Arrhythmia drugs Flashcards
Which class of drugs do procainamide and quinidine belong to?
Class 1a
What is the mode of action of class 1a drugs such as procainamide and quinidine? (3)
Moderate sodium channel blockers- slow depolarisation, slow conduction velocity and prolong repolarisation.
What class of drugs to propanolol, bisoprolol, atenolol and metoprolol belong to?
Class 2
Describe the mode of action of class 2 antiarrhythmics such as propanolol (3)
They are beta blockers- slows depolarisation and slow funny currents of SAN to slow HR, they also increase refractory period at AVN.
Name one class 1c antiarrhythmic.
Flecainide
What is the mode of action of class 1b drugs like lidocaine?
Class 1b dissociate from the sodium channels very quickly, so have no effect on sodium channels in normal tissue, but in ischaemic/ depolarised tissue they’ll inactivate the open sodium channels and repolarise the tissue.
What is the difference between mode of action of class 1 a and c drugs?
Class 1c drugs dissociate from the sodium channels more slowly so cause more marked increase in threshold and decreases in conduction velocity.
Give 2 examples of a class 3 anti- arrhythmic
amiodarone
How does amiodarone work?
Block K+ channels- alone this extends refractory period to slow conduction and terminate arrythmias, but may lead to early after depolarisations. For this reason it also has some Class 1, 2 and 4 actions as well
How does sotalol work?
Blocks K+ channels and is also has some beta- blocker properties
What class of drugs does verapamil and amlodopine belong to?
class IV
Other than verapamil and amlodipine, name one other class IV anti- arrhythmic?
Dilitazem
How do class IV anti- arrhythmics such as dilitazem and verapamil work?
Blocks Ca2+ channels- mainly in the AVN, to slow conduction and increase refractory period and increase the threshold for conduction.
How does adenosine work?
Binds to A1 receptors, activating K+ channels in SAN and AVN, causing hyperpolarisation and so a drop in HR, it also binds to Ca2+ channels in the AVN, increasing the refractory period.
How does vernakalent work?
Blocks K+ channels in the atria only- slowing atrial conduction, so helping to terminate atrial fibrillation
How does ivrabradine work?
Blocks HCN/ funny current channels in the SAN. This slows HR, but doesn’t affect contractility or work systemically so maintains BP- unlike B- blockers.
How does digoxin work? (2)
It is a cardiac glycoside, so increases vagal activity- increase k+ conduction, decrease Ca2+ channels and increase refractory period in AVN to slow HR.
It also inhibits Na/K/atpase so Na+ builds up, NCX swaps and Ca2+ enters, which increase contractility- thus maintaining good CO even though HR drop.
How does atropine work?
Muscarinic antagonist, so increases HR.
