Case 2 Physiology Flashcards

1
Q

What changes occur to ion channels in the phases of action potential generation in sinoatrial node pacemaker cells? (3 phases)

A

Phase 0: Ca2+ channels open
Phase 3: Ca2+ channels close, K+ channels open
Phase 4: HCN channels open, Ca2+ channels begin to reopen

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2
Q

What changes occur to membrane potential in the phases of action potential generation in sinoatrial node pacemaker cells? (3 phases)

A

Phase 0: membrane potential increases/depolarisation
Phase 3: membrane potential decreases/hyperpolarisation
Phase 4: membrane potential increases slowly/prepotential (funny current)

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3
Q

What major movements of ions occur in the phases of action potential generation in sinoatrial node pacemaker cells? (3 phases)

A

Phase 0: Ca2+ in
Phase 3: K+ out
Phase 4: Na+ in

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4
Q

Complete the sentences. Sinoatrial HCN channels are X-dependant and activated by Y. They permit the slow influx of ions in phase 4, mostly Z ions, to generate a prepotential.

A
X = cAMP
Y = hyperpolarisation
Z = Na+
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5
Q

What is the most important difference between Purkinje fibres and ventricular myocytes?

A

Purkinje fibres are intrinsic action potential firers (initiate depolarisation on their own through prepotential generation) whereas ventricular myocytes are not.

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6
Q

What changes occur to ion channels in the phases of action potentials in ventricular myocytes? (5 phases)

A

Phase 0: Na+ channels open
Phase 1: Na+ channels close, fast K+ channels open
Phase 2: Fast K+ channels close, Ca2+ channels (slow) open
Phase 3: Ca2+ channels close, slow K+ channels open
Phase 4: No changes (resting potential)
(Think ‘nakcak’ for order of channel opening)

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7
Q

Which is the slowest of the 4 major ion channels involved in ventricular myocyte action potentials?

A

Ca2+ channels

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8
Q

What major movements of ions occur in the phases of action potentials in ventricular myocytes? (5 phases)

A
Phase 0: Na+ in
Phase 1: K+ out
Phase 2: Ca2+ in
Phase 3: K+ out
Phase 4: No major changes (resting potential)
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9
Q

Which phase of the ventricular myocyte action potential is described as a ‘plateau’ and why?

A

Phase 2, there is (almost) an equilibrium of positive charge (K+, Ca2+) entering and leaving the cell (Cl- is also involved)

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10
Q

Which ion enables the functioning of the Na+/K+ ATPase pump to prevent cardiac arrhythmias?

A

Mg2+

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11
Q

An excess of which ion can cause increased depolarisation in phase 0, leading to more excitable myocytes?

A

Na+

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12
Q

An excess of which ion causes increased force of contraction and possible systolic cardiac arrest?

A

Ca2+

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13
Q

An excess of which ion disrupts phase 1 of the myocyte action potential, leading to possible diastolic cardiac arrest?

A

K+

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14
Q

How does acetylcholine lead to decreased cardiac output in terms of ion movement? (2 ways)

A
  • K(Ach) channels activated, increased K+ efflux in phase 3, greater hyperpolarisation, more Na+ needed to reach threshold, decreased heart rate
  • Ca2+ channels inhibited, decreased heart rate and contractility
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15
Q

How do the catecholamines lead to increased cardiac output in terms of ion movement?

A

Activate (phosphorylate) Ca2+ channels in the sarcoplasmic reticulum and myocyte cell surface membrane (especially in SAN), increasing contractility, conduction speed and heart rate.

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16
Q

What is the heterometric control mechanism of the heart?

A

Starling’s law – force of contraction is proportional to the initial diastolic fibre length (EDV, end diastolic volume)

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17
Q

What effect does underfilling of the heart have on contractility? Explain why.

A

According to Starling’s law, the overlap of actin and myosin is not optimal. Therefore, contractile ability is reduced.

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18
Q

What effect does overfilling of the heart, e.g. in heart failure, have on contractility? Explain why.

A

According to Starling’s law, actin and myosin become physically separated, cross-bridges cannot be formed and contractile ability is reduced.

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19
Q

A relatively high (but within normal range) end diastolic volume increases the contractility of cardiac muscle. True or false? Explain why.

A

True. According to Starling’s law, slightly increased distance between actin and myosin allows for more tension when cross-bridges form, leading to a more forceful contraction.

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20
Q

What is meant by cardiac homeometric control?

A

Extrinsic mechanisms to regulate cardiac output, independent of muscle fibre length changes (Starling’s law). This includes parasympathetic and sympathetic stimulation.

