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Pharmacology > Antiarrhythmic Medications > Flashcards

Antiarrhythmic Medications Flashcards

1
Q

What is “the ability of the heart to undergo spontaneous action potential?”

A

Automaticity

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2
Q

SA Node

  • Only a few _______ cells
  • Has _________ rate of automaticity
  • Intrinsic rhythm (“_______________”) — sets pace ( _________ bpm)
  • Sends action potential to _______
A
  • Only a few HUNDRED cells
  • Has HIGHEST rate of automaticity
  • Intrinsic rhythm (“PACEMAKER”) — sets pace ( 60 - 100 bpm)
  • Sends action potential to AV NODE
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3
Q

Atrial Muscle

  • Many _______
  • No _________ rhythm –> muscle must be __________/_________
A
  • Many CELLS

- No INTRINSIC rhythm –> muscle must be TRIGGERED/STIMULATED

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4
Q

AV Node

  • Has _________ rhythm, but slower than _____ node (_____ bpm)
  • Triggered/stimulated by _______ muscle cells
  • Can initiate own _________ if _____ node is not functioning properly
A
  • Has INTRINSIC rhythm, but slower than SA node (50 - 60 bpm)
  • Triggered/stimulated by ATRIAL muscle cells
  • Can initiate own ACTION POTENTIALS if SA node is not functioning properly
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5
Q

His Purkinje System

  • Has ________ rhythm, but slower than _____ and _______ nodes (_______ bpm)
  • Triggered/stimulated, then can trigger/stimulate other cardiac cell ______________
A
  • Has INTRINSIC rhythm, but slower than SA and AV nodes (30 - 40 bpm)
  • Triggered/stimulated, then can trigger/stimulate other cardiac cell DEPOLARIZATIONS
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6
Q

Ventricular Muscle

  • Has more cells than _______ muscle
  • No ________ rhythm
  • Must be _______ / _______
A
  • Has more cells than ATRIAL muscle
  • No INTRINSIC rhythm
  • Must be TRIGGERED / STIMULATED
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7
Q

Normal Sinus Rhythm — EKG

  • P wave = ____________________
  • PR interval = _________ conduction time
  • QRS complex = _________ muscle depolarization & _________ repolarization
  • T wave = __________________
  • PP interval = indicates _____________
A
  • P wave = ATRIAL MUSCLE DEPOLARIZATION
  • PR interval = AV NODE conduction time
  • QRS complex = VENTRICULAR muscle depolarization & ATRIAL repolarization
  • T wave = VENTRICULAR REPOLARIZATION
  • PP interval = indicates HEART RATE
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8
Q

Conduction Abnormalities

  • Most common conduction abnormalities involve _______ block (heart block)
  • Usually caused by localized or regional _______ from decreased coronary blood flow (ex. post MI, CHF patients at higher risk)
  • Hypoxia decreases action potential __________ and rate of __________
  • Areas of conduction block can lead to ________ circuits (major cause of ventricular and supra ventricular tachyarrhythmias)
A
  • Most common conduction abnormalities involve CONDUCTION block (heart block)
  • Usually caused by localized or regional HYPOXIA from decreased coronary blood flow (ex. post MI, CHF patients at higher risk)
  • Hypoxia decreases action potential AMPLITUDE and rate of DEPOLARIZATION
  • Areas of conduction block can lead to REENTRY circuits (major cause of ventricular and supra ventricular tachyarrhythmias)
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9
Q

Effective Refractory Period (ERP)

  • Period of time when a new action potential __________ be initiated
  • Protective mechanism to limit rapid ___________ depolarization (and HR)
  • Many anti arrhythmic drugs alter the _______
  • Prolonging the ERP can be effective for abolishing ________ currents
A
  • Period of time when a new action potential CANNOT be initiated
  • Protective mechanism to limit rapid SUCCESSIVE depolarization (and HR)
  • Many anti arrhythmic drugs alter the ERP
  • Prolonging the ERP can be effective for abolishing REENTRY currents
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10
Q

Antiarrhythmic Drug Classification

Vaughan Williams Classification

  • Class I = __________________ blockers
  • Class II = ____________ blockers
  • Class III = ____________ blockers
  • Class IV = ____________ blockers

Miscellaneous (add-ons)
- What are 4 add-ons?

