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Cardiology > Physiology > Flashcards

Physiology Flashcards

1
Q

What are the different cell types in heart?

A
  • Cardiomyocytes
  • Pacemaker cells
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2
Q

What is the function of cardiomyocytes?

A

Cardiomyocytes make up the atria and the ventricles. These cells must be able to shorten and lengthen their fibers and the fibers must be flexible enough to stretch. These functions are critical to the proper form during the beating of the heart

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3
Q

What is the function of the pacemaker cell?

A

The cells that create rhythmic impulses, setting the pace for blood pumping. They directly control the heart rate.

In most humans, the concentration of pacemaker cells in the sinoatrial (SA) node is the natural pacemaker, and the resultant rhythm is a sinus rhythm.

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4
Q

What is the resting membrane poterntial of cardiomyocytes?

A

-90mV - due to high resting potassium permeability

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5
Q

How does cardiac action potential move between cardiomyocytes?

A

Gap junctions between cells

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6
Q

Describe the process of depolarisation of cardiomyocytes

A
  • As membrane potential becomes more positive, voltage gated Na+ channels open -> Na+ enters the cell and rapidly depolarise it.
  • MP reaches about +20mV before the Na+ channels close.
  • Cell begins to repolarise as K+ begins to leave the cell .
  • Repolarisation plateaus due to two events:
    • K+ permeability decreases due to fast channels closing
    • Ca2+ permeability increases due to voltage gated calcium channels opening slowly
  • Following this, the calcium channels close and potassium channels reopen, and normal depolarisation takes place.
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7
Q

Why is repolarisation prolonged in cardiomyoctyes?

A

This helps prevent tetanus by allowing the muscle to almost completely relax before the next action potential can be fired

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8
Q

What is the resting membrane potential of pacemaker cells?

A

-60mV - partly due to specific sodium channels found in pacemaker cells

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9
Q

What is the depolarisation cycle of pacemaker cells?

A
  • Sodium channels (which open during the refractory period of the previous action potential) open, allowing influx of sodium.
  • As influx of sodium increases, channels close and large calcium channels open to continue depolarisation towards threshold.
  • When threshold is reached, smaller calcium channels open, and calcium rushes into the cell.
  • After depolarisation reaches its peak, calcium channels close, and slow potassium channels open, allowing efflux of K+ out of the cell
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10
Q

What are modulators of electrical activity in the heart?

A
  • Autonomic nervous system
  • Temperature
  • Hyper/hypokalaemia
  • Hyper/hypocalcaemia
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11
Q

Where does the electrical activity in the heart start?

A

Sinoatrial node

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12
Q

What is the speed of conduction of the SA node?

A

0.5 m/sec

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13
Q

What is the conduction speed of the AV node?

A

0.05 m/sec

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14
Q

What is the pathway of conduction of the cardiac action potential?

A

SA node -> AV node-> bundle of His -> right and left bundle branches -> purkinje fibres

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15
Q

Why does the heart conduct from the AV node down to the purkinje fibres?

A

So that the ventricles contract from the bottom up

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16
Q

Why does that AV node slow down the action potential?

A

To allow the atria to complete their contraction cycle

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17
Q

What is the 1st heart sound created by?

A

Mitral and tricuspid valves closing

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18
Q

What is the second heart sound created by?

A

Aortic and pulmonary valves closing

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19
Q

What is the 3rd heart sound?

A

Rapid filling phase

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20
Q

What is the fourth heart sound?

A

Atrial contraction

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21
Q

What is the sequence of changes in chamber contraction throught the cardiac cycle?

A
  • Late diastole
  • Atrial systole
  • Isovolumic ventricular contraction
  • Ventricular ejection
  • Isovolumic ventricular relaxation
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22
Q

What is end diastolic volume?

A

Volume in the ventricles when the end of diastole has been reached, and before the commencement of systolic contraction

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23
Q

What is end systolic volume?

A

Volume in the ventricles when the end of systole has been reached, when the ventricles have been emptied as much as the force of the contraction causes

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24
Q

What is stroke volume?

A

End diastolic volume - End systolic volume

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25
Q

How would you calculate the ejection fraction?

A

Stroke volume/End diastolic volume

This is the percentage of the EDV which is ejected with each contraction

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26
Q

What is the a-wave?

A

Representation of increase in left atrial pressure due to atrial contraction

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27
Q

What does the C-wave represent?

A

Bulging of the mitral valve back into the left atrium due to ventricular contraction

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28
Q

What does the V-wave represent?

A

Left atrial pressure continues to increase due to venous return from the pulmonary circulation

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29
Q

What is the isometric contraction phase?

A

The contraction phase between the mitral valve closing and the aortic valve opening

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30
Q

What is the isometric relaxation phase?

A

The relaxation phase between the aortic valve closing and the mitral valve opening

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31
Q

What is the rapid filling phase?

