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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
What are the therapeutic uses of Lidocaine?
* Terminating V-Tach and Preventing V-Fib AFTER cardioversion in acute ischemia * **Prophylactic use may actually INCREASE mortality → not advised**
26
What are the cardiac effects of Mexiletine?
* 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
27
What are the extracardial effects of Mexiletine?
Significantly effective at relieving chronic pain, especially due to Diabetic neuropathy and nerve injury (off-label use)
28
What are the pharmacokinetics of Mexiletine?
* 90% oral absorption * Peak plasma concentration @ 2-3 hours * low first pass metabolism
29
What are the potential symptoms of Mexiletine toxicity?
* 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
What are the therapeutic uses of Mexiletine?
* Tx of documented life-threatening ventricular arrhythmias (sustained V-tach) * not for less severe arrhythmias
31
What are the cardiac effects of Tocainide?
* 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
What are the pharmacokinetics of Tocainide?
no significant 1st pass metabolism
33
What are the potential symptoms of Tocainide toxicity?
* Lidocaine analog * Parasthesias, tremor, nausea, light headedness, hearing disturbances, slurred speech and convulsions (mostly elderly or vulnerable patients)
34
What are the therapeutic uses of Tocainide?
No longer sold in the USA.
35
What are the Class IC Antiarrhythmic drugs that we need to know?
* Flecainide * Propafenone * Moricizine
36
What are the cardiac effects of Flecainide?
* 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
What are the pharmacokinetics of Flecainide?
* Rapidly and completely absorbed via GI * Peak plasma concentration @ 2-3 hours * no significant 1st pass metabolism
38
What are the potential toxicities associated with Flecainide?
* New/more severe arrhythmias * Potential to exacerbate CHF * especially in those with Cardiomyopathy or CHF
39
What are the therapeutic uses of Flecainide?
* Suppression and prevention of recurrent life threatening arrhythmias * Prevention of paroxysmal supraventricular tachycardias * AV nodal reentrant tachycardia & Wolff-Parkinson-White syndrome
40
What are the cardiac effects of Propafenone?
* Slows Upstroke of AP * Slows conduction * **Weak beta-blocking activity** * similar to quinidine w/out AP prolongation
41
What are the extracardiac effects of Propafenone?
Bradycardia and bronchospasm | (Beta blocker)
42
What are the pharmacokinetics of Propafenone?
* Rapidly and completely absorbed via GI * extensive 1st pass metabolism via hydroxylation (CYP2D6)
43
What are the toxicities associated with Propafenone?
* 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
What are the therapeutic uses of Propafenone?
* Prolong time to recurrence of symptomatic PSVT * Conversion of rapid onset (\<48hrs) A-fib * Suppresses/prevents recurrence of life-threatening Ventricular arrhythmias
45
What are the cardiac effects of Moricizine?
* Inhibits rapid inward Na+ current in myocardial cells * Minimal effect on AP duration
46
What are the pharmacokinetics of Moricizine?
Significant 1st pass metabolism by liver
47
What are the toxicities associated with Moricizine?
* Vomiting * LOC * Severe hypotension
48
What are the therapeutic uses of Moricizine?
* Tx arrhythmias and maintain normal sinus rhythm
49
What are the Class II Antiarrhythmic Drugs that we need to know?
Beta-Adrenoceptor Blockers * Propranolol * Acebutolol * Esmolol * Sotalol
50
What are the cardiac effects of Propanolol?
* 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
What are the Pharmacokinetics of Propranolol?
* Complete Oral absorption w/wide bodily distribution * Metabolized by liver
52
What are the toxicities associated with Propranolol?
* Inhibits Bronchodilation * causes bronchospasm * Possible intensification of AV block, AV dissociation and AV conduction delays * Bradycardia * Fatigue
53
What are the therapeutic uses of Propranolol?
* 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
What are the cardiac effects of Acebutolol?
* 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
What are the pharmacokinetics of Acebutolol?
* Well absorbed from GI * Extensive 1st pass metabolism
56
What are the toxicities associated with Acebutolol?
* Avoid use in Patients w/decompensated HF * Possible decreased signs and sx of Hypoglycemia
57
What are the therapeutic uses of Acebutolol?
* HTN * Angina * Tx of frequent PVCs
58
What are the cardiac effects of Esmolol?
* 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
What are the pharmacokinetics of Esmolol?
* Rapid onset and remission * Renally excreted
60
What are the therapeutic uses of Esmolol?
* HTN * SVT
61
What are the toxicities associated with Esmolol?
* Hypotension, dizziness, diaphoresis, headache, somnolence, confusion, agitation, nausea
62
What are the cardiac effects of Sotalol?
* Non-selective B-blocking drug * Prolongs AP * delays the slow outward current of K+
63
What are the pharmacokinetics of Sotalol?
* Readily absorbed orally * Peak plasma concentration @ 2.5-4 hrs * Renally excreted
64
What are the toxicities associated with Sotalol?
* Sinus Bradycardia, chest pain, palpitations, hypotension, fatigue, dizziness, asthenia, lightheadedness, dyspnea, N/V
65
What are the therapeutic uses of Sotalol?
* Ventricular Arrhythmias * Supraventricular tachycardias

CRRAB Week 4 - WLB (5 decks)

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