A

Vaughan Williams Classification

  • Class I = Na+ CHANNEL blockers
  • Class II = BETA blockers
  • Class III = K+ CHANNEL blockers
  • Class IV = Ca2+ CHANNEL blockers

Miscellaneous (add-ons)
- (1) ATROPINE, (2) ADENOSINE, (3) DIGOXIN, (4) ELECTROLYTES

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11
Q 
Vaughan Williams Classification of Antiarrhythmic
Class Ia = \_\_\_\_\_\_\_\_ channel blockers
- blocks \_\_\_\_\_\_\_\_\_\_
- \_\_\_\_\_\_\_\_\_\_ ERP
Ex. \_\_\_\_\_\_\_\_\_\_\_\_\_\_
A

Class Ia = Na+ channel blockers
- blocks CONDUCTION
- INCREASES ERP
Ex. QUINIDINE

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12
Q 
Vaughan Williams Classification of Antiarrhythmic
Class Ib = \_\_\_\_\_\_\_\_ channel blockers
- blocks \_\_\_\_\_\_\_\_\_\_
- \_\_\_\_\_\_\_\_\_\_ ERP
Ex. \_\_\_\_\_\_\_\_\_\_\_\_\_\_
A

Class Ib = Na+ channel blockers
- blocks CONDUCTION
- DECREASES ERP
Ex. LIDOCAINE

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13
Q 
Vaughan Williams Classification of Antiarrhythmic
Class Ic = \_\_\_\_\_ channel blockers
- blocks \_\_\_\_\_\_\_\_\_\_
- \_\_\_\_\_\_\_\_\_\_ ERP
Ex. \_\_\_\_\_\_\_\_\_\_\_\_\_\_
A

Class Ic = Na+ channel blockers
- blocks CONDUCTION
- NO EFFECT ON ERP
Ex. FLECAINIDE

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14
Q

Vaughan Williams Classification of Antiarrhythmic
Class II = _______ blockers
- Decreases _________ node automaticity / _________ activity
- Ex. ______________

A

Class II = BETA blockers

  • Decreases SINUS node automaticity / SYMPATHOLYTIC activity
  • Ex. METOPROLOL
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15
Q 
Vaughan Williams Classification of Antiarrhythmic
Class III = \_\_\_\_\_\_\_ channel blockers
- no effect on \_\_\_\_\_\_\_\_
- delays \_\_\_\_\_\_\_\_\_\_\_\_\_
- Ex. \_\_\_\_\_\_\_\_\_\_ & \_\_\_\_\_\_\_\_\_\_\_\_\_
A

Class III = K+ channel blockers

  • no effect on CONDUCTION
  • delays REPOLARIZATION
  • Ex. AMIODARONE & DOFETILIDE
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16
Q

Vaughan Williams Classification of Antiarrhythmic
Class IV = _______ channel blockers
- slows _________ velocity in the _____ node
- Ex. ________ & _________

A

Class IV = Ca2+ channel blockers

  • slows CONDUCTION velocity in the AV node
  • Ex. VERAPAMIL & DILTIAZEM
17
Q

Class Ia: Na+ Channel Blockers
Ex. Quinidine
- _________ ERP
- _________ block Na+ channels undergoing depolarization of non-nodal action potentials at high rate
- Slow __________ velocity
- Depress ___________ in depolarized tissue b/c of a small component of _____ blockade

A

Ex. Quinidine

  • INCREASES ERP
  • SELECTIVELY block Na+ channels undergoing depolarization of non-nodal action potentials at high rate
  • Slow CONDUCTION velocity
  • Depress AUTOMATICITY in depolarized tissue b/c of a small component of K+ blockade
18
Q

Class Ib: Na+ Channel Blockers
Ex. Lidocaine
- ______________ ERP
- No activity on _______ channels like seen /c class Ia drugs
- less effective in blocking _________ of sodium channels during phase 3

A
  • DECREASE ERP
  • No activity on K+ channels like seen /c class Ia drugs
  • less effective in blocking OPENING of sodium channels during phase 3
19
Q

Class Ic: Na+ Channel Blockers
Ex. Flecainide
- Very little effect (if any) on ______________ duration
- ___________ to ERP (/c potential for minimal prolongation)
- avoid in patients /c _______________ or _______________

A

Ex. Flecainide

  • Very little effect (if any) on ACTION POTENTIAL duration
  • NO CHANGE to ERP (/c potential for minimal prolongation)
  • avoid in patients /c CORONARY ARTERY DISEASE (CAD) or HEART FAILURE (HF)
20
Q

Flecainide (Tambour)

