By Francisco Baigorri, MD, PhD
Reversible myocardial dysfunction may be much more common in critical illness than has been generally appreciated.1 Moreover, a significant proportion of patients admitted to medical ICUs due to noncardiac illnesses have underlying cardiac abnormalities, which can be detected with surveillance echocardiography at time of admission.2 In this essay I will consider some aspects of this phenomenon to warn about its early recognition and appropriate therapy during hemodynamic resuscitation.
A broad array of conditions associated with tissue inflammation and metabolic stress may be associated with reversible myocardial dysfunction. Such conditions include massive neurologic injury (stroke and cranial trauma), severe acute respiratory failure, anaphylaxis, trauma, postorgan transplant, severe pancreatitis, postcardiac arrest, and a variety of other severe illnesses.1 Reversible myocardial dysfunction also is a key component of the cardiovascular dysfunction of sepsis and septic shock. It may occur in up to 40% of cases of sepsis.3
The pathogenic mechanisms that may underlie this phenomenon are not fully understood. Potential pathogenic mechanisms include the following:1,4
1. direct ischemic injury to the heart (eg, myocardial infarction, chronic myocardial ischemia, postcardiac arrest);
2. free radical injury (eg, myocarditis, reperfusion injury);
3. cytokine-mediated myocardial injury (eg, septic shock, myocarditis) associated with nitric oxide and peroxynitrite generation; and
4. noncytokine-related mediator injury (eg, anaphylaxis-associated leukotriene production) among others.
This dysfunction is frequently associated with an increase in enzyme markers5 and electrocardiographic changes.6 It can worsen the prognosis. Interestingly, it has been shown that the cardiac ejection fraction of nonsurvivors was higher than of survivors of septic shock. In addition, end-diastolic volume was increased in the survivors but was not increased in the nonsurvivors of septic shock. How can we reconcile these apparently contradictory observations? It was put, with commendable clarity, by Walley in a classic essay on this subject some years ago.7 During sepsis, a decrease in systolic contractility results in a shift to the right of the end-systolic pressure/volume relationship and, if not compensated for, would result in a decrease in stroke volume and cardiac output. Compensatory mechanisms must act to account for the more common hyperdynamic circulation of early sepsis.
Three such compensatory mechanisms exist. First, when patients are seen early and are adequately volume resuscitated, an increase in end-diastolic pressure is one mechanism that may help maintain stroke volume and cardiac output. Second, the decrease in afterload of sepsis is also a compensatory response to some extent in that it improves stroke volume and can prevent a decrease in ejection fraction.8 Third, dilation of the diastolic ventricle due to decreased diastolic stiffness is the expected response to the decrease in systolic contractility. When this occurs, stroke volume and cardiac output can be maintained even in the face of relatively low filling pressures. This third compensatory response is associated with improved survival rates.9
Thus, myocardial depression could exist in the absence of depression of cardiac output. On the other hand, if the ventricle cannot increase volume, or volume decreases during diastole, then the ability to generate a stroke volume is impaired at both ends (see Figure 1). Lack of this normal response to decreased systolic contractility accounts for progressively decreasing cardiac output and hypotension and is associated with nonsurvival.9,10
Increased cardiac index and oxygen delivery with a pulmonary arterial occlusion pressure of < 18 mm Hg have been suggested as therapeutic goals for resuscitation and subsequent management.11 A meta-analysis of hemodynamic optimization in high-risk patients suggests that, when implemented early and aggressively, goal-directed therapy reduces mortality and the prevalence of organ failures.11 Rivers and colleagues12 specifically studied whether a goal-directed therapy before admission to the intensive care unit could reduce mortality and multi-organ dysfunction in patients with sepsis and septic shock. They also found that early goal-directed therapy provides significant benefits in terms of outcome in this kind of patients. Interestingly, the monitoring of patients randomly assigned to early goal-directed therapy included a central venous catheter capable of measuring central venous oxygen saturation. Moreover, during the initial 6 hours, these patients more frequently received inotropic support. This makes me think about the possibility that measuring central venous saturation allowed the identification of inappropriate cardiac output in a significant proportion of studied patients and that this could be an important aspect to improve the outcome.
