High cardiac output & low peripheral resistance shock

(C) Septic shock# SEPTIC SHOCK: An inflammatory stimulus (eg, a bacterial toxin) triggers production of proinflammatory mediators, including I NF and IL-1. These cytokines cause neutrophil-endothelial cell adhesion, activate the clotting mechanism, and generate microthrombi> Initially, arteries and arterioles dilate, decreasing peripheral arterial resistance; cardiac output typically increases. This stage has been referred to as warm shock.> Later, cardiac output may decrease, BP falls (with or without an increase in peripheral resistance), and typical features of shock appear.> With sepsis, patients typically have fever, tachycardia, diaphoresis, and tachypnea; BP remains normal. Other signs of the causative infection may be present.