Abstract
BACKGROUND: The purpose of this article is to examine the systemic circulation and left ventricular (LV) performance by alternative, nonconventional approaches: systemic vascular conductance (G (SV) ) and the head-capacity relation (ie, the relation between LV pressure and cardiac output), respectively; in so doing, we aspired to present a novel and improved interpretation of integrated cardiovascular function. METHODS: In 16 open-chest, anaesthetized pigs, we measured LV pressure (P (LV) ), central aortic pressure (P (Ao) ), and central venous pressure (P (CV) ) and aortic flow (Q (Ao) ). We calculated heart rate (HR), stroke volume, cardiac index (CI = cardiac output/body weight), mean P(LV) ( P¯LV) , and the average arteriovenous pressure difference ( ΔP = P¯Ao - P¯CV ); G (SV) = CI/( P¯Ao - P¯CV ). We studied the effects of changing loading conditions with the administration of phenylephrine (Δ P¯Ao ≥ +25 mm Hg), isoproterenol (ΔHR ∼+25%), sodium nitroprusside (Δ P¯Ao ≥ -25 mm Hg), and proximal aortic constriction (to maximize developed P (LV) and minimize Q (Ao) ). RESULTS: Sodium nitroprusside and isoproterenol increased G (SV) compared with phenylephrine and constriction. A maximum head-capacity curve was derived from pooled data using nonlinear regression on the maximum P¯LV values in Q (Ao) bins 12.5 mL/min/kg wide. The head-capacity relation and the plots of conductance were combined using CI as a common axis, which illustrated that CI is the output of the heart and the input of the circulation. CONCLUSIONS: Thus, at a given CI, G (SV) determines the driving pressure and, thereby, P (Ao) . We also demonstrated how decreases in G (SV) compensate for arterial hypotension by restoring the arteriovenous pressure difference and arterial pressure.