Week 2: Cardiac Physiology Flashcards

1
Q

Name 2 types of myocytes and their differences

A

conductive myocytes: specialised cells which conduct action potentials but can not contract contractile myocytes: contract when stimulated by an AP and conduct the action potential through intercalated discs

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

Fill the blanks

A
  1. sinoatrial node (SA) (aka sinus node) 2. internodal pathways 3. atrioventricular (AV) node 4. AV bundle (bundle of his) 5. left bundle branch 6. right bundle branch 7. purkinje fibres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is the automaticity of cardiac contraction produced?

A

Conductile myocytes spontaneously depolarise

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

Comment of the frequency differences of action potentials between different major regions of the heart

A

SA node cells: fastest with depolarisation of 60-100 AP/min with parasympathetic output AV node cells: depolarise at 40-60 AP/min at rest Purkinje fibres: depolarise at 15-40 AP/min at rest

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

Fill the blanks

A
  1. SA node 2. atrial fibres 3. AV node 4. ventricular fibres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe action potentials of pacemaker cells

A

The resting membrane potential of the sinoatrial node cells are -60mV

At this membrane potential, slow sodium channels (or pacemaker/funny channels) open at -60mV, triggering a slow depolarisation of the cell. Sodium released slowly.

These pacemaker channels dictate when to cause depolarisation to -40mV, which coincidentally is the threshold for the L type voltage gated calcium channels (are those channels that open at a particular voltage, they are triggered by the voltage)

Calcium then comes in, depolarising the membrane to about 0mV which then causes the inactivation of the calcium channels (closing (inactivation) of inactivation gate)

Slow potassium channels are triggered at 0mV resulting in the positive potassium ions travelling from inside to outside (diffusing across the cell membrane) causing repolarisation to resting membrane potential (-60mV) as there has being a build up finally big enough to repolarise it.

Once again, this -60mV resting membrane potential immediately reactivates the slow sodium channels which cause the pacemaker potential

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

Describe the sequence of depolarisation of the heart muscle

A

SA node -> atria contract -> AV node -> AV bundle -> bundle branches (left faster than right) -> purkinje fibres -> apex of ventricles -> superior area of ventricle

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

Describe the proportion of K+ Na+ and Ca2+ inside and outside contractile myocytes

A

Na+ and Ca2+ are higher outside, K+ is higher inside, however a large amount of Ca2+ is stored in the SR

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

Describe the phases of contractile myocyte action potentials

A

0: an influx of cations through intercalated discs from neighbouring cells raises the resting membrane potential from -90mV to the threshold of -60mV and fast voltage-gated Na+ channels open. Depolarisation inactivates Na+ channels. At -40mV slow L-type Ca2+ and K+ channels open 1. At peak depolarisation, K+ eflux briefly dominates causing a dip in potential 2. Slow Ca2+ channels are still open and balance the potential against the open K+ channels causing a plateau in potential and increased intracellular Ca2+ until Ca2+ channels inactivate. (High Ca2+ concentration in the cell during the plateau phase cause calcium-induced calcium release from the SR to allow muscle contraction.) 3. Rapid depolarisation due to active K+ channels. 4. Resting potential of -87mV is restored and maintaind by potassium K1/KIR channels. Ionic concentrations are resored via active ion pumps

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

Compare skeletal muscle contraction length with cardiac muscle contraction length

A

Cardiac muscle contracts much longer due to the plateau phase, which is necessary to expel blood from the chambers

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

Compare the length of the absolute refractory period in cardiac and skeletal muscle. Why is timing of this period critical in cardiac muscle?

A

Skeletal muscle only has an aboslute refractory period (ARP) of about 1ms whereas cardiac muscle has a 250ms ARP. This is necessary to allow chambers to fully relax between beats and to avoid wave summation and tetanus which would stop the heart from beating (fibrilation)

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

During which stages is the ARP active in contractile cardiac myocytes?

A

From depolarisation to about half-way through the repolarisation phase (Phase 0-half way through phase 3). The Second half of the repolarisation phase makes up the Relative refractory period

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

How does the parasympathetic nervous system slow the heart rate?

A

-ACh-sensitive K+ channels are activated hyperpolarising the membrane -muscarinic receptors are activated by ACh which lower the pacemaker current in the SA node

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

How does the sympathetic system increase the heart rate?

