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Hypoxemia alone does not explain blood pressure elevations after obstructive apneas.

J Ringler1, R C Basner, R Shannon

  • 1Charles A. Dana Institute, Boston, Massachusetts.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|December 1, 1990
PubMed
Summary

Obstructive sleep apnea (OSA) causes blood pressure spikes after apneas. These elevations are not mainly due to low oxygen but likely linked to arousal from sleep and breathing changes.

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Area of Science:

  • Cardiovascular Physiology
  • Sleep Medicine
  • Respiratory Physiology

Background:

  • Obstructive sleep apnea (OSA) is linked to significant blood pressure (BP) increases and oxyhemoglobin saturation (SaO2) drops after apnea events.
  • The precise mechanisms driving nocturnal hypertension in OSA remain unclear.

Purpose of the Study:

  • To investigate the role of arterial hypoxemia in causing post-apneic blood pressure elevations in patients with OSA.
  • To differentiate the effects of hypoxemia, apnea, and arousal on systemic BP changes during sleep.

Main Methods:

  • Mean arterial pressure (MAP) was monitored in 11 OSA patients during non-rapid-eye-movement (NREM) sleep.
  • Experimental conditions included: apneas with oxygen supplementation, isolated hypoxemia without apnea, and auditory arousal without respiratory events.

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Main Results:

  • Post-apneic MAP elevations were similar whether oxygen was supplemented or not (18.8 vs. 21.3 mmHg).
  • Isolated hypoxemia did not cause significant BP elevations (-5.4 mmHg change).
  • Auditory arousal alone induced MAP elevations comparable to those following apneas (24.0 mmHg).

Conclusions:

  • Post-apneic blood pressure elevations in NREM sleep are not primarily driven by arterial hypoxemia.
  • Arousal from sleep, lung reinflation, and intrathoracic pressure changes are likely contributors to post-apneic BP surges in OSA.