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YFRM 300 > Drugs used in arrhythmias > Flashcards

Drugs used in arrhythmias Flashcards

1
Q

Atrial rhythms
(Supraventricular tachycardia SVT)

A
  • Atrial flutter * Atrial fibrillation
  • AV nodal re-entrant tachycardia
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2
Q

Sinus rhythm

A
  • Sinus bradycardia <60
  • Sinus tachycardia >100
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3
Q

Ventricular rhythm

A
  • Ventricular tachycardia (V-tach) * Ventricular fibrillation (V-fib)
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4
Q

General principles for the treatment of cardiac arrhythmias.

A

particularly chronic therapy should be
instituted only for haemodynamically important sustained
arrhythmias, after a search for correction of any simple precipitating
factors and consideration of alternative treatment (e.g. catheter
ablation, implantable cardioverter / defibrillator). * Only use Class I and III agents in consultation with an arrhythmia
expert

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5
Q

Antiarrhythmic drug classes

A
  • Class I: drugs that block voltagesensitive sodium channels. They are subdivided: Ia, Ib and Ic
  • Class II: β-adrenoceptor
    antagonists
  • Class III: drugs that substantially
    prolong the cardiac action
    potential
  • Class IV: calcium antagonist
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6
Q

1a…..Sodium channel block (intermediate
dissociation) – prolong action potential
duration

A

Disopyramide,
quinidine,
procainamide

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7
Q

Sodium channel block (fast dissociation) –
shorten action potential duration

A

Lidocaine…….1b

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8
Q

Sodium channel block (slow dissociation) –
do not affect action potential duration

A

Flecainide…..1c

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9
Q

Class Ia

A

phase 0 depolarization and phase 3
repolarization, thereby increasing the QRS duration and the QT
interval.

  • Not available in
    SA
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10
Q

Class Ib

A
  • MOA: inhibit fast sodium channels
    and shortens action potential
    duration, thereby inhibiting ectopic beats and re-entry circuits
  • little effect on normal cardiac
    tissue, but they can accelerate phase 3
    repolarization and decrease the QT
    interval slightly.
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11
Q

Class Ib: Lidocaine

A

Amide-type local anaesthetic –
* MOA: inhibit fast sodium channels and shortens action potential
duration, thereby inhibiting ectopic beats and re-entry circuits
* Indication: suppression of symptomatic ventricular arrythmias
associated with MI, cardiac surgery and other acute situations
* Note: evidence show trials of prophylactic lidocaine use routinely
show increased mortality

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12
Q

Lidocaine: pharmacokinetics

A

Onset of action: IV administration = immediate, IM = 5-15 minutes
* Duration of action: IV= 10-20 minutes after initial bolus. IM = 1-1.5
hours
* 90% rapidly metabolised in the liver and excreted in the kidneys
(<10% as unchanged drug) * Hepatic clearance is decreased in hepatic disease and CCF

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13
Q

Lidocaine: cautions

A

Contraindications
* Severe sinus node dysfunction, 2nd or 3rd degree heart block,
hypersensitivity to amide type local anaesthetics (LAs )
Cautions
* Respiratory depression, other cardiac dysfunction
* Do not use in pregnancy
Drug interactions
* Other arrhythmias, anticonvulsants, cimetidine

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14
Q

Lidocaine: adverse effects

A
  • Neurological effects (seizures) * Common: drowsiness, confusion, dizziness
  • Uncommon: cardiac effects.
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15
Q

Class Ic

A

MoA: greatest effect on phase 0
depolarization and increase the
QRS duration markedly, but
they have little effect on phase 3
and the QT interval

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16
Q

Class III

A

MoA: no effect on
phase 0, but they markedly
prolong phase 3 and
increase the QT interval.

17
Q

Class III: amiodarone.

A

Use is limited due to side effects (including inducing tachy
arrhythmias) * One of the safest antiarrhythmic agent after B-blockers for oral use
* Indication: prophylaxis and treatment of supra ventricular and
ventricular arrhythmias. * Note: Amiodarone is an organic iodine compound that is structurally
related to thyroid hormone.

