Understanding Atropine

As requested, during our previous Adenosine discussion, we will briefly review, Parasympathetic stimulation and Atropine pharmacodynamics on the heart.

ACETYLCHOLINE (ACh) is one of the Neurotransmitters, a chemical signal, used by the Central Nervous System, which has many effects on the body, from stimulating muscle contraction, inducing peristalsis (digestion), Bile release by the liver, and as discussed here, decreasing Sinoatrial Node (SAN) and Atrioventricular Node (AVN) stimulation. When the later occurs, often we encounter its effect recorded on the ECG, seen as:

  • Sinus Bradycardia
  • SA Blocks
  • AV Blocks

The most common symptoms of Vagal stimulation include:

  • Vasovagal Syncope
  • Nausea and vomiting
  • Dizziness

ACh is released during Vagus Nerve (Cranial Nerve X) stimulation ,which in the heart, binds to M2 Muscarinic Receptors, one of the 5 types of Muscarinic Receptors, which mainly work in CNS and skeletal muscle. Out of all these receptors, binding of ACh to M2 receptors affects the heart and its overall conductivity.

How does this work?

  • Decrease Cyclic Adenosine Monophosphate (cAMP) intracellular
  • This slows down L-type Calcium Channel opening, leading to decreased automaticity and slightly decreasing contractility
  • Potassium (K+) efflux (leaving the cell) is delayed, which prolongs repolarization, delaying the next action potential

The combination of all these actions, hyperpolarize the cells, increasing SA Nodal and AV Nodal threshold, which decreases the overall conduction, mainly through the AVN. This is known as Negative Dromotropic Effect.




Atropine, an antichollinergic, derived from the plant, Atropa Belladonna, or “Deadly Nightshade flower”,  blocks ACh binding to M2 receptors, giving it the “Parasympatholytic” property. The goal is not necessarily to increase SAN function, but rather, block the parasympathetic  response produced by M2 receptor stimulation, leading to normal SAN and AVN function.

 Now that we understand how Vagal Stimulation affects our cardiac function, the use of Atropine makes a bit more sense during suspected bradycardia induced symptoms.



  • James M says:

    I love these drug summaries. Thanks a lot, Ivan, for taking the time to do them. I look forward to seeing more! Perhaps amiodarone?

  • Tony Correia says:

    Looking for an opinion. Had a pt. who was unconscious from unknown etiology, Agonal respiration = 6, SPO2 = 59, heart rate =37 sinus bradycardia, B/P = 137/80 . We ventilate the pt. approx for 2 minutes without change in status. Would you have administered atropine or continue with BVM to attempt to correct hypoxia, that in turn would hopefully increase heart rate?

    • Ivan Rios says:

      Hi Tony, thank you for writing. It’s always a bit of a gamble to give opinion in such topics without being there, however, addressing ventilation is a must. The rate could be secondary to vagal stimulation and/or respiratory depression, but it sounds like the patient is compensating pretty well when it comes to the hemodynamic aspect. If you have the extra hands, giving a trial of ATropine might help with the rate, but I would not bet on the Heart Rate as being the cause of the problem, so that would not be my priority. I would definitely address the Respiratory Rate to increase SPo2 and if PETCO2 monitoring available, titrate to achieve a value > 35 mmHg. But again, if you have the extra hands, giving a trial of Atropine won’t hurt, but then again, sounds like it wouldn’t have fixed the problem either.

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