Atropine

Atropine

Anticholenerigic

May 5, 2023

Dear colleagues:

 

Welcome to UH EMS Institute’s Pharmacy Phriday! Over the next month, our intent is to review medications within the protocols that directly affect and treat heart arrhythmias. In this installment, we focus on Atropine Sulfate. 


Atropine is indicated in the UH protocols for use in cases of symptomatic bradycardia. The medication is also useful in cases of various toxic ingestions, exposures, and overdoses. In this installment, we limit our focus to its use for bradycardia within the “cardiac” protocol pages. For more information on its use in poisonings and overdoses, check out UH EMS-I’s Prehospital Paradigm Podcast from this past week, “Cardiotoxins & The Drug Box, Part 1”. Dr. Singer joins the podcast to discuss this topic.  ( https://www.youtube.com/watch?v=n0i8bQQmARE )


Sinus bradycardia is defined as a heart rate of less than sixty beats per minute. Another definition sometimes taught is severe sinus bradycardia, which is a heart rate of forty beats or less. Regardless of the rate, a question the provider must always ask themselves is whether the patient is symptomatic. 


Bradycardia can occur at rest or in well-conditioned athletes and does not require treatment. There are also patients who may meet the criteria for bradycardia, i.e., a heart rate less than sixty beats per minute, but would be considered stable and not require treatment. Treatment of bradycardia is often based on the absence or presence of hypotension. Symptomatic typically refers to a patient who is experiencing dizziness, weakness, hypotension, shortness of breath, altered mental status, fainting, chest pain, etc. 


Another question to ask in treating bradycardia is what the possible cause may be. Bradycardia due to hypoxia, a conduction defect caused by structural heart disease (think Mobitz Type II or Complete Heart blocks), an MI, a toxicological emergency, hypothermia, a failed implanted pacemaker, increased cranial pressure from a trauma to the brain, or a cause other than the parasympathetic tone may not respond to Atropine and another treatment may be more appropriate.   Always consider the list of differential diagnoses for each patient encounter!


Atropine is often beneficial in bradycardia caused by excessive parasympathetic tone via the vagus nerve. You may recall that the parasympathetic nervous system restores the body to a state of calm, sometimes referred to as “rest and digest” or “breed and feed” activities. Other examples of stimulation of the vagus nerve may include coughing, vomiting, bowel movements, standing for long periods, cold water to the face, a tight collar (similar to carotid massage), etc.


When activated, the parasympathetic nervous system releases the hormone acetylcholine to, among other effects in the body, slow down the heart rate. Atropine blocks acetylcholine at the ends of the vagus nerve, allowing the heart to return to a normal intrinsic rate. As a result, the SA node increases its rate of electrical discharge, and the AV junction allows impulses to pass with minimal pause, that in turn, results in an increased heart rate. 

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Atropine is indicated for sinus bradycardia at a dosage of 1 mg IV/IO every 3-5 minutes to a max dose of 3 mg. Pediatric patients may also benefit from Atropine at 0.02mg/kg, but only secondary to the administration of Epinephrine (another example of the potential cause, likely hypoxia or hypoventilation in the pediatric patient, indicating another treatment other than Atropine is needed).    The minimum dose in the pediatric patient should be 0.1 mg, and the maximum dose of 0.5 mg. 


Contraindications to the use of Atropine may be overridden by the clinical need, especially in the unstable patient, but do include the concern of its use in the advanced Mobitz II- and Third-degree heart blocks. Some of the side effects of the use of Atropine can include increased oxygen demand, ischemia, dysrhythmias, pupil dilation, and dry mouth, to name a few. Tachycardia is the most common side effect. Once again, the provider should be sure to monitor the patient’s vitals and ECG during and after the administration of the medication.


Remember that when symptomatic bradycardia occurs, the primary goal should include identifying and treating the cause. In cases where bradycardia cannot be corrected by treating an underlying cause or if the cause cannot be determined, Atropine is the medication of choice. 


