IBHRE CEPS TEST LATEST
UPDATED
Class 1 Anti-Arrhythmic Mechanism: Sodium (Na) Channel Blockers
Class II Anti-Arrhythmic Mechanism: Beta Blockers
Class III Anti-Arrhythmic Mechanism: Potassium (K) Channel Blockers
Class IV Anti-Arrhythmic Mechanism: L-Type Calcium (Ca) Channel Blocker
Class Ia medicines - ANSWER: Quinidine (rarely used).
- Procainamide - Disopyramide.
Na Channel Blockers that Increase APD
Class Ib medications include lidocaine, mexiletine, and phenytoin.
Na channel blockers that modestly reduce APD
Class Ic medications include propafenone and flecainide.
Na Channel Blockers That Do Not Change APD
Class II drugs include propranolol, atenolol, esmolol, and metoprolol.
Beta-Blockers. (β-blockers)
Class III drugs include amiodarone, dronedarone, sotalol, ibutilide, and
bretylium.
Prolong APD (K Channel Blocker).
Class IV drugs include verapamil and diltiazem.
, L-Type Calcium Channel Blockers
During Phase 0 AP, the cell experiences depolarization, which causes rapid
opening of Na+ channels and flooding with positive sodium ions.
-The depolarization of one cell causes the Na+ channels of adjacent cells to
open, resulting in a wave of propagation.
Phase 1 AP: Initial Repolarization and Inactivation of Fast Na+ Channels.
Phase 2 AP: ANSWER-Plateau The phase is sustained by a balance of Ca2+
inward movement through L-type calcium channels (opened during
depolarization) and K+ outward movement through the slow K+ channel.
-Lower potassium ion permeability
Phase 3 AP - ANSWER: Rapid Repolarization Phase: Ca2+ channels close,
slow K+ remains open, and ionic pumps restore ion concentrations to pre-AP
levels.
Phase 4 AP - ANSWER: Resting Membrane Potential.
Vasoconstriction is the effect of the alpha adrenergic receptor site.
Beta-1 Adrenergic Receptor Site Effect - Cardiac Stimulation
We have one heart and two lungs.
Beta-2 Adrenergic Receptor Site Effect - ANSWER: Lung Bronchodilation
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