CVS session 8: the special circulations Flashcards

1
Q

What are the two circulations of the lungs?

A

Bronchial: part of systemic circulation; meets metabolic requirements of the lungs (parts not regularly perfused with oxygen)

Pulmonary: blood supply to alveoli, required for gas exchange, in series with the rest of the systemic circulation. Must accept the entire cardiac output

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2
Q

Pressure values for the heart, pulmonary artery and aorta

systole/diastole where relevant

A
Right atrium: 0-8 mmHg
Left atrium: 1-10 mmHg (slightly higher than RA as more resistance)
Right ventricle: 15-30 mmHg/0-8 mmHg
Left ventricle: 100-140 mmHg/1-10 mmHg
Pulmonary artery: 15-30 mmHg/4-12 mmHg
Aorta: 100-140 mmHg/60-90 mmHg
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3
Q

Pressures and resistances in the pulmonary circulation?

A
  1. Low pressure: MAP ~12-15 mmHg, mean capillary pressure ~9-12 mmHg, mean venous pressure ~5 mmHg
  2. Low resistance: short, wide vessels, many capillaries (so many parallel elements), arterioles have relatively little smooth muscle
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4
Q

Adaptations for efficient gas exchange in the pulmonary circulation

A
  • high density of capillaries in alveolar wall: large surface area
  • short diffusion distance as very thin layer of tissue that separates gas from plasma
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5
Q

What is the ventilation-perfusion ratio?

A

Need to match ventilation of alveoli with perfusion of alveoli in order to allow efficient oxygenation. Optimal V/Q ratio is 0.8. This is achieved when:

  • ventilation ~4L/min
  • perfusion (cardiac output) ~5L/min

Maintaining this means diverting blood from alveoli which are not well ventilated

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6
Q

What is the most important mechanism regulating pulmonary vascular tone? How does it work?

A

Hypoxic pulmonary vasoconstriction
Maintains an optimal V/Q ratio: alveolar hypoxia causes vasoconstriction of pulmonary vessels (opposite of in systemic where metabolites cause vasodilation to increase perfusion). Poorly-ventilated alveoli are less perfused, which prevents deoxygenated blood from returning to the left side of the heart

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7
Q

What can chronic hypoxic vasoconstriction lead to and why?

A

Right ventricular failure
At altitude or due to a lung disease (e.g. emphysema), chronic increase in vascular resistance causes chronic pulmonary hypertension. The high after load on the right ventricle can therefore lead to right ventricular heart failure

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8
Q

Effects of gravity on the lungs

A

Strong influence due to the low pressure of the vessels:

  • upright (orthostasis) there is a greater hydrostatic pressure on vessels in the lower part of the lung, so vessels are distended
  • at the level of the heart the vessels are continuously patent
  • vessels at the apex collapse during diastole
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9
Q

Effect of exercise on the pulmonary circulation

A

Increased CO increases flow to lungs ,causing a small increase in pulmonary arterial pressure which opens apical capillaries which have a faster transmit time as blood flow increases. This increases oxygen uptake by the lungs

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10
Q

Describe how Starling forces regulate tissue fluid locations

A

No1. Capillary hydrostatic pressure: pushes fluid out of capillary into interstitium normally (as is normally greater than tissue hydrostatic pressure). Main influence is by the venous pressure

  1. Tissue hydrostatic pressure
  2. Capillary plasma oncotic pressure: large molecules e.g. plasma proteins within draw fluid into the capillary normally
  3. Tissue interstitial oncotic pressure: usually lower than capillary oncotic pressure

In normal situations, tissue fluid is kept at a constant level by the capillary hydrostatic pressure pushing fluid out and the capillary oncotic pressure drawing fluid in

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11
Q

Does hypertension result in peripheral oedema?

A

No
No symptoms: silent killer

Oedema caused by heart failure due to increased pressure at venous ends of capillaries

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12
Q

How does a low capillary pressure minimise the formation of lung lymph?

A

Oncotic pressure of TF in lungs > in periphery

Capillary hydrostatic pressure in lungs

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13
Q

How does pulmonary oedema form?

A

Increased capillary pressure (usually venous end) resulting in filtration > reabsorption

Caused by left-sided heart failure, as blood backs up into the lung vessels

Left atrial pressure increased due to mitral valve stenosis of left ventricular hypertrophy: left ventricle can’t pump out as much so its harder for blood to move from LA to LV and from PV to LA
This causes capillary hydrostatic pressure to be increased, so fluid moves out of capillaries into interstitium
Gas exchange is therefore impaired

Use diuretics to relieve symptoms (reduce blood volume and venous pressure), treat underlying cause if possible

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14
Q

How does posture affect oedema of the lungs?

A

When upright it forms mainly at the bases so doesn’t cause as severe symptoms
When lying down, gravity causes redistribution of fluid when lying down so it is present throughout the lungs. Gravity increases venous pressure so increases capillary hydrostatic pressure causing fluid to move out into lungs
Leads to shortness of breath

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15
Q

What is the oxygen demand of the brain?

A

~15% of cardiac output even though only ~2% of body mass
O2 consumption of grey matter (cell bodies) accounts for ~20% of whole body oxygen consumption at rest, so secure oxygen supply is vital (neurones irreversibly damaged by hypoxia in ~4 minutes)

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16
Q

How does the cerebral circulation meet its demand?

A

High capillary density: large SA for gas exchange
Low diffusion density
High basal flow rate: x10 average for whole body
Blood supply secured by anastomoses between the basilar and internal carotid arteries: circle of Willis

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17
Q

What is myogenic auto regulation?

