Anti-Arrhythmic Drugs Flashcards

1
Q

What are the different normal variations in sinus rhythm?

A

sinus tachycardia
- heart rate is too fast = more than 100bpm

sinus bradycardia
- heart rate is too slow = less than 50bpm

sinus arrhythmia

  • R-R intervals vary between beats
  • can have multiple P waves
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2
Q

What are the two main types of arrhythmia?

A

supraventricular - originates in the atrial tissues

ventricular - originates in the ventricles

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3
Q

What are the main causes of arrhythmia?

A

abnormalities in the conduction - rate, direction and path
abnormalities in automaticity - rate of discharge
damage to the SA node

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4
Q

What are the three main mechanisms of abnormalities of conduction?

A

rate - slowed conduction/spread of depolarisation

direction - unidirectional block in the conducting pathway

path - anatomical abnormalities may produce an accessory pathway to allow conduction from the ventricle to the heart (can bypass some paths, results in tachycardia)

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5
Q

What are the mechanisms is abnormalities of automaticity?

A

change in the rate of discharge from the SAN can result in

early after depolarisation - membrane potential oscillations during plateau/repolarisation phase

delayed after depolarisation - spontaneous depolarisation after AP depolarisation

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6
Q

What is ectopic focus? What is its effects?

A

ectopic focus are abnormal pacemaker sites outside of the SAN
- can lead to dys-synchronisation of the heart beat = due to premature beats outside of the SAN function

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7
Q

What are the factors affecting choice of pharmacological treatment?

A

identification of the cause of the arrhythmia

identification of the site within the heart that is the initiator of the arrhythmia

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8
Q

What are the different classes of anti-arrhythmic drugs?

A

Class II - beta blockers = affect membrane potential
Class I - sodium channel blockers = affect depolarisation
Class IV - calcium channel antagonists = affect the plateau
Class III - potassium channel blockers = affect repolarisation

adenosine
digoxin

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9
Q

What is Class I of the anti-arrhythmic drugs?

A

sodium channel blockers

Ia - treats ventricular dysrhythmia, atrial fibrillation = quinidine, procainamide

Ib - treats ventricular tachycardia and fibrillation, digitalis induced arrhythmia = lignocaine, tocainide

Ic - treats resistant ventricular tachycardia, paroxysmal atrial fibrillation = flecainide

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10
Q

What is Class II of anti-arrhythmic drugs?

A

beta blockers - atenolol, propranolol

blocks the effects of catecholamines (adrenaline/noradrenaline) at the beta-1 adrenoceptors
- decreases sympathetic activity

decreases rate of automaticity - less firing from the SAN
prolongs refractoriness - prolongs depolarisation

treats supraventricular tachycardia

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11
Q

What is Class III of the anti-arrhythmic drugs?

A

potassium channel blockers - bretylium, sotalol, amiodarone

prolongs the refractory period

prevents delayed after depolarisations (occur after phase 3)

treats Wolff-Parkinson White Syndrome (accessory pathway bypasses the AVN resulting in fast HR)

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12
Q

What is Class IV of the anti-arrhythmic drugs?

A

calcium channel antagonists

  • verapamil, diltiazem
  • nifedipine and dihydropyridine derivatives are only used in hypertension as they have no anti-arrhythmic effects

treats supraventricular arrhythmia

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13
Q

How does adenosine act?

A

acts on receptors on the AV node

has negative chronotropic and dromotropic effects

  • chronotropic = reduces heart rate
  • dromotropic = reduces conduction velocity

decreases AP duration

  • prolongs the PR interval = holds the impulse at the AVN
  • transient complete AV block = slows impulse
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14
Q

What are the side effects of adenosine?

A
flushing 
dyspnoea - shortness of breath
bronchospasm = is contraindicated in asthmatics 
vomiting 
headaches
characteristic feeling of impending doom
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15
Q

How does digoxin act?

A

inhibits the Na/K ATPase pump

  • reversible inhibition
  • increases force of contraction as intracellular sodium increases

AVN inhibition

  • has vagomimetic effects = stimulates the parasympathetic nervous system by increasing vagal activity
  • slows conduction of electrical impulses at the AVN therefore decreasing heart rate

treats atrial flutter, atrial fibrillation and heart failure

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16
Q

What are the effects of digoxin toxicity?

A

increased frequency of ventricular ectopics
paroxysmal atrial tachycardia with AV block
marked ST segment depression - ischaemia
can cause ventricular tachycardia or ventricular fibrillation