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