A

The initial rapid filling of the ventricles after systole has completed along with isometric relaxation. This is associated with diastole. This is important as if heart rate increases, stroke volume is maintained.

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32
Q

What is the slower filling phase?

A

The 2/3rds of diastole where the rate of filling is slower than the initial rapid filling phase

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33
Q

What is the rapid ejection phase?

A

The initial rapid ejection of blood from the ventricle into the aorta

34
Q

What is the rapid ejection phase?

A

The initial rapid ejection of blood from the ventricle into the aorta

35
Q

What is the slow ejection phase?

A

The slower ejection of blood following the rapid ejection phase

36
Q

What is a pressure volume loop?

A

A plot of a system’s pressure versus volume which provides a framework for understanding cardiac mechanics in experimental animals and humans

37
Q

What is the equation for calculating cardiac output?

A

CO = HR x SV

38
Q

What happens to cardiac output at rates above 150 bpm?

A

Decreases due to the rate of depolarisation cutting into the rapid filling phase due to shortened cardiac interval. This results in a reduction in EDV, which reduces preload, thus reducing amount of stetch occuring in the cardiac muscle. This reduces resultant contraction, leading to a decrease in stroke volume

39
Q

What happens phsyiologically to increase CO?

A
  • HR increases
  • Contractility increases
  • Venous return increases - due to venoconstriction, skeletal and resp pump
  • TPR decreases - due to arteriolar dilatation which reduces afterload
40
Q

What is preload?

A

The degree of myocardial stretch before contraction - the load placed on the cardiac muscle before contraction causes the sarcomeres to stretch. The greater the stretch, the greater the contractile force

41
Q

What are factors which influence venous return?

A
  • Skeletal muscle pump
  • Respiratory muscle pump
  • Sympathetic innervation of veins
42
Q

How does preload compensate for a loss of pumping ability e.g. in an MI where muscle dies?

A

EDV is increased, which increases the preload. So, for a healthy heart, there will be a given stroke volume for an EDV. In a damaged heart, it will take a larger EDV to acheive the same SV as the larger EDV causes the remaining cardiac muscle to stretch more.

43
Q

What happens to the ejection fraction after someone has an MI?

A

Ejection fraction is reduced, as is exercise capacity

44
Q

What is afterload?

A

This is the load against which the muscle tries to contract. This is primarily the pressure within the aorta

45
Q

What factors contribute to afterload?

A
  • Pulmonary and systemic resistance (TPR)
  • Physical Characteristics of the vessels
  • The volume of blood that is ejected
46
Q

What happens to SV if afterload increases?

A

SV decreases due to the ventricles having less energy to eject the blood

47
Q

What is the spontaneous rhytm set by pacemaker cells with no autonomic input?

A

90-100 Bpm

48
Q

What effect does sympathetic activity have on the heart?

A

Increases HR

49
Q

How does the sympathetic nervous system influence HR?

A

Via sympathetic release of noradrenaline, which act on Beta 1 receptors in pacemaker cells in the SA node. This is also influenced by adrenaline from the adrenal gland.

Stimulation of the pacemaker cells increase the speed at which the cells depolarise by increasing ion flow through Ir and Ca2+ channels

50
Q

How does the parasympathetic influence HR?

A

Via release of acetylcholine by the vagus nerve (CN X). ACh activates muscarinic receptors in the SA node that influence K+ and Ca2+ channels, causing increased K+ influx, which hyperpolarises the cell, and decreased Ca2+ channel permeability.

The combination of the two leads to pacemaker cells taking longer to depolarise

51
Q

What is Starling’s law?

A

The energy of contraction is proportional to the initial length of the cardiac muscle fibre

52
Q

How does the sympathetic nervous system influence stroke volume?

A

Beta-1 activation increases the storage of Ca2+ in the cell. This makes more Ca2+ available for release, meaning more is available for contraction.

The compound effect of this is a stronger contraction, with increased contractility (inotropic effect), but the contraction is shorter due to increased removal of calcium from the cytosol.

53
Q

How does the parasympathetic nervous system influenve stroke volume?

A

This system has little effect on stroke volume. This is thought to be due to the fact the vagus nerve does not innervate the ventricular muscles.

54
Q

How does hypercalcaemia influence HR and contractility?

A

Shifts curve up and left - Hypercalcemia can result in an increase in heart rate and a positive inotropic effect (increase in contractility).

55
Q

How would hypocalcaemia influence HR and contractility?

A

Shifts curve down and right - Contractility and HR decreases

56
Q

How would you calculate mean arterial pressure?

A

MAP = CO x TPR

57
Q

Where are carotid sinus baroreceptors located?

A

In the walls of the carotid arteries and the aorta

58
Q

What is the function of the carotid sinus?

A

Monitoring blood pressure flowing to the brain. When the receptors are stretched, the rate of firing of action potentials increases.

