Université Paris-Sud, Faculté de Médecine, EA4533, Le Kremlin Bicêtre, France.
Hôpitaux Universitaires de Strasbourg, Service de Reanimation Medicale, Strasbourg, France.
Chest. 2013 May;143(5):1343-1350. doi: 10.1378/chest.12-1880.
The mean pulmonary artery pressure (mPAP) replaces mean systolic ejection pressure (msePAP) in the classic formula of right ventricular stroke work (RVSW) = (mPAP - RAP) × stroke volume, where RAP is mean right atrial pressure. Only the steady work is thus taken into account, not the pulsatile work, whereas pulmonary circulation is highly pulsatile. Our retrospective, high-fidelity pressure study tested the hypothesis that msePAP was proportional to mPAP, and looked at the implications for RVSW.
Eleven patients with severe, precapillary pulmonary hypertension (PH) (six patients with idiopathic pulmonary arterial hypertension and five with chronic thromboembolic PH; mPAP = 57 ± 10 mm Hg) were studied at rest and during mild to moderate exercise. Eight non-PH control subjects were also studied at rest (mPAP = 16 ± 2 mm Hg). The msePAP was averaged from end diastole to dicrotic notch.
In the full data set (53 pressure-flow points), mPAP ranged from 14 to 99.5 mm Hg, cardiac output from 2.38 to 11.1 L/min, and heart rate from 53 to 163 beats/min. There was a linear relationship between msePAP and mPAP (r² = 0.99). The msePAP matched 1.25 mPAP (bias, -0.5 ± 2.6 mm Hg). Results were similar in the resting non-PH group and in resting and the exercising PH group. This implies that the classic formula markedly underestimates RVSW and that the pulsatile work may be a variable 20% to 55% fraction of RVSW, depending on RAP and mPAP. At rest, RVSW in patients with PH was twice as high as that of the non-PH group (P < .05), but pulsatile work fraction was similar between the two groups (26 ± 4% vs 24 ± 1%) because of the counterbalancing effects of high RAP (11 ± 5 mm Hg vs 4 ± 2 mm Hg), which increases the fraction, and high mPAP, which decreases the fraction.
Our study favored the use of an improved formula that takes into account the variable pulsatile work fraction: RVSW = (1.25 mPAP - RAP) × stroke volume. Increased RAP and increased mPAP have opposite effects on the pulsatile work fraction.
在右心室射血做功（RVSW）的经典公式中，平均肺动脉压（mPAP）取代了平均收缩期射血压力（msePAP），公式为 RVSW = （mPAP - RAP）× 心搏量，其中 RAP 为平均右心房压力。该公式仅考虑了稳定工作，而没有考虑脉动工作，而肺循环是高度脉动的。我们的回顾性高保真压力研究检验了 msePAP 与 mPAP 成正比的假设，并研究了这对 RVSW 的影响。
11 例严重的毛细血管前肺动脉高压（PH）患者（6 例特发性肺动脉高压和 5 例慢性血栓栓塞性 PH；mPAP = 57 ± 10 mm Hg）在休息和轻度至中度运动时进行了研究。还对 8 例非 PH 对照组在休息时进行了研究（mPAP = 16 ± 2 mm Hg）。msePAP 从舒张末期到二尖峰平均。
在全数据集（53 个压力-流量点）中，mPAP 范围为 14 至 99.5 mm Hg，心输出量为 2.38 至 11.1 L/min，心率为 53 至 163 次/min。msePAP 与 mPAP 呈线性关系（r² = 0.99）。msePAP 与 1.25 mPAP 相匹配（偏差，-0.5 ± 2.6 mm Hg）。在休息时的非 PH 组和休息及运动时的 PH 组中，结果相似。这意味着经典公式明显低估了 RVSW，而脉动功可能是 RVSW 的一个变量，占 20%至 55%，取决于 RAP 和 mPAP。在休息时，PH 患者的 RVSW 是非 PH 组的两倍（P <.05），但两组的脉动功分数相似（26 ± 4%对 24 ± 1%），因为高 RAP（11 ± 5 mm Hg 对 4 ± 2 mm Hg）的平衡作用增加了分数，而高 mPAP 降低了分数。
我们的研究倾向于使用一种改进的公式，该公式考虑了可变的脉动功分数：RVSW = （1.25 mPAP - RAP）× 心搏量。增加 RAP 和增加 mPAP 对脉动功分数有相反的影响。
