Cardiovascular Flashcards

1
Q

What forms intercalated disks

A

Desmosome
Gap junction

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2
Q

What causes the rapid depolarisation phase of cardiac muscle

A

Sodium influx

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3
Q

What causes the slow repolarisation phase of cardiac muscle

A

Calcium Influx

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4
Q

What condition is described as sawtooth pattern on an ECG

A

Atrial flutter

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5
Q

What condition is no P waves on an ECG

A

Atrial fibrillation

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6
Q

What is a normal PR interval

A

> 0.12s - <0.2s

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7
Q

What is a normal QRS complex

A

<0.12s

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8
Q

What is normal QT interval at 60bpm

A

<0.42s

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9
Q

What is Standard limb lead 1

A

RH -
LH +

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10
Q

What is Standard limb lead 2

A

RH -
LF +

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11
Q

What is Standard limb lead 3

A

LH -
LF +

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12
Q

What are the possible systolic murmurs

A

Aortic/pulmonary stenosis
OR
Mitral/Tricuspid Regurgitation

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13
Q

What are the possible diastolic murmurs

A

Mitral/Tricuspid stenosis
OR
Pulmonary/Aortic regurgitation

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14
Q

What could cause a continuous murmur

A

Patent ductus arteriosus

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15
Q

How is cardiac output calculated

A

HR x SV

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16
Q

What is a normal ejection fraction

A

60%

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17
Q

How is ejection fraction calculated

A

SV/EDV

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18
Q

How is heart rate regulated

A

Controlled by pacemaker cells
ANS
- Sympathetic B1 receptors on SA node
- Parasympathetic muscarinic receptors on SA node

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19
Q

What 3 factors affect Stroke volume

A

Preload
Afterload
Neural - Contractility

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20
Q

What ion allows variable contractility of cardiac muscle

A

Ca2+

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21
Q

What 5 factors affect venous return

A

Gravity
Skeletal muscle pump
Respiratory pump
Venomotor tone
Systemic filling pressure

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22
Q

What are the 3 types of capillary

A

Continuous
Fenestrated
Discontinuous

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23
Q

What 4 things can cause oedema

A

Raised venous pressure
Lymphatic obstruction
Hypoproteinaemia
Increased capillary permeability

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24
Q

How is mean arterial pressure calculated

A

CO x TPR

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25
Q

What are the 4 causes of local hyperaemia

A

Metabolite hyperaemia
Reactive hyperaemia
Pressure autoregulation
Injury response

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26
Q

What is the mechanism of injury response hyperaemia

A

C-Fibres activated
Release of substance P
Mast cell activation

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27
Q

What is the mechanism of metabolite hyperaemia

A

Cell metabolites move into blood
Endothelium releases EDRF/NO
Causes dilatation

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28
Q

What is the mechanism of reactive hyperaemia

A

Decreased blood flow
=> flow increased
Extreme version of pressure autoregulation

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29
Q

What is the mechanism of pressure autoregulation

A

Increased MAP decreases flow
=> metabolites accumulate
=> NO/EDRF released
Dilatation

30
Q

What effect does noradrenaline have on systemic arterioles

A

Vasoconstriction

31
Q

What receptor does noradrenaline act on in systemic arterioles

A

Alpha-1

32
Q

Which 2 areas blood flow is affected by the parasympathetic nervous system

A

Genetalia
Salivary glands

33
Q

Where is adrenaline released

A

Adrenal medulla

34
Q

What receptor does adrenaline act on in systemic arterioles

A

Alpha-1

35
Q

How does hypoxia differ in pulmonary vessels to systemic vessels

A

Systemic hypoxia - dilation
Pulmonary hypoxia - constriction

36
Q

What 3 areas have very good blood pressure control

A

Coronary circulation
Cerebral circulation
Renal circulation

37
Q

Where are baroreceptors located

A

Aortic arch
Carotid sinus

38
Q

What is the function of baroreceptors

A

Detect changes in blood pressure

39
Q

What nerve communicates information from aortic baroreceptors

A

Vagus

40
Q

What nerve communicates information from carotid sinus baroreceptors

A

Glossopharyngeal

41
Q

Where do the vagus and glossopharyngeal nerves communicate information to

A

Medullary cardiovascular centres

42
Q

How do baroreceptors work

A

Releases action potentials when stretched

43
Q

Which organ controls long term blood pressure control

A

kidneys

44
Q

Where is renin produced

A

Juxtaglomerular (granule) cells

45
Q

What triggers renin production

A

Sympathetic innervation of juxtaglomerular apperatus
Renal baroreflex
Decreased delivery of Na/Cl through tubule

46
Q

What does renin do

A

Convert angiotensin to angiotensin I

47
Q

What converts angiotensin I to Angiotensin II

A

Angiotensin converting enzyme

48
Q

What effect does angiotensin have systemically

A

Increased MAP

49
Q

What 2 substances are released by angiotensin

A

Aldosterone
Anti diuretic hormone

50
Q

Where antidiuretic hormone produced

A

Hypothalamus

51
Q

Where antidiuretic hormone released

A

Posterior pituitary

52
Q

What systemic effects does antidiuretic hormone have

A

Increased MAP

53
Q

Where is Atrial Natriuretic Peptide produced

A

Atria

54
Q

Where is Brain Natriuretic Peptide produced

A

Ventricles

55
Q

What systemic effects do ANP and BNP have

A

Reduce MAP

56
Q

What are stage 1, 2 and 3 hypertension classified as

A

1 - 140/90
2 - 160/100
3 - 180/120

57
Q

What is the name of the risk calculator for blood pressure

A

Assign risk calculator

58
Q

Contradictions to ACEi

A

Impaired renal function
Hyperkalaemia
Fertile Female
Taking NSAIDS

59
Q

How is a complicated plaque defined

A

Plaque rupture/fissuring
Thrombosis

60
Q

Most important risk factor in atheroma

A

Hypercholesterolaemia

61
Q

Signs of hyperlipidaemia

A

Bloods - LDL, HDL, total cholesterol
Corneal arcus
Xanthelasmata/Xanthomata
Family History

62
Q

Prevention of atheroma

A

Smoking cessation
BP control
Weight loss
Diet modification
Exercise

63
Q

Treatment of atheroma

A

Cholesterol lowering drugs
Blood thinners
Surgical options

64
Q

Other risk factors of atheroma

A

Smoking
hypertension
Diabetes
Male
Elderly

65
Q

Most common cause of mitral stenosis

A

Rheumatic fever

66
Q

4 types of hypoxia

A

Hypoxic
Anaemic
Stagnant
Cytotoxic

67
Q

What is hypoxic hypoxia

A

Due to respiratory causes

68
Q

What is anaemic hypoxia

A

Blood cant carry enough O2

69
Q

What is stagnant hypoxia

A

Abnormal blood delivery

70
Q

What is cytotoxic hypoxia

A

Abnormal O2 delivery at tissue level