Martins S, do Rosário L, Soares R M, Sequeira A, Sousa M J, Sousa L, Oliveira M, Ferreira R, Branco L, Ferreira L, Ramos S, Antunes A M
Serviço de Cardiologia, Hospital de Santa Marta., Lisboa.
Rev Port Cardiol. 1998 Jun;17(6):515-22.
To assess the influence of inotropic IV therapy--dobutamine and/or dopamine--versus vasodilator therapy--nitroprusside, captopril or hydralazine--in aortic flow ejection phase indexes obtained by pulsed Doppler echocardiography.
In 17 patients admitted to the ICU (11 males, 62 +/- 14 years, 9 with ischemic cardiomyopathy and 8 with dilated cardiomyopathy, all in sinus rhythm), with congestive heart failure, and submitted to tailored therapy, 53 serial pulsed Doppler and hemodynamic evaluations were made as the therapy changed the hemodynamic and clinical status. Considering serial consecutive evaluations, a hemodynamic improvement was obtained only with inotropics in 13 (group A), and with vasodilators in only 15 (group B). The following ejection phase indexes were calculated from Doppler registers: average acceleration (AvAc) and ejection force (EFor), calculated according to the formula: Efor = 1.06 x Aortic Orifice Area x AvAc x Acceleration Velocity Time Integral.
Arterial blood pressure increased in gr A (76.2 +/- 14.1 to 81.4 +/- 14.8 mm Hg, p < 0.05) and decreased in gr B (85.1 +/- 12.6 to 76.2 +/- 9.7 mm Hg (p < 0.05). In both groups there was a significant (p < 0.05) increase in cardiac output (CO)-from 3.9 +/- 1.1 to 4.9 +/- 1.4 L/min in group A, and from 3.9 +/- 1.2 to 4.4 +/- 1.2 L/min in group B. CO increased 18.7% in group A and 13.8% in group B (NS). There was a decrease in pulmonary capillary wedge pressure (PCWP) from 19.5 +/- 6.0 to 15.1 +/- 5.8 mm Hg in group A (p < 0.05), and from (16.9 +/- 5.7 to 12.1 +/- 4.6 mm Hg in group B (p < 0.05). PCWP decreased 19.7% in group A and 27.8% in group B (NS). Systemic vascular resistance (SVR) changed from 18.2 +/- 7.0 to 16.2 +/- 7.1 Wood U in group A (p < 0.05), and from 22.3 +/- 9.3 to 17.7 +/- 5.7 Wood U in group B (p < 0.05). In group A, AvAc increased-from 1347 +/- 611 cm.s-2 (p < 0.05), as did Efor-from 15.4 +/- 10.7 to 20.2 +/- 11.0 g.cm,s-2 (p < 0.05), whereas in group B there was no significant change in either AvAc-from 1337 +/- 284 to 1277 +/- 256 cm.s-2, or Efor-from 22.7 +/- 17.0 to 23.8 +/- 15.0 g.cm.s-2.
Vasodilator therapy, although inducing hemodynamic changes similar to inotropics, does not alter the ejection phase indexes. Therefore, AvAc and Efor, in spite of being calculated from the aortic flow, are independent of the changes in PCWP and SVR and seem to reflect changes in inotropism in the clinical setting.
评估正性肌力静脉治疗(多巴酚丁胺和/或多巴胺)与血管扩张剂治疗(硝普钠、卡托普利或肼屈嗪)对经脉冲多普勒超声心动图获得的主动脉血流射血期指标的影响。
17例入住重症监护病房的患者(11例男性,62±14岁,9例缺血性心肌病,8例扩张型心肌病,均为窦性心律),患有充血性心力衰竭,并接受了针对性治疗,随着治疗改变血流动力学和临床状态,进行了53次连续的脉冲多普勒和血流动力学评估。考虑连续评估,仅使用正性肌力药物时13例患者血流动力学得到改善(A组),仅使用血管扩张剂时15例患者血流动力学得到改善(B组)。根据多普勒记录计算以下射血期指标:平均加速度(AvAc)和射血力(EFor),根据公式计算:Efor = 1.06×主动脉口面积×AvAc×加速度速度时间积分。
A组动脉血压升高(从76.2±14.1 mmHg升至81.4±14.8 mmHg,p<0.05),B组动脉血压降低(从85.1±12.6 mmHg降至76.2±9.7 mmHg,p<0.05)。两组心输出量(CO)均显著增加(p<0.05)——A组从3.9±1.1 L/min增至4.9±1.4 L/min,B组从3.9±1.2 L/min增至4.4±1.2 L/min。A组CO增加18.7%,B组增加13.8%(无显著性差异)。A组肺毛细血管楔压(PCWP)从19.5±6.0 mmHg降至15.1±5.8 mmHg(p<0.05),B组从(16.9±5.7 mmHg降至12.1±4.6 mmHg(p<0.05)。A组PCWP降低19.7%,B组降低27.8%(无显著性差异)。A组全身血管阻力(SVR)从18.2±7.0 Wood U变为16.2±7.1 Wood U(p<0.05),B组从22.3±9.3 Wood U变为17.7±5.7 Wood U(p<0.05)。在A组中,AvAc增加——从1347±611 cm·s⁻²(p<0.05),EFor也增加——从15.4±10.7变为20.2±11.0 g·cm·s⁻²(p<0.05),而在B组中,AvAc从1337±284变为1277±256 cm·s⁻²,EFor从22.7±17.0变为23.8±15.0 g·cm·s⁻²,均无显著变化。
血管扩张剂治疗虽然诱导出与正性肌力药物相似的血流动力学变化,但并未改变射血期指标。因此,尽管AvAc和EFor是根据主动脉血流计算得出的,但它们独立于PCWP和SVR的变化,似乎反映了临床环境中变力性的变化。