Symptomatic Bradycardia in the Field

Atropine or Pacing?

heart made of blocks
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In most prehospital emergency medical service systems around the United States, there are two options for direct treatment of symptomatic bradycardia available to paramedics: transcutaneous pacing (TCP) or the intravenous administration of atropine sulfate. In many systems, there is debate about which treatment modality is preferred. This is a great example of the way evidence-based medicine vacillates between treatments for some conditions based on the pile of data that builds up on one side of the debate or the other.

Symptomatic Bradycardia

Bradycardia (slow heart rate) is typically defined as a pulse rate of less than 50 beats per minute (BPM). We get concerned when a patient with bradycardia has symptoms that might be caused by the slow pulse rate—or—the patient has symptoms that are caused by the same thing that is causing the bradycardia. Either way, the patient is said to have symptomatic bradycardia. Symptoms that accompany bradycardia and are considered significant include:

Some folks, particularly endurance athletes, can have resting heart rates that are slower than 50 BPM and while that is technically a bradycardia, it comes without symptoms (asymptomatic).

Unstable or Stable Symptomatic Bradycardia

These symptoms can be split into two categories: hemodynamically unstable versus hemodynamically stable. Hemodynamically unstable bradycardias refer to those that lead to a loss of perfusion and are accompanied by hypotension or symptoms that show a lack of brain perfusion (dizziness, syncope, and confusion).

Usually, these symptoms are a result of the bradycardia, so fixing the bradycardia might resolve the symptoms.

Chest pain and shortness of breath can accompany either hemodynamically stable or unstable bradycardia. In unstable bradycardia, the lack of perfusion could be the cause of the chest pain or dyspnea.

In stable bradycardia, other cardiac conditions could be leading to both the symptoms and the bradycardia. Some emergency medical service systems consider bradycardia stable if the only accompanying symptoms are chest pain or shortness of breath. Other systems consider it unstable. Paramedics should always follow their local protocols.

Atrioventricular Block (AVB)

Some bradycardia can be a result of poor conduction through the atrioventricular (AV) node, which transfers the impulse telling the heart to contract from the atria (top two chambers) to the ventricles (bottom two chambers). The AV node provides a minuscule pause in the conduction of the impulse to give time for blood to be squeezed from the atria and completely fill the ventricles. After the pause, the impulse is sent down the Bundle of His and on to the Purkinje fibers, where it causes the ventricles to contract and push blood into the arteries (the pulse). Heart blocks (another term for AVB) come in three degrees.

First degree AVB simply increases the natural pause that the AV node is supposed to create. A first degree AVB does not have much, if any, effect on the heart rate. The rate in this case is still set by the sinus node situated in the left atrium.

Most first degree blocks are considered harmless.

There are two types of second degree AVB:

  1. Second degree Type I (also known as Wenckebach) is a progressive slowing of conduction through the AV node until an impulse doesn’t make it through from the atria to the ventricles. Once that happens, the conduction starts over faster and then progressively slows down again. If the dropped impulses happen frequently enough, it can reduce the BPM to less than 50. For example, if a patient has type 1 second degree AVB and every third heart beat doesn’t happen but the sinus node is sending 70 impulses per minute, the resulting pulse rate will be 46 per minute.
  1. Second degree Type II is not progressive like Type I, but it still results in some impulses not being conducted through the AV node and a missed beat. The missed beats can happen in a pattern or in a random way. Either way, the loss of enough beats per minute can cause the pulse to be less than 50 BPM and would be considered bradycardia.

Third degree AVB (also called complete AVB or complete heart block) occurs when impulses don’t appear to make it through the AV node at all. In this case, the atria will beat to the sinus node’s drum but the ventricles will do their own thing. The ventricles, not having any faster pacemaker to follow, will beat somewhere between 20-40 BPM, plenty slow enough to be considered bradycardia. Despite being called a complete block, during third degree AVB there might still be some conduction through the AV node. If conduction is too slow, the ventricles will not wait to see if anything’s coming through and will behave the same way they would if conduction was completely blocked. This nuance is very important when debating whether or not to try atropine at all for complete heart blocks.

Treatment of Symptomatic Bradycardia

Stable bradycardia is addressed by treating the underlying cause of the bradycardia. If it is related to an acute myocardial infarction (AMI), treating the AMI should have a positive effect on the bradycardia. If it’s medication-related, removing or adjusting the medication should help.

