Introduction: Obstructive sleep apnea is associated with atrial fibrillation. The mechanisms remain poorly understood.
Hypothesis: Apnea induces consistent intrinsic and extrinsic cardiac autonomic nerve responses that culminate in atrial fibrillation (AF) susceptibility.
Methods: Sixteen dogs were anesthetized and mechanically ventilated. In seven dogs, microelectrode recordings of the left and right cervical vagus nerves, anterior right ganglionated plexus (GP) and left stellate ganglion (SG) were performed during apnea. In nine dogs, left atrial (LA) single extrastimulation was performed in 3 sites before and after apnea. Apnea was induced by plugging the endotracheal tube as long as needed to reach oxygen saturations of 80%.
Results: Apnea induced a mild steady decline in heart rate (HR) and in blood pressure (BP). As oxygen saturation (SaO2) declined, phasic bursts of vagal discharges coincided with HR and BP oscillations, followed by tonic increase SG activity and increases in HR and BP. GP activity increased throughout apnea. (Figure). Apnea induced shortening of effective refractory period (ERP) from 110.20±31.3 ms to 90.6±29.1 ms (p<0.001) and AF induction with single extrastimulation in all 9 dogs vs 0/9 at baseline.
Conclusion: Oxygen desaturation during apnea leads to a complex response of the cardiac autonomic nervous system. Phasic vagal bursts coincide with HR and BP oscillations and simultaneous tonic SG firing lead to ERP shortening and AF vulnerability.