Zwissler B
Klinik für Anästhesiologie, Klinikum der Ludwig-Maximilians-Universität München.
Anaesthesist. 2000 Sep;49(9):788-808. doi: 10.1007/s001010070052.
Impaired right ventricular (RV) function may be caused by pulmonary hypertension or myocardial ischemia. It is characterized by a dilation of the RV, which is followed by an increase of wall tension and O2-consumption and a decrease of RV ejection fraction (RV 'dysfunction'). If a drop of arterial pressure occurs this my precipitate RV failure and shock (RV 'insufficiency'). Diagnosis of RV failure and monitoring of RV function is difficult. Sometimes, even a severe impairment of RV function goes undetected or is misinterpreted. Patients in the operating room or on intensive care units seem to be especially prone to RV dysfunction and failure. Since a causative therapy often is not readily available, adequate symptomatic therapy is of utmost importance. Four basic principles have to be considered: 1) Optimizing preload: The failing RV requires adequate filling for preservation of stroke volume. On the other hand, overdistension of the RV may result in RV ischemia, thereby further deteriorating RV function Hence, volume loading is important, but requires continuous monitoring. 2) Maintenance of aortic pressure: Vasopressors are indicated if there is a critical drop of coronary perfusion pressure. Norepinephrine presently is the drug of choice for this purpose. 3) Reduction of RV afterload: Whereas intravenous vasodilators are limited in their efficacy in dilating pulmonary vessels due to systemic side effects, inhaled vasodilators result in selective pulmonary vasodilation and may improve RV function. 4) Increase of RV contractility: In RV failure and shock, norepinephrine and epinephrine are the drugs of choice. Inodilators are well suited for reducing pulmonary vascular resistance due to their positive inotropic and vasodilating effects. Since systemic vasodilation may occur, these drugs must only be used in hemodynamically stable patients.
右心室(RV)功能受损可能由肺动脉高压或心肌缺血引起。其特征是右心室扩张,随后壁张力和氧消耗增加,右心室射血分数降低(右心室“功能障碍”)。如果动脉压下降,这可能会引发右心室衰竭和休克(右心室“功能不全”)。右心室衰竭的诊断和右心室功能的监测很困难。有时,即使右心室功能严重受损也未被发现或被误诊。手术室或重症监护病房的患者似乎特别容易出现右心室功能障碍和衰竭。由于通常难以立即进行病因治疗,充分的对症治疗至关重要。必须考虑四个基本原则:1)优化前负荷:衰竭的右心室需要足够的充盈以维持每搏输出量。另一方面,右心室过度扩张可能导致右心室缺血,从而进一步恶化右心室功能。因此,容量负荷很重要,但需要持续监测。2)维持主动脉压:如果冠状动脉灌注压严重下降,应使用血管升压药。去甲肾上腺素目前是用于此目的的首选药物。3)降低右心室后负荷:静脉血管扩张剂由于全身副作用在扩张肺血管方面的疗效有限,而吸入性血管扩张剂可导致选择性肺血管扩张并可能改善右心室功能。4)增强右心室收缩力:在右心室衰竭和休克中,去甲肾上腺素和肾上腺素是首选药物。由于其正性肌力和血管扩张作用,心肌收缩力增强剂非常适合降低肺血管阻力。由于可能发生全身血管扩张,这些药物仅应在血流动力学稳定的患者中使用。