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What is the basic mechanism of the 4 classes of anti-arrhythmic drugs?
What is the basic mechanism of the 4 classes of anti-arrhythmic drugs?
Class 1: Sodium Channel Blockers. Class 2: Beta Blockers. Class 3: Drugs that prolong cardiac action potential. Class 4: Calcium channel blockers.
Of the 4 classes of anti-arrhythmic drugs, which ones affect the electrical activity of the heart and which ones modify the myocardial response to electrical activity?
Of the 4 classes of anti-arrhythmic drugs, which ones affect the electrical activity of the heart and which ones modify the myocardial response to electrical activity?
Class 2 & 4 (Beta Blockers & Calcium Blockers) modify electrical activity; Class 1 & 3 modify myocardial response.
Which classes of anti-arrhythmic drugs affect the nodes and which ones affect the myocardium?
Which classes of anti-arrhythmic drugs affect the nodes and which ones affect the myocardium?
Class 2 & 4 affect the nodes; Class 1 & 3 affect the myocardium.
What are the Class 1a drugs, what is their mechanism of action, and how do they influence the myocardial action potential?
What are the Class 1a drugs, what is their mechanism of action, and how do they influence the myocardial action potential?
With regards to myocardium, what subclass of Class 1 drugs results in a decreased phase 0 slope and can potentially increase action potential duration?
With regards to myocardium, what subclass of Class 1 drugs results in a decreased phase 0 slope and can potentially increase action potential duration?
Given the effects of Class 1a anti-arrhythmic drugs on myocardial action potentials, how do you expect them to alter the EKG?
Given the effects of Class 1a anti-arrhythmic drugs on myocardial action potentials, how do you expect them to alter the EKG?
What are the Class 1b drugs, what is their mechanism of action, and how do they influence the myocardial action potential?
What are the Class 1b drugs, what is their mechanism of action, and how do they influence the myocardial action potential?
With regards to the myocardium, which subclass of Class 1 drugs results in a shortening of the action potential duration?
With regards to the myocardium, which subclass of Class 1 drugs results in a shortening of the action potential duration?
Given the effects of Class 1b anti-arrhythmic drugs on myocardial action potentials, how do you expect them to alter the EKG?
Given the effects of Class 1b anti-arrhythmic drugs on myocardial action potentials, how do you expect them to alter the EKG?
What are the Class 1c drugs, what is their mechanism of action, and how do they influence the myocardial action potential?
What are the Class 1c drugs, what is their mechanism of action, and how do they influence the myocardial action potential?
With regards to the myocardium, what subclass of Class 1 drugs will result in a slower myocardial depolarization, but not affect the action potential duration?
With regards to the myocardium, what subclass of Class 1 drugs will result in a slower myocardial depolarization, but not affect the action potential duration?
Given the effects of Class 1c anti-arrhythmic drugs on myocardial action potentials, how do you expect them to alter the EKG?
Given the effects of Class 1c anti-arrhythmic drugs on myocardial action potentials, how do you expect them to alter the EKG?
Given that Class 1 anti-arrhythmic drugs are sodium channel blockers, what conformational state do these drugs bind most strongly to the sodium channel?
Given that Class 1 anti-arrhythmic drugs are sodium channel blockers, what conformational state do these drugs bind most strongly to the sodium channel?
Explain why Procainamide increases repolarization time (increased action potential duration) if this drug is a sodium channel blocker associated with depolarization?
Explain why Procainamide increases repolarization time (increased action potential duration) if this drug is a sodium channel blocker associated with depolarization?
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Study Notes
Overview of Anti-Arrhythmic Drug Classes
- Four classes of anti-arrhythmic drugs:
- Class 1: Sodium Channel Blockers
- Class 2: Beta Blockers
- Class 3: Drugs prolonging cardiac action potential
- Class 4: Calcium Channel Blockers
Effects on Electrical Activity vs. Myocardial Response
- Class 2 (Beta Blockers) and Class 4 (Calcium Channel Blockers) primarily influence the conduction system's electrical activity, mainly at SA and AV nodes.
- Class 1 (Sodium Channel Blockers) and Class 3 drugs affect myocardial response to electrical depolarization.
Classification Based on Tissue Effects
- Class 2 and 4 reduce conduction velocity of the SA and AV nodes.
- Class 1 and 3 drugs modify myocardial action potentials.
Class 1a Drugs
- Examples: Disopyramide, Quinidine, Procainamide
- Mechanism: Sodium channel blockers that decrease the slope of phase 0 depolarization.
- Effect on Action Potential: Increase action potential duration.
Class 1a Effects on EKG
- Prolong phase 0 depolarization, leading to:
- Widening of the QRS complex (indicates altered phase 0)
- Lengthening of the QT interval (indicates increased action potential duration)
Class 1b Drugs
- Examples: Lidocaine, Mexiletine, Tocanide, Phenytoin
- Mechanism: Sodium channel blockers that decrease the slope of phase 0 depolarization.
- Effect on Action Potential: Shorten action potential duration.
Class 1b Effects on EKG
- Slow phase 0 depolarization and shorten myocardial action potential:
- Typically results in a normal QRS complex duration.
- Decrease in QT interval (due to shortened action potential duration).
Class 1c Drugs
- Examples: Flecainide, Propafenone, Moricizine
- Mechanism: Sodium channel blockers that decrease the slope of phase 0 depolarization.
- Effect on Action Potential: Do not increase action potential duration.
Class 1c Effects on EKG
- Slowing of phase 0 depolarization without affecting action potential duration:
- Widening of the QRS complex.
- QT interval remains unchanged or slightly altered.
Sodium Channel Binding Dynamics
- Class 1 anti-arrhythmic drugs bind sodium channels most effectively when they are activated or in their refractory state, rather than in the resting state.
Unique Effects of Procainamide
- Although it's a sodium channel blocker, procainamide prolongs repolarization time (increased action potential duration) due to secondary blockade of potassium efflux channels, affecting phases 2 and 3 in myocardium and phase 3 in nodes.
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