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Cardiac Antiarrhythmics Flashcards

1
Q

Cardiac Antiarrhythmics

  • Antiarrhythmic medications
  • Tachyarrhythmias occur as a result of abnormal impulse formation due to…
A
  • Antiarrhythmic medications
    • Suppress ectopic foci that depolarize more rapidly than the intrinsic conduction system in tachyarrhythmias
    • Treat both ventricular & atrial tachyarrhythmias
  • Tachyarrhythmias occur as a result of abnormal impulse formation due to…
    • Increased automaticity
    • Triggered activity
    • Reentrant pathways
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2
Q

Tachyarrhythmias due to Increased Automaticity

  • Mechanism of arrhythmias
  • Examples
  • Treatment targets
A
  • Mechanism of arrhythmias
    • Caused by an increase in the slope of phase 4 of a pacemaker AP
      • Phase 4 depolarization is modulated by the If (“funny”) Na+ current
      • Increased transmembrane Na+ conductance –> increased phase 4 slope fo the pacemaker AP –> more rapid depolarization of ectopic pacemaker foci
      • If sufficiently rapid, ectopic foci override the intrinsic conduction system –> tachyarrhythmia
    • Originate from all conduction system levels (atria, AV node, & ventricles)
  • Examples
    • Paroxysmal atrial tachycardia
    • Accelerated junctional rhythms
    • Idoiventricular rhythms
  • Treatment targets
    • Decrease rate of spontaneous depolarization of the ectopic pacemaker foci by…
      • Reducing the phase 4 slope of the pacemaker potential
      • Hyperpolarizing the diastolic membrane potential
      • Increasing the threshold for phase 0 depolarization
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3
Q

Tachyarrhythmias due to Triggered Activity

  • Mechanism of arrhythmias
  • Early after-depolarizations (EADs)
    • During phase 2
    • During phase 3
    • Self-perpetuating
    • Common causes
  • Delayed after-depolarizations (DADs)
    • During phase 4
    • Common causes
  • Treatment targets
    • EADs
    • DADs
A
  • Mechanism of arrhythmias
    • Occur when an extra AP is generated before the phase 4 current of the normal AP crosses the usual depolarization threshold
    • 2 forms
      • Early after-depolarizations (EADs)
      • Delayed after-depolarizations (DADs)
  • Early after-depolarizations (EADs)
    • During phase 2
      • Related to perturbations in Ca2+ current
      • Na+ channels are largely inactivated at the higher transmembrane potentials during phase 2
    • During phase 3
      • Related to perturbations in Na+ current
      • Partial recovery of Na+ channels at lower transmembrane voltages during phase 3
    • Self-perpetuating
      • Result in sustained tachyarrhythmia
      • Torsade de pointes: polymorphic ventricular tachycardia associated w/ a long QT interval
    • Common causes
      • Hypoxemia
      • Hypokalemia
      • Drugs
      • Metabolic abnormalities
      • Recent MI
  • Delayed after-depolarizations (DADs)
    • During phase 4
      • Due to increased intracellular Ca2+
      • Occur after complete repolarization
      • Activate the Na/Ca exchanger &/or Cl currents
      • Generate brief inward transmembrane currents that trigger the DAD
    • Comon causes
      • Digoxin toxicity
      • Catecholamine/exercise induced VT in patients w/ structurally normal hearts
  • Treatment targets
    • EADs
      • Decreasing the duration of the AP
    • DADs
      • Correcting conditions causing intracellular Ca2+ overload
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4
Q

Tachyarrhythmias due to Reentrant Pathways

  • Mechanism of AV-nodal reentrant tachycardia (AVNRT)
    • Dual-nodal pathways
    • Premature atrial contraction (PAC): early
    • Premature atrial contraction (PAC): late
    • Premature atrial contraction (PAC): perfect timing
    • Similar conditions in the ventricle
  • Treatment targets
A
  • Mechanism of AV-nodal reentrant tachycardia (AVNRT)
    • Dual-nodal pathways
      • Fast limb: fast antegrade conduction velocity & slow recovery time
      • Slow limb: slow antegrade conduction velocity & rapid recovery time
      • Normally, angegrade conduction occurs across the fast limb
    • Premature atrial contraction (PAC): early
      • Early wave depolariztion
      • Occurs soon after ventricular activaiton
      • Arrives at the AV node when both fast & slow limbs are still refractory
      • Prevents the premature beat from crossing the AV node
      • –> “blocked PAC”
    • Premature atrial contraction (PAC): late
      • PAC occurs later
      • Slow (fast recovery) limb may no longer be refractory
      • Permits antegrade conduction of the premature beat across the slow limb
    • Premature atrial contraction (PAC): perfect timing
      • Depolarization across the slow limb arrives at the distal end of the fast limb just as the fast limb recovers
      • Retrograde conduction across the fast limb occurs
      • –> self-propagating reentrant arrhythmia
    • Similar conditions in the ventricle
      • Anatomically defined pathways occur
      • Seen w/ scar mediated monomorphic VT related to myocardial infarction or heterogenous pathways
      • Can present in ischemic myocardium
  • Treatment targets
    • Suppressing ectopic beats that may trigger a reentrant arrhythmia
    • Interrupting the reentrant loop by…
      • Slowing antegrade conduction time of the limbs
      • Increasing the effective refractory period of the limbs
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5
Q