  • Class _____: Na+ channel blocker
  • MOA: slows __________ in cardiac tissue. Also causes ________ prolongation (no effect) of ERP, _________ the rate of rise of the action potential w/o affecting its duration
  • ADR = can induce life-threatening ___________________ (“pill-in-pocket”), ______________ ADR minimal, __________, headache
  • Metabolized by _______ system; may be problematic if patient is also taking _______ b/c then Flecainide would stay in the bloodstream longer
A
  • Class Ic: Na+ channel blocker
  • MOA: slows CONDUCTION in cardiac tissue. Also causes SLIGHT prolongation (no effect) of ERP, DECREASES the rate of rise of the action potential w/o affecting its duration
  • ADR = can induce life-threatening VENTRICULAR ARRHYTHMIAS (“pill-in-pocket”), ANTICHOLINERGIC ADR minimal, DIZZINESS, headache
  • Metabolized by P450 system; may be problematic if patient is also taking SSRIs b/c then Flecainide would stay in the bloodstream longer
21
Q

Class II Antiarrhythmics - Beta Blockers

  • MOA: bind to B1 receptors and block the activity of __________ and ____________. Block B1 receptors in ______ and _____ nodes, __________ system, and contracting _______
  • Predominantly _____ receptors in cardiac tissue. Inhibits normal _____________ effects through these receptors
  • Increased SA node automaticity (pacemaker activity) — increased _____ rate
  • By decreasing __________ velocity beta-blockers abort reentry circuits
  • Beta-blockers also affect _________________ action potentials (increase ERP)
A
  • MOA: bind to B1 receptors and block the activity of EPINEPHRINE and NOREPINEPHRINE. Block B1 receptors in SA and AV nodes, CONDUCTING system, and contracting MYOCYTES
  • Predominantly B1 receptors in cardiac tissue. Inhibits normal SYMPATHETIC effects through these receptors
  • Increased SA node automaticity (pacemaker activity) — increased SINUS rate
  • By decreasing CONDUCTION velocity beta-blockers abort reentry circuits
  • Beta-blockers also affect NON-PACEMAKER action potentials (increase ERP)
22
Q

Metoprolol

  • the primary _______________ when used for arrhythmias
  • only use if hemodynamically ___________
  • caution in patients /c ____________ heart failure
A
  • the primary BEAT BLOCKER when used for arrhythmias
  • only use if hemodynamically STABLE
  • caution in patients /c DECOMPENSATED heart failure
23
Q

Class III Anti-arrhythmics

  • _____ channels responsible for cell _______________
  • K+ channel blockers _______ or _________ membrane repolarization
  • work both ______ and _________ tissue (“broad spectrum” antiarrhythmics)
  • Prolong ____________ duration; ________ ERP
  • After Na+ and Ca2+ channels are activated, K+ channels begin to _________. This allows K+ to _____ cells causing membrane potential repolarization. Repolarize fast response action potentials in ___________ tissue. Repolarize slow response action potentials in _________ tissues
A
  • K+ channels responsible for cell REPOLARIZATION
  • K+ channel blockers SLOWS or DELAYS membrane repolarization
  • work both NODAL and NON-NODAL tissue (“broad spectrum” antiarrhythmics)
  • Prolong ACTION POTENTIAL duration; INCREASE ERP
  • After Na+ and Ca2+ channels are activated, K+ channels begin to OPEN. This allows K+ to LEAVE cells causing membrane potential repolarization. Repolarize fast response action potentials in NON-NODAL tissue. Repolarize slow response action potentials in NODAL tissues
24
Q

Class III Anti-arrhythmias

  • on EKG, this will _________ QT interval (classic effect). Prolongs time the cell is not __________
  • by increasing the ERP, very useful for terminating ________ mechanisms
  • Ex drug?
A
  • on EKG, this will PROLONG QT interval (classic effect). Prolongs time the cell is not EXCITABLE
  • by increasing the ERP, very useful for terminating REENTRY mechanisms
  • Ex. AMIODARONE
25
Q

Class III antiarrhythmic — Amiodarone

  • Very long half life = _______ days
  • may be used in patients /c __________ heart disease or __________ dysfunction
  • Use for Life saving ______ situations
A
  • Very long half life = 50 - 60 days
  • may be used in patients /c STRUCTURAL heart disease or LEFT VENTRICULAR dysfunction
  • Use for Life saving EMERGENT situations
26
Q

Class III antiarrhythmic — Amiodarone
Contraindications: _______ allergy (anaphylactic), significant _____ node dysfunction, ______ degree heart block, __________, _______ shock

A

Contraindications: IODINE allergy (anaphylactic), significant SA node dysfunction, 2ND or 3RD degree heart block, BRADYCARDIA, CARDIOGENIC shock

