Although still incredibly uncommon, the incidence of drownings during the triathlon swim have gone up with the popularity of multisport. Nine cases of triathlon deaths were reported in the summer of 2011, yet there is little certainty about the cause of these sudden fatalities.
One possible cause could be ordinary drowning due to water inhalation as a result of physical contact during crowded mass starts and pack swimming.
More: Avoiding Rip Currents
Cardiac arrest is also a possible cause, especially if the fatality was associated with underlying heart disease. However, respiratory failure due to pulmonary edema (PE) is also known to occur during immersion and it should be considered a probable cause in healthy, experienced swimmers.
In cases where profuse frothy hemoptysis (blood coughed up from the lungs) was found, PE was the likely cause. Three female triathletes who experienced severe breathing restriction and cough in "near-drownings" within minutes of their swim start were reported to have hemoptysis and crackling breath sounds (Pulm Med 2011;2011: 261404. Epub 2011 Jun 1).
Hemoptysis in healthy swimmers almost certainly results from increased blood volume in the heart and lungs with immersion. The abnormally large central vascular volume acutely elevates blood pressure in the lungs that ruptures the alveolar capillaries.
Though it's a rare occurrence, and chances are, it won't happen to you, it doesn't hurt to educate yourself on causes and prevention.
These are among the factors that may increase the risk of PE in the swim of a triathlon race:
1. Immersion in general—and face immersion in particular
2. Cold water
3. A tight wetsuit
4. Physical exertion without a warm-up
5. Any personal behavior that might raise blood pressure on race morning, such as excessive hydration or anxiety.
Upon immersion, water pressure on the extremities and abdomen forces more blood than usual into the chest. Cold water enhances this effect on the central circulation as blood vessels in the skin constrict and further increase venous return. The increased central blood volume raises cardiopulmonary vascular pressure while altering regional lung volumes.