Session 7: Antiarrhythmics Flashcards
Where might you find arrhythmias in the heart?
When there is something wrong with either AV or SA node.
When there is a contraction impulse induction issue of the cardiac tissue.
A combination of the two.
When an abnormal impulse is generated in arrhythmias, what are the two types of rhythms?
Automatic rhythms such as enhanced normal automaticity where there are more action potentials from SA node, or ectopic foci.
Triggered rhythms where there is either delayed afterdepolarisation or early afterdepolarisation.
An arrhythmia doesn’t have to be due to an abnormal impulse generation but could be instead due to abnormal conduction.
What types of abnormal conductions are there?
Conduction block such as 1st, 2nd or 3rd degree heart block.
Reentry loops such as circus movements or reflections.
Explain the pathology in wolff-parkinson-white syndrome.
There is an accessory pathway in the heart called the bundle of kent. Here the impulse can re-enter the atrium and reach the AV node again.
Give another example of a cause of a re-entry loop.
An area of an infarct.
This can cause re-entry in the scar.
What part of action potential do you aim to target in the case of an abnormal impulse generation?
Decreasing phase 4 slope in the pacemaker cells.
or
Raising the threshold of action potential.
What part of the action potential do you aim to target in the case of an abnormal conduction?
Decreasing the conduction velocity in phase 0.
or
Increasing the effective refractory period so the cell won’t be re-excited again.
So why do arrhythmias occur?
Automatic or triggered activity
Re-entry due to scar, or WPW syndrome.
What are the broad functions of antiarrhythmic drugs?
Decrease conduction velocity
Change the duration of ERP
Suppress abnormal automaticity
Give examples of class 1A agents.
Procainamide
Quinide
Disopyramide
How are class 1A drugs administered?
Oral or IV
Actions of class 1A drugs?
Decreased conduction by decreasing phase 0.
Increasing refractory period by prolonging action potential duration and NA inactivation.
Target automaticity by decreasing the slope of phase 4 in fast potentials.
Increase the threshold.
Special properties of quinidine.
Anticholinergic to speed AV conduction used with digitalis, beta-blockers or CCBs.
Class 1A effects on ECG.
Increased QRS
Increased PR
Increased QT
Uses of class 1A drugs.
Quinidine: atrial fibrilliation, atrial flutter and preent recurrence. Also for Brugada syndrome.
Procainamide: acute IV treatment of supraventricular and ventricular arrhythmias.
Side effects of class 1A drugs.
Hypotension
Pro-arrhythmic like Torsades de Points
Dizziness, confusion, insomnia, seizures
GI effects
Lupus-like syndrome.
Give examples of class 1B drugs.
Lidocaine
Mexiletine
Administration of lidocaine and mexiletine.
Lidocaine is IV only
Mexiletine is oral.
Effects on cardiac activity by class 1B drugs.
No change in phase 0 in normal tissue
APD will slightly decrease
Increased threshold of action potential
Decrease in phase 0 conduction in fast beating or ischaemic tissue.
Effects on ECG of class 1B drugs.
No changes in normal tissue.
In fast beating or ischaemic tissue there will be an increase in QRS.
Uses of class 1B drugs.
Acute ventricular tachycardia
Not used in atrial arrhythmias or AV junctional arrhythmias
Side effects of class 1B drugs.
Proarrhythmic but less so than class 1A.
CNS effects such as dizziness or drowsiness
GI problems.
Give examples of class 1C drugs.
Flecainide
Propafenone
Administration of flecainide and propafenone.
Oral or IV
Effects on cardiac activity by class 1C drugs.
Decreases phase 0 in normal tissue substantially.
Decreases automaticity by increasing threshold.
Increases the APD and also the refractory period.
Effects on ECG of class 1C drugs.
PR, QRS and QT all increase
Uses of class 1C drugs.
Supraventricular arrhythmias, fibrillation, flutter
Premature ventricular contractions
WPW syndrome.
Side effects of class 1C drugs.
Proarrhythmia and sudden death especially in chronic use and in structural heart disease.
Supraventricular arrhythmias
CNS and GI effects
Give examples of class 2 drugs.
Beta-blockers such as propanolol
bisoprolol
metoprolol
esmolol
Administration of class 2 drugs.
Propanolol: oral or IV
Metoprolol: IV or oral
Bisoprolol: oral
Esmolol: IV only (quick acting)
Cardiac effects of class 2 drugs.
APD increasing and refractory period as well. This is mostly in AV node to slow AV conduction velocity.
Decrease in phase 4 depolarisation
Effects on ECG of class 2 drugs.
Increased PR and decreased HR
Uses of class II drugs.
Treating sinus and catcholamine dependent tachycardia
Treating re-entrant arrhythmias at AV node
Protecting ventricles from high atrial rates in atrial flutter or atrial fibrillation
Side effects of class 2 drugs.
Bronchospasm
Hypotension
Do not use in partial AV block or acute heart failure
However can be used in stable heart failure.
Give examples of class 3 agents.
Amiodarone
Sotalol
Administration of amiodarone.
Oral or IV with a half-life of about 3 months.
Cardiac effects of amiodarone.
A K+ channel blocker which causes an increase in the refractory period and increased APD.
Decrease phase 0 and conduction.
