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CRRAB Pharmacology > Antiarrhythmics: Na+ Channel and Beta-Adrenergic Blockers > Flashcards

Antiarrhythmics: Na+ Channel and Beta-Adrenergic Blockers Flashcards

1
Q

What class of antiarrythmics is a Na+ channel blocker?

A

Class I

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2
Q

What are the main effects of using a Na+ channel blockade?

A
  1. Increasing AP duration

2. Increasing effective refractory period (d/t non-specific secondary activity of drugs on K+ channels in phase 3)

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3
Q

How many subgroups are there in Na+ channel blockers?

A

3: Subgroup IA, IB, and IC

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4
Q

What is the main goal of any antiarrythmic drug?

A

Suppress ectopic automaticity and abnormal conduction occurring in depolarized cells, while minimally affecting the electrical activity of normally polarized parts of the heart

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5
Q

Which antiarrythmic drugs have the least channel specificity?

A

Na+ channel blockers

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6
Q

Which channels to Na+ channel blockers bind and block?

A

Fast Na+ channels which are responsible for rapid depolarization (phase 0) of fast response cardiac APs

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7
Q

What is the effect on the AP by blocking Na+ channels? Ultimate effect?

A
  1. Decreased slope of phase 0
  2. Decreased amplitude of the AP
    Ultimate effect- decreases velocity in non-nodal tissue.
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8
Q

How do the subclasses of Na+ channel blockers differ?

A

Differing effects on AP duration, effective refractory period, and efficiency for reducing the slope of phase 0

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9
Q

What is the order of the subgroups when looking at the efficiency with which the subgroup blocks Na+ channels?

A

IC > IA > IB

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10
Q

What is the order of the subgroups when looking at the increase in the ERP?

A

IA > IC > IB (decreases)

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11
Q

What drugs are in Subgroup IA?

A

Quinidine
Procainamide
Disopyramide

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12
Q

Quinidine

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Subgroup IA

Mechanism: Decrease ventricular conduction, slows upstroke of AP, increases QRS interval on ECG; prolong ventricular action potential (ADP) by non-specific K+ channel blockage; antimuscarinic effects

Clinical Use: rarely used d/t side effects

Pharmacokinetics: hepatic met –> renal excret.

Extracardiac Effects: adverse GI effects of nausea, vomiting, diarrhea. Cinchonism (HA and tinnitus)

Toxicity: increased QT interval –> induction of torsades de pointes

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13
Q

Procainamide

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Subgroup IA

Mechanism: Decrease ventricular conduction, slows upstroke of AP, increases QRS interval on ECG; prolong ventricular action potential (ADP) by non-specific K+ channel blockage

Clinical Use: Most atrial and ventricular arrythmias.

Pharmacokinetics: Drug metabolite (NAPA) has class III activity and can induce torsades. Hep met –> renal excret.

Extracardiac Effects: ganglion blocking properties –> reduces peripheral vascular resistance and can cause hypotension

Toxicity: Long term use –> drug-induced lupus; increased QT interval –> induction of torsades de pointes

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14
Q

Disopyramide

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Subgroup IA

Mechanism: Decrease ventricular conduction, slows upstroke of AP, increases QRS interval on ECG; prolong ventricular action potential (ADP) by non-specific K+ channel blockage; antimuscarinic effects

Clinical Use: in US only approved for ventricular arrythmias

Pharmacokinetics: Loading dose not recommended –> increase risk of heart failure; hep met –> renal excrete.

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

Toxicity: May precipitate heart failure (not first line drug in USA); increased QT interval –> induction of torsades de pointes

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15
Q

Lidocaine

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Subgroup IB

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

Clinical Use: Acute ventricular arrythmias and prevention of ventricular fibrillation after cardioversion of an acute ischemia. Prophylactic use may not actually increase total mortality –> not advised.

Pharmacokinetics: Extensive first pass hep met. Given parenterally.

Extracardiac Effects: CV and CNS depression with overdose.

