Electricity and the heart

Question 1

3 types of muscle

Answer 1

Smooth, skeletal and cardiac

Question 2

Na+ extra and intra cellular

Answer 2

E: 120
I: 10

Question 3

Ca2+ extra and intra cellular

Answer 3

2 and 0

Question 4

K+ extra and intra cellular

Answer 4

4 and 140

Question 5

What is resting potential of nerve cell?

Answer 5

-70 mV

Question 6

What causes depolarisation?

Answer 6

Sodium entering

Question 7

What causes depolarisation?

Answer 7

Potassium leaving

Question 8

Potential of cardiac myocyte

Answer 8

-85 to -90 mV

Question 9

How is potential in cardiac myocyte regulated?

Answer 9

• ATP driven pump exchanges sodium and potassium - high Na+ outside cell and high K+ inside
• Antiport system: establishes Ca2+ gradient - exchange of sodium and calcium needed

Question 10

Phase 0

Answer 10

Depolarisation

• Fast sodium channels open
• When cardiac cell is stimulated and depolarises, the membrane potential is more positive
• Voltage gated sodium channels open and allow Na+ into cell = depolarisation
• Membrane potential reaches +20 mV before Na+ channels close

Question 11

Phase 1

Answer 11

Repolarisation

Na+ channels close and cell repolarises, K+ leaves cell through K+ channels

Question 12

Phase 2

Answer 12

Plateau

• Ca2+ channels open and fast K+ channels close
• After initial repolarisation occurs, AP plateaus as a result of increased Ca2+ permeability and decreased K+ permeability

Question 13

Phase 3

Answer 13

Rapid repolarisation

• Ca2+ channels close
• Slow K+ channels open, K+ exits cell
• Plateau ends and resting level is re-established

Question 14

Phase 4

Answer 14

Resting potential

Averages -80 to -90 mVW

Question 15

Why is there a prolonged resting potential in cardiac myocytes?

Answer 15

Ion channel inactivation and prevents tetany

Question 16

Features of pacemaker cells

Answer 16

• Specialised cells in atria, especially SAN and AVN
• Autonomic firing without stimulus
• Results from continuous slow ionic leak
• Natural highest rate in SAN - others become active if SAN fails

Question 17

What does pacemaker AP start at?

Answer 17

-60 mv

Question 18

What causes depolarisation of pacemaker cells?

Answer 18

Ca2+ influx

Question 19

Sympathetic influence on HR

Answer 19

Slow Na+ channel permeability increases
Slope of phase 4 steeper
Threshold reached sooner, increasing HR

Question 20

Parasympathetic influence on HR

Answer 20

Increases resting K+ permeability
Trough potential is lowered and slope of phase 4 flatter
Threshold reached later, decreasing HR

Question 21

Intra-cardiac conduction

Answer 21

• Non-specific conduction in atria
• AVN: gate in firewall between atria and ventricles - slows conduction and allows time for atrial emptying, protects ventricles from atrial tachyarrhythmias, also affected by autonomic NS
• His-Purkinje system - ventricles - depolarise of myometrium from in to out (opposite of perfusion)
• Branching nature of cardiac muscle also enables synchronous ventricular contraction

Question 22

What are ECGs?

Answer 22

Surface recording of electrical activity

Polarity of impulses is +ve if moving towards electrode, -ve if away

Question 23

Axis of ECGs

Answer 23

Lead iii at 90 degrees to axis = isoelectric trace

Question 24

Characteristics of ischaemia/infarction on ECH

Answer 24

• Typically produces ST segment (with/without T wave) changes acutely
• Damaged cells repolarise early so ST segment is out of step with normal areas
• Division between ischaemia and infarction is now less clear (acute coronary syndrome can be reversible) but classically:
• Full thickness damage (ST elevation)
• Subendocardial damage (ST depression)

