Which of the following statements about septic shock are true?
- A circulating myocardial depressant factor may account for the cardiac dysfunction sometimes seen with shock due to sepsis or SIRS.
- A cardiac index (CI) of 6 liters per minute per square meter of body surface, a pulmonary capillary wedge pressure of 15 mm. Hg, and a systemic vascular resistance index (SVRI) of 800 dynes-sec/(cm 5-m 2) is a hemodynamic profile consistent with septic sh
- An increase in SvO 2 in septic patients may be explained by the finding of anatomic arteriovenous shunts.
- Results of human trials employing antimediator therapy, such as antiendotoxin antibodies, IL-1 receptor antagonist, and tumor necrosis factor (TNF) antibodies, have confirmed animal studies that demonstrate a significant improvement in survival with the u
A. A circulating myocardial depressant factor may account for the cardiac dysfunction sometimes seen with shock due to sepsis or SIRS.
B. A cardiac index (CI) of 6 liters per minute per square meter of body surface, a pulmonary capillary wedge pressure of 15 mm. Hg, and a systemic vascular resistance index (SVRI) of 800 dynes-sec/(cm 5-m 2) is a hemodynamic profile consistent with septic shock.
DISCUSSION: 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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