Single-beat estimation of right ventricular end-systolic pressure-volume relationship
Single-beat estimation of right ventricular end-systolic pressure-volume relationship
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DOI：
10.1152/ajpheart.01023.2002
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发表时间：
2003-05-01
影响因子：
4.8
通讯作者：
Naeije, R
中科院分区：
文献类型：
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作者：
Brimioulle, S;Wauthy, P;Naeije, R
由于测量 RV 瞬时容量的问题以及 RV 前负荷或后负荷变化的影响，从收缩末期压力-容积关系 (ESPVR) 评估右心室 (RV) 收缩力很困难。因此，我们在麻醉犬中研究了是否可以在不测量 RV 体积且不改变 RV 前负荷或后负荷的情况下确定 RV ESPVR 和收缩力。等容搏动的最大右心室压力 (P-max) 是根据射血搏动期间 RV 压力的等容部分预测的，并与肺动脉钳夹后第一次搏动期间测量的 P-max 进行比较。在从右心室压力和综合肺动脉流量获得的右心室压力-容积环中，收缩末期弹性（E-es）被评估为P-max衍生的ESPVR的斜率，肺动脉有效弹性（E-a）被评估为舒张末期与收缩末期关系的斜率，耦合效率被评估为E-es-与E-a比率（E-es/E-a）。预测的 P-max 与观察到的 P-max 相关 (r = 0.98 +/- 0.02)。多巴酚丁胺使 E-es 从 1.07 mmHg/ml 增加至 2.00 mmHg/ml，E-es/E-a 从 1.64 增加至 2.49，普萘洛尔使 E-es/E-a 从 1.64 减少至 0.91（均 P < 0.05）。肾上腺素能阻断后，前负荷减少并不影响 E-es，而缺氧和动脉收缩则显着增加 E-a，并且由于 Anrep 效应而稍微增加 E-es。低预载不影响 E-es/E-a，高后载则降低 E-es/E-a。总之，在右心室中，1) P-max 可以根据正常心搏计算出来，2) P-max 可用于在不改变负荷的情况下确定 ESPVR，3) P-max 衍生的 ESPVR 可用于评估心室收缩力和心室-动脉耦合效率。
Assessment of right ventricular ( RV) contractility from end-systolic pressure-volume relationships (ESPVR) is difficult due to problems in measuring RV instantaneous volume and to effects of changes in RV preload or afterload. We therefore investigated in anesthetized dogs whether RV ESPVR and contractility can be determined without measuring RV volume and without changing RV preload or afterload. The maximal RV pressure of isovolumic beats (P-max) was predicted from isovolumic portions of RV pressure during ejecting beats and compared with P-max measured during the first beat after pulmonary artery clamping. In RV pressure-volume loops obtained from RV pressure and integrated pulmonary arterial flow, end-systolic elastance (E-es) was assessed as the slope of P-max-derived ESPVR, pulmonary artery effective elastance (E-a) as the slope of end-diastolic to end-systolic relation, and coupling efficiency as the E-es-to-E-a ratio (E-es/E-a). Predicted P-max correlated with observed P-max (r = 0.98 +/- 0.02). Dobutamine increased E-es from 1.07 to 2.00 mmHg/ml and E-es/E-a from 1.64 to 2.49, and propranolol decreased E-es/E-a from 1.64 to 0.91 (all P < 0.05). After adrenergic blockade, preload reduction did not affect E-es, whereas hypoxia and arterial constriction markedly increased E-a and somewhat increased E-es due to the Anrep effect. Low preload did not affect E-es/E-a and high afterload decreased E-es/E-a. In conclusion, in the right ventricle 1) P-max can be calculated from normal beats, 2) P-max can be used to determine ESPVR without change in load, and 3) P-max-derived ESPVR can be used to assess ventricular contractility and ventricular-arterial coupling efficiency.