Pathophysiology of Arrhythmias Flashcards Preview

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Flashcards in Pathophysiology of Arrhythmias Deck (42)
1

What does Dysrhythmia/Arrhythmia describe?

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

2

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

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

Combinations of these

3

What are the main classifications of arrhythmias?

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

Note: the names suggest the origin of the abnormality

Tachycardia
Bradycardia

4

What is an ectopic beat?

Premature atrial or ventricular contraction

5

Give two common examples of tachyarrhythmia.

AF
Supraventricular tachycardia (SVT)

6

What are two examples of more serious tachycardia?

VF
VT

7

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

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

8

From what four categories of events do arrhythmias arise?

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

9

What does heart block normally result from?

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

10

Which region of the heart does heart block normally affect?

AVN

11

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

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)

12

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

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

13

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

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)

14

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

• A 2:1 block has two P waves for each QRS
• A 3:1 block has three P waves for each QRS

15

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

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

16

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

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

17

How does the SAN spontaneously depolarise?

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

18

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

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

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?

Beta-1

20

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

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

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.

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

22

When can early after depolarisation occur?

End of phase 2

23

How does early after depolarisation appear on an ECG?

Prolonged QT interval

24

How is early after depolarisation triggered?

Fluctuating increases in Ca2+ permeability

25

What can result from an early after depolarisation?

Can set off self-sustaining depolarisations

26

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

Ca2+/3Na+ exchange

27

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

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

28

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

Cardiac glycosides
Increased HR
High levels of noradrenaline or adrenaline

--> after depolarisations can become increasingly larger and eventually self perpetuating, triggering AP's

29

How can delayed after depolarisations arise?

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

30

Why can delayed after depolarisations be dangerous?

Can lead to dangerous ventricular dysrhythmias

31

What are circus re-entry movements?

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

32

How can circus re-entry movements cause arrhythmias?

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

33

How does normal conduction from the SAN down the branches work

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

34

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

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

35

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

The circuits are short in length

36

How does a transient block differ from a unidirectional block?

A transient block allows some, but not all impulses through

37

What is Wolf-Parkinson-White Syndrome?

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

38

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

Left

39

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

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)

40

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

Paroxysmal tachycardia

41

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

• 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

42

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

Adenosine
Digoxin

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