Friday, September 4, 2009

The Athlete's Heart: Syncope--Part 2


Last week we talked about the problem of syncope and described the various causes. This week we’ll talk about the medical evaluation and treatment for the athlete with syncope. As I explained last week, syncope can sometimes be explained simply by benign problems such as dehydration, but the majority of individuals should be evaluated carefully for an explanation. This is particularly true for the athlete because of the demands placed upon his cardiovascular system and the potential risk of sudden death from unrecognized underlying heart disease.


MEDICAL EVALUATION


In general, the medical evaluation of patients with syncope should seek to determine a specific cause, with a special emphasis on distinguishing heart-related (cardiac) from non-cardiac causes. And, as for the evaluation of most medical problems, your physician will want to gather information from a careful medical history, including the syncopal event itself, a physical examination, and then one or more diagnostic tests. Because syncope is a common problem in the general population, most primary care physicians are knowledgeable about the evaluation of patients with syncope, but sometimes referral to a cardiologist, neurologist, or other medical specialist may be necessary.


Medical History


Much information can be gathered from a careful medical history. Your physician will be particularly interested in the events leading up to, and immediately after, your episode of syncope. In some cases, information provided by bystanders may be very important. This is particularly true if you have experienced a loss of memory (amnesia) for the events immediately preceding the syncopal event. Syncope should be distinguished from near-syncope, or “almost blacking out.” For our purposes here, we’re considering only syncope, characterized by a true loss of consciousness. Your physician will also want to know about any previous episodes of syncope, about any medications you may be taking (especially beta-blockers or inhaled bronchodilators for asthma), and about any personal or family history of heart disease.

Athletes with neurocardiogenic syncope typically report that their syncope occurred in the standing position, often after exercise, and often in the setting of some degree of dehydration. The syncope is usually preceded by feelings of light-headedness, a warm feeling, or nausea. Athletes may have experienced episodes of near-syncope previously and learned that prolonged standing after exercise should be avoided.


Athletes with situational syncope often relate a history of a causative symptom that reproducibly produces syncope.


Athletes with orthostatic syncope typically report the development of syncope when they change from the sitting to standing position. Upon reflection, they may admit to some degree of dehydration.


Athletes with neurologic syncope often report neurologic symptoms (eg, vertigo, visual changes, or muscle movement clumsiness) that precede their syncopal event. These athletes might be well served by referral to a neurologist for further evaluation and treatment.


More worrisome is syncope that occurs during exertion or in the sitting or lying positions. Syncope that is preceded by palpitations or chest pain or discomfort is also worrisome. All of these features suggest a cardiac cause and merit a more thorough search for a cardiac cause.


Physical Examination


In many cases, the physical examination will be unremarkable and offer no clues to the cause of syncope. Nonetheless, in some small number of cases, though, there will be specific clues from the physical examination that point to an underlying condition that might be the cause of syncope.


Patients should have their vital signs (heart rate and blood pressure) measured in the supine, sitting, and standing positions. Findings here may point to orthostatic hypotension as a cause of syncope.


The body habitus (height and shape) may suggest Marfan’s syndrome and this can be evaluated further with genetic testing. Your physician may hear bruits (or turbulent blood flow) in the carotid arteries, suggesting underlying vascular disease. The heart sounds may be abnormal, including the presence of an S3 or S4 gallup, but these findings are common in athletes even without a history of syncope. A careful examination should be made for evidence of heart valve disease because specific murmurs may suggest a cause of syncope and prompt further testing.


Diagnostic Tests


Athletes with syncope should have a complete medical history and physical examination and then have an electrocardiogram (ECG) and echocardiogram to complete the initial evaluation. The resting ECG and echocardiogram will identify or exclude many of the potential cardiac causes of syncope. The information gathered from these tests will then be used to determine if any additional diagnostic testing is needed.


