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Antiarrythmics Flashcards

1
Q

Goals of antiarrythmic drugs

A

reduce ectopic pacemaker activity; modify conduction or refractoriness in re-entry circuits

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2
Q

Classes of antiarrythmic drugs

A

I (Na channel blockers), II (Beta blockers), III (K channel blockers), IV (Ca channel blockers), magnesium, adenosine, digoxin

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3
Q

Class IA antiarrythmics

A

QUINIDINE, PROCANIMIDE, DISOPYRAMIDE

  • Blocks fast Na+ current by blocking activated Na+ channels
  • weak Class III effect (block K+ which ↑ AP duration)
  • EKG: ↑QRS, ↑QT (↓K+) (↓phase 0)
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4
Q

QUINIDINE

A
  • Class IA antiarrythmic
  • Mechanism: -Blocks fast Na+ current by blocking activated Na+ channels
  • weak Class III effect (block K+ which ↑ AP duration)
  • EKG: ↑QRS, ↑QT (↓K+) (↓phase 0)
  • Use: all forms of arrhythmia, esp. atrial fibrillation, flutter
  • AE: Not considered first-line drugs.
  • The mechanism combo can lead to refractory heterogeneity (differential sensitivity of myocardium to ΔK channel activity) → torsade de pointes → quinidine syncope (recurrent lightheadedness)
  • anti-muscarinic (vagolytic) → ↑AV conduction, ↑SA pacing → tachycardia, arrhythmia
  • ↑[digoxin] → digitalis toxicity possibility
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5
Q

PROCANIMIDE

A
  • Class IA antiarrythmic
  • Mechanism: -Blocks fast Na+ current by blocking activated Na+ channels
  • weak Class III effect (block K+ which ↑ AP duration)
  • EKG: ↑QRS, ↑QT (↓K+) (↓phase 0)
  • Use: similar to Quinidine
  • Sustained Ventricular Arrhythmias post acute MI
  • AE: Not considered first-line drugs.
  • The mechanism combo can lead to refractory heterogeneity (differential sensitivity of myocardium to ΔK channel activity) → torsade de pointes → quinidine syncope (recurrent lightheadedness)
  • anti-muscarinic (vagolytic) → ↑AV conduction, ↑SA pacing → tachycardia, arrhythmia
  • long-term → lupus-like symptoms
  • anti-muscarinic effects
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6
Q

DISOPYRAMIDE

A
  • Class IA antiarrythmic
  • Mechanism: -Blocks fast Na+ current by blocking activated Na+ channels
  • weak Class III effect (block K+ which ↑ AP duration)
  • EKG: ↑QRS, ↑QT (↓K+) (↓phase 0)
  • Use: similar to Quinidine
  • Sustained Ventricular Arrhythmias post acute MI
  • AE: Not considered first-line drugs.
  • The mechanism combo can lead to refractory heterogeneity (differential sensitivity of myocardium to ΔK channel activity) → torsade de pointes → quinidine syncope (recurrent lightheadedness)
  • anti-muscarinic (vagolytic) → ↑AV conduction, ↑SA pacing → tachycardia, arrhythmia
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7
Q

Class IB antiarrythmics

A

LIDOCAINE, TOCAINIDE, MEXILETINE, PHENYTOIN

  • Inhibit Na+ channels in both activated and unactivated states
  • state-/use-dependent block: preferentially blocks depolarized or ischemic, arrhythmic tissue
  • no effect on normal tissue
  • Selective for Ventricles
  • ↓ ph. 0 depol
  • ↓AP duration
  • (↓ERP)
  • EKG: ↑QRS, ↓QT
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8
Q

