Clinical Autonomic Research

, Volume 2, Issue 3, pp 171–176

Parasympathetic hyperresponsiveness and bradyarrhythmias during apnoea in hypertension

Authors

  • Virend Kristen Somers
    • Departments of Internal Medicine, Physiology and Biophysics, and Neurology, and the Cardiovascular CenterUniversity of Iowa College of Medicine
    • the Department of Veterans Affairs Medical Center
  • Mark Eric Dyken
    • Departments of Internal Medicine, Physiology and Biophysics, and Neurology, and the Cardiovascular CenterUniversity of Iowa College of Medicine
    • the Department of Veterans Affairs Medical Center
  • Allyn Lewis Mark
    • Departments of Internal Medicine, Physiology and Biophysics, and Neurology, and the Cardiovascular CenterUniversity of Iowa College of Medicine
    • the Department of Veterans Affairs Medical Center
  • Francois Mitry Abboud
    • Departments of Internal Medicine, Physiology and Biophysics, and Neurology, and the Cardiovascular CenterUniversity of Iowa College of Medicine
    • the Department of Veterans Affairs Medical Center
Research Paper

DOI: 10.1007/BF01818958

Cite this article as:
Somers, V.K., Dyken, M.E., Mark, A.L. et al. Clinical Autonomic Research (1992) 2: 171. doi:10.1007/BF01818958

Abstract

Voluntary end-expiratory apnoea in a 23-year-old asymptomatic mild hypertensive patient consistently elicited bradyarrhythmias (complete heart block and sinus pause) and sympathetic activation to muscle blood vessels, indicating simultaneous sympathetic and parasympathetic activation during apnoea. The sympathetic bradyarrhythmic response to apnoea was potentiated by hypoxia and eliminated by atropine. Baroreflex activation also attenuated the bradycardic response to apnoea.

A 43-year-old hypertensive patient with sleep apnoea also exhibited bradyarrhythmias (sinus arrest for up to 10 s) and a fall in perfusion pressure to <50 mmHg during episodes of sleep apnoea. These cardiovascular changes were associated with a reduction in oxygen saturation to levels as low as 35%. Neither patient was on any medication.

Simultaneous sympathetic and parasympathetic activation during episodes of apnoea may predispose to cardiovascular catastrophe. These chemoreflex mediated autonomic changes are inhibited by baroreflex activation. We propose that patients with impaired baroreflexes (patients with hypertension or heart failure and premature infants) may be especially susceptible to excessive autonomic responses to chemoreflex stimulation during periods of apnoea. In these patient groups, brady-arrhythmias, hypoxia, hypoperfusion and sympathetic activation during apnoea may predispose to sudden death.

Key words

Sympathetic nerve activity Hypoxia Sleep apnoea Bradycardia Hypertension

Copyright information

© Rapid Communications of Oxford Ltd 1992