Electrocardiogram (ECG). The ECG is usually done in the physician’s office and the results are immediately available. Electrodes are attached to the chest, arms, and legs and are used to make recordings of the heart’s electrical activity measured at the skin surface. In athletes with syncope, the ECG may be abnormal in 50% of cases, but will point to a specific cause of syncope in only a very small number of cases. Abnormalities that can be identified on the ECG that may be responsible for syncope include: long QT interval, pre-excitation or Wolff-Parkinson-White syndrome, pauses in the electrical activity, or heart block. It’s not so important that the athlete understand each of these possibilities; instead, any of these findings will prompt your physician to do additional diagnostic testing or to provide a specific treatment.


Echocardiogram. The echocardiogram is usually ordered by the physician and done in a cardiologist’s office or at the hospital. With the use of ultrasound, images are made of the heart that show the anatomy (structure) of the heart in great detail. The size of the heart chambers and heart walls can be made, the structure and function of the heart valves (aortic valve, mitral valve, pulmonary valve, tricuspid valve) can be determined, and estimates of the pressures in each of the heart chambers can be made. In the athlete without a history or physical findings that suggest cardiac disease, the chances of finding an abnormality with echocardiography are low, but not zero. Cardiac conditions that may cause syncope and which can be diagnosed with echocardiography include: aortic stenosis (narrowing of the aortic valve), benign tumors of the heart (eg, myxomas that obstruct blood flow in the heart), or hypertrophic obstructive cardiomyopathy (HOCM).


Holter monitoring. If the athlete reports an abnormal history of palpitations or if palpitations have immediately preceded the syncopal event—and if the ECG and echocardiogram do not suggest other cardiac diseases—holter monitoring may be useful to diagnose arrhtyhmias (abnormal heart rhythms) that may be responsible for syncope. With this test, the patient wears a tape recorder and several electrodes for a period of 24-72 hours and a recording is made of the heart’s electrical activity. The patient can often press a button to indicate symptoms such as palpitations that may later be correlated to the heart’s electrical activity at that moment. The Holter monitor may uncover atrial arrhythmias (often responsible for near-syncope) or ventricular arrhythmias (often responsible for syncope). This test may also show periods of heart block or pauses in the electrical activity that are not evident on the resting ECG.

Tilt-testing. For the athlete with syncope, and for whom the ECG and echocardiogram do not suggest a cardiac cause, tilt testing is the next appropriate diagnostic test. This test is used to establish the diagnosis of neurocardiogenic syncope and is done in a cardiologist’s office or at the hospital. The patient is strapped to a tilt table and measurements are made of the vital signs in various positions. Intravenous medications may be given to exaggerate the effects of the test and help the physician establish a diagnosis.


Other cardiac tests. A variety of additional diagnostic tests are available for patients in whom a cause for syncope cannot be determined on the basis of history, physical examination, ECG, echocardiogram, Holter monitoring, and tilt-table testing alone. Additional underlying cardiac diseases (that may be responsible for syncope) can be identified or excluded using: stress testing, cardiac catheterization, more extensive electrophysiologic testing, or the use of an implantable loop recorder (to make more extensive recordings of the heart’s electrical activity). If an athlete’s cause of syncope remains uncertain after the more basic tests—and particularly if syncope occurs with exertion—he should be referred to a cardiologist for evaluation and, possibly, one or more of these additional diagnostic tests.


TREATMENT


The treatment for athletes with syncope will be individualized and targeted at the underlying cause. The goal of treatment will be to prevent (or reduce the frequency of) future episodes. For athletes in whom a cardiac cause is determined, there will be specific treatments for any of the myriad of responsible cardiac causes. We’ll discuss these treatments at another time and consider whether continued participation in athletic activity is prudent.
For athletes with situational syncope, the inciting cause should be avoided. For athletes with orthostatic syncope, dehydration should be avoided and medicines such as beta-blockers should be discontinued. For patients with neurologic syncope, further diagnostic testing under the direction of a neurologist may be needed.