Increase threshold
Decrease phase 4
Decrease speed of AV conduction
Effects on ECG of amiodarone.
Increased PR, QRS, QT and decreased HR
Uses of amiodarone.
Very wide spectrum and effective for most arrhythmias and ventricular tachycardia
Side effects of amiodarone
Pulmonary fibrosis
Hepatic injury
Increase LDL cholesterol
Thyroid disease
Photosensitivity
Optic neuritis
Interaction of amiodarone with digoxin and warfarin.
May have to reduce if they are on digoxin or warfarin as well.
Montoring.
Administration of sotalol.
Oral
Cardiac effects of sotalol.
Increase in APD and refractory period in atrial and ventricular tissue
Slow phase 4 down
Slow AV conduction
ECG effects of sotalol.
Increase in QT and decrease in HR
Uses of sotalol.
Wide spectrum but specifically supraventricular and ventricular tachycardia.
Side effects of sotalol.
Proarrhythmia
Fatigue
Insomnia
Give examples of class 4 drugs relevant to the heart.
Non-dihydropyridines such as verapamil (phenylalkylamine) and diltiazem (benzothiazapine).
Administration of class 4 drugs.
Verapamil either oral or IV
Diltiazem is oral
Cardiac effects of class 4 drugs.
Slows conduction through AV node (Ca2+)
Increased refractory period in AV node
Increases slope of phase 4 in SA to slow HR
Effects on ECG of class 4 drugs.
Increase in PR
Could either be an increase or decrease in HR.
Uses of class 4 drugs.
Supraventricular tachycardia
Treat re-entry around AV node
Side effects of class 4 drugs.
Caution when partial AV block is present because it can cause asystole if taken with beta-blockers.
Hypotension
GI (constipation)
Administration of adenosine.
Rapid IV bolus with a very short half-life of just a few seconds.
Mechanism of adenosine.
Bind to A1 receptors causing inhibition of adenylyl cyclase.
This inhibits opening of Ca2+ channels leading to an increase in refractory period in AV node.
It also activates K+ currents and increases the K+ conductance/permeability leading to K+ leaving the cell.
This will decrease APD but also hyperpolarize the cell leading to a drop in heart rate.
Effectively it causes a transient heart block.
Cardiac effects of adenosine.
Slows AV conduction by the hyperpolarisation of the AV node.
Uses of adenosine
Treat re-entrant supraventricular arrhythmias by blocking the AV node to allow normal sinus rhythm to resume.
Diagnosis of coronary artery disease.
Administration of Vernakalant.
IV bolus over 10 minutes.
Mechanism of action of Vernakalant.
Blocks atrial specific K+ channels
Cardiac effects of vernakalant.
Slows atrial conduction and the potency increases with higher heart rates.
Side-effects of Vernakalant.
Hypotension
AV block
Sneezing and taste disturbances
Uses of vernakalant.
Convert recent onset atrial fibrillation to normal sinus rhythm
Administration of Ivabradine.
Given orally in 2.5 mg dosing up to 10mg
Mechanism of action of Ivabradine
Blocks funny current especially in SA node
Cardiac effects of Ivabradine.
Slows the SA node however it doesn’t affect blood pressure.
Side effects of Ivabradine
Flashing lights
Teratogenicity not known but avoid in pregnancy
Uses of ivabradine.
Reduce inappropriate sinus tachycardia
Reduce heart rate in heart failure and angina
Vasovagal syncope
Postural orthostatic tachycardia syndrome
Mechanism of digoxin.
Enhances vagal activity by increasing K+ currents and decreasing Ca2+ and increasing refractory period.
This leads to a slower AV conduction and slower HR.
Uses of digoxin.
Treatment to reduce ventricular rates in atrial fibrillation and flutter.
When should digoxin not be used.
In kidney failure because it is excreted renally.
Mechanism of atropine.
Selective muscarinic antagonist
Cardiac effects of atropine.
Block vagal activity to speed AV conduction and increase heart rate.
What is atropine used for?
Treat vagal bradycardia
How does the efficacy of the different antiarrhythmic drugs relate to the safety of the drugs.
The more effective a drug is the less safe it is. An examples is amiodarone.
Which drugs could be used in AF?
Something to control the rate and slowing the conduction through AV node.
E.g. Bisoprolol, verapamil, diltiazem and maybe digoxin.
If wanting to control the rhythm then sotalol, flecainide with bisoprolol or amiodarone.
Which IV drug for ventricular tachycardia?
Metoprolol/bisoprolol
Lignocain/mexiletine
Amiodarone
IV metoprolol/lignocaine or amiodarone
Should flecainide be used alone in atrial flutter?
No. Give AV nodal blocking drugs to reduce ventricular rates in atrial flutter.
Best drugs for treatment of WPW?
Flecainide
Amiodarone
List drugs that could be used in re-entrant narrow complex tachycardia.
Acutely IV adenosine, verapamil or flecainide.
If chronic then bisoprolol, verapamil, sotalol, flecainide or procainamide orally.
Which drugs for ectopic beats?
Bisoprolol first line
Flecainide, sotalol or amiodarone
Which drugs to treat sinus tachycardia?
Ivabradine due to no drop in BP
Bisoprolol or verapamil.
