Circulation, Vol 73, 637-644, Copyright © 1986 by American Heart Association
RE Cunnion, GL Schaer, MM Parker, C Natanson and JE Parrillo
Reversible myocardial depression, manifested by ventricular dilatation and
decreased ejection fraction, is common in human septic shock. A proposed
mechanism, based on animal studies, is myocardial ischemia resulting from
inadequate coronary blood flow. Coronary flow observations have not been
reported for human septic shock. To determine whether myocardial depression
in human septic shock is associated with reduced coronary flow,
thermodilution coronary sinus catheters were placed in seven patients with
septic shock for measurements of coronary flow and myocardial metabolism.
Four of the seven patients developed myocardial depression. These patients
had coronary flow similar to or higher than that of control subjects and
similar to that of the other three patients, who did not develop myocardial
depression. None of the patients had net myocardial lactate production. In
general, compared with values in control subjects, the oxygen content
difference (arterial minus coronary sinus) was narrowed, and the fractional
extraction of arterial oxygen was diminished. This pattern of disordered
coronary autoregulation is analogous to the pattern of arteriovenous
shunting in other organs in patients with septic shock. The preservation of
coronary flow, the net myocardial lactate extraction, and the increased
availability of oxygen to the myocardium argue against global ischemia as
the cause of myocardial depression in human septic shock.
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The coronary circulation in human septic shock
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