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Systems 1a Revision Decks > CVS Physiology > Flashcards

CVS Physiology Flashcards

1
Q

What planes may a standard limb lead perceive events in?

A

Frontal or vertical

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2
Q

What structures are associated with the following SSLs:

SLL1
SLL2
SLL3

A

SLL1 - Right arm with respect to left arm

SLL2 - Left leg with response to right arm

SLL3 - Left leg with respect to left arm

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3
Q

What two basic principles are essential to understanding and ECG blip?

A
  • Approaching depolarisation causes and upward blip (visa versa)
  • Fast events are transmitted better than slow events
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4
Q

What is the most important SLL and why?

A

SLL2 - the main wave of depolarisation passes down the axis of the ventricles

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5
Q

What is represented by a P-wave?

A

Atrial depolarisation

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6
Q

What is represented by the QRS complex?

A

Ventricular depolarisation

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7
Q

What is represented by the T-wave?

A

Ventricular repolarisation

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8
Q

What is the PR intervals and what is its typical duration?

A

The length of time between atrial and ventricular depol. usually 0.12-0.2 seconds

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9
Q

What is the typical duration of the QRS complex

A

.08 s

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10
Q

What is the QT interval and what is its typical duration?

A

Time spend while ventricles are depolarised about 0.42 seconds

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11
Q

Why can’t we see atrial depolarisation on an ECG?

A

Hidden by QRS complex

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12
Q

Outline the components of the QRS complex

A

Q - Septal depolarisation
R - Bulk depolarisation
S - Upper part of the inter-ventricular septum depolarisation

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13
Q

What pathologies may cause axis deviation of the heart?

A

Rotation, hypertrophy of left/atrophy of right side of the heart

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14
Q

What do augmented limb leads tell you?

A

Gives another aspect of the heart

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15
Q

What do precordial leads give you?

A

Horizontal view of events in the heart

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16
Q

What kind of blips do the precordial chest leads produce?

A

Negative until about V3/4 then positive

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17
Q

What does the rhythm strip tell you?

A

Heart rate and regularity, PR interval, , QRS complex width, QT interval and the relationship between a P-wave and QRS complex

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18
Q

What is a STEMI, how does it differ from a NSTEMI?

A

ST- elevated MI

Non-ST-Elevated MI

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19
Q

How is heart rate regulated?

A

Neural control

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20
Q

How is stroke volume regulated?

A

Preload/afterload and neural control

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21
Q

What is the collective effect of regulation of heart rate and stroke volume?

A

Regulation of cardiac output

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22
Q

How does the sympathetic nervous system regulate heart rate?

A

Noradrenaline and circulating adrenaline from the adrenal glands act on Beta-1 receptors on the SA node - increasing the slope of the path maker potential and increasing heart rate

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23
Q

How does the parasympathetic nervous system regulate heart rate?

A

Vagus nerve releases ACh and acts on muscarinic receptors of the S node, hyperpolarising cells and decreasing heart rate

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24
Q

What does Starlings law state?

A

The force of cardiac contractility is proportional to the initially length of the cardiac muscle fibre

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25
Q

In vivo, what variable effects preload?

A

End diastolic volume

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26
Q

What effect does an increased venous return have on stroke volume?

A

Increases EDV, therefore increases stroke volume

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27
Q

What effect does a decreased venous return have on stroke volume?

A

Decreases preload therefore decreases stroke volume

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28
Q

What is afterload?

A

The load of blood against which the muscle tries to contract

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29
Q

What is TPR?

A

Total peripheral resistance - a measure of how easy it is for blood to get through the aorta

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30
Q

An increased after load will decrease stroke volume - how?

A
  • TPR increases
  • Aortic pressure increases
  • More energy required to open aortic valves
  • Less energy available to eject blood
  • Decreased stroke volume
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31
Q

Describe the neural effect on stroke volume?

A

Noradrenaline/circulating adrenaline increase contractility of myocytes by acting on Beta-1 receptors

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32
Q

What effect does the parasympathetic system have on regulation of stroke volume?