A

Mechanism to maintain cerebral perfusion during hypotension (when blood pressure falls below 50 mmHg)
Cerebral resistance vessels have a well-developed myogenic response & respond to changes in transmural pressure: decreased blood pressure causes vasodilation

18
Q

Metabolic regulation of the cerebral circulation

A

Vessels very sensitive to changes in arterial PCO2:

  • hypercapnia (increased PCO2) leads to vasodilatation
  • hypocapnia (decreased PCO2) leads to vasoconstriction

Regional activity of neurones produces local increases in blood flow: increases in K+, adenosine, CO2 and decreased O2 cause vasodilation

E.g. ATP breakdown produces adenosine

19
Q

Why can hyperventilation in a panic attack lead to dizziness/fainting?

A

Can cause hypocapnia so cerebral vasoconstriction, reducing cerebral supply. When lose consciousness the breathing goes back to normal

Raise feet and lie down to minimise effects of gravity on circulation and maintain cerebral flow

20
Q

What is the blood-brain barrier?

A

Cerebral capillaries form a tight blood-brain barrier:

  • lipid-soluble molecules such as O2 and CO2 diffuse freely
  • lipid-insoluble molecules e.g. K+, catecholamines can’t diffuse freely. Useful as these can interact with receptors in the brain and cause hyperactivity
21
Q

Describe Cushing’s reflex

A

The cranium is rigid so increased intracranial pressure (due to tumour or haemorrhage) will impair cerebral blood flow. Impaired flow to vasomotor control regions of the brainstem increases sympathetic vasomotor activity:

  • increase vasoconstriction so increase TPR therefore increase arterial BP
  • helps to maintain cerebral blood flow
  • increased BP detected by baroreceptors to activate bradycardia

Therefore, the bradycardia and acute hypertension should be recognised in emergency situation as they indicate a large lesion in the skull

22
Q

When does blood flow through the coronary arteries occur?

A

LCA: mainly during diastole
RCA: slightly more in systole than diastole

23
Q

How does the coronary circulation meet the needs of the heart?

A

High capillary density so efficient O2 delivery (1 capillary to 1 fibre)
Short diffusion distance
Capillaries continuously perfused due to continuous production of NO by coronary endothelium to maintain a high basal flow rate

24
Q

How does the coronary circulation respond to increased flow demand?

A

Increased blood flow, causes vasodilation due to metabolic hyperaemia

25
Q

What type of arteries are the coronary arteries and how can this be problematic?

A

Functional end arteries: few anastomoses

They are prone to atheroma, so narrowed CA leads to transient ischaemia in exercise in angina, and if suddenly occluded by a thrombus cause an MI

26
Q

Why does circulation to skeletal muscle have a very high vascular tone?

A

Permits lots of dilatation

27
Q

Perfusion of capillaries in skeletal muscle circulation

A

At rest about 1/2 are perfused. There is about 1 capillary per fibres but not all are open at once. Opening of pre capillary sphincters allows more capillaries to be perfused, which increases blood flow and decreases diffusion distance

28
Q

How does metabolic hyperaemia increase flow in skeletal muscle?

A

Vasodilators including K+, H+, adenosine, increased osmolarity, inorganic phosphates. Adrenaline also vasodilator by acting at beta 2 receptors (noradrenaline at alpha 1 receptors activates vasoconstriction)

29
Q

What doe cutaneous blood flow regulate?

A

Heat dissipating through the skin

30
Q

What are acral/apical skin areas?

A

Areas specialised for heat loss due to a high SA:V ratio. E.g. fingers, ears. Contain arteriovenous anastomoses

31
Q

What are arteriovenous anastomoses (AVAs) and how do they regulate heat loss from apical skin?

A

Allow heat to be lost quickly by blood quickly bypassing the capillary bed to get to the venous system which is close to the surface. AVAs open to allow heat loss through dissipation by skin. Regulate loss because:

  • have a high SA:V ratio
  • NOT regulated by local metabolites but by SNS
  • increased core body temperature opens AVAs by decreased sympathetic tone, allowing them dilate. Low resistance shunts blood to venous plexus, allowing a large increase in flow just beneath the skin so dissipates heat
  • decreased core temperature increases sympathetic tone in AVAs causing vasoconstriction so less blood flow to apical skin
32
Q

What causes vasodilation in non-apical skin?

A

Sympathetic actions of sweat glands releases ACh; sweat glands also release bradykinin which can also affect

33
Q

Why is the pressure in the left atrium of a normal individual higher than the pressure in the right atrium?

A

Resistance in the pulmonary circulation is low, so less pressure drop occurs as blood enters the left atrium. The greatest resistance and therefore greatest pressure drop occurs in the systemic arteries

34
Q

Changes in pressure from IVC to RA?

A

Minimal change: RA essentially a continuation of venous system, valves not needed for entry

35
Q

Changes in pressure from RV to PA?

A

Systole: same
Diastole: higher as need to bring blood in

36
Q

Why is it useful to know the pressure changes in the heart?

A

Can identify pulmonary hypertension

37
Q

What happens to the pressure in the LA on inspiration and expiration?

A

Inspiration decreases, expiration increases

38
Q

Pressure in PA if left heart is compromised?

A

Increase
This will lead to pulmonary oedema in the short term, and over time the resistance vessels of the pulmonary circulation will become permanently narrowed

39
Q

What will happen to the V/Q ratio if some part of pulmonary arterial tree is occluded by a thrombus?

A

Mismatched ratio: as normal blood flow but inadequate perfusion (pulmonary embolism)

40
Q

How could you assess V/Q matching?

A

Arterial blood gases indicate effectiveness

Areas of mismatch may be shown in a lung scan