basic & advanced hemodynamic monitoring part 2
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Advanced Hemodynamics PART 2
B. McLean, MN, RN, CCRN, CCNS-BC, ANP-BC, FCCM
Grady Memorial Hospital, Atlanta GA, USA
bamclean@mindspring.com www.barbaramclean.com
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Hemodynamic Monitoring Truth No monitoring device, no matter how simple or
complex, invasive or non-invasive, inaccurate or precise will improve outcome
Unless coupled to a treatment, which itself improves outcome
Pinsky & Payen. Func/onal Hemodynamic Monitoring, Springer, 2004
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Intravascular volume
Myocardial contraction and heart rate
Vasoactivity
4 factors that aec/ng the haemodynamic condi/ons
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Hemodynamic monitors Traditional invasive monitors: Static Measures
Arterial line CVP & ScvO2 PA catheter, CCO, SvO2
Functional variation: Dynamic measures Pulse pressure variation Stroke volume variation
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Why are we monitoring? Preload, contractility, afterload,
and oxygen transport are commonly abnormal in the critically ill
Inadequate resuscitation and failure to restore cellular oxygen delivery and organ perfusion results in multiple system organ dysfunction syndrome (MODS) and death
Optimization of critical illness reduces organ failure and improves survival
Accurate assessment of hemodynamic function and goal-directed resuscitation is essential to improving patient outcome
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Purpose of monitoring Evaluate cardiovascular system
Pressure, flow, resistance Evaluate blood flow and oxygen delivery Establish baseline values and evaluate trends
Determine presence and degree of dysfunction Implement and guide interventions
Provides criteria for determination of CV efficacy
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Hemodynamic measures Arterial pressure
Systolic, diastolic, PP, MAP, Cardiac output, SVV Central venous pressure
Mean pressure, Oximetry Pulmonary artery pressure
PA systolic, diastolic, mean PAOP Cardiac output Oximetry
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Arterial Pressure Monitoring Indications
Patient in shock not rapidly responsive to therapy Insertion Sites
Radial Brachial Axillary Femoral Dorsalis Pedis
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Arterial Pressure Monitoring Radial artery has the benefit of collateral
circulation from the ulnar artery Allen Test used to evaluate the collateral
flow prior to radial artery cannulation
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Invasive Monitoring Equipment Flush solution Continuous flush system (usually a pressure bag
or pump) Pressure transducer and pressure tubing Invasive catheter Monitor
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Transducers Convert one form of energy to another Sense pressure Convert it to an electrical signal Electrical signal causes monitor reading
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Pressure monitoring system Catheter placed in vessel Fluid filled, low compliance, tubing-transducer kit Amplifier-monitor
Oscilloscope Printer
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Phlebostatic Axis Located at the intersection of the 4th ICS and
midway between the anterior and posterior surfaces of the chest
Midaxillary line is NOT interchangeable with mid anteroposterior level in all persons Bartz, et al, 1988
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Phlebostatic Axis
As the pa/ent moves from at to upright, the phlebosta/c level rotates on the axis and remains horizontal. This posi/on conrmed by CT by Paolella, et al, 1988.
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Phlebostatic Axis
The phlebosta/c axis moves to midchest at the 4th ICS when pa/ent is in the lateral posi/on.
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Leveling, Referencing, Balancing Placing the air-fluid interface of the catheter
system at the phlebostatic axis This negates the weight effect of the fluid in the
catheter tubing (hydrostatic pressure) Setting the correct reference point is the single
most important step in setting up a pressure monitoring system. Gardner, 1993
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Leveling Air fluid interface is the point in the system that is
opened to air during zeroing Inaccuracies are produced if the air-fluid interface
is above or below the phlebostatic axis 1.86 mmHg/inch
Phlebostatic axis determined by Windsor and Burch (1945) as correct reference for measurement of venous pressures
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Zeroing Opening the system to air to establish atmospheric
pressure as zero (0) This negates all pressure contributions from the
atmosphere Allows only pressure values that exist within the
heart or vessel to be measured
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When to Zero Before insertion After disconnecting transducer from pressure cable When values are in question
Ahrens, T. et al. Frequency requirements for zeroing transducers in hemodynamic monitoring, Am J Crit Care, 1995;4:466-471
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What can we see. Arterial line
Real time SBP, DBP, MAP Pulse pressure variation (PP)
PP (%) = 100 (PPmax - PPmin)/([PPmax + PPmin]/2) >= 13% (in septic pts,) discriminate between fluid responder and non respondaer (sensitivity 94%, specificity 96%)
Am J Respir Crit Care Med 2000, 162:134-138
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Arterial Pressure Waveform
1. Systole 2. Dicro/c notch 3. Diastole
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Summary Perfusion is the goal Perfusion =
oxygenation + flow You cannot do it alone Less invasive is better Technology should make you a better clinician
(only as good as you can be)
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Pressure monitoring Principles
Unobstructed fluid filled system will reflect change in pressure at distal tip of system (catheter) throughout the system
Pressure change may be detected at proximal end of system, transformed into electrical signal and displayed as a waveform
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Principles Level the system
Level to remove effects of hydrostatic pressure Pressure caused by weight of the fluid in the tubing
Level with left atrium Transducer above pressure directed from
transducer to tip so measured pressures less than actual
Transducer below pressure directed from tip to transducer so measured pressures higher than actual pressure
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Connect and prime tubing system with solution Typically NS Use gravity flush to prevent
micro-bubbles all must be removed
Apply pressure bag to solution container and inflate to 300 mmHg
Automatic delivery of solution 3-5 ml/hr.