A

Very little because vagus nerve does not innervate ventricles

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33
Q

What pathologies have an effect on regulations of stroke volume?

A
  • Hypercalcaemia
  • Hypocalcaemia
  • Ischaemia
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34
Q

What effect does hypercalcaemia have on stroke volume/EDV graph?

A

Shifts up and left

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35
Q

What effect does hypocalcaemia and ischaemia have on the stroke volume/EDV graph?

A

Shifts down and right

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36
Q

Where would you find capillaries with no clefts and no channels?

A

The brain

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37
Q

What is a capillary cleft?

A

Gap between adjacent epithelial cells

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38
Q

What is a capillary fenestration?

A

Circular pore in capillary

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39
Q

Where would you find a capillary with clefts only?

A

Muscles

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40
Q

Where would you find fenestrated capillaries?

A

Intestines

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41
Q

What are discontinuous capillaries and where would you find them?

A

Large open pores, also known as sinusoidal capillaries, can be found in the liver and kidneys

42
Q

What two components to a blood clot must occur?

A

Platelet plug and fibrin clot

43
Q

What is a platelet plug?

A

Aggregation of platelets to an exposed area of damage

44
Q

What is a fibrin clot?

A

Protein mesh that caps the platelet plug

45
Q

What ways can the endothelium prevent clotting?

A
  • Production of prostacyclin and NO
  • Expresses thrombomodulin and heparin
  • Secretes t-PA (tissue plasminogen activator)
46
Q

What are the causes of oedema?

A

Imbalance of Starling forces due to:

  • Lymphatic obstruction
  • Raised CVP
  • Hypoproteinaemia
  • Increased capillary permeability
47
Q

What are the Starling forces?

A

The balance between hydrostatic and oncotic pressures of tissue fluid and blood vessels

48
Q

What laws of haemodynamics regulate arteriolar resistance?

A

Darcy’s and Poiseulle’s Laws

49
Q

How do you calculate MAP?

A

CO x TPR

50
Q

How do autonomic nerves have extrinsic control of arteriolar resistance?

A

Sympathetic - norepinephrine act on alpha-1 receptors and cause vasoconstriction

Parasympathetic - no effect

51
Q

How does epinephrine have extrinsic control of arteriolar resistance?

A

Acts on alpha-1 cells causing vasoconstriction

Some skeletal and cardiac muscles have beta-2 receptors which cause vasodilation

52
Q

What other hormones have extrinsic control on arteriolar resistance?

A

Angiotensin II - constriction

Vasopressin - constriction

Atrial and brain natriuretic peptide - dilation

53
Q

What local intrinsic controls are there?

A

Active hyperaemia

Pressure flow auto regulation

Reactive hyperaemia

54
Q

What is active hyperaemia?

A

Increased activity causes metabolite build up - triggers EDRF causing dilation

55
Q

What is EDRF?

A

Endothelium derived relaxing factor

56
Q

What is pressure autoregulation?

A

Decreased MAP causes metabolites to accumulate - causing EDRF release

57
Q

What is reactive hyperaemia?

A

Occlusion of flood supply causes increase in blood flow (extreme pressure auto regulation)

58
Q

What is special about the arteriolar regulation of the coronary arteries?

A

Blood supply is interrupted during systole

Show excellent pressure active hyperaemia

Expresses many B2 receptors to keep it dilated

59
Q

What is special about cerebral circulation?

A

Needs to be kept stable so demonstrates excellent pressure autoregulation

60
Q

What is special about renal circulation?

A

Main function is filtration - relies on good autoregulation of pressure to function

61
Q

What is meant by intrinsic effects?

A

Local

62
Q

What is meant by extrinsic effects?

A

Distant - concerned with TPR of whole body

63
Q

What are Korotkoff sounds?

A

Auscultated sounds of the heart

64
Q

What are Korotkoff sounds used to measure?

A

Arterial pressure

65
Q

Atrial pressure wave are affected by what four variables?

A
  • Stroke volume
  • Velocity of ejection
  • Elasticity of arteries
  • Total peripheral resistance
66
Q

What is considered to be a normal arterial pressure?

