Anti-Arrhythmic Drugs Flashcards by Caitlin Griffiths

What is an arrhythmia?

Arrhythmias are a group of conditions in which the heart beat is irregular, too fast or too slow - this results in the rate and/or timing of cardiac contraction that is insufficient to maintain normal cardiac output

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What are the symptoms of arrhythmias?

If any:

Palpitations, syncope, dizziness

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What are the 4 main types of arrhythmia?

Supraventricular tachycardia (eg a fib, atrial flutter)
Ventricular arrhythmias (eg v fib, ventricular tachycardia)
Extra beats (premature atrial or ventricular contractions)
Bradyarrhythmias

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What happens in phase 0 of the fast cardiac action potential?

Influx of Na+ - depolarisation

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What happens in phase 1 of the fast cardiac action potential?

Rapid inactivation of Na+ channels

Transient opening of K+ channels, K+ out of cell

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What happens in phase 2 of the fast cardiac action potential?

Opening of L type calcium channels
Movement of Ca2+ into the cell, which is very very slowly repolarising
This phase is responsible for the large duration of the AP

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What happens in phase 3 of the fast cardiac action potential?

Rapid repolarisation phase

L type calcium channels close

K+ moves out of the cell

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What is happening in phase 4 of the fast cardiac action potential?

This is diastole

In the standard non-pacemaker cell the voltage is roughly -90mV

Maintained by Na/K/ATPase which moves 3 Na+ out of the cell and 2 K+ in

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Which cardiac cells do fast action potentials occur in?

Non pacemaker cells eg ventricular myocytes

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What are Class I antiarrhythmics?

Sodium channel blockers

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Give 3 examples of Class I antiarrhythmics

Quinidine (class Ia)
Lidocaine (class Ib)
Flecainide (class Ic)

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What are class II antiarrhythmics?

Beta blockers

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Give two examples of class II antiarrhythmics

Propranolol, bisoprolol

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What are class III antiarrhythmics?

Potassium channel blockers

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Give 2 examples of class III antiarrhythmics

Amiodarone, sotalol

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What are class IV antiarrhythmics?

Calcium channel blockers

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Give an example of a class IV antiarrhythmic

Verapamil

What are class V antiarrhythmics?

Additional antiarrhythmic drugs like adenosine and digoxin

What is meant by use-dependent block?

Only blocks voltage gated Na+ channels in open or inactive state so preferentially blocks damaged depolarised tissue

Describe the action of Class I antiarrhythmics on depolarisation

Block the fast sodium channels responsible for the rapid depolarisation (phase 0) of the fast cardiac APs.

Decreases amplitude of AP as reduces slope

Decreases conduction velocity in non-nodal tissue

Why do class I agents have no effect on nodal tissue?

Act on sodium channels that are responsible for phase 0 of the fast action potential, nodal tissue uses slow action potential

Why are there 3 subtypes of class I antiarrhythmics?

This is because some sodium channel blockers increase the effective refractory period, some decrease it and some have no effect

Class Ia - increase ERP
Class Ib - decrease ERP
Class Ic - no effect on ERP

What are the overall mechanisms of action of class I antiarrhythmics?

Block sodium channels
Class Ia increases ERP, class Ib decreases ERP, class Ic has no effect on ERP
Decrease automaticity

How do the subtypes of class I antiarrhythmics differ in their efficacy for reducing the slope of phase 0?

Ic > Ia > Ib

What are the side effects of class I antiarrhythmics?

Class Ia - hypotension, proarrythmia, GI effects Class Ib - Abdominal upset, dizziness Class Ic - proarrythmia, CNS and GI effects

What effects can quinidine (class Ia) have on an ECG?

Increased QRS Longation of QT +/ PR prolongation

What effects can lidocaine (class Ib) have on an ECG?

Increased QRS in fast beating/ischaemic tissue

What is the mechanism of action of lidocaine?

Class Ib - sodium channel blocker Increased depolarisation threshold making the heart less likely to initiate or conduct early APs that may cause an arrythmia

How does flecainide work?

Class Ic - sodium channel blocker, slows upstroke of cardiac AP Greatest effect on His-Purkinje system and ventricular myocardium Effect increases as the HR increases (use-dependence)

How do propanolol and bisoprolol differ in terms of selectivity?

Propanolol affect b1 and b2 but bisoprolol mostly affects b1 (more cardioselective)

What are the cardiac effects of class II agents?

Increased APD and refractory period in AV node to slow AV conduction velocity Decrease phase 4 depolarisation (catecholamine dependent)

What effects can a class II agent have on ECG?

Increased PR, decreased HR

What are the side effects of class II agents?

Bronchospasm (beware patients with asthma) Hypotension *Don't use in partial AV block

What are the cardiac effects of amiodarone?

Increase refractory period Increased APD Decreased speed of AV conduction

What effects can amiodarone have on ECG?

Increased QT, increased PR, increased QRS, decreased HR

What are the side effects of amiodarone?

Pulmonary fibrosis, hepatic injury, increased LDL, thyroid disease, photosensitivity

What are the cardiac effects of class IV agents?

Slows conduction through AV node Increases refractory period in AV node Increases slope of phase 4 in SAN to slow HR

What effects can a class IV agent have on ECG?

Increased PR | Increased or decreased HR depending on blood pressure response and baroreflex

What are the side effects of class IV agents?

GI effects, hypotension

How is adenosine administered?

Rapid IV bolus

What are the cardiac effects of adenosine?

Decreases APD, hyperolarisation, increases refractory period in AV node Slows AV conduction!

How does digoxin work as an antiarrhythmic?

Slows AV conduction and HR Inhibits Na/K/ATPase - increases intracellular Na+ which decreases NCX and increases Ca2+ This lengthens phase 4 and phase 0 of AP which decreases HR