Question 25

Full thickness STEMI on ECH

Answer 25

ST elevation | Q wave

Question 26

Subendocardial damage on ECG

Answer 26

ST wave depression | With or without T wave inversion

Question 27

Coronary artery to inferior heart

Answer 27

Right

Question 28

Coronary artery to antero-septal heart

Answer 28

Left anterior descending

Question 29

Coronary artery to antero-apical heart

Answer 29

Left anterior descending - distal

Question 30

Coronary artery to antero-lateral heart

Answer 30

Circumflex

Question 31

Coronary artery to posterior heart

Answer 31

Right

Question 32

Inferior MI on ECG

Answer 32

ST elevation in leads II, III and aVF (inferior leads)

Question 33

Anterior/septal MI on ECH

Answer 33

ST elevation in V2/3/4 - tombstoning

Question 34

What is the Q wave?

Answer 34

First downwards deflection in PQRS pathology | Seen in lateral leads as septal depolarisation

Question 35

What does deep Q wave indicate?

Answer 35

STEMI

Question 36

Hyperkalaemia on ECG

Answer 36

High, peaked T waves and QRS widening

Question 37

Hypertrophy on ECG

Answer 37

- LVH = large amplitude QRS complexes - Negative deflection in V1, positive deflection in V5 - Add the negative deflection to the positive deflection, want it to be less than 35

Question 38

Fibrillation on ECG

Answer 38

- Rapid, uncoordinated contraction - Atrial fibrillation: AVN prevents VF, cardiac output less than 30%, thrombo-embolism risk - Ventricular fibrillation: No cardiac output, fatal if not treated quickly

Question 39

AF on ECG

Answer 39

- No P waves - QRS normal but irregularly irregular - To confirm irregularity, mark consecutive r peaks on paper and compare down the line

Question 40

Management of AF

Answer 40

- Anti-thrombotics: warfarin, dabigatran, rivaroxaben, aspirin - Rhythm: cardioversion (synchronised shock to prevent VF), rate control ( beta blocker, Ca2+ antagonist, amiodarone, digoxin) - Plus any underlying causes

Question 41

Mechanism of digoxin

Answer 41

- Slows conduction through AVN - reduces ventricular rate in AF - Increases myocardial contractility - Na+/K+ pump inhibited, increasing [Na+] - Na+/Ca2+ exchange mechanism now less efficient, raising [Ca2+] - stored in sarcoplasmic reticulum - Force of subsequent contraction enhanced

Question 42

Ventricular fibrillation

Answer 42

- Continuous, bizarre, irregular trace | - No P wave

Question 43

Management of VF

Answer 43

- Defibrillation: unsynchronised (150-200J, biphasic) - Treat underlying causes - Automated function - AED (paramedics, airports) and AID (implanted, high risk patients) - Sudden death is often VF

Question 44

Conduction defects

Answer 44

- SAN: pacemaker failure, lower site normally takes over - AVN: heart block - Intra-ventricular - bundle branch block - Heart block: - Problem with conduction through AVN

Question 45

1st degree block

Answer 45

PR interval, prolonged but all eventually conducted

Question 46

2nd degree block

Answer 46

Some P waves not conducted, here in 2:1 ratio (type ii)

Question 47

3rd degree block

Answer 47

P waves unrelated to QRS complexes, usually bizarre in nature

Question 48

Bundle branch blockages

Answer 48

- Problem with circulation through R or L branch - 1 ventricle depolarises after the other - Wide QRS complex after normal P wave - RBBB: M pattern in V1, W pattern in V6 - LBBB: M pattern in V6

Question 49

ventricular ectopic

Answer 49

- One-off can be normal - Ventricle contracts after stimulus transported throughout heart - Wide QRS complex - Abnormalities in repolarisation - No P wave

Question 50

Pacing impulse

Answer 50

- Very brief impulse external impulse stimulates ventricle (with or without atrium) - Wide QRS - Short, sharp pacing spike