Arrhythmias & Drugs Flashcards
1
Q
What does Ectopic pacemaker activity cause
A
- Tachycardia
- Damaged area of myocardium becomes depolarised and spontaneously active
- Latent pacemaker region activated due to ischaemia - dominates over SA node
2
Q
What are the effects of afterdepolarisations
A
- Tachycardia
- Abnormal depolarisations
- Delayed after-depolarisation following the action potential (triggered activity)
- More likely to happen if intracellular calcium high
- Early after-depolarisation - oscillation during action potential
- More likely to happen if action potential prolonged
- Longer AP - longer QT interval
- Delayed after-depolarisation following the action potential (triggered activity)
3
Q
Explain the different re-entry loop mechanisms
A
- Re-entrant mechanism for generating arrhythmias
- Normal excitation spreads both ways and cancel each other out
- Refractory period prevents further depolarisation
- Block of conduction still normal conduction
- Incomplete conduction damage - Re-entry loop
- Can cause atrium to be overstretched and atrial fibrillation
- Normal excitation spreads both ways and cancel each other out
- AV nodal re-entry causes supraventricular tachycardia
- Fast and slow pathways in AV node cause re-entry loop
- Ventricular pre-excitation
- Accessory pathway between atria and ventricles
- Leads to tachycardia and possible fibrillation
- Drop in cardiac output as heart not filling completely
- Eg. Wolff-Parkinson-White syndrome
4
Q
What are some causes of sinus bradycardia
A
- Sick sinus syndrome - intrinsic SA node dysfunction
- Extrinsic factors such as drugs (beta blockers, Ca channel blockers)
5
Q
What are some causes of conduction block
A
- Problems at AV node or bundle of His
- Slow conduction at AV node due to extrinsic factors (drugs)
6
Q
Explain the therapeutic use of Class I anti-arrhythmic drugs
A
- Drugs which block voltage dependent sodium channels
- Local anaesthetic - eg. Lidocaine
- Use dependent - only block Na channels in open or inactivated state
- Little effect on normal cardiac tissues - dissociates quickly
- Does not affect closed channels
- Blocks during depolarisation in damaged areas but dissociates in time for next action potential
- Sometimes used following MI - only if patient shows ventricular tachycardia signs
- Damaged areas of myocardium may be depolarised and fire automatically
- More sodium channels are open in depolarised tissue - prevents automatic firing
- Not used prophylactically following MI - even in patients showing VT generally use other drugs
7
Q
Describe the therapeutic use of Class II anti-arrhythmic drugs
A
- Beta-adrenoceptor antagonists
- Block sympathetic action - eg. Propranolol, atenolol
- Decrease slope of pacemaker potential in SA and slow conduction at AV node
- Reduce funny current and reduce opening of Ca channels
- Beta-blockers
- Slow conduction in AV node - prevent supraventricular tachycardias
- Used following MI - sometimes causes increase sympathetic activity
- Prevent ventricular arrhythmias due to sympathetic activity
- Reduce oxygen demand
- Reduce MI
8
Q
Describe the therapeutic use of Class III anti-arrhythmic drugs
A
- Block potassium channels
- Prolong the action potential - lengthens absolute refractory period to prevent another action potential
- However can be pro-arrhythmic
- Amiodarone - not only blocks K channels, but also blocks Ca channels and beta blocker
- Treat tachycardia with re-entry problems (Wolff-Parkinson-White syndrome)
- Suppressing ventricular arrhythmias post MI
9
Q
Describe the therapeutic use of Class IV anti-arrhythmic drugs
A
- Block calcium channels
- Verapamil
- Decrease slope of action potential at SA node
- Decrease AV nodal conduction
- Decrease force of contraction (negative inotropy) - decrease plateau phase
- Dihydrophridine Ca channel blockers not effective in preventing arrhythmias
- Act on vascular smooth muscle
10
Q
Explain the therapeutic use of adenosine
A
- Produce endogenously but also can be administered IV
- Acts on A1 receptors at AV node
- Very short half life - 10 seconds
- Enhance potassium conductance - hydropolarises cells
- Anti-Arrhythmic - useful in treating re-entrant supraventricular tachycardia
11
Q
What type of drugs are used to treat heart failure
A
- Positive inotropes to increase cardiac output (not often used)
- Eg. Cardiac glycosides - treat symptoms but not long term outcome
- Eg. ß-adrenoceptor agonists - dobutamine
- Drugs which reduce work load of heart - better in the long run
12
Q
Explain the mechanism of cardiac glycosides
A
- Digoxin - blocks Na/K ATPase
- By blocking Na/K ATPase, sodium concentration inside increases
- NCX activity decreases leads to increase in calcium concentration inside
- Calcium becomes stored in SR via SERCA
- Increase calcium available to be released in action potential and increase force of contraction
- Glycosides also act on neurones in cardiac control centre to increase vagal activity
- Slows AV conduction and slows heart rate
- Used when patients have heart failure and arrhythmias such as AF
13
Q
Explain the mechanism of ß-adrenoceptor agonists
A
- Act on ß1 receptors in heart
- Stimulate Gαs stimulates adenylyl cyclase to convert ATP to cAMP
- Made into PKA which phosphorylates L-type calcium channels, thereby increase calcium in SR available for contraction
- Also opens VOCC responsible for pacemaker currents in SA node
- Patients in cardiogenic shock, acute but reversible heart failure (following cardiac surgery)
14
Q
What are drug types which reduce workload
A
- ACE inhibitors - prevent conversion of angiotensin I to angiotensin II
- Reduce sodium and water retention - reduce preload of heart
- Reduce vasoconstriction (reduce blood pressure) - reduce afterload of heart
- Less blood returning to heart - due to starlings law, reduces cardiac output
- Or use angiotensin II blocker
- Could also use beta-blockers or diuretics
15
Q
What types of drugs can alleviate angina
A
- Reduce workload of the heart - ß-blockers, Ca channel antagonists, organic nitrates
- Improve blood supply to the heart - Ca channel antagonists, organic nitrates
