Cardiac Rhythm

Question 1

What maintains the -ve resting membrane potential in cardiac cells?

Answer 1

Leak channels

Question 2

Briefly describe which channels re involved in depolarisation of cardiac cells.

Answer 2

Opening of transient-type Ca channels, closure of K channels and opening of fast and slow Na channels.

Question 3

Where can an AP be initiated in the cardiac system?

Answer 3

SAN/AVN
Atrial muscle
Purkinjie fibres
Ventricular muscle
Each varies in size, duration and ion control

Question 4

How is a contraction initiated in cardiac muscle?

Answer 4

Uses Excitation - contraction coupling which is the conversion of an electrical stimulus into a mechanical response.

Question 5

Why is cardiac muscle special?

Answer 5

Myogenic - can produce its own AP for contraction without stimulation from extrinsic nerve fibres

Question 6

How does depolarisation spread in the heart?

Answer 6

Begins in the atria within SAN, travels to bundle of His and the L+R bundle branches to the purkinjie fibre and into ventricular muscles depolarising from endocardium to epicardium.

Question 7

What is the pace-maker rate?

Answer 7

The rate of the fastest AP produced in cardiac muscle. Usually produced by the SAN at 100AP.min. The muscle always beats to the fastest pace maker.

Question 8

Why is the SAN highly excitable and what does this mean for the pace maker?

Answer 8

Has a resting membrane potential of -55mV, lying close to the threshold. It will spontaneously depolarise after repolarisation.

Question 9

What sequence of events generate the pacemaker potential of the SAN?

Answer 9

1) Inward movement of Na through Slow VGNC
2) K channels close
3) Inward movement of Ca through transient Ca channels

Question 10

How is the atria depolarised once the pacemaker potential reaches the threshold?

Answer 10

Produces a Ca mediated AP:

1) Inward movement of Ca through L type channels
2) Further decrease in K conductance

Question 11

What causes repolarisation?

Answer 11

Outward movement of K (reducing +ve charge inside)

Question 12

What is the pacemaker potential?

Answer 12

The slow increase in voltage across a cell membrane that occurs at the end of one AP and the start of another.

Question 13

If the SAN has an intrinsic rate of 100AP.min why is the resting HR 60-70bpm?

Answer 13

Vagal activity reduces HR by innervating SAN and AVN to alter their pacemaker potential.

Question 14

How does vagal activity reduce the pacemaker potential?

Answer 14

ACh acts via M2 receptors to open K channels and cause hyperpolarisation. This elongates the pacemaker potential and increases the time taken to reach the threshold, therefor less AP are produced per minute.

Question 15

How does sympathetic activity increase the HR?

Answer 15

NAd acts at beta1 receptors to increase Na and Ca conductance to shorten the pacemaker potential and increase the number of AP generated per minute.

Question 16

How do AP spread through the cardiac cells?

Answer 16

Spread via GAP junctions to create a functional syncytium.

Question 17

Although atrial myocytes have the potential to contract intrinsicly, why do they not depolarise until told so by neighbouring cells?

Answer 17

Due to the -ve resting membrane potential.

Question 18

What is the function of AVN?

Answer 18

It connects the conductance from the atria to the ventricles and ensures depolarisation occurs in the correct sequence.

Question 19

What is different about AVN pacemaker potential compared to SAN?

Answer 19

AVN pacemaker rate is less steep and takes longer to reach the threshold and so produces 40AP.min

Question 20

What influence does the SAN have on AVN?

Answer 20

AVN only produces 40AP.min so the SAN influences AVN to beat faster.

Question 21

What happens if the SAN fails or there is a block in conductance from SAN?

Answer 21

The SAN is responsible for the AP the produce ventricular contraction so without it the ventricular myocytes will take over, causing the heart to beat at 20-40bpm

Question 22

What is an ectopic pacemaker?

Answer 22

Random ventricular cells that contract out of phase.

Question 23

How are the ventricles adapted to prevent contraction without stimulation?

Answer 23

The ventricles are highly permeable to K and this keeps a low resting potential of -90mV.

Question 24

Describe the sequence of events that occur in ventricular depolarisation and repolarisation

Answer 24

1) Fast VGNC open for rapid depolarisation
2) Na channels spontaneously close at high voltage
3) Inward Ca and outward K movement balances the ions to steady the potential into a plateau
4) Outward K movement causes repolarisation

Question 25

Why is Ca needed to produce an AP in cardiac muscle?

Answer 25

Ca release from SR requires Ca to enter the cell in order to allow crossbridge formation for contraction.

Question 26

What is the absolute refractory period?

Answer 26

A state of a membrane in which no AP can be generated despite any stimulation. Lasts for 200ms

Question 27

What is the relative refractory period?

Answer 27

If enough stimuli is received and AP can be produced.

Question 28

Why is it necessary for cardiac cells to have longer AP than skeletal muscle?

Answer 28

The length of AP determines the length of refractory period. The long refractory period ensures that diastole is completed before the next contraction.

Question 29

How does the long AP prevent another contraction and why is it important?

Answer 29

In cardiac muscle the twitch lasts as long as the electrical event. This prevents the muscle from being stimulated immediately after the twitch and therefore prevents TETANY and TEMPORAL SUMMATION as the muscle fully relaxes during the refractory period.

Question 30

How is the AP different in skeletal muscle?

Answer 30

The twitch lasts longer than the electrical event, allowing for fast restimulation as the muscle is still contracting in the refractory period.