Antiarrhythmic drugs Flashcards
Which ion channel/receptor do class 1 agents block?
Voltage gated sodium channels
Which ion channel/receptor do class 2 agents block?
Beta 2 adrenoceptors
Which ion channel/receptor do class 3 agents block?
Voltage activated K+ channels
Which ion channel/receptor do class 4 agents block?
Voltage activated Ca++ channels
Give an example of a class 1A agent and what does it do?
Disopyramide
Causes a slow rise of AP and prolongs the refractory period
Give an example of a class 1B agent and what does it do?
Lignocaine
Prevents premature beats and causes a slow rise of the AP
Give an example of a class 1C agent and what does it do?
Flencainide
Greatly slow rise of the AP and depress conduction
Give an example of a class 2 agent and what does it do?
Metoprolol
Decrease the rate of depolarisation in SA and AV nodes
Give an example of a class 3 agent and what does it do?
Amiodarone
Prolong the AP and increase the refractory period
Give an example of a class 4 agent and what does it do?
Verapamil
Slow conduction in SA and AV nodes and decrease the force of contraction
What is the difference between Class 1 A, B and C agent?
Related to the speed at which the drug associates and dissociates from the voltage activated sodium channels
1A = moderate rate
1B = Fast rate
1C = Slow rate
Class 1 agents work in a use dependent manor. What does this mean?
During tachyarrythmias relatively more time is spent with Na+ channels in the open or inactivated state. Class 1 agents will block the Na+ channel in the open state or they stabilise the inactivated state preventing another AP. Overall, class 1 agents have little effect on myocardium beating at normal frequency, but a big effect when its beating fast.
Is the association or dissociation rate of class 1 agents the more important determinant of steady state block (bad thing generally) of Na+ channels and why?
Dissociation rate as class 1 agents dissociate when Na+ channels are in the resting state (diastole) If heart rate increases, less time is available for dissociation and more time available for association => steady state block increases, especially for agents with a slow dissociation rate (class C)
When the myocardium is ischemic, does action potential firing increase or decrease and why?
Why is it good?
Increase because the myocytes are partially depolariesed and the AP is a longer duration. This means the inactivated state of the AP is available for a longer period of time and the rate of channel recovery from block is decreased. Good because class 1 agents can block arrhythmia at its source
Which anti arrhythmic drug classes are used in atrial arrhythmias and give examples of these?
Class 1C = Flecainide
Class 3 = Amiodarone
Which anti arrhythmic drug classes are used in ventricular arrhythmias and give examples of these?
Class 1A = Disopyramide
Class 1B = Lignocaine
Class 2 = Metoprolol
Which anti arrhythmic drug classes are used in AV nodal arrhythmias and give examples of these?
Class 2 = Metoprolol
Class 4 = Varapamil and diltiazam
Adenosine and Digoxin
Which anti arrhythmic drug classes are used in atrial + ventricular + AV accessory pathway arrhythmias and give examples of these?
Class 1A = Disopyramide
Class 1C = Flencainide
Amiodarone and Setalol
What is Adenosine used for?
Terminate Paroxysmal Supraventricular Tachycardia caused by re-entry involving the SA or AV node or atrial tissue
What is the pharmacological action of adenosine?
Activates A1 adenosine receptors coupled to Gi/o
Opens ACh sensitive K+ channels (GIRK)
Hyperpolarises the AV node briefly suppressing impulse conduction.
How is adenosine administered?
IV bollus injection of 6mg
What is digoxin used for?
To treat atrial fibrilation
What is the pharmacological action of digoxin?
Stimulates vagal activity. Slows conduction and prolongs refractory period in AV node and bundle of His
How is digoxin administered?
IV infusion or oral. You must monitor the levels of digoxin in the blood because it has a narrow therapeutic index
