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Anatomy & Physiology - Medications

Review of Medications and how the different classes of meds affects cardiac conduction.

          While medications are often used as a part of both diagnostic and therapuetic electrophysiology, it may be appropriate to cover the different classifications of meds and how they affect the heart in this section. There are five different classifications of cardiac medications. Each group exerts an affect on a different portion of the cardiac anatomy and/or physiology. How the various medications exert an influence on cardiac function is described below. The information in this section was found in Richard Fogoros text on Electrophysiology Testing (see below).

 

Classification of Antiarrhythmic Drugs1

Class I - Medications that bind to the sodium channel decreasing the speed of depolarization. There are two gates that regulate rapid sodium channels in the cardiac cells, the M gate on the outer cell boundary and the H gate found on the inner cell lining. During phase 4, or the resting phase, the M gate is closed while the H gate remains open. At the onset of depolarization, the M gate opens allowing positively charged sodium ions to rush into the cell. This correlates to phase 0 of the cardiac action potential. The H gate closes after a few milliseconds ending phase 0.

          The mechanism of class I medications causes them to bind to the H gate in such a manner that it does not open to the fullest extent there by limiting the amount of Na+ ions that can enter the cell. This causes phase 0 of the action potential to happen slightly slower than it would without the medications affect.

Class Ia Medications
    Slow upstroke of action potential / Prolong duration of action potential / decrease conduction velocity / Increase the refractory period

  • Quinidine
  • Procainamide
  • Disopyramide

Class Ib Medications
          Have minimal effect on phase 0 of the action potential in systemic doses / Shorten duration of action potential / Decrease refractoriness

  • Lidocaine
  • Mexilitine
  • Tocanimide
  • Phenytoin

Class Ic Medications
          Strong slowing of upstroke of action potential / Minimal effect on duration of action potential / strong decrease in conduction velocity / little effect on refractory periods

  • Flecainide
  • Propafenone
  • Encainimide

Class II - Medications that are Beta blockers and thus decrease sympathetic tone. Remember that sympathetic tone involves the sympathetic nervous system. A decrease in sympathetic tone causes a decrease in response to sympathetic input. This effect helps to reduce the hearts response to nerve signals that would otherwise increase the heart rate. These medications have little effect on the cardiac action potential.

  • Atenolol
  • Labetolol
  • Metropolol
  • Propanolol

Class III - Medications that increase the duration of the action potential while having very little effect on conduction velocity.

  • Sotalol
  • Bretylium
  • Ibutilide
  • Amiodarone

Class IV - Medications that block the calcium channels and thus primarily effect the sinus and AV nodes.

  • Verapamil
  • Diltiazem

Class V - Medications that increase the response to parasympathetic activity and thus cause an indirect affect on the SA and AV nodes.

  • Digitoxin
  • Digoxin

 

Source 1: Electrophysiology Testing - Practical Cardiac Diagnosis Series 3rd Edition; Richard N Fogors M.D. ISBN # 0-632-04325-3           The Fogoros book is probably in more EP libraries than any other cardiac text. Dr. Fogoros takes a direct approach at cover all the basics of electrophysiology testing.
Order these books at Cardiotext.com            If you are looking to add any of these texts to your library, click on the link above to visit the Cardiotext website. Select the section on Electrophysiology to see some of the latest titles available.
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