Published: 8 September 2020
Authors: Simon R. Schneider, MA Laura C. Mayer, MD Mona Lichtblau, MD Charlotte Berlier, MD Esther I. Schwarz, MD Stéphanie Saxer, MSc Michael Furian, PhD Konrad E. Bloch, Prof. MD Silvia Ulrich, Prof. MD
Source: This abstract has been sourced from NZ Respiratory Research Review Issue 195
Many patients with pulmonary arterial or chronic thromboembolic pulmonary hypertension (PH) wish to travel to altitude or by airplane, but their risk of hypoxia-related adverse health effects is insufficiently explored.
How does hypoxia, compared with normoxia, affect constant work-rate exercise test (CWRET) time in patients with PH, and which physiologic mechanisms are involved?
Stable patients with PH with resting Pao2 ≥ 7.3 kPa underwent symptom-limited cycling CWRET (60% of maximal workload) while breathing normobaric hypoxic air (hypoxia; Fio2, 15%) and ambient air (normoxia; Fio2, 21%) in a randomized cross-over design. Borg dyspnea score, arterial blood gases, tricuspid regurgitation pressure gradient, and mean pulmonary artery pressure/cardiac output ratio (mean PAP/CO) by echocardiography were assessed before and during end-CWRET.
Twenty-eight patients (13 women) were included: median (quartiles) age, 66 (54; 74) years; mean pulmonary artery pressure, 41 (29; 49) mm Hg; and pulmonary vascular resistance, 5.4 (4; 8) Wood units. Under normoxia and hypoxia, CWRET times were 16.9 (8.0; 30.0) and 6.7 (5.5; 27.3) min, respectively, with a median difference (95% CI) of –0.7 (–3.1 to 0.0) min corresponding to –7 (–32 to 0.0)% (P = .006). At end-exercise in normoxia and hypoxia, respectively, median values and differences in corresponding variables were as follows: Pao2: 8.0 vs 6.4, –1.7 (–2.7 to –1.1) kPa; arterial oxygen content: 19.2 vs 17.2, –1.7 (–3 to –0.1) mL/dL; Paco2: 4.7 vs 4.3, –0.3 (–0.5 to –0.1) kPa; lactate: 3.7 vs 3.7, 0.9 (0.1 to 1.6) mM (P < .05 all differences). Values for Borg scale score: 7 vs 6, 0.5 (0 to 1); tricuspid pressure gradient: 89 vs 77, –3 (–9 to 16) mm Hg; and mean PAP/CO: 4.5 vs 3.3, 0.3 (–0.8 to 1.4) Wood units remained unchanged. In multivariable regression, baseline pulmonary vascular resistance was the sole predictor of hypoxia-induced change in CWRET time.
In patients with PH, short-time exposure to hypoxia was well tolerated but reduced CWRET time compared with normoxia in association with hypoxemia, lactacidemia, and hypocapnia. Because pulmonary hemodynamics and dyspnea at end-exercise remained unaltered, the hypoxia-induced exercise limitation may be due to a reduced oxygen delivery causing peripheral tissue hypoxia, augmented lactic acid loading and hyperventilation.
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