CVS 15 - Special Circulations Flashcards

1
Q

What are the 2 circulations that supply the lungs?

A

1) Bronchial circulation - part of systemic circulation, provides oxygen to parts of lungs not in close contact to pulmonary circulation.
2) Pulmonary circulation - blood supply to alveoli required for gas exchange. Pulmonary circulation must accept the entire cardiac output.

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2
Q

What are the key features of the pulmonary circulation?

A
  • Pumps blood from RV to the lungs via pulmonary artery + back to LA via the pulmonary vein.
  • Therefore works under low pressure (MAP = 12-15mmHg) + low resistance (short, wide vessels, lots of capillaries + arterioles with little SM).
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3
Q

What are the adaptions of the pulmonary circulation that enable efficient gas exchange?

A

1) High capillary density in alveolar wall - large capillary SA for diffusion
2) Short diffusion distance - combined endo+epithelium (type 1 pneumocyte) layer just 0.3um.

  • Large SA + short diffusion distance produce high O2 + CO2 transport capacity.
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4
Q

What is the ventilation-perfusion ratio (V/Q)?
What is the optimal V/Q ratio?
What ensures an optimal V/Q ratio during hypoxia?

A
  • For efficient oxygenation, ventilation (oxygen) of alveoli must match perfusion (blood) of alveoli.
  • Optimal ratio is 0.8
  • This means when the alveoli is not well ventilated, blood must be diverted away.
  • Hypoxic pulmonary vasoconstriction - alveolar hypoxia results in vasoconstriction of pulmonary vessels (opposite to whats seen in systemic circulations) to ensure that perfusion then matches ventilation.
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5
Q

How does chronic hypoxic vasoconstriction lead to RV heart failure?

A
  • Chronic hypoxia can occur at altitude or as a consequence of lung disease such as emphysema.
  • Causes chronic increase in vascular resistance due to vasoconstriction (chronic pulmonary hypertension)
  • High afterload then on RV, leading to RV HF.
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6
Q

What is the effect of exercise on pulmonary blood flow?

A
  • Increased CO, causing small increase in pulmonary arterial pressure, opening apical capillaries + O2 uptake by lungs.
  • As blood flow increases, capillary transit time is reduced, can fall to 0.3 seconds (normally 1 second) - why we require very efficient gas exchange.
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7
Q

What is the mechanism by which tissue fluid forms?
Is capillary hydrostatic pressure influenced more by venous pressure or arterial pressure?
Therefore, what prevents pulmonary oedema?

A
  • Capillary hydrostatic pressure (pushing fluid out) exceeds the oncotic pressure of plasma proteins (pulling fluid in). This results in oedema.
  • Venous pressure, as venous pressure is downstream and doesn’t offer much resistance (compared to arterial).
  • Low capillary hydrostatic pressure (normally 9-12mmHg), but can cause pulmonary oedema if raises to 20-25, e.g.: in mitral valve stenosis or LV failure (both increase LA pressure).
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8
Q

What are the consequences of pulmonary oedema?

How are symptoms relieved?

A
  • Impairs gas exchange. Affected by posture, so worst at base when upright, forms throughout lung when lying down (so they’ll complain it gets worse when lying down at night).
  • Diuretics relieve symptoms, try to treat underlying cause.
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9
Q

The cerebral circulation has a high O2 demand (15% of CO), what 3 adaptations allows for this demand?

A

1) High capillary density - large SA for gas exchange + reduced diffusion distance.
2) High basal flow rate - x10 greater than whole body average.
3) High O2 extraction - maintains concentration gradient for O2.

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10
Q

Why is a secure O2 supply to the brain vital?

How is a secure cerebella blood supply ensured?

A
  • Neurones sensitive to hypoxia, loss of consciousness after few seconds of ischaemia, irreversible brain damage after 4 minutes.

1) Structurally - anastomoses between basilar and internal carotid arteries (forming circle of willis). Allows circulation of blood if blockage in an area.
2) Functionally - Myogenic autoregulation maintains perfusion in hypotension.

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11
Q

Describe the response of cerebral blood vessels to hyper + hypotension (myogenic autoregulation) as well as hyper + hypocapnia (metabolic regulation).

A

BP increases = vasoconstriction
BP decreases = vasodilation
Hypercapnia = vasodilation (increasing blood flow to meet metabolic demands)
Hypocapnia = vasoconstriction

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12
Q

Why do areas with increased neuronal activity receive increased blood flow?

A
  • Areas of high neuronal activity produce a lot of metabolites (CO2, K+, adenosine etc), which are arteriolar vasodilators allowing for increased blood flow.
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13
Q

What is Cushing’s reflex?

A
  • A response to a space blocking lesion in the brain
  • Impaired blood flow to vasomotor control regions of the brainstem increase sympathetic vasomotor activity, helping maintain cerebral blood flow but also causing acute hypertension + reflex bradycardia (typical signs of a space-occupying lesion).
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14
Q

What specialisation does the coronary circulation have to maintain a high basal rate of O2 delivery + meet increased demands during exericse?

A

1) High capillary density (3000/mm^2)
2) Short diffusion distance (<9um)
3) Continous production of NO by coronary endothelium - vessels are continually patent maintaining high basal flow.

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15
Q

Why does coronary blood flow increase with increased myocardial O2 demand?

A
  • Metabolic hyperaemia - adenosine, K+, decreased pH act as vasodilators, increasing blood flow.
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16
Q

What specialisations of the skeletal muscle circulation allow for increased O2 + nutrient delivery during exercise? (4)

A

1) Very high vascular tone (rich sympathetic innervation), permits lots of dilation. Flow can increase >20 times in active muscle.
2) At rest, only 1/2 capillaries are perfused, allowing for increased recruitment (by pre-capillary sphincters)
3) Metabolic hyperaemia - K+, adenosine, H+ all act as vasodilators to increase blood flow.
4) Adrenaline can also act as a vasodilator at arterioles in skeletal muscle on B2-adr’s.

17
Q

What does the cutaneous circulation play an important role in?
How does it achieve this?

A
  • Temperature regulation - skin is main heat dissipating surface, regulated by cutaenous blood flow.
  • Artereovenous anastomoses (AVA’s) - spiral like structures connecting arterioles and venules allowing for heat loss via cutaneous blood flow.
  • Decreased body temp increases sympathetic tone in AVA’s, increased core temp reduces vasomotor tone, dilating them, diverting blood to veins near surface.

NB: This is only in apical skin, in non-apical skin sympathetic cholinergic fibres activate sweat glands that release vasodilators such as bradykinin.