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CRRAB Week 4 - WLB > Sodium Channel Blockers & Beta-Blockers - Nordgren > Flashcards

Sodium Channel Blockers & Beta-Blockers - Nordgren Flashcards

1
Q

What are the Class I Antiarrhythmic Drugs?

A

Na+ Channel Blockers

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2
Q

What are the subclasses of Na+ Channel Blockers?

A
  • IA:
    • moderate Na+-channel blockade
    • largest increase in effective refractory period
    • e.g. quinidine
  • IB:
    • Weak Na+-channel blockade
    • decreases effective refractory period
    • e.g. lidocaine
  • IC:
    • Strong Na+-channel blockade
    • moderate increase in effective refractory period
    • e.g. flecainide
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3
Q

How do the subclasses of Na+ Channel Blockers compare on duration of Fast-Response AP’s?

A
  • IA:
    • slows rate of rise (phase 0)
    • prolongs AP → increases refractory period
  • IB:
    • shortens refractory period/increases repolarization (phase 3)
    • decreases duration of AP
  • IC:
    • markedly slows depolarization (phase 0)
    • no effect on refractory period.
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4
Q

What are the Class IA Antiarrhythmic drugs that we need to know?

A
  • Procainamide
  • Quinidine
  • Disopyramide
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5
Q

What are the cardiac effects of Procainamide?

A
  • Slows upstroke of AP
  • Slows conduction
  • Prolongs QRS on EKG
  • Prolongs AP by non-specific blockade of K+ channels
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6
Q

What are the extracardiac effects of Procainamide?

A
  • Ganglion-blocking properties → reduces peripheral vascular resistance
    • can cause hypotension
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7
Q

What are the potential symptoms of Procainamide toxicity?

A
  • Excessive AP prolongation
  • QT interval prolongation
  • Induction of torsades de pointes arrhythmia
  • Syncope
  • Excessive slowing of conduction
  • Long-term
    • syndrome resembling lupus erythematosus
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8
Q

What are the pharmacokinetics of Procainamide?

A
  • Drug metabolite (NAPA) has class III activity
    • associated with torsades
  • Eliminated by hepatic metabolism to NAPA
    • NAPA → renal elimination
    • NAPA half-life is longer than procainamide
  • Plasma binding 15-20%
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9
Q

What are the therapeutic uses of Procainamide?

A
  • Atrial & Ventricular arrhythmias
  • DO NOT USE for long-term therapy (SLE)
  • 2nd or 3rd choice drug for Tx of sustained ventricular arrhythmias associated with acute MI
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10
Q

What are the cardiac effects of Quinidine?

A
  • Slows Upstroke of AP
  • Slows conduction of impulse
  • Prolongs QRS
  • Prolongs AP duration by blocking K+ channels
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11
Q

What are the extracardiac effects of Quinidine?

A
  • Antimuscarinic effects
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12
Q

What are the potential symptoms of Quinidine toxicity?

A
  • Adverse GI effects = diarrhea, N/V
  • Cinchonism observed at toxic concentrations
    • headache, dizziness, tinnitus
  • Excessive QT interval prolongation
  • Induction of torsades de pointes
  • Arrhythmia
  • Syncope
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13
Q

What are the pharmacokinetics of Quinidine?

A
  • Readily absorbed GI
  • Hepatic Metabolism
  • Renally excreted
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14
Q

What are the therapeutic uses of Quinidine?

A
  • Rarely used due to toxic effects
    • availability of better tolerated drugs
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15
Q

What are the cardiac effects of Disopyramide?

A
  • Slows Upstroke of AP
  • Slows conduction of impulse
  • Prolongs QRS
  • Prolongs AP duration by blocking K+ channels
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16
Q

What are the extracardiac effects of Disopyramide?

A
  • Antimuscarinic effects
  • Atropine-like activity:
    • urinary retention
    • dry mouth
    • blurred vision
    • constipation
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17
Q

What are the potential symptoms of Disopyramide toxicity?

A
  • Same as quinidine
  • May precipitate heart failure:
    • de novo
    • in pts with preexisting depression of LV function
  • NOT first line drug in US or pts with heart failure
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18
Q

What are the pharmacokinetics of Disopyramide?

A
  • Loading doses NOT recommended
    • risk of precipitating heart failure
  • Hepatic metabolism
  • Renal excretion
  • Protein binding = 50%-65%
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19
Q

What are the therapeutic uses of Disopyramide?

