The Hemodynamic Effects of Hypoxemia in Anesthetized Pigs

UNLABELLED During hypoxemia, hypoxic pulmonary vasoconstriction and tachycardia are often observed in association with increases in pulmonary artery pressure and cardiac output. Nevertheless, the hemodynamic consequences of hypoxemia have never been evaluated by echocardiography and simultaneously compared with invasive hemodynamic variables. Fourteen open-chest, anesthetized piglets (weight 29-36 kg) were submitted to progressive hypoxemia and reoxygenation. Usual invasive hemodynamic variables were obtained from peripheral and central heart catheters. Direct epicardial echocardiography was used to measure right and left ventricular areas on a short-axis view at mid-papillary level. The mean pulmonary artery pressure (MPAP) increased with pulmonary vascular resistance in a dose-related manner as the fraction of inspired oxygen (FIO2) declined from 0.5 to 0.12. The MPAP correlated with right ventricular end-diastolic area (RVEDA) only at FIO2 0.08. There was a 49% reduction in left ventricular end systolic wall stress (LVESWS) between FIO2 0.5 and 0.08. Left ventricular ejection fraction area (LVEFA) increased by 33% above baseline and correlated with the decrease in LVESWS. No correlation was observed between left ventricular end-diastolic area and pulmonary artery occlusion pressure or left atrial pressure and between cardiac output and LVEFA. Systemic vascular resistance underestimates the magnitude of changes in LVESWS but overestimates the afterload compared with LVESWS. This study demonstrates that, for the lowest FIO2 (0.08), changes in MPAP correlated with changes in RVEDA but not in pulmonary vascular resistance. Moreover, LVESWS decreases significantly in a dose-related manner under progressive hypoxemia and normalizes immediately after reoxygenation. This study also shows that, under hypoxemic conditions, echocardiography enhances understanding of hemodynamic changes compared with right heart catheterization alone. IMPLICATIONS Acute hypoxemia in pigs is responsible for pulmonary vasoconstriction-induced pulmonary hypertension (which is restricted by the right ventricular failure), as well as a PaO2-dependent decrease in left ventricular afterload. These changes are better displayed by echocardiography than by right heart catheter.