Unit 6 - Cardiovascular - Arrhythmia

Question 1

What causes arrhythmias?

Answer 1

Acquired
- changes to heart muscle
- damage
- ischaemia
- infarct
Genetic
- mutation
- polymorphism
- causing structural or ionic changes

Question 2

How can a post mortem diagnose arrhythmia?

Answer 2

Structural abnormalities
Molecular abnormalities
- ion channel changes

Question 3

Why is the duration of diastole important to allow filling of the ventricle?

Answer 3

Ventricles have to work harder if not stretched

- more inefficient

Question 4

What do alterations in timing of the cardiac cycle lead to?

Answer 4

Loss of efficiency

Complete failure to pump

Question 5

What is the natural prevention of arrhythmia?

Answer 5

Refractory period

• time in which myocyte cannot conduct or initiate action potential
• determined by voltage gated Na+ channel

Question 6

What is the re-entrant circuit movement?

Answer 6

Action potentials not triggered by the SAN

Question 7

What is WPW syndrome?

Answer 7

Wolff-Parkinson-White syndrome

- genetic condition

Question 8

What are the effects of Wolff-Parkinson-White syndrome?

Answer 8

SA node impulses overwhelmed by discharges in atria and parts of the pulmonary veins
- circus movement
- no P waves
Ventricular contraction
- AC escape
- idiopathic ventricular rate
- irregular frequency of QRS
Survivable
- ventricles protected by AV node
If AV node bypassed fibrillation can access the ventricle
- Wolff-Parkinson-White syndrome
- diagnosed by ECG
- no delay at AV node

Question 9

What is the treatment for Wolff-Parkinson-White syndrome?

Answer 9

Ablation of heart muscle

Question 10

What are the classes of cardiac arrhythmias?

Answer 10

Classified according to the site of origin of the problem
- atrial fibrillation
- ventricular ectopic beat
Classified according to the change in heart produced
- tachycardia
- bradycardia

Question 11

What are the types of cardiac arrhythmias?

Answer 11

Modified nodal automaticity
- normal variation
Ectopic pacemaker activity
Delayed after-depolarisation
Early after-depolarisation
- long QT syndrome
Re-entry
Heart block

Question 12

What is modified nodal automaticity?

Answer 12

Sinus arrhythmia
- normal waxing and waning of heart rate in phase with breathing in and out
- heart rate increases on inspiration
- heart rate decreases on expiration
Fluctuations in autonomic tone

Sinus bradycardia

• heart rate < 60 bpm during the day
• < 50 bpm when in deep sleep

Sinus tachycardia

• heart rate > 100 bpm
• rare that it is due to intrinsic sinus node factors
• causes include hyperthyroidism, fever, infection

Question 13

What are ectopic foci?

Answer 13

Action potentials generated outside the SA node

• increased rate of depolarisation during phase 4 due to overactivity of If
• causes include sympathetic overstimulation
• dobutamine

Question 14

What are delayed afterdepolarisations (DADs)?

Answer 14

Afterdepolarisations are depolarisations caused by excessively large inward currents carried by the Na+/Ca2+ exchanger
- if afterdepolarisations are large enough to reach threshold, premature ectopic action potentials result before the next expected normal action potential

Question 15

What is the ionic cause of DADs?

Answer 15

The Na+/Ca2+ exchanger produces an inward current which depolarises cells
Overactivity caused by Ca2+ overload causes depolarisation
Causes
- ischaemia (low ATP compromises Ca2+ pump)
- some forms of inherited arrhythmias
- digitalis
- block of Na+/K+ exchanger

Question 16

What are early afterdepolarisations (EADs)?

Answer 16

One cell fails to repolarise essentially resulting in prolongation of action potential
Long QT syndrome
- genetic mutations in genes encoding K+ channel subunits resulting in defective repolarisation lengthens the QT interval and can lead to arrhythmia

Question 17

What is drug induced long QT syndrome (LQTS)?

Answer 17

Drugs with inadvertently block hERG cause aquired LQTS sometimes leading to Torsades de Points (TdP)
No one structural class of drug responsible
- antibiotics
- antihistamines
- antifungals
- antipsychotics
- GI prokinetic agents
- antiarrhythmics
Polymorphisms in genes can predispose to problems with some drugs

Question 18

What is re-entry?

Answer 18

Essentially circus movement of cardiac action potentials
Requires
- a bifurcation
- two separate pathways of conduction which join
- an area of slow conduction and unidirectional block
Where depolarisation wavefront meet they cancel each other out
If tissue is damaged and refractory it stops a re-entrant circuit
If tissue is damaged by excitable in only the retrograde direction then depolarising wavefront may travel around and because of slowed conduction in the damaged area reaches an area no longer refractory to set up a self-sustaining circuit

Question 19

What is heart block?

Answer 19

Major damage in the conducting system has occurred

- most striking example is block at the AV node

Question 20

What is first degree AV block?

Answer 20

Excessive slowing of conduction through the AV node

- affecting the PQ/PR interval

Question 21

What is second degree AV block?

Answer 21

There may be missed beats

Question 22

What is third degree AV block?

Answer 22

There can be complete breakdown of conduction between the atria and ventricles

• here the ventricle would be driven by an intrinsic pacemaker
• ventricular escape
• much slower than normal heart rate
• 30 - 40 bpm
• bradycardia