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First Year > Cardio Misc. > Flashcards

Cardio Misc. Flashcards

1
Q

Where is the sinoatrial node located?

A

In the upper right atrium

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2
Q

What is the sinoatrial node?

A

It is the pacemaker of heart and site of origin of electrical excitation

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3
Q

How is the sinoatrial node capable of auto-rhythmicity?

A

As a result of pacemaker potential

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4
Q

What channel is responsible for pacemaker potential?

A

The hyper polarization activated cyclic nucleotide gated (HCN) channel

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5
Q

What is the process of HCN channels opening?

A

Following the action potential, the spontaneous opening of these channels in response to hyper polarization takes the pacemaker cells to threshold independent of a stimulus

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6
Q

How does action potential spread?

A

Via cell-to-cell conduction across gap junctions

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7
Q

What is the route of action potential spreading?

A

Atria – AV node – Bundles of His – Purkinjie fibers – Ventricles

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8
Q

What is the of the AV node?

A

It is the only point of electrical contact between the atria and ventricles

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9
Q

What is the role of the AV node?

A

To slow electrical action potential conduction between the atria and ventricles in order to allow the atria to fully contract and the ventricles fully fill before ventricular contraction

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10
Q

What is the resting membrane potential of ventricular myocytes?

A

-90mV

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11
Q

What is phase 0 of ventricular action potential?

A

Depolarization via influx of sodium

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12
Q

What is phase 1 of ventricular action potential?

A

Slight hyperpolarization due to close of sodium channels

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13
Q

What is phase 2 of ventricular action potential?

A

Plateau phase due to influx of calcium, which is responsible for calcium induced calcium release

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14
Q

What is phase 3 of ventricular action potential?

A

Hyperpolarization due to closure of calcium channels and efflux of potassium

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15
Q

What is phase 4 of ventricular action potential?

A

Resting membrane potential

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16
Q

What is meant by the term Chronotropic?

A

Increased rate of contraction

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17
Q

What is meant by the term Inotropic?

A

Modifying the force or speed of contraction of muscles

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18
Q

What is the parasympathetic effect on electrical activity?

A

Negative inotropic

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19
Q

What is the parasympathetic effect on electrical activity?

A

Positive inotropic

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20
Q

Where is parasympathetic innervation in the heart?

A

In the SA node only

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21
Q

Where is sympathetic innervation in the heart?

A

At the SA/AV nodes and ventricles

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22
Q

What is the parasympathetic receptor in the heart?

A

Muscarinic M2

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23
Q

What is the sympathetic receptor in the heart?

A

Adrenergic B1

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24
Q

What is the impact of the parasympathetic nervous system on the slope of pacemaker slope?

A

It reduces it

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25
Q

What is the impact of the sympathetic nervous system on the slope of pacemaker slope?

A

It increases it

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26
Q

What mediates the parasympathetic innervation in the heart?

A

Ach

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27
Q

What mediates the sympathetic innervation in the heart?

A

Noradrenaline

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28
Q

How are myocytes coupled?

A

Via desmosomes

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29
Q

How is force generated in the heart?

A

Via calcium and ATP dependent cross bridge cycles

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30
Q

Why is the plateau phase essential in ventricular potential?

A

It allows for calcium induced calcium release and therefore enough calcium to be present for the cross bridge cycle to occur

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31
Q

What is meant by the term excitation contraction coupling?

A

It is the physiological process of converting an electrical stimulus to a mechanical response

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32
Q

What is the refractory period?

A

It is the period in which it is not possible to produce another action potential due to inactivation of sodium channels

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33
Q

What is the importance of the refractory period?

A

Essential for preventing tetanic contraction of the heart

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34
Q

What is meant by the term stroke volume?

A

The volume of blood ejected from the heart with each beat

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35
Q

What is the average stroke volume?

A

70mls

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36
Q

What is the frank starling law?

A

It describes the mechanisms of intrinsic control of SV, stating that increasing venous return will increase stroke volume

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37
Q

What is afterload?

A

The pressure in which the heart is pumping out against

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38
Q

What is the relationship between the frank starling law and afterload?