Preparation
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Phlebostatic Axis
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Arterial pressure Continuous pressure evaluation
Tissue perfusion status Trends in blood pressure Efficacy of drugs, interventions Frequent blood samples required
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Arterial pressure Placement of catheter
Radial Brachial Axillary Femoral Dorsalis pedis
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Arterial waveform Morphology (shape) of waveform
Depends on force generated by ventricle Speed of ejection Volume of blood ejected Compliance of arterial vessels Rate of forward blood runoff dependent on resistance to
forward flow or systemic vascular resistance
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Measures Systolic pressure
Reflects volume and speed of ejection, compliance of aorta
Diastolic pressure Reflects vascular resistance and competence of aortic
valve
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Other? Pulse pressure
Reflects difference in volume ejected from LV into arterial vessels and volume that exits simultaneously
Function of SV and SVR Wide PP increase in SV and decrease in SVR Narrow PP Decreased SV and increased SVR
Mean Arterial Pressure (MAP) Best indicator of tissue perfusion Average driving pressure of blood during cardiac cycle Time weighted diastole is longer
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Arterial line Advantages
Easy setup Real time BP monitoring Beat to beat waveform display Allow regular sampling of blood for lab tests
Disadvantages Invasive Risk of haematoma, distal ischemia, pseudoaneurysm
formation and infection
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Review of physiology
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Increase venous pressure (preload) leads to a rise in stroke volume and therefore cardiac output
End diastolic volume causes stroke volume The energy of contraction of a cardiac muscle fiber,
like that of a skeletal muscle fiber, is proportional to the initial fiber length at rest.
Stroke volume increase due to increased force of contraction
Frank-Starling mechanism or Starlings Law of the Heart
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Preload
Stroke Volume
0 0
Cardiac Ouput Maximization
Cardiac Output Optimization Concept
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Current state of monitoring
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Preload Definition
The degree that the myocardial fiber is stretched prior to contraction at end diastole
The more the fiber is stretched, the more it will contract. However, if it is overstretched the amount of contraction goes down.
(Think rubber band) On right side of heart Right Ventricular End
Diastolic Volume which is reflected by Right Atrial Pressure or Central Venous Pressure (CVP)
On left side, the LVEDV is reflected by the PCWP.
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Afterload Definition
The force against which the ventricles must work to pump blood
The ventricular wall tension generated during systole Determined by:
Volume and viscosity of blood Vascular resistance Heart valves
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Vascular Resistance Derivation of Ohms Law
The resistance in a circuit is determined by the voltage difference across the circuit and the current flowing through the circuit.
Resistance = D Pressure Flow Vascular Resistance = D Blood Pressure (mmHg) Cardiac Output (L/min) Where D Blood Pressure is the highest pressure
in the circuit minus the lowest pressure in the circuit.
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Pulmonary Vascular Resistance (PVR) Key Components:
Highest Pressure MPAP Lowest Pressure LAP or PCWP Flow Cardiac Output
Formula PVR = (MPAP-PCWP)/CO x 80
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Systemic Vascular Resistance (SVR) Key Components
Highest Pressure MAP Lowest Pressure RAP or CVP Flow Cardiac Output
Formula SVR = (MAP-CVP)/CO x 80
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Contractility Definition
The force generated by the myocardium when the ventricular muscle fibers shorten.
Positive Inotropic effect ( force of contraction) Negative Inotropic effect ( force of contraction)
Contractility is affected by: Drugs Oxygen levels within the myocardium Cardiac muscle damage Electrolyte imbalances
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The Central Venous Catheter in Critical Care
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Central venous pressure
Indication of RVEDV Preload of RV Indication of fluid volume state
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Catheter insertion Percutaneous technique
Seldinger technique Exploring needle, guide or J wire, dilator, catheter system
2-3 cm above junction of SVC and atrium ideally
Most common sites Internal jugular vein Subclavian vein
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Central Venous Line Indications:
CVP monitoring Advanced CV disease + major operation Secure vascular access for drugs: TLC Secure access for fluids: introducer sheath Aspiration of entrained air: sitting craniotomies Inadequate peripheral IV access Pacer, Swan Ganz
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Central Venous Line: RIJ IJ vein lies in groove between sternal + clavicular
heads of sternocleidomastoid muscle IJ vein is lateral + slightly anterior to carotid Aseptic technique, head down Insert needle towards ipsilateral nipple Seldinger method: 22 G finder; 18 G needle,
guidewire, scalpel blade, dilator + catheter Observe ECG + maintain control of guide-wire Ultrasound guidance; CXR post insertion
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CVP Monitoring Reflects pressure at junction of vena cava +
RA CVP is driving force for filling RA + RV CVP provides estimate of:
Intravascular blood volume RV preload
Trends in CVP are very useful Measure at end-expiration Zero at mid-axillary line
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Zero @ Mid-Axillary Line
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Mark JB, CV Monitoring, in Miller 5th Edi/on, 2000, pg 1153
CVP Waveform Components
Component Phase of Cycle Event
a wave End diastole Atrial cont
c wave Early systole Isovol vent cont
x descent Mid systole Atrial relaxation
v wave Late systole Filling of atrium
y descent Early diastole Vent filling
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Right Atrial Pressure Tracing
a wave results from atrial systole
c wave occurs with the closure of the tricuspid valve and the initiation of atrial filling
v wave occurs with blood filling the atrium while the tricuspid valve is closed
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Timing of the positive deflections
a wave occurs after the p wave during the PR interval
c wave when present occurs at the end of the QRS complex (RST junction)
v wave occurs after the T wave
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Right Atrial Chamber Height of the v wave is
related to the atrial compliance and the volume of blood returning from the periphery
Height of the a wave is related to the pressure needed to eject forward blood flow The v wave is usually
smaller than the a wave in the right atrium
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Right atrial hemodynamic pathology Elevated a wave
Tricuspid stenosis Decreased RV
compliance e.g. pulm htn, pulmonic
stenosis
Cannon a wave AV asynchrony
atrium contracts against a closed tricuspid valve
e.g. AVB, Vtach
Absent a wave
Atrial fibrillation or standstill
Atrial flutter Elevated v wave
Tricuspid regurgitation RV failure Reduced atrial
compliance e.g. restrictive
myopathy
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Right atrial hemodynamic pathology
Note the Cannon a wave that is occurring during AV dysynchrony
atrial contrac/on is occurring against a closed tricuspid valve.
