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Anti-Arrythmic Agents Flashcards

1
Q

Incidence of Cardiac Arrythmias

A

5% of population
25% of patients under general anesthesia
80% of patients with acute myocardial infarction

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2
Q

All Arrhythmias result from

A

1) Disturbed impulse formation
2) Disturbed impulse conduction
3) Combination of 1 and 2

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3
Q

EAD

A

Early after depolarization
Usually at slow heart rates
Depolarizes on repolarization plateau (before it gets all the way down)

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4
Q

DAD

A

Delayed afterdepolarization
usually at fast heart rates
From resting potential

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5
Q

Re-entry

A

1) Block
2) Unidirectional conduction
3) Slow conduction through the block

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6
Q

Anti-arrhythmic therapy

A

Reduce ectopic pacemaker activity an/or modify conduction characteristic to disable re-entry circuit

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7
Q

Possible pharmacological mechanisms

A

1) Na channel blockade
2) Blockade of sympathetic autonomic effects (B-receptors)
3) Prolongation of the effective refractory period
4) Ca channel blockade

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8
Q

Ways to reduce rate of abnormal pacemaker activity

A

1) Reduction of phase 4 slope (B=blockers)
2) Increase of max. Em (hyperpolarize membrane with adenosine)
3) Increase of threshold potential (Na or Ca channel blockers)
4) Increase of AP duration (K channel inhibitors)

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9
Q

Use-dependent/state-dependent drug action

A

Selective blockade of depolarized cells
Channels that are used frequently/inactivated are more susceptible (ie during tachycardia or in ischemic/infarcted tissues)
Whereas channels in normal cells loose drug during resting phase
(anti-arrhythmics are no specific though, so can induce arrhythmias in normal cells)

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10
Q

Should you treat aymptomatic or minimally symptomatic arrhythmias?

A

NO

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11
Q

Class I

A

Na channel blockers

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12
Q

Class II

A

B-adrenocepto blockers

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13
Q

Class III

A

Prolongation of AP duration (usually K channel blockers)

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14
Q

Class IV

A

Ca channel blockers

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15
Q

Class I

MoA

A

Block fast Na channels (Phase 0)
Actions depend on HR and membrane potential
(Faster HR have less diastolic resting time, less time for drug to dissociate, more Na channels are blocked)
Can also have effects on K channels (APD)

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16
Q

Class IA

A

Intermediate kinetics, inc. APD
Procainamide
Quinidine
Disopyramide

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17
Q

Class IB

A

Fast kinetics, dec. APD
Lidocaine
Mexiletine

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18
Q

Class IC

A

Slow kinetics, does not change APD
Flecainidine
Propafenone

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19
Q

Procainamide

A

Class IA
Intermediate kinetics, inc. APD
Slows upstroke of AP, prolonges QRS, depressed SA and AV nodes

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20
Q

Procainamide Indications

A

Atrial and ventricular arrhythmias

2nd/3rd line drug for ventricular arrhythmias after acute MI (lidocain and amiodarone first)

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21
Q

Procainamide

Pharmacokinetics

A

IV, IM, PO
NAPA metabolite
Elimination via liver and kidney (NAPA)
1/2life 3-4 hours

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22
Q

Procainamide

Adverse Effects/toxicity

A 
Anticholinergic effects, hypotension
Torsade de pointes (NAPA!)
Lupus erythematousus (long term)
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23
Q

Quinidine

A

Class IA
Intermediate kinetics, inc. APD
Similar action and indications to procainamide
Rarely used because cardiac and other severe effects greater than procainamide
Cinchonism: headache, dizziness, tinnitus

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24
Q

Lidocaine

A

Class IB
Fast kinetics, dec. APD
Use/state dependent
Depression of conduction in ischemic cells

