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Anti Arrhythmic Drugs Flashcards

1
Q

Properties of cardiac cells?

A
  1. excitability
    - changes in resting membrane potential
  2. Conduction
    - slope of phase 0 (mass Na influx reaching threshold)
  3. Refractory period
    - phases 1-3
  4. Automaticity
    - slope of phase 4
    - increased slope = increase automaticity
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2
Q

Factors that increase automaticity?

A
  • Na/Ca influx
  • sympathetic stimulation (beta receptor stimulation increases PKA and opening of calcium channels)
  • ischemia
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3
Q

Factors that decrease automaticity?

A
  • K+ efflux

- parasympathetic stimulation (opens K+ channels causing hyperpolarization)

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4
Q

Mechanisms of cardiac arrhythmias?

A
  1. abnormal automaticity
    - sinus tachycardia at SA node
    - sinus bradycardia at SA node
    - latent pacemaker driven
    - escape beats (ectopic)
  2. triggered automaticity
    - afterdepolarizations, AP triggered directly after effective refractory period (ERP) or before start of phase 4
    - early afterdepolarizations (EAD) arise from plateau after ERP, class Ia and III antiarrhythmic drugs predispose person to EAD
    - delayed afterdepolarization (DAD) arise from resting potential due to Ca build up in cell from Na/K ATPase inhibitor (Digoxin)
  3. Reentry
    - develop self sustaining electrical circuit with depolarization of surrounding tissue, leading to tachycardia
    - conduction block (ischemia, fibrosis)
    - bypass track (parkinson’s bypass AV node)
    - treatment is ablation (burn excess track)
  4. Supraventricular tachycardia
    - paroxysmal atrial tachycardia (PAT) ectopic foci in atria
    - beat is somewhere other than SA node
    - HR increased
  5. Premature ventricular contractions (PVC)
    - beat arises from ectopic foci in ventricle
  6. Ventricular tachycardia
    - torsade de pointes
    - treat with lidocaine or amiodarone
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5
Q

What class of drugs predispose a person to EADs?

A

class III and Ia

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6
Q

Why is digoxin used instead of Ouabain?

A
  • Ouabain results in a bunch of DADs

- Digoxin stimulates PSNS via Vagus nerve slowing HR and contractility which offsets buildup of calcium

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7
Q

Classification of Antiarrhythmic drugs?

A
  1. Na channel blockers (class Ia, Ib, Ic)
    - decrease phase 0 upstroke rate and phase 4 slope, increase threshold
  2. Beta blockers (class II)
    - decrease phase 4 slope
  3. K channel blockers (class III)
    - increase action potential duration
  4. Ca channel blocker (class IV)
    - decreases phase 4 slope
  5. Adenosine
    - increase diastolic potential
    - opens K channels
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8
Q

Na channel characteristics?

A
  1. resting state is closed
  2. active state is open and Na comes in, reaching threshold
  3. inactivated channel, no ion conduction (occurs with lidocaine in system)
  4. USE-DEPENDENT BLOCKADE
    - more channel is activated the more drug will block it
    - antiarrhythmic effects faster during faster HR
  5. drugs have high affinity for inactivated channels and low affinity for resting state channels
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9
Q

Class 1 (a,b,c) anti arrhythmics?

A
  • Na channel blockers minimize Na reentry for AP
  • all depress phase 0 slope from Na block
  • Ia and Ic bind active channels
  • Ib bind inactive channels
  • Ia increased refractory period due to K channel block
  • Ib reduced refractory period b/c they bind inactive channels, do not block K channels
  • Ic normal refractory period due to limited K block
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10
Q

Class Ia anti arrhythmics common features?

A
  • Quinidine, Procainamide, Disopyramide
  • common features:
    1. block fast influx of Na channels during phase 0 and block K channels to PROLONG REFRACTORY PERIOD
    2. HYPERKALEMIA
  • increased K in blood
    3. ECG effects:
  • increases QRS and QT intervals (block K channels)
  • PR interval varies due to anticholinergic effects (increases HR and AV conduction)
    4. anti cholinergic effects
  • initial HR increase
    5. clinical use:
  • supraventricular (AV node and above) and ventricular arrhythmias
  • procainamide is used most
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11
Q

Quinidine?

A
  • class Ia
  • D isomer of antimalarial alkaloid Quinine

Clinical use:

  • supraventricular and ventricular arrhythmias
  • has some alpha adrenergic activity (PR)
  • use PO, can cause hypertension with IV administration due to alpha blocking

ADR:

  • diarrhea
  • cinchonism (hearing disorders)
  • torsades de pointes
  • interact with Digoxin by decreasing Digoxing clearance, which increases toxicity of Digoxin
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12
Q

Procainamide?

A
  • class Ia
  • less anticholinergic effects than Quinidine, no alpha block, safer for IV

Clinical use:

  • ventricular arrhythmias
  • good to take PO, short half life (3-4 hours), sustained release
  • active metabolite produces class III antiarrhythmic effects (blocks K channel to prolong AP)

ADR:

  • antinuclear antibody formation (ANA) in 80% of people, Lupus like symptoms in 15% of patients (blood disorder)
  • rash, fever, hepatitis, arthralgia
  • infrequent progress to pleural effusion and pericardial tamponade
  • agranulocytosis
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13
Q

Disopyramide?

A
  • class Ia
  • 2nd line drug only used when other drugs are not effective

clinical use:

  • ventricular arrhythmias (life threatening)
  • negative inotropic effects causing cardiac depression, CHF, and hypotension
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14
Q

Lidocaine?

