arrhythmia drugs Flashcards
what is an arrhythmia?
examples?
an anormality in heart rate or rhythm
atrial fibrillarion, ventricular fibrillation, tachycardias (supraventricular and ventricular)
some causes of arrhythmias- specifically tachycardias?
- ectopic pace maker activity (a damaged area depolarises or ischaemia causes latent pacemaker)
- afterdepolarisations - abnormal depolarisation following the AP
- atrial flutter and AF - creates many depolarisations - some will get transmitted
- re entry loop
some causes of arrhythmias? specifically brady cardia?
- conduction block e.g. heart block = slows conductions, also some drugs slow contraction (extrinsic factors)
- sinus bradycardia - sick sinus syndrome (SA node is dysfunctional) and also some drugs (extrinsic factor)
what are early after depolarisations?
EADs occur when thre is a prolonged QT wave - this give more tome for Ca2+ channels to recover and fire again creating an oscillation
e.g. hypokalaemia
what are delayed after depolarisations?
when is it more likely to happen?
what can it cause?
when there is a depolarisation after the repolarisation and its not meant to be there
more likely to happen in high intracellular ca2+ - can involve NCX which can cause depolaristion to threshold and create AP and tachycradia
tachycardia ans oscillations
what are re entrant mechanisms that generate arrhythmias?
what can multiple re-entrant circuits in the atria lead to?
when there is incomplete conduction damage the electric signal is not completing the normal circuit, but rather an alternative circuit looping back upon itself - set sup a circus of excitation
atrial fibrilation - irregularly irregular tachycardia
what does AV nodal re-entry cause?
what does an accessory pathway between atria and ventricles cause?
what syndrome?
loop in AV node = tachycardia
creates a re entry pathway between atria and ventricles = supraventricular tachycardia
cuases Wolff-Prkinson-White syndrome
what are the 4 classes of drugs to treat arrhythmia ?
- volatge gated sodium channel blockers
- B adrenoreceptor antagonists
- postassium channel blockers
- calcium channel blockers
exampe of class 1 drug? (Na+ channel blocker)
what state does the channel have to be in to be blocked?
what kind of tissue does it block?
what effect does it have?
use?
what other use does lidocane have?
lidocane
open or inactive
therefore it blocks damaged and depolarised tissue (will be open or inactive)
bound for long enough to prevent inappropriate depolarisations, and will quickly dissociate in time for the next AP - slows upstroke and shortens AP and slows conduction velocity
Can be used after an MI or VF but not often
local anaesthetic as well as an anti-arrhythmic.
example of a class 2 drug (B antagonists)
why do they do?
when is it used?
proppranolol, anteolol (beta blockers)
bind to B1 in the heart and reduce the SNS- NA cannot activate - this decreases slope of pace maker potential and less L type ca channels can open
after an MI as sympathtic activity is usually high, reduce O2 demand to stop ischaemia after MI, prevent supraventricular tachycardia (AF - slows conduction at AV so allows ventricles to recover snd refill)
give an example of class 3 drug? (block K+ channels)
what do they do?
what are the issues with this?
why is amiodarone used then?
amiodarone
prolong AP
pro-arrhythmic as it creates a longer QT interval
it has other actions as well as blocking K+ channels - treat Wolff-Parkinson-White syndrome tachycardia (re entry thing) and supress ventricular arrhythmia post MI
example of class 4 drug? (block Ca2+ channels)
what do they do?
what does non - dihydropyridine type mean?
verapamil, diltiazem (non - dihydropyridine)
decrease slope of AP at SA node, decrease AV conduction, slow conduction, it decreases introtopic and chondrotropic effects
it means that they effect cardiac muscle where dihydropyridine type act on vascular smooth muscle
what is adeosine?
when is it amdministed intravenously?
why is it used?
it is a substance produced endogenously?
it is given to a patient at high concentrations and enhances the K+ conductance meaning it will hyperpolarise well = allows the heart to stop and reset with proper timings
it is anti-arrhythmic ans useful for supraventricular re entrants