Note the large V wave that occurs with Tricuspid
regurgita/on
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Hemodynamic Pathology Tricuspid Stenosis
Large jugular venous a waves on noted on exam
Notable elevated a wave with the presence of a diastolic gradient - >5mmHg gradient is considered signficant
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Limitation of CVP
Systemic venoconstriction
Decrease right ventricular compliance
Obstruction of the great veins
Tricuspid regurgitation
Mechanical ventilation
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Central venous catheter Advantages
Easy setup Good for medications infusion
Disadvantages Cannot reflect actual RAP in most situations Multiple complications
Infections, thrombosis, complications on insertion, vascular erosion and electrical shock
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Static indicators have been shown to be poor predictors of fluid responsiveness central venous pressure(CVP) pulmonary capillary wedge pressure (PCWP) left ventricular end diastolic area
Dynamic indicators demonstrated to be better predictors of fluid responsiveness in patients during mechanical ventilation.
During positive pressure ventilation, the inspiratory right ventricular stroke volume (SV) decrease is proportional to the degree of hypovolemia and is transmitted to the left heart after two or three beats (pulmonary transit time)
Michard F, Boussat S et al. Am J Respir Crit Care Med 2000;162:1348 Feissel M, Michard F, et al. Chest 2001; 119:86773 Tavernier B, Makho/ne O, et al. Anesthesiology1998;89:131321 Rex S, Brose S, et al. Br J Anaesth 2004;93:7828 Wiesenack C, Fiegl C, et al.. Eur J Anaesthesiol 2005;22:65865 Michard F. Anesthesiology 2005;103:419 28,
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Neither CVP or Ppao reflect Ventricular Volumes or tract preload-responsiveness
Kumar et al. Crit Care Med 32:691-9, 2004
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Neither CVP or Ppao reflect Ventricular Volumes or tract preload-responsiveness
Kumar et al. Crit Care Med 32:691-9, 2004
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Marik PE: Techniques for assessment of intravascular volume in critically ill patients. J Intensive Care Med 2009; 24:329337 studies have shown that the CVP often does not
accurately reflect end-diastolic volume and right ventricular preload.
Dynamic responses to volume challenge by using either stroke volume variation or pulse pressure variation are both highly sensitive and specific for preload responsiveness in mechanical ventilated patients, whereas the
passive straight leg test should be used in spontaneously breathing patients
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The CVP Assumption
Preload = CVP = PAOP= LAP = LVEDP All equal volume??!!!???
Is ventricular geometry
unchanged?
Is ventricular compliance unchanged?
Is there valve
disease?
Are intrathoracic or intra-abdominal
pressures elevated?
Catheter properly
positioned?
CVP is accurate ONLY when these potential sources of error have been eliminated
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CVP Variability
CVP clearly has limitations Respiratory variability may be an option >1 mm change with inspiration consistent with fluid
responsiveness
Magder S ,et al, Respiratory varia/ons in right atrial pressure predict the response to uid challenge, Journal of Cri/cal Care, Volume 7, Issue 2, June 1992, Pages 76-85
INSP
EXP EXP
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Emerging data show that the choice, timing and amount of fluid therapy may affect clinical outcomes
Early administration of fluid therapy in sepsis may improve survival
Later fluid therapy in acute lung injury patients will increase the duration of ventilator dependence without achieving better survival
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Complications Pneumothorax
Incidence 0.5 to 6% Intervention
None Needle decompression Tube thoracostomy
Sudden dyspnea, chest pain, absent breath sounds, tachycardia, asymmetrical chest wall movement
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The Pulmonary Artery Catheter in Critical Care
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Connors et al 1996 JAMA
5734 adult ICU pa/ents 1989-1994, 5 ICUs at 15 ter/ary med centers
PA cath = 30 day mortality, ICU LOS, costs of care
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Harvey et al: PAC-Man 2005 Lancet - Game Over?
1014 pa/ents at 65 UK ins/tu/ons: NO DIFFERENCE between PA cath versus no PA cath
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Cochrane R & R: 2006 (Review and Reappraisal)
The PAC is a monitoring tool; if it is used to direct therapy and there is no
improvement in outcome, then the therapy does not help.