A
  • class Ib anti arrhythmic
  • must administer IV

Effects:

  • acts on inactivated Na channels
  • minimal K channel block
  • decreases excitability, phase 4 automaticity and afterpotentials

ECG effects:

  • PR and QRS unaffected
  • QT and AP duration decreased
  • ERP/APD ratio is increased (delay of AP)

Clinical use:

  • ventricular arrhythmias
  • one of two options for MI

ADR/Toxicity:

  • cardiac depression (decreased contractility), this is good
  • narrow therapeutic window, can cause mix of CNS stimulation and depression if above therapeutic levels, blocks Na in CNS (death from anaesthetic properties at high concentrations)
  • generally safe
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15
Q

Mexiletine/Tocainide?

A
  • oral forms of lidocaine, similar effects
  • does not undergo first pass effect

Tocainide

  • associated with agranulocytosis, blood dyscriasias and pulmonary fibrosis, give only fro life threatening arrhythmias
  • only for ventricular arrythymias and ventricular tachycardia
  • has a higher incidence of agranulocytosis

ADR:
-GI and CNS disturbances

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16
Q

Flecainide?

A

-class Ic

Effects:

  • decreases depolarization/conduction (His, purkinje)
  • increased PR
  • QRS, QT unchanged

Clinical use:

  • supraventricular and life threatening arrhythmia
  • paroxysmal atrial fibrillation

ADR:

  • negative inotropic, potential lethal arrhythmias after recovering from MI
  • blurred vision, dizziness, headache, CHF, bradycardia, neutropenia
17
Q

Propafenone and Moricizine?

A
  • Propafenone similar to Flecainide, same effects on heart, weak beta blocking activity
  • Moricizine mainly used in life threatening ventricular arrhythmias
  • both increases the mortality rate of patients recovering from MI versus placebo control group in CAST trial
18
Q

Class II drugs?

A
  • beta blockers
  • propanolol, metoprolol, atenolol, emolol

Effects:

  • decreases SNS stimulation of SA, AV, purkinje
  • decreases automaticity, especially AV, ventricles, this decreases O2 requirement

ECG:

  • increase PR
  • QRS, QT unaffected

Clinical use:

  • supraventricular and ventricular tachyarrhythmias
  • PVCs
  • prevent recurrent MI’s, sudden death patients recovering from MI

Esmolol:

  • used IV emergency treatment (atrial flutter/fibrillation, sinus tachycardia) to decrease ventricular rate
  • half life 9 mins, metabolized by RBC esterase
19
Q

Class III drugs?

A
  • K channel blockers
  • treat arrhythmias by increasing action potential duration (prevent K efflux)
  • extend QT by preventing K from leaving cell

Amiodarone

Sotalol

  • nonselective beta blocker with class III properties
  • increases refractory period, slows HR
  • used for ventricular arrhythmias
  • risk of proarrhythmias

Bretylium

  • class III drug that also depletes neuronal release of catecholamines
  • increases refractory period and action potential
  • used IV to treat emergency ventricular fibrillation

Ibutilide
-IV for rapid conversion atril fibrillation/flutter to normal sinus rhythm

Dofetilide

  • PO to maintain sinus rhythm in patients with atrial fibrillation
  • generally used inpatient setting due to risk of proarrhythmias
20
Q

Amiodarone?

A
  • class III
  • structural analog thyroxine, contain iodide
  • one of two options for MI
  • master arrhythmic

Effects:

  • increase refractory period, ERP, action potential duration
  • has class I, II, IV effects
  • slow onset, half life 50 days, give loading dose

ECG:
-increases PR, QRS, and QT

Clinical use:

  • mainly use for ventricular
  • supraventricular arrhythmias (use Na or Ca blocker first)

ADR:

  • deposits in eye/skin/ blue discoloration
  • pulmonary fibrosis
  • GI/liver disturbances
  • neurologic
  • thyroid dysfunction due to iodide component
  • bradycardia
  • CHF
  • hypotension
21
Q

Class IV drugs?

A
  • calcium antagonists
  • blocks calcium influx

Verapamil and Diltiazem

ECG effects:

  • slow sinus rate at SA and AV conduction
  • PR interval increased (slows HR)
  • suppresses ventricular rate in atrial flutter/fib
  • decreased myocardial contractility with increased dose
  • decreased phase 2 plateau

Clinical use:
-mainly used for supraventricular arrhythmias

ADR:

  • GI constipation with verapamil
  • hypotension
  • decreased HR
  • AV block
  • potential for CHF
22
Q

Adenosine?

A
  • endogenous nucleoside
  • half life, 10 seconds, due to carrier mediated uptake

Effects:

  • stimulates P1 purinergic receptor to open K channel which increases K efflux (hyperpolarization)
  • decreased calcium influx due to decreased cAMP
  • decreased automaticity and conduction through AV node
  • vasodilator, may cause hypotension
  • decreases pacemaker potential, making threshold farther away

Clinical use:
-used rapid bolus IV to halt reentrant paroxysmal supra ventricular tachycardia (PSVT) during emergencies

ADR:

  • hypotension
  • may precipitate brief bronchospasm
23
Q

Magnesium Sulfate?

A
  • deficiency can contribute to development of arrhythmias especially with loop diuretics (cause Mg loss)
  • administer IV for torsades de pointes
  • used for Digoxin induced ventricular arrhythmias
  • use for arrhythmias associated with Mg deficiency

Pharmacology (9 decks)

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