What is the expected hemodynamic change in septic or anaphylactic shock?

In septic or anaphylactic shock, the primary hemodynamic changes include decreased systemic vascular resistance (SVR) and compensatory mechanisms that can lead to increased cardiac output in early stages. However, the confusion arises from how these changes manifest in different types and stages of shock.

In the context of septic shock, there is significant vasodilation due to the release of inflammatory mediators, leading to a decrease in total peripheral resistance. In response to the decreased vascular tone and hypotension, the heart may initially increase its output due to compensatory mechanisms; however, as the shock progresses, myocardial dysfunction can occur, potentially leading to a decrease in cardiac output.

In early septic shock, elevated cardiac output might be seen alongside decreased peripheral vascular resistance, contributing to further hemodynamic instability. However, as the shock state becomes more severe, the cardiac output can drop due to cardiac dysfunction and inadequate preload.

Pulmonary capillary wedge pressure (PCWP) typically remains low or decreases in the context of vasodilation and low venous return, especially when fluid resuscitation is inadequate and there is significant peripheral pooling of blood.

In summary, during septic or anaphylactic shock, there is indeed a drop in cardiac output in cases of