Electrical activity of the Heart Flashcards

1
Q

How does excitation contraction coupling occur in cardiac muscle

A

working as functional syncytium of intercalated discs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is interlaced discs composed of and what is there individual function

A

electrically connected via gap junctions

physically connected by desmosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does it mean is cardiac muscle is myogenic

A

can contract without nervous stimulation - autorhymicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why is there a long refractory period in cardiac muscle

A

Lots of calcium entry from outside the cell which does not fully saturate troponin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The Regulation of calcium from outside the cell allows control over what

A

Strength of heart contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the length of action potential in cardiac muscle compared to skeletal muscle

A

250milli seconds compared to 2mill seconds

longer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do cells with unstable resting membrane potential acts as

A

Pacemaker cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In non pacemaker cells what causes the increase in resisting membrane potential

A

Increased permeability of potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In non pacemaker cells what causes the initial slight depolarisation

A

An increase in sodium permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In non pacemaker cells what causes the the plateau in polarisation

A

Increase in calcium permeability

Decrease in potassium permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

in non pacemaker cells what causes the re-polorisation

A

decrease in calcium permeability

Increase in potassium permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes pacemaker cells pre potential to depolarise

A

gradual decrease in Permeability of K+
early increase in Permeability of Na+ (= PF)
late increase in Permeability Ca2+ (T-type)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What then causes the action potential of pacemaker cells

A

increase in PCa2+ (L-type)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what triggers pF sodium permeability and why is that useful

A

Voltage dependant sodium current opened by the re-polarisation of previous channel which thens allows this early increase sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the major difference in pacemaker potential and no pacemaker potential

A

Pacemaker is the same as before but without fast depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the steps in cardiac muscle contraction

A

The action potential spreads from the cell membrane into the T tubules.
Calcium enters the cell from the ECF (this doesn’t happen in skeletal muscle).
This triggers the release of even more calcium from the SR.
Intracelllular calcium increases.
Calcium binds to the troponin/tropomysin complex, and tropomysin moves out of the way of the active site on the actin filament.
Actin and myosin bind, and the thick and thin filaments slide past each other
the myocyte contracts.
Relaxation occurs when calcium is actively transported back into the SR (by calcium-ATPase pump) or out of the cell into the ECF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is example of modulators of electrical activity of the heart

A
Sympathetic & parasympathetic systems 
Ca2+-channel blockers 
cardiac glycocides
Temperature
Hyperkalemia (high plasma K+)
Hypokalemia (low plasma K+)
Hypercalcemia (high plasma Ca2+)
Hypocalcemia (low plasma Ca2+)
18
Q

What is the effect of calcium channel blockers

A

decreases force of contraction

19
Q

What is the effect of cardiac glycosides

A

Increases force of contraction

20
Q

How much does 1ºC increase the heart rate

A

increases ~10 beats/min/ºC

21
Q

What is Hyperkalemia (High K) and hypokelimia (Low K) effect on the heart

A

Fibriltion and heart block

22
Q

What is unusual about the affect of Hyperkalemia and hypokelimia affect on the heart

A

should oppose each other, but don’t = anomalous

23
Q

What is the affect if Hypocalcemia (low Ca) and hypercalcemia (High Ca) affect on the heart

A

Hyper - increase heart rate and force of contraction

Hypo - decrease heart rate and force of contraction

24
Q

Why does hyerkalemia cause a heart block and fibrillation

A

increase potassium means heart with depolarises opening lots of channel therefore firing AP in an unorganised fashion = fibrillation

constant depolarisation than can eventual cause the heart to stop

25
Q

What are the three types of cardiocytes found in the myocardium

A

Sinoatrial nodes
Purkinje fibres
Contractile cells

26
Q

How are the SAnodes triggered to conduct

A

Influx of sodium makes cells more negative - pacemaker cell potential
AP threhsold is then reached
AP tiggere propagation of cells opening sodium channels, potassium channels and so-called FAST calcium channels

This causes further depolarisation of neighbouring cells

27
Q

What is the annulus fibrosis and is it conducting tissue?

A

tough circular exterior of the intervertebral disc that surrounds the soft inner core, the nucleus pulposus
is the only non conducting part of the heart

28
Q

Where is the SA node located and how long does it take to pass signal

A

found at the junction at the top of the right atrium

0.5m/s

29
Q

What is responsible for slowing down the heart rate i.e. the delay box

A

Atrioventricular node

30
Q

Where is the Atrioventricular node located

A

centre of the heart

31
Q

What is the functions of the AV node

A

Regulates signals from the SA node
sends the electrical impulses from the atria to the ventricles - prevent rapid conduction
makes sure that the atria are empty and closed before stimulating the ventricles

32
Q

How long does the function of the AV valve take

A

0.05 m/sec

33
Q

Define fibrillation

A

rapid, unsynchronised contractions of muscle fibre

34
Q

where is the only nonconducting part of the heart

A

Annulus fibrosus

35
Q

What does the bundle of his allow

A

Signal form AV to Purkinje fibres

36
Q

what is the function of Purkinje fibres

A

conduct APs in ventricle walls

37
Q

Why is purknje fibres cause a rapid conduction, what is the time of conduction

A

Ð to make sure ventricles depolarise at same time

Ð ~ 5 m/sec

38
Q

what rhythm does the heart beat to

A

The rhythm of the SA pacemakers

39
Q

what does a single AP in a single myocyte evoke

A

a very small extracellular (cf transmembrane) electrical potential

40
Q

What creates the large extracellular wave that is recorded on the periphery of an ECG

A

lots of small extracellular electrical potentials being evoked by many cells depolarising and repolarising at the same time and summating

41
Q

Why is tetnus impossible for cardiac muscle

A

As the action potential lasts nearly as long as the contraction and relaxation periods, a cardiac muscle cell will have nearly completed its relaxation period before it can respond to a subsequent stimulus.

42
Q

What would happen if tetnus was to occur in the heart

A

If tetanus could occur in cardiac muscle, it would stop the heartbeat and therefore the flow of blood