Pulmonary circulation Flashcards

1
Q

What are the two circulations of the lungs

A

The lung has two circulations:
§ Bronchial circulation.
§ Pulmonary circulation.

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2
Q

Describe the pulmonary circulation

A

Pulmonary artery carries low-oxygen blood
Pulmonary vein carries high-oxygen blood
Blood goes to gas exchange surfaces (alveoli)
It is not the bronchial circulation

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3
Q

Compare pulmonary arteries to systemic arteries

A

§ The pulmonary arteries have a greater lumen to wall thickness ratio à greater compliance.
§ The pulmonary arteries still need to be elastic to convert the pulsatile flow into continuous flow.
Need to be compliant and stretch- to reduce the risk of pulmonary hypertension

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4
Q

Compare the pressures of the pulmonary circuit to the systemic circuit

A

Systemic circuit is at a higher pressure- LV is thicker than the RV- it has to pump blood all around the body
RV- only needs to pump blood to lungs- local effects

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5
Q

Quantify the pressures of the pulmonary and systemic circulation

A

Pulmonary:
RV- 25/0—– 25
Pulmonary artery- 25/8 —- 13

Systemic:
LV- 120/0 —- 120
Aorta—- 120/80 —- 93

Right pressure is relative pressure

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6
Q

Compare these differences on the mechanics of flow for each circuit

A

 The cardiac output is the same on both sides but the volume contained in systemic is much higher (pulmonary contains 10% of volume)
 Less pressure is needed in the pulmonary because there is less distance to cover.
 Compliance is higher in the pulmonary circulation.
o Compliance = willingness to distend.

Mean arterial pressure of pulmonary circuit is 15% of that of the systemic (13/93)

Mixed venous pressure is 1mmHg in systemic and 4 in pulmonary

Pressure gradient is 92 in systemic, compared to 9 of pulmonary (pulmonary operates at 10% of gradient)

Resistance ( change in p/volume) less in pulmonary (1.8 vs 18.4)

BUT due to the lower gradient- blood moves at a lower velocity in the pulmonary circuit

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7
Q

Why is it important that the blood moves at a lower velocity in the pulmonary circuit

A

More time for gas exchange to take place

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8
Q

Describe the bronchial circulation

A

Part of systemic circulation; the bronchial arteries are branches of the descending aorta.
It’s function is to supply oxygen, water and nutrients to the:
lung parenchyma
airways- smooth muscle, mucosa and glands
pulmonary arteries and veins
pleurae

An additional function is to condition the inspired air

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9
Q

What are the airways distal to the terminal bronchiole supplied by

A

Alveolar wall capillaries- for this reason a pulmonary embolus may result in infarction of the tissue supplied by the alveolar wall tissues, shown as a wedge-shaped opacity on the lung periphery of a chest X-Ray

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10
Q

Describe the venous drainage of the lungs

A

Drained by pulmonary veins- carry oxygenated blood from the lungs into the left atrium of the heart ( also some deoxygenated from bronchial veins which drain into the pulmonary veins)

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11
Q

Describe the role of the pulmonary circulation in gas exchange

A

 CO2 and O2 are the main exchanged gases.
 Pulmonary transit time is 0.75s.
o Gas is usually equilibrated in 0.25s.

(or CO/anaesthetics/etc.) N2 comes in- but is chemically inert and so comes back out

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12
Q

Describe the role of the pulmonary circulation in metabolising vasoactive substances

A

 ACE is exhibited within pulmonary endothelium.
o ACE can mediate production of ANG-II.
o ACE can degrade bradykinin.

Bradykinin is a vasodilator
ANG-II is a vasoconstrictor - therefore leading to overall vasoconstriction

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13
Q

Define embolus and embolism

A

DEFINITION: An embolus is a ‘mass’ within the circulation capable of causing obstruction
DEFINITION: An embolism is an ‘event’ characterised by obstruction of a major artery

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14
Q

Describe the role of the pulmonary circulation in filtration of the blood

A

Thrombi have to go through the lung- if small- they can be broken down there- or if it’s gas it can diffuse out slowly
Eliminated in pulmonary microcirculation

However it the embolus is large:
Trapped in pulmonary microcirculation, obstructing local perfusion- dramatic consequences for V/Q and lung function

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15
Q

What can result in an embolus

A

Venous thrombosis
Ruptured fatty plaques
Air bubbles
 The pulmonary circulation acts as a good defence against emboli heading to the brain to cause a stroke.

