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

atropine

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.

 

2 Comments

  • 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?

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Comments
Kevin
44 year old male CC: Palpitations
Why on earth would you risk VF, by giving Adenosine to rule out rhythms.. This is dangerous, and foolish. There might be a slight chance that this is WPW.. You might as well just give him Cardizem, they are both AV nodal blockers... I don't know why the AHA even added this stupid idea..
2014-10-22 13:31:06
Vince DiGiulio
The 360 Degree Heart – Part II
It is standard practice in electrocardiography to label the first 90 degrees counter-clockwise from "zero" that way. When you see a patient with "left axis deviation" you'll see that their measured QRS axis is somewhere between -30 and -90 degrees. Imagine if you saw someone with a mean QRS axis at 5 degrees. Now imagine…
2014-10-21 14:00:37
Bryan
The 360 Degree Heart – Part II
I don't understand why (-)III and aVL are be labeled -60 and -30 degrees instead of 300 and 330 degrees?
2014-10-21 13:43:29
The 360 Degree Heart – Part II | EMS 12 Lead
The 360 Degree Heart – Part I
[…] first post in our “360 Degree Heart” series attempted to visualize how the different frontal plane […]
2014-10-21 12:50:56
Eric Strong
Axis Determination – Part VI
This is a great discussion of axis determination. One minor suggestion: I think it's potentially misleading to refer to an axis between 0 and -30 as "physiologic left axis deviation", since "axis devitation" implies deviation from normal, and axes between 0 and -30 are perfectly normal, (depending on age and body habitus). It may be…
2014-10-05 17:09:00

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