A

120/80mmHg

67
Q

What effect does age have on pulse pressure?

A

Increases

68
Q

Veins are distensible and collapsable; what five factors can effect this?

A
  • Gravity
  • Skeletal pump
  • Respiratory pump
  • Venomotor tone
  • Systemic filling pressure
69
Q

What is mean arterial pressure?

A

The main force driving blood through the circulation

70
Q

What happens if MAP is too low?

A

Syncope

71
Q

What happens if MAP is too high?

A

Hypertension

72
Q

What two locations for baroreceptors are there in the body in terms of blood pressure?

A

Aortic arch and carotid sinus

73
Q

What nerve transmits impulses from the aortic baroreceptors?

A

Sensory branch of the vagus nerve

74
Q

What nerve transmits impulses from the carotid sinus baroreceptors?

A

The glossopharyngeal nerve

75
Q

Where do both the vagus and glossopharyngeal nerve transmit impulses to in the brain?

A

The cardiac regulatory centre in the medulla

76
Q

Outline the motor side of regulation of blood pressure?

A

Vagus nerve innervates the SA node, causes hyper polarisation and the speed of depolarisation decreases therefore so does heart rate

Sympathetic has opposite effect

77
Q

What else occurs during activation of sympathetic nervous system?

A

Release of epinephrine from adrenal glands

Ventricles innervated to increased contractility

Vasoconstriction

78
Q

What effect does activation of central chemoreceptors have on the CVS?

A

Increases both heart rate and strength of contraction to accommodate increased PaO2

79
Q

Increased use of joints/muscles causes what?

A

Receptors to be activated to effect CVS

80
Q

What function do higher centres serve?

A

Feed-forward system to prepare body for physical activity

81
Q

What are the two reflexes occur to produce an increased blood pressure?

A

Decrease vagal tone and increase sympathetic tone

82
Q

What is the Valsalva manoeuvre?

A

Forced expiration against a closed glottis

83
Q

Outline the mechanics of the Valsalva manoeuvre?

A

Increase in thoracic pressure transmitted through pulmonary veins

Reduces venous return and decreases EDV

Produces weaker strength of contraction

Lowers MAP

Baroreceptors detect decrease in pressure and triggers reflex

84
Q

What is probably not the main gringo in long term blood pressure control?

A

The arterial baroreflex

85
Q

What three hormone systems are involved in long term blood pressure control?

A

RAAS
Antidiuretic hormone
Atrial natriuretic peptide

86
Q

What factors effect long term control of blood pressure?

A

Blood volume

87
Q

Where is renin produced?

A

Juxtaglomerular cells in the kidneys

88
Q

What triggers the release of renin?

A

Activation of the sympathetic nerves to the juxtaglomerular apparatus

Decreased distention afferent arterioles to glomerulus

Decreased delivery of Na+ and Cl- to kidneys

89
Q

What are the three triggers of renin production indicative of?

A

Decreased MAP

90
Q

What does renin do?

A

Causes angiotensinogen to be converted to angiotensin I

91
Q

What does angiotensin II do?

A

Vasoconstriction and stimulates the release of aldosterone and reduces diuresis

92
Q

What kind of system is the RAAS?

A

Negative feedback

93
Q

Where is ADH produced?

A

Pre-synthesised in the hypothalamus then released from the posterior pituitary gland

94
Q

What triggers ADH release?

A

Reduced MAP, Angiotensin II and increased osmolarity of interstitial fluid

95
Q

What does ADH do?

A

Causes water retention and vasoconstriction

96
Q

Where is ANP produced?

A

Myocytes of the atria

97
Q

What stimulates ANP release?

A

Increased distention of the atria

98
Q

What does ANP do?

A

Increases natriuresis, inhibits the release of renin and acts on CV centres in the medulla to reduce MAP

99
Q

What percentage of hypertensive patients are classed as secondary?

A

5-10%

100
Q

What pharmacological approach to management of blood pressure are there?

A

CCBs
Beta-blockers
Thiazide type diuretics
ACE inhibitors

Systems 1a Revision Decks (22 decks)

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