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Pulmonary Artery Catheterization Initially devised by Swan and Ganz. Allows for view of Left Ventricular function by using
extrapolation of right heart measurements. Catheter is floated into right side of the heart and
into a small pulmonary arteriole. Catheter is then wedged and a pressure is
measured. Pulmonary Capillary Wedge Pressure (PCWP) or
Pulmonary Occlusion Pressure (POP)
PCWP reflects Left Atrial Pressure (LAP) which reflects Left Ventricular End Diastolic Pressure (LVEDP) which reflects Left Ventricular End Diastolic Volume (LVEDV)
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Pulmonary arterial catheter
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Indications for PAP monitoring Shock of all types Assessment of cardiovascular function and
response to therapy Assessment of pulmonary status Assessment of fluid requirement Perioperative monitoring
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2011 Lippincoi Williams & Wilkins, Inc. 3
Pulmonary artery catheter monitoring in 2011. Richard, Chris/an; Monnet, Xavier; Teboul, Jean-Louis Current Opinion in Cri/cal Care. 17(3):296-302, June 2011. DOI: 10.1097/MCC.0b013e3283466b85
Box. 1 No cap/on available.
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Cardiac Output
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Stroke volume
Cardiac Output
L/ min
ml/ beat
Compensatory Mechanisms
Heart rate
beats/min
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Heart Rate heart rate increase in response to stress and tissue demands
for oxygen maximum heart rate and VO2 baroreflex control of BP increase in ejection fraction
dependence on Frank-Starling mechanism to maintain stroke volume vagal tone increases
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Stroke Volume Range of normal at rest is 60 100 ml/b Max. SV is 120 200 ml/b, depending on size, heredity, and
conditioning. Increased SV due to complete filling of ventricles during
diastole and/or complete emptying of ventricles during systole Rate of rise Vascular tone
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Cardiac Output: Heart Rate X Stroke Volume
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Heart rate
Stroke volume
Cardiac Output
beats/min
L/ min
ml/ beat
Compensatory Mechanisms
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Stroke Volume Index Stroke index is defined as the amount of blood
pumped with each beat indexed to BSA Normal 35-45 ml's/m2 Low values require treatment, especially if SvO2 is
low
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Cardiac Output Typically determined via thermodilution
A change in temperature of a known volume of cooled infusate is used to calculate CO
How quickly or slowly the cooled infusate mixes with blood determines the CO
Accuracy altered by conditions affecting the mixing of infusate and blood
Tricuspid regurgitation, intracardiac shunts, cardiac arrhythmias, positive pressure ventilation
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Main circumstances in ICU Positive pressure ventilation Severe pulmonary embolism ARDS Sepsis induced RV dysfunction Exacerbation of medical conditions leading to
chronic pulmonary hypertension Right ventricle infarction Pericardial diseases RV failure after cardiac surgery After cardiac transplant
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Physiology of the normal pulmonary circulation Low pressure system: PRV (syst) = 25 mmHg
versus PLV (syst) = 120 mmHg The pressure in the pulmonary system depends on
cardiac output, resistance and compliance Normally very compliant pulmonary vessels with large
diameter and thin wall Normal RV afterload very low
alveolar hypoxia leads to pulmonary arterial vasoconstriction and pulmonary vascular resistance
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Management strategies for patients with pulmonary hypertension in the intensive care unit *. Zamanian, Roham; Haddad, Francois; Doyle, Ramona; Weinacker, Ann Critical Care Medicine. 35(9):2037-2050, September 2007.
RV Dysfunction in ICU
Figure 2. Implica/ons of pulmonary hypertension on right ventricular (RV) func/on and hemodynamics. Development and progression of pulmonary hypertension leads to right ventricular pressure overload, which impacts right ventricular systolic and diastolic func/on. Len ventricular (LV) dysfunc/on also can result in the seong of right ventricular failure. The physiologic consequence of ventricular dysfunc/on in conjunc/on with development of arrhythmias, tricuspid regurgita/on (TR), and worsening hypoxemia ul/mately lead to hypotension and circulatory collapse.
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Effects of mechanical ventilation Increased RV afterload due to positive pressure
ventilation Hemodynamic failure frequently refractory in PAH
patient put on MV In ARDS increase in mPAP while increasing tidal
volume and PEEP Permissive hypercapnia is deleterious (increase in
mPAP)
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Effect of MV on venous return
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Effect of high PEEP on RV
Monitoring of right-sided heart function. Jardin, Francois; Vieillard-Baron, Antoine Current Opinion in Critical Care. 11(3):271-279, June 2005.
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O2 requirements and blood supply to the RV Less O2 requirements than the LV : myocardial
mass due toafterload Vascularisation : 2/3 RCA, 1/3 left branches RV perfused in both systolic and diastolic phases
low systolic pressure (25 mmHg) does not compress vessel
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Vicious cycle of auto-aggravation
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Ventricular interdependence
During systole, LV protrudes in RV Surrounding pericardium with limited distensibility Compliance of one ventricle can modify the other =
Diastolic ventricular interaction
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PA Catheter Pressures Impacted by circumstances altering ventricular
compliance Ischemia, LVH, hypertension, tamponade, AS
PEEP applied during mechanical ventilation Once greater than 10 cm H2O pressures transmit across
vasculature and elevate PAWP
Changes during respiratory cycle Intrathoracic pressure varies with inhalation/ exhalation,
impacting the PA catheter readings Measure readings at end exhalation
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Ventricular Function Left ventricular function Right ventricular function Depressed right ventricular function was further
linked to more severely compromised left ventricular function.
Nielsen et al. Intensive care med 32:585-94, 2006
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3
Pulmonary artery catheter monitoring in 2011. Richard, Christian; Monnet, Xavier; Teboul, Jean-Louis Current Opinion in Critical Care. 17(3):296-302, June 2011.
