The Hemodynamic Puzzle

O2ER

NIRS

SVV

Lactate

Ene

rgy

Met

abo

lism

(Oxy

gen

Co

nsu

mp

tio

n)

(Ml/

min

/m2)

Delayed Repayment of O2 Debt

Full Recovery Possible

Excessive O2 Deficit Produces Lethal Cell Injury

with Non-recovery Recovery Possible

Time

Oxygen Deficit

Oxygen Deficit

Oxygen Deficit

Oxygen Debt: To Pay or Not to Pay?

The principle task of acute care is

to avoid or correct oxygen debt

by optimization of the oxygen

supply and consumption.

Providing the right amount of fluid is vital in a critically ill patient, as both too little and too much can result in poor outcomes

Under Resuscitation Over Resuscitation

It is just as important to recognize that DO2 and tissue perfusion has

normalized, therefore any further measures to increase DO2 may do harm

by unnecessary over resuscitation

HR and BP as Resuscitation Endpoint

NIRS

SVV SvO2Heart Rate

Urine OutputMental Status

OPSI

GEDV

SV

DO2 ml*m-2*min-1

100 300 500 700 900 1100

n= 123230

60

90

120

150

180

MA

P m

mH

g

Correlation Between Arterial Pressure And Oxygen Delivery

DO2 ml*m-2*min-1

100 300 500 700 900 1100

n= 123630

60

90

120

150

180

HR

b/m

in

Correlation Between Heart Rate And Oxygen Delivery

CVP as a Resuscitation Endpoint

NIRS

SVV SvO2Heart Rate

Urine OutputMental Status

OPSI

GEDV

SV

Passive leg raising (PLR)Volume of blood transferred (usually 200-300 mL) to the heart during PLR is sufficient to increase the left cardiac preload and thus challenge the Frank-Starling curve.

Maximal effect occurs at 30-90 seconds and assess for a 10% increase in stroke volume (cardiac output monitor) or using a surrogate such as pulse pressure (using an arterial line)

Diagnostic Accuracy of Passive Leg Raising for Prediction of Fluid Responsiveness in Adults: Systematic Review and Meta-analysis of Clinical Studies.

• Meta-analysis 9 studies

• PLR changes in CO predicts fluid responsiveness

• Regardless of ventilation mode and cardiac rhythm

• Difference in CO of 18% distinguished responder from NR

Cavallaro, F. et al. Intensive Care Med. 2010 Sep;36(9):1475-83

The pooled sensitivity and specificity of PLR-cCO were

89.4% (84.1-93.4%) and 91.4% (85.9-95.2%) respectively

AUC= 0.96

CVP as a Resuscitation Endpoint

NIRS

SVV SvO2Heart Rate

Urine OutputMental Status

OPSI

GEDV

SVCVP

• European survey:

More the 90% of intensivist or anesthesiologists used the CVP to guide fluid management.

• Canadian survey:

90% of intensivists used the CVP to monitor fluid resuscitation in patients with septic shock.

Crit Care Med 2013; 41:1774–1781)

Paul E. Marik, MD, FCCP; Michael Baram, MD, FCCP; Bobbak Vahid, MD Chest. 2008;134(1):172-178.

Osman D1, Ridel C, Ray P, Monnet X, Anguel N, Richard C, Teboul JL. Crit Care Med. 2007 Jan;35(1):64-8.

The study demonstrates that cardiac filling pressures are poor

predictors of fluid responsiveness in septic patients. Therefore,

their use as targets for volume resuscitation must be

discouraged, at least after the early phase of sepsis has concluded

There are no data to support the widespread practice of using central venous pressure to guide fluid therapy. This approach to fluid

resuscitation should be abandoned.

Marik PE, Cavallazzi R . Crit Care Med. 2013 Jul;41(7):1774-81..

IVC Diameter and Collapsibility as End Point

NIRS

SVV SvO2Heart Rate

Urine OutputMental Status

OPSI

GEDV

CVP

Simultaneous measurements of the central venous pressure (CVP) and IVC diameter at the end of expiration in 108 mechanically ventilated patients

Collapsibility Index = 𝑰𝑽𝑪

𝒎𝒂𝒙−𝑰𝑽𝑪𝒎𝒊𝒏

𝑰𝑽𝑪𝒎𝒂𝒙

>12% = responders(PPV 93% and NPV92%).

