Vasoplegia is considered as a key factor responsible for the death of patients with septic shock, due to persistent and irreversible hypotension. The latter associated with vascular hyporeactivity to vasoconstrictors is a significant independent prognostic factor of mortality in severe sepsis. Loss of control of the vascular tone occurs through the complex, multifactorial mechanism and implicates deeply disrupted balance between vasoconstrictors and vasodilators.
View Article and Find Full Text PDFPatients with septic shock frequently develop myocardial dysfunction evidenced by severely depressed ejection fraction with ventricular dilatation, as measured by an increase in mean systolic and end diastolic ventricular volumes. The pathophysiology of myocardial dysfunction is complex and involves a multitude of factors. The current review describes individual contributing factors and mechanisms such as upregulation of proinflammatory cytokines (IL-1, TNFα, IL-2, IL-6, IFN-γ), reduced myocardial responsiveness to ß-adrenergic stimulation, elevated circulating endothelin levels, Impaired calcium uptake and release from calcium sarcoplasmic reticulum storage, and decreased calcium channel sensitivity, overexpression of inducible NOS and increased production of Nitric oxide.
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