Reprinted from Lawrence L. Creswell, M.D.
Introduction by Don Macdonald: I recently had a sudden cardiac event, collapsed, received life saving help immediately and found to have arrhythmia problems perhaps brought on by exercise, Well I survived and now find myself with an implanted ICD to prevent such future events. I was running, which I jokingly say was the problem, instead of swimming. I think ICD stands for "I Can't Die".
However my experience now takes me down a path relatively untraveled since only about 1% of such incidents leave survivor's. So onto the next chapter of my swimming journey just One Stroke At A Time.
Cardiac rehab has me exercising already and I am hopeful to return to the pool in the near future.
We've talked previously here at the blog about the general issue of sports-related sudden cardiac death (SCD). And we've also talked about the specific issue of swimming fatalities during triathlons and open water swims.
But what triggers a sudden, fatal arrhythmia during open water swimming?
The answer isn't known and perhaps it will never be known with certainty. But a recent report from a group of scientists in the U.K., though, suggests a very plausible mechanism. Their idea is worth considering.
What's been learned from studies on runners?
As I've mentioned previously here at the blog, sports-related SCD has been best studied in the setting of long-distance running events. Last year, Dr. Kim and colleagues in Boston reported on a decade-long study of runners with race-related SCD . These investigators found that fatalities during marathons are not distributed uniformly along the race distance. Instead, they predominate during the final 3 miles or so. And interestingly, fatalities during half marathon events also predominate during the closing miles. But why?
In the running population, we know from autopsy studies that the majority of victims have some sort of (often previously unknown) heart disease. And something happens during the closing miles of the race. In the words of the investigators, their "findings suggest that demand ischemia (i.e., ischemia due to an imbalance between oxygen supply and demand) may be operative in exercise-related acute coronary events during long-distance running races." The leading hypothesis is that this mismatch in blood (or oxygen) supply and demand in the heart occurs when the runner picks up the pace, producing an adrenaline surge and increased physiologic demands on the heart, once the finish line is mentally within sight.
Based on this hypothesis, the International Marathon Medical Directors Association issued an advisory in March, 2010 that recommended, among other things, that athletes "not sprint the last part of the race unless you have practiced this in your training."
The concept here is that a susceptible heart (in a susceptible athlete) is triggered at a particular moment in the race to have a fatal arrhythmia because of a specific trigger. The surge hypothesis might not explain all running race-related deaths, but is a plausible explanation for the physiology behind the majority of the deaths that occur late in a race.
It's very likely that the same concept is in play in triathlon-related sudden cardiac death.
What's going on in triathlon?
In triathlon, athletes have died at any point during the race--from the first few strokes of the swim through the final strides of the run. And a couple athletes have collapsed with SCD even a few hours after the finish. But the majority of deaths have occurred during the swim. USA Triathlon issued a report last year that summarizes these facts.
What might be the trigger for sudden cardiac arrest during the swim portion of a triathlon?
Recently, two researchers in the U.K.--Michael Shattock and Michael Tipton--have offered a new hypothesis that they have labeled autonomic conflict [2,3]
To understand their hypothesis, we first need to talk for a moment about some features of the heart's physiology.
Sympathetic and Parasympathetic Influences
One component of our nervous system is called the autonomic system. This portion of the nervous system is involuntary, responding to internal and external stimuli below the level of our consciousness. The autonomic nervous system has 2 different divisions--the sympathetic and parasympathetic systems. Each of these divisions can operate independently, often with opposite effects on the body's organs, including the heart.
We often think of the sympathetic nervous system as being excitatory--providing the so-called "fight or flight" response. When activated, the sympathetic nervous system has several effects on the heart: an increase in heart rate, vasodilation of the coronary arteries (leading to more blood flow), and increased contractility (contraction strength) of the heart muscle. And importantly for athletes, activation of the sympathetic nervous system also increases the blood flow to the skeletal muscles, decreases blood flow to the abdominal organs, and opens up the airways of the lungs.
In contrast, the parasympathetic nervous system has an inhibitory effect on the heart, acting to restore a baseline heart rate after sympathetic activation and by slowing electrical conduction in the specialized areas of the heart's electrical system known as the sino-atrial (SA) node and the atrio-ventricular (AV) node. In well-trained endurance athletes, the parasympathetic nervous system is often highly developed, and is one cause of a very low resting heart rate.
Drs. Shattock and Tipton have proposed a mechanism where sudden activation or sudden increase in activation of both the sympathetic and parasympathetic nervous systems can produce a fatal arrhythmia. This idea is supported by studies in isolated hearts as well as in healthy volunteers.
Let's say that an athlete's heart might be predisposed to an arrhythmia because of one or more anatomic or physiologic conditions such as: congenital or inherited long QT syndrome, coronary artery disease, myocardial hypertrophy, ischemic heart disease, or pathologic hypertrophy (eg, hypertrophic cardiomyopathy).
During an open water swim, an athlete's sympathetic nervous system is activated because of physical exertion, (relatively) cold water temperature, anxiety, or even anxiety or overcompetitiveness. The parasympathetic nervous system is activated because of facial wetting, water entering the mouth, nose, and pharynx, and extended breath holding--and particularly so, just at the moment of breaking a breath hold. At that very moment, there can be maximal parasympathetic activation.
These scientists suggest that this autonomic conflict--between the sympathetic and parasympathetic nervous systems--is what triggers a sudden, potentially fatal arrhythmia.
This is a plausible hypothesis. It fits with the observations that have been made on victims of sudden cardiac death during open water swimming. And it fits with the general concept of a susceptible heart and an arrhythmia trigger that seems to be in play in victims of SCD in other sports.
1. Kim JH et al. Cardiac arrest during long-distance running races. N Engl J Med 2012;366:130-140.
2. Shattock MJ, Tipton MJ. 'Autonomic conflict': a different way todiedu ring cold water immersion? J Physiol 2012;590:3219-3230.
3. Tipton MJ. Sudden cardiac death during openwater swimming. Br J Sports Med 2013. Online in advance.
1. Sports-relatd sudden cardiac death in the general population
2. Athletes, sudden death, and CPR