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lecture 19 Flashcards

1
Q

Lidocaine / Mexiletine

A

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

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2
Q

MOA of lidocaine

A

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

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3
Q

CA of lidocaine

A

Acute treatment of ventricular arrhythmias from
myocardial infarction or cardiac manipulation

Treatment of digitalis-induced arrhythmias

little effect on atrial arrhythmia

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4
Q

AE of lidocaine

A

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

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5
Q

Mexiletine

A

Class IB

Management of severe ventricular arrhythmias

AE: CNS and GI

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6
Q

Flecainide / Propafenone

A

Class IC drugs

depress of phase 0 of AP
slowing of conduction

no change in repolarization

marked Na channel block
Significant increase in QRS

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7
Q

CA of flecainide

A

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

Severe symptomatic supraventricular arrhythmias &
prevention of paroxysmal atrial fibrillation

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8
Q

AE of flecainide

A
  • Negative inotropic efffect (aggravates CHF)
  • CNS effects: dizziness, blurred vision, headache
  • GI effects: nausea, vomiting, diarrhea
  • Life-threatening arrhythmias & ventricular tachycardia
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9
Q

Propafenone CA

A

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

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10
Q

AE of propafenone

A

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

similar to flecainide

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11
Q

Quinidine, procainamide, disopyramide

A

Class IA

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

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12
Q

beta blockers as anti-arrhythmic drugs

A

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

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13
Q

CA of beta blockers (metro and prop)

A

Reduce incidence of sudden arrhythmic death after MI

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

Ventricular tachycardias

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14
Q

esmolol as anti-arrhythmic

A

treatment of acute arrhythmias occurring during surgery or in emergency situations

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15
Q

AE of the Class II drugs

A

Bradycardia, hypotension, CNS effects etc.

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

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16
Q

Class III anti-arrhythmic

A

block of the repolarizing K channels

prolonged repolarization

17
Q

Amiodarone MOA

A

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

most prominent is K channel blockade

18
Q

CA of amiodarone

A

commonly used

Used in the management of ventricular &
supraventricular arrhythmias

the drug of choice for acute VT refractory to cardioversion shock

19
Q

AE of amiodarone

A

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

20
Q

contraindications of amiodarone

A
  • Patients taking:
  • Digoxin, theophylline, warfarin, quinidine
Patients with:
• Bradycardia
• SA or AV block
• Severe hypotension
• Severe respiratory failure
21
Q

Sotalol MOA

A
  • Potent non-selective b-blocker
  • Inhibits rapid outward K+ current
  • Prolongs repolarization & duration of action potential
  • Lengthens refractory period
22
Q

CA of sotalol

A

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

23
Q

AE of sotalol

A

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

24
Q

Dofetilide

A

potent and pure K channel inhibitor

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

25
AE of dofetilide
* Headache, chest pain, dizziness, ventricular tachycardia | * Torsade de Pointes (prolongs QT interval)
26
Class IV anti-arrhythmics
Ca channel blockers | slow rise in the AP
27
verapamil and diltiazem
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)
28
MOA of verapamil and diltiazem
Slow conduction & prolong effective refractory period inhibits the Ca channels
29
CA of verapamil and diltiazem
• More effective against atrial than ventricular arrhythmias • Supraventricular tachycardia is major arrhythmia indication • Reduction of ventricular rate in atrial fibrillation & flutter • Hypertension, angina
30
AE of verapamil and diltiazem
* 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
31
digoxin and arrhythmia
• 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
32
MOA of digoxin in arrhythmia
• 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
33
adenosine and arrhythmia
High doses = decreases conduction velocity & prolongs refractory period as well as decreasing automaticity in AV node
34
MOA of adenosine
* Enhances K+ conductance * Inhibits cAMP-mediated Ca2+ influx * Leads to hyperpolarization esp. in AV node
35
CA of adenosine
drug of choice for abolishing acute supraventricular tachycardia
36
AE of adenosine
``` • Flushing • Burning • Chest pain • Hypotension • Bronchoconstriction in asthmatics (may persist up to 30 min) ```
37
magnesium
Functional Ca2+ antagonist uses: • Torsades de pointes • Digitalis-induced arrhythmia • Prophylaxis of arrhythmia in acute MI
38
atropine and arrhythmia
Used in bradyarrhythmias to decrease vagal tone

CRS (16 decks)

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