2. Heart Rate and Rhythm

Question 1

What happens when the heart contracts?

Answer 1

The muscle thickens and ventricular cavity reduces in size to eject blood

Question 2

What is activation of the heart controlled by?

Answer 2

Heart is an excitable tissue, activation is controlled by changes in membrane potential

Question 3

What are the stages of the cardiac action potential?

Answer 3

Phase 0 - Rapid depolarisation
Phase 1 - Partial repolarisation
Phase 2 - Plateau 
Phase 3 - Repolarisation 
Phase 4 - Pacemaker potential

Question 4

Describe Phase 0 - Rapid depolarisation.

Answer 4

Depolarisation occurs when membrane potential reaches threshold (-60mV) and is mediated by rapid sodium influx

Question 5

Describe Phase 1 - Partial repolarisation.

Answer 5

Rapid sodium influx deactivation by closure of voltage-gated Na channels

Question 6

Describe Phase 2 - Plateau.

Answer 6

Depolarisation maintained by slow calcium influx and initial fall in potassium efflux
Allows time for heart to eject blood and then refill (prevents AP firing at very high rates)

Question 7

Describe Phase 3 - Repolarisation.

Answer 7

Slow calcium influx deactivation and increased potassium efflux resets membrane potential to resting potential

Question 8

Describe Phase 4 - Pacemaker potential.

Answer 8

Gradual depolarisation of resting potential towards threshold by increasing sodium and calcium influx and decreasing potassium efflux
When membrane potential reaches threshold the next cardiac action potential will fire

Question 9

Describe the pathway for depolarisation through cardiac conduction tissue.

Answer 9

• Sinoatrial node - main pacemaker in right atrium
• Depolarisation rushes across conducting tissue in atria to cause atrial contraction
• Depolarisation reaches AV node - conduction is slow to ensure atria have fully contracted to fill ventricles with blood
• Depolarisation conducted through His bundle, Left and Right bundles and then Purkinje fibres
• Rapid conduction through Purkinje fibres ensures ventricles contract as one to maximally eject blood

Question 10

Where are pacemaker potentials found in cardiac tissue?

Why is this important?

Answer 10

• SA node (depolarises fastest = dominant pacemaker), AV node and Purkinje fibres
• If SA node fails still have pacemakers downstream to compensate

Question 11

Where is rapid sodium influx not found in cardiac tissue?

What mediates depolarisation instead?

Answer 11

• SA node and AV node

- Slow calcium influx mediates depolarisation in nodal tissue

Question 12

Where are long action potentials (plateaus) and refractory periods found in cardiac tissue?

Answer 12

• Purkinje fibres and ventricles depolarisation maintained by slow calcium influx

Question 13

What are the 2 general mechanisms of arrhythmia?

Answer 13

1. Abnormal impulse generation

2. Abnormal impulse propagation

Question 14

What is triggered activity?

Answer 14

• When muscle is stimulated, get depolarisation and then shortly after get delayed after-depolarisation
• If 2 stimuli are applied, the delayed after-depolarisation increases in size
• Closer the 2 stimuli are, the larger the delayed after-depolarisation
• Certain point at which delayed after-depolarisation is large enough to reach threshold and triggers and additional depolarisation

Question 15

What is increased automaticity?

Answer 15

• Due to biochemical upsets which cause patients to fire ectopic beats
• Normal rhythm is followed by a single irregular rhythm (ectopic beat)

Question 16

What is re-entry?

Answer 16

• Normally, an impulse is propagated down myocardial tissue but cannot propagate back on itself due to tissue behind being refractory
• In damaged heart, can get abnormal impulse propagation
• If there is unidirectional block, impulse can propagate back on itself to depolarise tissue that has just repolarised due to time delay, causing another depolarisation
• Creates a re-entrance circuit leading to tachycardia

Question 17

What is the normal delay between atrial depolarisation (P wave) and ventricular depolarisation (QRS complex)?

Answer 17

200m/s

Question 18

Describe 1st degree heart block.

Answer 18

Delay between atrial depolarisation and ventricular depolarisation is >200m/s but all impulses get through

Question 19

Describe 2nd degree heart block.

Answer 19

Intermitted dropped beat i.e. ventricular depolarisation does not follow atrial depolarisation as impulse is blocked

Question 20

Describe 3rd degree heart block.

Answer 20

Atrial and ventricular depolarisation is totally dissociated - impulses do not reach ventricles due to complete heat block

Still get ventricular depolarisation due to AV node pacemaker potential but this is slower and therefore QRS complex is wider

Question 21

Describe normal sinus rhythm.

