The coronary circulation in human septic shock.
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TLDR
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.Abstract:
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.read more
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Pathogenetic Mechanisms of Septic Shock
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TL;DR: With a canine model of septic shock that is very similar to human sepsis, myocardial depression was confirmed using load-independent measures of ventricular performance and Pharmacologic or immunologic antagonism of endotoxin or other mediators may prove to enhance survival in this highly lethal syndrome.
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Endotoxin and tumor necrosis factor challenges in dogs simulate the cardiovascular profile of human septic shock.
Charles Natanson,P. W. Eichenholz,Robert L. Danner,Peter Q. Eichacker,W. D. Hoffman,G. C. Kuo,Steven M. Banks,Thomas J. MacVittie,Joseph E. Parrillo +8 more
TL;DR: The hypothesis that the action of endogenous mediators (TNF) responding to bacterial products (endotoxin) is the common pathway that produces the serial cardiovascular changes found in septic shock is supported.
References
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Profound but Reversible Myocardial Depression in Patients with Septic Shock
Margaret M. Parker,James H. Shelhamer,Stephen L. Bacharach,Michael V. Green,Charles Natanson,Terri M. Frederick,Barbara A. Damske,Joseph E. Parrillo +7 more
TL;DR: To characterize the role of cardiac function in septic shock, serial radionuclide cineangiographic and hemodynamic evaluations were done on 20 patients with documented septicShock, finding that nonsurvivors had normal initial ejection fractions and ventricular volumes that did not change during serial studies.
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Measurement of Coronary Sinus Blood Flow by Continuous Thermodilution in Man
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A circulating myocardial depressant substance in humans with septic shock. Septic shock patients with a reduced ejection fraction have a circulating factor that depresses in vitro myocardial cell performance.
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TL;DR: The quantitative and temporal correlation between the decreased left ventricular EF and this serum myocardial depressant substance argues for a pathophysiologic role for this depressant substances in producing the reversible cardiomyopathy seen during septic shock in humans.
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