Vaughn-Williams Classification System

  • Class I
  • Class II
  • Class III
  • Class IV
  • Other
A
  • Class I
    • Predominant Na-channel blockers
  • Class II
    • Beta-adrenergic receptor antagonists
  • Class III
    • Predominant K-channel blockers
  • Class IV
    • Ca-channel blockers
  • Other
    • Digoxin
    • Adenosine
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6
Q

General Antiarrhythmic Concepts

  • Na+ channel blockade
  • K+ channel blockade
  • Anti-cholinergic effects
  • Anti-adrenergic effects
A
  • Na+ channel blockade
    • Slows the phase 0 upstroke of the AP
    • May lead to an increase in QRS duration
  • K+ channel blockade
    • Slows phase 3 repolarization of the AP
    • May lead to an increase in QT duration
  • Anti-cholinergic effects
    • May lead to changes in SA & AV node function
  • Anti-adrenergic effects
    • May lead to changes in SA & AV node function & peripheral vasodilation / BP
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7
Q

Class I Antiarrhythmics

  • Strength
    • Defined by…
    • Potent (strong)
    • Weak
  • Use-dependency
  • 3 categories based on receptor kinetics
A
  • Strength
    • Defined by the avidity w/ which the drug binds to the Na+ channel
    • Potent (strong): slow receptor kinetics
      • Drug binds avidly to & disassociates slowly from the Na+ channel
    • Weak: rapid receptor kinetics
      • Drug binds loosely to & releases rapidly from the Na+ channel
  • Use-dependency
    • Characteristic demonstrated by potent class I agents
    • Drugs have a greater inhibitory effect on the Na+ channel during prolonged periods of elevated HRs
      • The more the Na+ channel is used, the more potent the clinical effect
    • Occurs b/c there’s less time for the drug to diassociate from the target receptor during the shorter diastolic interval associated w/ tachycardia
  • 3 categories based on receptor kinetics
    • Class 1A: moderate Na+ channel blockers
    • Class IB: weak Na+ channel blockers
    • Class IC: strong Na+ channel blockers
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8
Q

Class IA Antiarrhythmics

  • Examples
  • General
  • Effects on APs
  • Most dreaded adverse effect
A
  • Examples
    • Quinidine
    • Procainamide
    • Disopyramide
  • General
    • Moderate Na+ channel blockers
    • Variable effects on K+ channels, muscarinic receptors, & adrenergic receptors
  • Effects on APs
    • Inhibition of fast Na+ channels –> decreased phase 0 slope –> slows conduction through reentrant circuits
    • Na+ channel blockade –> inhibition of If current –> decreased phase 4 upstroke slope –> decreased automatcitiy of ectopic pacemaker foci
    • K+ channel activity –> increase refractory period
    • Greater effect on the Purkinje system & ectopic pacemakers than on normally funcitoning SA nodes
  • Most dreaded adverse effect
    • Proarrhythmia related to QT interval prolongation
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9
Q

Class IA Antiarrhythmics: Quinidine

  • Characteristics
  • Adverse effects
A
  • Characteristics
    • Limited direct effect on SA node pacemaker AP
    • Anti-cholinergic effects may accelerate conduction across the AV node
      • Important to use an AV nodal blocking agent (ex. beta blockers, Ca2+ channel blockers) when using quinidine in the management of atrial arrhythmias (ex. AFib)
    • Alpha-adrenergic antagonist effects may cause hypotension
      • Esp when administered IV
    • Hepatically metabolized
      • Should be used w/ caution in patients w/ liver disease
  • Adverse effects
    • GI: common, esp diarrhea & nausea
    • Neurotoxicity (“cinchonism”): tinnitus, hearing loss, confusion, visual disturbances, flushing
    • Increase serum digoxin via decreased renal clearance
      • Follow serum drug levels if used in combination
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10
Q

