Abstract
BackgroundPure oxygen breathing (hyperoxia) may improve hemodynamics in patients with pulmonary hypertension (PH) and allows to calculate right-to-left shunt fraction (Qs/Qt), whereas breathing normobaric hypoxia may accelerate hypoxic pulmonary vasoconstriction (HPV). This study investigates how hyperoxia and hypoxia affect mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance (PVR) in patients with PH and whether Qs/Qt influences the changes of mPAP and PVR.Study Design and MethodsAdults with pulmonary arterial or chronic thromboembolic PH (PAH/CTEPH) underwent repetitive hemodynamic and blood gas measurements during right heart catheterization (RHC) under normoxia [fractions of inspiratory oxygen (FiO2) 0.21], hypoxia (FiO2 0.15), and hyperoxia (FiO2 1.0) for at least 10 min.ResultsWe included 149 patients (79/70 PAH/CTEPH, 59% women, mean ± SD 60 ± 17 years). Multivariable regressions (mean change, CI) showed that hypoxia did not affect mPAP and cardiac index, but increased PVR [0.4 (0.1–0.7) WU, p = 0.021] due to decreased pulmonary artery wedge pressure [−0.54 (−0.92 to −0.162), p = 0.005]. Hyperoxia significantly decreased mPAP [−4.4 (−5.5 to −3.3) mmHg, p < 0.001] and PVR [−0.4 (−0.7 to −0.1) WU, p = 0.006] compared with normoxia. The Qs/Qt (14 ± 6%) was >10 in 75% of subjects but changes of mPAP and PVR under hyperoxia and hypoxia were independent of Qs/Qt.ConclusionAcute exposure to hypoxia did not relevantly alter pulmonary hemodynamics indicating a blunted HPV-response in PH. In contrast, hyperoxia remarkably reduced mPAP and PVR, indicating a preserved vasodilator response to oxygen and possibly supporting the oxygen therapy in patients with PH. A high proportion of patients with PH showed increased Qs/Qt, which, however, was not associated with changes in pulmonary hemodynamics in response to changes in FiO2.
Highlights
Pure oxygen breathing may improve hemodynamics in patients with pulmonary hypertension (PH) and allows to calculate right-to-left shunt fraction (Qs/Qt), whereas breathing normobaric hypoxia may accelerate hypoxic pulmonary vasoconstriction (HPV)
We aim to investigate the effect of hypoxia (FiO2 0.15) and hyperoxia (FiO2 1.0) on pulmonary hemodynamics in a large cohort of patients with PH assessed by right heart catheterization (RHC) as well as the influence of fraction of right-to-left shunt (Qs/Qt) on hemodynamic parameters, which might provide insight on physiological mechanisms supporting the use of therapeutic oxygen in this patient collective
We included men and women, aged ≥18 years with mean pulmonary arterial pressure (PAP) > 20 mmHg, pulmonary artery wedge pressure (PAWP) ≤15 mmHg) and revealing a pulmonary vascular resistance (PVR) > 2.0 wood unit (WU) [20,21,22] referred to our clinic between March 2016 and June 2020 for RHC and who had undergone measurements of hemodynamic parameters while breathing ambient air, hypoxia (FiO2 0.15), and hyperoxia (FiO2 1.0) and who were classified as pulmonary arterial hypertension (PAH) or chronic thromboembolic pulmonary hypertension (CTEPH) according to a thorough investigation, including pulmonary function tests, CT-pulmonary angiography, ventilation-perfusion scan, serology, and other measures as required
Summary
Pure oxygen breathing (hyperoxia) may improve hemodynamics in patients with pulmonary hypertension (PH) and allows to calculate right-to-left shunt fraction (Qs/Qt), whereas breathing normobaric hypoxia may accelerate hypoxic pulmonary vasoconstriction (HPV). This study investigates how hyperoxia and hypoxia affect mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance (PVR) in patients with PH and whether Qs/Qt influences the changes of mPAP and PVR. A low inspired and alveolar oxygen concentration causes hypoxic pulmonary vasoconstriction (HPV), which in turn increases pulmonary vascular resistance (PVR) and pulmonary arterial pressure (PAP) [1]. Acute exposure to high fractions of inspiratory oxygen (FiO2) may reduce PAP and PVR in patients with PH through pulmonary vasodilation, though there are only few studies with hemodynamic data obtained during RHC [6,7,8]. Pulmonary vasodilation by oxygen supplementation might provide a physiological basis for supporting long-term oxygen therapy in PH, which was shown to improve exercise capacity and symptom relief in domiciliary and nocturnal settings [9, 10]
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