screen-shot-2016-09-09-at-9-37-40-pmIn the figure cited and the preceding dicussions in thread "Pathophysiology of the Circulation" at http://www.tomhsiung.com/wordpress/2016/08/pathophysiology-of-the-circulation/, values of Pms and Pra were expressed relative to atmospheric pressure. However, the transmural pressure of the right atrium exceeds the Pra by the subatmospheric value (about -4 mm Hg) of the Ppl surrounding the heart. Consider the effect of opening the thorax, which raises Ppl from -4 to 0 mm Hg: VR decreases from point A to point B in Figure 31-9 because Pra increases. This is indicated by the interrupted cardiac function curve shifted to the right by the increase in pressure outside the heart but parallel to the normal cardiac function curve (continuous line through point A). Normal VR can be restored (point B to point C) by increasing Pms by an amount equal to the increase in Ppl and Pra induced by thoracotomy. Then transmural Pra will be the same as at point A, and Pra will have increased from point A to point C at the same QT.

This mechanism for the decrease in QT with thoracotomy also partly explains the decrease in QT with PEEP. The Ppl within an intact thorax increases with passive positive-pressure ventilation, thereby increasing Pra and decreasing VR. When 8 mm Hg of PEEP (10 cm H2O) is added to the ventilator, the end-expiratory value of Ppl increases by about half that amount, for example, from -4 to 0 mm Hg. Accordingly, VR decreases with PEEP from point A to pint B in Figure 31-9, with no change in cardiac function or Pms. QT is returned to normal volume infusion or vascular reflexes that increase Pms by an amount equal to the increases in Ppl and Pra. Greater PEEP (20 cm H2O, as in the dotted line shown in Figure 31-8) decreases VR further (from point A to point D) and requires greater increases in Pms to return it to normal (from point D to point E). In one canine study, Pms increases as much as Pra when PEEP is added, so the observed decrease in VR must be due to an increase in RVR with PEEP. In either event, VR can be restored on PEEP by increasing Pms.

QT is much less suceptible to the deleterious effects of PEEP and increased mean intrathoracic pressure when Pms is high. In patients with reduced circulatory volume, vascular reflexes are already operating to maintain VR and Pms by reducing unstressed volume or vascular compliance. Such patients have little vascular reflex reserve and poorly tolerate intubation and positive-pressure ventilation without considerable intravenous infusion to increase vascular stressed volume. In contrast, well-hydrated or overhydrated patients may tolerate even large amounts of PEEP or increased mean intrathoracic pressure from elevated mechanical tidal volumes (VT) with no reduction in QT because their previously inactive vascular reflexes can increase Pms in well-filled systemic vessels by the amount that Ppl increases with PEEP. These considerations allow the physician to anticipate and treat the hypotension induced by ventilator therapy; the concept should not be interpreted as an indication for maintaining high circulatory volume in critical ill patients on ventilators because this often increases lung edema and provides even more QT than was already deemed sufficient. Further, pressure outside the heart can be increased by a variety of other concomitant conditions and complications of critical illness; all these actions increase pressure measured in the heart chambers and decrease heart volume and, as a consequence, are often interpreted as diastolic dysfunction.