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    2. “Pressure is not flow” Accurate assessment and monitoring of cardiac function in the intensive care unit (ICU) is essential, as the heart is one of the commonest organs to fail during critical illness. In addition, other failing organs as well as therapies supporting these organs may have an indirect effect on myocardial performance. The need to monitor cardiac function is underlined by the fact that a low flow state carries a higher mortality in certain diseases. As flow cannot be consistently estimated clinically, we often titrate therapies to maintain an acceptable blood pressure. While maintenance of an adequate perfusion pressure to organs is vital, it can be seen from table 1 and equation 1 that blood pressure is affected by cardiac output (CO) and systemic vascular resistance (SVR). Thus a low blood pressure may be secondary to a low CO, low SVR, or both. Conversely a normal blood pressure can exist in the face of decreased CO if SVR is high. A low CO may occur for many reasons including inadequate vascular volume, excessive afterload, poor contractility, myocardial restriction, diastolic dysfunction, valvular stenosis/insufficiency, or an arrhythmia. Accurate assessment and monitoring of cardiac function in the intensive care unit (ICU) is essential, as the heart is one of the commonest organs to fail during critical illness. In addition, other failing organs as well as therapies supporting these organs may have an indirect effect on myocardial performance. The need to monitor cardiac function is underlined by the fact that a low flow state carries a higher mortality in certain diseases. As flow cannot be consistently estimated clinically, we often titrate therapies to maintain an acceptable blood pressure. While maintenance of an adequate perfusion pressure to organs is vital, it can be seen from table 1 and equation 1 that blood pressure is affected by cardiac output (CO) and systemic vascular resistance (SVR). Thus a low blood pressure may be secondary to a low CO, low SVR, or both. Conversely a normal blood pressure can exist in the face of decreased CO if SVR is high. A low CO may occur for many reasons including inadequate vascular volume, excessive afterload, poor contractility, myocardial restriction, diastolic dysfunction, valvular stenosis/insufficiency, or an arrhythmia.

    3. What is cardiac function? Cardiac systolic function is the net product of four interrelated variables: heart rate, preload, contractility, and afterload.8 Quantification of these individual components of cardiac function in the clinical setting poses two major problems. First, the methods used require either invasive (usually ventricular) pressure and volume measurements, or highly specialised echocardiographic techniques. The invasive methods usually entail manipulation of one of the elements while measuring another (for example, altering preload to calculate contractility from either end systolic elastance9 or preload recruitable stroke work), which is impractical in the critically ill patient. Second, all components display a degree of interdependence, thus an apparent deficiency in one element of cardiac function may actually be secondary to a problem with one or more of the other facets. A simple example involves a tachyarrhythmia (heart rate) reducing the time for diastolic ventricular filling (preload). Here preload restoration involves treating the arrhythmia, rather than volume replacement. Early work aimed at quantifying myocardial performance centred on systolic function, however it is now known that diastolic mechanics are also crucial.11 Diastolic function encompasses both the rate and degree of ventricular relaxation, containing active and passive components. Like systolic performance, this parameter is not easily interpreted at the bedside. Cardiac systolic function is the net product of four interrelated variables: heart rate, preload, contractility, and afterload.8 Quantification of these individual components of cardiac function in the clinical setting poses two major problems. First, the methods used require either invasive (usually ventricular) pressure and volume measurements, or highly specialised echocardiographic techniques. The invasive methods usually entail manipulation of one of the elements while measuring another (for example, altering preload to calculate contractility from either end systolic elastance9 or preload recruitable stroke work), which is impractical in the critically ill patient. Second, all components display a degree of interdependence, thus an apparent deficiency in one element of cardiac function may actually be secondary to a problem with one or more of the other facets. A simple example involves a tachyarrhythmia (heart rate) reducing the time for diastolic ventricular filling (preload). Here preload restoration involves treating the arrhythmia, rather than volume replacement. Early work aimed at quantifying myocardial performance centred on systolic function, however it is now known that diastolic mechanics are also crucial.11 Diastolic function encompasses both the rate and degree of ventricular relaxation, containing active and passive components. Like systolic performance, this parameter is not easily interpreted at the bedside.

    4. When to measure cardiac output?

    5. Estimation of CI in infants: Is it possible for the clinician? Estimates of cardiac index were made on ventilated patients in whom objective measurement of cardiac index by femoral artery thermodilution (COLD Z-021, Pulsion Medical Systems, Munich, Germany) was undertaken for clinical reasons. One hundred and twelve estimates of cardiac index were made by 27 clinicians on 36 patients Our results show clinicians’ inaccuracies in estimating cardiac index in children. Futhermore, these inaccuracies appear to be spread across disciplines and levels of seniority. Estimates of cardiac index were made on ventilated patients in whom objective measurement of cardiac index by femoral artery thermodilution (COLD Z-021, Pulsion Medical Systems, Munich, Germany) was undertaken for clinical reasons. One hundred and twelve estimates of cardiac index were made by 27 clinicians on 36 patients Our results show clinicians’ inaccuracies in estimating cardiac index in children. Futhermore, these inaccuracies appear to be spread across disciplines and levels of seniority.

