physiology

Update on Swimming Induced Pulmonary Edema (SIPE)

May 26, 2015 By Larry Creswell, MD 6 Comments

I saw this week that there was an important new paper on swimming induced pulmonary edema (SIPE). Richard Moon, MD, and his colleagues at Duke University published a report entitled, “Immersion Pulmonary Edema and Comorbidities: Case Series and Updated Review” in a recent edition of the sports medicine journal, Medicine & Science in Sports & Exercise (1).

SIPE is known to occur not only in recreational or competitive swimmers, but also in divers. In fact, the condition was first recognized because of breathing difficulties encountered by military divers. As triathlete and swimmer readers here will know, there are many reasons why an athlete might develop shortness of breath during an open water swim. Water conditions, water and air temperature, exertion, and anxiety all play a role. SIPE is something different, altogether, though. This is a condition that develops because of immersion in the water, in which fluid builds up in the lungs and makes breathing difficult. The condition is believed to be self-limiting; if a swimmer gets out of the water, the condition will resolve. The underlying mechanisms and risk factors are not completely understood.

I’ve written about this condition in 2 previous blog posts….SIPE and More on SIPE. These posts might be a good starting point.

The newly published report is important because it reviews the medical literature and gathers all of the pertinent information about pre-existing medical conditions, or so-called comorbidities, in victims of SIPE. Dr. Moon is probably the world’s foremost authority on the topic of SIPE, so this new report deserves our attention.

The Study

There are 2 parts to the study: 1) a look at the Duke University experience with recreational swimmers who’ve had a SIPE episode and 2) a review of the medical literature on SIPE cases, both in military and recreational divers and swimmers.

In the first part, the investigators collated information on 41 swimmers who, over the past several years, had been studied at Duke University after reporting a SIPE episode. The mean age was 50.1 +/- 10.8 years (range, 25-71 years). Complete medical history data was available for 36 of the 41 swimmers.

In the second part, the investigators collected 45 previously published articles in the medical literature that reported on 292 cases of SIPE. There were 156 recreational swimmers or divers (89 men and 67 women), with a mean age of approximately 47.8 +/- 11.3 years. There were also 136 military swimmers or divers (135 men and 1 woman), with a mean age of approximately 23.3 years (range, 18-47 years).

For each of these groups, the investigators gathered information about pre-existing medical conditions in order to determine potential risk factors for the development of SIPE, focusing on: hypertension (high blood pressure), lung disease, overweight/obesity, sleep apnea, hypothyroidism, and cardiac abnormalities).

The Results

Among the Duke University group, 9 (25%) of the 36 swimmers with available health history were completely healthy. The remaining 27 (75%) had 1 or more medical/health conditions, including:

overweight/obesity in 12
hypertension in 7
cardiac arrhythmias in 4
heart valve problem (mitral valve prolapse) in 1
reduced heart function in 2
repaired congenital heart conditions in 2
asthma in 3
COPD in 1
reactive airways disease in 1
hypothyroidism in 3
diabetes in 2
polycystic ovary syndrome in 1
obstructive sleep apnea in 2

Twelve subjects had more than one of these conditions.

In the literature review, all of the 136 military swimmers and divers were healthy; they had none of the pre-existing medical/health conditions that were surveyed. In contrast, 70 (45%) of the 156 recreational swimmers or divers had one or more significant pre-existing risk factors:

asthma in 4
enlarged heart in 2
arrhythmias in 2
coronary artery disease in 3
diabetes in 4
exercise-induced cough in 1
Elevated serum lipids in 22
hypertension (high blood pressure) in 25
thickening of the left ventricle in 9
peripheral vascular disease in 1
sleep apnea in 6

As a side note, approximately 17% of cases in the literature review reported similar previous episodes or follow-up episodes that were suggestive of SIPE, giving an important look at the potential recurrence rate. And in total, 6 fatal cases of SIPE were identified in the literature review.

My Thoughts

How can all of this collated information be useful to us?

First, it’s important to note that all of the military swimmers and divers included in the literature review were healthy. We shouldn’t overlook the possibility that even completely healthy swimmers may experience SIPE.

Second, the recurrence rate of ~17% in the literature review is probably an underestimate. No doubt, some swimmers who experienced a worrisome episode of SIPE might avoid future swimming altogether. It’s very important to remember that this condition may recur.

Third, it’s very apparent that, among recreational swimmers who experience SIPE, the prevalence of important pre-existing medical conditions is rather high, at 75% in the Duke group and 45% in the recreational swimmers in the literature review. I suspect that the Duke investigators were more thorough in their history-taking and the 75% is probably more reflective of the reality.

