Anti-arrhythmic drugs Flashcards

1
Q

Flecainide MOA

A

block of open sodium channels
causes increase in effective refractory period and slowed AV conduction

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2
Q

How is Flecainide given and how is it excreted?

A

oral or IV
mostly excreted in urine

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3
Q

Clinical use of Flecainide

A

prevention of AF and ventricular tachyarrhythmias
cardioversion of acute onset AF

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4
Q

Adverse effects and cautions with Flecainide

A

suitable only for patients without ischaemic or structural heart disease
increases likelihood of dysrhythmia
may increase mortality due to ventricular fibrillation post-infarction

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5
Q

Beta blocker actions

A

antidysrhythmic, antihypertensive and antianginal
blocks actions of catecholamines on beta adrenoceptors

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6
Q

Beta blockers MOA

A

beta-adrenoceptor antagonist
block sympathetic drive , reducing pacemaker activity and increasing AV conduction time

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7
Q

Beta blockers examples

A

bisoprolol
propranolol (has additional class 1 action)

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8
Q

Clinical use of beta blockers

A

atrial fibrillation
supraventricular and ventricular tachyarrhythmias
reduction of mortality after infarct

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9
Q

Adverse effects of beta blockers

A

bronchoconstriction in asthma
bradycardia and heart block

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10
Q

Class 3 (amiodarone, sotalol etc) MOA

A

potassium channel blockers
increases refractory period

amiodarone also blocks sodium channels and beta adrenoceptors

sotalol is a beta adrenoceptor antagonist with class 2 actions

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11
Q

Clinical use of amiodarone and sotalol

A

atrial fibrillation and flutter
ventricular tachyarrhythmias

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12
Q

Amiodarone adverse effects

A

serious toxicity: pulmonary fibrosis, liver damage, photosensitive skin rashes and thyroid malfunction

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13
Q

Sotalol adverse effects

A

Torsades de pointes
less likely with amiodarone

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14
Q

Calcium channel blocker examples

A

Verapamil
Diltiazem

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15
Q

Calcium channel blocker MOA

A

blocks L-type voltage-gated calcium ion channels which are important in the action potential plateau
decreases automaticity and slows AV conduction

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16
Q

Clinical use of calcium channel blockers

A

supraventricular tachycardias
control of ventricular rate in AF

17
Q

Adverse effects of calcium channel blockers

A

side effects due to smooth muscle relaxation:
- hypotension + dizziness
- ankle oedema
- constipation

unwanted cardiac actions:
- heart block
- bradycardia

18
Q

Half-life of adenosine

A

10 seconds

19
Q

Adenosine MOA

A

ADP receptor agonist
activates G protein-coupled adenosine (A1 receptors)
inhibits calcium ion channel open whilst increasing potassium channel opening
negative chronotropic effect on SA node with slowed AV conduction

20
Q

Adenosine administration route

A

IV

21
Q

Clinical use of adenosine

A

termination of paroxysmal SVT
slowing of AV conduction to enable more precise diagnosis of SVTs

22
Q

Adverse effects of adenosine

A

flushing
chest pain
dyspnoea
bronchospasm

transient because rapid elimination of adenosine

23
Q

Actions of Digoxin

A

slows heart
slows AV conduction
prolongs AV node refractory period
increased force of contraction in failing heart

24
Q

Digoxin MOA

A

inhibits sodium/potassium ATPase in plasma membrane
increased intracellular sodium ions reduces calcium ion extrusion thus increasing intracellular calcium

25
Q

Clinical use of Digoxin

A

atrial fibrillation
heart failure (if diuretics and ACE inhibitors have not worked)

26
Q

Digoxin adverse effects

A

dysrhythmias (due to block of AV conduction and ectopic pacemaker action)
yellow vision
nausea
vomiting

27
Q

What kind of therapeutic window does Digoxin have?

A

narrow

28
Q

What symptoms/signs would suggest a life-threatening arrhythmia?

A

hypotension
pulmonary oedema
loss of consciousness due to arrhythmia

29
Q

What electrical methods can be used to treat life-threatening arrhythmias?

A

tachy = D/C cardioversion
brady = temporary external pacing or cardiology referral for emergency pacemaker fitting

30
Q

When is Digoxin used over a beta blocker?

A

beta blocker adverse effects (eg. fatigue, cold limbs, wheezing)
older, sedentary
no other compelling reason for beta blocker use (eg. angina, migraine)

31
Q

Adenosine administration instructions

A

rapid injection
as proximal as possible
immediately followed by saline flush

32
Q

Chronic AF in well patient Digoxin dosing schedule

A

start oral digoxin 125mg once daily
takes 9 days to reach steady state therapeutic level

33
Q

Fast AF in unwell patient Digoxin dosing schedule

A

rapid treatment
loading dose 750-1500 micrograms over 24 hours
maintenance 125mg after that

34
Q

Example of a drug with a high volume of distribution

A

amiodarone
- large amounts retained in thyroid, heart, fat etc