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We often treat patients with heart failure in the intensive care unit (ICU) setting, and clearly, severe heart failure carries a very high mortality rate. However, non-fatal heart failure commonly accompanies processes that cause patients to become critically ill. In these cases, heart failure becomes a co-morbidity. Although intuitively obvious that one needs forward blood flow to sustain life, it is not clear to what extent decreased cardiac reserve impairs outcome from acute illness other than acute coronary syndrome. It is important, therefore, to consider the impact that heart failure may have on outcome from critical illness.

Vascular reactivity has a fundamental role in regulating blood flow and tissue oxygen consumption. Vascular tone is regulated by receptors in endothelial and smooth muscle cells which can be stimulated by biochemical signals or a physical stimulus []. Receptor abundance and their response to stimuli is different among the different vascular beds, which enables fine tuning between organ perfusion and oxygen consumption according to different metabolic needs []. Vascular reactivity contributes to maintain the adequacy of tissue perfusion in response to acute injury such as sepsis and trauma []. This compensatory response can redirect regional blood flow towards organs where a decrease in oxygen consumption would have detrimental consequences for the organism such as the brain and the coronary arteries [].

Echocardiography continues to exert an increasing influence in the practice of intensive care medicine. Rapidly and non-invasively obtaining diagnostically accurate pictures of the heart can lead to major management changes when treating critically ill patients. Most intensivists regularly encounter its use, either in receiving a report after the study is performed by someone else, or by personally engaging in the acquisition of the required hemodynamic information. A number of hemodynamic and cardiac function parameters can be measured including cardiac output, pulmonary artery pressure, left atrial pressure, transvalvular pressures, in addition to evaluating the presence of underlying myocardial ischemia. At the very least, an intensivist training today should, from viewing a study, be comfortable in differentiating a well volumed, strongly contracting left ventricle from an underfilled, functionally impaired heart. This chapter is a brief outline of the many applications of echocardiography that are helpful in the intensive care unit.

Optimization of volume status to improve cardiac performance in critically ill and in high risk patients requires adequate preload monitoring. The pulmonary artery catheter (PAC) has been a milestone in the management of the hemodynamically unstable patient in the intensive care unit (ICU) for the last 30 years. Recently, the therapeutic utility of the PAC has been challenged based on studies (whose primary objective was ‘presumed’ to be patient outcome) suggesting an unfavorable balance of risk and benefits [, ]. Kern and Shoemaker in a meta-analysis reviewed 21 randomized controlled trials with various approaches to treatment and revealed statistically significant mortality reductions with hemodynamic optimization when patients with acute critical illness were treated early to achieve optimal goals before the development of organ failure, when there were control group mortalities of more than 20%, and when therapy produced differences in oxygen delivery between the control and protocol group []. However, that paper stressed the timing of treatment and not the technique used for monitoring. Squara and colleagues performed a study to look at the variability of treatment with the PAC and concluded that the problem lies in the users []. Kumar and colleagues in a prospective, nonrandomized, non blinded interventional study demonstrated that neither central venous pressure (CVP) nor pulmonary artery occlusion pressure (PAOP) appeared to be useful predictors of ventricular preload with respect to optimizing cardiac performance .

The use of esophageal Doppler is aimed at monitoring cardiac output by continuously measuring the blood flow in the descending thoracic aorta. Initially, the Doppler technique attempted to measure the blood flow in the part of the vessel. A Doppler probe was positioned on the skin at the level of the supra-sternal notch and manually moved until a correct positive signal was obtained []. Although it provided a reliable estimation of cardiac output [, ], this technique was never widely adopted because it did not allow continuous monitoring and because the position of the supra-sternal probe was unstable [].

