Reversible biventricular dysfunction secondary to ischemia in a patient with acute airway obstruction: a case report and review of the literature on reversible causes of acute ventricular dysfunction.

Reversible causes of acute myocardial dysfunction are important for clinicians to recognize. Reversible biventricular dysfunction secondary to myocardial ischemia is presented in a patient with acute upper airway obstruction. The differential diagnosis of reversible acute myocardial dysfunction is reviewed.

A re-evaluation of the hemodynamic consequences of intermittent positive pressure ventilation.

The hemodynamic effects of intermittent positive pressure ventilation (IPPV) have generally been considered straightforward, being dominated by the inspiratory reduction in systemic venous return. Paradoxically, there is considerable debate regarding the effects of PEEP. We have studied both right ventricular (RV) and left ventricular (LV) performance during a single IPPV respiratory cycle in dogs with intact circulatory systems or the right heart bypassed in open and closed chest conditions. We have found that the "reverse pulsus paradoxus" during inspiration reflects both transmission of the increased intrathoracic pressure to the thoracic aorta and an increase in LV stroke volume (SV). This inspiratory increase in LVSV has been found to be influenced by, but not dependent on: (a) respiratory variations in RVSV; (b) variations in functional residual capacity or tidal volume altering pulmonary venous return and the degree of physical compression of the heart by the lungs; (c) an inspiratory decrease in RV volume, increasing LV diastolic compliance and, thus, probably improving pulmonary venous return; (d) a decreased transmural aortic diastole pressure reflecting an effective decrease in LV afterload produced by both the general increase in intrathoracic pressure and the direct compression of the heart; and (e) variations in the pulmonary vascular volume as indicated by changes in the transmural LV end-diastolic pressure. An understanding of IPPV during a single respiratory cycle facilitates an appreciation of the steady state hemodynamic effects of IPPV with or without PEEP. Our results imply that measurements made only at end-expiration, ignoring inspiratory events, may have serious limitations. Furthermore, they suggest that IPPV with PEEP should be evaluated as a form of LV assist in LV failure.

The effects of positive end-expiratory pressure on right and left ventricular performance.

The cardiovascular effects of positive end-expiratory pressure (PEEP) were studied in mechanically ventilated, vagotomized, Beta-blocked, anesthetized dogs. To compensate for the effect of PEEP on decreasing systemic venous return, acute plasma volume expansion was accomplished returning stroke volume and cardiac output to control values. Left and right ventricular filling pressures (LVFP and RVFP) and aortic pressure were measured relative to pressure (transmural pressure). Ventricular performance was assessed by comparing the transmural ventricular filling pressures at similar stroke volumes. Studies were performed on individual dogs with increasing LVFP produced by Beta-blockade, volume expansion, and obstruction of the descending thoracic aorta. Utilizing these methods we observed that for a given cardiac output, transmural LVFP was higher on PEEP compared to a control state with both normal and elevated control LVFP. On the right side, for a given cardiac output, RVFP was elevated only when the control LVFP was elevated. Our results suggest a nonneuronal adverse effect of PEEP on both left and right ventricular performance. This effect is probably due to mechanical heart-lung interaction since left ventricular (LV) dp/dt showed no change.