Among the many physiological responses to swimming in cold water that have been suspected of contributing to the high incidence of deaths in the swim portion of triathlon are three unusual entities: two of which are uncommon (less than 2% of the population), and one which is quite rare. Now, take a deep breath: no need to be afraid of either of these, but the medical terminology gets thick here.
The Long QT Syndrome/Torsades de Pointes.
The “LQTS” is an uncommon electrical disturbance of the heart that can be inherited or acquired, that can adversely affect the contractile functions of the heart. It is often referred to as a “channelopathy”, as it is characterized by abnormalities of the ion channels that pass ions (such as potassium, sodium, calcium and chloride) across the cell membranes in the process of depolarization and repolarization. When these channels operate abnormally, the repolarization of the cardiac process on an EKG is prolonged (the QRS complex, followed by the T wave), hence the name long QT interval. When the repolarization process is prolonged, the risk of re-entrant ventricular arrhythmias is increased; the most dangerous one is called torsade de pointes, so-called because it looks like twisting up and down spikes, an unstable cardiac rhythm which is usually symptomatic (dizziness, fainting or seizure) and can just as quickly revert back to normal or lead to a fatal arrhythmia called ventricular fibrillation. Symptomatic LQTS is more common after age 40, and is somewhat more common in women.
Most people who have the LQTS are unaware that they have this vulnerability, but it is relatively easy to screen for it, with 85% of them appearing on a routine EKG, and simple genetic blood testing can be considered in other suspected cases. If there is any family history of LQTS, of sudden death, or other genetic cardiac abnormality, a cardiac assessment including an EKG and possibly a stress test would be a good first step in most cases.
However, where LQTS gets interesting is when it is realized that the majority of LQTS incidence is acquired. According to the Mayo Clinic, more than 50 medications are known to lengthen the QT interval (many more are suspected): Antihistamines, decongestants, antidepressants, some antibiotics (macrolides and quinolones), cocaine, diuretics, heart medications, cholesterol-lowering medications, some diabetes medications, some antifungals and some antipsychotic drugs make the list. Electrolyte imbalances such as low levels of potassium, magnesium, and calcium are also common triggers of LQTS, and can be the result of poor nutrition, anorexia nervosa, and even a simple diarrheal illness.
Besides a pre-screening EKG, a medication review with a physician or pharmacist is useful to confirm that there is no risk from medication use and a consideration of a stress test to see if the LQTS or any cardiac ischemia develops under conditions of increasingly intense exercise. With both training and racing, be well nourished, and avoid discretionary medication use, especially on the same day of your activity. And if you have been ill, potentially starting your event energy- or nutrient-depleted, dehydrated or exhausted, you should reconsider your participation until you are better.
Wolf-Parkinson-White (WPW) Syndrome.
This cardiac syndrome is a congenital cardiac disorder that is relatively common and usually asymptomatic; it is found in about 2-4 people per 1000 population and is more common in males—and it is suspected that many do not know that they have it. In WPW, there is an extra connecting pathway between the atria and the ventricles in the heart, that can at times “pre-excite” the ventricles to contract prematurely, leading to palpitations, tachycardia, dizziness, weakness, and shortness of breath. These symptoms can first appear at almost any age: The tachycardia can be provoked by exercise, and can provoke various secondary arrhythmias, including supraventricular tachycardia, atrial fibrillation, and atrial flutter – these in turn increase the risk of ventricular fibrillation and sudden death. WPW is usually easily detected on a routine EKG, and symptoms can be elucidated further in a cardiac stress test.
Becoming dizzy, short of breath and with low blood pressure while swimming can be disastrous, especially when at race pace, since it not easy to rest, recover, or get help quickly; being at risk of ventricular fibrillation because of an abnormal congenital electrical pathway as in the case of WPW while in open water is potentially lethal.
If you have had previous undiagnosed spells of dizziness, fainting, palpitations, or tachycardia, having a routine EKG is prudent. If you have further suspicions, then seeing a cardiologist for more testing would be useful to confirm the diagnosis. Once familiar with the diagnosis, there are several treatments available, including cardiac medications, or electrical cardioversion; if the WPW is persistent or recurrent, there is a definitive, potentially curative treatment: the destruction of the abnormal electrical pathway by radiofrequency catheter ablation.
This is a Latin term meaning “concussion of the heart”, and is a very unusual event caused by direct, blunt, non-penetrating trauma to the chest, perfectly timed to a vulnerable phase of the cardiac cycle (such as when ventricular polarization occurs), causing a spontaneous, sudden, fatal arrhythmia. It is suspected that the blunt force causes a significant transfer of kinetic energy to the heart, enough to disrupt the cardiac rhythm. Resuscitation of this event has been poor, even on land-based occurrences, such as with a baseball, a hockey puck or other blow striking the chest.
Although such a blow has never been witnessed in a mass start swimming event (frankly, it is hard for anything to be observed out in open water), open water swimmers need to be aware that being struck on the chest by another swimmer’s heel kick could, at least in theory, have lethal consequences. The solution: steer clear of other swimmers, especially when overtaking someone slower.
Photo Credit: Lambrini2010