Collapsibility Index = 𝑰𝑽𝑪

𝒎𝒂𝒙−𝑰𝑽𝑪𝒎𝒊𝒏

𝑰𝑽𝑪𝒎𝒂𝒙

<12% = non-responders (PPV 93% and NPV92%).

Zhongheng Zhang, Xiao Xu, Sheng Ye, Lei Xu. Ultrasound in Medicine and Biology. Volume 40, Issue 5, Pages 845–853, May 2014

Total of 8 studies/235 Pts

ΔIVC measured is of great value in predicting fluid responsiveness, particularly in patients on

controlled mechanical ventilation

CO/SV as a Resuscitation Endpoint

NIRS

SVV SvO2Heart Rate

Urine OutputMental Status

OPSI

SV/CO

CVP

GEDV

Effects of Cardiac Output and Stroke Volume Guided Hemorrhage and Fluid Resuscitation

CI-group SVI-group

Tbsl T0 tend Tbsl T0 Tend

SVI (ml/m2) 33.6 ± 6.2 14.6 ± 10.1 23.4 ± 7.9 26.8 ± 4.7 13.4 ± 2.3 26.6 ± 4.1

CI (l/min/m2) 2.88 ± 0.42 1.79 ± 0.53 2.73 ± 0.35 2.6 ± 0.4 1.8 ± 0.3 2.9 ± 0.5

MAP (mmHg) 127 ± 13.07 75 ± 25 85 ± 22 112 ± 23 74 ± 18 91 ± 19

Heart rate (beats/min) 87 ± 16 140 ± 40 124 ± 37 95 ± 12 131 ± 27 107 ± 16

Central venous oxygen saturation (%)

81 ± 8 58 ± 18 64 ± 15 78 ± 7 61 ± 5 73 ± 9

Venous to arterial carbon dioxide gap (mm Hg)

3.3 ± 3.1 8.9 ± 3.3 7.8 ± 4.8 5.3 ± 2 9.6 ± 2.3 5.1 ± 2.6

GEDV (ml/m2) 317 ± 36 198 ± 57 249 ± 46 309 ± 57 231 ± 61 287 ± 49

Stroke volume variation (%) 10.8 ± 5.5 17.3 ± 5.1 16.4 ± 8.2 13.6 ± 4.3 22.6 ± 5.6 12.2 ± 4.3

Nemeth, M. et al. Acta Anaesthesiol Scand (2014). doi:10.1111/aas.12312

21 animal subjects were bled until CI (n=9) or SVI (n=12) decreased by 50% then resuscitated during 60 minutes with LR till target is achieved

SVV & PPV as End Point

SvO2

Heart Rate

Urine OutputMental Status

OPSI

SV

GEDV

SVVCVP

Hemodynamics During Positive Pressure Ventilation: SVV and PPV

Preload

Stroke

Volume

0

0

Higher PVI = More likely to respond to fluid administration

24 %

10 %Lower PVI = Less likely to respond

to fluid administration

PVI to Help Clinicians Optimize Preload / Cardiac Output

Frank-Starling Relationship

Determine success of fluid by the response in stroke volume/index and SvO2

30

Stroke Volume

End-Diastolic Volume

D < 10%

D > 10%

D 0%

Fluid Responders

Fluid Non-Responders

Dynamic parameters should be used preferentially to static parameters to

predict fluid responsiveness in ICU patients

Dynamic Changes in Arterial Waveform Derived Variables and Fluid Responsiveness in Mechanically Ventilated Patients: A Systematic Review of Literature

Marik, PE et al. (2009). Citi Care Med. 37: 2642-2647

Sens. 0.89Spec. 0.88AUC= 0.94

Lactic Acid as Endpoint Resuscitation

Heart Rate

Urine OutputMental Status

OPSI

SV

Lactate

CVP

GEDV

SVV

Oxygen consumption

VO2 mls/min

Oxygen delivery

DO2 mls/min300mls/min

Lactate

Critical DO2

Oxygen Debt

DO2 independent in normal patients

DO2 dependent in septic patients

Prolonged lactate clearance is associated with increased mortality in the surgical intensive care unit

J. McNelis et al. The American Journal of Surgery 182 (2001) 481–485

Early lactate-guided therapy in intensive care unit patients: a multicenter, open-label, randomized controlled trial.