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RA
LA
LV
Alveoli Sv02 :0.6 0.8
Sa02 :0.95 1.0 Scv02 :0.65- 0.85
Oxygenation Patterns with Normal Function
Cell
RV
St02 :0.80- 0.90
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What are the Normal Post Cell Reads? 60-80% sat PA (mixed venous reading) 65-85% sat central venous reading 75-85 % thenar eminence When all numbers low, failure to deliver oxygen Not all patients are the same
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SCVO2 Monitoring
Surrogate of global tissue hypoxia Sepsis results in increased metabolic stress at the tissue level Response is to increase cardiac output and/or O2 utilization When O2 supply is overwhelmed by the disease, SCVO2 continues to
decrease (O2 demand > supply) Thus, SCVO2 is proposed to be a marker of adequate O2 utilization at the
tissue level as a response to metabolic stress
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Central Venous O2 Saturation (SCvO2)
Measures O2 saturation in the superior vena cava May be measured continuously with available fiberoptic catheters or
intermittently with venous blood gases More readily available as does not require a PA catheter Reflects CvO2 of blood returned from upper body SCvO2 typically higher than SvO2 but trend track in parallel
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SvO2 v. ScvO2
100%
VO2
75% StiO2
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Managing Tissue Oxygenation
OxyHemoglobin Dissociation
OXYGEN Delivery
OXYGEN Consump/on
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Understanding Tissue Oxygen Tissue Oxygenation The single MOST important issue is tissue
oxygenation. All physiologic components are designed to
maintain balanced tissue oxygen consumption (demand).
What are the components of Oxygen Consumption? Oxygen delivery Metabolic demand at the cellular level Blood flow through the capillary Ability to dissociate oxygen from hemoglobin
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Understanding Tissue OxygenComponents of Oxygen Delivery 1. Cardiac Output = Heart rate x stroke volume 2. Total hemoglobin (02 carrying capacity) 3. Saturation of hemoglobin First line compensatory mechanism ( patient)
Increase the heart rate and stroke volume to increase delivery when cells are hypermetabolic and/or when oxygen is not functionally dissociating from its transporter, hemoglobin.
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Understanding Tissue Oxygen The amount of oxygen required by the cells
changes every second" When demand/consumption increases, hemoglobin
releases oxygen more rapidly" Shift to the right: release"
When demand/consumption decreases, hemoglobin decreases release or latches on to oxygen"
Shift to the left: latched on" Second compensatory mechanism: hemoglobin
more aggressively releases oxygen to dissolve in the blood (partial pressure) to be used by the cells"
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Understanding Tissue Oxygen What is the purpose of saturating hemoglobin?
Hemoglobin is the transporter of oxygen Each heme molecule binds 1.34 mLs of oxygen
When oxygen is bound it is not usable Measure of bound oxygen in the arterial blood is the Sa02
(indirectly reflected by pulse oximetry Sp02) Only oxygen dissolved in blood can be used
Measure of dissolved oxygen in the arterial blood is the Pa02
The rate of oxygen use at the cell determines the Pa02 which in turn affects the dissociation
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Understanding Tissue Oxygen Oxygen dissociation as a compensatory response Shifts in the bound oxygen mean that there is a
change in the way oxygen is Taken up by the hemoglobin molecule at the alveolar
level (Sa02) Depends on the partial pressure of alveolar gas (PA02)
Released related to the partial pressure of capillary oxygen (Pa02, Pcap02)
Capillary oxygen depends on the tissue oxygen (Pti02) Tissue oxygen goes down when cells are hypermetabolic
and/or the delivery is inadequate
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Continuous SvO2 Monitoring Incorporated into PA catheter SvO2 changes rapidly when DO2 altered May allow for rapid interventions as patients
condition changes
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Global Tissue Hypoxia: A More Sensitive Measure of Shock
OxyHemoglobin Dissociation
OXYGEN Delivery
OXYGEN Consump/on
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Understanding Tissue Oxygen Tissue Oxygenation There are two mechanisms designed to meet
oxygen consumption (demand) Increase oxygen delivery Increase the release (dissociation) of oxygen from
hemoglobin
In the best of critical situations, both delivery and dissociation increase to maintain cells
failure of one mechanism will be supported by compensation by the other
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Managing Tissue Oxygenation
OxyHemoglobin Dissociation
OXYGEN Delivery
OXYGEN Consump/on
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Dissociation must be measured in the venous compartment
Pv02
Sv02 Scv02
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RA
LA
LV
Alveoli Sv02 :0.6 0.8
Sa02 :0.95 1.0 Scv02 :0.65- 0.85
Oxygenation Patterns with Normal Function
Cell
RV
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OXYGEN release
OXYGEN Demand &
Consump/on
OXYGEN Delivery
Compensation in attempts to sustain Tissue Oxygen
COMPENSATION: Shin to the right Release oxygen to save the cells MEASURE: Scv02 Always Compensatory Always an EMERGENCY
PROBLEM Oxygen delivery inadequate for oxygen demand Primary failure
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Sv02 Scv02 Low
Pv02
Compensation Oxygenation
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Compensation in attempts to sustain Tissue Oxygen
OXYGEN Demand &
Consump/on
OXYGEN Delivery
OXYGEN release
COMPENSATION: Cardiac output increases Despite increase, /ssue hypoperfusion persists (LA)
PROBLEM Scv02 normal to in the face of
suspicion (HR, RR persistent acidosis (LA))
MUST BE considered as failure to release oxygen (in the presence of LA)
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Sv02 Normal to High With Persistent Lactic Acidosis
Pv02
Compensation in attempts to sustain Tissue Oxygen
Cells do not need it!
