Acute respiratory failure is followed by decreased left ventricular performance probably due to the right ventricle dilatation induced by pulmonary hypertension and intraventricular septal shift to the left. An anacrotic notch on the upstroke slope of the carotid curve was detected in 22 of 36 hemodynamic studies with simultaneous ECG, PCG and external pulse carotid curve recording in 7 burned patients with acute respiratory failure. Comparing the values (x +/- SEM) obtained in group with notch and in group without notch, PAPs, PAPm, PVRI were higher (56 +/- 2.30 mmHg; 32 +/- 0.99 mm Hg; 543 +/- 56.8 dyn x s/cm5/m2 versus 32 +/- 1.08 mm Hg; 20 +/- 0.9 mm Hg; 173 +/- 14.7 dyn x s/cm5/m2) and CI and LVSWI were lower (2.6 +/- 0.17 l/min/m2; 25.8 +/- 2.41 g x m/m2; versus 3.8 +/- 0.26 l/min/m2; 38.3 +/- 2.82 g x m/m2) in group with notch. As it is shown by 11 paired measurements where the notch disappeared immediately after starting vasodilator therapy PAPs, PAPm, PVRI decreased (from 54 +/- 3.1, 35 +/- 0.8 mm Hg, 498 +/- 64.1 dyn x s/cm5/m2 to 35 +/- 0.8, 21 +/- 1.1 mmHg, 189 +/- 18.4 dyn x s/cm5/m2 respectively) and heart performance improved. Since the left ventricle contractility (characterized by EF, PCWP, ICT) was normal in both groups, our findings suggest that critically high PAPs values (over 40 mmHg) cause a septal bulging at the beginning of the systole which in turn narrows the left ventricle outflow tract. Regarding to the clinical importance of the deteriorated biventricular function at the critically high PAPs evidenced by notch phenomenon on carotid curve but measurable only by indwelling pulmonary arterial catheterization always being a source of infection, the noninvasive parameters as independent variables were entered into canonical discriminant analysis. The ratio of the correctly classified cases was 89%.

译文

急性呼吸衰竭后,左心室性能下降,可能是由于肺动脉高压和室间隔向左移位引起的右心室扩张。在36项血流动力学研究中,有22项同时记录了7例急性呼吸衰竭烧伤患者的ECG,PCG和外脉冲颈动脉曲线,在颈动脉曲线的上冲程斜率上检测到一个明显缺口。比较notch组和无notch组的值 (x/- SEM),PAPm,PVRI较高 (56/- 2.30 mmHg; 32/-0.99毫米Hg; 543 +/- 56.8 dyn x s/cm5/m2与32 +/-1.08毫米Hg; 20 +/-0.9毫米Hg; 173 +/- 14.7 dyn x s/cm5/m2) 和CI和LVSWI较低 (2.6 +/- 0.17 l/min/m2; 25.8/- 2.41g x m/m2; 与3.8/- 0.26 l/min/m2相比; 38.3/- 2.82g x m/m2)。如11对测量结果所示,在开始血管扩张治疗后,PAPs、PAPm、PVRI立即消失 (从54 +/- 3.1、35 +/-0.8毫米Hg、498 +/- 64.1 dyn x s/cm5/m2降至35 +/- 0.8,分别为21/- 1.1 mmHg,189/- 18.4 dyn x s/cm5/m2) 和心脏性能得到改善。由于两组的左心室收缩力 (以EF,PCWP,ICT为特征) 均正常,因此我们的发现表明,极高的PAPs值 (超过40 mmHg) 会导致收缩期开始时间隔膨胀,从而使左心室变窄流出道。关于在颈动脉曲线上的notch现象证明但仅通过留置肺动脉导管才能测量的临界高PAPs上的双心室功能恶化的临床重要性始终是一个传染源,将非侵入性参数作为独立变量输入到典型判别分析中。正确分类的病例比例为89%。

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