Pulmonary capillary wedge pressure augments right ventricular pulsatile loading.
Pulmonary capillary wedge pressure augments right ventricular pulsatile loading.
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DOI：
10.1161/circulationaha.111.051540
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发表时间：
2012-01-17
期刊：
影响因子：
37.8
通讯作者：
Kass DA
中科院分区：
文献类型：
--
作者：
Tedford RJ;Hassoun PM;Mathai SC;Girgis RE;Russell SD;Thiemann DR;Cingolani OH;Mudd JO;Borlaug BA;Redfield MM;Lederer DJ;Kass DA
肺血管负荷增加所致的右室衰竭是发病率和死亡率的主要原因，但疾病对右室功能的调节作用尚不清楚。我们验证了这样的假设：与体循环不同，肺血管阻力(RPA)和顺应性(CPA)与年龄、肺动脉高压(PH)或间质纤维化无关，而且这种关系可能会因肺毛细血管楔压(PCWP)的升高而改变，从而增加RV的脉动负荷。分析了几个有右心/肺插管数据的大型临床数据库，以确定RPA-CPA与PH、肺纤维化、患者年龄和不同的PCWP的关系。可疑或确诊的PH患者和正常的PCWP患者表现出一致的RPA-CPA双曲线(反向)依赖关系，CPA=0.564/(0.047+RPA)，阻力顺应性乘积(RC)接近恒定(0.48±0.17秒)。在相同的患者中，系统RC是高度可变的。重度肺纤维化(n=89)不改变RPA-CPA关系。随着患者年龄的增加，这种关系发生了很小的变化，但在统计学上有显著意义。然而，PCWP的升高有更大的影响，显著降低了任何RPA的CPA，并与RC负相关(p<；0.0001)。PH和肺纤维化不能显著改变RPA和CPA之间的双曲线依赖关系，而患者的年龄只有很小的影响。这种固定的关系有助于解释通过对平均RPA影响不大的治疗来减少总RV后负荷的困难。与阻性负荷相比，较高的PCWP似乎通过提高搏动性来增加RV净后负荷，并可能导致RV功能障碍。
Right ventricular (RV) failure from increased pulmonary vascular loading is a major cause of morbidity and mortality, yet its modulation by disease remains poorly understood. We tested the hypotheses that, unlike the systemic circulation, pulmonary vascular resistance (RPA) and compliance (CPA) are consistently and inversely related regardless of age, pulmonary hypertension (PH), or interstitial fibrosis, and that this relation may be changed by elevated pulmonary capillary wedge pressure (PCWP), augmenting RV pulsatile load. Several large clinical databases with right heart/pulmonary catheterization data were analyzed to determine the RPA-CPA relationship with PH, pulmonary fibrosis, patient age, and varying PCWP. Patients with suspected or documented PH (n=1009) and normal PCWP displayed a consistent RPA-CPA hyperbolic (inverse) dependence; CPA=0.564/(0.047+RPA), with a near constant resistance-compliance product (RC) (0.48±0.17 seconds). In the same patients, the systemic RC was highly variable. Severe pulmonary fibrosis (n=89) did not change the RPA-CPA relation. Increasing patient age led to a very small though statistically significant change in the relation. However, elevation of the PCWP (n=8142) had a larger impact, significantly lowering CPA for any RPA, and negatively correlating RC (p<0.0001). PH and pulmonary fibrosis do not significantly change the hyperbolic dependence between RPA and CPA, while patient age has only minimal affects. This fixed relationship helps explain the difficulty of reducing total RV afterload by therapies that have modest impact on mean RPA. Higher PCWP appears to enhance net RV afterload by elevating pulsatile, relative to resistive load, and may contribute to RV dysfunction.