A

-Norepinephrine (NE) activates beta-1 adrenergic receptors in the SA and AV nodes. Stimulation of these receptors increases Ca2+ channel activity, producing more rapid APs - beta-1 adrenergic receptors in ventricular muscle increases contraction force via an increase in Ca2+ currents, through a higher rate of Ca2+ influx during depolarisation

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

What is an inotropic effect?

A

This is a mechanism which changes the strength of contraction.

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

What is a chronotropic effect?

A

This is a mechanism which alters the heart rate.

17
Q

What is a dromotropic effect?

A

This is a mechanism which changes the speed of the electrical impulse

18
Q

Which effect on the heart is visualised here?

A

chronotropic effects - slower rate of automaticity

19
Q

Which effect on the heart is visualised here?

A

dromotropic effect - slower conduction

20
Q

Which phases in the contractile myocytes depolarisation are in absolute refractory state?

A

0, 1, 2 and first part of 3

21
Q

Explain the depolarisation (including absolute refractory period and relative refractory period) in terms of the activation and inactivation gate opening and closing.

A
  • When it depolarises to about -60mV, the gate has become sufficiently positive to repel those positively charge amino acids, the activation gate opens and sodium can enter, this causes the depolarisation to go to about +20mV, that is too positive for the inactivation gate which is also positively charged and therefore shuts the channel trying to get away from the positive anterior. Even though the activation gate is open, the inactivation gate is closed and therefore, sodium cannot pass causing a depolarisation. Cannot have another depolarisation until the inactivation gate recovers. - This ARP is caused by the closing of a positively charged Sodium inactivation gate which moves away when Na moves into the cell (closing the gate and stopping the Na current) - Whilst the activation gates are open and the inactivation gates are closed, there is no way another action potential can occur meaning it is in an ARP -Then as the cell becomes more negative, the inactivation gate will open and the activation gate will close. The activation gate is capable of opening now.
22
Q

If the inactivation gate is open, is it in an activated or inactivated state?

A

activated

23
Q

Which phases are the relative refractory period in?

A

Late phase 3 and phase 4

24
Q

How is a negative chronotopic and domotropic effect created on the heart? (what is the sequence to of stimulation)

A

Vagus nerve releases ACh which bind to Muscarinic cholinergic receptors in the SA node. This activates the ACh-sensitive K+ channels which hyperpolarise the membrane. Negative domotropic effect from ACh from vagus nerve at AV node

25
Q

How is a positive chronotopic and domotropic effect created on the heart? (what is the sequence to of stimulation

A

Norepinephrine released which activates beta 1 adrenergic receptors –> increases ability of caclium channels to open –> causes more action potentials. Positive domotropic by increased velocity of action potentials from step 1 above.

26
Q

How is a positive inotropic effect created on the heart?

A

Beta 1 adrenergic receptors on contractile myocytes. Norepinephine when released from sympathetic nervous system acts on these receptors. Allows fore more calcium to enter the cell and therefore, form more cross bridges.

27
Q

Fill the blanks

A
28
Q

Fill the blanks

A
29
Q

What would happen if the AV node depolarised quicker thant he SA node?

A

There would be a resistance of blood flow as the papillary muscles would be contracting closing the atrio-ventricular cusps.

30
Q

Why is the resting membrane potential (phase 4) of a contractile myocyte stable compared to that of a conductile myocyte?

A

A conductile myocyte has funny channels which control when it can spontaneously depolarise. Whereas the contractile myocytes receive their depolarisation.

31
Q

Explain inactivation and recovery from inactivation using voltage gated sodium channel of a contractile myocyte action potential as your model.

A

Inactivation of the gate means it has closed (inactivated state). Recovers from K+ diffusing across cell membrane, making the cell more negative. The inactivation gate opens and the activation gate closes (inactivated). The cell is ready is now ready for a depolarisation.

32
Q

Why is the wave of excitation unidirectional in the heart?

A

Because the contractile myocyte before the one depolarising will be in absolute refractory period.

33
Q

Does increased parasympathetic input affect inotropy?

A

No as it does not target L gated calcium channels therefore cannot increase levels of calcium in the cell. It targets ACh-sensitive potassium channels.

34
Q

What change in luistropy would occur with an increase of decrease of chronotropy, domotropy and inotropy?

A

If luistropy increases, inotropy would increase as it removes more calcium therefore more chance for greater efflux of calcium back into cell.

Would only be affected with sympathetic input to heart due to calcium channels. An increase in calcium would decrease luistropy as it has to remove more calcium to recover etc.