Abstract

Summary The hemodynamic consequences of acute obstruction of the pulmonary arterial tree result from physiologic changes in the pulmonary circulation. Normal mean pulmonary arterial pressure, about 12 to 15 mm Hg, is one-sixth to one-eighth the systemic pressure. Acute reduction in pulmonary vascular cross-sectional area creates a sudden increase in output load on the right heart chambers resulting in right heart failure. In the absence of preexisting cardiovascular disease, right ventricular decompensation sets in at a mean pressure in the pulmonary artery of approximately 40 mm Hg. At this point, performance of the thin-walled right ventricle deteriorates dramatically. Support of the pulmonary circulation begins with volume resuscitation and inotropic support for the right ventricle. Right coronary perfusion should also be optimized through support of aortic root pressure. Afterload stress to the right ventricle may be reduced with oxygen therapy. There are no other reliable selective pulmonary vasodilators available at this time. The impact of pulmonary embolization and therapy supportive of right ventricular function have recently been studied through assessment of incremental resistance in pulmonary vascular pressure flow curves. The utility of agents such as norepinephrine was confirmed in this model that revealed improved right ventricular function without deterioration in pulmonary vascular bed response. More recent studies utilizing thrombolytic therapy also suggest improved response of the right ventricle and pulmonary vascular bed with immediate administration following pulmonary embolic events. Finally, there are few data describing the utility of different anesthetic regimens in the management of patients during acute cardiopulmonary compromise secondary to pulmonary thromboembolism. Based on the limited data available, a narcotic technique with supplementation using nitrous oxide in inspired concentrations that allows adequate oxygenation can be recommended.

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