Hyperoxia Reduces Oxygen Consumption in Children with Pulmonary Hypertension

Abstract

High inspired oxygen concentration (FiO₂ > 0.85) is administered to test pulmonary vascular reactivity in children with pulmonary hypertension (PH). It is difficult to measure oxygen consumption (VO₂) if the subject is breathing a hyperoxic gas mixture so the assumption is made that baseline VO₂ does not change. We hypothesized that hyperoxia changes VO₂. We sought to compare the VO₂ measured by a thermodilution catheter in room air and hyperoxia. A retrospective review of the hemodynamic data obtained in children with PH who underwent cardiac catheterization was conducted between 2009 and 2014. Cardiac index (CI) was measured by a thermodilution catheter in room air and hyperoxia. VO₂ was calculated using the equation CI = VO₂/arterial–venous oxygen content difference. Data were available in 24 subjects (males = 10), with median age 8.3 years (0.8–17.6 years), weight 23.3 kg (7.5–95 kg), and body surface area 0.9 m² (0.4–2.0 m²). In hyperoxia compared with room air, we measured decreased VO₂ (154 ± 38 to 136 ± 34 ml/min/m², p = 0.007), heart rate (91  \(\pm\)  20 to 83  \(\pm\)  21 beats/minute, p=0.005), mean pulmonary artery pressure (41  \(\pm\)  16 to 35  \(\pm\)  14 mmHg, p=0.024), CI (3.6  \(\pm\)  0.8 to 3.3  \(\pm\)  0.9 L/min/m², p = 0.03), pulmonary vascular resistance (9  \(\pm\)  6 to 7  \(\pm\)  3 WU m², p = 0.029), increased mean aortic (61  \(\pm\)  11 to 67  \(\pm\)  11 mmHg, p = 0.005), pulmonary artery wedge pressures (11  \(\pm\)  8 to 13  \(\pm\)  9 mmHg, p = 0.006), and systemic vascular resistance (12  \(\pm\)  6 to 20  \(\pm\)  7 WU m², p=0.001). Hyperoxia decreased VO₂ and CI and caused pulmonary vasodilation and systemic vasoconstriction in children with PH. The assumption that VO₂ remains unchanged in hyperoxia may be incorrect and, if the Fick equation is used, may lead to an overestimation of pulmonary blood flow and underestimation of PVRI.

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