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Hyperoxia Reduces Oxygen Consumption in Children with Pulmonary Hypertension
Long Guo1,2, Prashant Bobhate1,2,3, Shine Kumar1,2,4
1Pediatric Cardiac Intensive Care, Mazankowski Alberta Heart Institute, Stollery Children's Hospital, Edmonton, Canada.
Insights
High oxygen levels decrease oxygen consumption (VO2) and cardiac index (CI) in children with pulmonary hypertension (PH). This challenges the assumption that VO2 is constant during hyperoxic testing, potentially affecting pulmonary blood flow calculations.
Area of Science:
- Pediatric Cardiology
- Pulmonary Hypertension Research
- Cardiopulmonary Physiology
Background:
- High inspired oxygen concentration (FiO2 > 0.85) is used to assess pulmonary vascular reactivity in pediatric pulmonary hypertension (PH).
- Measuring oxygen consumption (VO2) during hyperoxia is challenging, leading to the assumption that VO2 remains constant.
- This assumption may impact the accuracy of hemodynamic calculations, particularly pulmonary blood flow and resistance.
Purpose of the Study:
- To investigate the effect of hyperoxia on oxygen consumption (VO2) in children with PH.
- To compare VO2 measured via thermodilution catheter in room air versus hyperoxic conditions.
- To evaluate the potential inaccuracies in pulmonary blood flow and resistance calculations under hyperoxia.
Main Methods:
- Retrospective review of hemodynamic data from pediatric cardiac catheterizations (2009-2014).
- Measurement of cardiac index (CI) using a thermodilution catheter in room air and hyperoxia.
- Calculation of VO2 using the Fick equation: CI = VO2 / (arterial-venous oxygen content difference).
Main Results:
- Hyperoxia significantly decreased VO2 (154 to 136 ml/min/m2) and CI (3.6 to 3.3 L/min/m2) in children with PH (p < 0.05).
- Hyperoxia induced pulmonary vasodilation (decreased mean pulmonary artery pressure and pulmonary vascular resistance) and systemic vasoconstriction (increased systemic vascular resistance).
- Heart rate and pulmonary artery wedge pressures also showed significant changes under hyperoxia.
Conclusions:
- The assumption that VO2 remains unchanged during hyperoxia in children with PH is incorrect.
- Hyperoxia alters VO2, CI, and vascular tone, potentially leading to overestimation of pulmonary blood flow and underestimation of pulmonary vascular resistance when using the Fick equation.
- These findings necessitate a re-evaluation of hyperoxic testing protocols in pediatric PH assessment.
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 [Formula: see text] 20 to 83 [Formula: see text] 21 beats/minute, p=0.005), mean pulmonary artery pressure (41 [Formula: see text] 16 to 35 [Formula: see text] 14 mmHg, p=0.024), CI (3.6 [Formula: see text] 0.8 to 3.3 [Formula: see text] 0.9 L/min/m2, p = 0.03), pulmonary vascular resistance (9 [Formula: see text] 6 to 7 [Formula: see text] 3 WU m2, p = 0.029), increased mean aortic (61 [Formula: see text] 11 to 67 [Formula: see text] 11 mmHg, p = 0.005), pulmonary artery wedge pressures (11 [Formula: see text] 8 to 13 [Formula: see text] 9 mmHg, p = 0.006), and systemic vascular resistance (12 [Formula: see text] 6 to 20 [Formula: see text] 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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