A
  • Supraventricular arrhythmias
  • ONLY approved for ventricular arrhythmias in USA
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20
Q

What are the Class IB Antiarrhythmic drugs that we need to know?

A
  • Lidocaine
  • Mexiletine
  • Tocainide
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21
Q

What are the cardiac effects of Lidocaine?

A
  • Selective depression of conduction in depolarized cells
    • decrease AP duration
  • Little effect seen on EKG in normal sinus rhythm
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22
Q

What are the extracardiac effects of Lidocaine?

A
  • Block generation & conduction of nerve impulses
    • increase the threshold excitation → slows propagation = no Pain
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23
Q

What are the potential symptoms of Lidocaine toxicity?

A
  • Minimal
  • Parasthesias, tremor, nausea, light headedness, hearing disturbances, slurred speech and convulsions
    • Sx mostly in elderly or vulnerable patients
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24
Q

What are the pharmacokinetics of Lidocaine?

A
  • Extensive first-pass hepatic metabolism
    • only 3% of orally administered appears in plasma
  • MUST give parenterally
  • Half life = 1-2hrs
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25
Q

What are the therapeutic uses of Lidocaine?

A
  • Terminating V-Tach and Preventing V-Fib AFTER cardioversion in acute ischemia
  • Prophylactic use may actually INCREASE mortality → not advised
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26
Q

What are the cardiac effects of Mexiletine?

A
  • Mexiletine = orally active congener of lidocaine
  • Selective depression of conduction in depolarized cells
    • Preferentially affects ischemic/depolarized purkinje and ventricular tissue
  • Little effect seen on EKG in normal sinus rhythm
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27
Q

What are the extracardial effects of Mexiletine?

A

Significantly effective at relieving chronic pain, especially due to Diabetic neuropathy and nerve injury (off-label use)

28
Q

What are the pharmacokinetics of Mexiletine?

A
  • 90% oral absorption
  • Peak plasma concentration @ 2-3 hours
  • low first pass metabolism
29
Q

What are the potential symptoms of Mexiletine toxicity?

A
  • Development/exacerbation of arrhythmias (monitor before and during use)
  • Possible exacerbation of Hypotension and CHF
  • Possible decreased liver function
  • Possible leukopenia, agranulocytosis and thrombocytopenia
30
Q

What are the therapeutic uses of Mexiletine?

A
  • Tx of documented life-threatening ventricular arrhythmias (sustained V-tach)
    • not for less severe arrhythmias
31
Q

What are the cardiac effects of Tocainide?

A
  • Selective depression of conduction in depolarized cells
    • Preferentially affects ischemic/depolarized purkinje and ventricular tissue
  • Little effect seen on EKG in normal sinus rhythm
32
Q

What are the pharmacokinetics of Tocainide?

A

no significant 1st pass metabolism

33
Q

What are the potential symptoms of Tocainide toxicity?

A
  • Lidocaine analog
    • Parasthesias, tremor, nausea, light headedness, hearing disturbances, slurred speech and convulsions (mostly elderly or vulnerable patients)
34
Q

What are the therapeutic uses of Tocainide?

A

No longer sold in the USA.

35
Q

What are the Class IC Antiarrhythmic drugs that we need to know?

A
  • Flecainide
  • Propafenone
  • Moricizine
36
Q

What are the cardiac effects of Flecainide?

A
  • Significantly prolongs refractory period in AV node
  • Slows upstroke of AP
  • Slows conduction
  • Potent blocker of Na+ and K+ channels with slow unblocking kinetics
    • ​but does not prolong the AP or QT interval
37
Q

What are the pharmacokinetics of Flecainide?

A
  • Rapidly and completely absorbed via GI
  • Peak plasma concentration @ 2-3 hours
  • no significant 1st pass metabolism
38
Q

What are the potential toxicities associated with Flecainide?

A
  • New/more severe arrhythmias
  • Potential to exacerbate CHF
    • especially in those with Cardiomyopathy or CHF
39
Q

What are the therapeutic uses of Flecainide?

A
  • Suppression and prevention of recurrent life threatening arrhythmias
  • Prevention of paroxysmal supraventricular tachycardias
    • AV nodal reentrant tachycardia & Wolff-Parkinson-White syndrome
40
Q

What are the cardiac effects of Propafenone?

A
  • Slows Upstroke of AP
  • Slows conduction
  • Weak beta-blocking activity
  • similar to quinidine w/out AP prolongation
41
Q

What are the extracardiac effects of Propafenone?

A

Bradycardia and bronchospasm

(Beta blocker)

42
Q

What are the pharmacokinetics of Propafenone?

