Physiology of the heart 1

Question 1

How does the heart control heart rate / rhythm

Answer 1

Autonomic nervous system, muscles and nerve interacting, spontaneous contraction

Question 2

How many bpm on average, how is direction of flow maintained an what happens to heart muscle upon contraction?

Answer 2

Around 70bpm
Direction of flow maintained by valves
Muscle thickens upon contraction

Question 3

Cardiac action potential - PHASE 0

Answer 3

Rapid depolarisation - this is allowed due to the low IC K+ –> influx of Na+ –> membrane potential moves from -70 towards 0

Question 4

Cardiac action potential - PHASE 1

Answer 4

Deactivation of Na+ influx, stops Na+ conductance further.

Partial repolarisation occurs

Question 5

Cardiac action potential - PHASE 2

Answer 5

Plateau phase - slow inward current of Ca2+ which is slow so that the heart can properly fill with blood

Question 6

Cardiac action potential - PHASE 3

Answer 6

Repolarisation –> outwards current K+. Ca2+ becomes deactivated

Question 7

Cardiac action potential - PHASE 4

Answer 7

Decrease in the conductance of K+. Pacemaker potential causes gradual increase in the conductance of Ca2+/K+.

Question 8

What is the importance of the pacemaker potential?

Answer 8

Gradual increase in Ca2+ and K+ allows sequential of action potentials, mediated by the SA node

Question 9

What is the pathway of the cardiac action potential?

Answer 9

Starts at the SA node –> travels down the bachmann’s bundle –> delay, to allow the ventricles to fill, then hits the AV node

Question 10

Why is the AP long and what is the need for the absolute refractory period?

Answer 10

This means that there can be no second action potential fired in this time.

Question 11

What is a triggered activity heart block??

Answer 11

Action potential impulse is triggered by several impulses of the same size, close together, causing a large depolarisation

Question 12

What characterises an increased automaticity heart arrhythmia?

Answer 12

Ectopic beat from different part of the heart causing an ectopic impulse

Question 13

What characterises a re-entry arrhytmia (circus movement)?

Answer 13

Most common type –> impulse is fired and is only propogated down one half of the heart so the impulse is blocked
The impulse can fire back and reactivates muscle that has been repolarised and triggers another AP, causing an ectopic beat

Question 14

1st degree heart block

Answer 14

Atrial and ventricular depolarisation occurs, but there is a delay of around 200ms seen between the two (greater P-R interval)

Question 15

2nd degree heart block

Answer 15

Failure of conduction to the AV node even though impulses are propogated –> missed heart beat

Question 16

3rd degree heart block

Answer 16

Complete dissociation between atria and ventricles, pacemaker activity takes too long, longer wider QRS complexes seen

Question 17

What characterises atrial tachycardia

Answer 17

Rapid contraction of the atria –> this causes a delay at the AV node as full sequence signal isn’t propagated quickly enough

Question 18

What characterises venctricular tachycardia

Answer 18

Impulses don’t come though from the SA node quickly enough – causes widening of complexes.
V serious

Question 19

What characterises atrial fibrillation

Common treatment?

Answer 19

P waves hit the SA node but no propagation of impulse is seen, causing disorganised contraction of the heart
Anti-coagulants commonly used to treat

Question 20

What characterises ventricular fibrillation?

Answer 20

Impulses not propogated through the ventricles –> no cardiac output therefore
No defined rhythm, so can cause sudden death
SHOCK FIBRILLATOR NEEDED

Question 21

Autonomic control - parasympathetic impact on HR?? Via what receptors?

Answer 21

Reduced HR, decreased slope of pacemaker potential. Occurs via M2 muscarinic receptors

Question 22

Autonomic control - sympathetic impact on HR?? Via what receptors?

Answer 22

Increased HR, positive chronotrophic effects, increased slope of pacemaker potential
Occurs via B1 adrenergic receptors

Question 23

Anti-arrhythmic drugs - class 1 - how do they work and provide example

Answer 23

Na+ channel blockers
QUINIDINE
Use - dependant!! Means that drug attaches to the effected area of the heart at the resting state and only impacts the effected channels

Question 24

Anti-arrhythmic drugs - class 2 - how do they work and provide example

Answer 24

B - adrenoreceptor antagonists - non selective

PRONANOLOL

Question 25

Anti-arrhythmic drugs - class 3 - how do they work and provide example

Answer 25

Work by prolonging the refractory period of an action potential to prevent new impulses from coming along
AMIODARONE

Question 26

Anti-arrhythmic drugs - class 4 - how do they work and provide example

Answer 26

Ca2+ channel blockers! Prevent contraction of the heart

VERAPAMIL

Question 27

Digoxin - where is it derived from? Mechanism of action? Adverse effects?

Answer 27

Derived from the foxglove flower
Used to treat atrial fibrillation and heart failure
Inhibits the Na+/K+ pump –> this maintains the resting potential. This causes increase in force of contraction of the heart, bradycardia, slowed AV conduction and increased ectopic activity
Adverse effects –> nausea, vomiting, diarrhoea. Due to narrow therapuetic range

Question 28

How does inhibiting the Na+/K+ pump caused increase contraction of the heart?

Answer 28

Inhibiting this pump causes inhibition of the Na+ gradient outside the cell.
This decreases the activity of Ca2+ pump (pumping out of the cell)
Ca2+ remains in cell for longer and increases contraction force

Question 29

AMIODARONE - where is it derived from? Mechanism of action? Adverse effects?

Answer 29

Works to prolong the QT period, increasing the amount of time taken to repolarise the heart cells
Adverse effects - slate grey skin, increased UV sensitivity, hypo/hyperthyroidism, abnormal liver function, corneal microdeposits, impacts other drug interactions (eg warfarin), optic neuropathy