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Cardiovascular System > Session 8 > Flashcards

Session 8 Flashcards

1
Q

What are the 2 circulations of the lungs?

A
  • Bronchial circulation

- Pulmonary circulation

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2
Q

What is the function of the pulmonary circulation?

A
  • Directs output of right heart
  • Must accommodate entire cardiac output
  • Needs gas exchange
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3
Q

What is the function of the bronchial circulation?

A
  • Infuses parts of the lungs that are too far from the alveoli with O2
  • Meets metabolic requirements of lungs
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4
Q

What kind of pressures and resistance does the pulmonary circulation work at?

A

Low pressure and low resistance

- Pressure in the arteries and ventricles are very similar in systole

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5
Q

Why are the atria at a much lower pressure than the ventricles?*

A
  • Atria do not undergo the same level of systole as ventricles
  • RA: 0-8mmHg
  • LA: 1-10mmHg
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6
Q

Why is the diastolic pressure in the aorta so high (60-90mmHg)?

A

There is much more elastic recoil in the aorta which allows the maintenance of a higher pressure.

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7
Q

Why is the pressure in the pulmonary circulation so low?

A

Low resistance - ready flow is needed to deliver all the blood to the lungs for oxygenation

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8
Q

What contributes to the low resistance?

A
  • Short, wide vessels
  • Lots of capillaries
  • Less smooth muscle in the arterioles which keeps lumen open and allows flow (no constriction)
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9
Q

What promotes efficient gas exchange in the lungs?*

A
  • High density of capillaries in the alveolar wall (high SA)
  • Short diffusion distance as endothelium + epithelium thickness is around 0.3 micrometres
  • High transport capacity
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10
Q

What is the meaning of perfusion and ventilation?

A

Perfusion: blood flow
Ventilation: air flow

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11
Q

What is needed for efficient oxygenation?

A
  • Ventilation and perfusion of alveoli must be matched
  • Alveoli that are not being ventilated must have blood flow diverted from them
  • V/Q ration = 0.8
  • Mismatch will result in hypoxia as blood leaving the lungs will have less oxygen
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12
Q

What ensures the optimal ventilation/perfusion ratio?

A

Hypoxic pulmonary vasoconstriction that regulates pulmonary vascular tone (degree of vessel constriction)

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13
Q

What will alveolar hypoxia result in?

A
  • Vasoconstriction of pulmonary vessels

- Narrows lumen of vessels that lead to poorly ventilated alveoli to ensure that perfusion = ventilation

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14
Q

Why is blood flow diverted from poorly ventilated alveoli?

A

Optimising gas exchange

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15
Q

What is the issue with chronic hypoxic vasoconstriction?

A
  • Can occur at altitude or because of COPD/emphysema
  • Chronic increase in vascular resistance contributes to chronic pulmonary hypertension
  • Right ventricle pumps blood at a higher pressure
  • High afterload
  • Right ventricular heart failure
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16
Q

What is the influence of gravity on low pressure vessels?*

A
  • Greater hydrostatic pressure on vessels in lower lung during orthostasis
  • Those vessels are distended
  • Vessels at the level of the heart are continuously open
  • Vessels at the apex of the lungs have a lower hydrostatic pressure and therefore are only open during systole and collapse during diastole
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17
Q

What is the effect of exercise on pulmonary blood flow?

A
  • Increased CO
  • Increase in pulmonary arterial pressure opens apical capillaries that usually collapse in diastole
  • More O2 taken up by lungs
  • Capillary transient time reduced but gas exchange not compromised
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18
Q

How does tissue fluid form?

A

STARLING FORCES

  • Hydrostatic pressure within capillary pushes fluid out into the tissues
  • Oncotic/colloid osmotic pressure that is exerted by large plasma proteins draws fluid back into the capillary
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19
Q

What influences hydrostatic capillary pressure?

A

Venous pressure in the systemic circulation (5x greater effect)

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20
Q

How can you tell that hydrostatic pressure is not greatly influenced by arterial pressure?

A
  • Hypertension is high arterial blood pressure
  • Patients with hypertension do not present with peripheral oedema
  • If it was affected, they would have it
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21
Q

How is the formation of lung lymph minimised?*

A

Filtration = reabsorption, so most forces are equivalent

  • OP lungs > OP periphery
  • CHP lungs < CHP systemic
  • Plasma oncotic pressure same
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22
Q

What is the reason for formation of oedema?*

A
  • Filtration rate exceeds reabsorption

- Increased capillary pressure causes more fluid to be filtered out

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23
Q

Why is the pulmonary capillary pressure between 9-12 mmHg?

