Class I antiarrhythmics: Sodium channel blockers

00:00 / 00:00


Class I antiarrhythmics: Sodium channel blockers


0 / 32 complete


Class I antiarrhythmics: Sodium channel blockers

of complete

External References

First Aid








Sodium channel blockers p. 328


Antiarrhythmic drugs help control arrhythmias or abnormal heartbeats.

There are four main groups of antiarrhythmic medications: class I, sodium-channel blockers; class II, beta-blockers; class III, potassium-channel blockers; class IV, calcium-channel blockers; and miscellaneous antiarrhythmics, or unclassified antiarrhythmics.

We’ll focus on class I antiarrhythmics which are further broken down into 1a, 1b, and 1c. All three groups work on Na+ channels in the cardiac myocytes, so class I medications are also called Na+ channel blockers.

Normally, an electrical signal starts at the sinoatrial or SA node in the right atrium, then propagates throughout 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 a heartbeat doesn’t follow this path, it’s 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. This creates a reentry circuit that causes extra contractions that occur in between the signals coming from the SA node.


  1. "Katzung & Trevor's Pharmacology Examination and Board Review,12th Edition" McGraw-Hill Education / Medical (2018)
  2. "Rang and Dale's Pharmacology" Elsevier (2019)
  3. "Pharmacological Effects of Antiarrhythmic Drugs" Archives of Internal Medicine (1998)
  4. "Pharmacology and Toxicology of Nav1.5-Class 1 Antiarrhythmic Drugs" Cardiac Electrophysiology Clinics (2014)
  5. "Modernized Classification of Cardiac Antiarrhythmic Drugs" Circulation (2018)
  6. "Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th Edition" McGraw-Hill Education / Medical (2017)

Copyright © 2023 Elsevier, its licensors, and contributors. All rights are reserved, including those for text and data mining, AI training, and similar technologies.

Cookies are used by this site.

USMLE® is a joint program of the Federation of State Medical Boards (FSMB) and the National Board of Medical Examiners (NBME). COMLEX-USA® is a registered trademark of The National Board of Osteopathic Medical Examiners, Inc. NCLEX-RN® is a registered trademark of the National Council of State Boards of Nursing, Inc. Test names and other trademarks are the property of the respective trademark holders. None of the trademark holders are endorsed by nor affiliated with Osmosis or this website.