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. 2022 Feb 11:9:791423.
doi: 10.3389/fmed.2022.791423. eCollection 2022.

The Impact of Breathing Hypoxic Gas and Oxygen on Pulmonary Hemodynamics in Patients With Pulmonary Hypertension

Arcangelo F Carta  1 , Mona Lichtblau  1 , Charlotte Berlier  1 , Stéphanie Saxer  1 , Simon R Schneider  1 , Esther I Schwarz  1 , Michael Furian  1 , Konrad E Bloch  1 , Silvia Ulrich  1
Affiliations

The Impact of Breathing Hypoxic Gas and Oxygen on Pulmonary Hemodynamics in Patients With Pulmonary Hypertension

Arcangelo F Carta et al. Front Med (Lausanne). .

Abstract

Background: 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.

Study design and methods: Adults 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.

Results: We 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.

Conclusion: Acute 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.

Keywords: chronic thromboembolic pulmonary arterial hypertension (CTEPH); hypoxia; oxygen; pulmonary arterial hypertension (PAH); right heart catheterization; right to left shunting.

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Conflict of interest statement

SU reports grants from Johnson and Johnson SA, Switzerland, during the conduct of the study; grants from the Swiss National Science Foundation, grants from Zurich Lung, grants from Orpha Swiss, personal fees from Actelion SA, Switzerland, personal fees from MSD Switzerland, outside the submitted work. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Patient flow is shown. No pulmonary hypertension classified patients with a mean pulmonary artery pressure <25 mmHg and a pulmonary vascular resistance <2 WU.
Figure 2
Figure 2
Boxplots showing mean pulmonary artery pressure (mPAP) (A) and pulmonary vascular resistance (PVR) (B) under normoxia (FiO2 0.21), hypoxia (FiO2 0.15), and hyperoxia (FiO2 1.0). The horizontal lines represent the median values, upper and lower box edges represent the 25th and 75th percentiles, and “x” indicates the mean. FiO2: fraction of inspired oxygen.
See this image and copyright information in PMC

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