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CRAAB 2 > Nordgren: Na +- Channel Blockers > Flashcards

Nordgren: Na +- Channel Blockers Flashcards

1
Q

What does a Na channel blockade do?

A

Alters the AP duration and kinetics of Na channel blockade

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2
Q

Which class is the largest and oldest group of antiarrhythmic drugs?

A

Class I- Na channel blockers

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3
Q

What do Na channel blockers do?

A

Bind to and block FAST Na channels.

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4
Q

What are FAST Na channels responsible for?

A

Rapid depolarization (phase 0) of fast response cardiac APs.

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5
Q

What affect does a Na channel blocker have on an AP?

A
  1. Decreased slope of phase 0 and amplitude of the AP.

2. Reduces the rate and magnitude of depolarization and leads to a decrease in conduction velocity in non-nodal tissue.

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6
Q

Do Na channel blockers have an effect on nodal tissue?

A

NO because those AP are dependent on Ca to depolarize.

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7
Q

Why are there subdivisions of class I drugs?

A

Because they have differing effects on AP duration and effective refractory period.

  • subclasses differ in eff
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8
Q

How do the subdivisions of class I differ?

A

Some effect ERP adue to non-specific secondary activity of drugs on efflux of K in phase 3.

Some subclasses also differ in efficiency for reducing the slope of phase 0.

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9
Q

How do the three class I Na channel blockers differ in terms of increasing the ERP (effective refractory period)?

A

IA- Increase ERP
IB- Decreases ERP
IC- maintains ERP

IA>IC>IB

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10
Q

Class IB drug?

A

lidocaine

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11
Q

How does the rate of association of the Na blocker drug with the channel differ?

A

IA- immediate rate of association
IB- rapid rate of association
IC- slow rate of association

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12
Q

What is the effect of a IA drug?

A
  1. Slows the rate of rise (phase 0) of AP.

2. Prolongs AP (increases the ERP)

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13
Q

What is the effect of drug IB?

A

Shortens the refractory period (phase 3 repolarization) and decreases duration of the AP.

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14
Q

What is hte effect of drug IC?

A

Markedly slow phase 0 depolarization and has no effect on the refractory period.

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15
Q

What drugs are used to treat atrial fibrillation, flutter; supraventricular and ventricular tachyarrhythmias?

A

Class IA

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16
Q

What are the three class IA drugs? How do these drugs differ in terms of anticholinergic activity?

A

QPD
quinidine
procainamide
disopyramide

All three are anticholinergic but D>Q>P.

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17
Q

What are the SE of qunidine?

A

Cinchonism (blurred vision, tinnitus, HA, psychosis)
Cramping and nausea
Enhances digitalis toxicity

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18
Q

What is the SE of procainamide?

A

lupus like syndrome in 25-30% of pts

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19
Q

What is the SE of disopyramide?

A

Negative inotropic effect

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20
Q

What drug class treats ventricular tachyarrhythmias?

A

Class IB

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21
Q

What are the three drugs in class IB?

A

Lidocaine- IV only; VT and PVCs
tocainide
mexiletine

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22
Q

Which class IB drugs are orally active lidocaine analogs?

A

tocainide

mexiletine

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23
Q

Which class IB drugs have good efficacy in ischemic myocardium?

A

Lidocaine

Mexiletine

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24
Q

Which class IB drug can cause pulmonary fibrosis?

A

Tocainide

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25
Q

What drug class is used for life-threatening supraventricular tachyarrhythmias and ventricular tachyarrhythmias?

A

Class IC

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26
Q

What are the three class IC drugs? What type of arrhythmia do they treat?

A

flecainide- SVT
Propafenone-SVT adn VT
moricizine- VT; IB activity

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27
Q

Which class IC drug can induce life-threatening VT?

A

flecainide (usually used to treat SVT)

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28
Q

Which Class IC drug causes beta blocking and Ca channel blocking activity that can worsen heart failure?

A

propafenone

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29
Q

What are class II Na blockers?

A

Beta adrenoceptor blockers

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30
Q

What are class II drugs used for?

