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BMS10 > Regulation of Cardiac Function 2 > Flashcards

Regulation of Cardiac Function 2 Flashcards

1
Q

Describe a ventricular action potential

A

Rapid depolarisation

Long plateau phase

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2
Q

What is the resting membrane potential in the ventricles?

A

-90mV

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3
Q

What is the resting membrane potential in the atria?

A

-90mV

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4
Q

What is the resting membrane potential in the Purkinje fibres?

A

-90mV

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5
Q

Describe the ionic currents during a ventricular action potential (3)

A

Opening of Na+ channels = rapid depolarisation (voltage-gated Na+ channels and positive feedback) due to Na+ influx

Ca2+ channels open at peak depolarisation and Na+ channels close = plateau due to Ca2+ influx

K+ channels open after plateau and Ca2+ channels close = repolarisation due to K+ efflux

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6
Q

What occurs in skeletal muscle when there is insufficient time to remove Ca2+?

A

Tetany

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7
Q

Why is tetany not desirable in cardiac muscle?

A

Discrete contractions

Maximise volume of blood pumped

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8
Q

How are discrete cardiac muscle contractions achieved?

A

Length of action potential and length of contraction and relaxation is synonymous

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9
Q

How does lowering the Ca2+ concentration affect the ventricular action potential/contraction?

A

Shorter plateau

Less tension generated

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10
Q

What is the decaying pacemaker potential?

A

Describes the SAN membrane potential

Gradual spontaneous depolarisation to allow spontaneous action potential to be generated

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11
Q

What cells have a decaying pacemaker potential?

A

SAN

AV node and Purkinje fibres have some in case SAN is damaged

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12
Q

Is the upstroke/depolarisation faster in the SAN or the ventricles?

A

Ventricles

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13
Q

Describe the currents underlying the SAN action potential (4)

A

Long-acting Ca2+ channels generate slow-rising action potential by Ca2+ influx

At peak, K+ channels open and Ca2+ channels close = repolarisation by K+ efflux

Closure of K+ channels and opening of ‘funny current’ Na+ channels = start of pacemaker potential by Na+ influx

Towards end of pacemaker potential, transient and long-acting Ca2+ channels open = depolarisation

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14
Q

What kind of ion channel is mostly absent in nodal cells?

A

Voltage-gated Na+ channels

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15
Q

Why is it called the ‘funny current’ Na+ channel?

A

Opens on hyperpolarisation rather than depolarisation

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16
Q

What is the difference between transient and long-acting Ca2+ channels?

A

Transient = open for less time but let in more Ca2+ at one time

Long-acting = open for longer but let in less Ca2+ at one time

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17
Q

What drugs inhibit long-acting Ca2+ channels in the SAN?

A

Verapamil

Nifedipine

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18
Q

What inhibits K+ channels in the SAN?

A

Barium

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19
Q

What drug inhibits the ‘funny current’ Na+ channels in the SAN?

A

Ivabradine

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20
Q

What type of agents modulate the pacemaker potential decay rate?

A

Chronotropic agents

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21
Q

What do chronotropic agents modulate and how?

A

Decay of pacemaker potential

Affect ion conductance of channels

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22
Q

What are two examples of chronotropic agents and what do they do?

A

Noradrenaline (sympathetic) = faster decay = faster heart rate

Acetylcholine (parasympathetic) = slower decay = slower heart rate

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23
Q

What are the units that make up a gap junction?

A

Connexons

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24
Q

What are the subunits of a connexon?

A

6 connexins

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25
Q

Where are the gap junctions in the heart?

A

Intercalated discs

26
Q

Why are there gap junctions in the heart?

A

Allow ions to move between cells/electrically coupled

So act as an electrical syncitium

Smooth contraction = maximum blood ejection

27
Q

What two factors affect the rate of action potential conduction?

A

Resistance of gap junctions

Membrane capacitance

28
Q

How can you change a gap junction to give faster action potential conduction?

A

More connexons (less resistance)

29
Q

What is the conduction pathway in the heart?

A

SAN

AVN

Bundle of His

Left and right bundles

Purkinje fibres

30
Q

How fast is action potential conduction in the atria?