Cardiac output is monitored in critically ill patients in the intensive care unit (ICU) and during anesthesia to maintain and improve cardiac function with the primary goal of adequate tissue perfusion. Since the introduction of the pulmonary artery catheter (PAC) into clinical practice in 1970, this invasive technique has been considered to be the gold standard for cardiac output measurement. However, its risk-to-benefit ratio has been increasingly questioned in recent years based on conflicting study results. Connors et al. [] showed that the use of the PAC was associated with a higher mortality in a large series of critically ill medical patients with organ failure. Comparable results were found in patients with myocardial infarction [] and in surgical patients with organ failure []. By contrast, some studies reported no difference in relation to mortality [] or even an improved outcome when a PAC was used . Apart from the inherent potential risk of morbidity in association with the PAC [] differences in outcome observed in these studies may be related to differences in hemodynamic changes between medical and surgical patient groups and the presence or lack of defined treatment concepts based on hemodynamic findings. Several less invasive cardiac output monitoring techniques have been advanced in recent years with the aim of avoiding the risk associated with PAC use. These less-invasive techniques have the potential to replace the current gold standard for a variety of established indications. Furthermore, they may be applied earlier in situations at risk for hemodynamic instability to a larger patient population than the PAC. However, before these alternative techniques can be generally applied, their safe and easy handling, as well as their accuracy in providing hemodynamic data, needs to be demonstrated compared with the PAC.

Cardiac output monitoring is part of routine practice in the critically ill patient. Recently, there has been increasing interest in continuous cardiac output monitoring, which has seen the development of new devices less invasive than the pulmonary artery catheter (PAC). The insertion of a PAC allows semi-continuous monitoring of cardiac output using the thermodilution technique but these new devices allow continuous monitoring by analyzing the arterial pressure wave. This analysis is known as pulse pressure analysis. This chapter explores the issues associated with pulse pressure analysis and presents the mathematical basis for the devices available.

Mechanical ventilation in controlled mode has long been known to induce cyclic changes in systolic blood pressure. This occurrence was first described by Massumi et al. as an increase in systolic blood pressure related to lung inflation, followed by a decrease during expiration, and called “reverse pulsus paradoxus” [] (Fig. 1). These changes stem from cyclic modifications in systemic venous return [] and in right ventricular (RV) afterload [] related to alterations in intrathoracic pressure and in transpulmonary pressure, respectively. Indirectly, this reflects cyclic changes in left ventricular (LV) stroke volume induced by positive-pressure ventilation. Such a phenomenon is always present but is limited in a patient with a normal hemodynamic status. Coyle et al. were probably the first to use these variations to detect hypovolemia []. Using the baseline value of systolic blood pressure observed at end-expiration, they also separated systolic blood pressure variations into two components, delta Up (dUp) and delta Down (dDown) (4) (Fig. 1), the latter being closely correlated with the level of induced hemorrhage in dogs and with fluid responsiveness in septic patients [].

The commonly employed reference techniques for assessment of cardiac output are represented by the direct Fick method in physiology, and by intermittent thermodilution in clinical practice. According to the Fick principle, cardiac output is determined by the ratio of oxygen uptake to the difference in oxygen content between arterial and mixed venous blood []. The validity of the method depends on the assumption that pulmonary blood flow closely approximates systemic blood flow and that lungs themselves do not extract oxygen. The major limitations of the method are the need for right heart catheterization to obtain truly mixed venous blood, the availability of techniques for measuring oxygen uptake and content, and the attainment of a steady state in which oxygen consumption matches tissue oxygen utilization [, ]. Likewise, the intermittent thermodilution method requires fulfillment of several conditions, such as complete mixing of the thermal indicator with blood, no loss of indicator within the dilution volume, and constant blood flow during the dilution time []. Inconsistency of these assumptions may occur in many clinical conditions, leading to inaccuracy in cardiac output measurements. In particular, variability of blood flow may result from hemodynamic instability related to changes in heart rate, cardiac arrhythmias, valvular or congenital heart disease, and application of mechanical ventilation []–[].

Since the first descriptions of haemolytic-uremic syndrome (HUS) by Moschowitz and thrombotic thrombocytopenic purpura (TTP) by Gasser, our knowledge about thrombotic microangiopathy (TMA) has grown considerably []. TMA now refers to a group of diseases comprising mechanical hemolytic anemia, peripheral thrombocytopenia, and varying degrees of organ failure. The incidence of TMA is increasing in the USA. Considerable progress has recently been made in the understanding of the pathophysiological mechanisms of TMA. These rare diseases, characterized by platelet thrombi in the microcirculation, are responsible for often serious organ dysfunction leading to the admission of these patients to intensive care units (ICUs). The prognosis of TMA was extremely poor prior to plasma therapy and especially plasma exchange. TMA is a serious, life-threatening disease that requires early diagnosis and urgent specialized therapeutic management.