A

To prevent and treat supraventricular arrhythmias and to reduce ventricular ectopic depolarizations and sudden death in pts w/ MI.

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31
Q

Why do Beta blockers have antiarrhythmic effects?

A

Because of their ability to INHIBIT sympathetic activation of cardiac automaticity and conduction.

32
Q

What do Beta blockers do?

A
  1. Slow the heart rate
  2. Decrease the AV node conduction velocity
  3. Increase the AV node refractory period
  4. Have little to no effect on ventricular conduction and repolarization
33
Q

Cardiac effects: Procainamide (IA)

A

Slow upstroke of AP, slows conduction, prolongs QRS on ECG, prolongs ADP by non-specific blockade of K channels

**NO antimuscarinic effects

34
Q

Extracardiac effects: Procainamide (IA)

A

Ganglion blocking properties> reduce peripheral vascular resistance and can cause hypertension.

35
Q

Toxicity: Procainamide (IA)

A

Excessive AP prolongation, QT interval prolongation, induction of TORSADAS DE POINTES arrhythmia and syncope, excessive slowing of conduction. Long term can cause SYNDROME RESEMBLING LUPUS.

36
Q

Pharmacokinetics: Procainamide

Drug metabolism
T1/2
PPB

A 
Drug metabolite (NAPA)
Hepatic metabolism to NAPA, NAPA via renal elimination.

T1/2 of NAPA is longer than procainamide.

Plasma protein binding 15-50%

37
Q

TU: procainamide

A

Atrial and ventricular arrhythmias

2nd or 3rd choice drug for sustained ventricular arrhythmias associated w/ acute MI.

38
Q

Why do you want to avoid long term therapy with procainamide?

A

It can lead to frequent dosing and lupus related events.

39
Q

CE: Quinidine (IA)

A 
Slows upstroke of AP
slows conduction
prolongs QRS on ECG
prolongs ADP by nonspecific blockade of K channels
Antimuscarinic effects
40
Q

ECE: Quinidine (IA)

A

GI effects of diarrhea, nausea and vomiting obeseved in 1/3-1/2 of pts. Cinchonism observed at toxic conc.

41
Q

Toxicity: Quinidine

A

Excessive QT interval prolongation, induction of TORSADAS DE POINTES arrhythmias and syncope

42
Q

Pharmacokinetics: Quinidine (IA)

A

Readily absorbed from GI tract and eliminated by hepatic metabolism and renal excretion.

43
Q

TU: Quinidine (IA)

A

RARELY used b/c of cardiac and extracardiac adverse effects and the availability of better tolerated drugs.

44
Q

CE: Disopyramide (IA)

A 
Slows upstroke of AP
slows conduction
prolongs QRS on ECG
prolongs ADP by nonspecific blockade of K channels
Antimuscarinic effects
(Same as Quinidine)
45
Q

ECE: Disopyramide (IA)

A

Atropine-like activity–> urinary retention, dry mouth, blurred vision, constipation

46
Q

Toxicity: Disopyramide (IA)

A

Same as quinidine. May precipitate heart failure de novo or in pts w/ pre-existing depression of left ventricular function. Not to be used as a first line drug in USA or in pts w/ heart failure.

47
Q

Pharmakokinetics: Disopyramide (IA)

A

LOADING DOSES NOT RECOMMENDED b/c of risk of precipitating heart failure.

Hepatic metabolism, renal excretion.

Protein binding 50-65%

48
Q

TU: Disopyramide (IA)

A

Effective for many supraventricular arrhythmias, but only used for ventricular arrhythmias in US.

49
Q

CE: Lidocaine (IB)

A

Selective depression of conduction in depolarized cells.

Little effect seen on ECG in normal sinus rhythm.

50
Q

Toxicity: Lidocaine (IB)

A

One of the least cardiotoxic Class I drugs.

Most common adverse effects: paresthesias, termor, nausea of central origin, lightheadedness, hearing disturbances, slurred speech, convulsions.

These effects occur most commonly in elderly or vulnerable patients.

