Hyperoxia and the cardiovascular system: experiences with hyperbaric oxygen therapy

Area of Science:

• Physiology
• Cardiovascular Research
• Oxygen Therapy

Background:

• Hyperoxia is known to potentially induce bradycardia through parasympathetic stimulation and increased vascular resistance.
• Increased vascular resistance can also lead to bradycardia via baroreceptor reflex activation.
• The precise mechanism linking oxygen administration, blood pressure, and heart rate requires further investigation.

Purpose of the Study:

• To evaluate the correlation between oxygen (O2) administration and heart rate changes over time.
• To investigate the relationship between hyperbaric oxygen therapy, blood pressure, and heart rate.
• To determine if direct vagal activation or baroreceptor reflex is responsible for bradycardia during hyperbaric oxygen therapy.

Main Methods:

• A single-arm, monocentric retrospective study design.
• Data collected from 23 patients undergoing hyperbaric oxygen therapy (2.4 bar).
• Monitoring of transcutaneously measured partial pressure of O2, arterial blood pressure, and heart rate during oxygen administration.

Main Results:

• Hyperbaric oxygen therapy increased transcutaneously measured partial pressure of O2.
• Arterial blood pressure increased while heart rate decreased during oxygen surges.
• The decrease in heart rate followed the increase in O2 pressure with a slow decline, suggesting baroreceptor reflex involvement.

Conclusions:

• The observed heart rate decrease during hyperbaric oxygen therapy is primarily mediated by the baroreceptor reflex due to increased blood pressure.
• Direct vagal activation does not appear to be the main mechanism for bradycardia in this context.
• Oxidative stress and reduced endothelial-derived vasodilators contribute to vasoconstriction, increased blood pressure, and subsequent heart rate reduction.