Answer 21

Atrial depolarisation (P wave) followed by AV node delay (200m/s) followed by ventricular depolarisation (QRS complex) followed by ventricular repolarisation (T wave)

Question 22

Describe sinus bradycardia.

Answer 22

Origin of rhythm is still sinus (P wave present)

Increased interval between QRS complexes slows heart rate (Bradycardia)

Question 23

Describe sinus tachycardia.

Answer 23

Origin of rhythm is still sinus (P wave present)

Decreased interval between QRS complexes accelerates heart rate (Tachycardia)

Question 24

Describe atrial tachycardia.

Answer 24

Atria contracting very rapidly, but due to AV node delay not all impulses get through to ventricles
Decreased interval between QRS complexes accelerates heart rate (Tachycardia)

Question 25

Describe ventricular tachycardia.

Answer 25

Impulse comes from ventricles, as this is not propagated through fast channels QRS complexes are wider Decreased interval between QRS complexes accelerates heart rate (Tachycardia)

Question 26

Describe atrial fibrillation.

Answer 26

- Atria do not contract in an organised way so there is no atrial output - No true P waves only fibrillation waves - Depolarisations reach AV node but only some get through to ventricles leading to irregular heart rhythm - Makes heart inefficient as lose atrial output and irregular heart rate

Question 27

What is a risk in atrial fibrillation patients? | What are these patients therefore given?

Answer 27

- If atria stand still develop atrial thrombus, which can break of and cause stroke - Anti-coagulants

Question 28

Describe ventricular fibrillation.

Answer 28

- Wide QRS complexes (Ventricular rhythm) - No cardiac output (Sudden death) - No pattern of ventricular rhythm

Question 29

What can save someone's life in ventricular fibrillation?

Answer 29

Defibrillation restores normal ventricular rhythm

Question 30

What is the intrinsic heart regulated by?

Answer 30

Intrinsic heart rate is continuously suppressed by vagal tone

Question 31

What is the effects of sympathetic stimulation of the heart? What mediates this effect? How does it cause this effect?

Answer 31

- Increased heart rate (positive chronotropic) and force of contraction (positive inotropic) - Increases automaticity (increases risk of arrhythmias) - Mediated by Adrenaline (from adrenal glands) and Noradrenaline (from sympathetic neurones) at B1-adrenoceptors - Increases the slope of pacemaker potential, therefore threshold is reached quicker and heart rate increases

Question 32

What is the effects of parasympathetic stimulation of the heart? What mediates this effect? How does it cause this effect?

Answer 32

- Decreases heart rate (negative chronotropic) - Decreases automaticity (decreases risk of arrhythmias) - Mediated by Acetylcholine (from parasympathetic neurones) at M2 muscarinic receptors - Decreases slope of pacemaker potential, thereofore threshold is reached slower and heart rate decreases

Question 33

What are the 4 classes of drugs in the Vaughan Williams classification?

Answer 33

1. Na+ channel blockers 2. B-adrenoceptor antagonists 3. Prolong AP 4. Ca2+ channel blockers

Question 34

How do Na+ channel blockers treat arrhythmias?

Answer 34

- Use dependent i.e. drugs are specific to refractory-state Na+ channels but do not affect resting Na+ channels - During tachycardia, there is increased AP firing, meaning increased Na+ channel activation - when these become refractory blockers will bind to channel and inhibit AP firing

Question 35

Describe the mechanism of action of Digoxin.

Answer 35

- Digoxin is a cardiac glycoside that inhibits the Na+/K+ pump - Normally, Na+/K+ pump maintains a low [Na+]i and high [Na+]o which creates a driving force for inward Na+ movement - Na+/Ca2+ pump uses this driving force to extrude Ca2+ from the cell - When inhibit Na+/K+ pump, this decreases the driving force for Na+ movement therefore decreases Na+/Ca2+ pump activity - Leads to increased [Ca2+]i

Question 36

What are the main effects of Digoxin?

Answer 36

- Bradycardia (increased vagal tone) - Slowing of atrioventricular conduction (increased vagal tone) - Increased ectopic activity (pro-arrhythmic) - Increased force of contraction (increased [Ca2+]i)

Question 37

What is significant about Digoxin's narrow therapeutic range?

Answer 37

- Need to achieve a certain level to see beneficial effects, but this is close to level that causes adverse effects

Question 38

What is Digoxin used in?

Answer 38

- Atrial fibrillation to decrease ventricular response rate by increasing AV node delay - Severe heart failure as increases force of contraction

Question 39

What can be caused by drugs that delay repolarisation and therefore prolong QT interval?

Answer 39

Ventricular polymorphic tachycardia - lethal