Goertz A W, Lindner K H, Schütz W, Schirmer U, Beyer M, Georgieff M
Department of Anesthesiology, University of Ulm, Germany.
Anesthesiology. 1994 Jul;81(1):49-58. doi: 10.1097/00000542-199407000-00009.
Left ventricular diastolic function is known to be impaired in patients with coronary artery disease and patients with valvular aortic stenosis. Phenylephrine is frequently administered as an intravenous bolus in these patients perioperatively to increase coronary perfusion pressure. Although this is common practice, there is no information about the effect of phenylephrine bolus administration on left ventricular filling dynamics.
Twenty patients with coronary artery disease (group 1), 15 patients with valvular aortic stenosis (group 2), and 10 subjects without cardiovascular disease (group 3, control) entered the study. Left ventricular filling was evaluated using transesophageal pulsed Doppler echocardiography before and after phenylephrine injection given to patients whose mean blood pressure has decreased by more than 20% (and was not higher than 90 mmHg). We recorded the transmitral blood flow velocity curve and measured peak early and peak atrial flow velocity, acceleration and deceleration time of the early flow velocity peak, and mitral valve diameter. We calculated the ratio of peak early to peak atrial flow velocity (PE/PA), acceleration and deceleration rate of the early flow peak, and peak filling rate.
Phenylephrine effectively restored arterial pressure in all three groups. However, in group 1, phenylephrine administration resulted in a reduction of PE/PA, acceleration rate of the early flow peak, and peak filling rate from 1.25 (mean) to 0.75 (P < 0.001), 411 to 276 cm/s2 (P < 0.001), and 439 to 305 ml/s (P < 0.001), respectively. In contrast, in group 2, intravenous phenylephrine increased PE/PA, acceleration rate of the early flow peak, and peak filling rate from 0.76 to 0.97 (P < 0.001), 365 to 503 cm/s2 (P < 0.05), and 321 to 388 ml/s (P < 0.01), respectively. In the control subjects, phenylephrine caused a transient reduction of PE/PA and peak filling rate from 1.71 to 1.39 (P < 0.001) and 618 to 524 ml.s-1 (P < 0.001), respectively.
Phenylephrine bolus administration causes an alteration of left ventricular filling in coronary artery disease patients that seems to be more marked than that seen in normal subjects. In patients with aortic stenosis no deleterious effects were observed in response to phenylephrine.
已知冠状动脉疾病患者和主动脉瓣狭窄患者存在左心室舒张功能受损。在这些患者围手术期，常静脉推注去氧肾上腺素以增加冠状动脉灌注压。尽管这是常见做法，但关于静脉推注去氧肾上腺素对左心室充盈动力学的影响尚无相关信息。
20例冠状动脉疾病患者（第1组）、15例主动脉瓣狭窄患者（第2组）和10名无心血管疾病的受试者（第3组，对照组）进入本研究。对平均血压下降超过20%（且不高于90 mmHg）的患者，在注射去氧肾上腺素前后，采用经食管脉冲多普勒超声心动图评估左心室充盈情况。我们记录二尖瓣血流速度曲线，测量早期峰值和心房峰值流速、早期流速峰值的加速和减速时间以及二尖瓣直径。我们计算早期峰值与心房峰值流速之比（PE/PA）、早期流速峰值的加速和减速速率以及峰值充盈率。
去氧肾上腺素有效恢复了所有三组患者的动脉压。然而，在第1组中，静脉注射去氧肾上腺素导致PE/PA、早期流速峰值的加速速率和峰值充盈率分别从1.25（平均值）降至0.75（P<0.001）、从411降至276 cm/s²（P<0.001）以及从439降至305 ml/s（P<0.001）。相比之下，在第2组中，静脉注射去氧肾上腺素使PE/PA、早期流速峰值的加速速率和峰值充盈率分别从0.76升至0.97（P<0.001）、从365升至503 cm/s²（P<0.05）以及从321升至388 ml/s（P<0.01）。在对照组受试者中，去氧肾上腺素使PE/PA和峰值充盈率分别从1.71短暂降至1.39（P<0.001）以及从618降至524 ml·s⁻¹（P<0.001）。
静脉推注去氧肾上腺素会导致冠状动脉疾病患者左心室充盈改变，这种改变似乎比正常受试者更为明显。在主动脉瓣狭窄患者中，未观察到去氧肾上腺素产生有害影响。
