Published in:
01-06-2006 | Seminal Study in Intensive Care
Septic shock: a heart story since the 1960s
Published in: Intensive Care Medicine | Issue 6/2006
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Before the advent of pulmonary arterial catheter two distinct clinical profiles of septic shock had been described [1, 2]. One was characterized by warm, dry skin and a bounding pulse despite hypotension (“warm” shock) and the other by cold skin (“cold” shock). Authors were under the impression that “warm” shock was seen in the initial phase of hospitalization in septic shock patients while “cold” shock was more often observed later, before patients died. Invasive measurements were available in few patients showing that “warm” shock was associated with high cardiac output (CO) and “cold” shock with a low CO (Fig. 1a). It was then concluded that patients in septic shock initially went through an early hyperdynamic phase after the onset of illness and eventually either recovered or deteriorated into heart failure or myocardial depression related to sepsis leading to hypodynamic shock and death [3]. The latter concept was supported by animal models designed by Weil (Fig. 2) using intravenous bolus injections of high doses of endotoxin or live organisms [4, 5] (Fig. 1b), showing septic shock characterized by reduced CO and elevated systemic vascular resistance (SVR) leading to animal death (Fig. 1b).
Fig. 1
General hemodynamic in septic shock as viewed before the advent of pulmonary arterial catheter. a Description in 1967 of a case of a hyperdynamic or “warm” shock (high cardiac index, CI; hypotension) and a case of hypodynamic or “cold” shock (low CI, hypotension). (From [1] with permission) b Experimental model supporting the “cold” shock model. (From [4] with permission) c First description showing that normal or elevated CI is present predominantly in septic shock patients. This view was fully adopted after the widespread of pulmonary artery catheters with thermodilution capacity. (Adapted from [7])
Fig. 2
Photograph of M.H. Weil
Fig. 3
Photograph of J.E. Parrillo
Fig. 4
Sepsis-induced cardiac dysfunction in septic shock. a Time-course of left ventricular ejection fraction (LVEF) in dogs implanted with a viable Escherichia coli clot into the peritoneum [15]. b Dose-response curve of LVEF after septic inoculation with increasing inoculum of alive bacteria (surv) or dead bacteria (dead) [16]. c Left and right ventricular ejection fraction in survivors (LV/S, RV/S, respectively) and in nonsurvivors (LV/NS and RV/NS, respectively) from septic shock (adapted from [19]). d Left and right ventricular end diastolic volume index in survivors (LV/S and RV/S, respectively) and in nonsurvivors (LV/NS, and RV/NS, respectively) patients before and after treatment of septic shock (adapted from [28]). Clinical data confirm that sepsis-induced cardiac dysfunction is reversible with time
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