Class III antiarrhythmics: Potassium channel blockers

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Class III antiarrhythmics: Potassium channel blockers

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Amiodarone p. 327

hypothyroidism p. 248

hypothyroidism with p. 345

photosensitivity p. 249

pulmonary fibrosis p. 250

restrictive lung disease p. 694

Bradycardia

amiodarone and p. 327

Haptens

amiodarone as p. 327

Heart failure p. 316

amiodarone p. 327

Hepatotoxicity

amiodarone p. 327

Hyperthyroidism p. 344, 346, 665

amiodarone and p. 327

Hypothyroidism p. 344, 345

amiodarone and p. 327

Pulmonary fibrosis

amiodarone and p. 327

Transcript

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Antiarrhythmic medications help control arrhythmias, or abnormal heart beats.

There are five main groups of antiarrhythmic medications: class I, also known as sodium-channel blockers; class II, also called beta-blockers; class III, also known as potassium-channel blockers; class IV, also called calcium-channel blockers; and miscellaneous antiarrhythmics, or unclassified antiarrhythmics. Now, we’ll focus on class III antiarrhythmic medications.

Normally, an electrical signal starts at the sinoatrial or SA node in the right atrium, then propagates out through both atria, making them contract.

The signal gets delayed a bit as it goes through the atrioventricular or AV node, then goes through the Bundle of His to the Purkinje fibers of both ventricles, making them contract as well.

When the signal doesn’t follow this pathway, we get abnormal heartbeats called an arrhythmia, and there are two main causes - abnormal automaticity and abnormal reentry.

Abnormal automaticity is when an area of the heart, say, a part of the ventricle, begins to fire off action potentials at a rate that’s even faster than the SA node.

As a result, this area of the heart essentially flips roles with the SA node, firing so fast that the pacemaker cells in the SA node don’t get a chance to fire. At that point, the heartbeat is being driven by the ventricles.

Alternatively, there can be an abnormal reentry which often results from scar tissue in a ventricle after a heart attack.

Scar tissue doesn’t conduct electricity, so the signal just goes around and around the scar, and each cycle can cause the ventricles to contract.

Alternatively, there might be an accessory, or extra pathway between the atria and the ventricles, like the bundle of Kent in Wolff-Parkinson-White syndrome.

Here, the signal might move back up the accessory pathway, since oftentimes it’s bidirectional, meaning the signal can go from atrium to ventricle as well as from ventricle to atrium.

Sources

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  2. "Rang and Dale's Pharmacology" Elsevier (2019)
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  4. "Effects of amiodarone on short QT syndrome variant 3 in human ventricles: a simulation study" BioMedical Engineering OnLine (2017)
  5. "Dronedarone for the treatment of atrial fibrillation and atrial flutter: approval and efficacy" Vascular Health and Risk Management (2010)
  6. "Dronedarone for the treatment of atrial fibrillation and atrial flutter" Health Technology Assessment (2010)
  7. "Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th Edition" McGraw-Hill Education / Medical (2017)
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