Class IA Antiarrhythmics: Procainamide

  • Characteristics
  • Adverse effects
A
  • Characteristics
    • Less anti-cholinergic & anti-adrenergic effects when compared to quinidine
    • Hypotension occurs less frequently w/ procainamide than quinidine
    • Both hepatically & renally metabolized
      • ~50% of procainamide is excreted by the kidneys
      • Rest is acetylated by the liver to an active metabolite (N-acetyl procainamide (NAPA)) which is then excreted by the kidneys
    • Exhibits genetic variability in rates of drug acetylation
      • In “fast acetylators” who have renal insufficiency, NAPA can accumulate more rapidly –> drug toxicity, so procainamide shouldn’t be used
  • Adverse effects
    • Lupus-like syndrome: more common in slow acetylators
      • _​_Positive serological markers (anti-nuclear antibody (ANA))
      • Systemic inflammatory response
      • Pleuropericarditis (inflammation fo the pleura & pericardium
      • Fever
      • Rash
      • Arthralgias (achiness of the joints)
    • Hypersensitivity reactions: drug fvere, agranulocytosis (low WBCs), & rash independent of a lupus-like syndrome
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11
Q

Class IA Antiarrhythmics: Disopyramide

  • Characteristics
  • Adverse effects
A
  • Characteristics
    • More potent anti-cholinergic & negative inotropic effects than quinidine & procainamide
    • Renally excreted
      • Should be avoided in aptients w/ kidney disease
  • Adverse effects
    • Anti-cholinergic: urinary retention, constipation, dry mouth
      • Contraindicated in patients w/ glaucoma
    • Anti-adrenergic: CHF
      • Contraindicated in patients w/ severe LV systolic dysfunction
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12
Q

Class IB Antiarrhythmics

  • Examples
  • General
A
  • Examples
    • Lidocaine
    • Mexiletine
    • Phenytoin
  • General
    • Weak Na+ channel blockers
    • Less heterogeneous activity than class IA –> fewer electrophysiological effects
    • Exert greater effect on diseased or ischemic myocardium than on normal myocardium
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13
Q

Class IB Antiarrhythmics: Lidocaine

  • Mechanism of action
  • Adverse effects
A
  • Mechanism of action
    • Decreases phase 0 slope of the ventricular AP
    • Inhibits small Na+ currents that persist throughout phase 2
      • –> no net change or mild decrease in QRS & QT intervals
    • Decreases phase 4 slope of ectopic pacemaker potentials, EADs, & DADs
      • Potentially effective drug for treating ventricular arrhythmias associated w/ digoxin toxicity
    • Only available IV (oral is unreliable)
  • Adverse effects
    • Hepatically metabolized
      • Drug half-life may increase in patients w/ CHF & hepatic congestion –> toxicity
      • Monitor serum drug levels in these patients
    • Neurotoxicity: most common
      • Confusion, seizures, paresthesia, coma
    • Heart block: rare
      • Occurs primarily in patients w/ intrinsic conduction disease
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14
Q

Class IB Antiarrhythmics: Mexiletine

  • Mechanism of action
  • Adverse effects
A
  • Mechanism of action
    • Oral equivalent of lidocaine
    • Use-dependent inhibition of Na+ channels
    • Not particularly effective as an antiarrhythmic when used in isolation
      • May be effective as an adjunctive agent
      • May be effective in patients w/ congenital long QT, type 3 (associated w/ SCN5A mutation for cardiac Na+ channel)
  • Adverse effects
    • Neurological: tremor, dizziness, dysarthria (speech difficulties), confusion, nystagmus (eye oscillations), diplopia (double vision)
    • GI: nausea & vomiting
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15
Q

Class IC Antiarrhythmics

  • Examples
  • General
  • Electrophysiological effects
  • Efects on APs
  • Adverse effects
A
  • Examples
    • Flecainide
    • Propafenone
  • General
    • Strong Na+ channel blockers
    • Increase QRS, QT, & PR intervals
    • Decrease HR
  • Electrophysiological effects
    • Potent Na+ channel blockers
    • Mild K+ channel blockers
    • Increase the refractory period of the AV node & accessory bypass tracts
    • Variable effects on beta-adrenergic receptors (propafenone > flecainide)
  • Efects on APs
    • Slow phase 0 upstroke to a greater degree than other class I agents
    • Delay repolarization during phase 3 –> prolong relative refractory period
  • Adverse effects
    • Increase mortality in post-MI patients
    • Rarely used to treat ventricular dysrhythmias in patients w/ underlying structural heart disase
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16
Q

