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AY Cardiovascular > Physiology continued > Flashcards

Physiology continued Flashcards

1
Q

What is the QRS complex?

A

Ventricular depolarisation (masks atrial repolarisation)

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2
Q

What is T?

A

Ventricular repolarisation

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3
Q

What is the ST segment?

A

Ventricular systole

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4
Q

What is the TP interval?

A

Diastole

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5
Q

Where does lead I go

.

A

Right arm - left arm

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6
Q

Where does lead II go?

A

Right arm - left leg

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7
Q

Where does lead III go?

A

Left arm - left leg

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8
Q

In an ECG what is the right leg used for?

A

Earth

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9
Q

What is the difference between positive and negative chronotropic effect?

A 
Positive = increase in heart rate 
Negative = decrease in heart rate
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10
Q

What are gap junctions?

A

Protein channels which form low resistance electrical communication pathways between neighbouring myocytes - ensure that electrical stimulation reaches all cardiac myocytes

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11
Q

What adheres cardiac cells together?

A

Desmosomes

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12
Q

What is the structure of striated muscle fibre?

A

Myofibrils - contractile units of muscle
- Actin (thin filaments) cause lighter appearance
- Myocjn (thick filaments) cause darker appearance
Within each mock rip actin and Myocjn are arranged in sarcomere so

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13
Q

What causes muscle tension in the heart?

A

Sliding of actin filaments on myocin filaments

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14
Q

What activates ventricular muscle contraction?

A

Ca2+ influx during plateau phase of AP

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15
Q

What is the refractory period?

A

A period of time following an action potential in which it is not possible to produce another action potential

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16
Q

What is tetany?

A

Spasm and twitching of cardiac muscle caused by reduced calcium influx

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17
Q

How do you calculate stroke volume?

A

SV = EDV - ESV

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18
Q

Intrinsic control of stroke volume

A

Changes in diastolic length of cardiac muscle fibres - EDV

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19
Q

What is the EDV a determined by?

A

Venous return to the heart

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20
Q

What is the frank starling law of the heart?

A

The more the ventricle is filed with blood during diastole (EDV) the greater volume of ejected blood during the resulting systolic contraction

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21
Q

Why’s is afterload?

A

The resistance into which the heart is pumping

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22
Q

Sympathetic influence on stroke volume

A

Noradrenaline acts on B1
Increases the force of contraction
Positive inotropic effect

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23
Q

What is the effect of sympathetic stimulation on the frank starling curve?

A

Crude is shifted to the left

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24
Q

Where does the left ventricle pump blood?

A

The aorta

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25
Q

Where does the RV pump blood?

A

Pulmonary artery

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26
Q

What drains into the RA?

A

SVC

IVC

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27
Q

What drains into the LA?

A

Pulmonary veins

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28
Q

What are the stages of the cardiac cycle?

A

1) passive filling
2) atrial contraction
3) isovolumetric ventricular contraction
4) ventricular ejection
5) isovolumetric ventricular relaxation

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29
Q

What happens in passive filling?

A

Mitral & tricuspid valves open - venous return goes into ventricles

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30
Q

Which side of the heart is higher pressure?

A

Left

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31
Q

What happens in atrial contraction?

A

P wave - atrial depolarisation

Atria contracts between P wave and QRS

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32
Q

What happens in isovolumetric ventricular contraction?

A 
Starts after the QRS 
Ventricular pressure rises 
When ventricle pressure > atrial pressure AV VALVES SHUT 
This produces the first heart sound
All valves are shut so pressure builds
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33
Q

What happens in ventricular ejection?

A 
When ventricular pressure > aorta/pulmonary artery pressure
Valves open (silent) 
Aortic pressure rises 
T wave =!ventricular repolarisation 
Ventricular pressure
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34
Q

What is P?

A

Atrial depolarisation

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35
Q

What happens in isovolumetric ventricular relaxation?

A

Ventricle is closed box again
When ventricular pressure falls below atrial pressure
AV valves open again (silent)

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36
Q

What causes the first heart sound?

A

Closure of mitral & tricuspid valve

(beginning of systole!

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37
Q

What causes the second heart sound?

A

Closure of aortic & pulmonary valves

end of systole, beginning of diastole

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38
Q

Where are the baroreceptors?

A

Aortic arch

Carotid sinus

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39
Q

What causes postural hypotension?