Most commonly, however, athletes will be found to have neurocardiogenic syncope and there is a variety of treatment options.


Avoidance. The most important “treatment” will be to avoid situations that predispose the athlete to developing syncope. And the most common situation to avoid is prolonged standing after exercise—particularly strenuous exercise. It is important for the athlete to recognize their own specific premonitory symptoms (eg, light-headedness, nausea) and remember to sit down or lie down to prevent a syncopal episode.


Blood volume. Anything that produces a relative or absolute decrease in the circulating blood volume (eg, dehydration, certain medications) should be avoided. Compression stockings in the post-exercise period may be helpful in this regard.


Drugs. Many different medications have been used to treat patients with neurocardiogenic syncope, including beta-blockers (eg, propranolol, atenolol), alpha-agonists (eg, midodrine), and calcium channel blockers (eg, disopyramide). Unfortunately, long-term studies have often failed to show a convincing benefit. Importantly, beta-blockers may be poor choice in athletes because these medications limit the heart rate.


NEXT WEEK

Next week, I'll be back to talk about what I've called the athlete's cardiac paradox. Until then....

Sunday, August 30, 2009

VSA Open Water Swim Race


I traveled to Eagle Lake, north of Vicksburg, for the 1st annual Vicksburg Swim Association (VSA) Open Water Swim Race. It turns out this is Mississippi's first-ever open water swim race.
Congrats to VSA and coach Mathew Mixon for making this event happen. I know that it's hard sometimes to get good ideas off the drawing board and into action. The event was well-organized and I heard many positive comments from the participants and the spectators.
It turns out that Eagle Lake is a fair drive from Jackson....152 miles round-trip for me! But the lake was a beautiful setting for the race. Actually, 3 races: a 1-mile (1600 m) swim, a 1/2-mile swim, and a 1/4-mile swim. The event was sanctioned by USA Swimming and there were probably equal numbers of adults and children participating. It was mostly sunny, with high overcast clouds, the lake was calm, and there was no boating activity to mess things up!
Each of the 3 races featured a time-trial start from the end of a pier....from the seated position. That's a first! The course was triangular. I started 9th, following 8 children. I tried to gain ground from the get-go, but even the little kids were too quick, it turned out. We struggled on the backstretch to see the far turning buoy....and on the inbound leg we probably added 300m to the course....when I couldn't see the buoys (or the starting/finishing pier) I just followed the people in front. Stupid!
Finished in about 28 minutes. Almost hard to believe it took that long, but I'm sure we swam a fair distance more than 1600m! Finished 7th overall and 1st for the adults.
I hope there is a 2nd annual edition of this race. I heard from Mathew Mixon today that he was pleased with yesterday's races and already looking forward to next year. They've tentatively scheduled the event for August 28, 2010. Perhaps it will become a tradition. I also spoke with the Makos coach, Eddie, yesterday about the possibility of a similar race here in Jackson next year. For the triathlete community, it would be great to have an open water swim race sometime in advance of the major local triathlons next summer. We'll see.
Next up for me....Nation's Tri (olympic distance) in Washington, D.C., in 2 weeks. Combining race with visit with my sister, Lori. Looking forward to the trip.

Friday, August 21, 2009

The Athlete's Heart: Syncope--Part 1



Some of you will know about professional triathlete Joanna Zeiger’s recent troubles with syncope. Her trials and tribulations with race-related dizziness are summarized in a nice article at Slowtwitch, “Zeiger sidelined by dizziness.” Her story is typical. This week and next week, we’ll talk about the causes, medical evaluation, and treatment options for syncope.

Syncope (syn' ko pee) is the medical term used to describe a brief period of loss of consciousness (either partial or complete) that is due to insufficient blood flow to the brain. This process is temporary and followed by spontaneous recovery. Patients often use different terms such as “dizziness”, “light-headedness”, “blacking out”, “passing out”, or “falling out” to describe this problem. This is a common medical condition that affects approximately 3% of the population at some point during life. It is increasingly common as we age, affecting 6% of individuals over the age of 75. It’s not surprising, then, that this is a fairly common problem among athletes.

Syncope may occur without warning or may be preceded by warning signs that are called premonitory symptoms. Typical premonitory symptoms include palpitations, light-headedness, grogginess, feeling warm, or experiencing nausea.


Types of Syncope

There are many types or causes of syncope and it can be useful to categorize the types as: 1) cardiac (heart-related), 2) non-cardiac, or 3) unknown. This framework helps the physician sort out an individual’s cause among the many possibilities and then provide any needed treatment.

Cardiac syncope

A variety of cardiac disorders can produce syncope, but cardiac causes account for the explanation in only 10% of cases. As patients age, it is more likely that a cardiac cause is responsible for their syncope. Some of the cardiac causes are potentially life-threatening, but most are less serious; all can be treated.

Life-threatening cardiac causes. Acute myocardial infarction (“heart attack”) or aortic dissection (tearing apart of the layers of the aorta) can produce syncope or other changes in the level of consciousness. Both of these conditions are usually accompanied by chest or back pain and can also be associated with shortness of breath. In these situations, syncope is the result of decreased blood pressure and/or decreased blood flow to the brain. Both of these conditions can result in sudden death and affected individuals require urgent medical attention.

Arrhythmias. The most common cardiac cause of syncope, though, is an abnormal heartbeat, or arrhythmia—either atrial (from the upper heart chamber) or ventricular (from the pumping chamber of the heart). Syncope can be the result of an abnormally fast (tachy-) or slow (brady-) arrhythmia. Bradyarrhythmias are usually found in patients with known, pre-existing heart disease, but they sometimes occur because of unwanted side effects of medicines (eg, beta-blockers for high blood pressure). It’s important to remember that the well-trained athlete typically has a baseline slow heart rate and this can sometimes confuse the picture. Syncope is more common with atrial or ventricular tachyarrhythmias, though. The atrial tachyarrhythmias include atrial fibrillation (A-fib), atrial flutter (A-flutter), and supraventricular tachycardia (SVT). These arrhythmias may be accompanied by chest discomfort, palpitations, or shortness of breath. With persistent arrhythmias, syncope often occurs when moving from the sitting to standing position (postural) due to decreased blood pressure. Ventricular tachyarrhythmias include ventricular fibrillation (V-fib) and ventricular tachycardia (V-tach). These arrhythmias are usually associated with known, pre-existing heart disease. Syncope due to ventricular tachyarrhythmias is not usually related to posture.

Cardiac blood flow obstruction. A third set of cardiac causes of syncope are due to obstruction to blood flow in the heart. This can be due to narrowing (stenosis) of the aortic, mitral, or pulmonary valves, hypertrophic obstructive cardiomyopathy (HOCM, one of the most common causes of sudden death in athletes), or to tumors of the heart. With these conditions, syncope is often sudden, without any preceding symptoms.

Low cardiac output. The last set of cardiac causes are those due to decreased pumping function, or cardiac output, from the heart. Long-standing congestive heart failure (CHF) or leaking (regurgitant) heart valves may lead to a low blood pressure that limits blood flow to the brain.

Non-cardiac syncope

Neurocardiogenic syncope. The most common type of syncope is termed neurocardiogenic, or vasovagal syncope. The term vasovagal conveys the association of “vaso,” for vasodilation of arterial system (leading to a decrease in blood pressure) and “vagal,” for the accompanying slow heart rate (sometimes produced by decreased activity in the vagal nerves). This type of syncope usually occurs in the standing position and is usually preceded by symptoms such as light-headedness, nausea, or sweating.

Situational syncope. A variety of precipitating factors, such as emotional stress, anxiety, pain, cough, urination, or defecation can lead to syncope. In this situation, the resulting syncope is thought to be due to a reflex, sudden decrease in heart rate that produces a transient reduction in blood flow to the brain.

Orthostatic syncope. Syncope can be caused by a sudden drop in the blood pressure as we rise from a sitting to standing position. The medical terms for this situation are orthostasis, or orthostatic hypotension (reduced blood pressure). Ordinarily, the body adjusts to this change in position by increasing the heart rate and increasing motor tone in the blood vessels to keep the blood pressure constant. When these mechanisms fail, the sudden (relative) drop in heart rate and blood pressure may produce syncope. This problem can be made worse by dehydration or medications that reduce the circulating blood volume or by medications that limit the blood pressure response (eg, beta-blockers).

Neurologic syncope. One last, unusual category of causes is termed neurologic. In this situation, the syncope is caused by a sudden decrease in blood flow to the brain in conditions such as stroke, transient ischemic attack (TIA, or “near-stroke”), or seizures. In one variant, syncope is due to a sudden decrease in blood flow to the posterior portion of the brain called the cerebellum. This is often due to pre-existing vascular disease in the vertebral arteries that supply this portion of the brain. Patients with neurologic syncope often experience other neurologic symptoms such as vertigo, visual changes, or muscle movement clumsiness immediately before the syncopal event.


Medical Evaluation

Syncope can sometimes easily be explained by benign problems such as dehydration, but the majority of individuals with syncope should be evaluated carefully for an explanation. Because of the demands on the athlete’s cardiovascular system during exercise, it is particularly important for the athlete with syncope to be evaluated completely.

Next week, we’ll talk about the medical evaluation of patients with syncope and discuss the various treatment options.

Sunday, August 16, 2009

The Athlete's Heart


Over the past few weeks, I've done a bit of reading about heart disease in athletes. And you'll recall that I promised to be back to report what I learned.
I could probably write a book....so if anybody out there wants to share their literary agent with me, drop me a line!
The outline would look like:
I. Introduction
II. Your Cardiovascular System
III. Symptoms of Cardiovascular Disease
IV. Cardiovascular Diseases
V. Diagnosis and Screening for Cardiovascular Disease
VI. Nutrition and the Cardiovascular System
VII. Vitamins, Supplements, and Alternative Therapies
VIII. Athletes Living with Cardiovascular Disease
IX. Resources
In the absence of a book deal, I'll serialize things here at the blog. I'll try to write a short section weekly about one specific topic. I'll even take suggestions about which topic to do next. Again, drop me a line with suggetions or questions.
Back next week with the first report!

Saturday, August 15, 2009

Triathlon Overhead

I was thinking the other day about the "overhead" associated with triathlon.


A few weeks ago, I finished up my first 12 months with Justin Daerr as my coach....and I was reflecting on the year. A year ago, we planned to devote 750 hours per year to training, or ~15 hours per week. As it turns out, we spent 655 hours on training....logging 540,000 yards of swimming, 4900 miles of riding, and 780 miles of running. I was sidelined for several weeks last summer and again this January because of running injuries or we might have reached the goal of 750 hours. Along the way, there were 5 triathlons (1 sprint, 3 Olympic, 1 IM), 1 duathlon, 1 tri relay (as the swimmer), 1 long open water swim race, and 1 training camp with Endurance Corner. There were 151 swim workouts, 175 bike workouts, 197 run workouts, 66 strength workouts, and 23 days off. A modest amount of time and training by Ironman standards, I suppose, but that's not what I was thinking about.....

Today, I'm thinking about the overhead....the additional time and energy that were needed to support those 655 hours. By my reckoning, the overhead for this past year included:

Showers. I like to get up and shower even before the first workout of the day, but I won't count this in the overhead....just the showers after the workouts (9x/week @ 10 minutes each = 78 hours/year).


Laundry. I've got a housekeeper to do the regular laundry, but I do all of the workout laundry (9x/week @10 minutes each time = 78 hours/year).


