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Pharmacology > Arrhythmia > Flashcards

Arrhythmia Flashcards

1
Q

Aim of therapy

A

To reduce ectopic pacemaker activity

To modify conduction or refractoriness in reentrant circuits to disable the circular movement

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2
Q

Antiarrhythmic agents generally alter:

A

Diastolic potential in pacemaker cells and/or resting membrane potential in ventricular cells (phase 4)
Phase 4 depolarization
Threshold potential
Action potential duration

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3
Q

Effect on Automaticity:

A
  • Can slow spontaneous discharge by:
    Depressing diastolic depolarization
    Otherwise known as phase 4
    Shifting threshold voltage to zero
    Hyperpolarizing resting membrane potential
  • Affects ectopic sites more than sinus node
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4
Q

Effect on Reentry:

A
  • Improves or depresses conduction
    Eliminate unidirectional block
    Facilitate conduction so returning wavefront reenters when cells still refractory
    Depress conduction to transform unidirection to bidirectional block
  • Prolong refractoriness relative to action potential duration
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5
Q

Vaughan Williams Classification of Antiarrhythmic Drugs Class I

A

block sodium channels

 works mostly on Phase 0, but also works on the latter parts

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6
Q

T/F: Vaughan Williams Classification of Antiarrhythmic Drugs Class Ia example: Lidocaine

A

F:
Ia (quinidine, procainamide, disopyramide)
Ib (lidocaine)
Ic (flecainide)

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7
Q

Vaughan Williams Classification of Antiarrhythmic Drugs Class II

A

β-adrenoreceptor antagonists
works on Phase 4, keeps slope less steep (flattens the slope)
Atenolol, sotalol

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8
Q

Vaughan Williams Classification of Antiarrhythmic Drugs Class III

A

prolong action potential and prolong refractory period
Works on Phase 0 to 3
Amiodarone, sotalol

Drugs which prolong ERP (effective refractory period) by prolonging action potentials

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9
Q

Vaughan Williams Classification of Antiarrhythmic Drugs Class IV

A

Calcium channel antagonists
Works on Phase 2
verapamil

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10
Q

T/F: Lidocaine Low toxicity high effectiveness in arrhythmias associated with MI

A

T

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11
Q

Lidocaine toxicity

A

Toxicity: one of the least cardiotoxic drugs
May precipitate hypotension by depressing myocardial contractility in large doses in patients with heart failure
Neurologic: parethesias, convulsions, dizziness

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12
Q

T/F Flecainide is a potent Na and K channel blocker

A

T

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13
Q

Very effective in suppressing premature ventricular contractions and  premature atrial contractions

A

Class Ic: Flecainide

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14
Q

T/F Class Ic May exacerbate arrhythmias in patients with ventricular arrhythmias + patients with previous MI and ventricular ectopy

A

T

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15
Q

Flecainide route, half-life, metabolism

A

oral, 20 hours, hepatic and renal metabolism

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16
Q

main use is for patients with paroxysmal AF and those without structural heart diease

A

Class Ic: Flecainide

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17
Q

Prototype of Class II

A

propranolol, esmolol

18
Q

MOA of class II

A

indirectly reduce the phase 4 slope by blocking positive chronotropic action of norepinephrine

19
Q

therapeutic use of class II

A

suppression of ventricular ectopic depolarizations

20
Q

Amiodarone cardiac effect

A

Broad spectrum of cardiac actions, high efficacy
Markedly prolongs APD (QT interval)
Significantly blocks inactivated Na channels
Has weak β-adrenergic and calcium channel blocking actions

21
Q

Indications of amiodarone

A

Preventing recurrent VT
Adjuvant therapy in patients with ICD
Maintaining sinus rhythm in atrial fibrillation patients with structural heart disease

22
Q

Amiodarone cardiac toxicity

A

Symptomatic bradycardia and heart block in patients with preexisting sinus or AV node disease
Prolongs QT interval

23
Q

Amiodarone toxicity

A

Pulmonary fibrosis (dose-related)
Hypothyroidism or hyperthyroidism
Amiodarone has iodine in it, so you have to check the patient’s thyroid function every so often.
Abnormal liver function tests and hepatitis
Skin deposits, photodermatitis

24
Q

T/F: Sotalol is not cardioselective

A 
T
 both class II and class III effects
25
Q

Sotalol route, half-life, excretion

A

oral, 12 hours, renal excretion

26
Q

Sotalol toxicity

A

further depression of LV function

27
Q

Sotalol use

A

life-threatening ventricular arrhythmias maintaining sinus rhythm in AF

28
Q

Class IV prototype

A

Verapamil

29
Q

Effects of verapamil

A

Block both activated and inactivated L-type Ca channels
Prolongs AV nodal conduction time and ERP
Slows the SA node
Peripheral vasodilation

30
Q

Verapamil indication

A

Termination of SVT (if adenosine not available)

Control heart rate in AF

31
Q

Verapamil toxicity

A

Dangerous in patients with VT misdiagnosed as SVT, may cause hypotension and VF
Negative inotropic effects
Can induce AV block

32
Q

Adenosine half life

A

<10 seconds

33
Q

Adenosine cardiac effect

A

Marked hyperpolarization
Suppression of Ca-dependent AP
Directly inhibits AV nodal conduction

34
Q

DOC for prompt conversion of SVT to sinus

A

Adenosine

35
Q

Magnesium MOA

A

not well known

36
Q

use of magnesium

A

Digitalis-induced arrhythmias if low Mg

Torsade de pointes even if Mg normal (1g/IV)

37
Q

Main indication of digoxin

A

Slow the ventricular rate in chronic AF (not very effective in acute setting)

38
Q

MOA of digoxin

A

Slowing the sinus node discharge rate

Prolonging AV nodal refractoriness

39
Q

Toxicity of digoxin

A

Headache, nausea/vomiting, diarrheas and arrhythmias

40
Q

Pharmacologic Treatment of Arrhythmias

A 
Eliminate the cause if possible
Make a firm diagnosis
Determine baseline condition
Evaluate need for therapy
Weigh benefits vs risks of therapy
41
Q

T/F Antiarrythmics can be proarrhythmics.

A

T

Pharmacology (11 decks)

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