In the next installment of Pharmacy Phriday, we will focus on the use of Adenosine for tachycardia. Until then, stay safe!



Sincerely,



The UH EMS-I Team

University Hospitals

August 19, 2022

Dear Colleagues,


Welcome back to UH EMS Institute’s Pharmacy Phriday!  This week’s focus is on Atropine Sulfate.  Atropine is indicated in the UH protocol for use in cases of symptomatic bradycardia, organophosphate poisoning, and nerve agent exposure. In this installment, the focus will be limited to its use in bradycardia.


Within the body, the sympathetic and parasympathetic nervous systems are constantly working to control vital functions.  Through various biochemicals, body functions are either enhanced or suppressed based on needs. The sympathetic nervous system activates the fight or flight response during a threat or perceived danger, and the parasympathetic nervous system restores the body to a state of calm (“rest and digest” or “breed and feed”). 


With regards to the heart, the sympathetic nervous system releases the hormones epinephrine and norepinephrine that accelerate the heart rate. The parasympathetic nervous system releases acetylcholine, the hormone that slows down the heart rate.


Atropine is a parasympatholytic which means it inhibits, or blocks, the actions of the parasympathetic system allowing the preexisting sympathetic stimulation to dominate.  In the case of the heart, Atropine blocks the effects of the vagus nerve and subsequent acetylcholine release acting on the SA node and AV junction, which would normally slow the heart rate. When this occurs, the SA node increases its rate of electrical discharge, and the AV junction allows impulses to pass with a minimal pause that, in turn, results in an increased heart rate. 


Because of its actions, Atropine is indicated in cases of symptomatic bradycardia.  Symptomatic typically refers to a patient experiencing hypotension, altered mental status, chest pain, etc.  Remember there are patients who may meet the criteria for bradycardia, i.e., a heart rate less than 60 beats per minute, but would be considered stable and not be experiencing symptoms as listed above. Conversely, there may be the patient that is experiencing “relative” bradycardia at a near normal heart rate but is unstable and experiencing symptoms that would require treatment. 


Another consideration before the use of Atropine is the potential cause of the bradycardia.  In the 2020 ACLS provider manual, we are reminded that the “key clinical question is whether the bradycardia is causing the patient’s symptoms, or some other illness is causing the bradycardia.” Atropine is beneficial in bradycardia caused by excessive parasympathetic tone.  If the bradycardia is due to hypoxia, a conduction defect caused by structural heart disease (think Mobitz Type II or complete heart blocks), a toxicological emergency, hypothermia, or a cause other than the parasympathetic tone discussed above, then the patient will often not respond to Atropine, and another treatment may be more appropriate.  


Atropine is indicated for sinus bradycardia at a dosage of 1 mg IV/IO every 3-5 minutes to a max dose of 3 mg. Pediatric patients may also benefit from Atropine at 0.02mg/kg, but only secondary to the administration of Epinephrine (another example of the potential cause, likely hypoxia or hypoventilation in the pediatric patient, indicating another treatment other than Atropine is needed). The minimum dose in the pediatric patient should be 0.1 mg and the maximum dose of 0.5 mg. 


Contraindications to the use of Atropine may be overridden by the clinical need, especially in the unstable patient, but do include the concern of its use in the advanced Mobitz II- and Third-degree heart blocks.  Some of the side effects to the use of Atropine can include increased oxygen demand, ischemia, dysrhythmias, pupil dilation, and dry mouth, to name a few of the most common. Tachycardia is the most common side effect.  Once again, the provider should monitor the patient’s vitals and ECG during and after the medication administration. 


Remember that when symptomatic bradycardia occurs, the primary goal should include identifying and treating the cause.  In cases where that bradycardia cannot be corrected by treating an underlying cause or if the cause cannot be determined, Atropine is the medication of choice. 


Check in next week when we will review Atropine’s use in organophosphate poisoning and nerve agent exposure.  Till then, stay safe!!




Sincerely,


The UH EMS-I Team

University Hospitals