The investigators’ aim was to identify risk factors for SIPE. Sadly, there’s obviously no single, unifying thread here. Hypertension (high blood pressure) was the most commonly identified condition among the cases, but this accounted for only ~15% of the cases. As I mentioned at the top, the physiologic underpinnings of SIPE are not completely understood and indeed there may be more than one responsible mechanism leading to some common final pathway by which fluid accumulates in the lungs. All of the various cardiovascular abnormalities identified in the cases might conceivably play a role. There’s more to learn.

It’s worth noting that the long list of medical conditions that were identified deserve careful medical attention before participating in recreational swimming events.

Advice

I’ll reprint here my best advice to athletes and event organizers regarding SIPE. I originally included this in another blog post, but this is still my best advice!

Triathletes and open water swimmers should be aware of SIPE and the possibility that this condition can be lethal.
Symptoms of SIPE can manifest for the first time even in experienced swimmers. Symptoms may develop rapidly, be unexpected, and confuse the athlete about the cause.
The development of SIPE does not appear to be confined to cold water swims or only to victims who are wearing a wetsuit at the time.
SIPE appears to be self-limiting–that is, the symptoms will subside if the victim stops exercising and gets out of the water.
Because of #2, #3, and #4, athletes who experience breathing difficulties in the open water should treat the problem like a medical emergency and STOP swimming and SEEK immediate assistance. Because of the challenges of rescue in the open water, your life could depend on recognizing a problem early and getting out of the water. I would encourage affected athletes to get complete medical evaluation as soon as possible after an episode.
There appear to be no effects on lung function after an episode of SIPE, but repeat episodes of SIPE may occur.
Affected athletes have described a variety of strategies for preventing repeat episodes of SIPE. From athlete accounts, no single strategy appears to be universally successful.
Affected athletes should use EXTREME CAUTION in subsequent open water training and races, being hypervigilant for warning signs.
Event organizers and on-water rescue personnel should be familiar with SIPE. The safety plan should allow for athletes with breathing difficulties to be removed from the water as quickly as possible.

Reference

1. Peacher DF, Martina S, Otteni C, et al. Immersion pulmonary edema and comorbidities: Case series and updated review. Med Sci Sports Exerc 2015;47(6):1128-1134.

2. More on Swimming Induced Pulmonary Edema (SIPE)

Exercise and Acute Heart Injury: An Introduction

October 23, 2013 By Larry Creswell, MD Leave a Comment

I’ve talked here at the blog on many occasions about the health benefits of exercise. Once again, I’ll point out that those many benefits are undeniable.

Over the years, many studies have been devoted to questions like:

How little exercise is needed to produce those benefits?

What intensity is needed to enjoy those benefits?

Answers to those questions have guided the development of the various consensus guidelines about exercise as a part of healthy living. Check out the guidelines from the American Heart Association, World Health Organization, or the U.S. Centers for Disease Control.

Recently, though, there’s been increased attention paid to the potential issue of harm that might come to the heart because of too much exercise. The surprising–and rather serendipitous–finding of unusual scarring, or fibrosis, in the hearts of long-time marathoners has raised many important questions. In clinical practice, we usually associate such findings with serious heart problems. Yet the affected athletes may have gone a lifetime without any indication of a heart problem.

At least a couple working hypotheses have emerged:

1, Repeated episodes of seemingly routine, but intense exercise produces the harm, or
2. Increased inflammation from each episode, or a prolonged inflammatory state, produces the harm.

For now, let’s focus on the first hypothesis. And let’s consider the possibility that with even just a short period of intense exercise, a small amount of harm, or damage might come to the heart….and that little by little this damage accumulates over the years.

In today’s blog post, we’ll lay the necessary foundation for our discussion by developing some of the vocabulary we’ll need. In my next two posts, I’ll talk about what’s known regarding acute heart injury after running and after triathlon, specifically.

Skeletal Muscle and CPK

It’s long been known that periods of exercise can lead to skeletal muscle injury. In the early 1970s it was recognized that this injury was associated with release of proteins from the muscle cells into the bloodstream where they could be detected and quantified. The primary example is creatine phosphokinase (CPK), an enzyme that catalyzes the reversible reaction between creatine and phosphocreatine and is central to the muscle’s energy metabolism. When CPK is measured in the bloodstream as an indicator of muscle injury, we call the CPK a biomarker for muscle injury.

By the late 1970s enough investigation had been completed to know that elevation of the CPK could be mild in the case of recreational exercise or quite severe after efforts such as marathon running.

Heart Muscle and CPK-MB

It turns out that there are actually 3 different forms, or isoenzymes, of CPK. One of those forms, the CPK-MB is found almost exclusively in heart muscle. More than 98% of the body’s CPK-MB is found in the heart, while the remaining 2% is found in skeletal muscle. As a result, the CPK-MB can be used as a specific biomarker for heart muscle injury.

