Active Voice: Triathlon Swim Deaths: Initial Steps Toward Prevention
By Rudy Dressendorfer, P.T., Ph.D., FACSM
Viewpoints presented in SMB commentaries reflect opinions of the authors and do not necessarily reflect positions or policies of ACSM.
Rudy Dressendorfer, P.T., Ph.D., FACSM is an accomplished scientist, educator and clinician with a career focused on clinical exercise physiology. He is an ACSM Program Director and has served on ACSMís certification and education committee. He retired as full professor of human performance and sport at New Mexico Highlands University and subsequently taught exercise physiology and did collaborative research with faculty at the University of Alberta in Canada. Currently, he practices sports medicine as a licensed physical therapist in California. Rudy has published extensively on physical conditions, injuries and related prevention strategies for endurance athletes. He also has direct experiences with these issues, as he is a highly successful amateur triathlete.
A disturbing number of drownings have occurred during triathlon swims in recent years: 14 deaths were reported between 2006 and 2008, and nine more in the summer of 2011. Prevention is indicated, but there is little certainty about the causes of these unexplained deaths. Drowning due to water inhalation could occur, given that physical contact during mass starts and pack swimming is the norm in triathlon races. However, rescue craft are typically close by, and trained swimmers usually tolerate catching a mouthful of water or missing a breath or two without the need for emergency help. In the absence of other limitations to breathing, ordinary drowning seems an unlikely cause for most triathlon swim deaths. Sudden cardiac death remains a possibility to be ruled out.
Profuse frothy hemoptysis (coughing up blood) was found in some of these cases, making acute pulmonary edema (APE) an apparent cause. In a recent report of three female triathletes, symptoms of APE (breathing restriction, cough, hemoptysis and rales) occurred within minutes of immersion (Pulm Med 2011;2011:261404. Epub 2011 Jun 1). The probable pathophysiological mechanism of APE in swimmers is elevated blood volume in the heart and lungs due mainly to immersion. The abnormally increased central vascular volume can produce high blood pressure in the lungs. Capillary hemorrhage then results from pulmonary overperfusion.
Contributors or triggers to the development of APE in the swim of a triathlon race might include whole-body immersion per se, cold water, face immersion, tight wetsuit, sudden physical exertion and any personal behavior that could raise central blood pressure on race morning, such as excessive hydration or anxiety. Upon immersion to the neck, hydrostatic pressure on the extremities and trunk forces more blood than usual into the chest, thereby increasing central vascular volume and blood pressure while altering regional lung volumes. Cold water enhances this effect on the cardiopulmonary circulation by causing cutaneous vasoconstriction and increasing venous return. Face immersion, especially in cold water, can dramatically slow heart rate, thereby prolonging diastolic filling time. A tight wetsuit around the chest and neck could further increase resistance to inspiration as well as alter arterial baroreflex function. Failure to warm up before the swim could increase the hypertensive response to immersion. Heightened stress because of an unfamiliar swim venue or darkness might raise plasma catecholamines and also increase blood pressure. In addition, drinking just before the swim will increase abdominal volume and thus augment the fluid shift into the chest upon immersion.
Assuming that APE is the correct diagnosis and can be prevented, the following seven precautionary steps are recommended to lessen the risk of triathlon swim deaths: