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Sudden Cardiac Death

Some of the causes of Sudden Cardiac Death in young athletes.

Rich Peverley
Rich Peverley
Jerome Miron-USA TODAY Sports

First, if you don't know CPR, please learn.  You might save someone's life. 
Contact the American Heart Association to find a class near you.

Rich Peverley had Sudden Cardiac Death Monday night in Dallas.  By coincidence, I got a flyer in the mail from Duke on Wednesday.


Sudden Cardiac Death and "heart attack" are not quite the same thing.  When people say "heart attack" they usually mean a myocardial infarction.  Myocardial infarction is a blockage in an artery.  If your heart is like a house, a myocardial infarction is plumbing problem.  Sudden Cardiac Death is a problem with your electricity.  A myocardial infarction can lead to Sudden Cardiac Death, but other conditions can lead to it too.

Normal Cardiac Physiology.

The heart beats using electricity.  A normal heartbeat starts at the top of the heart in the Sinus (SA) node.  It spreads across the top of the heart to the Atrioventricular (AV) node.  It pauses there a while, then travels to the bottom of the heart via the Bundles of His, which function like wires carrying the electrical impulse.  The Right Bundle Branch and the Left Bundle Branch are the two parts of the Bundles of His.

The EKG tracing shows the electrical impulses as they move through the heart.  The first small blip is the P wave.  It represents the top part of the heart contracting.  The next, largest blip, is the QRS complex.  It is the bottom part of the heart contracting.  Finally, the T wave is the final blip.  It is the bottom part of the heart repolarizing.


When muscles contract, there are pores in the cell membrane that open up and let sodium ions flow into the cell and potassium and calcium flow out.  When the cell repolarizes, and gets ready to contract again, sodium gets pumped out of the cell and potassium and calcium get pumped back inside.

Atrial Fibrillation

Atrial Fibrillation is a very common type of abnormal heart rhythm.  In "A fib", the top part of the heart basically just jiggles.  Electrical impulses hit the AV node irregularly.  As a result the bottom part of the heart fires irregularly.  However, the AV node slows the frequency down.  If the AV node is seeing 300 impulses a minute it is generally sending far fewer impulse down the Bundles of His.

Rich Peverley has atrial fibrillation.  By itself, this would not normally be a reason for your heart to stop.  Millions of people have A fib.  You probably know people who have it.  A fib is not a good thing, as it can lead to strokes, but most people with it suffer no ill effects.

Wolff-Parkinson-White Syndrome

Wolff-Parkinson-White Syndrome, or WPW, is an abnormal "wire" (called an "accessory pathway") in the heart that bypasses the AV node. 

Again, by itself, this is no big deal.  It causes an abnormal EKG, where the first part of the QRS complex slopes upward in a way that looks like the Greek letter Delta, creating the "Delta wave". 


By itself, WPW will not kill you.  Put A fib and WPW together, though, and now you have a potentially fatal combination.  If a normal person goes into A fib, the AV node slows down the electrical impulses so that the bottom part of the heart beats much slower than the upper part.  If you have WPW and and go into A fib, the extra wire takes the electrical impulses right to the bottom part of the heart.  The bottom part begins to quiver.  This is Ventricular Fibrillation.  Ventricular fibrillation kills people unless you "defibrillate" them and shock their heart back into rhythm.

WPW can be cured with an ablation.  A Cardiologist can thread catheters into the heart, find the location of the accessory pathway, and destroy it with radio waves, heat, or chemicals.

Long QT syndromes

The "QT interval" is the length of time from the start of the QRS complex to the end of the T wave.  It measures how long it takes for the bottom part of the heart to depolarize and, more importantly, repolarize.  Some people inherit ion pumps that don't work very well.  As a result it takes longer than normal for the heart to return to its baseline.  This becomes a problem if the next heart beat happens while the bottom part of the heart is still recovering.  This is called "R on T".  If the next QRS complex happens while the last T wave is still going on, it can lead to a potentially fatal rhythm called "Torsades de Pointes".  Like Ventricular Fibrillation, Torsades de Points can result in death.  Stopping it often requires defibrillation.

People sometimes kill themselves demonstrating defibrillators.  If you shock yourself at the wrong moment with an unsynchronized defibrillator, you can give yourself "R on T" and create Torsades de Pointes.  The Automatic Defibrillators you see in malls, etc. WILL NOT DO THIS!  They are designed to be smart enough not to shock the heart during the T wave (even if the people operating them aren't).

Long QT syndromes can be managed with medicines.  Most people with these syndromes will have surgery to implant a defibrillator in their chest.  Long QT syndromes generally are a contra-indication to athletic participation.

Hypertrophic Cardiomyopathy

Hypertrophic Cardiomyopathy (HCM), also known as Hypertrophic Obstructive Cardiomyopathy (HOCM), Idiopathic Hypertrophic Subaortic Stenosis (IHSS), etc. is an abnormal thickening of part of the heart muscle.


Blood travels from the lungs to the left atrium to the left ventricle and out the left ventricular outflow tract (LVOT) to the aorta and on to the body.  In HCM, the contraction of the left ventricle causes dynamic obstruction of the LVOT.   As a result, the flow of blood is dramatically reduced.  I recently treated an older lady who had HCM.  At rest, the gradient across her LVOT was around 100.  That means if the blood pressure in her arm was 130, the pressure in her left ventricle was 230.  With just the effort of walking around, the gradient went up to 180!  Fast heart rates make HCM worse.  Adrenaline makes HCM worse.  In an athlete with HCM, during exertion the pressure in the heart can go so high that the heart is unable to pump the blood out.  At that point, the athlete will pass out.  Sometimes, the heart will go into ventricular fibrillation.

HCM is treated with medicines that slow the heart and make the contractions of the heart less forceful.  There are surgical procedures that can open up the LVOT.  Like people with Long QT Syndromes, many people with HCM will have surgery to implant a defibrillator in their chest.  HCM generally is a contra-indication to athletic participation.

Preventing Sudden Death

Athletes usually have pre-participation screening exams.  Unfortunately, these may not help that much.  If an athlete has HCM, they may have a heart murmur (although at rest they may not).  WPW and Long QT syndromes would not necessary have any physical exam findings.  A routine EKG will pick up WPW and Long QT syndromes and may show changes that can occur with HCM.  Echocardiogram is needed to diagnose HCM.  Personal and Family History can help find athletes at risk for sudden death.  Any athlete with a history of passing out, especially during exercise, needs further evaluation.  An athlete with a family member who had Sudden Cardiac Death also needs further evaluation.