fluid optimization concept based on dynamic parameters of hemodynamic monitoring

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Fluid Optimization Concept Based On Dynamic Parameters Of HDM DR. SURENDRA KUMAR FNB-CCM RTIICS KOLKATA

Transcript of fluid optimization concept based on dynamic parameters of hemodynamic monitoring

Page 1: fluid optimization concept based on dynamic parameters of hemodynamic monitoring

Fluid Optimization Concept Based On Dynamic Parameters

Of HDM

DR. SURENDRA KUMAR

FNB-CCM

RTIICS KOLKATA

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Hemodynamic Truths

• Tachycardia is never a good thing

• Hypotension is always pathological

• There is no normal cardiac output

• CVP is only elevated in disease• Peripheral edema is of cosmetic

concern

CONSIDER OF A CASE OF SEPSIS

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Routine Haemodynamic Monitoring

Mandatory

Clinical Examination

ECG

Pulse Oxymetry

End Tidal CO2 Monitoring

Blood Pressure Monitoring

Non-invasive

Invasive

Urine output

ABG

Non-mandatory

Central Venous Pressure

Pulmonary Artery pressure

Cardiac Output

Ultrasound

Novel Technologies

Functional HD Monitoring

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Protocol for Early Goal-directed Therapy

• Rivers protocol for hemodynamic management in severe sepsis or septic shock.

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What do we expect from a hemodynamic monitoringsystem?

•This question depends on the monitor. •At least, we expect a monitor to accurately measure

•CO •fluid responsiveness

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Integrative hemodynamic monitoring approach

Ramsingh et al. Critical Care 2013, 17:208

• The goal of most functional HDM parameters is to

predict fluid responsiveness in critically ill pts

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Is cardiac output responsive to intravascular fluid loading?

• Assumes that venous return and LV preload are the primary determinants of cardiac output (Starling’s Law of the Heart)

• Assumes low LV end-diastolic volume (EDV) equals preload-responsiveness

• Attempts to assess EDV through surrogate measures• CVP, PAOP, LV end-diastolic area, RV EDV, intrathoracic blood volume

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Determinants of Cardiac Output

• CO = HR x SV

• Stroke Volume is determined by:• Preload

• Afterload

• Contractility

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What is Preload?

• Preload is the force or “load” which stretches the ventricle of the heart, that determines the force-length relationship

• Preload can be measured only in lab

• We measure surrogates for preload

• Pressure vs Volume

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Frank Starling Curves

Factors Affecting Preload

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Fluid optimization concept based on stroke volume monitoring.

The concept of cardiac output maximization based on fluid administration and stroke volume monitoring. Small boluses of fluid are administered intravenously (200 to 250 ml at a time) until the stroke volume increases by <10%.

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Assessment of volume responsiveness Fluid responsiveness should be detected before deciding to administer volume expansion, especially in patients in whom fluid overload should be particularly avoided, i. e., patients with septic shock and/or ARDS.

For this purpose, ‘static markers ’ of cardiac preload have been used for many years.

Nevertheless, a very large number of studies clearly demonstrate that neither pressure nor volume markers of preload can predict fluid responsiveness

• -CVP and PAOP poor predictors of fluid status

• Cardiac filling pressures did not predict fluid responders from non-responders. [Osman, et al. CCM 2007 ]

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Preload ( Filling Pressures) Assessment

CVP

RAP

RVEDP

PCWP

LVEDP

LVEDV

LVEDV determines LVEF

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dynamic approach

a ‘dynamic approach’ has been developed for assessing volume responsiveness.

The concept is to assess preload dependency by observing the effects on cardiac output of changes in cardiac preload induced by various tests.

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Dynamic parameters

• Systolic pressure variation

• Pulse pressure variation

• Stroke volume variation

• Passive leg raising

• Pleth variability index

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Normal Spontaneous Breathing

Variation of peak systolic pressure by < 5 mm Hg

Pulsus Paradoxus : Adolf Kussmual

‘Disappearing pulse during inspiration and return in expiration’

Exaggeration of this response - constrictive pericarditis

- Cardiac Tamponade

- Severe lung disease

Arterial Pressures and Respiration

Swing!

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Morgan et al: Anesthesiology: 1966

Effect of Positive Pressure on Blood flows

Aortic Blood Flow

Pulmonary Artery Flow

Vena Cava Flow

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Arterial Pressures and IPPV

Inspiratory increase in SBP

followed by

a decrease on expiration

Also known as

Systolic Pressure Variation

Pulse Pressure Variation

Reverse Pulsus Paradoxus Reverse swing!