LIDOCAINE

A
  • Class IB antiarrythmic
  • Inhibit Na+ channels in both activated and unactivated states
  • state-/use-dependent block: preferentially blocks depolarized or ischemic, arrhythmic tissue
  • no effect on normal tissue
  • Selective for Ventricles
  • ↓ ph. 0 depol
  • ↓AP duration
  • (↓ERP)
  • EKG: ↑QRS, ↓QT
  • Admin: IV only – only used in acute situations
  • Use: Ventricular tachycardia
  • Digitalis-induced arrhythmia
  • Acute Suppression Ventricular Arrythmias w/ MI esp. after cardioversion
  • Promotes conduction block, terminates re-entry, ↓ automacity of ectopic pacemaker
  • DOC for ventricular arrhythmias
  • AE: CNS effects
  • beta blockers block clearance of lidocane clearance
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9
Q

TOCAINIDE

A
  • Class IB antiarrythmic
  • Inhibit Na+ channels in both activated and unactivated states
  • state-/use-dependent block: preferentially blocks depolarized or ischemic, arrhythmic tissue
  • no effect on normal tissue
  • Selective for Ventricles
  • ↓ ph. 0 depol
  • ↓AP duration
  • (↓ERP)
  • EKG: ↑QRS, ↓QT
  • Admin: IV only – only used in acute situations
  • Use: Ventricular tachycardia
  • Digitalis-induced arrhythmia
  • Acute Suppression Ventricular Arrythmias w/ MI esp. after cardioversion
  • Promotes conduction block, terminates re-entry, ↓ automacity of ectopic pacemaker
  • AE: CNS effects
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10
Q

MEXILETINE

A
  • Class IB antiarrythmic
  • Inhibit Na+ channels in both activated and unactivated states
  • state-/use-dependent block: preferentially blocks depolarized or ischemic, arrhythmic tissue
  • no effect on normal tissue
  • Selective for Ventricles
  • ↓ ph. 0 depol
  • ↓AP duration
  • (↓ERP)
  • EKG: ↑QRS, ↓QT
  • Admin: IV only – only used in acute situations
  • Use: Ventricular tachycardia
  • Digitalis-induced arrhythmia
  • Acute Suppression Ventricular Arrythmias w/ MI esp. after cardioversion
  • Promotes conduction block, terminates re-entry, ↓ automacity of ectopic pacemaker
  • AE: CNS effects
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11
Q

PHENYTOIN

A
  • Class IB antiarrythmic
  • Inhibit Na+ channels in both activated and unactivated states
  • state-/use-dependent block: preferentially blocks depolarized or ischemic, arrhythmic tissue
  • no effect on normal tissue
  • Selective for Ventricles
  • ↓ ph. 0 depol
  • ↓AP duration
  • (↓ERP)
  • EKG: ↑QRS, ↓QT
  • Admin: IV only – only used in acute situations
  • Use: Ventricular tachycardia
  • Digitalis-induced arrhythmia
  • Acute Suppression Ventricular Arrythmias w/ MI esp. after cardioversion
  • Promotes conduction block, terminates re-entry, ↓ automacity of ectopic pacemaker
  • AE: CNS effects
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12
Q

Class IC antiarrythmics

A

FLECANIDE (don’t use), PROPAFENONE

  • Inhibit fast Na+ channels and IloK+ currents
  • esp. effective @His-Purkinje, QRS widening
  • ↓↓ph. 0 depol
  • ↑AP duration (↑ERP)
  • EKG: ↑PR, ↑QRS, ↑QT → torsade
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13
Q

FLECANIDE

A

-Class IC antiarrythmic, DONT USE
-Mechanism: Inhibit fast Na+ channels and IloK+ currents
- esp. effective @His-Purkinje, QRS widening
- ↓↓ph. 0 depol
- ↑AP duration (↑ERP)
- EKG: ↑PR, ↑QRS, ↑QT → torsade
-Use: life threatening ventricular arrythmias (chronic v-tach)
- recurrent atrial fibrillation- rhythm control
- PSVT
- if pt. can’t tolerate Class III
AE:contraindicated in left ventricular disease or coronary heart disease
- does not reduce mortality
- proarrthymic

