Sudden Cardiac Death While Running

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Illustration by Heikenwaelder Hugo, wikimedia commons

The Tell-Tale Heart

Examining your risk for sudden cardiac arrest while running

DAVID ROCHE FEBRUARY 2ND, 2017

My wife and I have only one rule when it comes to running through pain. If either of us ever feels any unusual sensation in our heart, we promise to stop and walk home.

Initially, that philosophy was motivated not by science, but by fear. We had read the news stories about cardiac arrest in otherwise healthy athletes, and the tragedies stuck with us. You may have read about Micah True—also known as “Caballo Blanco,” of Born to Run fame—who died of cardiac arrest on a trail run in 2012, and every so often a similar story crops up in the local or national press.

In reality, sudden cardiac arrest in runners is much rarer than the hype machine suggests, but it is a serious risk that is important to understand.

Most cases arise from a heart condition known as hypertrophic cardiomyopathy, or HCM. “Many runners think they’re in the clear from chronic diseases solely because they run,” says Emily Kraus, a sports-medicine doctor at Stanford University. “Although physical activity is an excellent cardio-protective practice, it can’t always shield from those underlying, non-modifiable risk factors.”

Here are five questions to help you understand your risk of sudden cardiac arrest from HCM.

What causes cardiac arrest in healthy athletes?

HCM is a genetic condition that causes progressive thickening of the heart tissue. According to the American College of Sports Medicine (ACSM), when the muscle gets large enough, during exercise it “can start to quiver in ventricular fibrillation, which is the cause of sudden death.”

“Imagine the heart as an inflatable bouncy castle,” says Robyn Reed, a pathologist at Children’s Hospitals and Clinics of Minnesota. “The kids ricocheting around inside are the blood. If you get the castle too pumped up, the doorway gets squeezed shut and the kids have trouble squeezing their way out. It can even get so pumped up that it cuts off its own air supply (or blood supply), leading to tissue damage.”

Reed adds that HCM can interfere with heart-muscle contraction and even result in the muscle cells no longer “correctly conducting the electrical signals that tell your heart how to beat. They’ll still try to contract, but they’ll do it in a disorganized way.”

How common is HCM?

According to the ACSM, about one in 500 people have HCM. The condition is more common in men and in families with a history of the diagnosis.

How often does HCM lead to sudden death?

A 2012 study in the New England Journal of Medicine found that one out of every 259,000 marathon and half-marathon participants died of sudden cardiac arrest. For cases where data was available, 23 of 31 were due to HCM.

To put that in perspective, your odds of being struck by lightning this year are 1 in 960,000. So even though both events seem unlikely, just as you wouldn’t venture outside with a metal umbrella during a thunderstorm, you shouldn’t expose yourself to unnecessary risk from HCM.

While no statistics are available for lifetime mortality risk, most people with HCM never know. It’s a time bomb with a fuse that may never be lit. But when it is, it often ends quickly and tragically.

What can I do to understand my risk?

You wouldn’t drive 50,000 miles without taking your car in for a checkup. The same goes for your body—the ACSM recommends regular physical exams to screen for things like HCM. People with HCM “may develop a heart murmur or arrhythmia,” according to the organization.

Not all people with HCM get a “check-engine-light” warning, but some do. Symptoms include “chest discomfort with exertion, unreasonable breathlessness (this is not the same as the breathlessness experienced from hill or sprint repeats—that’s normal), dizziness, fainting or blacking out,” says Kraus. If one of those lights pops on, see a doctor before continuing activity.

Kraus identifies additional heart-related risk factors as “a family history of a blood relative who had a heart attack before the age of 55 years (father or brother) or age 65 years (mother or sister), or an unexplained sudden death before age 50 (including drowning, unexplained car accident or sudden-infant-death syndrome).”

A sure diagnosis requires an electrocardiogram or echocardiogram. Some universities, like Rice, now require these tests before an athlete competes in intercollegiate athletics. Consider having your heart tested before embarking on a grueling training regimen.

 What should I do if I have HCM?

If you have HCM, it’s not the end of the world. The risk of death for people with HCM is 2 to 4 percent per year.

There are a few different approaches to living with HCM. In general, says Kraus, “If a runner has been diagnosed with HCM, they should not run due to the risk of sudden cardiac death.” She adds that “depending on the severity of the diagnosis,” a doctor may prescribe low-to-moderate-intensity activity or install an implantable defibrillator. Treatment plans are highly personal and should be determined by a cardiologist.

David Roche is a two-time USATF trail national champion, the 2014 U.S. Sub-Ultra Trail Runner of the Year and a member of team Hoka One One and Team Clif Bar. He works with runners of all abilities through his coaching service, Some Work, All Play. Follow David’s daily training on Strava here, and follow him on Twitter here.

Why hypokalemia causes tachycardia

Principles of Critical Care, 4e >

Potassium is the most common cation in the body.Normal serum potassium ranges from 3.5 to 5.2 mmol/L. The molecular weight of potassium is 39.1, so a daily potassium intake of 80 mmol is roughly equivalent to 3.1 g of potassium.

