Antiarrhythmic Drugs Flashcards

1
Q

Describe the ventricular action potential

A

Phase 0 - rapid depolarisation when Na+ enters

Phase 1 - partial depolarisation where Na+ channels become inactivated

Phase 2 - plateau caused by inward Ca2+ currents opposing the outwards K+ movement

Phase 3 - repolarisation due to closing of the L-type and unopposed K+ current

Phase 4 - resting membrane potential determined by K+ permeability

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2
Q

Describe the pacemaker potential

A

No resting membrane potential. The funny current is activated by HCN channels moving Na+ into the cell and when this reaches -50mv it reaches the threshold to generate an action potential. HCN channels inactivate and the upstroke is caused by opening of L-type Ca2+ channels. The downstroke is caused by opening of K+ channels.

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3
Q

What is the difference between atrial fibrillation and supra ventricular tachycardia?

A

Atrial fibrillation is irregularly irregular whereas supra ventricular tachycardia is regular but tachycardic

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4
Q

What are delayed after-depolarisations?

A

Mainly caused by an increase in Ca2+ which reverses NCX allowing Na+ to enter and depolarise the cell early.

Early after-depolarisation occurs before the action potential has completed and can be potentates by hypokalaemia or drugs that increase the QT interval (class III antiarrhythmics)

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5
Q

What are re-entry loops?

A

An impulse re-excites regions after the refractory period has subsided causing a continuous circulation of action potentials that would usually cancel each other out. As a result of structural abnormality or MI

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6
Q

What physiological action can cause ectopic pacemaker activity and what does this cause?

A

Activation of the sympathetic system and can cause tachycardias

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7
Q

What causes heart block?

A

Fibrosis/ischaemic damage to the conducting system

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8
Q

How do class I drugs work?

A

Na+ channel blockers - bind to open Na+ channels and keep them inactivated but dissociates in time for the next action potential so prevents early APs

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9
Q

Name a class IA drug

A

Quinidine, procainamide

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10
Q

Name a class IB drug

A

Lidocaine, phenytoin

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11
Q

Name a class IC drug

A

Flecainide, propafenone

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12
Q

What are the ADRs for flecainide?

A

Pro arrhythmic

CNS - dizziness, drowsiness

GI - nausea, vomiting

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13
Q

Describe the pharmacokinetics for flecainide

A

Oral, CYP2D6, renal excretion

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14
Q

How do beta blockers achieve a chronotrophic effect?

A

They decrease the slope of the pacemaker potential

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15
Q

Name the major class III antiarrhythmic

A

Amiodarone - binds to K+ channels and prolongs the refractory period

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16
Q

What are the ADRs of amiodarone?

A

Hepatic injury, pulmonary fibrosis, thyroid disease, increased LDLs

17
Q

Name a Ca2+ channel blocker

A

Verapamil, diltiazem - decrease the inwards current of Ca2+ causing a decrease in the slope of the action potential and also reduces the force of contraction

18
Q

How would you treat a supra ventricular tachycardia?

A

Vagal manoeuvres

IV adenosine/verapamil

19
Q

How does adenosine work?

A

Binds to A1 receptor which is Gi and reduces cAMP thus increases K+ efflux and leads to hyperpolarisation

20
Q

How would you manage chronic AF?

A

Anticoagulant

Rate control - beta blocker/verapamil (consider adding digoxin/amiodarone)

Rhythm control - cardioversion (+amiodarone) or pharmacological cardioversion (flecainide)

21
Q

How would you treat acute AF?

A

Anti coagulation

Emergency cardioversion (+amiodarone) or pharmacological cardioversion (flecainide)

Control rate - verapamil/bisprolol (digoxin/amiodarone second line)

22
Q

How would you treat ventricular tachycardia?

A

Amiodarone/lidocaine, shock

23
Q

What are the ADRs for verapamil?

A

Constipation, hypotension, ankle swelling, heart failure

24
Q

How does digoxin work? (Cardiac glycoside)

A

Has a positive inotrphic effect by blocking Na+/K+ ATPase. This increases intracellular Na+ which reverses the NCX pump so more Ca2+ is stored in the SER and available during contraction

It also has a negative chronotrophic effect by increasing vagaries activity g