OR
Cells need it but cannot get it!
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Monitoring Venous Oxygenation ScvO2 is usually less than SvO2 by about 23% but
two change in parallel In septic shock ScvO2 often exceeds SvO2 by
about 8% -correlation between these two parameters may worsen
ScvO2/SvO2 should not be used alone in assessment of cardiocirculatory system
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The Research Chawla et al. Lack of equivalence between central and mixed
venous oxygen saturation. Chest 2004; 126:18911896 -------- 53 critically ill patients that SvO2 was consistently lower than ScvO2 (P < 0.0001), with a mean bias of 5.2 5.1%, ScvO2 was not a reliable surrogate
Tahvanainen J, Can central venous blood replace mixed venous blood samples? Crit Care Med 1982; 10:758761 ------ ScvO2 is equivalent to SvO2
Dueck MH et al. Trends but not individual values of central venous oxygen saturation agree with mixed venous oxygen saturation during varying hemodynamic conditions. Anesthesiology 2005; 103:249257
----- 70 neurosurgical patients, trends of ScvO2 and SvO2 are interchangeable
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Why do we need dynamic fluid measures
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What about other information? With a thermaldilution, transpulmonary system, it is
possible to calculate and index: Global end diastolic volume Extravascular lung water
Measurements of extravascular lung water (EVLW) correlate to the degree of pulmonary edema and have substantial prognostic information in critically ill patients.
normal EVLW (defined as < 10mL/kg)
Mar/n GS, Eaton S, Mealer M, Moss M. Extravascular lung water in pa/ents with severe sepsis: aprospec/ve cohort study. Crit Care 2005;9:R74R82. Kuzkov VV, Kirov MY, Sovershaev MA, et al. Extravascular lung water determined with single transpulmonary thermodilu/on correlates with the severity of sepsis-induced acute lung injury. CritCare Med 2006;34:16471653. [ Groeneveld AB, Verheij J. Extravascular lung water to blood volume ra/os as measures of permeability in sepsis-induced ALI/ARDS. Intensive Care Med 2006;32:13151321. Patroni/ N, Bellani G, Maggioni E, Mano A, Marcora B, Pesen/ A. Measurement of pulmonary edema in pa/ents with acute respiratory distress syndrome. Crit Care Med 2005;33:25472554.
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Newer Methodologies for Obtaining CO Data The arterial pressure wave form results from
interactions of the vascular system and the ejected SV
Analyzing the waveform allows for determination of SV
CO then simply calculated by equation: CO = HR x SV
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Heart rate
Stroke volume
Cardiac Output
beats/min
L/ min
ml/ beat
Compensatory Mechanisms
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Why do we give volume
Increase stroke volume (SV) and cardiac output (CO) Only 50% of patients respond to a fluid challenge Cumulative fluid balance may affect outcome Whether the patient is responsive to fluid or not? Optimal strategy of increasing CO and oxygen delivery
Volume expasion for hemodynamically unstable paQents
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Newer Methodologies for Obtaining CO Data Stroke volume variation
Determined with arterial pressure cardiac output monitors Shown to predict volume responsiveness in mechanically
ventilated patients An algorithm utilizing this concept follows
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Systolic pressure
Diastolic pressure
Average pressure
Pulse pressure = systolic pressure - diastolic pressure
80
100
120
1 second
Pressure [m
mHg]
Aortic pulse wave
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40
PPmax
PPmin
PPmax - PPmin
(PPmax + PPmin) /2
PP =
Am J Respir Crit Care Med 2000; 162:134-138
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Use of Heart Lung Interactions to Diagnose Preload-Responsiveness
ValSalva maneuver Ventilation-induced changes in:
Right atrial pressure Systolic arterial pressure Arterial pulse pressure Inferior vena caval diameter Superior vena caval diameter
Sharpey-Schaer. Br Med J 1:693-699, 1955 Zema et al., D Chest 85,59-64, 1984 Magder et al. J Crit Care 7:7685, 1992
Perel et al. Anesthesiology 67:498-502, 1987
Michard et al. Am J Respir Crit Care Med 162:134-8, 2000
Jardin & Vieillard-Baron. Intensive Care Med 29:1426-34, 2003
Vieillard-Baron et al. Am J Respir Crit Care Med 168: 671-6, 2003
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Preload
Stroke Volume
0
0
Normal
Heart Failure
Frank-Starling relationship
-
Fluid Responsiveness % increase in stroke volume after volume
expansion.
Responders 15 % Non Responders < 15%
The Goal is to Improve Oxygen Delivery
-
Respiratory Variations in LV Stroke Volume
Venous Return RVEDV
RVSV
pulmonary venous return
LVEDV
LVSV
Pulmonary Vascular transit Time
Static Parameters vs. Dynamic Parameters
Airway pressure up Ventricular compliance and volume load down
Ventricular pressure up (resistance )
CVP, PA , PaOP
-
Preload
Stroke Volume
0
0
ExhalaQon
inspiraQon
Frank-Starling relationship
Stroke volume varia/on occurring with ITP change
-
Preload
Stroke Volume
VariaQon opQmized
Frank-Starling relationship
normal
hypovolemic
-
Preload
Stroke Volume
0 0
PP /POP Minimization
Preload Dependence Optimization Concept
-
Cardiopulmonary Interactions
The more sensitive a ventricle is to preload, the more the stroke volume will be impacted by changes in preload due to positive pressure ventilation.
