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Southfield, MI
Dr. Puri is Director of Critical Care Services, Providence Hospital and Medical Center.
Correspondence to: Vinod K. Puri, MD, Director Critical Care Services, Providence Hospital and Medical Center, 16001 West Nine Mile Rd, Southfield, MI 48037-2043; e-mail: vinodpuri{at}providencehospital.org
The oft-repeated adage that we have gained the ability to keep critically ill patients alive longer is valid for the complication of cardiogenic shock. So the next question is, has the disease state changed in the last 40 years? The breathtaking advances in cardiology that have focused on reperfusion of the myocardium after an infarct are supplemented by intensive care to preserve the myocardium. The exhaustive review by Hollenberg and colleagues1 estimated the incidence of cardiogenic shock at 5 to 10% after myocardial infarction, a value that has remained stable in other studies since 1975.2 The reviewers emphasized that myocardial dysfunction due to ischemia worsens the ischemia that creates the "downward spiral."1 The study by Lim and associates in this issue (see page 1885) seems to suggest that the pathophysiology of cardiogenic shock may have changed in some patients. They present a provocative idea that a group of patients who were significantly younger and were kept alive for 4 to 5 days actually may have experienced a distributive form of shock. Their hypothesis is based on data from nine nonsurvivors in whom cardiac index (CI) levels were restored to > 2.2 L/min/m2. These patients had no clinical or bacteriologic evidence of sepsis, including nosocomial infections. In comparison, patients with low CI values died rapidly from either the classic downward spiral or malignant arrhythmias. They speculate from an analysis of a subgroup of patients in the retrospective study about the role of cytokines, tissue mediators, and nitric oxide in cardiogenic shock. These authors, interestingly, do not consider the important role of myocardial stunning or hibernation that contribute to the pathogenesis of cardiogenic shock.1
Some details in the present study are worth pondering. Consider the fact that the authors of the current study restored normal CI levels of 2.5 to 2.7 L/min/m2 with high doses of pressors and inotropes. They also used aortic balloon counterpulsation in almost one third of the patients. A single patient in both groups experienced shock after undergoing cardiopulmonary bypass. The suggestion that a cardiac index of 2.6 L/min/m2, which is barely in the normal range with maximum therapy, represents an inflammatory response may arouse some skepticism. Similarly, values of what the authors call "low systemic vascular resistance" fall within the normal range. Admittedly, these values are lower than those observed in patients who are unable to increase their cardiac output. An astute clinician would consider such a response if the values were associated with a good clearance of lactate. Why would a decrease in systemic vascular resistance to low normal levels be considered pathologic? To quote Kuhn3 from his 1967 article: "It is reasonable to relate the initiation of arterial hypotension to an acute reduction of cardiac output. However, in several instances, the ‘normal’ response to such an acute cardiac output (ie, a compensatory rise of systemic vascular resistance) has not occurred in acute myocardial infarction." On the other hand, high doses of pressors and inotropes have been found to be detrimental to myocardial oxygen consumption and lactate production.4 The work of Mueller et al4 established a long time ago that whole-body oxygen consumption or blood lactate levels might not reflect the true metabolic state of the myocardium. Thus, the change in thinking of the clinicians who, with a great deal of supportive therapy, were able to sustain a subset of cardiogenic shock patients for a few days and then were surprised when the patients died may be real "hubris"!
The authors of the current study have used a relatively new concept that they have developed (ie, the use of a CI/oxygen extraction [O2ER] ratio to document adequacy of oxygen delivery and oxygen consumption). Vincent5 in a previous publication has proposed the use of the CI/O2ER ratio. In cardiogenic shock, a ratio of < 5 has been identified as being indicative of poor outcome. In all likelihood, the low levels of CI mostly determine the low levels of CI/O2ER. In the present study, O2ER values are quite similar in patients with low CI and normalized CI values. One surely would consider the separate contributions of CI and O2ER in this ratio.
Lim and colleagues deserve credit for looking at an old problem and attempting to provide new explanations. They have generated a new hypothesis. We must await further work to delineate the mechanism of death in some patients with cardiogenic shock in whom cardiac output seems to have been restored to normal. Meanwhile, we should heed Kuhn,3 who emphasized that specific hemodynamic derangements may vary considerably among different patients who may present similar clinical appearances.3 What is more remarkable is that he made these observations when data on only 72 patients with cardiogenic shock were available.
References
This article has been cited by other articles:
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  A. Joffe, N. Lim, M.-J. Dubois, D. De Backer, and J.-L. Vincent Cardiogenic Shock: Nothing Has Changed Chest, August 1, 2004; 126(2): 652 - 653. [Full Text] [PDF]
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