51
Q

Pharmacokinetics: Lidocaine (IB)

A

Extensive first pass hepatic metabolism> only 3% of orally administered appears in plasma.

Must give parenterally.

T1/2 1-2 hrs.

52
Q

TU: Lidocaine (IB)

A

Good for termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in the setting of acute ishemia.

PROPHYLATIC USE MAY ACTUALLY INCREASE TOTAL MORTALITY > NOT ADVISED!

53
Q

CE: Mexiletine (IB)

A

Selective depression of conduction in depolarized cells. Little effect seen on ECG in normal sinus rhythm.

54
Q

Extracardiac effects: Mexiletine (IB)

A

SIGNIFICANT EFFICACY IN RELIEVING CHRONIC PAIN, ESPECIALLY D/T DIABETIC NEUROPATHY AND NERVE INJURY.

55
Q

Toxicity: Mexiletine (IB)

A

Tremor, blurred vision, lethargy, nausea.

56
Q

Pharmacokinetics: Mexiletine (IB)

A

Hepatic metabolism, renal excretion.

Protein binding 50-60%. T1/2 8-20 hrs.

57
Q

TU: Mexiletine (IB)

A

Ventricular arrhythmias

58
Q

CE: Tocainide (IB)

A

Selective depression of conduction in depolarized cells. Little effect seen on ECG in normal sinus rhythm.

59
Q

Toxicity: Tocainide (IB)

A

Lidocaine analog.

60
Q

Pharmacokinetics: Tocainide (IB)

A

GLUCORONIDATION METABOLISM, renal excretion (30-50% unchanged). Protein binding 10-20%.

61
Q

TU: Tocainide (IB)

A

No longer sold in the US.

62
Q

CE: Flecainide (IC)

A

Slows upstroke of AP, slows conduciton. Potent blocker of Na and K channels w/ SLOW UNBLOCKING KINETICS (but doesn’t prolong AP or QT interval)

63
Q

Toxicity: Flecainide (IC)

A

Severe exacerbation of arrhythmia even when normal doses adminsitered to patients with preexisting ventricular tachyarrhythmias and those w/ previous MI and ventricular ectopy.

64
Q

Pharmacokinetics: Flecainide (IC)

A

Metabolism and elimination both hepatic and renal.

Protein binding 40%.

65
Q

TU: Flecainide (IC)

A

Supraventricular arrhythmias. Very effective in suppressing premature ventricular contractions.

66
Q

CE: Propafenone (IC)

A

Slos upstroke of AP, slows conduciton. WEAK BETA BLOCKIGN ACTIVITY. Spectrum of action similar to quinidine, but does not prolong AP.

67
Q

Toxicity: Flecainide (IC)

A

Metallic taste and constipation. Arrhythmia and exacerbation can also occur.

68
Q

Pharmacokinetics: Flecainide (IC)

A

Hepatic metabolism, renal excretion. Protein binding 97%.

69
Q

TU: Flecainide (IC)

A

Supraventricular arrhythmias.

70
Q

CE: Moricizine (IC)

A

Slows upstroke of AP, slows conduction. Does not prolong AP duration.

71
Q

Pharmacokinetics: Moricizine (IC)

A

Extensive first pass hepatic metabolism

Protein binding 95%

72
Q

TU: Moricizine (IC)

A

Ventricular arrhythmias. Phenothiazine derivative. NO longer sold in US.

73
Q

What are some examples of class II beta adrenoceptor blockers?

A

PASE

Propanolol
acebutolol
sotalol
esmolol

74
Q

What are the adverse affects of propanolol?

A

Bronchospasm, bradycardia, fatigue.

It also has some class I activity.

75
Q

In what pts is acebutolol good for?

A

Acebutolol is a cardioselective beta-blocking drug so it’s good for pts w/ asthma (avoid adverse effects like bronchospasm).

76
Q

What is sotalol good for?

A

It is a nonselective beta blocking drug that prolongs the action potential (delays the slow outward current of K)

77
Q

What do we use esmolol for?

A

It’s a short acting blocker used for intraoperative and acute arrhythmias.

CRAAB 2 (9 decks)

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