A

1m/s

31
Q

How fast is action potential conduction via the AVN?

A

0.05m/s

32
Q

How fast is action potential conduction through the Bundle of His, left and right bundles and Purkinje fibres to the ventricular mass?

A

4m/s

33
Q

How fast is action potential conduction from the endocardium to the epicardium?

A

0.3m/s

34
Q

Why is conduction speed so slow in the AVN?

A

Allow last of atrial blood to enter ventricles

35
Q

What type of cells make up the conduction pathway in the heart?

A

Muscle

36
Q

What part of the nervous system modulates heart rate?

A

Autonomic NS

37
Q

What is Ca2+-induced Ca2+ release?

A

Action potential causes long-acting Ca2+ channels to open in T-tubules = Ca2+ influx

Ca2+ binds to ryanodine receptors on sarcoplasmic reticulum to allow Ca2+ release from internal store

38
Q

What receptor do Ca2+ ions bind to on the sarcoplasmic reticulum?

A

Ryanodine

39
Q

What protein does Ca2+ bind to in muscle contraction?

A

Troponin

40
Q

Why must Ca2+ be removed after heart contraction?

A

Allow relaxation before the next contraction

41
Q

How is Ca2+ removed after heart contraction?

A

Active Ca2+ uptake into sarcoplasmic reticulum via SERCA pump

Ca2+ removal by Na-Ca exchanger

42
Q

What pump is used in the uptake of Ca2+ into the sarcoplasmic reticulum?

A

SERCA

43
Q

How many ions are transported by the Na-Ca exchanger at one time?

A

1 Ca2+ out

3Na+ in

44
Q

How does noradrenaline act as an positive inotropic agent?

A

Faster decay of pacemaker potential = faster heart rate (positive chronotropic agent)

Less time to remove Ca2+ so builds up

Ca2+ required for contraction so increased contractile force (staircase/Treppe effect)

45
Q

What is the Treppe effect?

A

Increased heart rate increases contractile force

46
Q

What is the difference between chronotropic agents and inotropic agents?

A

Chronotropic agents affect rate

Inotropic agents affect contractility

47
Q

Give an example of a positive chronotropic agent

A

Noradrenaline

48
Q

Give an example of a negative chronotropic agent

A

ACh

Propanolol (b-blocker)

Atenolol (b1-blocker)

Adenosine

Digoxin (glycosides)

49
Q

How does adenosine decrease heart rate?

A

Activates nodal K+ channels = hyperpolarisation

50
Q

How do glycosides decrease heart rate?

A

Increase vagal tone

51
Q

Give an example of a positive inotropic agent

A

Noradrenaline

Isoprenaline, adrenaline (b-agonists)

Digoxin (glycosides)

52
Q

How does digoxin increase contractility?

A

Inhibits Na-K ATPase

Na+ not removed = Ca2+ not removed

53
Q

What can act as a negative inotropic agent?

A

Ischaemia

Hypoxia

Acidity

54
Q

How does an electrocardiogram work?

A

Measures alterations in currents at skin’s surface to detect de/repolarisation of heart muscle

55
Q

What is Einthoven’s triangle?

A

Placement of electrodes in a 3-lead ECG

56
Q

Which type of 3-lead ECG is used most often and why?

A

Lead II

Depolarisations measured are parallel to the interventricular septum (best view of PQRST waves)

57
Q

What is the positioning of electrodes in the Lead II 3-lead ECG?

A

Cathode on right clavicle

Anode on last left rib

Earth on left clavicle

58
Q

What is the positioning of electrodes in the Lead III 3-lead ECG?

A

Cathode on left clavicle

Anode on last left rib

Earth on right clavicle

59
Q

What is the positioning of electrodes in the Lead I 3-lead ECG?

A

Cathode on right clavicle

Anode on left clavicle

Earth on last left rib

60
Q

Why do we take 6 or 12 lead ECGs?

A

Allows us to see different planes of heart to determine where a blockage in conduction is

61
Q

In a Lead II 3-lead ECG, why is there positive and negative deflection?

A

Positive = depolarisation in same direction of anode

Negative = depolarisation in opposite direction to anode

BMS10 (13 decks)

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