Septic shock is almost uniformly associated with an increased cardiac outpu
t and decreased systemic vascular resistance when patients are adequately V
olume resuscitated. Despite the increased cardiac output, septic myocardial
depression is common. Most patients experience biventricular dilatation, a
decrease in ejection fraction, and a depressed Frank-Starling response. In
addition, diastolic compliance abnormalities may be seen. These responses
may be adaptive and can herald a good outcome. The mechanism underlying sep
tic myocardial depression is not myocardial hypoperfusion but rather the di
rect cellular effects of circulating or local mediators, particularly the c
ytokines TNF-alpha and IL-1 beta. These cytokines may depress baseline and
catecholamine stimulated myocardial contractility by a variety of mechanism
s. Nitric oxide generation is one such mechanism.