Cardio L3 ECG Flashcards Preview

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Flashcards in Cardio L3 ECG Deck (36):
1

Electrical Conducting system:
consists of and function

1. Consists of modified myocytes with few contractile filaments.
 Function: Generates and conducts the electrical impulses that trigger contraction

2

Valsalva manouevure 

Exhale against closed glottis therefore increase intrathoracic pressure and impeding return of blood to heart.

3

Sinoatrial node: (5)

1. Physiological pacemaker
2. Excitability (generates AP
3. Automaticity (spontaneous – separate from CNS)
4. Rhythmicity (regular)
5. Dominance over other potential pacemakers by overdrive suppression.

4

Electrophysiology of the SA Node:

1. Several currents are involved
2. No “fast” sodium channels (unlike neurone)
3. Unstable resting membrane potential or pacemaker potential – as membrane drifts towards threshold AP will occur.

5

Process: of SA node

a. During pacemaker potential slow Na influx (funny current)
b. Upstroke  Calcium influx
c. Repolarisation  K current.

6

Control of Heart rate:

1. Resting adult Human has a heart rate of 60-100 beats per minute
2. Autonomic control
3. Temperature

7

a. Sympathetic 

Innervates large areas of heart and the artrioventricular and sinoatrial nodes.

8

parasympathetic

 Carried in vagus nerve predominatly innervates sinoatrial node and atrioventricular node.

9

Parasympathetic System and Acetylcholine: SLOW HR process
Blocked by

1. Fibres in the vagus (left and right) nerves
2. Release Ach
3. Ach binds to muscarinic receptors
4. Pacemaker cells become hyperpolarised
a. Decreases rate at which pacemaker potential reaches threshold (Negative chronotropism) -> decreases heart rate.
b. Block: atropine

10

Sympathetic: SPEEDDS HR

1. Postganglionic fibres originate T1 to T5 and synapse in the paravertebral ganglia
2. Postganglionic fibres release noradrenaline]Noradrenaline agonises Beta-1 adrenoceptors
3. Increases slope of pacemaker potential
4. Increases heart rate (Positive chronotropism)

11

Intrinsic Heart Rate:

1. At rest parasympathetic and sympathetic systems are tonically active.
2. Pharmacological blockade of both systems causes 50% increase in intrinsic heart rate, thus at rest the parasympathetic effects are dominant
a. Tachycardia  >100/min
b. Bradycardia  <60/min

12


Atrial Conduction:

1. Atria acts as a syncytium  cells physically separate but electrically act together:
2. Myocytes are joined by intercalated dics containing gap junctions
3. Rapid propagation as myocytes have fast sodium channels.

13

Atrioventricular Node: Calcium current
located at
lacks

1. Located in the right atrium
2. Lacks fast sodium channels
3. Dromotropism

14

Atrioventricular Node: function

: A slow conduction velocity ensures that atria contract and fill the ventricles before the ventricles contract.

15

Dromotropism

change in conduction velocity
a. Positive  during exercise
b. Negative  decrease in rate of conduction between two nodes.

16

His Bundle, bundle Branches and purkinje Fibres:

1. All are formed from Purkinje cells
2. The bundle of His is the only electrical connection between the atria and ventricles.
3. Pathological connections such as the Bundle of Kent may predispose to arrhythmias (WPW syndrome)  extra pathological connection between atria and ventricles.

17

Purkinje cells:

1. These are cells adapted for rapid conduction (200 cm//sec)
2. Wide diameter
3. Few myofibrils
4. Numerous gap junctions

18

SA node and atrioventricular node channel typr

 shallow up stoke as they lack fast sodium channels and depend on calcium channels

19

channel type
Atrial mycocytes, ventricular myocytes and purkinje

fast upstroke as they have fast Na channels.

20

Chain of events:

1. SA Noda
2. Atrial
3. AV Node
4. Purkinje Fibres
5. Endocardial
6. Midmyocardial
7. Epicardial

21

Ventricular myocyte AP: phase 0

Rapid depolarisation due to opening sodium channels (Na)

22

Ventricular myocyte AP: phase 1

Inactivation of sodium channels

23

Ventricular myocyte AP: phase 2

Slow inward calcium channels (L-type) (Ica). Also known as the Plateau phase – contraction of myocyte.

24

Ventricular myocyte AP: phase 3

Rapid repolarisation including IK via delayed rectifier potassium channels

25

Ventricular myocyte AP: phase 4

Resting membrane potential

26

ECG Flat
description

Isoelectric line

27

ECG pwave
description

Atrial depolarisation

28

ECG PR segment
description

Delay due to atrial-ventricular node

29

ECG P-R interval
description
Clinical

0.12-0.2s Atrioventricular conduction
Clinically affected by diseases that affect conduction between atria and ventricle = heart block and increase in PR interval.

30

ECG QRS complex
description

<0.10s
Generated by depolarisation of ventricles.

31

ECG S-T segment
description
Clinical

Period that the ventricles are depolarised. Clinically:
1. ST elevation = can be an indicated of MI
ST depression – indicator of myocardial ischemia in angina

32

ECG T wave
description
Clinical

Repolarisation of ventricles – same as depolarisation as it occurs from the outer surface (epi) to endocardial.

Can be altered with electrolyte disturbance – hyperkalaemia = tall peak T waves. (arryhtmias causing)

33

ECG QT interval
description
Clinical

<0.44s duration of ventricular activation
Varies with heart weight
Inherited disorders
Prolonged = major risk factor for arrhythmias.
Combination of antihistamines and grapefruit juice to causes prolonged QT intervals

34

ECG U wave
description
Clinical

Not in every ECG (more common in younger) or a sign hypokaelaemia (U prominent and T wave flatten)

35

Sinus rhythm

 The heart rate is between 60-100 bpm.
 Regular
 Every P wave is followed by a QRS complex

36

Sinus arrhythmia

Normal in young adults and children:
 Can alter in expiration and inspiration
 Inspiration – HR increased (QRS shorter)
Expiration – HR reduced R waves further apart

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