Jansen TC,van Bommel J, Schoonderbeek FJ,Sleeswijk Visser SJ, vander Klooster JM, Lima AP, et al. Am J Respir Crit Care Med (2010) 182:752–

61.doi:10.1164/rccm.200912-1918OC

Effects of Cardiac Output and Stroke Volume Guided Hemorrhage and Fluid Resuscitation

CI-group SVI-group

Tbsl T0 tend Tbsl T0 Tend

Oxygen delivery (ml/min/m2)

335 ± 63 158 ± 62 284 ± 52 419 ± 62 272 ± 56 341 ± 62

VO2 (ml/min/m2) 44 ± 25 62 ± 38 76 ± 34 77 ± 26 96 ± 19 82 ± 27

Oxygen extraction (VO2/DO2)

0.13 ± 0.08 0.38 ± 0.19 0.32 ± 0.14 0.20 ± 0.07 0.36 ± 0.05 0.24 ± 0.09

Central venous oxygen saturation (%)

81 ± 8 58 ± 18 64 ± 15 78 ± 7 61 ± 5 73 ± 9

Venous to arterial carbon dioxide gap (mm Hg)

3.3 ± 3.1 8.9 ± 3.3 7.8 ± 4.8 5.3 ± 2 9.6 ± 2.3 5.1 ± 2.6

Lactate (mmol/L) 3.6 ± 1.1 5.0 ± 1.6 4.6 ± 2.0 1.62 ± 0.43 3.86 ± 1.49 3.54 ± 1.9

Hemoglobin (g/L) 9.0 ± 0.7 8.0 ± 2.7 6.9 ± 1.3 12.05 ± 1.37 11.22 ± 1.39 8.45 ± 1.1

Nemeth, M. et al. Acta Anaesthesiol Scand (2014). doi:10.1111/aas.12312

Oxygen Extraction-based Resuscitation

SVVHeart Rate

Urine OutputMental Status

SV

GEDV

SVV

O2ER

SvO2

ScvO2

CVP

DO2= CO x [CaO2]

CaO2= [Hb X 1.34 x SaO2] + 0.003 x PaO2

VO2= CO x [CaO2-CvO2]

O2ER = 𝟏𝟎𝟎 𝐗 VO2 DO2

Oxygen Extraction-based Resuscitation

ScVO2

Effects of Cardiac Output and Stroke Volume Guided Hemorrhage and Fluid Resuscitation

CI-group SVI-group

Tbsl T0 tend Tbsl T0 Tend

Oxygen delivery (ml/min/m2)

335 ± 63 158 ± 62 284 ± 52 419 ± 62 272 ± 56 341 ± 62

VO2 (ml/min/m2) 44 ± 25 62 ± 38 76 ± 34 77 ± 26 96 ± 19 82 ± 27

Oxygen extraction (VO2/DO2)

0.13 ± 0.08 0.38 ± 0.19 0.32 ± 0.14 0.20 ± 0.07 0.36 ± 0.05 0.24 ± 0.09

Central venous oxygen saturation (%)

81 ± 8 58 ± 18 64 ± 15 78 ± 7 61 ± 5 73 ± 9

Venous to arterial carbon dioxide gap (mm Hg)

3.3 ± 3.1 8.9 ± 3.3 7.8 ± 4.8 5.3 ± 2 9.6 ± 2.3 5.1 ± 2.6

Lactate (mmol/L) 3.6 ± 1.1 5.0 ± 1.6 4.6 ± 2.0 1.62 ± 0.43 3.86 ± 1.49 3.54 ± 1.9

Hemoglobin (g/L) 9.0 ± 0.7 8.0 ± 2.7 6.9 ± 1.3 12.05 ± 1.37 11.22 ± 1.39 8.45 ± 1.1

