Cardiac Arrhythmia Classifications
There is quite a lot to be said about the medications we use for patients with arrhythmias. It’s easy to get lost as to what drugs do what and how, but thankfully there was a kind enough person by the name of Vaughan Williams, who actually broke them down into separate classes. Each class effects separate parts of the cardiac cycle, ultimately changing the electrical current of the heart.
Cardiac Action Potential
Before looking at the medications, we have to understand the cardiac cycle and how it actually works.
The above chart presents the four phases of an action potential in a ventricular myocardial cell and how the electrolytes are used to cause the depolarization and repolarization of myocardial cells.
Phase 0 begins with a slight influx of sodium until it passes the potential threshold. Once past the threshold, more sodium channels will open and flood the cell, causing it the depolarize.
Phase 1 is an efflux of potassium from the cell, causing the cell to reach 0mV.
Phase 2 happens at this point. This is when calcium influx happens, prolonging the repolarization period. This period also goes by the name of an absolute refractory period for the cell, since it cannot depolarize during this time.
Phase 3 Calcium channels close again and potassium continues to efflux from the myocardial cell until the internal cell voltage returns to -90mV. Majority of potassium channels then close and the heart enters phase 4, which potassium is allowed to continue to leak into from the cell.
This process happens anywhere from 60 to 100 times per MINUTE!
Vaughan Williams Classifications
The major purpose of the medications in this class effect they way the cardiac action potential works in the cells of the heart. The drugs usually help to slow down specific phase to the heart and allow the heart to fix itself a bit.
Class I - Sodium Channel Blockers
These medications are designed to disrupt phase 0, causing a prolongation of it. There are 3 subcategories (a,b,c) that are broken down into moderate, weak, and strong.
This article won’t go into great depths, but the major goal of the class is to prolong the QRS complex and prolong or shorten QTi.
Class II - Beta Blockers (-olol or -alol)
Quite commonly used out of hospital for patients with hypertension, beta blockers are actually a common antidysrhythmic. The basic pharmacology is: by blocking the beta-1 receptor sites, it prevents stimulation of the cardiac muscle to beat faster. The increase of sympathetic tone will decrease the rate the heart will beat.
- Propranolol
- Metoprolol
- Carvedilol
Class III - Potassium Channel Blockers
Similar to the Class Ia medications, potassium channel blockers are used to prolong APD, which can cause a prolongation of ERP. This class of medication is commonly known to treat different ventricular dysrhythmias (Vtach or Vfib). The most common medication for this class is Amiodarone and deserves a post of its own.
It’s most common use is during CPR, when the patient is in pulses Vtach or Vfib rhythm and is then followed by a drip with ROSC is achieved. An important note to make about Amiodarone is it can take 16 weeks to leave the system.
- Amiodarone
- Sotalol
- Ibutilide
Class IV - Calcium Channel Blockers
Commonly uses for Afib with RVR and PSVT, a calcium channel blocker will prolong phase 2 of the action potion in the cell. The goal is to slow the conduction through the atrioventricular (AV) node, slowing the ventricular tachycardia that is occurring. By prolonging the ERP in the AV node, the heart is able to regulate the rate better.
Calcium channel blockers are commonly prescribed by physicians to assist in the care of such arrhythmias. One side effect of these drugs is it may drop the patient’s BP, so ensure you have an SBP >100 or a MAP >65, prior to administering the medication
This is the mix bag class. These drugs do not truly fit in any category but are still highly important to mention anyways. Two of these medications are Adenosine and Digoxin.
Adenosine prevents the re-entry of a signal in a sinus rhythm, preventing SVT. A warning though is for patients that have WPW syndrome may cause an increase in heart rate instead, so make sure you’re reading the rhythm correctly.
Digoxin effects vagal tone and is seen less as an emergency drug and more as a maintenance drug for chronic heart issues. A major issue with this drug is it holds a very narrow therapeutic index. Toxicity is quite possible if given too much.
Summary
Each class works in its own way on the action potential in the cardiac conduction system. How they affect the heart greatly determines when and how the medication should be used in different medical scenarios. The point of this article is to help a bit with the pharmacodynamics involved with the medications and to hint at the situations a person in the medical field would use them?
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