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22 Cards in this Set
- Front
- Back
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Atrial/Ventricular AP phases |
0: rapid depolarization- Na influx 1: depolarization "overshoot"- Na channels close 2: plateau- Ca2+ open 3: repolarization- K+ rectifier 4: intrinsic depolarization- Na leak
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SA node AP phases: |
4: automaticity- Na leak 0: conduction velocity- Ca2+ influx 3: Repolarization- K+ rectifier |
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Vaughan-Williams classification |
Class 1: Na channel blockers Class 2: Beta blockers Class 3: K channel blockers Class 4: Ca2+ channel blockers |
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Class I effects |
slow intrinsic depolarization current--> reduce automaticity of AV, atria & ventricles
slow rate of phase 0 depolarization spike--> reduce conduction velocity in atria & ventricles |
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Class IA drugs & effects
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Quinidine, procainamide, disopyramide
reduce automaticity prolong AP duration reduce conduction velocity |
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Why is Quinidine not normally used? |
toxic effects--> cinchonism, lupid hepatitis, thrombocytopenia--> can actually cause V tach
-only moderately effective for atrial arrhythmia only |
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Pracainamide & Disopyramide are both moderately effective for atrial & ventricular arrhythmias. What are the side effects of each?
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procainamide- lupus symptoms
disopyramide- decreased contracility & urinary retention |
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Class IB drugs also, reduce automaticity & slow conduction velocity
How do they differ from class IA? |
-shorten AP duration -act on ventricles ONLY (do not effect atrial tissue) |
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Class IB drugs & side effects |
-lidocaine/Tocainamide/Mexiletine ^ cause CNS dysfunction
-Dilatin (used primarily for seizures) ^ CNS side effects more effective for atypical ventricular tachycardia |
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Class IC drugs have the same MOA as class IA, but are more potent (& toxic--> proarrhythmia)
What drugs belong to IC? |
Flecaininde Propaphenone Dofetilide |
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Class IC drugs (Flecaininde, Propaphenone, & Dofetilide) are VERY good inhibitors of ________ |
ventricular arrhythmia
-also effective at stabilizing atrial rhythm |
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Beta blockers ONLY work on arrhythmias that are caused by _________ |
catecholamines (overstimulation of sympathetics)
--> reduce sympathetics --> slow AV node conduction (for supraventricular rhythm disturbance) |
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What beta-blockers are cardioselective? what are the side effects? |
cardioselective: atenolol, metorpolol (nonselective- propranolol, timolol, carvedelol)
SE: bronchospasm (nonselective only) fatigue bradycardia/AV block decreased myocardial contractility |
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What class is the MOST potent antiarrhythmic agents & work on all tissue (atrial, ventricular, nodal, etc)?
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class III- potassium channel blockers (amiodarone, sotolol, dronedarone)
(mainly block potassium but also have effects of all other classes- calcium blocker, beta, etc) --> primary effect on repolarization current |
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What is the ONLY potassium blocker that can be used in patients w LV dysfunction? (OVERALL most effective arrhythmatic)
what are the possible side effects? |
Amiodarone
SE: hepatotoxicity hypo/hyper-thyroidism corneal deposits irreversible pulmonary fibrosis (^all common SE for potassium blockers) |
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Which potassium channel blocker is also a strong beta blocker?
SE? |
Sotolol
SE: bronchospasm, proarrhythmia, worsening heart failure (in addition to potassium blocker SE) |
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Dronedarone (or sotolol) are not quite as effective as amiodarone. However, what is the advantage of Dronedarone? |
- fewer side effects (no thyroid effects or pulmonary effect) - shorter half life |
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Class 4 calcium channel blockers primarily effect what phase? |
phase 0--> slow conduction velocity in NODAL tissue (prevents reentry arrhythmia)
*good for control of ventricular rate in supraventricular tachy arrhythmias
-NOT effective in direct atrial or ventricular arrhythmias |
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What are the 2 groups of class 4 drugs?
Which are more effective for rate control?
SE? |
1. dihyrdopyradine group: nifepidine, amlodipine, nitrendipine, isradipine, isoldipine SE: reflex tachycardia, edema, orthostatic hypotension (NOT for rate control)
2. Diltiazem & Verpamil SE: bradycardia (diltiazem), hypotensin, dec LV contracility, peripheral edema (verpamil) *MORE effective for rate control |
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Diltiazem & Verpamil both reduce ventricular response to supraventricular tachyarrhythmias. Which is more potent at slowing AV node conduction? |
Verpamil |
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Digoxin (not calcium blocker) also slows ventricular response to supraventricular tachyarrhythmias. How?
SE? |
vagotonic--> dec AV node conduction velocity
SE: may promote atrial & ventricular irritability |
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________ also slows AV node conduction, but only works for a very short amount of time |
Adenosine
(not very useful) |
