO2 for assessment of tissue perfusion
The higher initial lactate the higher mortality
Lactate changing over time is better than a single value for monitoring
The higher lactate clearance the better
outcome
At least 10 reduction of lactate during resuscitation should be achieved
Type of fluid
Colloids or Crystalloids
26 Randomized trials
BMJ 1998316961-4
RR of death
Trauma 130(095-177)
Burn 121(088-166)
Sepsis 108(073-161)
Pooled 119(098-145)
Crystalloid and colloid infusion over 90 min in sepsis and non sepsis cases with
fluid responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid Colloid P value
CI before
CI after
EVLW
beforeEVLW after
39(24-55)
41(25-59)
71(19-339)75(16-299)
34(20-82)
38(23-69)
71(26-213)71(25-196)
Plt001
Pgt005
P value between before and after
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
Crystalloid and colloid infusion over 90 min in
sepsis and non sepsis cases with fluid
responsivenessMelanie van der Heijden etal Crit Care Med 2009371275
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
19
Crystalloid VS Colloid
No difference in
PLI
EVLW
Gas exchange
If fluid is administered in septic
patients with
fluid responsiveness even in ALI
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
ARDS development and mortality
in hypoproteinemic stateManglialardi etal Crit Care Med 2000283137-45
Correction of albumin in ARDS
Refresher course ICM December 2008
Correction of albumin in ARDS
Refresher course ICM December 2008
Colloid solution
Albumin Artificial
Gelatins
Dextran
HES
Poor effective
Allergic reactionAltered hemostasis
Allergic reactionRenal dysfucntion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
20
Colloid solutions
Hypoalbuminemia tends to increase the incidence of ARDS and mortality in sepsis patients
More fluid required for correct hemodynamic abnormality
Poor response to Furosemide
More potential leakage at capillary site may lead to more lung injury
Correction of hypoalbuminemia in ARDS may be benefitial in terms of mortality but it must be used carefully
HES may cause renal failure and high dosage may lead to bleeding tendency
The benefit of artificial colloid solution over albumin is not known
Case
60 YO male patient 60 Kg
Pneumonia with septic shock on MV
VS BP 8040 mmHg HR 120 RR 26 BT 39oC
Heart normal S1S2 no murmur
Lungs crepitation RLL lingular segment
Liver and spleen not palpable
No edema
Neuro WNL
Case
Load NSS 1500 ml -gt PPV 14 -gt lung crepitation
BP 9040 mmHg (MAP = 57 mmHg)
Increase Nor-epinephrine
BP 8545 mmHg (MAP = 55 mmHg)
HR 90 -gt 110 min lactate 3 to 6 mmolL
Re-assessment
ABG
pH 71
pCO2 35 mmHg
pO2 70 mmHg
HCO3 15 mmolL
We corrected acidosis and start dobutamine
Can decrease dosage of NorE and lactate 41
The
EGDT
We need re-
assessment
here
These are causes of no
response to pressor
Acidosis
Poor LV contraction
RV dysfunction +- PE
Pneumothorax
Concealed hemorrhage
Relative adrenal insufficiency
Electrolyte imbalance
Severe sepsis
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
21
Norepinephrine in septic shock
Study Baseline CI(normal 25-4)
EM Redl-Wenzl et al 1993Claude Martin et al 1993BLevy et al 1997Daniel De Backer et al 2003
Jacques Albane`se et al 2004Franccedilois Lauzier et al 2006
38+1153+1340+134+1
47+0244+14
Blood transfusion in septic shockJean-Louis Vincent Pongdhep Theerawit Davide Simeon
Basic Principles of Oxygen Transport and Calculations
Alternatives to Blood Transfusion in Transfusion Medicine 2nd Ed
Chapter 17 Published Online 4 SEP 2010
Transfusions will obviously have opposite effects to
anemia increasing blood viscosity and reducing the adrenergic response It is intriguing to consider
that transfusions may result in a decrease in
myocardial contractility Hence cardiac output often decreases following transfusions in the
nomovolemic patient and the increase in DO2
can be minor or even absent For example Shah et al observed in resuscitated trauma patients
that blood transfusion of one unit of RBC increased hemoglobin from 92 plusmn 03 to 102 plusmn 03
gdL but decreased cardiac output so that DO2
did not change
Hb lt 10 gL goal 10-12 gL
Hb lt 7 gL goal 7-9 gL
N=418
N=420
A MULTICENTER RANDOMIZED CONTROLLED CLINICAL
TRIAL OF TRANSFUSION REQUIREMENTS IN CRITICAL CAREPAULC HEacuteBERT MD GEORGEWELLS PHD MORRISA BLAJCHMAN MD JOHNMARSHALL MD CLAUDIOMARTIN MD GIUSEPPEPAGLIARELLO MD MARTINTWEEDDALE MD PHD IRWINSCHWEITZER MSC ELIZABETHYETISIR MSC ANDTHETRANSFUSIONREQUIREMENTSINCRITICALCAREINVESTIGATORSFORTHECANADIANCRITICALCARETRIALSGROUP
NEJM 1999
(normovolemia)
Red blood cell transfusion during septic shock in the ICUA Perner etal Acta Anaesthesiol Scand 2012 56 718ndash723
The CRIT Study Anemia and blood transfusion in the critically illmdashCurrent clinical practice in the United States
(Observational study 284 ICU 4892 patients)
Crit Care Med 2004 3239 ndash52
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
22
Microvascular response to red blood cell
transfusion in patients with severe sepsisYasser Sakr MD PhDetal Crit Care Med 2007 351639ndash1644
Clinical practice guideline Red blood cell transfusion in
adult trauma and critical careLena M Napolitano MD Stanley Kurek DO Fred A Luchette MD Howard L Corwin MD
Philip S Barie MD Samuel A Tisherman MD Paul C Hebert MD MHSc Gary L Anderson DO
Michael R Bard MD William Bromberg MD William C Chiu MD Mark D Cipolle MD PhD
Keith D Clancy MD Lawrence Diebel MD William S Hoff MD K Michael Hughes DO
Imtiaz Munshi MD Donna Nayduch RN MSN ACNP Rovinder Sandhu MD Jay A Yelon MD
for the American College of Critical Care Medicine of the Society of Critical Care Medicine and the Eastern
Association for the Surgery of Trauma Practice Management Workgroup (Crit Care Med 2009)
we recommend that red blood cell transfusion occur
only when hemoglobin concentration decreases to
lt70 gdL to target a hemoglobin concentration of 70 ndash90 gdL in adults
The
EGDT
started at a dose of 25 microg per kilogram of body weight per
minute a dose that was increased by 25 microg per kilogram
per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a
maximal dose of 20 microg per kilogram per minute was given
Median max dose of dobutamine to reach CI gt 45 DO2 gt 600 VO2 gt 170
Control group 023 mcgkgmin (005-10)
Treatment group 12 mcgkgmin (002-166)
P = 0029
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion
060356
23
CI ge 45 CI = 25-35
in the presence of (a)myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output or
(b)ongoing signs of hypoperfusion