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F-65 Free Communication/Poster - Clinical Exercise Physiology - Other Friday, May 31, 2019, 1: 00 PM - 6: 00 PM Room: CC-Hall WA2

Cardiac Etiology of Exercise Induced Hypoxemia within Elite Athletes

3176 Board #222 May 31 3:30 PM - 5:00 PM

Dostal, Jiri1; Stasek, Josef1; Kockova, Radka2; Kocka, Viktor3

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Medicine & Science in Sports & Exercise: June 2019 - Volume 51 - Issue 6S - p 882
doi: 10.1249/01.mss.0000563134.67000.a1
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PURPOSE: Exercise induced hypoxemia (EIH) is common finding within a group of elite athletes. It is generally thought, that the causality lies in the pulmonary. We report a group of 8 elite athletes with severe EIH (SpO2 below 92%) examined for the origin of the EIH. The task was to perform differential diagnoses to locate the shunt into the pulmonary circulation or cardiac shunts.

METHODS: : Eight consecutive national level endurance athletes (cycling, running and rowing) with severe EIH (SpO2 reproducibly below 92) has been examined with stress transthoracic echocardiography with injection of agitated saline. The saline was administered via cubital vein during the last two steps of the stress echo and the presence of the hypoxemia. Differential diagnoses was based on previously published reports for evaluation of cardiac shunts - number of microbubbles and latency (number of cardiac cycles) between the injection and the appearance of the microbubbles in the left heart. Trans-esophageal echo has been performed in the follow up procedure to evaluate the anatomical etiology of the shunt.

RESULTS: Four athletes presented pulmonary etiology of the hypoxemia. Four athletes have presented cardiac origin with right to left shunt causing EIH. Concurrent transesophageal echocardiography discovered one atrial septal defect and three patent foramen ovale (PFO). One athlete with present PFO underwent successful catheterization closure of the PFO. Follow up exercise testing and stress echo confirmed no signs of shunt and no signs of presence of EIH in that patient. Also, performance measures of that athlete improved significantly. One athlete with present PFO/ASD underwent unsuccessful catheterization closure due to anatomical challenges.

CONCLUSIONS: : Exercise induced hypoxemia is generally thought to be caused by anatomical or functional shunts within the pulmonary circulation. Our findings suggest possibly higher prevalence than originally thought of cardiac etiology. Successful treatment by catheter-based closure device improves performance and eliminate other clinical signs of the right to left cardiac shunt. Further evaluation of larger group of elite athletes with EIH is warranted to understand better the real prevalence and possible treatment of the cardiac origin of the EIH.

Copyright © 2019 by the American College of Sports Medicine