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Systolic pressure variation

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• The SPV consists of an upward swing ( up) as well as a fall ( down)

• This phenomenon is an extension of the ‘pulsusparadoxux’

• Can be used only during IPPV

• If the sum of up + down > 15 mmHg, then that patient will respond to fluids (preload)

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if ∆PP is low (<13%), then a beneficial haemodynamic effect of volume expansion is veryunlikely, and inotropes or vasoactives drugs should be proposed in order to improve haemodynamics. In contrast, if ∆PP is high (>13%), then a significant increase in cardiac index in response to fluid infusion is very likely.

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Pulse pressure variation

The first application of this ‘dynamic’ concept consisted of quantifying the variations in stroke volume induced by positive-pressure ventilation

The arterial pulse pressure (systolic minus diastolic arterial pressure) as a surrogate of stroke volume has been proposed to predict fluid responsiveness through its respiratory variation .

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SVV to determine Preload Responsiveness

International Panel Point of View Article; 2009

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SPV /SVV AlgorithmF. Michard 2009

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Other surrogates of stroke volume• Aortic blood flow measured by esophageal Doppler

• Subaortic peak velocity measured by echocardiography

• Stroke volume estimated from pulse contour analysis

Finally,

• analysis of respiratory variations of the diameter of the IVC using TTE or of the SVC using TEE can also be used to assess fluid responsiveness in mechanicall y ventilated pts

• the non-invasive arterial pulse pressure estimated by the volume-clamp method or the amplitude of the plethysmographic waveform. All the se non-invasive methods still require confirmatory studies.

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PVI >17 %

Relation between respiratory variations in pulse oximetry plethysmographic waveform amplitude and arterial pulse pressure in ventilated patients.

Adapted from Cannesson et al., 2005

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Limitations of the respiratory variation in stroke volume for predicting fluid responsiveness

1. Spontaneous Breathing Activity

2. Cardiac Arrhythmias

3. High Frequency Ventilation

4. Presence Of Increased Abdominal Pressure

5. Open-chest Surgery

6. Low Tidal Volume

7. Low Compliance Of The Respiratory System[ < 30 ml/cm H2O] ...........recent clinical study

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Practical Limitations of PPV

• Requires fixed HR• Atrial fibrillation, frequent PVCs

• Requires no spontaneous ventilatory efforts• Can not use during CPAP, PSV

• Magnitude of PPV or SVV will change with changing tidal volume

• Heart failure may give false positive response!

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PPV and SVV during IPPV

• Reflect complex interactions between preload and afterload

• Potential false positive PPV with inspiration• Severe CHF-Reverse Bernheim Effect

• Cor pulmonale- Minimize ventricular interdependence

• Potential false positive SVP with inspiration• Stiff chest wall + large tidal volume: Valsalva Maneuver

• Whenever ITP increases rapidly

• These limitations dissolve with passive leg raising

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Limits of Preload-Responsiveness• Preload Preload-responsiveness

• Preload-responsiveness Need for fluids

• The means of altering preload matters• Size of Vt, passive leg raising, spontaneous breaths

• Different measures of pressure or flow variation will have different calibrations

• Pinsky Intensive Care Med 30: 1008-10, 2004

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Alternatives to the respiratory variation of hemodynamic signals: recent advances

Critical Care 2013, 17:217

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The end-expiratory occlusion test[EEO]

it was demonstrated that if a 15-sec EEO test increased the arterial pulse pressure or the pulse contour-derived cardiac output by more than 5 %, the response of cardiac output to a 500 ml saline infusion could be predicted with good sensitivity and specificity.

ADVANTAGE

is that it exerts its hemodynamic effects over several cardiac cycles and thus remains valuable in case of cardiac arrhythmias. [main]

can be used in pts with spontaneous breathing activity, unless marked triggering activity interrupts the test.

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Marik et al. Annals of Intensive Care 2011, 1:1

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The ‘mini’ fluid challenge

Obviously, the easiest way to test preload responsiveness is to administer fluid and to observe the resulting effect on cardiac output.

