Parasympathetic hyperresponsiveness and bradyarrhythmias during apnoea in hypertension

Virend Somers, Mark Eric Dyken, Allyn Lewis Mark, Francois Mitry Abboud

Research output: Contribution to journalArticle

82 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)171-176
Number of pages6
JournalClinical Autonomic Research
Volume2
Issue number3
DOIs
StatePublished - Jun 1992
Externally publishedYes

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Keywords

  • Bradycardia
  • Hypertension
  • Hypoxia
  • Sleep apnoea
  • Sympathetic nerve activity

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

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