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”!