COMPARATIVE HEMODYNAMIC EFFECTS OF INOTROPIC AND VASODILATOR DRUGS IN SEVERE HEART-FAILURE
COMPARATIVE HEMODYNAMIC EFFECTS OF INOTROPIC AND VASODILATOR DRUGS IN SEVERE HEART-FAILURE
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DOI：
10.1161/01.cir.56.4.528
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发表时间：
1977-01-01
期刊：
影响因子：
37.8
通讯作者：
FRANCIOSA, JA
中科院分区：
文献类型：
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作者：
MIKULIC, E;COHN, JN;FRANCIOSA, JA
对12例因缺血性心脏病或非缺血性心肌病所致的严重充血性心力衰竭(CHF)患者进行了静脉滴注血液动力学检查。硝普钠(N)与多巴酚丁胺(D)10微克/公斤/分钟输注进行比较。D组和N组的心输出量(CO)增加相似(分别为2.8-5.8 L/分钟和2.9-5.0 L/分钟)，但与N组相比，D组的动脉压(99.3vs.86.2 mm Hg，P<；0.0 1)和心率(102.5 vs.95.3，P<；0.0 5)明显升高，而肺楔压降低较小(2 8.9~2 0.2 mm Hgvs.2 9.1~16.6 mm Hg，P<；0.0 5)；0.05)。在另外5例患者中，分别研究N和D，然后一起输注。与单独用药相比，联合用药可导致更高的CO、更低的PWP以及更大程度的降低体循环和肺血管阻力。前臂动脉注射硝普钠的剂量为全身剂量的10%时，前臂血管显著扩张，而多巴酚丁胺的血管扩张作用仅在全身剂量的50%时才轻微。强效的正性肌力药物和血管扩张剂药物在心力衰竭时可产生类似的和相加的左心功能增强。多巴酚丁胺降低血管阻力可能主要是由反射引起的，但血管扩张本身可能是心输出量增加的重要决定因素。
In 12 patients with severe congestive heart failure (CHF) due to ischemic heart disease or nonischemic cardiomyopathy the hemodynamic response to i.v. infusion of sodium nitroprusside (N) was compared to that of dobutamine (D) 10 .mu.g/kg per min. D and N produced comparable increases in cardiac output (CO) (2.8-5.8 l/min and 2.9-5.0 l/min, respectively), but compared to N, D caused a higher arterial pressure (99.3 vs. 86.2 mm Hg, P < 0.01) and heart rate (102.5 vs. 95.3, P < 0.05) and less reduction in pulmonary wedge pressure (PWP) (28.9-20.2 mm Hg vs. 29.1-16.6 mm Hg, P < 0.05). In 5 additional patients N and D were studied separately and then were infused together. The combination resulted in a higher CO, lower PWP and greater reduction in systemic and pulmonary vascular resistances than either drug alone. Brachial arterial infusion of nitroprusside produced prominent forearm vasodilation in a dose < 10% of the systemic dose, whereas vasodilation with dobutamine was only modest even when 50% of the systemic dose was infused. Potent inotropic and vasodilator drugs produce similar and additive augmentation of left ventricular performance in heart failure. Reduction in vascular resistance with dobutamine probably is largely of reflex origin, but vasodilation itself may be an important determinant of rise in cardiac output.