Cardiac Arrhythmia Drugs Flashcards
What is torsades de pointes?
A life threatening form of ventricular tachycardia that arsises from long QT intervals
What can cause arrhythmia?
When there is a disturbance in:
- Pacemaker impulse formation
- Contraction impulse conduction (through tissues)
- Or both
What is the consequence of arrhythmia?
Results in rate/ timing of contraction of the heart that may be insufficient to maintain normal cardiac output
Identify the movement of ions in cardiac action potentials in the ventricles
What is the MoA of class 1 antiarrythmics?
block Na+ channel
slows conduction through the tissue
Name 2 class 1 antiarrhythmics
Flecainide (1c)
Lidocaine (1b)
What is the mechanism of action of class 2 antiarrhythmics?
Beta adrenoreceptors blockers
Diminish phase 4 depolarisation and automaticity
Name a class 2 antiarrhythmic
Bisoprolol
What is the MoA of class 3 antiarrhythmics?
Block the K+ channel
Extend the refractory period increasing action potential duration
Name 2 class 3 antiarrhythmics
Amiodarone
Sotalol
What is the MoA of class 4 antiarrhythmics?
Calcium channel blockers
Prolong the plateu of the action potential and decrease spontaneous depolarisations
Name 2 class 4 antiarrhythmics
Diltiazem
Verapamil
Descibe the movement of ions in the SA/ AV node (slow action potential)
How do calcium channel blockers affect the SA/AV node action potential?
Slow conduction velocity by slowing pace maker cell depolarisation
What is Wolf-Parkinson- White syndrome?
A condition where accessory pathways exist within the heart called The Bundle of Kent
Causes re-entry loops that avoid the AV node → tachycardia
How can tachycardias arrise following myocardial infarcts?
Following M.I, scar issue is imperfect
Allows micro-re entry loops
What are the aims of drugs given if an arrhythmia is due to abnormal generation?
- To decrease the action potentials in pacemaker cells (Beta blockers, Calcium channel blockers)
- Raise the threshold for action potentials to occur
What are the aims of drugs given if an arrhythmia is due to abnormal conduction?
- To reduce conduction velocity through the tissues (Class 1)
- Increase the refractory period so cell can’t be reexcited again (Class 3)
What drugs fall in to each category of the Vaugh Williams Classification?
What are the effects of class 1A agents antiarrhythmics? (Procainamide, quinidine, disopyramide)
- Decrease conduction of AP
- Increase refractory period
- Decrease autamaticity
- Increase threshold for AP
What are the side effects of Class 1A antiarrhythmics?
- Hypotension - reduced CO
- Proarrhytmic due to increased QT interval
- Dizziness, confusion, insomnia, seizure (at high doses)
- GI effects (common)
- Lupus like syndrome (esp procainamide)
What are the 2 class 1B antiarrhythmics, how must each be given?
Lidocaine: IV only
Mexiletine: oral
What are the effects on cardiac activity of class 1b antiarrhytmics?
- No change in phase 0 in normal tissue
- Increase threshold for action potnetials
- Decrease phase 0 in fast beating/ ischemic tissue
In which situations would you use class 1b antiarrhythmics?
Acute ventricular tachycardia (especially during ischemia)
What are some of the side effects of class 1b antiarrhythmics?
- GI upset (most common)
- CNS effects: dizziness, drowsiness
- Less proarrhythmic than class 1a
What are the effects of class 1c antiarrhythmics on cardiac activity?
- Substantial decrease of phase 0 in normal tissue
- decrease automacitiy
- Increase refractory period
What are the effects of class 1c antiarrhythmics on an ECG?
- Increase PR interval
- Increase QRS interval
- Increase QT interval
When would you use class 1C antiarrhythmics? (Flecainide, Propafenone)
- Supraventricular arrhythmias (fibrillation and flutter)
- Pemature ventricular contractions
- Wolf-Parkinson-White syndrome
What are the some the side effects of class 1C antiarrhythmics?
- Proarrthymic and sudden death especially with chronic use and strucutal heart disease
- Increase ventricular response to supraventricular arrhythmias
- CNS and GI effects
Describe the absorption and elimination of class 2 agents; propanolol, metoprolol, bisoprolol, esmolol
Propanolol: oral and IV
Metoprolol: oral (short acting), IV
Bisoprolol: oral only
Esmolol: IV only (v short acting t1/2 9 min)
What are the cardiac effects of class 2 antiarrhythmics?
- Increase refractory period in AV node to slow AV conduction velocity
- Decrease phase 4 depolarisation
When would you use class 2 antiarrhythmics?
- Sinus and catecholamine dependent tachycardias
- Converting reentrant arrhythmias at AV node
- Protect ventricles from high atrial rates (slow AV conduction) in atrial flutter/ fibrillation
What are some of the side effects of class 2 antiarrhythmics?
- Bronchospasm
- Hypotension
- Not to be used in partial AV block or acute heart failure
How can you administer amioderone (Class III agent)?
Oral or IV through a central line only
(T 1/2 of around 3 months)
Why can amioderone not be given by IV peripherally?
Thromboplebitic if given peripherally
What are the effects of giving amioderone (class 3 agent) on cardiac tissue?
- Increases refractory period
- Decreases phase 0 and conduction
- Increases threshold for next AP
- Decreased phase 4
- Decreases speed of AV condution
What are the effects of amioderone on the ECG?
- Increase PR
- Increase QRS
- Increase QT
- Decrease HR
In what circumstances would you give amioderone?
Very wide spectrum, effective for most arrthymias
(especially life threatening ventricular tachycardia)
What are some of the side effects of amioderone?
- Pulmonary fibrosis
- Hepatic injury
- Increase LDL cholesterol
- Thyroid disase
- Photosensitivity
- Optic Neuritis (transient blindness)
Risk of these increases with time
How do you administer Class III antiarrhythmic sotalol?
Oral only
What are the side effects of class III agent Sotalol?
- Proarrhythmic
- Fatgiue
- Insomnia
How do you administer the 2 class IV antiarrhythmics verapamil and diltiazem?
Verapamil: orally or IV
Diltiazem: orally only
When would you use class IV antiarrhythmics?
- Control the ventricles during supraventircular tachycardias
- Stop re-entry loops around AV node
What are some of the side effects of class IV antiarrhythmics?
- Use with caution when AV block present
- Can get asystole if given with Beta blockers
- Hypotension
- Decreased CO
- GI problems (constipation)
What is the mechanism of action of Adenosine in treating arrhythmia?
- natural nucleoside binds to A1 receptors at AV/ SA node
- Activates K+ currents
- Hyperpolarisation of cell
- Decreases heart rate by slowing AV conduction
When would you give adenosine as an antiarrhythmic?
- Re-entrant loops in supraventricular tachycardia
- When scanning the heart to diagnose coronary artery disease
What is the only way to administer adenosine
IV bolus dose
Very short acting half life of seconds
What is the mechanism of action of ivabradine?
Blocks the If ion highly expressed in SA node
Slows the SA node but does not affect blood pressure
When would you use ivabradine?
- Reduce innapropriate sinus tachycardia
- Reduce heart rate in heart failure and angina
What is the mechanism of action of digoxin?
Slows AV conduction and slows HR by enhancing vagal activity
Used to reduce ventricular rates in atrial fibrillation and flutter
What is the mechanism of action of atropine in treating bradycardia?
Selective muscarinic antagonist, blocks vagal activity to speed up AV conduction and increase HR
Why should flecainide not be used alone to treat atrial flutter?
Flecainide alone causes pro-arrhythmic effect
Need to give alongside AV node blocking durgs to reduce ventricular rate
What drug is used first line to treat ectopic beats?
Bisprolol
