Premium
Evolution of Human Pulmonary Hemodynamics during Severe Sustained Hypoxia
Author(s) -
Hoffmann Fabian,
Limper Ulrich,
Zaha Vlad,
Reuter Hannes,
Zange Leonora,
SchulzMenger Jeannette,
Hein Marc,
Sadek Hesham,
Baldus Stephan,
Levine Benjamin,
Jordan Jens,
Tank Jens
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.531.5
Subject(s) - medicine , pulmonary hypertension , hypoxia (environmental) , cardiology , effects of high altitude on humans , pulmonary artery , blood pressure , diastole , anesthesia , oxygen , anatomy , chemistry , organic chemistry
Background Susceptible individuals experience hypoxia‐induced pulmonary hypertension when ascending to high altitude. Descent is considered the primary intervention to treat this condition. A human feasibility study testing influences of severe sustained normobaric hypoxia corresponding to >7,000 m altitude on the heart allowed us to follow the evolution of pulmonary hypertension using state‐of‐the‐art cardiovascular imaging. Material & Methods Two healthy, professional mountaineers (subject A, male 57 years, subject B, female 50 years) first pre‐acclimatized for one week in the field at 4559 m altitude. Then, they stayed at the :envihab facility of the German Aerospace Center in Cologne where normobaric hypoxia was achieved by nitrogen dilution starting at 13.5% O2 to a minimum of 8% O2 over three weeks. Afterwards, 8.5% O2 during the daytime and 8.8% O2 at night was kept for another 14 days. Velocity encoded single plane phase contrast MRI of the pulmonary artery (PA) and echocardiography were performed 1 month before, during and 1 and 3 months after hypoxia for assessment of right ventricular (RV) function, PA pressure, area, flow and distensibility. Results Systolic PA pressure (PAPsys) was closely related to the decrease in oxygen during acclimatization. In subject B PAPsys peaked at 67 mmHg, 48 mmHg higher than baseline. PAPsys decreased steadily to a minimum of 44 mmHg after two weeks while still at 8.55% oxygen. Peak values occurred with clinical symptoms of acute mountain sickness and a drop in exercise capacity but without signs of cerebral or pulmonary edema. In subject A peak PAPsys was 44 mmHg and remained stable over the entire hypoxia exposure. Conclusion In healthy humans, severe normobaric hypoxia induces pulmonary hypertension with paradoxically preserved right ventricular function. Pulmonary hypertension may improve over time in some individuals, even in the face of sustained hypoxia. The findings attest to the remarkable physiological reserve of healthy human beings allowing for adaptation to massively increased pulmonary pressure. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .