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CPR II Exam 1 > Lecture 7: Drugs to Treat Cardiac Arrhythmias > Flashcards

Lecture 7: Drugs to Treat Cardiac Arrhythmias Flashcards

1
Q

Where are slow (2) and fast (3) cardiac action potentials found?

A

Slow: Sinoatrial Node and Atrioventricular Cells

Fast: Purkinje fibers, Ventricular cardiomyocytes, and Atrial cardiomyocytes

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2
Q

What is the MOA of Class 1A Drugs and what do they prolong (4)?

What are the 3 drugs of this family? (Q/P/D)

A

MOA: block sodium channels (prolong QRS and reduce phase 0 slope) and block potassium channels (prolong QT interval and action potential)

  • affects CARDIC MYOCYTES

D: Quinidine, Procainamide, Disopyramide

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3
Q

What are effects and adverse effects of:

  1. Procainamide (3 adverse effects)
  2. Quinidine (3 adverse effects)
  3. Disopyramide (3 adverse effects)
A
  1. directly depress SA and AV activity (infrequent use)
    • AE: torsades, syncope, and lupus erythematosus
  2. enhance AV conductance, hypotension (rarely used)
    • AE: torsades, GI, tinnitus/hearing loss/confusion
    • “Cinchonism” - neuro changes (Cinchona bark)
  3. strong antimuscarinic effect on heart
    • recurrent ventricular arrhythmias
    • AE: torsades, negative inotropic, atropine symptoms
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4
Q

What are the effects of Class 1, Class 2, Class 3, and Class 4 drugs used to treat Arrhythmias?

A

Class 1 = sodium channel blockers
Class 2 = beta blockers
Class 3 = potassium channel blockers
Class 4 = cardioactive calcium channel blockers

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5
Q

What is the MOA of Class 1B Drugs and what does it shorten?

What are the 2 drugs of this family? (L/M)

A

MOA: block sodium channels (bind to INACTIVATED channels) on damaged tissue (may shorten AP)
- dissociate with FAST kinetics = no effect on normal tissue

Drugs: Lidocaine and Mexiletine

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6
Q

What are effects and adverse effects of:

  1. Lidocaine (2 adverse effects)
  2. Mexiletine (3 adverse effects)
A
  1. terminate vent. tachycardia after acute MI
    • given IV only; least toxic of all Class 1 drugs
    • hypotension (HF) and neuro side effects
  2. ventricular arrhythmias, relieve chronic pain
    • ORALLY active congener of lidocaine
    • tremor, nausea, lethargy
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7
Q

What is the MOA of Class 1C Drugs and what do they prolong?

What are the 2 drugs of this family? (F/P)

A

MOA: block sodium channels (bind to open/activated channels) and block certain potassium channels

  • prolongs QRS interval duration
  • SLOW kinetics - does NOT dissociate completely

Drugs: Flecainide and Propafenone

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8
Q

What are effects and adverse effects of:

  1. Flecainide
  2. Propafenone
A
  1. normal hearts with supraventricular arrhythmias and refractory ventricular arrhythmias that are life-threatening
    • can exacerbate ventricular arrhythmias
    • in pts with preexisting problems
  2. similar to Flecainide (also weak B-blocker); treat supraventricular arrhythmias in normal hearts
    • can exacerbate ventricular arrhythmias
    • similar to Flecainide adverse effects
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9
Q

What is the MOA of Class 2 Drugs and how do they work?

What are the 2 drugs of this family? (P/E)

A

MOA: bind to GPCR and dec. the amount of cAMP that is created, dec. PKA activity

  • inc. threshold (effect on L-type Ca channels)
  • dec. slope (effect on If and T-type Ca channels)
  • SA node (dec. HR/inc. RR interval) and AV node (dec. conductance/inc. PR interval)

Drugs: Propranolol and Esmolol

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10
Q

What are the uses of Propranolol and Esmolol?

A

P: arrhythmias associated w/stress and thyroid storm, paroxysmal supraventricular arrhythmia

E: short-acting B1 selective; use as continuous IV infusion (in an in-patient setting)

  • thyrotoxicosis arrhythmias
  • control arrhythmias in perioperative period
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11
Q

What is the MOA of Class 3 Drugs and what do they prolong?