27
Q 
Class III antiarrhythmic — Amiodarone
Adverse effects
- B\_\_\_\_\_\_\_\_\_\_\_\_\_
- QT \_\_\_\_\_\_\_\_\_\_\_
- Extracardiac toxicities (including \_\_\_\_\_\_, liver, pulmonary, and \_\_\_\_\_ and \_\_\_\_\_\_\_ discoloration)
- \_\_\_\_\_\_\_ upset
- Constipation
- Photosensitivity
A

Adverse effects

  • BRADYCARDIA
  • QT PROLONGATION
  • Extracardiac toxicities (including THYROID, liver, pulmonary, and OCULAR and SKIN discoloration)
  • GI upset
  • Constipation
  • Photosensitivity
28
Q

Amiodarone (Class III antiarrhythmic)

  • Inhibits most ______
  • Interaction = increases concentrations of __________ (leading to easier bruising, and bleeding gums)
  • metabolized ________
A
  • Inhibits most CYPs
  • Interaction = increases concentrations of WARFARIN (leading to easier bruising, and bleeding gums)
  • metabolized HEPATICALLY
29
Q

Dronedarone (Class III)

  • another version of __________
  • benefit = no _______ allergy
A
  • another version of AMIODARONE

- benefit = no IODINE allergy

30
Q

Dofetilide (Class III)

  • Must be initiated in hospital /c constant _____ monitoring for ___ days
  • Used for chronic atrial ___________ or ____________
  • requires dose adjustment in ______ impairment and should be used /c caution in severe ________ impairment
A
  • Must be initiated in hospital /c constant EKG monitoring for 3 days
  • Used for chronic atrial FIBRILLATION or FLUTTER
  • requires dose adjustment in RENAL impairment and should be used /c caution in severe HEAPTIC impairment
31
Q

Class IV anti-arrhythmics

  • ______ channel blockers (only non-DHPs) = ___________ & _________
  • Block Ca2+ channels in cardiac _______ tissue, also causes peripheral ____________
  • slows conduction through _____ node, increases time needed for each _____, _________ myocardial oxygen demand, effective for __________ supra ventricular tachycardias
  • Negative __________ effects
  • contraindicated in ________________
A
  • Ca2+ channel blockers (only non-DHPs) = VERAPAMIL & DILTIAZEM
  • Block Ca2+ channels in cardiac NODAL tissue, also causes peripheral VASODILATION
  • slows conduction through AV node, increases time needed for each BEAT, DECREASES myocardial oxygen demand, effective for REENTRY supra ventricular tachycardias
  • Negative INOTROPIC effects
  • contraindicated in HEART FAILURE
32
Q

Digoxin

  • __________ effort
  • Check drug levels b/c can be ________
  • Used for __________ & _____________
A
  • LAST DITCH effort
  • Check drug levels b/c can be TOXIC
  • Used for HEART FAILURE & ACUTE ATRIAL FIBRILLATION
33
Q

Adenosine (Misc. anti-arrhythmic)

  • very short half life = ______ (given IV)
  • Use for: __________ & pharmacological __________ testing
  • ADRs: arrhythmias, chest pain/pressure, __________, _________, ____________, can see a transient heart block / sinus pause immediately after given
A
  • very short half life = 10 SECONDS (given IV)
  • Use for: PSVT (paroxysmal supra ventricular tachycardia) & pharmacological STRESS testing
  • ADRs: arrhythmias, chest pain/pressure, HEADACHE, DIZZINESS, FLUSHING, can see a transient heart block / sinus pause immediately after given
34
Q

Magnesium & Potassium

  • ___________ and _____/___________ can precipitate arrhythmias
  • can also potentiate ________ toxicity
A
  • HYPOMAGNESEMIA and HYPO/HYPOERKALEMIA can precipitate arrhythmias
  • can also potentiate DIGOXIN toxicity
35
Q

Atropine (Misc. Antiarrythmia)

  • DOC for ___________
  • anti-____________
A
  • DOC for BRADYCARDIA

- anti-CHOLENERGIC

36
Q

Anti-arrhythmic Summary

  • Anti-arrhythmias are all _____________
  • Various classes of anti arrhythmic agents require appropriate selection based on ________ specific characteristics
  • _______ is the mechanism responsible for most tachyarrhythmias
  • _________ is workhorse agent for most arrhythmias, but comes /c many toxicities
A
  • Anti-arrhythmias are all PRO-ARRHYTHMIC
  • Various classes of anti arrhythmic agents require appropriate selection based on PATIENT specific characteristics
  • REENTRY is the mechanism responsible for most tachyarrhythmias
  • AMIODARONE is workhorse agent for most arrhythmias, but comes /c many toxicities

Pharmacology (10 decks)

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