Parasympathetic hyperresponsiveness and bradyarrhythmias during apnoea in hypertension

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

Research output: Contribution to journalArticle

80 Citations (Scopus)

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

Fingerprint

Apnea
Bradycardia
Hypertension
Baroreflex
Sleep Apnea Syndromes
Heart Block
Sudden Death
Atropine
Premature Infants
Blood Vessels
Cardiac Arrhythmias
Heart Failure
Perfusion
Oxygen
Pressure
Muscles

Keywords

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

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Parasympathetic hyperresponsiveness and bradyarrhythmias during apnoea in hypertension. / Somers, Virend; Dyken, Mark Eric; Mark, Allyn Lewis; Abboud, Francois Mitry.

In: Clinical Autonomic Research, Vol. 2, No. 3, 06.1992, p. 171-176.

Research output: Contribution to journalArticle

Somers, Virend ; Dyken, Mark Eric ; Mark, Allyn Lewis ; Abboud, Francois Mitry. / Parasympathetic hyperresponsiveness and bradyarrhythmias during apnoea in hypertension. In: Clinical Autonomic Research. 1992 ; Vol. 2, No. 3. pp. 171-176.
@article{4925118b54e44dbb9855a6516eb1a522,
title = "Parasympathetic hyperresponsiveness and bradyarrhythmias during apnoea in hypertension",
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.",
keywords = "Bradycardia, Hypertension, Hypoxia, Sleep apnoea, Sympathetic nerve activity",
author = "Virend Somers and Dyken, {Mark Eric} and Mark, {Allyn Lewis} and Abboud, {Francois Mitry}",
year = "1992",
month = "6",
doi = "10.1007/BF01818958",
language = "English (US)",
volume = "2",
pages = "171--176",
journal = "Clinical Autonomic Research",
issn = "0959-9851",
publisher = "D. Steinkopff-Verlag",
number = "3",

}

TY - JOUR

T1 - Parasympathetic hyperresponsiveness and bradyarrhythmias during apnoea in hypertension

AU - Somers, Virend

AU - Dyken, Mark Eric

AU - Mark, Allyn Lewis

AU - Abboud, Francois Mitry

PY - 1992/6

Y1 - 1992/6

N2 - 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.

AB - 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.

KW - Bradycardia

KW - Hypertension

KW - Hypoxia

KW - Sleep apnoea

KW - Sympathetic nerve activity

UR - http://www.scopus.com/inward/record.url?scp=0026871378&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026871378&partnerID=8YFLogxK

U2 - 10.1007/BF01818958

DO - 10.1007/BF01818958

M3 - Article

C2 - 1498563

AN - SCOPUS:0026871378

VL - 2

SP - 171

EP - 176

JO - Clinical Autonomic Research

JF - Clinical Autonomic Research

SN - 0959-9851

IS - 3

ER -