15. Special Circulations Flashcards

1
Q

What are the purposes of the lung circulations - bronchial and pulmonary?

A

Bronchial circulation meets the metabolic requirements of the lungs. Pulmonary circulation is required for gas exchange.

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2
Q
What are the pressures in the following parts of circulation?
A. Pulmonary artery
B. Right ventricle
C. Left ventricle
D. Aorta
E. Right atria
F. Left atria
A

A. 15-30mmHg in systole, 4-12mmHg in diastole.
B. 15-30mmHg in systole, 0-8mmHg in diastole.
C. 100-140mmHg in systole, 1-10mmHg in diastole.
D. 100-140mmHg in systole, 60-90mmHg in diastole.
E. 0-8mmHg.
F. 1-10mmHg.

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3
Q

What are the two key features of the pulmonary circulation?

A

Low pressure and low resistance.

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4
Q

What are the pressure in pulmonary circulation? Mean arterial, mean capillary, and mean venous pressures.

A

Arterial 12-15mmHg.
Capillary 9-12mmHg.
Venous 5mmHg.

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5
Q

How does the pulmonary circulation have low resistance?

A

It has short, wide vessels. Lots of capillaries (parallel elements). Arterioles have relatively little smooth muscle.

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6
Q

What are the two circulations of the lungs?

A

Bronchial circulation and pulmonary circulation.

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7
Q

How has the pulmonary circulation adapted to promote efficient gas exchange?

A

Very high density of capillaries in alveolar wall so large capillary surface area and short diffusion distance.

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8
Q

What is the equation for calculating perfusion rate?

A

Ventilation/cardiac output = V/Q

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9
Q

What is the optimal perfusion rate?

A

0.8, ventilation = 4l/min, cardiac output = 5l/min.

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10
Q

How does hypoxic pulmonary vasoconstriction ensure optimal vetnilation/perfusion ratio?

A

Alveolar hypoxia results in vasoconstriction of pulmonary vessels, this ensures that perfusion matches ventilation as the alveoli get less well perfused when poorly ventilated. This optimises gas exchange.

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11
Q

What can the outcome of chronic hypoxic vasoconstriction be?

A

Right ventricular failure because there is a chronic increase in vascular resistance so pulmonary hypertension and high afterload on the right ventricle, which can lead to its failure.

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12
Q

What happens to pulmonary blood flow in exercise?

A

There is increased cardiac output and a small increase in pulmonary arterial pressure. This opens apical capillaries so there is increased O2 uptake by lungs. The capillary transit time is reduced due to faster blood flow.

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13
Q

How do hydrostatic pressure and oncotic pressure affect the formation of tissue fluid?

A

Hydrostatic pushes fluid out of the capillary.

Oncotic pressure draws fluid into the capillary.

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14
Q

How do oncotic pressure, capillary hydrostatic pressure and plasma oncotic pressure vary in the lungs and in the periphery?

A

Oncotic pressure of tissue fluid in the lungs > than in periphery.
Capillary hydrostatic pressure in lung

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15
Q

What happens when there is increased capillary pressure to tissue fluid?

A

Filtration > reabsorption o fluid moves out and oedema forms.

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16
Q

How does pulmonary oedema occur?

A

If capillary pressure increases. The left atrial pressure rises to 20-25mmHg, could be from mitral valve stenosis or left ventricular failure. The LV can’t pump out that much, so it’s harder for blood to move from LA to LV and then out of the heart. This leads to pulmonary oedema.

17
Q

What does pulmonary oedema impair?

A

Gas exchange.

18
Q

How is pulmonary circulation affected by posture?

A

There are changes in hydrostatic pressure due to gravity. It forms mainly at the base when upright and through lung when lying down.

19
Q

How is pulmonary oedema treated?

A

Diuretics relieve symptoms but the underlying cause should be treated.

20
Q

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

A

High capillary density so large surface area for gas exchange, High basal flow rate, and high O2 extraction.

