Sodium Channel Blockers: Fast Food and the ABCs
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Example Case
A male patient presents with palpitations and shortness of breath. Symptoms began approximately one hour ago after completing a bike ride. His symptoms were sudden onset and have been persistent.
He informs you he has a history of Wolff-Parkinson-White (WPW) syndrome. You obtain an immediate EKG and hook him up to cardiac monitor. He is tachycardic with a heart rate above 200 but blood pressure remains stable at this time.
Sodium Channel Blockers
Cardiac conduction abnormalities can result in many different abnormal heart rhythms.
Antiarrhythmic drugs can help suppress many of these abnormal dysrhythmias.
This lecture will focus on sodium channel blockers (class I antiarrhythmics), along with their 3 different subclasses.
EZmed always provides an easy way to remember and learn the content.
You will be provided with a simple mnemonic to help memorize the different sodium channel blocker medications in each subclass.
You will also receive a seamless method to remember the mechanism of action of each subclass and the effects they have on cardiac action potentials.
Sodium Channels - Action Potential
We learned in the cardiac action potential post that sodium channels were involved in depolarization (the “summit” phase of the action potential) of non-pacemaker cardiac myocytes, such as the atrial and ventricular muscle cells.
As the voltage across the cell membrane became more positive from a surrounding stimulus, sodium channels opened once a threshold voltage was met.
This allowed for sodium ions to enter the cell resulting in a rapid increase in voltage across the cell membrane.
This was referred to as depolarization, phase 0 of the action potential, and it ultimately led to cardiac contraction.
We also learned that sodium channels are not as important in pacemaker cells, which use mainly calcium for depolarization and potassium for repolarization.
Sodium channels are involved in phase 0 of the non-pacemaker atrial/ventricular myocyte action potential.
The influx of sodium when these channels are open increases the voltage across the cell membrane and the cell depolarizes ultimately leading to cardiac contraction.
Sodium Channel Blockers
Now that we have a good understanding how sodium channels are involved in generating an action potential, let’s discuss sodium channel blockers in more detail.
Sodium channel blockers are class I antiarrhythmic drugs; the others being class II beta blockers, class III potassium channel blockers, and class IV calcium channel blockers.
As the name says, sodium channel blockers are going to block sodium channels.
What part of the action potential did we say sodium is involved?
We know from above and in the cardiac action potential post that sodium channels are 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 blockers will reduce the influx of sodium during depolarization, thereby decreasing the phase 0 slope and decreasing depolarization amplitude/rate.
Class IA Sodium Channel Blockers
As mentioned above, there are 3 different subclasses to sodium channel blockers: Class IA, Class IB, and Class IC.
The subclasses are defined by their effects on repolarization.
Class IA sodium channel blockers prolong the repolarization phase leading to an increase in action potential duration and effective refractory period.
The way to remember this is IA = After; meaning repolarization occurs after the normal repolarization phase.
Example class IA medications include: procainamide, quinidine, and disopyramide.
Class IA = After
Class IA sodium channel blockers prolong repolarization leading to increased action potential duration and effective refractory period.
Class IB Sodium Channel Blockers
Class IB sodium channel blockers shorten the repolarization phase leading to a decrease in action potential duration and effective refractory period.
The way to remember this is IB = Before; meaning repolarization occurs before the normal repolarization phase.
Example class IB medications include: lidocaine, tocainide, phenytoin, and mexiletine.
Class IB = Before
Class IB sodium channel blockers shorten repolarization leading to decreased action potential duration and effective refractory period.
Class IC Sodium Channel Blockers
Class IC sodium channel blockers have no effect on repolarization, action potential duration, or effective refractory period.
The way to remember this is IC = Correct; meaning repolarization occurs as normal.
Example class IC medications include: flecainide and propafenone.
Class IC = Correct
Class IC sodium channel blockers have no effect on repolarization, action potential duration, or effective refractory period.
Sodium Channel Blocker Subclass Trick
Class IA = After; repolarization occurs after the normal repolarization phase
Class IB = Before; repolarization occurs before the normal repolarization phase
Class IC = Correct; repolarization occurs correctly with the normal repolarization phase
Sodium Channel Blocker Mnemonic
“Double Quarter Pounder, Lettuce Tomato Pickle Mayo, Fries Please”
Now that we have a good understanding of how sodium channel blockers work and the different subclasses of sodium channel blockers, let’s discuss an easy way to remember the different medications in each class.
The mnemonic that is helpful if you have not used this before is: “Double Quarter Pounder, Lettuce Tomato Pickle Mayo, Fries Please”.
Class 1A = “Double Quarter Pounder”
This will help you remember Disopyramide, Quinidine, and Procainamide are class IA sodium channel blockers.
Procainamide commonly shows up on medical tests and licensure exams, especially for the treatment of WPW.
Class IB = “Lettuce Tomato Pickle Mayo”
This will help you remember Lidocaine, Tocainide, Phenytoin, and Mexiletine are class IB sodium channel blockers.
Lidocaine and phenytoin are usually the class IB medications tested as they are more common.
Class IC = “Fries Please”
This will help you remember Flecainide and Propafenone are class IC sodium channel blockers.
Flecainide is the more common one and is what is usually tested.
Practical Applications
EKG
We know that sodium channel blockers will decrease the slope of phase 0 of atrial/ventricular myocyte action potentials.
This will decrease the depolarization rate and amplitude.
Let’s now correlate this with an EKG.
The QRS interval reflects ventricular depolarization. Therefore, sodium channel blockers can prolong or widen the QRS interval.
Sodium Channel Blocker Toxicity
This is especially appreciated in cases of sodium channel blocker toxicity or overdose in which the QRS can widen and lead to dysrhythmias.
EKG correlations and sodium channel blocker toxicity will be discussed in more detail in other posts.
Conclusion
Hopefully that provided you with a better understanding of sodium channel blockers and their mechanism of action on action potentials.
Using the mnemonic and the ABC trick can help you remember the different subclasses of medications and their effects on repolarization.
Remember A, B, C = After, Before, Correct in relation to the repolarization phase.
Remember “Double Quarter Pounder, Lettuce Tomato Pickle Mayo, Fries Please” for the different medications in each sodium channel blocker subclass.
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