Antiarrhythmics

Question 1

Which two neurotransmitters control the heart?

Answer 1

Ach (parasympathetic) and noradrenaline (sympathetic)

Question 2

What are the ways an arrhythmia can originate?

Answer 2

From and ectopic focus, or by a re-entry mechanism.

Question 3

How do you class antiarrhythmic drugs?

Answer 3

1) Supraventricular drugs
2) Ventricular drugs
3) Both types

Question 4

How would you treat arrhythmias triggered by stress conditions?

Answer 4

Beta-blockers

Question 5

How would you treat a sinus bradychardia and when do they commonly occur?

Answer 5

I.V. atropine, common after acute MI

Question 6

What is a problem common to many antiarrhythmics?

Answer 6

They can induce lethal arrhythmias

Question 7

How effective are antiarrhythmics?

Answer 7

Apart from b-blockers and maybe amiodarone in MI, there is no evidence that antiarrhythmics reduce mortality in any condition.

Question 8

What sort of intervention is preferable to drugs in arrhythmia?

Answer 8

Invasive procedures and devices are preferable in serious arrhythmias.

Question 9

What are the two depolarising currents in heart cells?

Answer 9

Na+, Ca++

Question 10

What is the single depolarising current in the SA and AN node?

Answer 10

Ca++

Question 11

What is significant about having a single current in the AN and SA nodes?

Answer 11

Ca ++ currents depolarise more slowly than NA+ currents so there is a delay between atrial and ventricular depolarisation and contraction.

Question 12

What type of calcium channels are present in the AV and SA node?

Answer 12

L-type calcium channels

Question 13

How does vagal stimulation of the heart reduce the heart rate?

Answer 13

Vagal fibres release ACh onto M2-type muscarinic receptors.

This opens a K+ channel via G-protein coupling.

The influx of K+ creates a hyper polarising current and decreases the slope of the pacemaker potential.

This the threshold for firing is reached later and the heart beat slows.

ACh also inhibits atrioventricular conduction.

Question 14

How does sympathetic stimulation increase heart rate?

Answer 14

Sympathetic fibres release noradrenaline onto Beta-1 receptors in the pacemaker tissues and myocardium.

Noradrenaline increases the inwards Na+ so threshold is reached earlier and the heart rate increases.

Noradrenaline also increases the force of contraction by increasing the amount of Ca++ to enter the cell during the plateau phase.

Question 15

Name the drugs used in supraventricular arrhythmias

Answer 15

Adenosine
Digoxin
Verapamil

Question 16

How does Adenosine work and how is it administered?

Answer 16

Adenosine stimulates Adenosine-1 receptors and opens ACh sensitive K+ channels.

This hyperpolarises the cell membrane in the AVN, and by inhibiting the Na+ channels, slows conduction.

To terminate paroxysmal supraventricular tachycardia it is administrated IV.

Question 17

How dies Digoxin work and how is it administered?

Answer 17

It stimulates vagal activity by causing the release of ACh, which slows conduction and prolongs the refractory period in the bundle of His.

Administered both orally and IV, depending on the severity and rate of the atrial fibrillation or flutter.

Question 18

How does Verapamil work and how is it administered?

Answer 18

It works buy blocking L-type channels, so has particularly powerful affects on the AVN where conduction is entirely dependent on Ca++ spikes.

It also has a negative inotropic effect as it blocks the of Ca++ during the plateau phase.

It has largely been replaced in IV form by Adenosine, which is much safer.

It is still administered orally for the prophylaxis of supraventricular tachycardia.

Question 19

When should Verapamil not be used?

Answer 19

It should not be used in conjunction with Beta-blockers or quinidine because of the cumulative negative inotropic effects.