Hyperoxia-induced alterations in cardiovascular function and autonomic control during return to normoxic breathing

Abstract

Hyperoxia causes hemodynamic alterations. We hypothesized that cardiovascular and autonomic control changes last beyond the end of hyperoxic period into normoxia. Ten healthy volunteers were randomized to breathe either medical air or 100% oxygen for 45 min in a double-blind study design. Measurements were performed before (baseline) and during gas exposure, and then 10, 30, 60, and 90 min after gas exposure. Hemodynamic changes were studied by Doppler echocardiography. Changes in cardiac and vasomotor autonomic control were evaluated through changes in spectral power of heart rate variability and blood pressure variability. Cardiac baroreflex sensitivity was assessed by the sequence method. Hyperoxia significantly decreased heart rate and increased the high frequency power of heart rate variability, suggesting a chemoreflex increase in vagal activity since the slope of cardiac baroreflex was significantly decreased during hyperoxia. Hyperoxia increased significantly the systemic vascular resistances and decreased the low frequency power of blood pressure variability, suggesting that hyperoxic vasoconstriction was not supported by an increase in vascular sympathetic stimulation. These changes lasted for 10 min after hyperoxia (p < 0.05). After the end of hyperoxic exposure, the shift of the power spectral distribution of heart rate variability toward a pattern of increased cardiac sympathetic activity lasted for 30 min (p < 0.05), reflecting a resuming of baseline autonomic balance. Cardiac output and stroke volume were significantly decreased during hyperoxia and returned to baseline values (10 min) later than heart rate. In conclusion, hyperoxia effects continue during return to normoxic breathing, but cardiac and vascular parameters followed different time courses of recovery.

Activation of the carotid chemoreflex secondary to muscle metaboreflex stimulation in men

“…These were not controlled because of the difficulty in determining an appropriate PET CO 2 set point for all exercise/PECO trials, and the practical difficulty of maintaining breathing frequency/PET CO 2 with changes in ventilation. In addition, hyperoxia can have the effect of reducing cardiac output (12,37,39), modifying ventilation/perfusion matching in the lung, and increasing alveolar deadspace, resulting in an increase in the alveolar to PET CO 2 difference. Indeed it appears as though this may have occurred during our hyperoxic PECO trials, as ventilation during hyperoxic PECO was similar to the normoxic PECO despite a lower PET CO 2 in hyperoxic PECO, Values are means Ϯ SE.…”

Beat:To:Beat Autonomic Cardiovascular Response to Short:Term 100%O2 Breathing: a Time:Frequency Analysis Approach

“…However, contradictory effects of hyperoxia have also been reported: reduction [6], no change [4] or increase [3] of AP; no change of BRS evaluated by alpha technique [7], and, when estimated by sequence analysis, increase [3] or reduction [2]; and either no change, decrease or increase of PV [5].…”

“…There is substantial consensus on the effects that longterm hyperoxia causes in healthy subjects: sympathetic activity decrease, as evaluated by muscular sympathetic nerve activity [4], by LFSP power [2] and by the LFRR/HFRR ratio [8]; augmented vagal activity as indicated by the increase of HFRR power [2,3,8], associated with HR reduction [2,3,4,8,9]; decreased stroke volume [2,9]; vasoconstriction due to a local effect [7,9], which has recently been considered the primary effect of hyperoxemia [1], eliciting an increase in peripheral resistance [2,3] and decreased blood flow to the limbs [4]. However, contradictory effects of hyperoxia have also been reported: reduction [6], no change [4] or increase [3] of AP; no change of BRS evaluated by alpha technique [7], and, when estimated by sequence analysis, increase [3] or reduction [2]; and either no change, decrease or increase of PV [5].…”

“…Moreover, the participation of either the baroreflex or the respiratory sinus arrhythmia (RSA) mechanisms in these effects remains unclear. Additionally, spectral analysis of cardiovascular variability under hyperoxemic conditions has only been performed using steady-state techniques [2,3,7,8], so the transient changes of the autonomic-cardiovascular variables in the first minutes of hyperoxemia are still unknown. To clarify these issues, by using a timefrequency spectral analysis approach, we assessed the instantaneous time course of the effects produced by short-term 100%O2 breathing on the spectral measures of heart rate variability (HRV) and systolic pressure variability, BRS, RSA sensitivity (RSAS), R-R intervals (RR), AP and respiratory variables.…”

“…On the one hand, there is consensus that hyperoxia directly causes vasoconstriction [1], vagal activity increase with heart rate (HR) reduction [2,3] and sympathetic activity decrease [2,4]; but on the other hand, contradictory effects of hyperoxia on pulmonary ventilation (PV) [5], arterial pressure (AP) [3,6] and baroreflex sensitivity (BRS) [2,3,7] have been reported. Apparently, hyperoxia produces various effects on different organs in a parallel manner, directly, and separately [1].…”