Dysrhythmias

Question 1

What are escape beats and rhythms?

Answer 1

Dysrhythmias caused by extra beats generated by other pacemakers in the heart (e.g. AVN).

Question 2

What are premature beats and extrasystole?

Answer 2

• If other tissues in the heart depolarise faster than the SAN, an ectopic focus is formed, resulting in ectopic beats.
• If the focus is above the ring of insulating tissue in the heart, depolarisation resets SAN, which starts normal pacemaker activity again.
• If ectopic focus below insulating tissue, atria may contract independent of ventricles.

Question 3

What is ectopic tachycardia?

Answer 3

Sequence of 3 or more ectopic beats.

Question 4

What are the types of supraventricular tachycardias?

Answer 4

1. Atrial paroxysmal tachycardia: Ectopic pacemaker gives rise to episodes of tachycardia (100-180 bpm).
2. Atrial flutter: Ectopic pacemaker gives rise to atrial beating of 250-350 bpm heart rate, with only around half of these being converted to ventricular beats.

Question 5

What is atrial fibrillation?

Answer 5

Uncontrolled atrial beating at 500-600 bpm, with only impulses occasionally being converted to ventricular beats.

Question 6

What is ventricular paroxysmal tachycardia?

Answer 6

Ectopic pacemaker in ventricles cause abnormally fast rate of ventricular beating, independent of atria, which is especially problematic if ventricular beating exceeds atrial beating, resulting in insufficient cardiac output.

Question 7

What is ventricular fibrillation?

Answer 7

Uncontrolled ventricular beating, resulting in ventricles ‘quivering’ instead of pumping blood, causing severely reduced cardiac output and death if untreated.

Question 8

Why do class I anti-dysrhythmics only affect myocardium and not pacemaker tissue?

Answer 8

Na_vs are absent in pacemaker tissue

Question 9

What are the subgroups of type I anti-dysrhythmics?

Answer 9

1. Class IA: Intermediate associating/dissociating
2. Class IB: Fast associating/dissociating
3. Class IC: Slow associating/dissociating

Question 10

What are the binding properties of type IB anti-dysrhythmics?

Answer 10

• Class IB drugs (e.g. lidocaine) associate when the heart is depolarising (i.e. phase 0) as it has a very high affinity for activated NaVs. It is also associated during refractory period (phase 2,3) as it has even higher affinity for inactivated channels.
• During diastole, it dissociates quickly from the channels between APs as it has very low affinity for channels in resting state.

Question 11

What are the effects of class IB anti-dysrhythmics?

Answer 11

The drug prevents premature AP from firing during refractory period (as it is still associated and inhibits AP Na+ current), but has little effect on the duration of APs or the cardiac rhythm.

Question 12

What are the affinities of class IB drugs for different states of class IB drugs?

Answer 12

States:

• Resting: Very low
• Activated: Very high
• Inactivated: Very high (higher than activated)

Dissociation time: Fast

Question 13

What are the clinical uses of class IB drugs?

Answer 13

Treatment of ventricular dysrhythmias

Question 14

What are the binding properties of type IC anti-dysrhythmics?

Answer 14

• They associate when the heart is depolarising as they have high affinity for activated NaVs.
• However, because of their slow dissociation time, they remain bound to the NaVs throughout the whole of the cardiac cycle.

Question 15

What are the affinities of class IC drugs for different states of class IC drugs?

Answer 15

States:

• Resting: None
• Activated: High
• Inactivated: None

Dissociation time: Very slow

Question 16

What are the clinical uses of class IC anti-dysrhythmics?

Answer 16

1. Prevent paroxismal atrial fibrillation
2. Recurrent tachycardias (e.g. in Wolff-Parkinson- White syndrome)

Question 17

What are the binding properties of type IA anti-dysrhythmics?

Answer 17

Class IA drugs also associate when the heart is depolarising, and has a dissociating time between that of IB and IC. However, they still remain bound throughout the whole of the AP cycle, and so increase the duration of APs.

Question 18

What are the affinities of class IA drugs for different states of Na_vs and their dissociation time?

Answer 18

States:

• Resting: None
• Activated: High
• Inactivated: None

Dissociation time: Slow

Question 19

What are the clinical uses of class IA anti-dysrhythmics?

Answer 19

1. Treat ventricular dysrhythmias
2. Prevent recurrent paroxysmal atrial fibrillation

Question 20

Why are class II anti-dysrhythmics (β-blockers) effective at treating dysrhythmias?

Answer 20

1. Adrenaline can have dysrhythmic effects by altering pacemaker current.
2. Sympathetic over-activity may be a cause of ventricular dysrhythmias post-MI.
3. Inhibition of sympathetic activity may inhibit conduction through AV node and thus prevent certain dysrhythmias (e.g. SVTs).

Question 21

What are the clinical uses of class II anti-dysrhythmics?

Answer 21

1. Prevent development of dysrhythmias post MI
2. To prevent recurrent tachyarrhythmias (e.g. recurrent paroxysmal atrial fibrillation)

Question 22

What are the mechanisms of action of class III anti-dysrhythmics?

Answer 22

• Outward current inhibition: Inhibits K⁺ channels and thus lengthens AP by slowing down rate of repolarisation. This increases the length of refractory period and prevents premature beats.

Inward current inhibition: Inhibits Na⁺ channels (as well as perhaps Ca²⁺ channels). This suppresses excitability of cardiac tissue (depend on I_Na and I_Ca for depolarisation).

Question 23

What are the functions of drugs involved myocardial salvage?

Answer 23

These drugs don’t directly have anti-dysrhythmic effects, but maximise the amount of myocardium saved post-MI. This indirectly minimises risk of dysrhythmias.

Question 24

What are anti-dysrhythmics outside the Vaughan William classification?

Answer 24

1. Adenosine: Causes opening of K⁺ channels (through action of A₁ receptors and cAMP), leading to hyperpolarisation of pacemaker and conductive tissue.
2. Cardiac glycosides (e.g. digoxin): Central action causes increased vagal activity, causing decreased heart rate and conduction through AV node.
3. I_f inhibitors: Decreases pacemaker rhythm and thus heart rate.

Question 25

What is the mechanism of action of nifedipine in myocardial salvage?

Answer 25

1. During myocaridal ischaemia, levels of ATP decrease, causing decreased activity of Na⁺/K⁺-ATPase, NCX and PMCA, resulting in ↑[Na⁺]_i and ↑[Ca²⁺]_i.
2. When tissue re-oxygenated, ↑[Ca²⁺]_i contributes to ischaemic-reperfusion injury.
3. Nifedipine decreases levels of Ca²⁺ during ischaemia and reduces effects of IRI.