L8- Arrythmias Flashcards
What are the causes of arrhythmia?
AMI Heart failure Hyperthyroidism Hypokalaemia Autonomic dysfunction Certain drugs Cardiac ion channel dysfunction Fever
How are arrhythmia initiated?
When the heart beat originates in a place other than the SA node it is due to abnormal pacemaking (automaticity) or failure of conduction to stop at the end of the heart beat (re-entry).
What is the mechanism of re-entry?
Caused by localised slow conduction due to depolarisation (sometimes in infarct tissue).
This makes wave front become jagged and split and then may circle around and re-enter original pathway. Causes slow retrograde conduction and a spiral wave front.
What are the types of ventricular arrhythmia?
Ventricular premature beat- mildest type, not treated
Ventricular fibrillation- severest type, rapidly lethal
How are arrhythmia’s maintained?
Via the mechanism of re-entry
Once re-entry loop starts it can be quite ‘stable’ and persistent.
What are the different classes of anti-arrhythmic drugs?
◘ Class I- Na channel blockers= Lidocaine, Quinidine, Flecainide
◘ Class II- B1 adrenoceptor antagonists= Atenolol, Metoprolol
◘ Class III- Depolarisation delay= Amiodarone, Sotalol
◘ Class IV- Ca antagonists= Verapamil, Diltiazem
Which classes of drugs are the most successful in treating ventricular arrhythmia’s?
Class I- Na channel blockers= Lidocaine, Quinidine, Flecainide
Class III- Depolarisation delay= Amiodarone, Sotalol
How are arrhythmia’s suppressed?
◘ Target re-entry or abnormal automaticity (not a major drug target)
◘ Re-entry is blocked by blocking conduction of the re-entry wave which can be done in 2 ways
◘ 1. Directly on the retrograde conduction region 2. Indirectly
How is re-entry blocked directly?
Achieved by localised blocking of ion channels responsible for depolarisation in damaged area.
Channel block makes damaged cells inexcitable (Na channels are targets in AV node, atria, ventricles)
Class I drugs e.g Lidocaine
What is the problem with direct blocking of re-entry?
Off-target effects of the drugs because they aren’t selective enough. They cause conduction slowing in surrounding healthy tissue.
Thus the drug may mimic ischaemia in healthy tissue and even cause re-entry there.
What is lidocaine?
Class 1b antiarrhythmic drug
Only given via I.V. (limitation)
More selective for Na channel than 1a drugs
Effective in VPB but no reduction in VF (death) in long term
What are the pros and cons of lidocaine?
+ Highly ischaemia selective
+ No effects in healthy heart regions
+ No tendency to increase risk of re-entry
- Has off-target effects on nerves
- Can cause paraesthesia and convulsions
- Only given by I.V.
How is indirect block of conduction achieved?
Delaying repolarisation anywhere in re-entry pathway (including healthy tissue)
Known as prolonging the ‘refractory period’ because cells are inexcitable during any AP. This means jagged wave fronts encounter fewer excitable cells and re-entry is blocked.
K channels mediate repolarisation so are the targets of Class III drugs.
What is amiodarone?
Class III antiarrhythmic drug which is used for VF prophylaxis
What are the pros and cons of amiodarone?
+ Little/no negative ionotropic effects
+ Reducess VF in MI
- Side (off-target) effects prevent long term use- corneal opacities, thyroid dysfunction