59
Q

What are carotid sinus baroreceptors?

A

Tonically active stretch receptors which fire action potentials continuously at normal blood pressures.

60
Q

How do signals from carotid sinus barorecepetors reach the brain?

A

Via the glossopharyngeal nerve

61
Q

How do signals from aortic baroreceptors travel to the brain?

A

Via the vagus nerve

62
Q

Where in the brain do signals from the carotid sinus and aortic baroreceptors travel to?

A

Medullary cardiovascular control centre

63
Q

What happens after baroreceptors are triggered by a drop in blood pressure?

A

Increased sympathetic activity, decreased parasympathetic activtiy

  • Increased HR - Beta 1 receptors in pacemaker cells
  • Increased contractility - Beta 1 receptors in ventricular cells
  • Vasoconstriction - alpha 1 receptors
  • Venoconstriction - alpha 1 receptors
64
Q

What happens after baroreceptors are triggered by an increase in blood pressure?

A

Increased parasympathetic output, decreased sympathetic tone

  • Parasympathetic effects
    • Decreased HR - muscarinic receptors in pacemaker cells
  • Sympathetic removal
    • Decreased contractility
    • Decreased vaso/venoconstriction
65
Q

What are the main inputs into the medullary cardiovascular centres which influence cardiovascular performance?

A
  • Cardiopulmonary receptors
  • Peripheral chemoreceptors - low O2
  • Central chemoreceptors - increased CO2
  • Muscle chemoreceptors - increased K+
  • Joint receptors
66
Q

What is the effect of moving from sitting to standing on the cardiovascular system?

A

Standing causes a decrease in venous return (as blood pools in the feet). The result is a drop in EDV, resulting in reduced preload, reduced SV and subsequently a drop in CO, resulting in a drop in MAP.

Baroreceptors register this drop in pressure, and medullary centres increase sympathetic output and decrease parasympathetic output, resulting in increased HR, contractility, and vaso and venoconstriction. Coupled with venoconstriction, the skeletal muscle pump also increases venous return.

67
Q

What happens to MAP if CO increases but TPR remains constant?

A

MAP increases

68
Q

What happens to MAP is CO increases, but TPR decreases to a similar extent?

A

MAP remains fairly constant

69
Q

How does the cardiovascular system respond to someone initiating exercise?

A

CO needs to be increased to supply muscles with adequate oxygen. The initial response is active hyperaemia in the muscles, which results in a drop in MAP. This leads the baroreceptor reflex response:

  • Increased HR
  • Increased contractility
  • Vaso/venoconstriction

Respiratory and muscle pumps increase venous return, which increases EDV and thus preload, leading to an increased stroke volume. This leads to increased CO (Increased SV and HR) to meet the demands of the muscle

70
Q

Where is renin produced?

A

Juxtaglomerular cells of the kidney

71
Q

What is renin produced in response to?

A
  • Activation of sympathetic nerves to JGA by baroreceptor response
  • Decreased distension of afferent arterioles
  • Decreased delivery of Na+/Cl- to the macula densa in the loop of henle
72
Q

What is the pathway of renin activation?

A

Renin is released, and converts angiotensinogen to angiotensin 1. Angiotensin 1 has little effect. However, it is then converted to angiotensin 2 by angiotensin converting enzyme (ACE). This then has a number of actions which increases fluid volume, and also acts as a vasoconstrictor.

It also stimulates the release of aldosterone.

73
Q

What is the action of Angiotensin II?

A
  • Aldosterone release
  • ADH release
  • Vasoconstriction
  • ANG II receptors in medullary CV centres
  • Antinatriuretic actions
74
Q

What is the action of aldosterone?

A
  • ­Increased Na+ reabsorption at distal tubule
  • Increased ­K+ secretion
  • ­Retention of H2O with ­Na+
  • Stimulation of release of ANP from atrial cell - due to volume expansion
75
Q

What is the function of ADH?

A
  • Increase the permeability of collecting ducts.
  • Vasoconstriction
76
Q

What is ADH released in response to?

A
  • Decrease in blood volume - cardiopulmonary baroreceptors
  • Increase in osmolarity of the interstitial fluid - osmoreceptors in the hypothalamus
  • Circulating angiotensin II
77
Q

Where is atrial natriuretic peptide produced?

A

Myocardial cells of the heart

78
Q

Where is brain natriuretic peptide produced?

A

Ventricular myocardial cells

79
Q

What causes release of ANP?

A

Increased distention of the atrium

80
Q

What are the actions of ANP?

A
  • Increases excretion of Na+ (natriuresis) - thus leading to less water reabsorption (DIURESIS)
  • Inhibits the release of renin
  • Acts on the medullary CV centre to reduce MAP - vasodilation

ALDOSTERONE ESCAPE - also opposes action of angiotensin II

Cardiology (29 decks)

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