    7. Intensive care physicians‘ insufficient knowledge of right-heart catheterization: time to act? „The proportion of incorrect answers to some basic items was disturbingly high. For instance, [approximately] 50% of the respondents, whether trained or in training, did not correctly identify pulmonary artery occlusion pressure from a clear chart recording.“ Eighty-six European university and nonuniversity intensive care units (ICUs). Subjects: One hundred thirty-four ICUs identified from the directories of two European intensive care medicine societies were asked to participate. Five hundred thirty-five critical care physicians working in 86 ICUs participated.Eighty-six European university and nonuniversity intensive care units (ICUs). Subjects: One hundred thirty-four ICUs identified from the directories of two European intensive care medicine societies were asked to participate. Five hundred thirty-five critical care physicians working in 86 ICUs participated.

    8. How to monitor CO in pediatric patients? Noninvasive Fick using CO2 Bioimpedance Transesophagel Echo (TOE) Transesophageal doppler Pulse contour analysis Clinical observation Dye dilution Pulmonary artery thermodilution Transpulmonary dilution Lithium dilution Mixed venous oxygenation

    9. Focus on Methods of hemodynamic assessment

    10. Transpulmonary Indicator Dilution (PiCCO)

    11. TOE Transgastric view, short axis

    12. TOE Transgastric view, long axis

    13. CO Measurement with TOE

    14. Markers of tissue perfusion

    15. Serum lactate as a predictor of mortality after pediatric cardiac surgery There are several confounding issues in the use of postoperative serum lactate to reflect mortality. We may not simply assume that hyperlactataemia reflects global tissue hypoxia and therefore tissue injury, as hyperlactataemia results from a net imbalance between production and hepatic clearance.10–12 Even if serum lactate were a consistent, accurate reflection of tissue hypoxia, it is limitation of tissue oxygen extraction despite increased oxygen delivery, not decreased oxygen supply per se, that is most closely related to mortality in critical illness.13 Moreover, studies have shown that critical oxygen supply limitation to the hepatosplanchnic circulation may occur at levels of global oxygen delivery which remain adequate for other tissue beds.1 There are several confounding issues in the use of postoperative serum lactate to reflect mortality. We may not simply assume that hyperlactataemia reflects global tissue hypoxia and therefore tissue injury, as hyperlactataemia results from a net imbalance between production and hepatic clearance.10–12 Even if serum lactate were a consistent, accurate reflection of tissue hypoxia, it is limitation of tissue oxygen extraction despite increased oxygen delivery, not decreased oxygen supply per se, that is most closely related to mortality in critical illness.13 Moreover, studies have shown that critical oxygen supply limitation to the hepatosplanchnic circulation may occur at levels of global oxygen delivery which remain adequate for other tissue beds.1

    16. Oxygen Delivery

    17. Oxygen Demand

    18. What affect sVO2 ?

    19. Relative change in CO vs. change in VO2 From the Fick principle (table 1) it can be seen that a low CO or excessive oxygen consumption can be partially compensated by an increase in the arteriovenous oxygen difference. This commonly translates into a fall in mixed venous saturation, as arterial blood is often almost fully saturated and the contribution of dissolved oxygen to total oxygen content is usually minimal. This is an early compensatory mechanism, and may precede a rise in blood lactate. Again, from the Fick equation, it can be seen that, at a constant oxygen consumption and arterial oxygen saturation, the relation between change in mixed venous saturation and CO is not linear, in other words a given decrease in mixed venous saturation may represent a comparatively larger decrease in CO. Mixed venous blood should ideally be taken from the pulmonary artery or the right ventricle43; however, these sites may be inaccessible in the small infant. Right atrial catheters may, in theory selectively sample desaturated coronary venous blood; however, in practice this does not seem to be the case.43 Central venous sites have been advocated, although this is subject to ongoing debate.44 The oxygen saturation of central venous blood from either the superior or inferior vena cavae Mixed venous blood should ideally be taken from the pulmonary artery or the right ventricle43; however, these sites may be inaccessible in the small infant. Right atrial catheters may, in theory selectively sample desaturated coronary venous blood; however, in practice this does not seem to be the case.43 Central venous sites have been advocated, although this is subject to ongoing debate.44 The oxygen saturation of central venous blood from either the superior or inferior vena cavae From the Fick principle (table 1) it can be seen that a low CO or excessive oxygen consumption can be partially compensated by an increase in the arteriovenous oxygen difference. This commonly translates into a fall in mixed venous saturation, as arterial blood is often almost fully saturated and the contribution of dissolved oxygen to total oxygen content is usually minimal. This is an early compensatory mechanism, and may precede a rise in blood lactate. Again, from the Fick equation, it can be seen that, at a constant oxygen consumption and arterial oxygen saturation, the relation between change in mixed venous saturation and CO is not linear, in other words a given decrease in mixed venous saturation may represent a comparatively larger decrease in CO. Mixed venous blood should ideally be taken from the pulmonary artery or the right ventricle43; however, these sites may be inaccessible in the small infant. Right atrial catheters may, in theory selectively sample desaturated coronary venous blood; however, in practice this does not seem to be the case.43 Central venous sites have been advocated, although this is subject to ongoing debate.44 The oxygen saturation of central venous blood from either the superior or inferior vena cavae Mixed venous blood should ideally be taken from the pulmonary artery or the right ventricle43; however, these sites may be inaccessible in the small infant. Right atrial catheters may, in theory selectively sample desaturated coronary venous blood; however, in practice this does not seem to be the case.43 Central venous sites have been advocated, although this is subject to ongoing debate.44 The oxygen saturation of central venous blood from either the superior or inferior vena cavae

    20. Example 1: Shivering

    21. Example 2: Endotrachel Suctioning

    22. Summary

    23. Intrauterine development: Michael Schumacher

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