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25
Lidocaine | Indications
Arrhythmias after MI First choice drug for v.tach and v.fib after cardioversion PROPHYLACTIC TX NOT RECOMMENDED
26
Lidocaine | Pharmacokinetics
IV ONLY First pass metabolism (cannot be taken orally) Half-life 1-2 hours
27
Lidocaine | Adverse effects/toxicity
``` Least cardiotoxic of the class I Hypotension (large doses may affect cardiac contractility) Neurologic SE: local anesthetic properties, paresthesia, tremors, nausea, lightheadedness, hearing disturbances, slurred speech, convulsions ```
28
Mexiletine
``` Class IB Fast kinetics, dec. APD Orally active lidocaine Half-life: 8-20 hours Off-label use: chronic pain in diabetic neuropathy/nerve injury (because of its loacl anesthetic properties) ```
29
Flecainide
Class IC Slow kinetics, similar APD Blocks K and Na channels No anti-cholinergic effects
30
Flecainide | Indications
Supraventricular arrhythmias in patients with normal hearts
31
Flecainide | Pharmacokinetics
Well absorbed Half-life 20 hours Eliminted via liver and kidney
32
Fleicainide | Adverse effects/toxicity
Do not give to patient with ventricular tachyarrhythmias, MI, ventricular ectopy
33
Propafenone
Class IC Blocks K and Na channels Structurally similar to propranol, thus weak B-blocking
34
Propafenone | Indications
Supraventricular arrhythmias in patients with otherwise normal hearts
35
Propafenone | Pharmacokinetics
PO Half-life 5-7 hours Liver elimination
36
Propafenone | Adverse effects/toxicity
Similar to flecainide (arrhythmogenic) Sinus bradycardia/bronchospasm (B-blockade) Metallic taste Constipation
37
Class II | MoA
Inhibit normal sympathetic effects that act through B-adrenoceptors Reduce Hr Decrease intracellular Ca Decrease pacemaker currents (SA node) Reduce conduction velocity Decrease catecholamine induced DAD and EAD mediated arrhythmias
38
Non-selective
B1 and B2 Propranolol Sotalol Timolol
39
Cardioselective
B1 Esmolol Acebutolol
40
B-blocker | Indications
``` Prevention of infarction/death after MI Exercise-induced arrhythmias A. fib A. flutter AV nodal reenty ```
41
B-Blocker | Adverse Effects
Bradycardia Reduced exercise capacity Heart failure Hypotension AV block (contraindicated in bradycardia and partial AV block) Bronchospasm (contraindicated in asthma and COPD) Masks tachy in hypoglycemia (risk for diabetics)
42
Class III | MoA
Block K currents in phase 3 repolarization QT prolongation Enhance inward current (Na channels) Delayed repolarization leads to AP prolongation Reverse use/state dependence: least effects at fast heart rates, strong effects at low (risk torsades)
43
Amiodarone | MoA
``` Class III Structural analogue of thyroid hormone Prolong AP Blocks K, Na, Ca, inhibits B-receptors Prolongs refractory Slows reduction Slow sinus rhythm ```
44
Amiodarone | Indications
Oral: v.tach or v. fib not treatable by other drugs, a.fib (maintains sinus) IV: 1ST CHOICE for out-of-hospital cardiac arrest, halting v.tach or v.fib
45
Amiodarone | Pharmacokinetics
IV or PO Hepatic metabolization Complex half life (stays in body for a while) Lipophilic, accumulates in organs (heart, lung, liver, cornea)
46
Amiodarone | Adverse Effects
``` Bradycardia and heart block in SA/AV node disease Pulmonary toxicity (fibrosis) Hepatic toxicity Photodermatitis (skin discoloration) Cornea microdeposits Blocks conversion of T4 to T3 (iodine) Hypo and hyperthyoridisms ```
47
Dronedarone
Class III Structural analogue of amiodarone Altered to reduce thyroid effects
48
Dronedarone | Indications
A.fib A. flutter CONTRAINDICATED in severe/recently decompensated heart failure
49
Class VI | MoA
Ca channel blockers (vascular smooth muscle, cardiac myocytes, SA/AV nodes) Ca influx is required for smooth muscle and cardiomyocyte contraction and phase 0 depolarization
50
Class IV | Dihydropyridines class
Nifedipine Nitrendipine High vascular selectivity Used for hypertenstion
51
Class IV | Non-dihydropyridines
Benzothiazepine (Diltiazem): intermediate selectivity, used for hypertension, angina pectoris, arrhythmia Pheylalkylamine (Verapamil): high cardiac selectivity, used for angina pectoris and arrhythmia
52
Verapamil
``` Class IV Ca channel blockers Blocks activated/inactivated Ca channels in heart Use/state-dependent action Major effects in slow-response tissues (SA/AV node) Directly slows AV Increases AV node refractoriness Slow SA node automaticity Lowers HR and increases PR interval ```
53
Verapamil | Indications
``` Supraventricular arrhythmias (drug of choice) Re-entry arrhythmias/tachycardias involving the AV node Slows ventricular rate in a.flutter/fib Makes everything slower because AV conduction is delayed ```
54
Verapamil | Pharmacokinetics
Extensively metabolized by liver | Half-life: 7 hours
55
Verapamils | Adverse Effects
Vasodilation Negative inotropic effects Constipation, nervousness, peripheral edema CONTRAINDICATED in v.tach or LV dysfunction(will cause hypotension and fibrillation) AV nodal disease (will cause AV block) B-Blockers (will cause heart blocks)
56
Adenosine
``` Endogenous purine nucleoside Acts via GPCR Increases K conductance (hyperpolarization) Inhibits cAMP- Ca currents Atrial tissues Similar actions to acetylcholine Slows AV node conduction, increases AV node refractoriness PRODUCES TRANSIENT CARDIAC ARREST ```
57
Adenosine | Indications
DRUG OF CHOICE FOR SUPRAVENTRICULAR TACHYCARDIA TO SINUS RHYTHM
58
Adenosine | Adverse Effects
``` Flushing SOB Sinus bradycardia Sinus pauses AV block Hypotension ```
59
Adenosine | Pharmacokinetics
Half-life of seconds Rapid IV bolus Less effective with theophylline/caffeine Potentiated by dipyridamole
60
A.fib/Supraventricular Tachycardia | Conversion to Sinus Rhythm
Adenosine/Amiodarone/Fecainide
61
A.fib/Supraventricular Tachycardia | Maintenance of Sinus Rhyhtm
Amiodarone/Dronedarone | Flecainide/Propafenone
62
A.fib/Supraventricular Tachycardia | Ventricular Rate Control
Diltiazem/Verapamil | Propranolol/Esmolol
63
Ventricular Tachycardia without Heart Disease
Amiodarone | Lidocaine

Pharmacology (44 decks)

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