Answer: ABDISCUSSION: Shock due to sepsis or SIRS frequently manifests as a hyperdynamic cardiovascular response, consisting of an elevated CI and a decreased SVR or SVRI. Occasionally, myocardial depression may be seen, characterized by increased ventricular volumes and decreased ejection fractions. A circulating myocardial depressant factor, possibly TNF, may be responsible for the cardiac dysfunction in such instances. The cause of the increased SvO 2 frequently observed in septic patients is unclear, but it may be secondary to bioenergetic failure, metabolic downregulation, or microcirculatory maldistribution leading to physiologic shunting. True anatomic arteriovenous shunting has not been demonstrated in humans in septic shock. Treatment of septic shock consists of appropriate antibiotic use and supportive therapy. Experimental antimediator therapies have not been encouraging thus far in human clinical trials, despite the promising results from many animal studies.
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Surgery MCQs
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