Nevertheless, the disadvantage of the ‘classical’ fluid challenge is that it consists of administration of 300–500 ml of fluid. Because it is not reversible, such a fluid challenge may contribute to fluid overload, especially when it is repeated several times a day

It consists of administering 100 ml of colloid over 1 min and observe the effects of this ‘mini’ fluid challenge on stroke volume, as measured by the sub aortic velocity time index using transthoracic echocardiography. In a clinical study, an increase in the velocity time index of more than 10 % predicted fluid responsiveness with a sensitivity of 95 % and a specificity of 78 %

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• Advantage

small volume of fluid is unlikely to induce fluid overload even if repeated several times a day

easy to perform and can be assessed in a non-invasive way

• Nevertheless, a strong limitation is that, even in cases of preload-dependency, such a small volume infusion will unavoidably induce only small changes in cardiac output. This test, therefore, requires a very precise technique for measuring cardiac output

Disadv.--------cannot be used in the presence of cardiac arrhythmias

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The passive leg-raising testpassively transfers a significant volume of blood from the lower part of the body toward the cardiac chambers: Passive leg-raising (PLR) partially empties the venous reservoir and converts a part of the unstressed blood volume to stressed volume. In this connection, PLR increases right and left cardiac preload. Eventually, the increase in left cardiac preload results in an increase in cardiac output depending upon the degree of preload reserve of the left ventricle. The increase in cardiac preload induced by PLR totally reverses once the legs are returned back to the supine position.

In summary, PLR acts like a reversible and short-lived ‘self ’ volume challenge

since the test exerts its effects over several cardiac and respiratory cycles, it remains a good predictor of fluid responsiveness in patients with spontaneous breathing activity (even non-intubated) or cardiac arrhythmias

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Passive leg raising: five rules, not a drop of fluid!

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Fluid challenges and PLR

45 degrees 45 degrees

Patients who are fluid responsive will show a 10% -15 % rise of SV in 30 to 90 seconds. SV % increase by 10-15% preload responsive.

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Benefits of Passive Leg Raising (PLR)In situations where it is not possible to use SVV, the effects of fluid loading can be replicated by using PLR.

PLR acts like a ‘self volume challenge’

Equivalent to 150 – 300 ml volume

if a patient is responsive to PLR, they will be responsive to fluid administration

The PLR test is reversible, and therefore useful in patients with fluid-loading related complications

If the increase in cardiac preload induced by PLR induces significant changes in SV (a to b), the patient will likely be fluid responsive

If the same changes in cardiac preload during PLR do not significantly change SV (a’ to b’), the heart is likely preload dependent and should not be administered

Examples

Sources:Michard, F. Touch Briefings 2007: 47-48

Monnet, X. Yearbook of Intensive Care & Emergency Medicine 2007: 542-548

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The postural change used for performing the PLR test is important

. If PLR is started from the 45° semirecumbent position, the induced increase in central venous pressure is larger than if started from the supine position Because mobilizes blood coming not only from the inferior limbs but also from the large splanchnic compartment.

As a consequence, starting PLR from the semi-recumbent posture is more sensitive than starting from the horizontal posture to detect fluid responsiveness , so that this method should be considered as a standard.

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• A real-time measurement able to track hemodynamic changes in the time frame of PLR effects, i.e., 30–90 s, must be used. Indeed, the increase in cardiac output during PLR is not sustained when the leg elevation is prolonged.

• Effects < 30 sec.. Not more than 4 minutes

This aspect is particularly true in septic patients in whom capillary leak may account for an attenuation of the PLR effects after one minute

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This is why clinical studies that have tested the value of PLR to predict volume responsiveness used real-time hemodynamic measurements, such as

Aortic blood flow measured by esophageal doppler,

Pulse contour analysis-derived cardiac output,

Cardiac output measured by bio reactance or endotrachealbioimpedance cardiography ,

Subaortic blood velocity measured by echocardiography,

Ascending aortic velocity measured by suprasternal doppler

End-tidal carbon dioxide---more recently

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Limitations:

• Its effects cannot be assessed by observing the arterial pressure. Because arterial pulse pressure is only a rough surrogate of stroke volume.

• It needs more direct estimation of cardiac output.

• Not be used when mobilizing the patient is difficult e. G., In the operating room or in the case of head injury

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How to assess the response to volume expansion?Effects of volume expansion on cardiac output

What is expected from fluid administration is a significant increase in cardiac output.

In this regard, it has been recently shown that changes in arterial pressure are relatively imprecise to estimate the effects of fluid infusion on cardiac output

In 228 patients who received a standardized saline infusion, fluid-induced changes in arterial pulse pressure were weakly correlated with the simultaneous changes in cardiac output (r = 0.56). Consequently, the changes in pulse pressure induced by volume expansion detected a positive response to fluid (i. e., an increase in cardiac output ≥ 15 %) with a specificity of 85 % but with a sensitivity of only 65 %; in other words, 20 % of cases were false negatives, meaning that in these patients, fluid administration significantly increased cardiac output whereas the arterial pulse pressure did not change to a large extent

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These results are explained by the fact that arterial pulse pressure is physiologically related to stroke volume but also inversely correlated with arterial compliance , which may differ among patients and may change over time in the same patient.

