Heart physiology

Question 1

What ions determine the SAN pacemaker potential?

Answer 1

Na+ in via voltage gated channels (NOT fast ones), Ca2+ (different ones to SAN action potential ones) in and decrease in K+ conductance

Question 2

What ions determine the SAN action potential?

Answer 2

Ca2+ moves in (different channels to SAN pacemaker potential ones) and further decrease in K+ conductance during the depolarisation phase, and outward movement of K+ later on in repolarisation phase.

Question 3

How long does the SAN action potential last in ms?

Answer 3

200ms

Question 4

How does autonomic control of heart rate occur?

Answer 4

By altering pacemaker potential

Question 5

How is heart rate decreased by the autonomic nervous system?

Answer 5

Heart has M2 parasympathetic system receptors and Ach –> decrease in HR via vagal. Reduces slope of pacemaker potential (becomes less vertical) + hyperpolarises. So action potentials space out in the graph.

Question 6

How is heart rate increased by the autonomic nervous system?

Answer 6

β1 receptors in the heart and NA via nerves lead to a steeper slope and more frequent action potentials so faster heart rate.

Question 7

What is the conduction rate through the atria?

Answer 7

0.5m/s, complete within 0.09s of the SAN firing

Question 8

Does atrial muscle electrical signals have resting or pacemaker potentials?

Answer 8

Resting membrane potential

Question 9

What is the conduction rate in AVN?

Answer 9

Falls to 0.05m/s (can be increased by SA)

Question 10

What potential does the AVN have; resting or pacemaker?

Answer 10

Pacemaker BUT less steep than SAN pacemaker potential

Question 11

Why is there an AV delay?

Answer 11

Ensures atrial depolarisation, contraction and ejection before ventricles depolarise

Question 12

How fast is conduction through Bundle of His?

Answer 12

2m/s

Question 13

How fast is conduction through Left and Right branches

Answer 13

2m/s

Question 14

How fast is conduction through Purkinje fibres and ventricular muscle?

Answer 14

4m/s, depolarisation takes place endocardium moving outwards to epicardium

Question 15

What does the ventricular myocyte action potential look like and what are the phases?

Answer 15

(Stable) resting potential (phase 4), straight line up (phase 0), small fall (phase 1), plateau a bit (phase 2), then falls not 100% vertically down but nearly to stable resting potential again (phase 4)

Question 16

How fast is the ventricular myocyte depolarisation?

Answer 16

250-300ms

Question 17

What ion movements are there in ventricular action potential?

Answer 17

Phase 0 - depolarisation - Na+ goes in via fast voltage gated channels, phase 1 Na+ fast voltage gated channels inactivate, there is partial repolarisation, phase 2 - plateau - inward movement of Ca2+ and outward of K+, phase 3 - repolarisation - outward movement of K+

Question 18

What are the classes of anti-dysrhythmic drugs?

Answer 18

Class I - Na+ channel blockers
Class II - β blockers
Class III - drugs that prolong cardiac action potential
Class IV - calcium antagonists

Question 19

How long is the absolute refractory period in ventricular myocytes?

Answer 19

200ms - Na+ channels are inactivated and unresponsive

Question 20

How long is the relative refractory period in ventricular myocytes?

Answer 20

50ms - Na+ channels are inactivated and recovering but cant’t yet really support an action potential

Question 21

What Class of anti-dysrhythmics can affect the ventricular action potential?

Answer 21

Class I can inhibit fast Na+ voltage gated channels only found in ventricular myocyte action potential to depolarise. In SAN depolarisation its Ca2+ that leads to depolarisation so don’t have an effect on those channels.

Question 22

What can Class IV anti-dysrhythmics block and in what action potential (s) of the heart?

Answer 22

Can affect SAN and ventricular action potentials; they are Ca2+ channel blockers.

Question 23

What are the 3 subdivisions of Class I antidysrhythmics?

Answer 23

Ia - disopyramide
Ib - lidocaine
Ic - flecainide

Question 24

Give an example of a Class III antidysrhythmic

Answer 24

Amiodarone
Effect: suppresses dysrhythmias
Mechanism of action: affects repolarisation prolonging cardiac action potential (more than one mechanism but) thought to be via blocking K+ channels involved in cardiac repolarisation (including outward delayed rectifier). Action potential prolongation increases the refractory period–>e.g. interrupts re-entrant tachycardias and suppressing ectopic activities.
Site of action: ventricular a.p.
Side effects: pro-arrhythmic; the increase in action potential duration can produce torsades de pointes (a type of ventricular tachycardia), especially in patients with long-QT syndrome. pulmonary fibrosis (late onset)
Need to monitor K+ levels
This drug increase the QT interval in an ECG
Contraindications: Amiodarone, because of its Class IV effects, can cause bradycardia and atrioventricular block, and therefore is contraindicated in patients with heart block, or sinoatrial node dysfunction