What are the 4 drugs of this family? (A/S/D/I)

A

MOA: block potassium channels, prolonging AP duration and QT interval due to a prolonged refractory period in myocytes

Drugs: Amiodarone, Sotalol, Dofetilide, Ibutilide

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12
Q

Amiodarone

What activity does it have in the heart?

What are 3 adverse reactions to drug use? (T/PF/HT)

A
  • blocks inactivated sodium channels, possesses adrenolytic activity, blocks potassium channels, AND blocks calcium channels
  • torsades de pointes incidence is LOWER compared to other class 3 drugs, but can cause fatal pulmonary fibrosis
  • can also cause hypo/hyperthyroidism (blocks thyroxine conversion to triiodothyronine)
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13
Q

Sotalol

What activity does it have in the heart?

What are 2 adverse effects to use?

A
  • has Class 2 (non-selective B blocker) and Class 3 (prolongs APD) effects

AE: depresses cardiac function and provokes torsades de pointes

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14
Q

Dofetilide and Ibutilide

What activity do they have on the heart and what are they clinically used for?

A
  • specifically block rapid component of the delayed rectifier potassium current

I: restore sinus rhythm in pts. with Atrial Fibrillation
D: maintain sinus rhythm after cardioversion in pts. with Atrial Fibrillation

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15
Q

What is the MOA of Class 4 Drugs and what do they prolong?

What are the 2 drugs of this family? (V/D)

What are two conditions they are used to control?

A

MOA: block L-type calcium channels in pacemaker cells

  • dec. Phase 0 slope (Slow SA = reduced HR/inc. R-R)
  • inc. L-type threshold potential (prolong conduction time and refractory period in AV node)

Drugs: Verapamil and Diltiazem

  • terminate paroxysmal supraventricular tachycardia
  • ventricular rate control in atrial fibrillation
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16
Q

What is the MOA of Adenosine and what does it prolong?

A

MOA: activates A1 adenosine receptor (Gi GPCR)

  • enhances potassium current
  • inhibits Calcium and Funny currents
  • inhibits AV conduction and inc. AV nodal refractory period (prolongs Action Potential
17
Q

What is the clinical use of Adenosine and what are its 3 adverse effects? (S/B/CB)

A

C: conversion to sinus rhythm in paroxysmal supraventricular tachycardia (IV gives RAPID relief)

AE: SOB, bronchoconstriction, chest burning

18
Q

What arrhythmias can these drug classes cause:

  1. Class 1A and Class 3 drugs
  2. Class 1A and Class 1C drugs
A
  1. torsades de pointes

2. persistent ventricular tachycardias

19
Q

Atrial Fibrillation

What are the 3 requirements for a Reentry Arrhythmia?

What is the BPM for the atrium/ventricle during Atrial Fibrillation?

A
  1. must be an obstacle to normal conduction
  2. there must be a unidirectional block at some point of the circuit
  3. conduction time around the circuit must exceed the effective refractory period

BPM: A = 350-600 bpm and V = 120-180 bpm

20
Q

What drug classes are used to treat Atrial Fibrillation and how do they achieve this?

A
  • *consider direct current cardioversion FIRST before treatment with pharmaceuticals**
    • CATHETER ABLATION

Class 1C agents

  • block fast Na channel to reduce retrograde signals
  • convert unidirectional block to bidirectional block
  • contraindicated in pts. with structural disease (HF)

Class 3 agents

  • block K channels = keep cells in refractory period
  • cannot stimulate cells still in refractory period
21
Q

What is Paroxysmal Supraventricular Tachycardia (PSVT)?

What does it look like on ECG?

How is it treated?

A
  • antegrade conduction through slow pathway and retrograde conduction along fast pathway of the AV node (abrupt onset and termination)

ECG: narrow QRS complex tachycardia with inverted or missing P wave (hidden by ventricular depol.)

  • Class 4 drugs (Verapamil/Diltiazem) preferred, but can use Beta Blockers (metoprolol, Atenolol, Propranolol)
22
Q

What is Torsades de pointes (TdP)?

What does it look like on ECG?

How is it treated?

A
  • rapid form of polymorphic VT in setting of prolonged ventricular repolarization (“long QT syndrome”) that can lead to sudden cardiac death

ECG: large QRS peaks that “twist” around isoelectric line

  • if drug induced = stop drugs; if hemo unstable = DCC; if hemo stable = correct electrolyte problems, IV magnesium sulfate, isoproterenol IV

CPR II Exam 1 (15 decks)

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