The normal physiologic handling of potassium can be viewed as a three-step process: 

1. ingestion
2. cellular distribution
3. excretion

Irregularities at any of these steps can result in pathologic serum potassium concentrations.

Cell Uptake: Following absorption, potassium distributes among the intracellular and extracellular compartments. The intracellular compartment acts as the primary buffer to changes in serum potassium concentration.

The Na-K-ATPase pump, driven by a ubiquitous cell surface enzyme, moves potassium into cells while pumping sodium out of cells. The pump is stimulated by β2-adrenergic activity, while α-adrenergic activity results in potassium efflux.53 Insulin also stimulates the activity of this pump and is independent of its hypoglycemic activity.54

Extracellular pH can affect the cellular distribution of potassium. Various explanations have been proposed, including a direct effect of pH on the Na-K-ATPase, or an H+-K+exchange to maintain electroneutrality. The effect of pH on potassium distribution varies depending on the nature of the acid-base disturbance. Respiratory acidosis, alkalosis, and organic acidosis all have minimal effect on potassium distribution. Inorganic acidosis can increase serum potassium, while metabolic alkalosis can lower potassium. Inorganic acidosis  (ie, non-Anion Gap). Diabetic ketoacidosis (DKA) often presents with hyperkalemia that does not parallel the acidosis; in this case, hyperkalemia results from insulin deficiency and the effects of hyperosmolality. Lactic acidosis and other forms of organic acidosis generally do not present with a significant potassium shift.

Hypokalemia is defined as a serum potassium concentration below 3.5 mmol/L, and is found among 20% of the hospitalized population. However, this high frequency probably does not reflect total body potassium depletion. In a review of 70 hospitalized patients with a potassium less than 2.8 mmol/L, the potassium rose toward normal regardless if they were given potassium or not. The authors suggested that hospitalization for acute illness was associated with increased adrenergic stimulation, resulting in intracellular movement of potassium and transient hypokalemia.60

Hyperkalemia is defined as a serum potassium concentration above 5.2 mmol/L

Increased Potassium Intake is one cause; e.g., KCl salt substitute

Transfusion of red blood cells

Intracellular Redistribution of Potassium - The Na-K-ATPase is critical in preventing intracellular potassium from causing hyperkalemia. Any factor that decreases the activity of this enzyme will cause potassium to leak from cells. A lack of insulin slows the Na-K-ATPase. In diabetic ketoacidosis hyperkalemia is typical.  β-Blockers inhibit the Na-K-ATPase activity and are associated with a mild increase in serum potassium. Uremia reduces Na-K-ATPase activity so that renal failure patients are less able to use the intracellular compartment to buffer potassium loads. Digitalis is an Na-K-ATPase antagonist. Digitalis toxicity can cause severe hyperkalemia.

Inorganic acids increase serum potassium. Decreases in pH due to respiratory or organic acidosis (e.g., lactic acidosis) have minimal effect on serum potassium.

Clinical Sequelae: The potassium concentrations inside and outside of the cell are the primary determinants of the cellular resting membrane potential (Em). Changes in the extracellular concentration can have dramatic effects on the resting membrane potential and the cell’s ability to depolarize. As extracellular potassium rises, the normally negative Em increases toward zero; this allows easier depolarization (ie, increased excitability). However, this excitability is short-lived as chronic hyperkalemia ultimately inactivates the sodium channels critical to producing an action potential. Hyperkalemia shortens the refractory period following depolarization by facilitating faster potassium uptake.

In the myocardium, inactivated sodium channels slow conduction velocity, and high serum potassium speeds repolarization. On ECG, hyperkalemia causes widened QRS complexes (slowed conduction velocity) and shortened ST intervals with tented T waves (rapid repolarization). The slowed conduction associated with rapid repolarization predisposes the myocardium to ventricular fibrillation.

During Phase 4 there is also a slow decline in the outward movement of K⁺ as the K⁺ channels responsible for Phase 3 continue to close. This fall in K⁺ conductance (gK⁺) contributes to the depolarizing pacemaker potential.

Hypokalemia increases the rate of phase 4 depolarization and causes tachycardia.  It apparently does this by decreasing gK during phase 4.

E_m = g'_K E_K  + ..................

The effects of hyperkalemia and hypokalemia on heart rate are explained by changes in membrane conductance rather than by changes in the potassium Nernst potential.  The increase in K conductance that occurs in hyperkalemia causes the maximum diastolic potential (MDP) to shift closer to EK. Accordingly, even though EK becomes more positive in hyperkalemia, the MDP becomes more negative.  This negative shift in MDP acts to slow heart rate by increasing the potential difference between MDP and the threshold for activation of the L-type calcium current.  In addition, the increased K conductance that occurs in hyperkalemia makes it more difficult for the funny sodium current to drive phase 4 depolarization.  Heart rate is also slowed by a decrease in the rate of phase 4 depolarization.   Just the opposite effects are produced by the decreased K conductance associated with hypokalemia.  The decreased conductance causes MDP to become more positive even though EK becomes more negative.  In addition, the decreased K conductance allows the funny sodium current to be more effective at driving phase 4 depolarization which results in a faster phase 4 depolarization.