Antiarrhythmic Drugs: “Some Block Potassium Channels” Mnemonic
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Example Case
A male patient presents with palpitations, chest pain, and shortness of breath that began 2 hours ago. Symptoms initially were intermittent but have become more constant over the past 30 minutes.
An EKG is obtained immediately on arrival and shows a wide complex tachycardia. The patient’s blood pressure is currently stable with a reading of 131/82. You begin to think through your options for treatment and management.
Antiarrhythmic Medications
Antiarrhythmic drugs are used to treat abnormal cardiac rhythms such as atrial fibrillation, atrial flutter, ventricular tachycardia, ventricular fibrillation, etc.
There are several different classes of antiarrhythmic medications, and each class acts on different phases of the action potentials of cardiac myocytes (heart muscle cells) and pacemaker cells.
EZmed always provides simple memory tricks to remember and learn medical topics.
In this lecture, you will learn the following classes of antiarrhythmic drugs along with an easy mnemonic to memorize them all!
Class I: Sodium Channel Blockers
Class II: Beta Blockers
Class III: Potassium Channel Blockers
Class IV: Calcium Channel Blockers
Let’s get right into it!
Cardiac Action Potentials
The myocardium is the middle layer of the heart and is made up of heart muscle cells called cardiac myocytes.
The cardiac myocytes function to contract the heart and pump blood to the lungs and the rest of the body.
The atrial myocytes contract the right and left atria, while the ventricular myocytes contract the right and left ventricles.
The atrial and ventricular myocytes are known as non-pacemaker cells because they do not have the ability to generate their own action potentials or electrical impulses.
Instead, they rely on electrical impulses from the pacemaker cells to become depolarized and are primarily involved in contracting the heart.
The non-pacemaker cells are commonly referred to as contractile cells as a result.
Some of the cardiac myocytes are specialized cells in that they can produce their own action potentials or electrical impulses.
These specialized cardiac myocytes are called pacemaker cells and are primarily found along the cardiac conduction system, or the electrical pathway of the heart.
The cardiac conduction system is primarily made up of the SA node, internodal pathways, AV node, bundle of His, right and left bundle branches, and the Purkinje fibers.
The action potentials of non-pacemaker cells compared to pacemaker cells are slightly different.
In the cardiac action potential lecture we learned a simple memory trick to remember these differences, along with the action potential phases and ions involved.
Understanding cardiac action potentials will help you better understand how antiarrhythmic drugs work.
Non-Pacemaker Cells: Action Potential
We used the following catchphrase to remember the action potentials of non-pacemaker cells (such as the atrial and ventricular cardiac myocytes):
“Summit, Plummet, Continue, Plummet”
This helped us remember the following action potential phases of non-pacemaker cells:
Phase 0: Summit = Sodium In
Phase 1: Plummet = Potassium Out
Phase 2: Continue = Calcium In
Phase 3: Plummet = Potassium Out
Phase 4: Resting Phase
Phase 0 is the “summit” phase in which the voltage across the cell membrane becomes more positive (depolarizes) due to the influx of sodium ions.
Phase 1 is a slight “plummet” phase in which the voltage across the cell membrane becomes slightly more negative (repolarizes) due to the efflux of potassium ions.
Phase 2 is the “continue” phase in which the voltage across the cell membrane remains constant (contraction) due to calcium influx to counteract potassium efflux.
Phase 3 is the major “plummet” phase in which the voltage across the cell membrane becomes more negative (repolarizes) due to the efflux of potassium ions.
Phase 4 is when the cell is at rest and the voltage remains at a fairly constant level until the next action potential occurs.
Pacemaker Cells: Action Potential
We used the following catchphrase to remember the action potentials of pacemaker cells (found primarily in the cardiac conduction system - SA node, AV node, etc.).
“Climb and Plummet”
This helped us remember the following action potential phases of pacemaker cells:
Phase 0: Climb = Calcium In
Phase 3: Plummet = Potassium Out
Phase 4: “Resting” Phase
Remember: Pacemaker cells do not have a phase 1 or phase 2 in their action potentials because they do not contract.
Instead, pacemaker cells generate spontaneous electrical impulses that depolarize the contractile non-pacemaker cells, which in turn leads to cardiac contraction.
Remember: Pacemaker cells do not have a true “resting phase”.
During phase 4, the pacemaker cells slowly become more positive on their own.
Once a threshold voltage (-40 mV) is met, a spontaneous action potential is generated.
