Right ventricular performance during acute hypoxic exercise

Author:

Forbes Lindsay M.1,Bull Todd M.1,Lahm Tim123,Sisson Tyler4,O'Gean Katie4,Lawley Justin S.56ORCID,Hunter Kendall7,Levine Benjamin D.89ORCID,Lovering Andrew10ORCID,Roach Robert C.1,Subudhi Andrew W.11,Cornwell William K.412

Affiliation:

1. Division of Pulmonary Sciences and Critical Care Medicine University of Colorado Aurora CO USA

2. Division of Pulmonary, Critical Care and Sleep Medicine National Jewish Health Denver CO USA

3. Rocky Mountain Regional Veterans Affairs Medical Center Aurora CO USA

4. Clinical Translational Research Center University of Colorado Anschutz Medical Campus Aurora CO USA

5. Department of Sport Science University of Innsbruck Innsbruck Austria

6. Institute of Mountain Emergency Medicine Eurac Research Bolzano Italy

7. Department of Bioengineering University of Colorado Anschutz Medical Campus Aurora CO USA

8. Division of Cardiology University of Texas Southwestern Medical Center Dallas TX USA

9. Institute for Exercise and Environmental Medicine Texas Health Presbyterian Hospital Dallas TX USA

10. Department of Physiology University of Oregon Eugene OR USA

11. Department of Physiology University of Colorado Colorado Springs CO USA

12. Division of Cardiology, Department of Medicine University of Colorado Aurora CO USA

Abstract

AbstractAcute hypoxia increases pulmonary arterial (PA) pressures, though its effect on right ventricular (RV) function is controversial. The objective of this study was to characterize exertional RV performance during acute hypoxia. Ten healthy participants (34 ± 10 years, 7 males) completed three visits: visits 1 and 2 included non‐invasive normoxic (fraction of inspired oxygen () = 0.21) and isobaric hypoxic ( = 0.12) cardiopulmonary exercise testing (CPET) to determine normoxic/hypoxic maximal oxygen uptake (). Visit 3 involved invasive haemodynamic assessments where participants were randomized 1:1 to either Swan–Ganz or conductance catheterization to quantify RV performance via pressure–volume analysis. Arterial oxygen saturation was determined by blood gas analysis from radial arterial catheterization. During visit 3, participants completed invasive submaximal CPET testing at 50% normoxic and again at 50% hypoxic ( = 0.12). Median (interquartile range) values for non‐invasive values during normoxic and hypoxic testing were 2.98 (2.43, 3.66) l/min and 1.84 (1.62, 2.25) l/min, respectively (P < 0.0001). Mean PA pressure increased significantly when transitioning from rest to submaximal exercise during normoxic and hypoxic conditions (P = 0.0014). Metrics of RV contractility including preload recruitable stroke work, dP/dtmax, and end‐systolic pressure increased significantly during the transition from rest to exercise under normoxic and hypoxic conditions. Ventricular–arterial coupling was maintained during normoxic exercise at 50% . During submaximal exercise at 50% of hypoxic , ventricular–arterial coupling declined but remained within normal limits. In conclusion, resting and exertional RV functions are preserved in response to acute exposure to hypoxia at an  = 0.12 and the associated increase in PA pressures. imageKey points The healthy right ventricle augments contractility, lusitropy and energetics during periods of increased metabolic demand (e.g. exercise) in acute hypoxic conditions. During submaximal exercise, ventricular–arterial coupling decreases but remains within normal limits, ensuring that cardiac output and systemic perfusion are maintained. These data describe right ventricular physiological responses during submaximal exercise under conditions of acute hypoxia, such as occurs during exposure to high altitude and/or acute hypoxic respiratory failure.

Funder

National Institutes of Health

Publisher

Wiley

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