Unstable bradycardia should be treated directly. Left untreated, hemodynamically unstable bradycardia can spiral out of control—the lack of perfusion could further impact cardiac blood flow. Decreased perfusion in the brain can lead to strokes, dizziness, or confusion.

There are three ways to treat unstable symptomatic bradycardia: increase the blood pressure (and therefore perfusion) by increasing fluid volume in the cardiovascular system, constricting peripheral blood vessels to push blood toward vital organs, or increasing heart rate. Most successful treatment uses a combination of all three.

A bolus of IV fluid infused can help increase the blood pressure and improve perfusion. Sympathomimetic drugs, such as dopamine, can help shunt blood away from the periphery and focus the pressure to the core, especially the brain and heart. Sympathomimetic drugs may also help increase heart rate, which is the most direct treatment possible. In most cases, significant increases in heart rate will only come from either administering atropine sulfate or therapeutic pacing.

And now, the debate.

Atropine or Transcutaneous Pacing

The American Heart Association recommends atropine sulfate as the first line of treatment for symptomatic bradycardia, regardless of whether it is due to AVB or not. This is where the nuance of complete heart blocks comes in. It is generally thought that while atropine improves conduction through the AV node, it won’t do anything for a true complete heart block.

Right about the time that transcutaneous pacing (the ability to temporarily apply an electric pacemaker externally using adhesive patches on the chest and/or back) became available to paramedics in the field, the use of atropine began to be challenged. There are several reasons given. The most common reason is that atropine increases oxygen use in heart muscle, which could worsen an AMI. The second most common reason given is that atropine doesn’t affect complete heart blocks.

Neither of those reasons holds up to scrutiny, however. There is no published evidence that atropine, when administered for symptomatic bradycardia, worsens myocardial infarction. Also, complete AVB is an extremely rare condition that is relatively easy to identify through ECG. Even if a third degree AVB is misidentified or unclear and atropine is administered, at worst there will be no change to the heart rate and at best, there will be some improvement.

The reluctance to use atropine is made worse by a belief that transcutaneous pacing is easy to apply in the prehospital setting and that it is a benign treatment with few side effects. In practice, TCP is often incorrectly applied by paramedics and patients do not always have positive results even when the paramedic believes the pacemaker is “capturing” (resulting in ventricular contraction and a pulse for every paced impulse). Using TCP is a high-acuity, low frequency skill with significant potential for improper application.

Bottom Line: Medicine Before Edison

In the mnemonic heavy field of emergency medical services, this debate is often couched as whether to use Edison (electricity) or medicine (atropine) in the treatment of unstable bradycardia. A similar discussion—without the debate part—exists in whether to use Edison or medicine for unstable tachycardia.

The best thing to remember is to follow the American Heart Association and give atropine a try. Evidence suggests that it won’t harm the patient. If atropine is going to work, it usually works within a minute of administration. If, two doses and two minutes later, atropine hasn’t done the trick, then it’s time to move on to TCP.

Sources:

Brady WJ Jr, Harrigan RA. Diagnosis and management of bradycardia and atrioventricular block associated with acute coronary ischemia. Emerg Med Clin North Am. 2001 May;19(2):371-84, xi-xii. Review.

Brady WJ, Swart G, DeBehnke DJ, Ma OJ, Aufderheide TP. The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: prehospital and emergency department considerations. Resuscitation. 1999 Jun;41(1):47-55.

Morrison LJ, Long J, Vermeulen M, Schwartz B, Sawadsky B, Frank J, Cameron B, Burgess R, Shield J, Bagley P, Mausz V, Brewer JE, Dorian P. A randomized controlled feasibility trial comparing safety and effectiveness of prehospital pacing versus conventional treatment: 'PrePACE'. Resuscitation. 2008 Mar;76(3):341-9. Epub 2007 Oct 22.

Sherbino J, Verbeek PR, MacDonald RD, Sawadsky BV, McDonald AC, Morrison LJ. Prehospital transcutaneous cardiac pacing for symptomatic bradycardia or bradyasystolic cardiac arrest: a systematic review. Resuscitation. 2006 Aug;70(2):193-200. Epub 2006 Jun 30. Review.

Swart G, Brady WJ Jr, DeBehnke DJ, MA OJ, Aufderheide TP. Acute myocardial infarction complicated by hemodynamically unstable bradyarrhythmia: prehospital and ED treatment with atropine. Am J Emerg Med. 1999 Nov;17(7):647-52.

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