Toxicity: One of least cardiotoxic drugs; paresthesias, tremor, nausea of central origin, lightheadedness, hearing disturbances, slurred speech, convulsions (most common in elderly and vulnerable)

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16
Q

Mexiletine

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Subgroup IB

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

Clinical Use: Ventricular arrythmias

Pharmacokinetics: hep met. –> renal excret.

Extracardiac Effects: significant efficacy in relieving chronic pain, especially due to diabetic neuropathy and nerve injury

Toxicity: tremor, blurred vision, lethargy, nausea

17
Q

Tocainide

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Subgroup IB

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

Clinical Use: no longer sold in USA

Pharmacokinetics: glucaronidation metabolism –> renal excret.

Extracardiac Effects:

Toxicity: lidocaine analog

18
Q

Moricizine

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Subgroup IC

Mechanism: decreases ventricular conduction, slows upstroke of AP (increased QRS interval on ECG); does NOT prolong APD

Clinical Use: no longer sold in USA

Pharmacokinetics: extensive first pass hep. met.

Extracardiac Effects:

Toxicity:

19
Q

Flecainide

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Subgroup IC

Mechanism: decreases ventricular conduction, slows upstroke of AP (increased QRS interval on ECG); does NOT prolong APD

Clinical Use: supraventricular arrythmias; very effective in suppressing premature ventricular contractions

Pharmacokinetics: hep met. –> renal excret.

Extracardiac Effects:

Toxicity: can cause exacerbation of arrythmias in pts w/ preexisting ventricular tachyarrythmia or post- MI

20
Q

Propafenone

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Subgroup IC

Mechanism: decreases ventricular conduction, slows upstroke of AP (increased QRS interval on ECG); does NOT prolong APD; weak beta blocking activity

Clinical Use: supraventricular arrythmias

Pharmacokinetics: hep met. –> renal excret.

Extracardiac Effects:

Toxicity: metallic taste and constipation; arrhythmia exacerbation

21
Q

Propanolol

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Class II

Mechanism: some class I activity, reduces O2 demand by decreasing HR and contractility d/t inhibiting SNS stimulation to the heart

Clinical Use: stable angina, NOT variant angina; ventricular and supra ventricular arrythmias; Contraindicated in sinus bradycardia

Pharmacokinetics: hep met. –> ren excret. good oral availability

Extracardiac Effects:

Toxicity: bradycardia (can precipitate CHF), bronchospasms and fatigue

22
Q

Acebutolol

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Class II

Mechanism: cardioselective, reduces O2 demand by decreasing HR and contractility d/t inhibiting SNS stimulation to the heart

Clinical Use: stable angina, NOT variant angina; ventricular and supra ventricular arrythmias; better for those w/ asthma –> no bronchospasm

Pharmacokinetics:

Extracardiac Effects:

Toxicity: precipitate of CHF, fatigue, HA, dizziness

23
Q

Esmolol

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Class II

Mechanism: short acting, reduces O2 demand by decreasing HR and contractility d/t inhibiting SNS stimulation to the heart

Clinical Use: intraoperative and acute arrythmias

Pharmacokinetics: IV administration; urine excrete.

Extracardiac Effects:

Toxicity: risk of hypotension; precipitate of CHF

24
Q

Sotalol

Mechanism
Clinical Use
Pharmacokinetics
Extracardiac Effects
Toxicity
A

Class II

Mechanism: non-selective, reduces O2 demand by decreasing HR and contractility d/t inhibiting SNS stimulation to the heart

Clinical Use: ventricular arrythmias, supraventricular tachycardia

Pharmacokinetics: no met. –> renal excret.

Extracardiac Effects:

Toxicity: bradycardia, prolonged QT –> torsades

25
Q

What is the pneumonic for Subgroup IA drugs?

A

The Queen Proclaimed Diso’s Pyramid!

26
Q

What is the pneumonic for Subgroup IB drugs?

A

IB is the Best post-MI

27
Q

What is the pneumonic for Subgroup IC drugs?

A

Can I have some More Fries Please?

28
Q

What is the pneumonic for Class II drugs?

A

APES

29
Q

What changes will you see in an ECG if you use a beta blocker?

A

Increased PR interval

CRRAB Pharmacology (3 decks)

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