Pathophysiology of Arrhythmias

Question 1

What does Dysrhythmia/Arrhythmia describe?

Answer 1

Conditions where the co-ordinated sequence of electrical activity in the heart is disrupted

Question 2

What are the two main changes that arrhythmias could arise from?

Answer 2

Changes in the heart cells
Changes in the conduction of the impulse through the heart

Combinations of these

Question 3

What are the main classifications of arrhythmias?

Answer 3

Atrial (supraventricular)
Junctional (associated with the AV node)
Ventricular

Note: the names suggest the origin of the abnormality

Tachycardia
Bradycardia

Question 4

What is an ectopic beat?

Answer 4

Premature atrial or ventricular contraction

Question 5

Give two common examples of tachyarrhythmia.

Answer 5

AF
Supraventricular tachycardia (SVT)

Question 6

What are two examples of more serious tachycardia?

Answer 6

VF

VT

Question 7

How do atrial and ventricular ectopic beats differ visually on an ECG?

Answer 7

Atrial - slightly smaller QRS complex than average for the specific ECG
Ventricular - markedly larger and broader QRS complex than average for the specific ECG

Question 8

From what four categories of events do arrhythmias arise?

Answer 8

• Heart block
• Ectopic pacemaker activity
• Delayed after-depolarisations
• Circus re-entry

Question 9

What does heart block normally result from?

Answer 9

Damage (usually ischaemia) to a part of the conducting system

Question 10

Which region of the heart does heart block normally affect?

Answer 10

AVN

Question 11

Describe 1st degree heart block, whether atrial depolarisations lead to ventricular depolarisations and how it affects the ECG trace.

Answer 11

AV node is only slightly affected and conduction is slowed
All atrial depolarisations lead to ventricular depolarisations
Abnormally long P-R interval (i.e. longer than 200ms)

Question 12

Describe 2nd degree heart block, whether atrial depolarisations lead to ventricular depolarisations and how it affects the ECG trace.

Answer 12

More serious damage to the AVN leads to partial AV block
Some, but not all atrial depolarisations lead to ventricular depolarisations
Multiple P waves to every QRS complex

Question 13

Moritz (Type 2) is a sub-type of 2nd degree AV block. How does this differ from normal 2nd degree AV block?

Answer 13

Most beats are conducted with a constant P-R interval, but occasionally there is an atrial depolarisation without a ventricular depolarisation (i.e. an unaccompanied P wave)

Question 14

What are the 2:1 and 3:1 2nd degree AV block subtypes?

Answer 14

• A 2:1 block has two P waves for each QRS

* A 3:1 block has three P waves for each QRS

Question 15

What is the Wenckebach (Type 1 Moritz) subtype of 2nd degree heart block?

Answer 15

Progressive lengthening of P-R interval until a P wave fails to produce a QRS complex (or T wave)
The P-R interval then shortens and normal conduction occurs before the P-R interval starts to lengthen again

Wenckle the wanker is a bit of a savage bastard - he really tests the limits of the poor PR interval until it’s follower (QRS) decides, screw that, I’m bailing and only rejoins when Wenckle backs off

Question 16

Describe 3rd degree heart block, whether atrial depolarisations lead to ventricular depolarisations and how it affects the ECG trace.

Answer 16

The AV node is completely blocked
No electrical activity from the atria progresses to the ventricles

The atria depolarise (and beat) at their inherent rate
The ventricles depolarise (and beat) at pace set by Purkinje fibres
Therefore no relationship between atrial depolarisation and ventricular depolarisation on an ECG

Question 17

How does the SAN spontaneously depolarise?

Answer 17

• Decrease in K+ outflow
• “funny” Na+ current
• Slow inward Ca2+ current

Question 18

By what methods can areas of the heart develop pacemaker activity?

Answer 18

If damaged
Increased sympathetic activity
Increased sensitivity to catecholamines (caffeine, hyperthyroidism, dopamine, etc)
Cardiac glycoside toxicity

Question 19

What type of receptors can catecholamines act on to increase the rate of depolarisation and cause pacemaker activity to arise from cells which are normally quiescent?

