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Acute 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 (FiO2${F_{{\mathrm{i}}{{\mathrm{O}}_{\mathrm{2}}}}}$) = 0.21) and isobaric hypoxic (FiO2${F_{{\mathrm{i}}{{\mathrm{O}}_{\mathrm{2}}}}}$ = 0.12) cardiopulmonary exercise testing (CPET) to determine normoxic/hypoxic maximal oxygen uptake (V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$). 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 V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$ and again at 50% hypoxic V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$ (FiO2${F_{{\mathrm{i}}{{\mathrm{O}}_{\mathrm{2}}}}}$ = 0.12). Median (interquartile range) values for non‐invasive V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$ 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% V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$. During submaximal exercise at 50% of hypoxic V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$, 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 FiO2${F_{{\mathrm{i}}{{\mathrm{O}}_{\mathrm{2}}}}}$ = 0.12 and the associated increase in PA pressures. Key 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. [ABSTRACT FROM AUTHOR]

This article, published in Pulmonary Circulation, discusses the potential benefits of combined chemotherapy and immunotherapy in improving the course of pulmonary arterial hypertension (PAH). The article presents a case study of a patient with PAH associated with connective tissue disease who received chemotherapy and immunotherapy for metastatic lung adenocarcinoma. The patient experienced improvement in functional class and risk score while on treatment, but experienced clinical deterioration after discontinuation. The article acknowledges the limitations of a single case study and the difficulty in determining the specific effects of the treatment on PAH. However, it provides valuable insights into the potential effects of antineoplastic and immunomodulatory therapy in PAH and calls for further research in this area. [Extracted from the article]