Positive end­ expiratory pressure (PEEP) is used in patients who are mechanically ventilated to prevent the alveoli from continuously opening and closing with each breath. Although this is beneficial from a respiratory mechanics standpoint, PEEP affects cardiac hemodynamic, sometimes in an unpredictable manner. Here are some important points:

PEEP will usually cause cardiac output (CO) to fall by a reduction in stroke volume (SV)

PEEP increases baseline intrathoracic pressure (as the name would imply)

This pressure is in turn, applied to the great vessels and percarium, the entirety of which lie in the thorax and therefore are subject to intrathoracic pressure.

PEEP will shift the Frank­Starling curve to the right, yielding a lower CO for a given

PEEP has two effects on RV afterload: 1.PEEP can afterload reduce the RV by decreasing the pulmonary vascular resistance (PVR) that occurs from hypoxic vasoconstriction. 2.PEEP can increase afterload by increasing lung volumes (which is variable)

LV preload is decreased mostly becuase of the decrease in RV preload

Ventricular interdependence starts to occur with high levels of PEEP (in much the same way as happens in pericardial tamponade)

Unlike the RV, PEEP can decrease LV afterload by increasing the pressure differential between the LVOT and the systemic vasculature.

Therefore: (here is the punch line for cardiologists) in critically ill cardiac patients who have high RA pressure and significant LV systolic dysfunction, CO could rise with PEEP because the failing heart is more sensitive to LV afterload reduction than it is to RV preload reduction. This does not apply in preload sensitive states such as tamponade, constriction and RV dysfunction.

Needless to say this is a very complex issue. For those wanting to dive into this issue more thoroughly (cardiology fellows and anyone interested in critical care), here is a link to the excellent review article I used to help me with this post.

Luecke and Pelosi. Critical Care December 2005 Vol 9 No 6