Class IC Antiarrhythmics: Flecainide

  • Characteristics
  • Adverse effects
A
  • Characteristics
    • Use-dependency
      • Stress test to assess extent of this effect once steady state drug levels are achieved
    • Both renally (40%) & hepatically (60%) metabolized
      • Hepatically metabolized into inactive metabolites
  • Adverse effects
    • Proarrhythmia
      • Variable effects on AP duration in different tissues (ex. Purkinje fibers vs. ventriuclar myocytes)
      • Variability can increase the electrical heterogeneity among cardiac cells –> enhances the substrate for reentrant circuits & proarrhythmia
    • Conduction abnormalities: bradycardia, AV block
      • Should be avoided in patients w/ underlying conduction disease unless they have a pacemaker
    • CHF exacerbation b/c it’s a negative inotrope
      • Should be avoided in patients w/ moderate to severe LV systolic dysfunction
    • Neurotoxicity: confusion, visual disturbances, dizziness
17
Q

Class IC Antiarrhythmics: Propafenone

  • Characteristics
  • Adverse effects
A
  • Characteristics
    • Hepatically metabolized
    • Significant genetic variability in rates of metabolism
      • Poor metabolizers –> increase drug elimination half-life –> increase risk for drug toxicity
  • Adverse effects
    • Neurological: dizziness & dysguesia (abnromal taste)
    • Arrhythmia: proarrhythmia & conduction abnormalities
      • Lower incidence than flecainide
    • CHF: more common
      • More potent negative inotrope than flecainide
18
Q

Class III Antiarrhythmics

  • Examples
  • General
  • Electrophysiological effects
A
  • Examples
    • Amiodarone
    • Dronedarone
    • Sotalol
    • Dofetilide
    • Ibutilide
  • General
    • K+ channel blockers
    • Heterogeneous group of medications
    • Treat both supraventricular & ventricular dysrhythmias
  • Electrophysiological effects
    • Delay repolarization during phase 3
    • May lead to QT interval prolongation
19
Q

Class III Antiarrhythmics: Amiodarone

  • General
  • Electrophysiological effects
  • Adverse effects
A
  • General
    • Most effective antiarrhythmic
    • Iodine-rich benzofuran derivative
    • Slowly absorbed by the GI tract
    • Achieves peak plasma concentrations 5-6 hours after oral administration
    • Highly lipophilic
    • Stored extensively in soft tissue –> long half-life (25-60 days)
  • Electrophysiological effects
    • Characteristics form all 4 Vaughn-William classes
    • Na+, Ca2+, & K+ channel blockade
    • Adrenergic receptor antagonism
    • Beta blocking effects: most commonly seen
  • Adverse effects
    • Increase PR, QRS, & QT intervals
    • Bradycardia
    • Hypo- > hyper-thyroidism: b/c it’s iodinated
    • GI: anorexia, nausea, elevated LFTs (reversible w/ discontinuation)
    • Pulmonary: most serious, associated w/ chronic use, may –> irreversible pulmonary fibrosis if detected late
    • Skin: photosensitivity, bluish hyperpigmentation (use sunscreen)
    • Eye: corneal deposits (don’t impair vision)
    • CNS: neuropahty, tremors, muscle weakness, alterations in sleep patterns (rare)
20
Q

Class III Antiarrhythmics: Dronedarone

  • General
  • Electrophysiological effects
  • Adverse effects
A
  • General
    • Non-iodinated oral analog of amiodarone
    • Associated w/ fewer side effects than amiodarone (less toxic)
    • Less potent & less effective
  • Electrophysiological effects
    • Characteristics form all 4 Vaughn-William classes
    • Na+, Ca2+, & K+ channel blockade
    • Adrenergic receptor antagonism
  • Adverse effects
    • Increase PR, QRS, & QT intervals
    • Bradycardia
    • Rash
    • Photosensitivity
    • Nausea, vomiting, & diarrhea
21
Q

Class III Antiarrhythmics: Sotalol

  • General
  • Electrophysiological effects
  • Adverse effects
A
  • General
    • Nonselective beta blocker w/ no ISA activity
    • Some K+ channel blockade
    • Renally excreted
      • Should be avoided in patients w/ renal disease
  • Electrophysiological effects
    • Nonselective beta blocker w/ no ISA activity
    • Some K+ channel blockade
  • Adverse effects
    • Proarrhythmia
      • _​_Related to QT prolongation (torsade de poitnes)
      • Esp in women & patietns w/ CHF
    • Bradycardia
    • AV block
22
Q

