Elsevier

American Heart Journal

Volume 139, Issue 1, January 2000, Pages 142-148
American Heart Journal

Relations among hypoxemia, sleep stage, and bradyarrhythmia during obstructive sleep apnea,☆☆

https://doi.org/10.1016/S0002-8703(00)90321-1Get rights and content

Abstract

Background Obesity, apneic hypoxemia, and rapid eye movement (REM) sleep are supposed to be the major causes for bradyarrhythmia in patients with obstructive sleep apnea. The aims of this study were to compare clinical findings and diagnoses in patients with obstructive sleep apnea with and without nocturnal bradyarrhythmia and to analyze the relations among hypoxemia, sleep stage, and bradyarrhythmia. Methods During a 17-month period 239 patients were found to have sleep apnea in an ambulatory study. Patients with nocturnal bradyarrhythmia were hospitalized for 3 days and polysomnographies were performed over 2 successive nights. A Holter electrocardiogram was recorded for 48 hours. Results Nocturnal episodes of bradyarrhythmia were identified in 17 (7%) of 239 patients. Body mass index (39 ± 7 vs 31 ± 5 kg/m2) and respiratory disturbance index (90 ± 36 per hour vs 24 ± 24 per hour) were significantly different (P < .01) between patients with (n = 17) and without bradyarrhythmia (n = 222). Bradyarrhythmia occurred significantly more often during REM than non-REM sleep (P < .01). There was a significant difference in end-apneic oxygen saturation in apnea/hypopnea episodes with and without bradyarrhythmia (71% ± 9% vs 75% ± 10%; P < .01). A linear relation between end-apneic oxygen saturation and number of sinus arrests and heart blocks could not be found. Conclusions Patients with apnea-associated bradyarrhythmia are more overweight than patients without bradyarrhythmia. The higher respiratory disturbance index measurements found in these patients may be caused by this difference. Bradyarrhythmia occurs predominantly during REM sleep and occurred independently from decrease in oxygen saturation; a threshold value as an upper limit could not be found. (Am Heart J 2000;139:142-8.)

Section snippets

Patients

During a 17-month period 239 patients were found to have sleep apnea in an ambulatory study. In addition to the clinical interview and physical examination, a visually analyzed ambulatory monitoring of breathing sounds, heart rate, oxygen saturation, and body position (MESAM IV, Madaus Schwarzer, Munich, Germany) from 6 PM until 8 AM and a 2-channel Holter electrocardiogram (ECG) (Oxford Medilog 4000, Abingdon, UK) from approximately 2 PM until 8 AM were recorded.

Patients with nocturnal

Clinical characteristics of all study patients

Twenty-one of 239 patients were women. Mean age was 52 ± 10 years (range 16 to 78 years), body mass index was 32 ± 5 kg/m2 (range 20 to 58 kg/m2). Arterial hypertension was found in 47.3%, diabetes mellitus in 6%, hyperlipidemia in 49%, and hyperuricemia in 19%. Three of the patients (1%) had a history of myocardial infarction and 9 patients (3%) had evidence of coronary artery disease determined by bicycle stress test. Mean RDI was 29 ± 25 per hour (range 10 to 158 per hour). Episodes of sinus

Discussion

The major findings of the study are: (1) Patients with apnea-associated bradyarrhythmias are more overweight than patients without bradyarrhythmia. The higher RDI found in these patients may be caused by this circumstance. (2) Bradyarrhythmia occurred predominantly during REM sleep. (3) Bradyarrhythmia were found independently from decrease in SaO2; a threshold value as an upper limit could not be defined.

Obesity has been shown to be a predisposing factor for the occurrence of bradyarrhythmia

References (19)

There are more references available in the full text version of this article.

Cited by (68)

  • Prevalence, types and treatment of bradycardia in obstructive sleep apnea - A systematic review and meta-analysis

    2022, Sleep Medicine
    Citation Excerpt :

    OSA is a condition that involves repeated upper airway collapse and oxygen desaturation during sleep [68]. It has been proposed that OSA causes bradycardia due to negative intrathoracic pressure from the stretch of thoracic cavity [69,70]; moreover, hypoxemia may also induce a vagally-mediated cardioprotective mechanism [71,72]. Furthermore, the cessation of breathing, together with hypoxemia seen in OSA, is necessary to cause bradycardia [73].

  • Sleep in infants with congenital myasthenic syndromes

    2017, European Journal of Paediatric Neurology
    Citation Excerpt :

    The role of oxygen desaturation as trigger of severe bradycardia during OSA is controversial, as the prolonged negative intrathoracic pressures during OSA may be more important as a trigger of increased vagal tone than oxygen desaturation.25,28 Bradycardia occurring during an apnoea represents a vagal response to hypoxaemia aiming at limiting the oxygen consumption of the heart.29,30 However some studies also reported the occurrence of tachycardia associated with respiratory events during sleep in infants or preschool children with OSA.31–34

  • Obstructive Sleep Apnea and the Metabolic Syndrome: Clinical Profiles and Relationships

    2015, Modulation of Sleep by Obesity, Diabetes, Age, and Diet
  • Sleep-Related Cardiac Disorders

    2012, Therapy in Sleep Medicine
View all citing articles on Scopus

Reprint requests: Ulrich Koehler, MD, Department of Internal Medicine, Medizinische Poliklinik, Philipps-University Marburg, Baldingerstrasse, 35033 Marburg, Germany.

☆☆

0002-8703/2000/$12.00 + 0   4/1/101492

View full text