What is the pathophysiology of cardiovascular dysfunction in sepsis/septic shock?

Updated: Oct 07, 2020
  • Author: Andre Kalil, MD, MPH; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, FAPS, MCCM  more...
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Answer

Significant derangement in the autoregulation of the circulatory system is typical in patients with sepsis. Vasoactive mediators cause vasodilatation and increase the microvascular permeability at the site of infection. NO plays a central role in the vasodilation of septic shock. Impaired secretion of vasopressin may also occur, which may permit the persistence of vasodilatation.

Changes in both systolic and diastolic ventricular performance occur in patients with sepsis. Through the Frank-Starling mechanism, cardiac output is often increased to maintain blood pressure in the presence of systemic vasodilatation. Patients with preexisting cardiac disease are unable to increase their cardiac output appropriately.

Because sepsis interferes with the normal distribution of systemic blood flow to organ systems, core organs may not receive appropriate oxygen delivery. The microcirculation is the key target organ for injury in patients with sepsis. A decrease in the number of functional capillaries leads to an inability to extract oxygen maximally; this inability is caused by intrinsic and extrinsic compression of capillaries and plugging of the capillary lumen by blood cells. Increased endothelial permeability leads to widespread tissue edema involving protein-rich fluid.

Hypotension is caused by the redistribution of intravascular fluid volume that results from reduced arterial vascular tone, diminished venous return from venous dilation, and release of myocardial depressant substances.


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