Right ventricular pressure overload during acute lung injury: Cardiac mechanics and the pathophysiology of right ventricular systolic dysfunction

Right ventricular (RV) pressure overload (PO) accompanying acute lung injury is associated with a poor prognosis. To determine if RV ischemia (RVI) is responsible for RV failure (RVF) during acute PO induced by an acute lung injury, a group of eight dogs was studied with the pericardia open after instrumentation with RV, left ventricular (LV), and pulmonary artery (PA) Millar catheters, a PA thermodilution catheter, an aortic fluid-filled catheter, and RV and LV septal-free wall segment length crystals. The animals were studied during baseline, and after infusing glass beads into the right atrium sufficient to first double the PA pressure (PAP), then triple the PAP, and finally to produce RVF (decreased cardiac output with increased RV preload). Transmural RV biopsies were obtained at each phase for adenosine triphosphate and creatine phosphate (CP) assays. To determine the mechanism of RVI, a second group of nine dogs was studied (with the pericardia closed) at baseline, after a doubling of PAP and during RVF. Right ventricular myocardial blood flow was determined by a microsphere technique at each phase and was correlated with the determinants of RV myocardial O₂ demand and supply. In the open pericardia group, RVF, but not doubling or tripling of PAP, was associated with a decrease in CP to 50% of baseline conditions, confirming RVI (4.82 ± 3.67 versus 10.39 ± 3.94 μmol/gm wet weight; P < .005). In the closed pericardia group, RV myocardial blood flow increased in response to myocardial O₂ demands (multiple R = .69 for endocardial and .64 for epicardial flow; P < .05), although the ratio for total RV blood flow to myocardial O₂ demand ratio (planimetered area beneath RV pressure tracing) decreased (4.88 ± 2.76 versus 2.08 ± 2.14; P < .05). In both groups of dogs, RVF was associated with a similar decrease in LV end diastolic segment length or preload (17% in open group and 10% in closed group; P = NS between groups) and stroke work. From these observations, we conclude that after an acute lung injury, RVPO induces RVF because RV myocardial O₂ demand outstrips RV myocardial O₂ supply. Coincidentally with RVF, LV function is depressed on a preload-mediated basis independent of the pericardium, suggesting a dominant “series” interaction between both ventricles. These observations suggest that therapy in patients with acute lung injury is better aimed at increasing RV myocardial blood flow and RV function.