Many methods to noninvasively measure cardiac output are currently available for use in the ICU. These include applications of the Fick principle, Doppler technology, thoracic-electrical bioimpedance, and pulse contour analysis devices (see Table 1).13
Each of the methods in the Table has advantages and disadvantages. The indirect Fick methods are convenient and relatively easy to apply to mechanically ventilated patients but may not be accurate enough for initial diagnostic information in a patient with significant lung disease or multi-organ failure. The esophageal Doppler monitor, although more invasive than others, may be a better alternative for the critically ill patient. The bioimpedance methods tend to lose accuracy in the setting of intrathoracic fluid shifts, which may limit its use in the intensive care setting. The pulse contour devices offer a beat-to-beat measurement of cardiac output and have shown good correlation with pulmonary artery thermodilution during times of stable hemodynamics. These devices should be recalibrated frequently in patients with unstable hemodynamics. Pulse contour devices also allow estimation of intrathoracic blood volume to assess cardiac preload. Provided that the clinician understands the strengths and limitations of each device to effectively use the information derived from them, it would be expected these methods help us in timing decision making in hemodynamic resuscitation.
Simplified treatment algorithms are now being proposed using some of these techniques, for instance, using the analysis of arterial pressure pulse variation in patients with mechanical ventilation14 and aortic flow measured with transesophageal pulsed Doppler.15 However, there is the risk that all these techniques may delay or prolong resuscitation of our patients. In the meantime, the early use of transesophageal echocardiography (when available) and pulmonary artery balloon-tip thermodilution catheter must be considered the gold standard for the evaluation of circulatory function in the ICU patient (see Figure 2).16
To summarize, reversible myocardial dysfunction may occur in cases of critical pathology. The true frequency of this phenomenon in the critically ill appears to be significantly higher than is generally appreciated. It seems to worsen the patient’s prognosis when it occurs, but an early and aggressive goal-directed therapy reduces mortality and the prevalence of organ failures. Many methods to noninvasively measure cardiac output are currently available for use in the ICU. It remains unknown whether these new monitoring techniques may help us in timing decision making in hemodynamic resuscitation and have an effect on patient outcome.
References
1. Ruiz Bailén M. Reversible myocardial dysfunction in critically ill, noncardiac patients: A review. Crit Care Med. 2002;30:1280-1290.
2. Bossone E, et al. Range and prevalence of cardiac abnormalities in patients hospitalized in a medical ICU. Chest. 2002;122:1370-1376.
3. Fernandes CJ, et al. Cardiac troponin: A new serum marker of myocardial injury in sepsis. Intensive Care Med. 1999;25:1165-1168.
4. Kumar A, Parrillo JE. Reversible myocardial dysfunction: A ubiquitous phenomenon in the critically ill? Crit Care Med. 2002;30:1392-1393.
5. Spies C, et al. Serum cardiac troponin T as a prognostic marker in early sepsis. Chest. 1998;113:1055-1063.
6. Sharkey SW, et al. Reversible myocardial contraction abnormalities in patients with an acute noncardiac illness. Chest. 1998;114:98-105.
7. Walley KR. Ventricular Dysfunction During Sepsis. Berlin, Germany: Springer, 1995:505-517.
8. Walley KR, et al Decrease in left ventricular contractility after tumor necrosis factor infusion in dogs. J Appl Physiol. 1994;76:1060-1067.
9. Parker MM, et al. Responses of left ventricular function in survivors and non-survivors of septic shock. J Crit Care. 1989;4:19-25.
10. Parker MM, et al. Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med. 1984;100:483-490.
11. Kern JW, Shoemaker WC. Meta-analysis of hemodynamic optimization in high-risk patients. Crit Care Med. 2002;30:1686-1692.
12. Rivers E, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368-1377.
13. Chaney JC, Derdak S. Minimally invasive hemodynamic monitoring for the intensivist: Current and emerging technology. Crit Care Med. 2002;30: 2338-2345.
14. Baigorri F. Applying heart-lung interactions physiology to assess fluid responsiveness. Crit Care Alert. 2002; 10:16-20.
15. Pinsky MR. Functional hemodynamic monitoring: Applied physiology at the bedside. Berlin, Germany: Springer, 2002;537-552.
16. Boldt J. Clinical review: Hemodynamic monitoring in the intensive care unit. Critical Care. 2002;6:52-59.
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