Introduction: Obstructive sleep apnea/hypopnea (OSAH) is strongly associated with atrial and ventricular arrhythmias yet exact underlying mechanisms remain unclear.
Hypothesis: Human authentic (non-simulated) OSAH episodes differentially affect sinoatrial node automaticity (RR interval), atrial conduction (P wave duration), atrioventricular nodal conduction (PR interval), ventricular conduction (QRS duration), ventricular repolarization (QT interval), and oxygen saturation (SpO2).
Methods: Sleeping patients (N=10) with moderate OSAH syndrome but no cardiopulmonary comorbidity were analyzed with expanded (8 lead) ECG montage during untreated isolated OSAH episodes (10 episodes per patient). Manual ECG measurements collected from pre-specified phases of the OSAH episode/recovery were compared to baseline (10s before episode onset).
Results: During OSAH, RR initially increased (p<0.01) then briskly declined, P wave increased (p=0.03), PR and QRS trended up (p=0.1), and QT increased (p=0.01). During 30 second recovery after OSAH, RR decreased below baseline (p<0.01) and then normalized, P wave remained increased (p=0.05), PR and QT returned to baseline, and QRS mildly increased with delay (p=0.03). The type of episode (apnea vs. hypopnea), magnitude of oxygen drop, and length of episode prominently affected ECG changes (p<0.01).
Conclusions: Increased atrial automaticity after the release of breathing obstruction in combination with concurrent slowing of atrial propagation may lead to substrate vulnerable to atrial fibrillation initiation. The type and magnitude of OSAH episodes markedly influence the gravity of ECG changes, suggesting that refinement of the standard apnea hypopnea index is needed to more accurately reflect pro-arrhythmic propensity of OSAH.