Nemeth, M. et al. Acta Anaesthesiol Scand (2014). doi:10.1111/aas.12312

Mixed Venous Saturation in Critically Ill Patient

Oxygen Supply: DO2 Oxygen Demand: VO2

SvO2/ScvO2

Low

↓DO2 ↑VO2

AnemiaBleedingHypovolemiaHypoxiaHeart faliure

PainAgitationShiveringSeizureFever

High

↑DO2 ↓VO2

HgOxygenFluidsInotropics

SedationAnalgesiaHypothermiaSepsis

SvO2 %

DO

2/ V

O2

25 705540 85 1001.0

2.8

4.6

6.4

8.2

10.0

r= 0.906

y= -9.58 + 0.19*x

n= 1149

Lee J et al. (1972) Anaesthesiology 36: 472

% S

svO

2

% SvO2

100

80

60

40

20

0 20 40 60 80 100

r= 0.73

r= 0.88

Shock

Normal

Reinhart K et al, Chest, 1989; 95:1216-1221

SvO2 closely correlates with ScvO2

Time (min)

% S

at

80

60

40

20

0

300 60 90 120 150 180 210 240

Normoxia Bleeding Volume Therapy (HAES) Bleeding

Hy

po

xia

No

rmo

xia

Hy

pe

rox

ia

Mixed venous

Central venous

Pope, J et al. Ann Emerg Med. 55:40-46

ScvO2 of > 90%, ScvO2 of < 70%,

Oxygen Parameters as Endpoint

SVVHeart Rate

Urine OutputMental Status

SV

GEDV

SVV

O2ER

SvO2

ScvO2

P(cv-a)CO2

CVP

P(cv-a)CO2

Normal is 2-5 mmHg.

Is not a marker of tissue hypoxia

but it is a marker of the adequacy of cardiac output

∆PCO2= K X 𝑽𝑪𝑶

𝟐

𝑪𝒂𝒓𝒅𝒊𝒂𝒄 𝑶𝒖𝒕𝒑𝒖𝒕

Persistently high venous-to-arterial carbon dioxide differences during early resuscitation are associated with poor outcomes in septic shock

Ospina-Tascón GA et al., Crit Care. 2013; 17(6)

The persistence of high Pv-aCO2during the early resuscitation of septic shock was associated with

more severe multi-organ dysfunction and worse outcomes at

day-28

H-H, mixed venous-to-arterial carbon dioxide difference (Pv-aCO2) high at Time 0 (T0) and 6 hours later (T6); L-H, Pv-aCO2 normal at T0 and high at T6; H-L, Pv-aCO2 high at T0 and normal at T6; and L-L, Pv-aCO2 normal at T0 and T6

Central Venous-to-Arterial Gap Is a Useful Parameter in Monitoring Hypovolemia-Caused Altered Oxygen Balance: Animal Study

ScvO2 < 73% and CO2 gap >6 mmHg can be complementary tools

in detecting hypovolemia-caused imbalance of oxygen

extraction.

Kocsi S et al, Crit Care Res Pract. 2013; 583-598.

The Hemodynamic Puzzle

SVVHeart Rate

Urine OutputMental Status

SV

GEDV

SVV

O2ER

SvO2

ScvO2

P(cv-a)CO2 NIRSOPSI

CVP

Near-infrared spectroscopy (NIRS)

NIRS

StO2 (at 20 mm, skeletal muscle) is an index of profusion that tracks DO2 during active resuscitation

Crit Care. 2009; 13(Suppl 5): S10.

Orthogonal Polarization Spectral Imaging (OPS): Sublingual capillaroscopy.

Orthogonal polarization spectral (OPS) imaging is an optical imaging technique that uses a handheld microscope and green polarized light to visualize the red blood cells in the microcirculation of organ surfaces

Orthogonal Polarization Spectral Imaging (OPS): Sublingual capillaroscopy.

Red blood cells are visualised as black-grey points flowing along the vessels. Up-right and up-left: normal findings; bottom-

left: septic shock; bottom-right: after cardiac arrest under therapeutic hypothermia

The Hemodynamic Puzzle

O2ER

NIRS

SVV SvO2

ScvO2

Heart Rate

Urine OutputMental Status

OPSI

GEDV

P(cv-a)CO2

Lactate

SV

CVP