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14
Q

PROPAFENONE

A

-Class IC antiarrythmic
-Mechanism: Inhibit fast Na+ channels and IloK+ currents
- esp. effective @His-Purkinje, QRS widening
- ↓↓ph. 0 depol
- ↑AP duration (↑ERP)
- EKG: ↑PR, ↑QRS, ↑QT → torsade
-Use: life threatening ventricular arrythmias (chronic v-tach)
- recurrent atrial fibrillation- rhythm control
- PSVT
- if pt. can’t tolerate Class III
AE:contraindicated in left ventricular disease or coronary heart disease
- does not reduce mortality
- proarrthymic

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15
Q

Class II antiarrythmics

A

ACEBUTOLOL (S), ESMOLOL (S), METOPROLOL (S), PROPANOLOL(NS), SOTALOL(NS) (C III)
-β-blockers

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16
Q

ACEBUTOLOL, ESMOLOL, METOPROLOL, PROPANOLOL, SOTALOL

A

Class II antiarrythmic, β-blocker
-Mechanism: -Blocks sympathetic effects
- mostly at SA/AV nodes
- ↓ph. 4 depol of SA → ↓HR
- ↑ERP of AV (& SA) by blocking K+ → ↓reentry
- ↓AV nodal conduction
- ↓O2 demand → ↓ischemia
- EKG: ↑PR, ↑RR
-Use: -control of ventricular rate @atrial fibrillation, flutter –> PVST
- arrythmias @excess catecholamines
-Ischemia-related v-tach
-reduce arrhythmia and arrhythmia assoc mortality
- ventricular arrythmias @reentry circuits w/ AV node
AE: - withdrawal → rebound hypersensitivity
- bradycardia
- negative inotropes
- contraindicated in asthma
- CNS effects (Propanolol)

17
Q

Class III antiarrythmics

A

Ibutelide (IV), Dofetilide (oral), Sotalol, Bretylium, Amiodarone, Dronedarone
-K+ channel blockers

18
Q

Ibutelide

A
  • Class III antiarrythmic
  • Mechanism: Blocks K+ channels
  • ↑AP duration, ↑ERP
  • acts only @repol phase (therefore has no effect on ph. 0 depol, no effect on conduction velocity)
  • EKG: ↑ PR, ↑ QRS, ↑↑ QT → torsade
  • Use: atrial fibrillation
  • Admin: IV
  • pure Class III effect
19
Q

Dofetilide

A
  • Class III antiarrythmic
  • Mechanism: Blocks K+ channels
  • ↑AP duration, ↑ERP
  • acts only @repol phase (therefore has no effect on ph. 0 depol, no effect on conduction velocity)
  • EKG: ↑ PR, ↑ QRS, ↑↑ QT → torsade
  • Use: atrial fibrillation
  • Admin: oral
  • pure Class III effect
20
Q

Sotalol

A
  • Class III antiarrythmic
  • Mechanism: Blocks K+ channels
  • ↑AP duration, ↑ERP
  • acts only @repol phase (therefore has no effect on ph. 0 depol, no effect on conduction velocity)
  • EKG: ↑ PR, ↑ QRS, ↑↑ QT → torsade
  • Use: VT, AF&F, bypass mediated PSVT
  • L isomer: some Class II @ [low]
21
Q

Bretylium

A
  • Class III antiarrythmic
  • Mechanism: Blocks K+ channels
  • ↑AP duration, ↑ERP
  • acts only @repol phase (therefore has no effect on ph. 0 depol, no effect on conduction velocity)
  • EKG: ↑ PR, ↑ QRS, ↑↑ QT → torsade
  • Use: rare!
    • ↓release of catecholamines (NE) from nerves (initial ↑release)
22
Q