A
  • Rapidly and completely absorbed via GI
  • extensive 1st pass metabolism via hydroxylation (CYP2D6)
43
Q

What are the toxicities associated with Propafenone?

A
  • New or worsened CHF in patients w/ HF or decreased EF
  • possible reversible granulocytopenia or agranulocytosis
  • Inhibition of bronchodilation (Beta blocker)
    • not recommended for those w/ asthma
44
Q

What are the therapeutic uses of Propafenone?

A
  • Prolong time to recurrence of symptomatic PSVT
  • Conversion of rapid onset (<48hrs) A-fib
  • Suppresses/prevents recurrence of life-threatening Ventricular arrhythmias
45
Q

What are the cardiac effects of Moricizine?

A
  • Inhibits rapid inward Na+ current in myocardial cells
  • Minimal effect on AP duration
46
Q

What are the pharmacokinetics of Moricizine?

A

Significant 1st pass metabolism by liver

47
Q

What are the toxicities associated with Moricizine?

A
  • Vomiting
  • LOC
  • Severe hypotension
48
Q

What are the therapeutic uses of Moricizine?

A
  • Tx arrhythmias and maintain normal sinus rhythm
49
Q

What are the Class II Antiarrhythmic Drugs that we need to know?

A

Beta-Adrenoceptor Blockers

  • Propranolol
  • Acebutolol
  • Esmolol
  • Sotalol
50
Q

What are the cardiac effects of Propanolol?

A
  • Non-selective Beta1/Beta2 blocker
  • Decrease SA & AV nodal activity via decreasing cAMP, decreasing Ca2+ currents
  • Decreases Conduction velocity through SA and AV Node
51
Q

What are the Pharmacokinetics of Propranolol?

A
  • Complete Oral absorption w/wide bodily distribution
  • Metabolized by liver
52
Q

What are the toxicities associated with Propranolol?

A
  • Inhibits Bronchodilation
    • causes bronchospasm
  • Possible intensification of AV block, AV dissociation and AV conduction delays
  • Bradycardia
  • Fatigue
53
Q

What are the therapeutic uses of Propranolol?

A
  • Preffered Tx for Stable, Narrow complex Supraventricular tachycardias
  • Tachycardia during CV surgery
  • Management of Supraventricular or ventricular tachycardia associated w/glycoside toxicity w/o AV block
  • HTN, Angina, MI
54
Q

What are the cardiac effects of Acebutolol?

A
  • Cardioselective Beta-blocking drug
    • better for use in patients with asthma
  • Suppress normal pacemakers by decreasing slope of phase 4
    • AV node particularily sensitive → increased PR interval
  • Decreases Conduction velocity through SA and AV Node
55
Q

What are the pharmacokinetics of Acebutolol?

A
  • Well absorbed from GI
  • Extensive 1st pass metabolism
56
Q

What are the toxicities associated with Acebutolol?

A
  • Avoid use in Patients w/decompensated HF
  • Possible decreased signs and sx of Hypoglycemia
57
Q

What are the therapeutic uses of Acebutolol?

A
  • HTN
  • Angina
  • Tx of frequent PVCs
58
Q

What are the cardiac effects of Esmolol?

A
  • Suppress normal pacemakers by decreasing slope of phase 4
    • AV node particularily sensitive → increased PR interval)
  • Short acting selective Beta1-blocker
  • Negative Chronotrope and ionotrope
59
Q

What are the pharmacokinetics of Esmolol?

A
  • Rapid onset and remission
  • Renally excreted
60
Q

What are the therapeutic uses of Esmolol?

61
Q

What are the toxicities associated with Esmolol?

A
  • Hypotension, dizziness, diaphoresis, headache, somnolence, confusion, agitation, nausea
62
Q

What are the cardiac effects of Sotalol?

A
  • Non-selective B-blocking drug
  • Prolongs AP
    • delays the slow outward current of K+
63
Q

What are the pharmacokinetics of Sotalol?

A
  • Readily absorbed orally
  • Peak plasma concentration @ 2.5-4 hrs
  • Renally excreted
64
Q

What are the toxicities associated with Sotalol?

A
  • Sinus Bradycardia, chest pain, palpitations, hypotension, fatigue, dizziness, asthenia, lightheadedness, dyspnea, N/V
65
Q

What are the therapeutic uses of Sotalol?

A
  • Ventricular Arrhythmias
  • Supraventricular tachycardias

CRRAB Week 4 - WLB (5 decks)

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