Race trip planning. Won't count any time for the local races....after all, it only takes a moment to fill out the registration form, etc. But the out-of-town trips took some time to plan....Hilton Head (1 hour), Chicago (3 hours), Disney World (twice, 2 hours each), Tucson (2 hours), Maryland (1 hour), Brazil (10 hours)....21 hours total.


Race travel. 80 hours total. The Brazil trip was a long one!


Buying triathlon supplies/equipment online. About 20 minutes each week (17 hours/year).


Buying triathlon supplies/equipment locally. About 10 hours for the new bike and ~17 hours total for everything else.


Bike maintenance/cleaning. About 20 minutes/week (17 hours/year).


Logging the workouts into TrainingPeaks (without technical difficulties....8 minutes per day, or 48 hours/year).


Talking with JD....phone/email/Twitter, etc....10 minutes/week, or 9 hours/year.


Volunteering at a couple triathlons. 3 hours for the local race, 8 hours for IM Florida 2008.


Driving to/from workouts. Jackson is small, so thankfully nothing's too far away. But the pool is a 20-minute drive and the closest of my gyms is an 8-minute drive. Usually ride from home. Conservatively, 1 hour 40 minutes each week, or 86 hours per year.


Tri Club. Not a big time consumer, but a couple meetings and social events, ~8 hours per year.


Reading magazines. Triathlete, Inside Triathlon, Bicycling, Runners World. About 25 minutes per week. Add in some online reading for another 15 minutes per weeek. About 35 hours/year.


Post-race celebration. There's some of this after every race, but I won't add this into the total. We'll say that celebration is just part of life!


And God only knows what I've left out....

So....getting out the calculator....that works out to 329 hours for the past year....or an overhead rate of about 50%. The tables in the triathlon books never seem to take this into account. So the next time you're talking to somebody about the 600 or 700 or 800 hours of training you've planned for the coming year, take a moment to think about the overhead.

At the Endurance Corner Tucson training camp in March, Jeff Shilt offered the advice that success in triathlon was related to one's ability in the area of "crap management." He's right! For the busy working triathlete, perhaps nothing is more important than managing the overhead. Something to keep in mind!


Toward more efficient management of triathlon overhead....

Thursday, August 6, 2009

Beach Bum Triathlon 2009


I raced in the Beach Bum Triathlon last Saturday in Hilton Head Island, South Carolina. I combined this with a trip to visit the parents....mom's birthday & dad recovering from eye surgery. Lori was also along, so we had a great weekend.
The race is produced by the local tri shop on Hilton Head, GoTriSports, and takes place two or three times each summer. The race seems to attract a fair number of out-of-town visitors in addition to the local triathletes. It's ultra-short: 500m swim in the ocean, 6 mi bike on the beach, and a 3 mi run on the beach. I'm calling it Ironman 9.3. Perhaps this is another brand that WTC could adopt!
This year I see that 215 people (or teams) completed the race. I finished 69th. But for a while, it looked like the prospects were much brighter....



The race starts with a mass start at the water's edge. As usual, I had a lackluster run into the waves and ended up behind ~50 people at the first turning buoy (only 50 meters from shore). I managed a good "backstretch" leg along the beach of ~400 meters, and got back to shore, and T1, in about 15th position.




I decided to use my moutain bike for the bike leg....and this was the most popular choice. I recall that Michael Lovato did the race (and won) the first time I did this race....and I seem to recall he used a tri bike. I did well on the bike, maintaining my position at about 15th in the race. I passed a couple people and was passed by a couple people. I was pretty happy. It's great to be near the front of the race!




I faded a bit in the run, though, losing 54 positions. In the end, I was 15th out of 45 men who were older than 40. I need to run better!



I've shared this already on Twitter, but this was my favorite bike at the race. Stylish and plenty of room for the athlete's nutritional products!

Next race....Nation's Tri in Washington, D.C., on Sept. 13th. Hoping for cooler weather and looking to have a better run.