A

Failure of baroreceptor responses to gravitational shifts

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40
Q

Summary of baroreceptor reflex

A 
Person stands up 
Venous return to the heart decreases 
MAP decreases 
Reduces rate of firing of baroreceptors
VAGAL TONE to the heart DECREASES
SYMPATHETIC tone INCREASES
- Increases TPR
- increases HR 
- increases SV 
Increases venous return
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41
Q

Which 2 main factors affect extracellular fluid volume?

A

Water (excess or deficit)

Na+ (excess or deficit)

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42
Q

Which hormones regulate extracellular fluid volume?

A

RAAS
ANP
ADH

43
Q

What is renin and what does it do?

A

Renin is released from the kidneys and stimulates formation of angiotensin I in the blood from angiotensin produced in the liver

44
Q

What is angiotensin I and what does it do?

A

Angiotensin I is converted to angiotensin II by ACE (produced by pulmonary vascular endothelium)

45
Q

What is angiotensin II and what does it do?

A

Stimulates the release of aldosterone from the adrenal cortex - causes sysstemic vasoconstriction - increases TPR

Also stimulates thirst and ADH release

46
Q

What is aldosterone and what does it do?

A

Steroid hormone that acts on the kidneys to increase sodium and water retention - increases plasma volume

47
Q

How is renin secretion regulated?

A
  1. Renal artery hypotension (systemic hypotension)
  2. Stimulation of renal sympathetic nerves
  3. Decreases NA in renal tubular fluid (sense by macula densa)
48
Q

What is Atrial Natriuretic Peptide (ANP)?

A

28 amino acid peptide synthesised and stored by atrial muscle cells (atrial myocytes)

49
Q

What causes the release of ANP?

A

Atrial distension

Hypervolaemic states

50
Q

What is hypervolaemia?

A

Increased volume of circulating blood

51
Q

What are the actions of ANP?

A

Excretion of salt and water in the kidneys
Reducing BP & blood volume
Acts as vasodilator - decreases BP
Decreases renin release

52
Q

What is ADH (vasopressin)?

A

Peptide hormone derived from a ore hormone receptor synthesised by the hypothalamus and stored in the posterior pituitary

53
Q

What stimulates ADH secretion?

A
  1. Reduced extracellular fluid volume

2. Increases extracellular fluid osmolarity (osmoreceptors)

54
Q

How does ADH act in the kidneys?

A

Acts in the kidney tubules
Increases water reabsorption
Causes vasoconstriction

55
Q

Where is the main site of TPR?

A

Arterioles

56
Q

What is the sympathetic control of vascular smooth muscles?

A

Sympathetic nerve fibres

Noradrenaline acting on aloha receptors

57
Q

Parasympathetic innervation of arterial smooth muscles

A

No significant innervation except penis & clitoris

58
Q

Where is adrenaline released from?

A

Adrenal medulla

59
Q

How does adrenaline act on vascular smooth muscle?

A

Adrenaline -> Beta receptors -> vasodilation

Adrenaline -> alpha receptors -> vasodilation

60
Q

Where are alpha raptors predominantly found?

A

Skin, gut, & kidney arterioles

61
Q

Where are beta receptors commonly found?

A

Cardiac & skeletal muscle

62
Q

Which 3 hormones cause vasoconstriction?

A

Angiotensin II
ADH (vasopressin)
Adrenaline (on alpha receptors)

63
Q

What chemical factors can cause vasodilation?

A 
Decreased local PO2 
Increased local PCO2 
Decreased pH 
Increased extracellular K+
Increased osmolarity of ECF
Adenosine release (from ATP)
64
Q

What humoral agents cause vasodilation?

A

Histamine
Prostaglandins
Bradykinin
NO

65
Q

What does NO do?

A

Potent vasodilator
Diffuses into adjacent smooth muscle where it activates a form of cGMP that serves as a second messages for signalling smooth muscle relaxation

66
Q

What humoral agents can cause vasoconstriction?

A

Serotonin
Thromboxane A2
Leukotrienes
Endothelium (potent vasoconstrictor released from endothelium stimulated by angiotensin II and vasopressin)

67
Q

Factors that influence increased venous return

A

Increased venomotor tone
Increased blood volume
Increased “skeletal muscle pump”
Increased “respiratory pump”

68
Q

What is a 3rd heart sound?