In clinical practice, a blood test showing elevation of the CPK-MB was used for many years as our way of confirming the diagnosis of acute myocardial infarction (MI), the condition that results from sudden, complete blockage of one of the coronary arteries. In the case of acute MI, there is a very characteristic pattern to the CPK-MB elevation found in the blood, with a rise in level very soon after the coronary artery becomes blocked, a peak level about 24 hours later, then a slow return to normal over several days’ time.

Exercise and the Cardiac Biomarkers

Around the time of the 1979 Boston Marathon, Dr. Arthur Siegel from Boston was interested in the newly available CPK-MB biomarker and enlisted 15 male marathoners to serve as subjects for a study. In their training leading up to the race, these runners were found to have borderline or slightly elevated blood levels of CPK-MB despite being completely healthy from a heart standpoint.
When their CPK-MB levels were checked 24 hours after the Marathon, there were elevations of up to 21 times normal, again without any other overt sign of a heart problem.

This was the first of many, many studies on cardiac biomarkers and exercise. We’ll talk about the results of these studies in more complete detail in my next two blog posts.

Today, the CPK-MB is seldom used clinically for the purpose of identifying cardiac injury. Instead, we measure cardiac troponin (cTn) which is even more specific for cardiac injury than the CPK-MB. But this newer biomarker works much the same way: with acute MI, there is a steady rise in the cTn to a peak level about 24 hours later, then a slow, gradual return to normal over several days’ time.

Exercise and Cardiac Structure and Function

In modern cardiology practice, we have many different diagnostic tests that help us define the heart’s structure and to asses its function. For the purpose of our discussion here, the important options are the echocardiogram (using ultrasound), the CT scan (using x-rays), and the MRI (using a powerful magnet).

Echocardiogram

Cardiac CT

In recent years, investigators have used these imaging tests to study the structure and function of the heart immediately after periods of intense exercise like marathon running or long-distance triathlon. The findings are intriguing.

Stay tuned for my next blog post devoted to acute heart injury–biomarkers and imaging tests–specifically after running events.

Fatal Arrhythmias in Open Water Swimming: What’s the Mechanism?

March 10, 2013 By Larry Creswell, MD Leave a Comment

We’ve talked preveiously 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 [1]. These investigators found that fatalities during marathons are not distributed uniformly along the race distance. Instead, they predominate duirng 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.

A Hypothesis

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.

It’s Plausible

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.

References

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.

2. Athletes, sudden death, and CPR

Does the Heart Get Tired?

January 16, 2013 By Larry Creswell, MD Leave a Comment

In my monthly column at Endurance Corner, I try to answer the question, “Does the Heart Get Tired?” Avoiding the notion of “tiredness,” I talk about the phenomenon of cardiac fatigue and relate that to endurance sport. This is useful reading for the endurance athlete because recent warnings about potential long-term health risks related to exercise often mention cardiac fatigue as one red flag.

More on Long-term Cardiac Risks of Endurance Sport

December 28, 2012 By Larry Creswell, MD 2 Comments

Last week I got an inquiry from Casey R. Ruff at the Simon Fraser University in Burnaby, British Columbia, Canada in response to my blog post, “Don’t Stop Running Yet!” from earlier this month.

Ruff wanted to share his report from earlier this year, entitled “Consequnces of decades of intense endurance training: Is there a cardiovascular overtraining phenomenon?” This is an excellent review of the data on this topic. If you’re scientifically-minded, I would encourage you to give it a read. If you’re interested in pursuing further reading, the reference list is extensive and useful.

The report makes the case for the hypothesis that intense endurance training over many years may produce unwanted heart disease. The situation is summed up well in this figure which suggests a sweet spot, or “healthy zone,” for training volume. Less or more exercise leads to greater heart disease risk over the long term.

I’ve noted before that many biological systems are known to have a “sweet spot” phenomenon. This may be no different.

For the sake of balance, I shared some of my questions with Ruff:

1. Is there any evidence for increased mortality rate or shorter life-expectancy because of participation in some sort of endurance sport?

2. What explanation would you provide for the observation that most incidents of sports-related sudden cardiac death (SCD) occur in NON-veteran athletes? And with autopsies that often show relatively unremarkable cardiac findings?

3. Do you believe that veteran endurance athletes are at increased risk of SCD compared to non-veteran athletes? And what is the magnitude of that risk?

4. What are the consequences to the athlete who develops atrial arrhythmias? How bad is that problem?

Ruff and his colleagues correctly suggest that further investigation with longitudinal studies are sorely needed. I’m hopeful that with increased participation in endurance sports and increasing public dialog about this issue that these studies will be undertaken.

My Related Posts and Articles:

1. Don’t Stop Running Yet!

2. Short-term and Long-term Injury to the Heart with Exercise

3. Ironman and Heart Health: My Take on Things