21
Q

Why is O2 delivery to the brain so vital?

A

Neurones are sensitive rapper to hypoxia. A few seconds into cerebral ischaemia leads to loss of consciousness. Irreversible damage to neurones is after 4 minutes so interrupted blood supply causes neuronal death.

22
Q

How is a secure blood supply to the brain ensured?

A

Structurally - anastomoses between basilar and internal carotid arteries.
Functionally - myogenic auto regulation maintains perfusion in hypotension, metabolic factors control blood flow and brain stem regulates other circulations.

23
Q

How does blood pressure affect vasoconstriction or vasodilatation?

A

High blood pressure leads to vasoconstriction, low blood pressure leads to vasodilatation.

24
Q

How are cerebral vessels regulated metabolically?

A

Hypercapnia, high PCO2, leads to vasodilatation.

Hypocapnia, low PCO2, leads to vasoconstriction.

25
Q

How can panic hyperventilation cause hypocapnia?

A

Breathing out too much CO2 so their levels drop, hypocapnia, and vasoconstriction in vasal vessels lead to fainting.

26
Q

What are four key vasodilator so in the cerebral blood flow?

A

Increased PCO2, [K+] or adenosine. Decreased PO2.

27
Q

What is the Cushing’s reflex in cerebral blood flow?

A

Rigid cranium protect the brain, but doesn’t allow for expansion of volume. This means increases in intracranial pressure impair cerebral blood flow. Impaired blood flow to vasomotor control regions of the brain stem increase sympathetic vasomotor activity and increase arterial blood pressure and maintain cerebral blood flow.

28
Q

What is the blood-brain barrier composed of?

A

Cerebral capillaries. Lipid soluble molecules like O2 and CO2 can diffuse across freely but lipid insoluble solutes like K+ can’t diffuse freely.

29
Q

What are the thee coronary arteries?

A

Right coronary, left anterior descending and circumflex.

30
Q

How does cardiac muscle differ from skeletal muscle in terms of fibre diameter, capillary density and capillary perfusion?

A

CM has a smaller fibre density, 18um, than SMm 50um.
CM has a higher capillary density, 3000/mm2, than SM, 400/mm2.
CM has it’s capillaries continuously perfused, but SM doesn’t at rest.

31
Q

What causes vasodilation in coronary blood flow?

A

Metabolic hyperaemia, also the vasodilators - adenosine, increased [K+] and decreased pH.

32
Q

What feature of coronary arteries makes them prone to atheromas?

A

They are functional end arteries, few arterio-atrial anastomoses.

33
Q

How do narrowed coronary arteries lead to angina in exercise?

A

Blood flow is mostly during diastole, this time is reduced as heart rate increases in exercise. So there is less blood flow, angina.

34
Q

What are three key features of skeletal muscle circulation?

A

Capillary density depends on the muscle type, postural muscle have a higher capillary density. They have very high vascular tone to permit lots of dilatation so flow can increase 20 time in active muscle. At rest, only half the capillaries area perfused.

35
Q

How do more capillaries get perfused in skeletal muscle?

A

The precapillary sphincters open to allow more capillaries to be perfused.

36
Q

which agents act as vasodilators in skeletal muscle?

A

High [K+], high osmolarity, inorganic phosphates, adenosine, high [H+] and adrenaline.

37
Q

How does adrenaline cause vasodilation of arterioles in skeletal muscle?

A

Act through B2 receptors and vasoconstrictor response via noradrenline on a1 receptors.

38
Q

What is the special role of cutaneous circulation?

A

Temperature regulation.

39
Q

How do artereovenous anastomoses regulate heat loss from apical skin?

A

Apical skin has a high surface area to volume ratio. AVAs are under neural control, sympathetic vasoconstrictor fibres. Decrease in core temperature increases sympathetic tone in AVAs so they decrease blood flow to apical skin. Increased core temperature opens AVAs.