A

Prevents formation of pulmonary oedema so that only small amounts of lung lymph leave the capillary

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24
Q

When can you get pulmonary oedema?

A
  • Mitral valve stenosis: buildup of pressure in LA
  • Left ventricular failure: more blood left over at the end of systole means that you need more diastolic pressure to compensate
  • Left atrial pressure rising to 20-25 mmHg
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25
Q

What problems does pulmonary oedema cause?

A

Impairment of gas exchange and fluid making it very difficult to breathe when patients sleep/lay down as the lymph then forms throughout the lung rather than mainly at bases

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26
Q

How is pulmonary oedema treated?

A
  • Diuretics (symptom relief)

- Underlying cause

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27
Q

Why do individuals who experience a reduced blood supply experience syncope?

A
  • Brain has a high O2 demand
  • Neurones are active all the time
  • Shortness of O2 for 3/4 minutes will lead to permanent brain damage and death
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28
Q

How does the cerebral circulation meet the high demand for O2?

A
  • High capillary density that provides a large SA for gas exchange and a short diffusion distance
  • High basal flow rate
  • High O2 extraction due to continuous O2 use so therefore a good diffusion gradient
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29
Q

How is a secure blood supply ensured structurally?

A

Anastomoses between basilar and internal carotid arteries that form a ‘circle’ so even when the blood supply is cut off from one side perfusion still occurs

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30
Q

How is a secure blood supply ensured functionally?

A
  • Myogenic autoregulation (perfusion during hypertension)
  • Metabolic factors
  • Brainstem regulates other circulations
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31
Q

What is myogenic autoregulation?

A
  • Smooth muscle cells in the cerebral resistance vessels responds to changes in transmural pressure
  • Maintains cerebral blood flow when BP changes
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32
Q

How does myogenic autoregulation work?*

A
  • Increased blood pressure = vasoconstriction

- Decreased blood pressure = vasodilation

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33
Q

Why does hypercapnia cause vasodilation while hypocapnia causes vasoconstriction?

A

High partial pressures of CO2 indicate that the neurones are very active, meaning that the blood flow must increase to provide oxygen

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34
Q

Why does panic hyperventilation cause syncope/dizziness?

A
  • Causes hypocapnia
  • This causes vasoconstriction
  • Blood supply to the brain becomes reduced
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35
Q

What causes vasodilation?

A

+ Adenosine
+ PCO2
+ K+ conc
- PO2

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36
Q

What is the function of the rigid cranium?

A

Protection

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37
Q

What happens when there is an increase in intercranial pressure and what causes the increase?

A
  • Can be caused by tumour/haemorrhage

- Impairs cerebral blood flow as the blood vessels may become compressed and the blood will not flow

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38
Q

What happens if blood flow to vasomotor control regions is reduced?

A
  • Increased sympathetic vasomotor activity
  • Powerful vasoconstriction occurs and BP rises to help maintain the cerebral blood flow
  • Increase in vagus activity due to baroreceptors sensing the pressure
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39
Q

What do patients present with that usually indicates the presence of a space-occupying lesion?

A

Bradycardia and hypertension

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40
Q

What is the function of the coronary circulation?*

A
  • Delivery of O2 at a high basal rate

- Meeting increased demands (eg. exercise)

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41
Q

When does flow to the coronary arteries (LEFT) mostly occur and why can this be a problem when a person has narrowing of the coronary arteries?*

A
  • Coronary arteries mostly fill with blood during diastole
  • Narrowing of arteries already compromises and prolongs their filling
  • During exercise, diastole is cut short and so the artery cannot receive as much blood
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42
Q

What determines the oxygen demand of the myocardium?

A
  • Metabolic work

- External work

43
Q

Why can coronary arteries not fill in systole?

A
  • Tension in walls compresses coronary vessels in ventricles

- Reduces blood flow

44
Q

What are the features of the coronary circulation?

A
  • High capillary density
  • Short diffusion distance
  • Continuous NO production by endothelium to maintain high basal flow
45
Q

What is metabolic hyperaemia?

A

An increase in blood flow that occurs when the tissue is metabolically active to provide more O2 via vasodilation

46
Q

Why are coronary arteries so prone to atheromas?

A

They have few anastomoses as they are end arteries

47
Q

Why can narrow coronary arteries lead to angina?

