Treatment of Dysrhythmias Flashcards
How can you classify dysrhythmias?
- atrial/supraventricular
- junctional (associated with AV node)
- ventricular
- tachycardia/bradycardia
What cardiac events can result in dysrhythmias?
- ectopic pacemaker activity
- delayed after-depolarisations
- circus re-entry
- heart block
What are the classes of antidysrhythmic drugs?
1: Na channel blockers
2: b-adrenoceptor blockers
3: K channel block
4: Ca channel block
Explain the mechanism of sodium channel blockers?
- can bind to channel to prevent other ligand from binding:
- inhibits AP propagation reducing rate of cardiac depolarisation
- can also bind to channel to keep it in its refractory period in a different conformation:
- maintains depolarisation keeping channels in inactive state
What subdivides the sodium channel blockers into different categories?
properties of the drugs in their binding to sodium channels in which state:
- open
- refractory
- resetting
What does ‘use-dependent’ mean?
- the drugs work more effectively if there is high activity so work better at abnormal high frequency and not well against normal beating rates
- applies to Na channel blockers
What is the clinical application of class 1 antidysrhythmics?
1a: disopyramide: ventricular dysrhythmias, prevents recurrent AF triggered by vagal over-activity
1b: lignocaine: treatment and prevention of ventricular tachycardia and fibrillation during and immediately after MI
1c: flecainide: suppresses ventricular ectopic beats, prevents paroxysmal AF and recurrent tachycardias associated with abnormal conducting pathways
Describe the mechanism of action of B-blockers
- block B-1 receptors to slow HR and decrease CO
- decreases rate of depolarisation of pacemaker cells and blocks calcium entry
- increases refractory period of AV node preventing recurrent supraventricular tachycardias
What are examples and clinical application of B-blockers?
- sotalol, bisoprolol, atenolol
- reduce mortality following MI and prevent recurrence of tachycardias provoked by increased sympathetic activity
Describe the mechanism of action of K channel blockers
prolongs the cardiac AP by prolonging the refractory period
What are the clinical applications of K channel blockers with specific examples?
- amiodarone: tachycardia associated with Wolff-Parkinson-White Syndrome and other supraventricular/ventricular tachyarrhythmias
- sotalol: combines class 2 and 3 actions, used in supraventricular dysrhythmias and suppresses ventricular ectopic beats
What is Wolff-Parkinson-White Syndrome?
- a heart condition featuring episodes of abnormally fast HR. Episodes can be for seconds/minutes/hours/days
- due to extra electrical conduction pathway in the heart
Describe the mechanism of action of CCBs
- blocks cardiac voltage gated L-type calcium channels
- slows conduction through SA and AV node
- shorten plateau of cardiac AP and decreases force of contraction
What is the clinical uses of CCBS with specific examples?
- verapamil: prevent recurrence of supraventricular tachycardias and ventricular rate in patients with AF (if they don’t have WPW Syndrome)
- diltiazem is similar to verapamil but has more effect on smooth muscle Ca channels
What does adenosine affect?
- breathing
- cardiac/smooth muscle
- vagal afferent nerves
- platelets
