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Original Research: Pulmonary Vascular Diseases |

Estimating Right Ventricular Stroke Work and the Pulsatile Work Fraction in Pulmonary HypertensionRight Ventricular Stroke in Pulmonary Hypertension

Denis Chemla, MD, PhD; Vincent Castelain, MD, PhD; Kaixian Zhu, MSc; Yves Papelier, MD; Nicolas Creuzé, MD; Susana Hoette, MD, PhD; Florence Parent, MD; Gérald Simonneau, MD, PhD; Marc Humbert, MD, PhD; Philippe Herve, MD, PhD
Author and Funding Information

From the Université Paris-Sud, Faculté de Médecine (Drs Chemla, and Papelier, and Mr Zhu), EA4533, Le Kremlin Bicêtre, France; Hôpitaux Universitaires de Strasbourg, Service de Reanimation Medicale (Dr Castelain), Strasbourg, France; Radiology Department (Dr Creuzé), Hopital Antoine Béclère, Clamart, France; Pulmonary Division (Dr Hoette), University of Sao Paulo, Sao Paulo, Brazil; AP-HP, Services des Explorations Fonctionnelles et de Pneumologie (Drs Parent, Simonneau, and Humbert), Hôpital Bicêtre, Le Kremlin Bicêtre, France; INSERM UMR_S999, Centre Chirurgical Marie Lannelongue (Dr Herve), Le Plessis-Robinson, France.

Correspondence to: Denis Chemla, MD, PhD, Service des Explorations Fonctionnelles-Broca 7, Hôpital de Bicêtre, 78 rue du Général Leclerc, 94 275 Le Kremlin Bicêtre, France; e-mail: denis.chemla@bct.aphp.fr


Part of this study was presented at the European Respiratory Society 2011 Annual Congress, Sepetember 24-28, 2011, Amsterdam, The Netherlands (abstract 2315).

Funding/Support: The authors have reported to CHEST that no funding was received for this study.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(5):1343-1350. doi:10.1378/chest.12-1880
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Background:  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.

Methods:  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.

Results:  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.

Conclusions:  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.

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