Phase 0 is the “climb” phase in which the voltage across the cell membrane becomes more positive (depolarizes) due to the influx of calcium ions.
Phase 3 is the “plummet” phase in which the voltage across the cell membrane becomes more negative (repolarizes) due to the efflux of potassium ions.
Phase 4 occurs when the voltage across the cell membrane slowly becomes more positive until the next action potential is generated.
If you have not checked out the cardiac action potential post, I highly recommend it as it simplifies the different phases of cardiac action potentials and the ions involved.
It will help you better understand the mechanism of action of antiarrhythmic drugs.
Antiarrhythmic Drugs: Mnemonic
“Some Block Potassium Channels”
Now that we have a good understanding of cardiac action potentials, let’s discuss how antiarrhythmics work by blocking different phases of these action potentials.
The mnemonic to remember the different classes of antiarrhythmic medications is “Some Block Potassium Channels”.
“Some” = Sodium channel blockers = Class I antiarrhythmics.
“Block” = Beta blockers = Class II antiarrhythmics.
“Potassium” = Potassium channel blockers = Class III antiarrhythmics.
“Channels” = Calcium channel blockers = Class IV antiarrhythmics.
Class I: Sodium Channel Blockers
As the name suggests, class I antiarrhythmics will block sodium channels.
What part of the action potential did we say sodium is involved?
We said it was involved in the “summit” phase (phase 0) of atrial and ventricular myocyte action potentials, in which the influx of sodium led to depolarization of the cell.
If sodium is blocked from entering the cell, then the myocyte will have a harder time becoming more positive and depolarizing.
Therefore, sodium channel blockers decrease the slope of phase 0, and the depolarization rate and amplitude will be reduced.
Cardiac myocyte conduction velocity and transmission will be decreased as a result.
This will decrease atrial and ventricular myocyte excitability and serve to suppress abnormal conduction rhythms.
Since pacemaker cells use calcium ions to depolarize, sodium channel blockers have little effect on the SA node and AV node (pacemaker cells).
For this reason, sodium channel blockers are useful in re-entry tachyarrhythmias where blocking the AV node could be detrimental.
Sodium Channel Blocker Subclasses
It is important to note that there are 3 main classes to sodium channel blockers: Class IA, Class IB, and Class IC.
The different class types are based on their effects on repolarization.
Some sodium channels increase action potential duration and effective refractory period by having a prolonged repolarization phase (class IA), some decrease action potential duration and effective refractory period by having a shortened repolarization phase (class IB), and some have no effect on either action potential duration, effective refractory period, or repolarization phase (class IC).
Examples of Class I Antiarrhythmics
Common examples of sodium channel blockers include procainamide (class IA), lidocaine and phenytoin (class IB), and flecainide (class IC).
Sodium channel blockers act on phase 0 of non-pacemaker cardiac myocyte action potentials by blocking the influx of sodium ions into the cell.
This decreases depolarization rate and amplitude thereby decreasing myocyte conduction velocity and transmission.
All sodium channel blockers decrease the phase 0 slope (in red).
Class IA sodium channel blockers prolong repolarization leading to increased action potential duration and effective refractory period.
Class IB sodium channel blockers shorten repolarization leading to decreased action potential duration and effective refractory period.
Class IC sodium channel blockers have no effect on repolarization, action potential duration, or effective refractory period.
Class II: Beta Blockers
We’re going to skip beta blockers briefly as they do not act directly on ion channels. We will first discuss class III and IV antiarrhythmics and finish with beta blockers.
Class III: Potassium Channel Blockers
As the name suggests, class III antiarrhythmics will block potassium channels.
What part of the action potential did we say potassium was involved?
We said it was involved in the “plummet” phase (phase 3) of both atrial/ventricular myocyte and pacemaker cell action potentials, in which the efflux of potassium led to repolarization of the cell.
If potassium is blocked from exiting the cell, then the repolarization phase will be prolonged. This will increase action potential duration and effective refractory period.
Since pacemaker cells and atrial/ventricular myocytes both use potassium ions to repolarize, potassium channel blockers will act on both types of action potentials.
They will reduce the excitability of atrial and ventricular myocytes as well as reduce conduction velocity through the conduction system.
This will serve to suppress tachyarrhythmias.
Examples of Class III Antiarrhythmics
Common examples of potassium channel blockers include: amiodarone, dofetilide, and ibutilide.
