True about Septic shock
The hallmark of septic shock is a decrease in peripheral vascular resistance that occurs despite increased levels of vasopressor catecholamines. Before this vasodilatory phase, many patients experience a period during which oxygen delivery to tissues is compromised by myocardial depression, hypovolemia, and other factors. During this "hypodynamic" period, the blood lactate concentration is elevated and central venous oxygen saturation is low. Fluid administration is usually followed by the hyperdynamic, vasodilatory phase during which cardiac output is normal (or even high) and oxygen consumption declines despite adequate oxygen delivery. The blood lactate level may be normal or increased, and normalization of central venous oxygen saturation may reflect either improved oxygen delivery or left-to-right shunting.Prominent hypotensive molecules include nitric oxide, b-endorphin, bradykinin, platelet-activating factor, and prostacyclin.Agents that inhibit the synthesis or action of each of these mediators can prevent or reverse endotoxic shock in animals. However, in clinical trials, neither a platelet-activating factor receptor antagonist nor a bradykinin antagonist improved survival rates among patients with septic shock, and a nitric oxide synthase inhibitor, L-N G -methylarginine HCl, actually increased the moality rate. Remarkably, recent findings indicate that exogenous nitrite can protect mice from challenge with TNF or LPS. Nitrite provides a storage pool from which nitric oxide can be generated in hypoxicand/or acidic conditions. These findings should renew interest in the possibility of exploiting nitric oxide metabolism to improve no survival rates among septic patients. ref:harrison&;s principles of internal medicine,ed 18,pg no 2226
| Cardiac output is initially present
Vascular dilation
Hypotension is a late sign
Widespread endothelial dysfunction
C.V.S