Answer 19

Beta-1

Question 20

What can ischaemic damage cause, predisposing to ectopic pacemaker activity?

Answer 20

Can cause cells to become leaky to Na+, thus developing a ‘funny’ current

Question 21

5 phases of cardiac muscle contraction (0 - 4). Use a word or two to describe what happens in each phase and state which ion channels open or close at each.

Answer 21

Phase 0: rapid depolarisation (F-type Na+ open)
Phase 1: partial repolarisation (F-type Na+ close)
Phase 2: plateau (Ca2+ open)
Phase 3: repolarisation (Ca2+ close, K+ open)
Phase 4: stable

Question 22

When can early after depolarisation occur?

Answer 22

End of phase 2

Question 23

How does early after depolarisation appear on an ECG?

Answer 23

Prolonged QT interval

Question 24

How is early after depolarisation triggered?

Answer 24

Fluctuating increases in Ca2+ permeability

Question 25

What can result from an early after depolarisation?

Answer 25

Can set off self-sustaining depolarisations

Question 26

Following an action potential, some of the Ca2+ has to be removed, back to the ECF. Through what system is this achieved?

Answer 26

Ca2+/3Na+ exchange

Question 27

What can the exchange of Ca2+/3Na+ cause?

Answer 27

Insignificant depolarisation, since overall net influx of +'ve ions

Question 28

How can intracellular Ca2+ be raised and what is the consequence of this?

Answer 28

Cardiac glycosides Increased HR High levels of noradrenaline or adrenaline --> after depolarisations can become increasingly larger and eventually self perpetuating, triggering AP's

Question 29

How can delayed after depolarisations arise?

Answer 29

``` Delayed repolarisation (increased QT interval) increases intracellular Ca2+ --> increased after depolarisations ```

Question 30

Why can delayed after depolarisations be dangerous?

Answer 30

Can lead to dangerous ventricular dysrhythmias

Question 31

What are circus re-entry movements?

Answer 31

When a electrical impulse can re-stimulate (re-enter) a region of the heart after its refractory period has passed

Question 32

How can circus re-entry movements cause arrhythmias?

Answer 32

Comes from an unusual direction and before the tissue would have been re-stimulated by the next normal impulse from the SAN

Question 33

How does normal conduction from the SAN down the branches work

Answer 33

The impulse originates in the SAN and is transmitted to the branches Each branch depolarises When the impulses meet, there is extinction by collision

Question 34

How does circus re-entry movement differ from normal conduction?

Answer 34

An area of damage with no full conduction in the orthodromic direction – cells unable to generate sufficient current to maintain the depolarisation to reach threshold The bigger current generation from the tissue on the other side of the block has enough strength to be transmitted through Sinus impulse extinguished

Question 35

Why is the frequency of impulses generated in circus re-entry movements high?

Answer 35

The circuits are short in length

Question 36

How does a transient block differ from a unidirectional block?

Answer 36

A transient block allows some, but not all impulses through

Question 37

What is Wolf-Parkinson-White Syndrome?

Answer 37

Condition where there is additional or “accessory” electrical connection between atria and ventricles

Question 38

On which side of the heart does Wolf-Parkinson-White Syndrome normally occur?

Answer 38

Left

Question 39

How can Wolf-Parkinson-White Syndrome be diagnosed from an ECG trace?

Answer 39

PR interval is short; QRS has early upstroke (delta wave) Second part of QRS normal as conduction via AVN “catches up” (looks like broad QRS complex with abnormal inverse and lengthy ST)

Question 40

What type of tachycardia can Wolf-Parkinson-White Syndrome cause, in addition to circuit re-entry?

Answer 40

Paroxysmal tachycardia

Question 41

What are the 4 classes of Vaughan Williams classification anti-dysrhythmic drug treatment?

Answer 41

• Class I: block fast sodium channels – Class now subdivided in Ia, Ib and Ic • Class II: block b-adrenergic receptors • Class III: prolong the duration of action potential repolarisation • Class IV: block Ca2+ channels

Question 42

Which two important drugs don't fit in the Vaughan Williams classification

Answer 42

Adenosine | Digoxin