pulmonary wedge pressure falls before 12

This motion allows for maximal chamber enlargement in the concentric LV. Normally, LV end-diastolic pressure (LVEDP) is greater than RVEDP, allowing the IVS to move toward the RV during diastole. The RV and LV share a common septum, and changes in pressures of one ventricle can be transmitted across the septum and affect the compliance of the other ventricle. In contrast, the pulmonary circulation has relatively low vascular tone, making it difficult to acutely increase or decrease PVR. A variety of vasoactive drugs can also be used to sharply increase or decrease systemic vascular tone. In the systemic circulation, muscularized resistor vessels allow for marked alterations in SVR via sympathetic stimulation or the release of endogenous catecholamines or vasodilators such as nitric oxide (NO) and prostaglandins. The difference between the 2 circulations is the relatively low degree of vascular motor tone in the proximal pulmonary vascular bed, and the ability of the lung to recruit partially collapsed or unused vessels as CO increases. In the systemic circulation, increased CO during exercise is associated with an increase in MAP. Despite a rise in CO during heavy exertion that may be 4-fold above baseline, PAP increases minimally and PVR falls. In the healthy adult, PVR is remarkably low, considering the drop in pressure across the pulmonary circulation is less than a tenth of that across the systemic circulation [MAP (90 mm Hg) − CVP (5 mm Hg) = 85 mm Hg, where MAP = mean systemic arterial pressure and CVP = central venous pressure. This is unfortunate because the pulmonary and systemic circulations are connected in series, and despite its smaller size, nearly the entire circulation must pass through the right heart and pulmonary vasculature before it reaches the systemic circulation.Īlthough the CO generated by the RV and LV is essentially the same, the vascular bed they pump it through is considerably different. 1–3 Whereas a considerable number of studies have examined left ventricular (LV) and systemic circulatory responses to sepsis, 4–6 relatively little attention has been directed at the RV and pulmonary circulation. As a group, these patients have a poor prognosis, with intensive care unit (ICU) mortality rates between 30% and 41%. As a result, the management of critically ill PAH patients can be extremely challenging.

Unfortunately for patients who suffer from pulmonary arterial hypertension (PAH), the ability to acutely increase CO may be severely limited, and significant pulmonary hypertension (PH) in the setting of acute illness can lead to rapid deterioration of right ventricular (RV) function, hemodynamic instability, and death. The inflammatory response to sepsis results in increased vascular permeability and vasodilation, leading to decreased intravascular volume and a fall in systemic vascular resistance (SVR) that must be compensated for by an increase in cardiac output (CO).

Pulmonary wedge pressure falls before 12