Stephen J Brown1, M J Barnes2, T Mündel2. 1. University of Ballarat School of Health Sciences Ballarat Victoria Australia. 2. Massey University College of Sciences Palmerston North New Zealand.
Abstract
PURPOSE: Hypercapnia increases minute ventilation (V’E) with little effect on heart rate (HR), whereas hypoxia may increase HR without affecting V’E. However, the effects of hypercapnia and hypoxia on both heart rate variability(HRV) and the clustering of heart beats during spontaneous breathing (respiratory sinus arrhythmia – RSA), are not clear. METHODS: In this study, 10 human volunteers breathed room air (RA), hypercapnic (5% CO2) or hypoxic (10%O2) gas mixtures, each for 6 min, while resting supine. ECG, mean arterial pressure (MAP), ventilatory flow, inhaled and exhaled fractions of CO2 and O2, were recorded throughout. RESULTS: Both V’E and MAP increased with 5%CO2, with no change in HR. Hypoxia did not change ventilation but increased HR. High frequency components of HRV, and the relative proportion of heart beats occurring during inhalation increased with 5% CO2, but neither changed with 10% O2. CONCLUSION: Increased RSA concomitant with increased MAP suggests RSA – vagal dissociation with hypercapnia. Elevated heart rate with acute hypoxia with no change in either frequency components of HRV or the distribution of heart beats during ventilation, suggested that clustering of heart beats may not be a mechanism to improve ventilation-perfusion matching during hypoxia.
PURPOSE:Hypercapnia increases minute ventilation (V’E) with little effect on heart rate (HR), whereas hypoxia may increase HR without affecting V’E. However, the effects of hypercapnia and hypoxia on both heart rate variability(HRV) and the clustering of heart beats during spontaneous breathing (respiratory sinus arrhythmia – RSA), are not clear. METHODS: In this study, 10 human volunteers breathed room air (RA), hypercapnic (5% CO2) or hypoxic (10%O2) gas mixtures, each for 6 min, while resting supine. ECG, mean arterial pressure (MAP), ventilatory flow, inhaled and exhaled fractions of CO2 and O2, were recorded throughout. RESULTS: Both V’E and MAP increased with 5%CO2, with no change in HR. Hypoxia did not change ventilation but increased HR. High frequency components of HRV, and the relative proportion of heart beats occurring during inhalation increased with 5% CO2, but neither changed with 10% O2. CONCLUSION: Increased RSA concomitant with increased MAP suggests RSA – vagal dissociation with hypercapnia. Elevated heart rate with acute hypoxia with no change in either frequency components of HRV or the distribution of heart beats during ventilation, suggested that clustering of heart beats may not be a mechanism to improve ventilation-perfusion matching during hypoxia.
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