lecture 19

Question 1

Lidocaine / Mexiletine

Answer 1

Class IB anti-arrhythmic

slow phase 0 and decrease the slope of phase 4
shorten phase 3

Little effect on depolarization phase of action
potential in normal cells

Rapidly associate and dissociate with Na+ channels

block the Na channels
Small increase in QRS. Clinically insignificant
decrease in QT

Question 2

MOA of lidocaine

Answer 2

Class IB
local anesthetic
useful for ventricular arrhythmias
little effect on the K channels

Question 3

CA of lidocaine

Answer 3

Acute treatment of ventricular arrhythmias from
myocardial infarction or cardiac manipulation

Treatment of digitalis-induced arrhythmias

little effect on atrial arrhythmia

Question 4

AE of lidocaine

Answer 4

CNS effects (drowsiness, slurred speech, agitation etc.)
• Little impairment of left ventricular function
• NO negative inotropic effect
• Cardiac arrhythmias (<10%)
• Toxic doses: convulsions, coma

Question 5

Mexiletine

Answer 5

Class IB

Management of severe ventricular arrhythmias

AE: CNS and GI

Question 6

Flecainide / Propafenone

Answer 6

Class IC drugs

depress of phase 0 of AP
slowing of conduction

no change in repolarization

marked Na channel block
Significant increase in QRS

Question 7

CA of flecainide

Answer 7

Severe symptomatic ventricular arrhythmias,
premature ventricular contraction or ventricular
tachycardia resistant

Severe symptomatic supraventricular arrhythmias &
prevention of paroxysmal atrial fibrillation

Question 8

AE of flecainide

Answer 8

• Negative inotropic efffect (aggravates CHF)
• CNS effects: dizziness, blurred vision, headache
• GI effects: nausea, vomiting, diarrhea
• Life-threatening arrhythmias & ventricular tachycardia

Question 9

Propafenone CA

Answer 9

Used for treatment of life-threatening ventricular
arrhythmias and the maintenance of normal sinus
rhythm in patients with symptomatic atrial fibrillation

Question 10

AE of propafenone

Answer 10

Also has b-blocking activity therefore bronchospasm, aggravation of underlying heart failure

similar to flecainide

Question 11

Quinidine, procainamide, disopyramide

Answer 11

Class IA

Block both Na+ and K+ channels
Increase both QRS and QT

Question 12

beta blockers as anti-arrhythmic drugs

Answer 12

reduce HR and contractility
slow conduction of impulses
reduce rate of depolarization
prolonged repolarization at AV node

Question 13

CA of beta blockers (metro and prop)

Answer 13

Reduce incidence of sudden arrhythmic death after MI

Control of supraventricular tachycardias (atrial
fibrillation & flutter, AV nodal re-entrant tachycardias)

Ventricular tachycardias

Question 14

esmolol as anti-arrhythmic

Answer 14

treatment of acute arrhythmias occurring during surgery or in emergency situations

Question 15

AE of the Class II drugs

Answer 15

Bradycardia, hypotension, CNS effects etc.

Contraindicated in acute CHF, severe bradycardia or
heart block and severe hyperactive airway disease

Question 16

Class III anti-arrhythmic

Answer 16

block of the repolarizing K channels

prolonged repolarization

Question 17

Amiodarone MOA

Answer 17

similar to thyroxine
shows MOA of multiple classes of drugs for arrhythmia

most prominent is K channel blockade

Question 18

CA of amiodarone

Answer 18

commonly used

Used in the management of ventricular &
supraventricular arrhythmias

the drug of choice for acute VT refractory to cardioversion shock

Question 19

AE of amiodarone

Answer 19

interstitial pulmonary fibrosis, GI intolerance, tremor,
ataxia, dizziness, hyper- or hypothyroidism, liver
toxicity, photosensitivity, neuropathy, muscle weakness,
hypotension, bradycardia, AV block, arrhythmias

