In most prehospital emergency medical service systems around the United States, there are two options for direct treatment of symptomatic bradycardia available toparamedics, transcutaneous pacing (TCP) or the intravenous administration of atropine sulfate. In many systems, there is a 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.
Deagreez / Getty Images
Symptomatic Bradycardia
Some folks, particularly endurance athletes, can have resting heart rates that are slower than 60 BPM and while that is technically bradycardia, it comes without symptoms (asymptomatic).
Unstable or Stable Symptomatic Bradycardia
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 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 theatrioventricular (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.
There are two types of second-degree AVB:
Third-degree AVB(also calledcomplete 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
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.
A bolus of IV fluid infused can help increase blood pressure and improve perfusion. Sympathomimetic drugs, such as dopamine, can help shunt blood away from the periphery and focus the pressure on 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 throughECG. 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.
Bottom Line
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 unstabletachycardia.
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
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
Meet Our Medical Expert Board
Share Feedback
Was this page helpful?Thanks for your feedback!What is your feedback?OtherHelpfulReport an ErrorSubmit
Was this page helpful?
Thanks for your feedback!
What is your feedback?OtherHelpfulReport an ErrorSubmit
What is your feedback?
