Arian Foster's Irregular Heartbeat: The Medicine Behind the Scare

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Arian Foster's Irregular Heartbeat: The Medicine Behind the Scare
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The Houston Texans (12-3) suddenly look vulnerable, and Arian Foster's irregular heartbeat scare didn't do anything to help.

According to Nick Scurfield of the official Texans website, Foster left the Texans' Week 16 23-6 loss to the Minnesota Vikings (9-6) in the third quarter due to the condition.

Scurfield also reports that team physicians cleared him to return to play later in the game, but head coach Gary Kubiak decided to hold him out as a precautionary measure.

Fortunately, it appears that everything is OK. On Monday, Foster tweeted:

 

 

Scurfield also tweeted that Foster should be back for Week 17.

The Texans looked nowhere near the same without their dynamic running back lined up in the backfield, so that is great news. It is also not terribly surprising. While an irregular heartbeat sounds scary—and it most certainly can be—it is usually of minimal concern in an athlete of Foster's caliber.

Also called a cardiac arrhythmia, an irregular heartbeat can be a sign of a number of underlying medical conditions. Yet before getting into the nature of an arrhythmia, it helps to understand the exact workings of a healthy heart.

Oh yes, it's science time, people. I promise to make this as painless as possible.

Under normal conditions, the heart paces itself. Each heartbeat starts with an electrical signal that arises at the very top of the heart from a source called the sinoatrial node, or SA node for short.

Next, the signal travels downward to the two atria—the upper-most, smaller chambers of the heart.  It then continues down to the very bottom of the ventricles—the large, strong chambers that send blood to the body and lungs—before making a U-turn and backtracking somewhat to finish at the top of the ventricles.

Diagram showing the electrical pathway of the heart. With each heartbeat, an electrical signal arises at the sinoatrial node and travels downward through the atria, past the atrioventricular node, down the right and left bundles, into the ventricles and back upward through the Purkinje fibers. As the electrical signal passes through muscle cells, they contract, causing the heart to squeeze. This pathway is highlighted by the red arrows. Photo from Wikimedia Commons and edited by the author.

As the electrical signal moves along its path, it activates the heart's muscle cells as it passes through them. This activation is what causes the heart to squeeze, or contract.

Additionally, following activation, a muscle cell must "reset" itself before squeezing again, a period of time called the "refractory period." Refractory periods of cells are what eventually cause the electrical signal to die out at the end of its circuit.

Because the signal takes time to travel from cell to cell, the atria contract first, followed by the bottom of the ventricles and lastly by the top of the ventricles. This smooth, coordinated and sequential contraction sends blood from the atria at the top of the heart, to the bottom of the ventricles and then out the top of the ventricles to the rest of the body. It also times up the refractory periods and allows the electrical signal to end in time for the next one's arrival.

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Arian Foster left the game on Sunday and did not return after being diagnosed with an irregular heartbeat.

For a brief period on Sunday, Foster's heart circuit, quite simply, went haywire. Any number of conditions can interfere with the usually rock-solid electrical circuit of the heart, from the very minor to the life-threatening. There are also many types of arrhythmias.

Foster's was of the minor variety.

Exact medical details are unavailable, but Foster likely suffered from an arrhythmia called "supraventricular tachycardia" (SVT). SVT is actually an umbrella term for a number of arrhythmia types that are caused by a circuit interruption above the ventricles, usually within the atria.

Dehydration, stress or even too much coffee (seriously!) can cause SVT, as any of these can cause a heart to beat fast. A heart beating too fast can lose the synchronization of its contraction and refractory periods within the atria by preventing the electrical signal from dying out or by causing it to arise from somewhere other than the SA node.

A brief but excellent overview of atrial fibrillation.

A continuously moving electrical signal without control from refractory periods can move anywhere it pleases within the atria. Among many other rhythms, it can cause them to quiver rather than strongly contract—called "atrial fibrillation"—or beat normally but very, very fast—called "atrial flutter".

Some educated speculation suggests that something minor caused Foster's SVT—such as the aforementioned dehydration or stress. His heart most likely switched into a rhythm such as atrial fibrillation, atrial flutter or any number of similar rhythms. He also likely removed himself from the game, as SVT often presents itself only as the sensation of a racing heart, without any other signs or symptoms.

It appears that Foster may be particularly susceptible to developing SVT. As Scurfield states in his previously mentioned report, Foster once had a bout of an arrhythmia during a practice, as well. Fortunately, atrial fibrillation or atrial flutter in an otherwise healthy person often resolve on their own once the cause is removed.

In addition, simple actions such as "bearing down" to perform the Valsalva maneuver—attempting to exhale against a closed mouth and pinched nose—or splashing the face with ice water can break the arrhythmia and restore a normal heartbeat.

Nevertheless, the consequences of not taking an arrhythmia seriously are quite severe. If the heart is not functioning properly, blood flow to the brain and body is decreased. Decreased blood flow can lead to loss of consciousness and other serious problems.

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Additionally, returning to the field too soon risks re-developing whatever condition led to the arrhythmia in the first place. For that reason, it is probably best that Foster did not return to play.

He will certainly be monitored throughout the week, but once an arrhythmia breaks, it usually leaves no lingering effects and should not limit him any way.

However, should Foster continually re-develop SVT, his cardiologist may decide to perform a procedure called an "electrophysiology study." This minor procedure allows him or her to see where Foster's heart's electrical signal is veering off course. It also allows for planning of future interventions.

Yet that is a discussion for another day. For now, expect to see Foster active for Week 17.

That is great news for the Texans, because as Sunday showed, they clearly need him. 

 

Dave Siebert is a medical/injury Featured Columnist for Bleacher Report who will graduate from medical school in June, 2013.  He plans to specialize in both Family Medicine and Primary Care (non-operative) Sports Medicine.  Anatomical and arrhythmia information discussed above is based on his own knowledge, and the above article represents only educated speculation and is not meant to suggest a diagnosis for Arian Foster or anyone else.

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