Understanding Amiodarone

Recently, I was part of a short discussion between fellow healthcare providers of different levels of care, about Amiodarone and its expected effects on the heart during Ventricular Tachycardia (VT). I figured, I could break it down and write a short summary of how it works.

bioniche_amiodarone

  Most healthcare providers are familiar, or at least have heard of AMIODARONE. We also know that it is one of the leading antiarrhythmics used for treating ventricular dysrhythmias. But the  reality is that, it can be used for more than just ventricular tachyarrhythmias.

Amiodarone is a Class III antiarrhythmic of the Vaughan-Williams Classification system. Class III antiarrhythmics, are Potassium Channel Blockers. This means they partially block Potassium efflux (intracellular to extracellular) by inhibiting Na-KAtpase channels, adenosine triphospatase mediated channels (utilizes ATP breakdown for opening) . However, Amiodarone has other familiar properties such as:

  • Beta Adrenergic Receptor Blocking
  • Slow Calcium Channel Blocking
  • Fast Sodium Channel Blocking

Pharmacodymanics:

  • Potassium (K+), which is a positive ion,  is responsible for cardiac repolarization (rest). As Sodium and Calcium  channels  become inactivated,  Potassium channels open, allowing  Potassium to exit the cell, causing the cell to return to its predominantly negative voltage state, leading  to cardiac relaxation. This portion is seen on the surface ECG as a the end of the ST segment and  the entire  T wave.

  The initial portion of the T wave (the upslope), represents the Absolute or Absolute Refractory Period (ARP), where it is physiologically impossible to stimulate another cardiac cycle, while the terminal portion (downslope), is the Relative Refractory Period (RRP), where the ventricles can be stimulated again, if a premature impulse causes ventricular depolarization.

“You can’t jump again (depolarization), until you have at least one foot back on the ground (RRP)”… a simple example  I often use!

  • Potassium Channel Blocking leads to increased repolarization phase, which is  the Phase 3 of the Action Potential (AP). This means that since Potassium efflux  is delayed, there is  a prolonged positive gradient intracellular, which delays the next AP, while delaying repolarization.  The result is a prolonged QT interval on the surface ECG, which is the beginning of ventricular depolarization, until the end of ventricular repolarization. Prolonged QT is the main electrophysiologic change secondary to Amiodarone administration, typically with prolonged use.
  • Amiodarone also delays fast Sodium Channel opening, again, by Na-Katpase inhibition, which delays fast sodium influx. This means that, Phase 0 of the Action Potential (which is the fast upstroke caused by sodium influx) is slowed down. This slows down the initiation of ventricular depolarization.
  • Because of the above mechanism, slow L-Type Calcium Channels are also inhibited, leading to slow calcium influx which reduces automaticity  in SA and AV node, as Calcium helps maintain depolarization and transmission. This also reduces contractility of cardiac tissue (decreased Cardiac Output), as well as decreasing systemic vascular resistance (decreased preload).
  • Because of Amiodarone’s effect on the Thyroid gland, hormonal and adrenergic receptor proteins, there is a “Beta blocker like” effect. That is, it does not bind to Beta adrenergic receptors, but can lead to reduced inotropic and chronotropic effect.

Because changes is heart rate such as tachycardias  shortening the QTI (QT Interval) and bradycardias appearing as prolonged QTI, the QTc (QT Corrected) should be evaluated over the QTI during abnormal rates.

  My goal is that more healthcare providers realize that, because of all these actions mentioned above, Amiodarone can be use for more than just VT, such as atrial arrhythmias (i.e. Atrial fibrillation), Cardiomyopathies or Heart Failure. It can also be effective terminating ventricular dysrhythmias in the presence of Hyperkalemia, as long as the Hyperkalemia is being treated.

http://www.ems12lead.com/2014/10/27/calcium-and-hyperkalemia/

https://www.aclsmedicaltraining.com/blog/wide-complex-tachycardia-treated-with-amiodarone-and-synchronized-cardioversion/

 

 

11 Comments

  • Placebo says:

    Great Stuff!!

    Anyone with an ERC ALS course (and I guess AHA ACLS?) should know that Amiodarone is good for more than just vT?

    • Ivan Rios says:

      I agree… Unfortunately, the majority of providers I encounter, have the “I’m not a doctor so I don’t need to know that” mentality or, “I don’t know, I just do what my protocols say”. Althought, understanding pharmacodynamic may not necessarily change our treatment, I believe we should at least have an idea of how our treatment works and what to expect.

  • Andrew says:

    Great post! Could you talk a little more about the use of amiodarone in heart failure? I have not encountered that before…

  • kyle says:

    I think it can absolutely change our treatment. Protocols in most states are sort of a minimum requirement. knowing something like this enables you to call up your med control and say”pt has been showing ekg changes consistent with severe hyper k+, is receiving treatment per protocol, and just entered afib. I’d like to try amio due to the K+ channel blocking”. This makes the difference between the cook book medics that say things like “treat the patient not the monitor” because they can’t read the EKG, and good quality medics.

  • Karl Brennan says:

    Great article , however in VF caused by hyperkalemia it should be avoided along with lidocaine , Since it shuts down the K channels, the eiteiology of the arrest hyper K, K channels are needed to exchange K in the cell. Calcium , Bicarbonate, dextrose and insulin should be used to decrease K levels along w defibrillation.

  • Ren says:

    I share Karl Brennan’s concern about use of Amio in setting of VF due to HyperK. Most of these rhythms progresses to wide complex bradycardias. Which intuitively would be worsened by an agent that blocks Na, K, and Ca channels. Furthermore, how is the myocardium suppose to be stabilized if the patient is being concurrently treated with IV Ca when you’ve initiated Ca channel blockade? Just my thoughts..I would love to review the literature that supports this. Thanks for the great post!

  • C galliher says:

    I hate cook book medics. I just do what my protocols say”.

  • Ivan Rios says:

    I like your thought process. A
    Its not that Amiodarone is contraindicated in Hyperkalemia. In the event of arrest, Hyperkalemia usually leads to PEA and asystole. The Hyperkalemic effects on Action potential and Sodium potassium atpase channels should be addressed first in order for Amiodarone to work effectively. Once this is achieved, proper depolarization and repolarization can be corrected.

  • Dean S says:

    Great article. I would have liked to have dosages for the alternate uses discussed. As well as knowing if it is superior to drugs like Diltiazem for AFib.

  • Eduard says:

    Arterioles have muscular walls (usually only one to two layers of smooth muscle) and are the primary site of vascular resistance.

    You wrote: ‘This also reduces contractility of cardiac tissue (decreased Cardiac Output), as well as decreasing systemic vascular resistance (decreased preload).’

    SVR = 70% Arterioles -> SVR = after load ? Or?

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