Question 20

contraindications of amiodarone

Answer 20

• Patients taking:
• Digoxin, theophylline, warfarin, quinidine

Patients with:
• Bradycardia
• SA or AV block
• Severe hypotension
• Severe respiratory failure

Question 21

Sotalol MOA

Answer 21

• Potent non-selective b-blocker
• Inhibits rapid outward K+ current
• Prolongs repolarization & duration of action potential
• Lengthens refractory period

Question 22

CA of sotalol

Answer 22

Treatment of life-threatening ventricular arrhythmias

Maintenance of sinus rhythm in patients with atrial
fibrillation & flutter who are currently in sinus rhythm

Due to pro-arrhythmic effects – do not use for
asymptomatic arrhythmias

Question 23

AE of sotalol

Answer 23

Lowest rate (of antiarrhythmics) of acute or long-term
adverse effects
Torsades de pointes (prolongs QT interval)
Use with caution in patients with renal impairment

similar AE as other beta blockers

Question 24

Dofetilide

Answer 24

potent and pure K channel inhibitor

CA:
Conversion of atrial fibrillation / flutter to normal
sinus rhythm

Question 25

AE of dofetilide

Answer 25

• Headache, chest pain, dizziness, ventricular tachycardia

* Torsade de Pointes (prolongs QT interval)

Question 26

Class IV anti-arrhythmics

Answer 26

Ca channel blockers

slow rise in the AP

Question 27

verapamil and diltiazem

Answer 27

Verapamil = relatively selective for the myocardium and is less effective as a systemic vasodilator drug

Diltiazem = intermediate selectivity for the myocardium
between verapamil and the dihydropyridines

effects:
Decrease contractility (negative inotropy)
Decrease heart rate (negative chronotropy)
Decrease conduction velocity (negative dromotropy)

Question 28

MOA of verapamil and diltiazem

Answer 28

Slow conduction & prolong effective refractory period

inhibits the Ca channels

Question 29

CA of verapamil and diltiazem

Answer 29

• More effective against atrial than ventricular arrhythmias
• Supraventricular tachycardia is major arrhythmia
indication
• Reduction of ventricular rate in atrial fibrillation &
flutter
• Hypertension, angina

Question 30

AE of verapamil and diltiazem

Answer 30

• Negative inotropes
• Transient decrease in BP
• CNS effects (headache, fatigue, dizziness)
• GI effects (constipation, nausea)

contra:
increase the concentrations of other cardiovascular drugs such as digoxin, dofetilide, simvastatin, & lovastatin

Question 31

digoxin and arrhythmia

Answer 31

• Shortens refractory period in atrial & ventricular
myocardial cells
• Prolongs effective refractory period & diminishes
conduction velocity in AV node

Control of ventricular response rate in atrial
fibrillation & flutter with impaired left ventricular
function or heart failure

Question 32

MOA of digoxin in arrhythmia

Answer 32

• Direct AV node blocking effects & vagomimetic
properties:
• Inhibition of Ca2+ currents in AV node
• Activation of Ach-mediated K+ currents in atrium

hyperpolarization
shorten atrial AP
increase AV node refract

Question 33

adenosine and arrhythmia

Answer 33

High doses = decreases conduction velocity & prolongs refractory period as well as decreasing automaticity in AV node

Question 34

MOA of adenosine

Answer 34

• Enhances K+ conductance
• Inhibits cAMP-mediated Ca2+ influx
• Leads to hyperpolarization esp. in AV node

Question 35

CA of adenosine

Answer 35

drug of choice for abolishing acute supraventricular tachycardia

Question 36

AE of adenosine

Answer 36

• Flushing
• Burning
• Chest pain
• Hypotension
• Bronchoconstriction in asthmatics (may persist up to
30 min)

Question 37

magnesium

Answer 37

Functional Ca2+ antagonist

uses:
• Torsades de pointes
• Digitalis-induced arrhythmia
• Prophylaxis of arrhythmia in acute MI

Question 38

atropine and arrhythmia

Answer 38

Used in bradyarrhythmias to decrease vagal tone