Amiodarone

A
  • Class III antiarrythmic
  • Mechanism: Blocks K+ channels
  • ↑AP duration, ↑ERP
  • acts only @repol phase (therefore has no effect on ph. 0 depol, no effect on conduction velocity)
  • EKG: ↑ PR, ↑ QRS, ↑↑ QT → torsade
  • ALSO: weak Class I, II, IV
    • ↓sinus rate
  • ↓automaticity: ↓Na, Ca
  • ↓ph. 4 in any automaticity focus
  • ↓reentry activity (↓Ca (@AV), Na)
  • negative inotrope and vasodilator
  • Use: -Acute & Chronic ventricular arrhythmias
  • Recurrent atrial fibrillation, flutter (rhythm control)
  • VF, VT, PSVT
  • AE: pulmonary fibrosis, hypothyroid (5%), hyperthyroid (rare), CNS effects (rare), ↓liver fxn (rare) → drug interaction
23
Q

Dronedarone

A
  • Class III antiarrythmic
  • Mechanism: Blocks K+ channels
  • ↑AP duration, ↑ERP
  • acts only @repol phase (therefore has no effect on ph. 0 depol, no effect on conduction velocity)
  • EKG: ↑ PR, ↑ QRS, ↑↑ QT → torsade
  • ALSO: weak Class I, II, IV
    • ↓sinus rate
  • ↓automaticity: ↓Na, Ca
  • ↓ph. 4 in any automaticity focus
  • ↓reentry activity (↓Ca (@AV), Na)
  • negative inotrope and vasodilator
  • *Dronedarone is Analogue of Amiodarone with a shorter half life (1-2 days instead of 180 days), and no thyroid side effects
  • Use: -Acute & Chronic ventricular arrhythmias
  • Recurrent atrial fibrillation, flutter (rhythm control)
  • VF, VT, PSVT
  • AE: pulmonary fibrosis, hypothyroid (5%), hyperthyroid (rare), CNS effects (rare), ↓liver fxn (rare) → drug interaction
24
Q

Class IV antiarrythmics

A

VERAPIMIL, DILTIAZEM

-Ca channel blockers (NOT dihydropiridines!)

25
VERAPIMIL
- Class IV antiarrythmic - Mechanism: Ca2+ channel blockers, so their effects are mostly on the SA and AV nodes! - ↓ SA node automaticity - ↓ AV nodal conduction (for PSVT) - EKG: ↑PR, ↑RR - Use: DOC Acute & Chronic PSVT - ↓ventricular rate @atrial fibrillation, flutter, multifocal AT - AE: - avoid with β-blocker use - like β-blocker, but
26
DILTIAZEM
- Class IV antiarrythmic - Mechanism: Ca2+ channel blockers, so their effects are mostly on the SA and AV nodes! - ↓ SA node automaticity - ↓ AV nodal conduction (for PSVT) - EKG: ↑PR, ↑RR - Use: DOC Acute & Chronic PSVT - ↓ventricular rate @atrial fibrillation, flutter, multifocal AT - AE: - avoid with β-blocker use - like β-blocker, but
27
Adenosine
- Antiarrythmic - Mechanism: Opens K channels in nodal tissues and indirectly inhibits Ca2 channels - ↓ adenyl cyclase → ↓Ca, If - ↓ ph. 4 depol (↓Ca, Na, ↑K): via adenosine-R → ↓sinus tachycardia - ↓AV nodal conduction, ↓SA rate - EKG: ↑PR - IV, t½ = 10 s; acute only - Use: PSVT Drug of choice! (terminates reentry pathways) - AE: vasodilation: flushing, headache, hypotension - bronchoconstriction (later & longer) - ↓effects w/ adenosine-R blockers, (caffeine, theophylline)
28
Magnesium
-Antiarrythmic -Mechanism: weakly blocks ICa, inhibits INa and IK Use: TORSADES DE POINTES -Can be used to slow ventricular rate, but not used for PVST
29
Digoxin
- Antiarrythmic - vagomimetic; ↓AV nodal conduction - Rarely used except in a-fib and heart failures

Cardio Pharm (5 decks)

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