Class III Antiarrhythmics: Dofetilide

  • General
  • Adverse effects
A
  • General
    • Potent oral K+ channel blocker
    • Treats arrhythmias by prolonging the effective refractory period
    • Renally excreted
      • Adjust dose in patients w/ renal insufficiency
      • Avoid in patients w/ severe kidney disease
  • Adverse effects
    • QT interval prolongation
    • Torsades de pointes
23
Q

Class III Antiarrhythmics: Ibutilide

  • General
  • Electrophysiological effects
  • Adverse effects
A
  • General
    • Administered IV
    • Treats arrhythmias by activating slow inward Na+ channels during phase 2
    • Rarely used
  • Electrophysiological effects
    • Activates slow inward Na+ current during phase 2
    • Increases the refractory period in the atrium & ventricle
  • Adverse effects
    • QT interval prolongation
    • Torsades de pointes
24
Q

Digoxin

  • General
  • Mechanism of action
  • Its effectiveness in treating supraventricular arrhythmias is a result of…
  • Effects on APs
    • Phase 4 resting potential
    • Phase 0 slope
    • AP duration
    • Triggered activity
    • Other
  • Adverse effects
  • Treatment of digoxin toxicity
A
  • General
    • Cardiac glycoside derived from teh foxglove plant
    • Increases cardiac contractility
    • Treats “dropsy” (edema / CHF) & AVNRT
    • Improves rate control in patients w/ rapid atrial fibrillation/flutter
    • Renally excreted
      • Avoid in patients w/ significant renal insufficiency
  • Mechanism of action
    • Na+/K+ ATPase inhibitor
      • Increases intracellular Na+
    • Activates the Na+/Ca2+ exchanger
      • Moves Na+ ions from intra- to extra-cellular in exchange for Ca2+
      • Increases intracellular Ca2+
      • Increases myofibril contractility & cardiac output
  • Its effectiveness in treating supraventricular arrhythmias is a result of…
    • Enhanced vagal tone (primary effect)
      • Increased CO –> carotid baroreceptor stimulation –> increased parasympathetic tone –> decreased sympathetic stimulation of the AV node –> slowed AV node conduction
    • Reduction in the relative refractory period (modest effect)
  • Effects on APs
    • Less negative phase 4 resting potential
      • Inhibition of the Na+/K+ ATPase pump –> decreased outward Na+ current –> less negative membrane potential
      • Hyperpolarization –> increased automaticity of non-pacemaker cells
    • Decreased phase 0 slope
      • Less negative resting potential –> parital inactivation of fast Na+ channels
      • Significant heterogeneity in the depolarizaiton of adjacent cardiac cells –> risk for reentrant arrhythmias
    • Decreased AP duration
      • Increased intracellular Ca2+
        • –> activated Ca2+ dependent K+ channel –> K+ efflux during phase 3
        • –> decreased Ca2+ influx shortening duration of phase 2
      • Decrease effective refractory period –> increase window where ventricle may be vulnerable to ectopic arrhythmic foci
    • Increased triggered activity
      • Intracellular Ca2+ overload –> trigger DADs –> sustained tachyarrhythmias
    • AV block
  • Adverse effects
    • Narrow therapeutic window
    • GI: anorexia, nausea, & emesis (vomiting)
    • Ophthalmologic: greenish-yellow visual halos
    • Cardiac: malignant tachy- &/or brady-arrhythmias
    • “Dig toxic” arrhythmias: arrythmias associated w/ digoxin toxicity
      • Low extracellular K+ –> suppressed Na+/K+ ATPase pump –> hypokalemia –> arrhythmia exacerbation
  • Treatment of digoxin toxicity
    • Correction of hypokalemia & hypomagnesemia
    • IV lidocaine suppress ventricular tachycardia
    • Digibind (digoxin specific antibodies) control malignant arrhythmias
25
Q

Adenosine

  • General
  • Mechanism of action
A
  • General
    • Endogenous nucleotide
    • Short half-life (~9 seconds), so few contraindications as an IV bolus
    • Treats AVNRTs
    • Used as a diagnostic tool in differentiating supraventricular arrhythmias
  • Mechanism of action
    • Activates K+ channels –> K+ efflux –> hyperpolarized cell membrane –> decreased automaticity
    • Inhibits adenylate cyclase –> decreases cAMP –> decreases If / Na+ current –> decreases automaticity
    • Inhibits protein kinases –> decreases Ca2+ influx –> slows AV node conduction

Cardiology (40 decks)

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