Moreover, the proportionality between pulse pressure and stroke volume is physiologically expected at the aortic level, but not at the peripheral arterial level because of the pulse wave amplification phenomenon.

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Another important point emphasized by the above cited studies, is that the fluid-induced changes in cardiac output are not reflected at all by the fluid-induced changes in mean arterial pressure (MAP).

Physiologically, the changes in MAP are dissociated from the changes in cardiac output because of the sympathetic modulation of the arterial tone, which tends to maintain MAP constant while cardiac output varies.

These results suggest that precise assessment of the effects of volume expansion should not rely on simple blood pressure measurements but should rather be based on direct measurements of cardiac output.

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The analysis of respiratory variation in stroke volume has received the largest level of evidence, but cannot be used in cases of

1. Spontaneous breathing activity, 2. Cardiac arrhythmias, 3. Low tidal volume or 4. Low lung compliance.

Some more recently developed tests, such as the end-expiratory occlusion test, the ‘mini’ fluid challenge and the PLR test can be used as alternative methods, solving the problem of prediction of volume responsiveness in cases of spontaneous breathing activity and/or cardiac arrhythmias

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Marik et al. Annals of Intensive Care 2011, 1:1

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Key principles of hemodynamic monitoring

• Principle 1: no hemodynamic monitoring technique can improve outcome by itself

• Principle 2: monitoring requirements may vary over time and can depend on local equipment availability and training

• Principle 3: there are no optimal hemodynamic values that are applicable to all patients

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• Principle 4: we need to combine and integrate variables

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Relationship between CO, SvO2 & O2delivery

• O2 delivery CO

• Since O2 extraction by peripheral tissues is independent of

O2 delivery,

CO SvO2

Cardiac Output SvO2

25% extraction in peripheral tissues

100% saturatedArterial blood

75% saturation of venous blood

SvO2 - global index of tissue oxygenation

Principle 5: measurements of SvO2 can be helpful

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Limitations of SvO2

• SvO2 may be normal in presence of tissue hypoxia & anaerobic metabolism Sr. lactate

• SvO2 may be normal in presence of requirement of O2

in tissues if there is maldistribution of blood flow shunts in ESLD

• SvO2 may be normal OR high if tissues are not able to extract O2 from arterial blood ( severe sepsis)

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SvO2 Vs ScvO2

• Though SvO2 is more appropriate guide to early resuscitation of critically ill pts, it is practically not justifiable to place a PAC in all pts for obtaining a blood sample to measure SvO2

• More convenient to measure ScvO2 from central venous blood

• Studies have shown that ScvO2 > SvO2 & hence not a true representative of global tissue oxygenation

• ScvO2 is 5 – 7% > SvO2

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• Principle 6: a high cardiac output and a high SvO2 are not always best

• Principle 7: cardiac output is estimated, not measured

• Principle 8: monitoring hemodynamic changes over short periods of time is important

This assessment of hemodynamic variations observed during the challenge of the cardiovascular system has been termed ‘functional hemodynamic monitoring’. Combining measures of multiple variables and their dynamic interactions in response to time and specific treatments often increases the sensitivity and specificity of these monitoring modalities to identify specific disease processes and quantify whether therapy is effective or not.

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• Principle 9: continuous measurement of all hemodynamic variables is preferable

• Principle 10: non-invasiveness is not the only issue

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MEASURING CARDIAC OUTPUT

The Fick Principle

Invasive methods• Pulmonary artery thermodilution (trans-right-heart thermodilution)• Pulse Pressure (PP) methods

• Calibrated PP – PiCCO, LiDCO• Non-calibrated PP - Statistical analysis of Arterial Pressure — FloTrac / Vigileo• Uncalibrated, pre-estimated demographic data-free — PRAM

Minimally invasive methods• Doppler ultrasound method• Echocardiography• Transcutaneous Doppler: USCOM• Transoesophageal Doppler: TOD

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Non-invasive methods• Pulse Pressure methods

• Non-invasive PP – Sphygmomanometry and Tonometry• Finapres methodology

• Impedance cardiography• Ultrasound dilution method• Electrical Cardiometry• Magnetic Resonance Imaging

MEASURING CARDIAC OUTPUT

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ACCURACY AND PRECISION OF CARDIAC OUTPUT MEASUREMENTS

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Critical Care 2013, 17:208

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Ramsingh et al. Critical Care 2013, 17:208

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Finally……………………..

‘Finally, no monitoring tool, no matter how accurate, by itself

has improved patient outcome’ Michael Pinsky and Didier Payen

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Thank you