A

The frank starling law helps to compensate for an increase in afterload, which is seen with the likes of hypertension

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39
Q

What mediates extrinsic control of stroke volume?

A

An increase in calcium-induced calcium release and contractility

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40
Q

What effect does the extrinsic control of stroke volume have on the frank starling curve?

A

It acts to shift it to the left

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41
Q

What is meant by the term cardiac output?

A

The amount of blood pumped from the heart per minute

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42
Q

What is the average cardiac output?

A

5l/min

43
Q

What is phase 1 of the cardiac cycle?

A

Passive filling

44
Q

What is phase 2 of the cardiac cycle?

A

Atrial contraction

45
Q

What is phase 3 of the cardiac cycle?

A

Isovolumetric ventricular contraction

46
Q

What is phase 4 of the cardiac cycle?

A

Ventricular ejection

47
Q

What is phase 5 of the cardiac cycle?

A

Isovolumetric ventricular relaxation

48
Q

What occurs during passive filling?

A

It is the phase of diastole in which both chambers of the heart are relaxed and there is passive filling of the ventricles

49
Q

What occurs during atrial contraction?

A

Depolarization and contraction of the atrium, which allows filling of the ventricles to be completed

50
Q

What occurs during isovolumetric ventricular contraction?

A

Depolarization and contraction of the ventricles, causing pressure inside the ventricles to exceeds that of the atria, resulting in the closure of the AV valve

51
Q

What occurs during ventricular ejection?

A

Pressure builds in the ventricles due to contraction and results in ejection of blood once the pressure exceeds that in the great vessels. Following ejection, the ventricles being to repolarize and relax and pressure drops below that of the great vessels, causing semi lunar valves to shut.

52
Q

What occurs during isovolumetric ventricular relaxation?

A

Commences when the semi lunar valve shuts and continues until passive filling commences again

53
Q

Why is there no actual movement of blood during isovolumetric ventricular contraction?

A

Because the pressure in the great vessels is still exceeding that of the ventricles.

54
Q

What is meant by the term blood pressure?

A

The outward hydrostatic pressure exerted against the vessels by the blood

55
Q

What does the 1st Korotkoff sound indicate?

A

Systolic pressure

56
Q

What does the 2nd Korotkoff sound indicate?

A

Diastolic pressure

57
Q

What is meant by the term mean arterial blood pressure?

A

The product of product of cardiac output and total peripheral resistance

58
Q

What is the equation for calculation mean arterial blood pressure?

A

(2 x diastolic + systolic) / 3

59
Q

What is a normal mean arterial blood pressure?

A

70 – 105 mmHg

60
Q

What is the average mean arterial blood pressure?

A

93mmHg

61
Q

What is minimal mean arterial blood pressure required to maintain perfusion to coronary arteries, brain and kidneys

A

60mmHg

62
Q

How is total peripheral resistance controlled?

A

Via altering the muscle tone of the smooth muscle within the arterioles

63
Q

What intrinsic metabolic changes and chemical mediators result in constriction of smooth muscle?

A

Serotonin, thromboxane A2

64
Q

What intrinsic metabolic changes and chemical mediators result in dilation of smooth muscle?

A

Acidosis, hypoxia, hypercapnia, increased temperature, nitric oxide, inflammatory mediators

65
Q

What is the myogenic response?

A

Reflex mechanism that overcomes slight changes in MAP that results in dilation or constriction, depending in the change, in order to maintain blood flow to brain and kidneys over a range of mean arterial blood pressures

66
Q

What is the principle extrinsic controller of smooth muscle tone?

A

The sympathetic nervous system

67
Q

How is basal tone in the blood vessels created?

A

Tonic sympathetic discharge to vascular smooth muscle

68
Q

What is the primary control of basal tone?

A

Noradrenaline action on alpha adrenoceptors causing dilation

69
Q

What is the effect of adrenaline acting on alpha receptors in the skin, gut and kidneys?

A

Constriction and reduced flow

70
Q

What is the effect of adrenaline acting on beta receptors in cardiac and skeletal ?

A

Dilation and increased flow

71
Q

What is the effect of parasympathetic activity on mean arterial blood pressure?

A

Reduces it by reducing cardiac output via negative inotropic effects

72
Q

What is the effect of sympathetic activity on mean arterial blood pressure?

A

Increases it by inducing Positive chronotropic and inotropic effects, which increases cardiac output, and by causing an increase in total peripheral resistance via stimulation of arteriolar constriction.

73
Q

How is short-term control of blood pressure achieved?

A

Via activity of the autonomic nervous system and the baroreceptor reflex.

74
Q

Where are baroreceptor found?

A

At the aortic arch and carotid sinus

75
Q

What is the short-term response to a decreased mean arterial blood pressure?

A
  • Decreased signalling from baroreceptors, which is detected by the medulla
  • This stimulates a decrease in parasympathetic and an increase in sympathetic output, which will increase MAP
76
Q

What is the short-term response to a increased mean arterial blood pressure?

A
  • Increased signalling from baroreceptors, which is detected by the medulla
  • This stimulates an increase in parasympathetic and a decrease in sympathetic activity, which will reduce MAP
77
Q

How is long-term control of blood pressure achieved?

A

Via the renin angiotensin system

78
Q

What is renin?

A

A hormone released from granular cells in the juxtamedullary apparatus of the kidneys

79
Q

When is renin released?

A

In response to:
- Reduced BP
- Low sodium
- Sympathetic stimulation

80
Q

What is angiotensinogen?

A

A protein released from liver and is acted upon by renin to produce angiotensin 1

81
Q

Where is angiotensinogen found?

A

In the liver

82
Q

What is the angiotensin converting enzyme?

A

An enzyme that converts angiotensin 1 to the effector protein called angiotensin 2

83
Q

Where is the angiotensin converting enzyme found?

A

Mainly in the lungs

84
Q

What is angiotensin 2?

A

An effector protein that acts to:
- Stimulate thirst
- Cause vasoconstriction
- Stimulation of aldosterone release

85
Q

What is aldosterone?

A

A hormone that acts to increase blood volume by increasing sodium resorption in the kidneys

86
Q

Where is aldoestrone found?

A

In the adrenal cortex

87
Q

What is the effect of aldosterone stimulation?

A

Increased fluid resorption, blood volume and BP & secretion of potassium and hydrogen.

88
Q

What is the atrial natriuretic hormone?

A

A peptide produced in the atria that is released in response to increase blood volume causing atrial distension

89
Q

What does the atrial natriuretic hormone stimulate?

A
  • Excretion of sodium and water
  • Reduce renin release
  • Vasodilation of blood vessels
90
Q

What is the anti diuretic hormone?

A

A hormone produced in hypothalamus and stored in posterior pituitary

91
Q

When is the anti diuretic hormone released?

A

In response to increased ECF osmolarity, which results in a reduced RCF volume.

92
Q

What does the anti diuretic hormone work to do?

A

Increase water reabsorption via aquaporins

93
Q

What are the ‘big 5’ cardiovascular risk factors?

A
  • Obesity
  • Smoking
  • Diabetes
  • Hypertension
  • Hyperlipidemia
94
Q

What are the ‘little 4’ cardiovascular risk factors?

A
  • Stress
  • Alcohol
  • Physical inactivity
  • Biological factors (age, gender, genetics, family/personal history)
95
Q

What are some cardiovascular chest pain differentials?

A

ACS, Angina, Pericarditis and Aortic dissection

96
Q

What are some respiratory chest pain differentials?

A

PE, Pneumonia and Pneumothorax

97
Q

What are some other chest pain differentials?

A

GORD, MSK chest pain and anxiety

98
Q

What are murmurs?

A

Audible turbulent blood flow as a consequence of valve disease

99
Q

When are systolic murmurs heard?

A

After the first heard sound

100
Q

When are diastolic murmurs heard?

A

After the second heart sound

101
Q

When are right sided murmurs heard?

A

Louder during inspiration and expiration

102
Q

What diagnostic investigations would be done for murmurs?

A

Echo

103
Q

What causes the first heart sound?

A

Closure of the mitral and tricuspid valves

104
Q

What causes the second heart sound?

A

Closure of the aortic and pulmonary valves

First Year (71 decks)

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