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21
Q

Complete the sentence. Catecholamines are X inotropes, Y dromotropes and Z chronotropes.

A

X = positive, Y = positive, Z = positive

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22
Q

How do catecholamines increase the speed of diastole? (5 steps)

A
  • Bind to ß1 receptors
  • Activate cAMP
  • Deactivate phospholamban
  • Upregulation of Ca2+ ATPase pumps in sarcoplasmic reticulum
  • Faster Ca2+ uptake into sarcoplasmic reticulum following systole
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23
Q

What effect does sympathetic activity have on cytosolic Ca2+ concentration in cardiac myocytes? Explain how.

A

Increase. Voltage-gated Ca2+ channels open, releasing Ca2+ from the sarcoplasmic reticulum.

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24
Q

Complete the sentences. In exercise, blood pressure increases. This is detected by X and leads to a compensatory response (involving process Y). However, this is over-ridden by Z as higher blood pressure is needed to meet the metabolic need of contracting skeletal muscle.

A
X = Baroreceptors
Y = Vasodilation
Z = Central nervous system (Sympathetic NS)
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25
Q

What causes increased venous return to the heart in exercise?

A

Greater pumping of skeletal muscle to squeeze blood through veins back to the right atrium.

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26
Q

Complete the sentence. Exercise leads to W stroke volume, X heart rate, Y cardiac output and Z length of the cardiac cycle.

A
W = increased
X = increased
Y = increased
Z = decreased
27
Q

Why is the cardiac cycle shorter in exercise?

A

Sympathetic stimulation, which leads to shorter length of diastole.

28
Q

What effects does repeated exercise (training) have on the cardiovascular system? (3 effects)

A
  • Increased cardiac muscle mass
  • Increased skeletal muscle mass
  • Increased venous return to heart (EDV increases, leading to lower BP and HR)
29
Q

What effect does increased rate and depth of ventilation in exercise have on the cardiovascular system? Explain why.

A

Blood is drawn to the heart (and lungs). This is due to negative pressure in the thorax.

30
Q

What is the sequence of tissues through which an impulse travels through the heart in one cardiac cycle? (6 steps)

A

Sinoatrial node, atrial myocardium/internodal pathways, AV node, bundles of His, left/right bundle branches, Purkinje fibres/ventricular myocardium

31
Q

At which point of the cardiac cycle’s electrical events is there a delay in transmission? Explain the benefit of this delay.

A

At the AV node. This delay allows extra time for ventricles to fill before ventricular systole.

32
Q

What structure ensures that ventricular depolarisation occurs from the apex of the heart upwards, rather than directly outwards from the interventricular septum?

A

Fibrous (non-conducting) skeleton of heart.

33
Q

Which type of cell-cell attachment enables synchronised contraction of cardiac muscle?

A

Connexons (gap junctions)

34
Q

What is the “Ca2+ sensor” in cardiac muscle that facilitates the formation of cross-bridges?

A

Troponin

35
Q

How does parasympathetic innervation slow the generation of prepotential in sinoatrial node cells? (2 points)

A
  • Decreased opening of HCN channels means decreased funny currents, therefore slower generation of prepotential occurs.
  • Ligand-gated K+ channels open, there is an efflux of K+, greater hyperpolarisation so slower generation of prepotential.
36
Q

Complete the sentence. Continuous X ensures that the sinoatrial node cells fire at a rate lower than their intrinsic firing rate of 110bpm.

A

X = vagal tone/parasympathetic innervation

37
Q

The electrical events of the cardiac cycle lags behind the corresponding mechanical events. True or false? Explain why.

A

False. The electrical events cause Ca2+ movement, leading to the formation of cross-bridges and mechanical events. Therefore, the mechanical events lag behind the electrical events.

38
Q

Complete the sentence. In sinoatrial node cells, the secondary chemical messenger X’s activity is Y by sympathetic innervation and Z by parasympathetic innervation, allowing heart rate to be controlled by various cellular effects.

A
X = cAMP
Y = increased
Z = decreased
39
Q

Put the mechanical events of the cardiac cycle in order: 1. ventricular ejection, 2. ventricular filling, 3. atrial contraction, 4. isovolumetric ventricular relaxation, 5. isovolumetric ventricular contraction.

A

2, 3, 5, 1, 4 (could start on any number as long as sequence is correct)
Ventricular filling, atrial contraction, isovolumetric ventricular contraction, ventricular ejection, isovolumetric ventricular relaxation

40
Q

In which mechanical event of the cardiac cycle is ventricular pressure

a) the highest
b) rising most rapidly?

