In the November 2003 issue of CHEST, Lim and colleagues1suggest that some patients initially presenting with cardiogenic shock actually succumb to a form of distributive shock. The idea of altered gut permeability and bacterial translocation in cardiogenic shock is not new. Brunkhorst et al2 reported patients presenting with cardiogenic shock surviving > 12 h were found to have elevated levels of procalcitonin, neopterin, tumor necrosis factor-α, interleukin-6, and C-reactive protein, suggesting exposure to bacterial endotoxin presumed to be of gut origin. However, evidence for this phenomenon in the patients reported by Lim et al1 is lacking and is not supported by the hemodynamic data. Using data presented in Table 2 of the article by Lim et al,1 stroke volume index and left ventricular stroke work index can be calculated. In addition, interpretation of the hemodynamic data within a “per-beat” rather than traditional “per-minute” framework using stroke systemic vascular resistance index in place of systemic vascular resistance index allows a more accurate assessment of the state of vasoactivity as the cardiac index used in the systemic vascular resistance index equation already includes chronotropic compensation by the heart rate.3The true nature of shock in both the low and normalized cardiac index groups is shown in Table 1
, and they are the same. All patients are hypodynamic (low stroke volume index), hypocontractile (low left ventricular stroke work index), and vasoconstricted (high stroke systemic vascular resistance index), a state compatible with progressive failure of the left ventricular pump. Not surprisingly, the younger normalized cardiac index group was better chronotropically compensated achieving heart rates of 5 to 17% in excess of their older low cardiac index counterparts. Both groups, however, achieved similar percentages of their age-predicted maximum heart rate, suggesting chronotropic competence appropriate for their age (Table 1). Although the difference in heart rate between groups did not reach statistical significance, the difference is clinically significant as elevated heart rate engenders proportional increases in cardiac index given a constant stroke volume index. Other than cardiac index, no other measure of myocardial function was returned to even near normal despite maximal therapy. Thus, it would appear both the low and normalized cardiac index groups represent one group exhibiting a narrow spectrum of hemodynamic derangements within the same clinical entity, cardiogenic shock, and succumb to the so-called downward spiral after all. Any thought to the contrary would be real “hubris”4 indeed.