18
Q

Amiodarone: pharmacokinetics

A

Oral absorption is slow with bioavailability of 20-55%
* Wide distribution in fat muscles and liver * Therapeutic response may take 3 weeks, with peak effect reached in
1-5 months
* Antiarrhythmic effect persist for 10 – 150 days after withdrawal of
long-term treatment * Onset of action: IV 10-15 minutes
* Extensive hepatic metabolism with biliary excretion (renal excretion
negligible)

19
Q

Amiodarone: cautions

A

Contraindications
* Cardiac bradycardia / block, hyperthyroidism, sensitivity to iodine,
hypokalemia
* Pregnancy and lactation
Cautions
* Heart failure, hepatic impairment
Drug interactions (may interact with other drugs for months after
discontinuation of treatment) * Other antiarrhythmics, b-blockers, digoxin, drugs causing QT prolongation,
phenytoin, simvastatin, warfarin, grapefruit juice

20
Q

Amiodarone: adverse effects

A

May take several weeks to appear and continue of months after
discontinuation of treatment * Torsades de Pointes
* Hyper/hypothyroidism (thyroid function monitoring necessary) * Neurotoxicity (including peripheral neuropathies) * Photosensitivity (warn to avoid exposure to sunlight) * GI * Uncommon: pulmonary fibrosis & hypersensitivity pneumoniti

21
Q

lass II: Propranolol

A

MoA:
* Inhibit sympathetic activation of cardiac automaticity and conduction, * Slow the heart rate, * Decrease the AV node conduction velocity, and * Increase the AV node refractory period, * Little effect on ventricular conduction and repolarization.

Indications:

  • Prevent and treat supraventricular dysrhythmias
  • Reduce ventricular ectopic depolarizations and sudden death in patients
    with myocardial infarction
22
Q

Class IV: Verapamil

A

MoA:
* Decrease the AV node conduction velocity and * Increase the AV node refractory period, * Smaller effect on the SA node and heart rate, * Little effect on the ventricular conduction velocity and refractory
period.

Indications:
* Controlling or converting certain supraventricular dysrhythmias, not
effective in treating ventricular dysrhythmias. * Control the ventricular rate in patients with atrial fibrillation

23
Q

Miscellaneous antiarrhythmics

A
  • Adenosine
  • Digoxin
  • Magnesium sulphate
  • Ivabradine & ranolazine
24
Q

Adenosine*

A

Acute management of paroxysmal supraventricular tachycardias –
convert to sinus rhythm
* Administer as rapid IV bolus
* Half-life <10 seconds
* Adverse effects: dyspnoea, flushing, chest pain are an indication the
bolus has reached the heart * Adverse effects are short lived <1 minute: bradycardia, prolonged
hypotension
* Only use when cardiac monitoring and resuscitation is available

25
Q

Management of dysrhythmias

A

Atrial fibrillation and flutter * Torsades de Pointes

26
Q

Atrial fibrillation and flutter

A

Pathology: disorganized form of re-entry in which atrial cells are
continuously re-excited by re-entrant stimuli as soon as they are
repolarized - AV node is continuously bombarded with atrial
impulses, some of which are conducted to the ventricles, so that the
ventricular rate is often rapid and irregular.

27
Q

Two general approaches to pharmacologic therapy: Atrial fibrillation and flutter

A
  • Ventricular rate control is essential for all patients to avoid symptoms
    and development of cardiomyopathy and is the first objective in
    treating acute atrial fibrillation: β -blockers and calcium channel
    blockers, which slow AV node conduction velocity and increase its
    refractory period, so that fewer atrial impulses are transmitted to the
    ventricles. * Preventing recurrences and maintaining normal sinus rhythm
    (rhythm control): amiodarone
  • Anticoagulant (warfarin) to prevent thromboembolism and stroke
28
Q

Torsades de Pointes

A

Polymorphic ventricular tachycardia (VT), associated with
QTc prolongation, which is the
heart rate adjusted lengthening of the QT interval.
Induced by: * Drugs (including tricyclic antidepressants and antipsychotic agents ) * Electrolyte abnormalities that prolong the QT interval and predispose cardiac cells to after- depolarizations
* Congenital p

29
Q

Torsades de Pointes

A

Treatments: * Withdrawal of the causative
agent, * Correction of any
electrolyte abnormalities,
such as hypokalemia, * Intravenous administration
of magnesium sulfate IV ,
and * Cardiac overdrive pacing. * These treatments act in part
by shortening the QT
interval

YFRM 300 (18 decks)

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