A
  • Diastole cut short during exercise
  • Hypoxia
  • Stress and cold causing sympathetic coronary vasoconstriction
48
Q

Why do skeletal muscles have a high vascular tone?

A
  • Permit lots of dilation
  • Flow can increase over 20x in active muscle
  • Increased recruitment allowed
49
Q

What are pre-capillary sphincters and why do they open?

A
  • Smooth muscles that adjust blood flow through capillaries
  • Allow more capillaries to be perfused when needed
  • Reduce diffusion distance
50
Q

What acts to promote vasodilation?

A
  • Inc. K+ conc.
  • High osmolarity
  • Adenosine
  • Low pH
  • Adrenaline (smooth muscle arterioles via B2 receptors)
51
Q

What is the role of the cutaneous circulation?

A

Maintaining a constant body temperature (37 degrees Celsius)

- Also maintains blood pressure

52
Q

How does blood flow through the skin?*

A

Arterio-venous anastomoses (precapillary communications between arteries and veins) in acral surfaces
- Heat lost as they’re close to the surface

53
Q

How are AVAs controlled?

A

Sympathetic vasoconstrictor fibres

  • Decreasing core temp. will increase sympathetic tone and reduce blood flow to apical skin
  • Reduced vasomotor drive allows dilation and diverting blood to veins near surface
54
Q

Where does most of the venous return come from?

A

Superficial veins

55
Q

How does blood move in the lower limb?

A

Superficial -> deep veins

56
Q

Where are deep and superficial veins found?

A

Deep: deep fascia
Superficial: subcutaneous tissue
All originate from INFERIOR VENA CAVA

57
Q

What are some deep veins in the lower limb?*

A
  • Popliteal vein
  • Femoral/deep femoral vein
  • Peroneal
  • Anterior/posterior tibial
58
Q

What are the superficial veins in the lower limb?*

A
  • Short saphenous vein

- Long saphenous vein (medial)

59
Q

Where does the long saphenous vein run down?

A
  • Medially

- In front of medial malleolus (anatomical landmark)

60
Q

What muscles push the blood back towards the heart and against gravity and how do they do that?*

A
  • Soleus
  • Gastrocnemius
    Muscles are constricted within the fascia and therefore pump blood
61
Q

How do valves allow the blood pumping?

A
  • Valves open to push blood through to deep vein and prevent retrograde movement
  • Perforating valves allow filling from superficial veins
62
Q

What is peripheral venous disease?

A

Varicose veins (common in saphenous veins) forming due to valves being ineffective and blood movement slowing or reversing

63
Q

Why do the varicosities develop?*

A

Vein walls weaken and the valve cusps separate, so blood pools in the veins

64
Q

Does peripheral venous disease cause problems?

A
  • Can present symptomatically

- Usually only removed due to aesthetic reasons

65
Q

What are the symptomatic developments in patients with peripheral venous disease?

A
  • Aching, cramping and throbbing along affected veins
  • Haemorrhage which can be reduced by placing legs above the level of the heart
  • Varicose eczema
  • Superficial vein thrombophlebitis
  • Chronic venous insufficiency
  • Haemosiderin staining
  • Lipodermatosis
  • Venous ulceration
66
Q

What is superficial vein thrombophlebitis?

A
  • Inflammatory process that causes clots in the veins

- Increases risk of DVT

67
Q

What is haemosiderin staining?*

A
  • Red blood cells are broken down
  • Haemoglobin stored as haemosiderin
  • ‘Rusty’ colour along affected vein
68
Q

What is lipodermatosclerosis?*

A

Inflammation and thickening of the fat layer under skin

69
Q

What is venous eczema/ulceration?*

A
  • Itchy, red, tight swelling
  • Hard to touch
  • Often around hard nodular areas
70
Q

Which patients commonly suffer from chronic venous insufficiency?

A

Patients who have had a DVT

71
Q

Why do calf muscle pumps fail?

A

Plantarflexion of the ankle joint during walking allows the muscles to be used properly

72
Q

Who is at risk of calf muscle failure?

A
  • Elderly people
  • Obese people
  • Injured people
  • People with Parkinson’s disease (shuffling gait means that there is no plantarflexion)
73
Q

What is the result of deep vein incompetence?

A

Flow backwards so the vessel gets overwhelmed.

74
Q

What is the result of superficial vein incompetence?*

A

Blood flow goes the wrong way, from deep to superficial vein and that makes the

75
Q

What treatment improves ulceration?