Preload Independent Preload Dependent
AP AP
= SVmax SV min (SVmax + SV min)/2
Dynamic change of SV inspira/on
-
Variation from Ventilation
SVV, PPV, and SPV are created by tidal volume-induced changes in venous return.
presumes a constant R-R interval and are measured from diastole to systole
+ presure ventilation causes changes in venous return, which is accentuated in hypovolemic patients
take advantage of the swings in venous return in order to determine the fluid responsiveness of hypotensive patients
Lose their predictive value under conditions of varying R-R intervals
(atrial fibrillation), tidal volume varies
from breath to breath (with assisted and spontaneous ventilation)
-
When do measures become less reliable? aortic insufficiency Peripheral vascular disease intra-aortic counterpulsation cardiac arrhythmias SIMV, other forms of ventilation that have limited
changes ( APRV,HFOV, ) or uncontrolled changes (SIMV)
-
.
Stroke Volume
Ventricular preload
Preload-dependence
Preload-independence
Normal heart
Failing heart
SVV physiology
SVV
-
Normal Variation & Pulsus Paradoxus
Arterial Pressure
Time
In a normal individual who is breathing spontaneously, blood pressure decreases on inspiration The exaggeration of this phenomenon is called pulsus paradoxus
F.Michard
Pulsus Paradoxus Expiration Inspiration
-
Reversed Pulsus Paradoxus
Arterial Pressure
Time
A phenomenon that is the reverse of the conventional pulsus paradoxus has been reported during positive pressure breathing
F. Michard
Expiration
Inspiration
-
Calculate is variability Assign PA label Go to the wedge window Edit and store trace Move my cursor High Systole: 154 Low Systole: 148 High diastole: 84 Low diastole: 80 High systole high diastole: MAX PP Low systole low diastole: MIN PP MAX PP= 154-84 = 70 MIN PP= 148-80= 68 MEAN PP Max + min/2= 69 MAX PP MIN PP/ mean PP 70-68=2/69 2% variation
-
Pulse Pressure Variation Pulse pressure variation (PPV)
Calculated in the same manner as SVV, Also predict preload responsiveness well.
A 13% PPV predicts a 15% increase in CO for a 500-mL volume bolus
ANY signal that gives pulse density REQUIRED
Controlled variables Ventilation Heart rate
-
What are the Limitations of SVV? Mechanical Ventilation
Currently, literature supports the use of SVV on patients who are 100% mechanically (control mode) ventilated with tidal volumes of more than 8cc/kg and fixed respiratory rates.
Spontaneous Ventilation Currently, literature does not support the use of SVV with
patients who are spontaneously breathing.
Arrhythmias Arrhythmias can dramatically affect SVV. Thus, SVVs
utility as a guide for volume resuscitation is greatest in absence of arrhythmias.
-
11
Emerging trends in minimally invasive haemodynamic monitoring and opQmizaQon of uid therapy. Benington S; Ferris P; Nirmalan M European Journal of Anaesthesiology. 26(11):893-905, 2009 Nov.
-
Are the pulse analysis techniques as accurate as the PAC for monitoring CO? Yes, (level of evidence, C) but it depends.
Not all monitors are the same. In stable patients they perform to a clinically acceptable level
and have other advantages. Continuous data Less invasive Offer other variables.
In shocked patients the evidence is less clear.
A. Rhodes , personal communication ESICM 2010
-
Why are we concerned about too much volume or volume that is in the wrong place?
-
What about other information? With a thermodilution, transpulmonary system, it is
possible to calculate and index: Intrathoracic blood volume Pulmonary vascular permeability index
Increased capillary permeability during the first 48 h in patients with sepsis was associated with a higher mortality rate during the intensive care unit (ICU) stay than those with decreased permeability 1, 2
1. Hotchkiss RS, Karl IE (2003) The pathophysiology and treatment of sepsis.N Engl J Med 348: 138150. 2. Abid O, Sun Q, Sugimoto K, Mercan D, Vincent JL (2001) Predic/ve value of microalbuminuria in medical ICU pa/ents: results of a pilot study. Chest 120:19841988.
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What does thermodilution do for me Fluid responsiveness: PPV and SVV CO measurement
Transpulmonary thermodilution Pulse contour analysis
Extravascular lung water index (EVLWI): a good surrogate assessment of pulmonary edema
Global end-diastolic volume index (GEDI): a volumetric preload assessment
Cardiac function index: a calculated index of cardiac function
Pulmonary vascular permeability index (PVPI)
-
7
Emerging trends in minimally invasive haemodynamic monitoring and opQmizaQon of uid therapy. Benington S; Ferris P; Nirmalan M European Journal of Anaesthesiology. 26(11):893-905, 2009 Nov.
-
What am I looking for? Indices of hypovolemia: SVV > 13% volume loading should decrease SVV. If not
Stop fluid administration Inotropic support initiated
- Goals for cardiocirculatory therapy ScvO2 >70% or SvO2 >65% MAP (mean arterial pressure) >65 mmHg Cardiac Index >2.0 l/min/m2 CVP 815 mmHg (dependent on ventilation mode) SVV < 13 % ITBVI 8501000 ml/m2 GEDVI 640800 ml/m2 PAOP 1215 mmHg Diuresis >0.5 ml/kgBW/h Lactate
-
Preload
Stroke Volume
0 0
Cardiac Ouput Maximization
Cardiac Output Optimization Concept
EVLW
-
Why do we need EVLWI Diagnosis Prognosis Goal to aggressive therapy Better guide to resuscitation in patients at risk for
pulmonary edema (anyone with high permeability index) Shock or severe sepsis ALI CHF
-
Case Presentation 1 54 year old man with fever and
abnormal liver function for liver biopsy Biopsy well tolerated until 3 hours
afterwards when he developed abdominal distension , with systolic BP 60 and Hg 8.6
-
Case Presentation 1a HR 128, RR 26 22% SVV what now? EVLWI < 8 Next?
