4.5 Article

Case Studies in Physiology: Is blackout in breath-hold diving related to cardiac arrhythmias?

Journal

JOURNAL OF APPLIED PHYSIOLOGY
Volume 134, Issue 4, Pages 951-956

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00708.2022

Keywords

bigeminy; freediving; static apnea; syncope; unconsciousness

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Blackout in breath-hold diving is commonly attributed to hypoxia, but it has been suggested that cardiac arrhythmias may also play a role. In this study, heart rate recordings during a static apnea competition revealed that the diver who experienced blackout displayed a different heart rate pattern, including persistent alterations in R-R intervals and ectopic beats. This suggests that arrhythmia may have contributed to the blackout by affecting cardiac pumping function and brain perfusion.
Syncope or blackout (BO) in breath-hold diving (freediving) is generally considered to be caused by hypoxia. However, it has been suggested that cardiac arrhythmias affecting the pumping effectivity could contribute to BO. BO is fairly common in competitive freediving, where athletes aim for maximal performance. We recorded heart rate (HR) during a static apnea (STA) competition, to reveal if arrhythmias occur. Four male freedivers with STA personal best (PB) of 349 +/- 43 s, volunteered during national championships, where they performed STA floating face down in a shallow indoor pool. A non-coded Polar T31 chest strap recorded R-R intervals and a water- and pressure-proof pulse oximeter arterial oxygen saturation. Three divers produced STA near their PB without problems, whereas one diver ended with BO at 5 min 17s, which was 12 s beyond his PB. He was immediately brought up by safety divers and resumed breathing within 10 s. All divers attained similar lowest diving HR (47 +/- 4 beats/min), but HR recordings displayed a different pattern for the diver ending with BO. After a short tachycardia, the three successful divers developed bradycardia, which became more pronounced during the second half of the apnea. The fourth diver developed pronounced bradycardia earlier, and at 2.5 min into the apnea, HR started alternating between approximately 50 and 140 beats/min, until the diver lost consciousness. At resumed breathing, HR returned to baseline. Nadir oxygen saturation was similar for all divers. We speculate that arrhythmia could have contributed to BO, by lowering stroke volume leading to a systolic blood pressure drop, affecting brain perfusion. NEW & NOTEWORTHY Heart rate during prolonged breath-holding until the point of loss of consciousness has not previously been published. The recordings show that blackout was preceded by a period of persistent alterations in R-R intervals, whereby an ectopic beat followed every normal heartbeat. Explanations for this deviating heart rate pattern could be either premature atrial contractions or premature ventricular contractions following every atrial beat, i.e., bigeminy, which could have compromised cardiac pumping function and caused/contributed to blackout.

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