Circulation · 1997
Nitric oxide inhalation in the treatment of right ventricular dysfunction following left ventricular assist device implantation.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wagner F, Dandel M, Günther G, Loebe M, Schulze-Neick I, Laucke U, Kuhly R, Weng Y, Hetzer R
Аннотация
BACKGROUND: Following left ventricular assist device (LVAD) implantation in end-stage heart failure, the management of right ventricular dysfunction presents a therapeutic problem unresolved by conventional drug therapy (catecholamines, nitrates, and prostacyclin). This study was performed to investigate the effects of supplemental inhalation of nitric oxide (NO), a selective pulmonary vasodilator, postoperatively and prospectively.
METHODS AND RESULTS: Intraindividual dose titration of NO was performed (0 to 40 ppm) according to a standardized protocol. Thereafter treatment was continued with the individually most effective dose of NO (25 to 40 ppm). In 8 consecutive male patients presenting with right ventricular dysfunction postoperatively, a significant dose-dependent improvement in hemodynamic function was observed: pulmonary vascular resistance decreased from 336+/-110 to 210+/-59 dynes x s x cm(-5) (P<.0001), cardiac index rose from 2.0+/-0.4 to 2.7+/-0.4 L x min(-1) x m(-2) (P<.003) at 40 ppm; doses of >20 ppm were effective in increasing cardiac index (P<.05). With continuous NO inhalation up to 48 hours, pulmonary vascular resistance decreased further to 155+/-33 dynes x s x cm(-5) (P<.0001) as the cardiac index increased to 3.3+/-0.6 L x min(-1) x m(-2) (P<.003). Pulmonary artery pressure decreased (P<.0001) as did systemic vascular resistance with hemodynamic improvement (P<.01). Central venous pressure and mean arterial pressure remained unchanged. Right ventricular ejection fraction at transesophageal echocardiography increased from 24+/-7% to 44+/-7% (P<.01) at the end of the study, and right ventricular end-diastolic volume decreased (P<.05). Weaning from NO therapy was successful at 2 to 8 days, and all patients were extubated. Right ventricular function remained stable thereafter.
CONCLUSIONS: In the treatment of right ventricular dysfunction following LVAD implantation, inhalation of NO markedly decreased right ventricular afterload by its selective vasodilating effects on the pulmonary circulation without producing systemic hypotension; this merits further evaluation.
METHODS AND RESULTS: Intraindividual dose titration of NO was performed (0 to 40 ppm) according to a standardized protocol. Thereafter treatment was continued with the individually most effective dose of NO (25 to 40 ppm). In 8 consecutive male patients presenting with right ventricular dysfunction postoperatively, a significant dose-dependent improvement in hemodynamic function was observed: pulmonary vascular resistance decreased from 336+/-110 to 210+/-59 dynes x s x cm(-5) (P<.0001), cardiac index rose from 2.0+/-0.4 to 2.7+/-0.4 L x min(-1) x m(-2) (P<.003) at 40 ppm; doses of >20 ppm were effective in increasing cardiac index (P<.05). With continuous NO inhalation up to 48 hours, pulmonary vascular resistance decreased further to 155+/-33 dynes x s x cm(-5) (P<.0001) as the cardiac index increased to 3.3+/-0.6 L x min(-1) x m(-2) (P<.003). Pulmonary artery pressure decreased (P<.0001) as did systemic vascular resistance with hemodynamic improvement (P<.01). Central venous pressure and mean arterial pressure remained unchanged. Right ventricular ejection fraction at transesophageal echocardiography increased from 24+/-7% to 44+/-7% (P<.01) at the end of the study, and right ventricular end-diastolic volume decreased (P<.05). Weaning from NO therapy was successful at 2 to 8 days, and all patients were extubated. Right ventricular function remained stable thereafter.
CONCLUSIONS: In the treatment of right ventricular dysfunction following LVAD implantation, inhalation of NO markedly decreased right ventricular afterload by its selective vasodilating effects on the pulmonary circulation without producing systemic hypotension; this merits further evaluation.