Volume responsive!
-
Case Presentation 1b SVV 13% BP 80/40 EVLWI > 12 Next?
Vasopressor
-
Case Presentation 1c SVV 20% EVLWI 10% Next?
Volume, inotrope
-
Newer Methodologies for Obtaining CO Data The arterial pressure wave form results from
interactions of the vascular system and the ejected SV
Analyzing the waveform allows for determination of SV
CO then simply calculated by equation: CO = HR x SV
-
Newer Methodologies for Obtaining CO Data Stroke volume variation
Determined with arterial pressure cardiac output monitors Shown to predict volume responsiveness in mechanically
ventilated patients An algorithm utilizing this concept follows
-
Hemodynamic Monitoring Truth No monitoring device, no matter how simple or complex, invasive or non-invasive, inaccurate or precise will improve outcome Unless coupled to a treatment, which itself improves outcome
Pinsky & Payen. Func/onal Hemodynamic Monitoring, Springer, 2004
-
0
Volts
Io
Vo
Io
Vo
0
Amp.
Bioimpedance
Bioreactance
-
Perfusion Index Perfusion Index is an objective method for
measuring a patients peripheral perfusion Perfusion Index is an early indicator of
deterioration
-
Perfusion Index
Infrared
Satura/on
Red
-
108 healthy, 37 critically ill adults (finger sensors)
PI range: 0.3% to 10%, median 1.4% ROC used to determine the cutoff value 1.4% PI best discriminated normal from
abnormal
What is a Normal PI ?
Lima, et al. CCM 2002
-
Clinical Uses for PI Normals have been suggested to be:
>1.4% adults, >1.27% neonates 1.Site selection (varies between patients and sites) 2.Chorioamnionitis (placental membrane/amniotic fluid
infection) 3.Effectiveness of Servoflorane anesthesia 4.Monitor onset/effectiveness of epidural anesthesia 5.Predict illness severity scores (good correlation) 6.Monitor/quantify peripheral perfusion 7.Detect shock states 8.PI trend may best reflect changes in condition
-
Photoplethysmography
Abso
rptio
n
Time
R IR
Photodetector
Pleth Waveform
-
Pleth Waveform
-
A-line versus Pulse Ox Pleth
-
McLean Method
Cardiac
Heart Rate
SV
SVV
PPV Systolic pressure
Echo Oxyhemoglobin Dissocia/on
Volume
IOS
PPV SVV SV
EVLW U/O ml/kg
Echo Oxyhemoglobin Dissocia/on
Vascular Tone
Respiratory Rate
PPV
SVV
PPV/SVV Diastolic pressure
Echo
Oxyhemoglobin Dissocia/on
Tissue Anion Gap, Serum C02, Base, pH, Lac/c acid, Ketones, S/0
-
What do these patients have in common? PaQent 1 PaQent 2 PaQent 3
HR 127 133 113
RR 34 28 18
Pa02 70 PaC02 23 Fi02 1.0 PEEP 12 Rate 20 ACMV
91 PaC02 35 0.70 PEEP 15 Rate 15 SIMV
100 PaC02 39 0.5 PEEP 20 Rate 10 SIMV
BPS 80 BPD 55
BPS 80 BPD 40
BPS 100 BPD 60
-
What do these patients have in common? PaQent 1 PaQent 2 PaQent 3
HR 127 133 113
RR 34 28 18
Pa02 70 PaC02 23 Fi02 1.0 PEEP 12 Rate 20 ACMV
91 PaC02 35 0.70 PEEP 15 Rate 15 SIMV
100 PaC02 39 0.5 PEEP 20 Rate 10 SIMV
BPS 80 BPD 55
BPS 80 BPD 40
BPS 100 BPD 60
Sv02 45% Sv02 70% Sv02 65
-
What do these patients have in common? PaQent 1 PaQent 2 PaQent 3
HR 127 133 113
RR 34 28 18
Pa02 70 PaC02 23 Fi02 1.0 PEEP 12 Rate 20 ACMV
91 PaC02 35 0.70 PEEP 15 Rate 15 SIMV
100 PaC02 39 0.5 PEEP 20 Rate 10 SIMV
BPS 80 BPD 55
BPS 80 BPD 40
BPS 100 BPD 60
PP 25 SVV 16%
PP 40 SVV 21%
PP 40 SVV 15%
Sv02 45% Sv02 70% Sv02 65
-
What do these patients have in common? PaQent 1 PaQent 2 PaQent 3
HR 127 133 113
RR 34 28 18
Pa02 70 PaC02 23 Fi02 1.0 PEEP 12 Rate 20 ACMV
91 PaC02 35 0.70 PEEP 15 Rate 15 SIMV
100 PaC02 39 0.5 PEEP 20 Rate 10 SIMV
BPS 80 BPD 55
BPS 80 BPD 40
BPS 100 BPD 60
PP 25 PPV 16%
PP 40 PPV 21%
PP 40 PPV 15%
Sv02 45% Sv02 70% Sv02 65
AG 34 AG 41 AG 13
LA 6.1 LA 7.2 LA 2.8
-
Remember A searchlight cannot be used effectively without a
fairly thorough knowledge of the territory to be searched.
Fergus Macartney, FRCP
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