A

a) ventricular ejection

b) isovolumetric ventricular contraction

41
Q

In which mechanical event of the cardiac cycle is ventricular volume lowest?

A

Isovolumetric ventricular relaxation

42
Q

Between which two of the mechanical events of the cardiac cycle do the semilunar valves close?

A

Ventricular ejection, isovolumetric ventricular relaxation

43
Q

Between which two of the mechanical events of the cardiac cycle do the semilunar valves open?

A

Isovolumetric ventricular contraction, ventricular ejection

44
Q

Between which two of the mechanical events of the cardiac cycle do the AV valves close?

A

Atrial contraction, isovolumetric ventricular contraction

45
Q

Between which two of the mechanical events of the cardiac cycle do the AV valves open?

A

Isovolumetric ventricular relaxation, ventricular filling

46
Q

What is the origin of the first heart sound “lub” in the cardiac cycle?

A

Closing of AV valves (mitral, tricuspid)

47
Q

What is the origin of the second heart sound “dub” in the cardiac cycle?

A

Closing of semilunar valves (aortic, pulmonary)

48
Q

Which parameters determine stroke volume? (3 factors)

A

Contractility, preload, afterload

49
Q

What is the difference between preload and afterload?

A

While preload is pressure exerted by blood entering the heart is diastole, afterload is pressure exerted by the blood ejected into the arteries in systole.

50
Q

What equation connects heart rate, cardiac output and stroke volume?

A

Cardiac Output = Heart Rate x Stroke Volume

51
Q

Complete the sentence. Stroke volume is measured per X, whereas cardiac output is measured per Y.

A
X = (each) contraction of the heart
Y = minute
52
Q

Stroke volume is equal to the difference between EDV and ESV. True or false? Explain why.

A

True. Stroke volume is the volume of blood ejected per contraction of the heart, so it equal to the difference in ventricular volume between the end of diastole and the end of systole.

53
Q

Why can peripheral oedema be observed in patients with heart failure?

A

Heart failure is the inability of the heart to function effectively as a pump – if blood cannot be pumped, fluid will “back up” through the venous system, increasing hydrostatic pressure in the venous end of capillaries. This will lead to reduced reabsorption of interstitial fluid and therefore oedema.

54
Q

In terms of Starling’s forces, how does oedema arise? (2 ways)

A
  • Increase in hydrostatic pressure (e.g. due to heart failure) inside the capillary increases fluid loss to/reduces fluid reabsorption from the interstitial fluid
  • Decrease in oncotic pressure (e.g. due to albumin loss in kidney disease) inside the capillary reduces fluid reabsorption from the interstitial fluid
55
Q

What is haemorrhage?

A

Bleeding due to damaged blood vessels.

56
Q

How is a decrease in effective circulating volume detected? (3 ways)

A
  • Chemoreceptors (measure H+) more stimulated
  • Baroreceptors (measure stretch) and renal baroreceptors less stimulated
  • Atrial and venous volume receptors less stimulated
57
Q

What are the cardiovascular compensatory mechanisms to hypovolaemic shock resulting from sympathetic activation? (3 mechanisms)

A
  • Vasoconstriction, increased BP
  • Release of catecholamines, increased heart rate/contractility, increased cardiac output
  • Release of ADH, fluid retained, BP maintained
58
Q

How does autotransfusion result from sympathetic activation in hypovolaemic shock compensation? (3 steps)

A
  • Glycogenolysis (increased glucose production)
  • Increased plasma and interstitium osmolarity
  • Up to 500ml water moves from cells to interstitium to plasma
59
Q

How is cardiogenic shock different to hypovolaemic shock?

A

Cardiogenic shock results from a failure of the ventricles (mechanical/electrical), whereas hypovolaemic shock results from an actual loss in effective circulating volume, e.g. due to haemorrhage.

60
Q

What is the basis of defibrillation?

A

It uses an electrical shock to reset the electrical state of the heart so that it may beat to its own rhythm, as set by the pacemaker cells.

61
Q

How does the amount of tissue affect the ECG wave?

A

The greater the amount of tissue, the larger the deflection.

62
Q

How does the direction of depolarisation affect the ECG wave?

A

Depolarisation towards the viewpoint (positive electrode): upwards wave.
Depolarisation away from the viewpoint: downwards wave.

63
Q

How does the direction of repolarisation affect the ECG wave?

A

Repolarisation towards the viewpoint (positive electrode): downwards wave.
Repolarisation away from the viewpoint: upwards wave.