Hypoxic tachycardia is not a result of increased respiratory activity in healthy subjects

What is the central question of this research? Does increased ventilation contribute to the increase in heart rate during the transient exposure to hypoxia in humans? What is the main finding and its importance? Voluntary suppression of the ventilatory response to transient hypoxia does not affect the magnitude of the heart rate response to the stimulus. This indicates that the hypoxic‐tachycardia is not secondary to hyperpnoea in humans. Better understanding of the physiology behind cardiovascular response to hypoxia may help in identifying novel markers of elevated chemoreceptors activity, which was proposed as a target in treatment of sympathetically mediated diseases.

Abstract

Animal data suggest that hypoxic‐tachycardia is secondary to hyperpnoea, and for years this observation has been extrapolated to humans, despite the lack of experimental evidence. We addressed this thesis in 17 volunteers aged 29 ± 7 y. The transient hypoxia test comprising several nitrogen‐breathing episodes was performed twice in each subject. In the first test the subject breathed spontaneously (spontaneous‐breathing). In the second test the subject was repeatedly asked to adjust his/her depth and rate of breathing according to visual (real‐time inspiratory flow) and auditory (metronome sound) cues, respectively (controlled‐breathing), to maintain respiration at resting level during nitrogen‐breathing episodes. Hypoxic responsiveness, including: minute ventilation [Hyp‐VI, L min⁻¹/SpO₂%], tidal volume [Hyp‐VT, L/SpO₂%], heart rate [Hyp‐HR, bpm/SpO₂%], systolic [Hyp‐SBP, mmHg/SpO₂%] and mean blood pressure [Hyp‐MAP, mmHg/SpO₂%] and systemic vascular resistance [Hyp‐SVR,<dyn*s/cm⁵>/SpO₂%] was calculated as the slope of the regression line relating the variable to SpO₂%, including pre‐ and post‐hypoxic values. Hyp‐VI and Hyp‐VT were reduced by 69 ± 25% and 75 ± 10%, respectively in the controlled‐ vs spontaneous‐breathing (Hyp‐VI: −0.30 ± 0.15 vs −0.11 ± 0.09, Hyp‐VT: −0.030 ± 0.024 vs −0.007 ± 0.004, both p < 0.001). However the cardiovascular responses did not differ between spontaneous‐ and controlled‐breathing (Hyp‐HR: −0.62 ± 0.24 vs −0.71 ± 0.33, Hyp‐MAP: −0.43 ± 0.19 vs −0.47 ± 0.21, Hyp‐SVR: 9.15 ± 5.22 vs 9.53 ± 5.57; all p≥0.22), indicating that hypoxic‐tachycardia is not secondary to hyperpnoea. Hyp‐HR correlated with Hyp‐SVR (r = −074 and ‐0.80 for spontaneous‐ and controlled‐breathing, respectively, both p < 0.05) and resting barosensitivity assessed with the sequence technique (r = ‐0.60 for spontaneous‐breathing, p < 0.05). This may suggest that the baroreflex mechanism is involved.

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