Potassium channel blockers act on phase 3 of atrial/ventricular myocyte and pacemaker cell action potentials by blocking the efflux of potassium ions out of the cell.
This prolongs repolarization thereby increaseing cardiac myocyte and pacemaker cell action potential duration and effective refractory period.
Class IV: Calcium Channel Blockers
As the name suggests, class IV antiarrhythmics will block calcium channels.
What part of the action potential did we say calcium was involved?
We said it was involved in the “climb” phase (phase 0) of pacemaker cell action potentials, in which the influx of calcium led to depolarization of the cell.
We also said calcium was involved in the “continue” phase (phase 2) of atrial/ventricular myocyte action potentials, in which the influx of calcium led to contraction.
If calcium is blocked from entering the pacemaker cells, then the depolarization rate and amplitude will be decreased thereby decreasing SA node automaticity and AV node conduction velocity.
This will ultimately decrease heart rate (negative chronotropy).
If calcium is blocked from entering the atrial/ventricular myocytes, then decreased cardiac contraction will occur (negative inotropy).
Both of these effects will help to suppress tachyarrhythmias.
Examples of Class IV Antiarrhythmics
Common examples of calcium channel blockers include: verapamil and diltiazem
Calcium channel blockers act on phase 0 of pacemaker cell action potentials by blocking the influx of calcium ions into the cell.
This decreases depolarization rate and amplitude thereby decreasing SA node automaticity, AV conduction velocity, and ultimately heart rate (negative chronotropy).
Calcium channel blockers also act on phase 2 of atrial/ventricular myocyte action potentials by blocking the influx of calcium ions into the cell.
This will decrease cardiac contractility (negative inotropy).
Class II: Beta Blockers
Beta blockers do not act directly on ion channels.
Rather they act by antagonizing beta adrenergic receptors.
The heart predominately has beta1 adrenergic receptors. These receptors are located on both atrial/ventricular myocytes and pacemaker cells.
Normally catecholamines such as norepinephrine and epinephrine will bind to beta1 adrenergic receptors in the heart to increase heart rate and cardiac contractility, part of the sympathetic response.
Since beta receptors are located on both non-pacemaker myocytes and pacemaker cells, beta blockers will have effects on both the atrial/ventricular myocytes and SA/AV node.
By blocking the beta adrenergic receptors on pacemaker cells, this will prolong and decrease the slope of phase 4 of the action potential leading to decreased heart rate (negative chronotropy).
Furthermore, blocking beta adrenergic receptors on non-pacemaker myocytes will decrease phase 2 cardiac contractility (negative inotropy).
Both of these effects will help to suppress tachyarrhythmias.
Examples of Class II Antiarrhythmics
Common examples of beta blockers include: metoprolol, propranolol, esmolol, atenolol, and timolol.
Beta blockers will antagonize beta1 adrenergic receptors in the heart.
This will prolong and decrease the slope of phase 4 pacemaker cell action potentials thereby leading to decreased heart rate (negative chronotropy).
This will also decrease cardiac contractility of non-pacemaker myocytes (negative inotropy).
Conclusion
Hopefully this helped clarify antiarrhythmic medications.
Use the mnemonic “some block potassium channels” to remember the different classes of antiarrhythmic medications.
Class I sodium channel blockers act by reducing the influx of sodium ions during phase 0 of the atrial/ventricular myocyte action potential. This decreases depolarization rate and amplitude thereby decreasing conduction velocity and myocyte excitability.
Class II beta blockers act by antagonizing beta adrenergic receptors. This decreases heart rate (pacemaker cell phase 4) and cardiac contractility (atrial/ventricular myocyte phase 2).
Class III potassium channel blockers act by reducing the efflux of potassium ions during phase 3 of the atrial/ventricular myocyte and pacemaker cell action potentials. This prolongs repolarization thereby increasing action potential duration and effective refractory period; both will lead to decreased excitation of the cells.
Class IV calcium channel blockers act by reducing calcium influx of calcium ions during phase 0 of the pacemaker cell action potential and phase 2 of the atrial/ventricular myocyte action potential. This will decrease SA/AV node automaticity/conduction velocity and decrease cardiac myocyte contractility respectively.
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https://www.cvpharmacology.com/antiarrhy/sodium-blockers
https://www.cvpharmacology.com/antiarrhy/potassium-blockers
https://www.cvpharmacology.com/vasodilator/CCB
https://www.cvpharmacology.com/cardioinhibitory/beta-blockers