Session 7: Cardiac Arrhythmias and CVS Drugs CHECK CARD 22 AGAIN Flashcards
What are cardiovascular drugs used to do?
To treat arrhythmias, heart failure, angina, hypertension and risk of thrombus formation.
Causes of tachycardia.
Ectopic pacemaker activity Afterdepolarisations Atrial flutter/fibrillation Re-entry loop by conduction delay or accessory pathway
Causes of bradycardia.
Sinus bradycardia like sick sinus syndrome or extrinsic factors such as drugs like beta-blockers and some Ca2+ blockers. Conduction block like problems at AV node or bundle of His.
Common cause of delayed after-depolarisation?
If intracellular Ca2+ high but it happens after repolarisation.
Explain re-entrant mechanism leading to the generation of an arrhythmia.
When there is incomplete conduction damage also called uni-directional block the excitation can take a long route to spread the wrong way through the damaged area setting up a circus of excitation. Multiple small re-entry loops in the atria can lead to atrial fibrillation.
Cause of AV nodal re-entry loop.
Fast and slow pathways in the AV node create a re-entry loop.
Cause of ventricular pre-excitation.
If there is a breach in the fibrous ring leading to an accessory pathway between ventricles and atria. This can cause an re-entry loop called Wolff-Parkinson-White syndrome
There are 4 basic classes of anti-arrhythmic drugs. Which?
I - Drugs that block voltage-sensitive sodium (Na+) channels II - Antagonists of B-adrenoceptors III - Drugs that block potassium (K+) channels IV - Drugs that block calcium (Ca2+) channels
Give an example of Class I which block voltage-dependant Na+ channels.
Local anaesthetic lidocaine
Explain how Class I drugs work.
They only block voltage gated Na+ channels in open or inactive state. This means that they preferentially block damaged depolarised tissue like in an MI.
Does class I drugs work on normal cardiac tissue?
It has little to no effect because it dissociates rapidly.
Explain use of lidocaine.
Can be used sometimes following an MI however only if patient shows signs of ventricular tachycardia. This is given intravenously. Damaged areas of myocardium may be depolarised and fire automatically and randomly independent on any other input. More Na+ channels are open in depolarised tissue so lidocaine works by blocking these Na+ channels and prevents the automatic firing of depolarised ventricular tissue.
Give example of Class II b-adrenoceptor antagonists.
Propanolol and atenolol.
Briefly explain how Class II drugs work.
Block sympathetic action on b1-adrenoreceptors in the heart. They decrease slope of pacemaker potential in SA node and slows conduction at AV node.
What are Class II drugs used for?
It can prevent supraventricular tachycardia to slow down the heart rate. It also slows ventricular rate in patients with atrial fibrillation. Can be used following MI because MIs often causes increased sympathetic activity. They also prevent ventricular arrhythmias. Also reduces O2 demand.
Explain how Class III K+ channel blockers work.
They prolong action potential by blocking K+ channels to lengthen the absolute refractory period.
In theory this should prevent another AP occuring to son but instead in reality it can be pro-arrhythmic instead by prolonging QT interval.
Class III K+ blockers are not used a lot because of the risk of being pro-arrhythmic instead of helping.
However there is an exception of something used. Which drug?
Amiodarone.
Explain why amiodarone is used.
It is called a dirty drug because it doesn’t only have one action.
It has other actions as well as blocking K+ channels.
It can be used to treat tachycardia associated with Wolff-Parkinson-White syndrome (re-entry loop disease).
It is also effective for suppressing ventricular arrhythmias after an MI.
Give examples of Class IV Ca2+ channel blockers.
Verapamil and diltiazem which are non-dihydropyridine types.
Explain how non-dihydropyridine class IV drugs work lie verapamil and diltiazem.
They decrease the slope of action potential at the SA node.
They decrease AV nodal conduction as well (same slope as in SA node)
Decrease force of contraction and also some coronary and peripheral vasodilation.