The effect of sudden drop in partial pressure of oxygen during ascent on heart function

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Diving, Sudden Cardiac Death, ECG, Transient Ischemia, Drop in O2

Background: Cardiovascular disease is the second leading cause of diving deaths. Scarcity of 12 lead ECG recordings during dives leaves many questions unanswered about cardiac function during ascent. I hypothesized that decreased oxygen partial pressure (PpO2) initiates cardiac arrhythmia on ascent. I examined heart rate variability (HRV), rhythm and circulating markers of cardiac damage in the blood in response to submersion, increased pressure and reduction in the partial pressure of oxygen during the ascent. Methods: Experiments were performed in the wet pot of the hyperbaric chamber. Participants (N=19) were occupational and scientific divers, age 39.3 years, BMI 26.5 kg/m2, 3 females. Each completed two dives in a drysuit while swimming in 8oC water outfitted with a 12 lead ECG holter recorder. A 30-minute swim was performed at ambient pressure followed by a dive to 5 atmospheres absolute (ATA) with a direct ascent to surface pressure. The experimental exposure held the PpO2 at 1.0 ATA for the ascent. Blood samples were drawn at baseline, immediately after the dive and one-hour post dive. ECG analysis was performed for 5 epochs of 5 minutes each. Results: Diving increased heart rate and decreased HRV (p<0.05). The change in heart rate variability time domain was increased on ascent with oxygen clamping over the control (P=<0.004). Diving increased markers of cardiac vagal tone (P=<0.02) and decreased markers of sympathetic tone (P=<0.003). Diving caused QTc prolongation, particularly in the control (P=0.021) on ascent. No ST depression was observed, and ST elevation was present in the anterior leads with no differences between epochs or conditions. Diving increased the number of atrial ectopics (PAC) particularly with oxygen clamped on ascent (P=0.002). There was no troponin (cTnI) or significant change in pH or Lactate however there was a significant increase in B-Type natriuretic peptide (BNP) production with the oxygen clamped on ascent (P=<0.0001). Discussion: This is the first study to examine the effect of submersion and diving on HRV using 12 lead ECG while exercising in a controlled study, and unlike previous studies without exercise I saw an increase in HR and a significant decrease in heart rate variability. This agrees with the effect of exercise alone. The effect of clamping oxygen on the ascent eliminated the reduction of HRV from control. Submersion and diving both increase markers of cardiac vagal tone unlike the effect of exercise. Markers of sympathetic tone were decreased during submersion but not during the 5 ATA dive. This suggests an autonomic conflict not observed when no exercise is present during a dive. The ST segment elevation showed the typical “early repolarization syndrome” of young, athletic, healthy, males with physically demanding jobs. Under conditions of high oxygen pressure an increase in the QT interval from baseline was observed along with a significant increase in PACs and BNP levels. Its relation to the observed PAC’s and QTc is unclear.

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Peter Ruben
Michael Koehle
Science: Department of Biomedical Physiology and Kinesiology
Thesis type: 
(Thesis) M.Sc.