A

Ligation and vein stripping

76
Q

What is arterial thrombosis?*

A
  • Most commonly caused by atheromas
  • Platelet rich and pale
  • Activated
  • Aggregate
  • ‘Plug hole’
77
Q

What is venous thrombosis?*

A
  • Caused by stasis
  • Usually another factor too (trauma, chemo, dehydration, pregnancy)
  • Low flow
  • Little platelet
  • Fibrin rich
  • Dark red
78
Q

What is the Virchow’s triad?

A

Any of the three can contribute to a thrombotic state:

  • Stasis
  • Vessel wall damage
  • Hypercoagulability
79
Q

What is deep vein thrombosis (DVT)?

A

Clotting of blood in a deep vein (commonly calf) which causes impaired venous return and hypercoagulability

80
Q

What are the features of DVT?*

A
  • Inflammatory response following thrombosis
  • Pain, swelling, redness
  • Signs vary in severity and frequency
  • Calf tenderness
  • Warmth
  • Visible superficial veins
  • Oedema
  • Pyrexia with no obvious cause
  • Asymmetry in leg size
81
Q

What are the differential diagnoses for DVTs?

A
  • Soft tissue trauma
  • Cellulitis
  • Lymphatic obstruction
82
Q

How is DVT prevented after surgery?

A
  • Promote mobility soon after surgery
  • Prophylaxis to lower DVT
  • Anticoagulant agents
83
Q

What is a fatal consequence of DVT?*

A

Pulmonary embolism

84
Q

How does the body adapt to stenosis?*

A

Occlusion in the main vessel promotes collateral arteries forming to provide an alternative route around the occlusion to ensure that blood flow is maintained.

85
Q

What is acute limb ischaemia?

A
  • Occlusion that develops acutely over minutes/days

- No chance to develop collaterals

86
Q

What can cause acute limb ischaemia?

A
  • Popliteal artery aneurysm
  • AF
  • Sudden atherosclerotic plaque rupture
87
Q

What are the 6 Ps of leg ischaemia?

A
  • Pain
  • Pallor
  • Perishing with cold
  • Pulseless
  • Paraesthesia
  • Paralysis/reduced power
88
Q

What is the treatment of acute limb ischaemia?

A
  • Vascular surgery unit referral
  • Extent of threat assessed
  • Imaging done
  • Decides if angioplasty/thrombectomy/thrombolysis/amputation
89
Q

What is chronic peripheral arterial disease similar to?

A

Coronary artery disease and stable angina, as intermittent claudication only happens on exertion (same as stable angina)

90
Q

What is intermittent claudication?

A

Cramping pain in the leg that is induced by exercise, usually intermittent (comes and goes), and goes away upon rest

91
Q

What causes intermittent claudication?

A

Atherosclerosis

92
Q

How is chronic peripheral arterial disease treated?

A

Exercise, smoking cessation, antiplatelet drugs, angioplasty and bypass graft (saphenous vein)

93
Q

What is critical ischaemia and what is it similar to?

A
  • Similar to STEMI/unstable angina

- Blood supply so poor that pain is felt even at rest

94
Q

What does untreated critical ischaemia lead to?

A

Ulceration and gangrene

95
Q

How is critical ischaemia treated?

A
  • Assess extent of threat of limb survival
  • Imaging needed
  • Angioplasty/thrombectomy/intra-arterial thrombolysis/amputation
96
Q

What is the pathology of claudication?*

A
  • Atheroma most common
  • Becomes ischaemia if untreated
  • Stenosis will dictate where claudication presents
97
Q

Where can the femoral pulse be palpated?*

A
  • Mid inguinal point

- Midway between anterior superior iliac spine and pubic symphysis

98
Q

Where can the popliteal pulse be felt?*

A

Deep in popliteal fossa

99
Q

Where can the dorsalis pedis pulse be felt?*

A

Lateral to extensor hallucis longus tendon

100
Q

Where can the posterior tibial pulse be felt?*

A

Behind the medial malleolus?

101
Q

What is Doppler sonography?*

A

Sonogram using ultrasound and Doppler effect to measure real-time flow and velocity
- Flow and velocity change with atheromas and stenosis

102
Q

What is the ankle-brachial pressure index (ABPI)?*

A

The systolic pressure recorded in brachial artery of arm and systolic pressure in the arteries of the ankle

103
Q

How is ABPI calculated?

A
  • Ankle systolic pressure divided by brachial systolic pressure
  • If <0.9 = peripheral artery disease

Cardiovascular System (11 decks)

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