Regulation of Cardiac Function 2 Flashcards

(61 cards)

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
Where are the gap junctions in the heart?
Intercalated discs
26
Why are there gap junctions in the heart?
Allow ions to move between cells/electrically coupled So act as an electrical syncitium Smooth contraction = maximum blood ejection
27
What two factors affect the rate of action potential conduction?
Resistance of gap junctions Membrane capacitance
28
How can you change a gap junction to give faster action potential conduction?
More connexons (less resistance)
29
What is the conduction pathway in the heart?
SAN AVN Bundle of His Left and right bundles Purkinje fibres
30
How fast is action potential conduction in the atria?
1m/s
31
How fast is action potential conduction via the AVN?
0.05m/s
32
How fast is action potential conduction through the Bundle of His, left and right bundles and Purkinje fibres to the ventricular mass?
4m/s
33
How fast is action potential conduction from the endocardium to the epicardium?
0.3m/s
34
Why is conduction speed so slow in the AVN?
Allow last of atrial blood to enter ventricles
35
What type of cells make up the conduction pathway in the heart?
Muscle
36
What part of the nervous system modulates heart rate?
Autonomic NS
37
What is Ca2+-induced Ca2+ release?
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
What receptor do Ca2+ ions bind to on the sarcoplasmic reticulum?
Ryanodine
39
What protein does Ca2+ bind to in muscle contraction?
Troponin
40
Why must Ca2+ be removed after heart contraction?
Allow relaxation before the next contraction
41
How is Ca2+ removed after heart contraction?
Active Ca2+ uptake into sarcoplasmic reticulum via SERCA pump Ca2+ removal by Na-Ca exchanger
42
What pump is used in the uptake of Ca2+ into the sarcoplasmic reticulum?
SERCA
43
How many ions are transported by the Na-Ca exchanger at one time?
1 Ca2+ out 3Na+ in
44
How does noradrenaline act as an positive inotropic agent?
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
What is the Treppe effect?
Increased heart rate increases contractile force
46
What is the difference between chronotropic agents and inotropic agents?
Chronotropic agents affect rate Inotropic agents affect contractility
47
Give an example of a positive chronotropic agent
Noradrenaline
48
Give an example of a negative chronotropic agent
ACh Propanolol (b-blocker) Atenolol (b1-blocker) Adenosine Digoxin (glycosides)
49
How does adenosine decrease heart rate?
Activates nodal K+ channels = hyperpolarisation
50
How do glycosides decrease heart rate?
Increase vagal tone
51
Give an example of a positive inotropic agent
Noradrenaline Isoprenaline, adrenaline (b-agonists) Digoxin (glycosides)
52
How does digoxin increase contractility?
Inhibits Na-K ATPase Na+ not removed = Ca2+ not removed
53
What can act as a negative inotropic agent?
Ischaemia Hypoxia Acidity
54
How does an electrocardiogram work?
Measures alterations in currents at skin's surface to detect de/repolarisation of heart muscle
55
What is Einthoven's triangle?
Placement of electrodes in a 3-lead ECG
56
Which type of 3-lead ECG is used most often and why?
Lead II Depolarisations measured are parallel to the interventricular septum (best view of PQRST waves)
57
What is the positioning of electrodes in the Lead II 3-lead ECG?
Cathode on right clavicle Anode on last left rib Earth on left clavicle
58
What is the positioning of electrodes in the Lead III 3-lead ECG?
Cathode on left clavicle Anode on last left rib Earth on right clavicle
59
What is the positioning of electrodes in the Lead I 3-lead ECG?
Cathode on right clavicle Anode on left clavicle Earth on last left rib
60
Why do we take 6 or 12 lead ECGs?
Allows us to see different planes of heart to determine where a blockage in conduction is
61
In a Lead II 3-lead ECG, why is there positive and negative deflection?
Positive = depolarisation in same direction of anode Negative = depolarisation in opposite direction to anode