A

Early diastolic low frequency filling sound (passive filling of ventricle)

69
Q

What is a 3rd heart sounds indicative of?

A

Can be normal finding

Can indicate heart failure in a patient with evidence of heart failure, especially if the patient is older

70
Q

What is a 4th heart sound?

A

Late diastolic low frequency sound which relate to the active filling of a stuff non-compliant ventricle by atrial contraction

71
Q

What does a 4th heart sound indicate?

A 
Ventricular stiffness (e.g. Left ventricular hypertrophy) 
Almost always pathological
72
Q

What intrinsic mechanisms control coronary blood flow?

A

Decreased PO2 causes vasodilation
Metabolic hyperaemia matches flow to demand
Adenosine (from ATP) is a potent vasodilator

73
Q

Extrinsic mechanisms to control coronary blood flow

A

Sympathetic stimulation causes vasodilatation

In exercise - circulating adrenaline activates B2 adrenergic receptors

74
Q

What arteries supply the brain?

A

Carotid and vertebral arteries

75
Q

What is the main adaptation of the cerebral circulation to prevent ischaemia?

A

Circle of Willis

76
Q

What does MABP drop below to cause confusion, fainting and brain damage if not quickly corrected?

A

50mmHg

77
Q

How does pCO2 affect cerebral circulation?

A

Increased PCO2 -> vasodilation

Decreased PCO2 -> vasoconstriction

78
Q

What is the normal range of intracranial pressure?

A

8-13mmHg

79
Q

How do you calculate cerebral perfusion pressure?

A

COO = MAP - ICP

80
Q

How does raised ICP affect cerebral blood flow?

A

Decreases cerebral blood flow

81
Q

How does glucose cross the BBB?

A

By facilitated diffusion

82
Q

What is the skeletal muscle pump?

A

Large veins in limbs lie between skeletal muscles

Contraction of muscles aids venous return

83
Q

What conditions can failure in the skeletal muscle pump cause?

A

Postural hypotension

Fainting

84
Q

What causes varicose veins?

A

Incompetence of venous valves

85
Q

Why do varicose veins not lead to a reduction in cardiac output?

A

Chronic compensatory increase in BP

86
Q

What are capillaries?

A

Kringle layer of endothelial cells

87
Q

What is the function of capillaries?

A

Allow rapid exchange of gases, water and salutes with interstitial fluid
Delivery of nutrients and O2 to cells
Removal of metabolites from cells

88
Q

What regulates blod flow to the capillary bed?

A

Terminal arterioles

89
Q

When capillaries join together what do they form?

A

Venules

90
Q

How do substances transport across the capillary wall?

A

Fluid - follows pressure gradient

Gas - Ficks law of diffusion (I.e. downhill)

Lipid soluble - go through endothelial cells

Water soluble - through water filled pores

Large molecules can generally not cross the capillary wall

91
Q

What are the forces involved in transcript liars fluid flow called?

A

Starling forces

92
Q

What forces favour filtration?

A

Pc - capillary hydrostatic pressure

interstitial fluid osmotic pressure

93
Q

What forces oppose filtration?

A

Capillary osmotic pressure

Interstitial fluid hydrostatic pressure

94
Q

Overall what do the starling forces do?

A

Favour filtration at arteriolar end
AND
Reabsorption at venular end

95
Q

How is excess fluid returned to the circulation in capillaries?

A

Via the lymphatics as lymph

96
Q

What role do the starling forces have in pulmonary capillaries?

A

Prevent oedema

97
Q

What is oedema?

A

Accumulation of fluid in interstitial space

98
Q

What causes oedema?

A

Reduced capillary pressure
Reduced plasma osmotic pressure
Lymphatic insufficiency
Changes in capillary permeability

99
Q

How does raised capillary pressure cause pulmonary oedema?

A 
Causes arteriolar dilatation 
Raised venous pressure 
LV failure - pulmonary oedema 
RV failure - peripheral oedema 
Prolonged standing - swollen ankles
100
Q

What causes lymphatic insufficiency leading to oedema?

A

Lymph node damage
Filariasis
Elephantiasis

101
Q

What causes changes in capillary permeability?

A

Inflammation

Histamine - increases leakage of protein

102
Q

Where can you get pitting oedema?

A

Ankles

Sacrum

103
Q

What does pulmonary oedema look like on a CXR?

A

Haziness in peri hilar region

AY Cardiovascular (28 decks)

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