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16
Q

Essentially, what is a pulmonary shunt

A

‘…circumstances associated with bypassing the respiratory exchange surface…’

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17
Q

Describe the bronchial circulation as a pulmonary shunt

A

blood from left side of the heart supplies the parenchyma but drains back to pulmonary veins to re-enter left side of heart
1. Bronchial Circulation – The blood goes through the left side of the heart twice (bronchial and systemic circulations) without getting oxygenated.
Weak shunt- may ‘escape’ being drained into the lung parenchyma and continue through systemic circulation- where it may return to the right side- question of probability

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18
Q

Describe the foetal circulation as a pulmonary shunt

A
  1. Foetal Circulation – Has two shunts:
    a. Foramen Ovale.
    i. Hole between the left and right atria with low resistance.
    b. Ductus Arteriosus.
    i. Between aorta and pulmonary arch. This is because O2 is from mother’s placenta, not the lungs.
19
Q

Describe congenital defects as a pulmonary shunt

A
  1. Congenital Heart Defect – 2 forms:
    a. Atrial Septal Defect or Patent Foramen Ovale.
    b. Ventricular Septal Defect.
20
Q

Describe the consequences of a ventricular septal defect

A

mixing of blood across the septum
will increase pressure in right atria and ventricle
RV hypertrophy- will become stronger than the left
the shunt will reverse- but we will be pushing mixed blood out of the right hand side- CdO2 will decrease

21
Q

Describe the consequences of atrial septal defects

A

Thromboses may bypass lungs and get into the systemic circulation- dramatic consequences

22
Q

What should happen as we increase cardiac output

A

MAP will increase
Therefore fluid leakage will increase
Pulmonary oedema will increase
Therefore decreasing pulmonary function

23
Q

What actually happens in response to an increase in cardiac output

A

Pulmonary arteries distend more
We recruit hypoperfused tissue beds- to improve V/Q
This leads to negligible changes in MAP
Minimal fluid leakage
No onset of pulmonary oedema and therefore no loss in function
Huge capacity for increasing throughput without increasing pressure- important as you don’t want your lungs to fill with fluid during exercise

24
Q

Which regions become more perfused as we increase cardiac output

A

The apex

25
Q

What determines whether a vessel distends or compresses

A

the transmural pressure
positive pressure outside- collapse
negative pressure outside- distension

26
Q

Describe the alveolar capillaries

A

Dense network in alveolar wall, the external pressure impacting these is the alveolar pressure
Lungs expand- capillaries compressed (transpulmonary pressure more positive)
Diameter is dependant on transmural pressure (difference between hydrostatic pressure in capillaries and pressure in the alveolus)
If alveolar pressure greater- collapse of capillaries- can happen in the apex when the alveoli expand - more likely during diastole

27
Q

Describe the extra-alveolar capillaries

A

Arteries and veins in the lung tissue
As the lungs expand, they are distended by radial traction.
The external pressure is subatmospheric pressure ( which is negative, therefore transmural pressure tends to distend these vessels)
Will distend even further in inspiration as intrapleural pressure becomes more negative, reducing vascular resistance and increasing pulmonary blood flow
Radial traction is greater at greater volumes- more distension

28
Q

Describe the effect of lung volumes on the capillaries

A

Hydrostatic pressure is lowered in capillaries during deep inspiration (due to negative intra-pleural pressure around the heart- changing transmural pressure- increasing compression- increasing resistance
Large lung volumes- alveolar wall is stretched and becomes thinner- compressing the capillary and becoming compressed (no cartilage)
This is a key feature of COPD- leading to pulmonary hypertenstion- more resistance to push against

Extra-alveolar (at RV- more distended)
But at TLC (compressed- due to less negative intrapleural pressure)- see graph

29
Q

Summarise the effects of hypoxia in the lungs

A

Systemic vascular response to hypoxia is vasodilation

Pulmonary response to hypoxia is vasoconstriction

30
Q

Describe the mechanism that leads to hypoxic vasoconstriction

A
Hypoxia
Closure of O2-sensitive K+ channels
Decreased K+ efflux
Increased membrane potential 
Membrane depolarisation
Opening of voltage-gated Ca2+ channels
Vascular smooth muscle constriction
31
Q

When is hypoxic vasoconstriction beneficial

A

During foetal development
Blood follows the path of least resistance
High-resistance pulmonary circuit means increased flow through shunts
First breath increases alveolar PO2 and dilates pulmonary vessels

32
Q

When is hypoxic vasoconstriction detrimental

A

Chronic obstructive lung disease
Reduced alveolar ventilation and air trapping
Increased resistance in pulmonary circuit
Pulmonary hypertension (Cor pulmonale)
Right ventricular hypertrophy
Congestive heart failure

33
Q

Summarise the importance of hypoxic vasoconstriction

A

The aim of breathing is to oxygenate the blood sufficiently
This is achieved by efficient gas exchange in the alveoli and the bloodstream
If an area of lung is poorly ventilated and the alveolar partial pressure of oxygen is low, perfusion would be wasted due to inefficient gas exchange- it would be more beneficial to perfuse an area that is well ventilated
this is the basis of hypoxic vasoconstriction

34
Q

Summarise the distribution of blood in the lung

A

P = p x g x h
vessel at base subjected to hydrostatic pressure- this increased hydrostatic pressure will distend the vessels- lowering the resistance to blood flow= therefore blood flow will be greater at the base

35
Q

Describe the vessels in zone 3

A

venous pressure greater than alveolar pressure, so vessels always distended ( flow depends on arteriovenous pressure difference in systemic circulation

36
Q

What is flow determined by in zone 2 and 1

A

1- no flow (arterial pressure less than alveolar pressure)
2- flow determined by arterial-alveolar pressure difference - postcapillary venules open and close depending on hydrostatic pressure

37
Q

Give the starling equation for fluid balance

A
Jv = Kf  [(Pc - Pi) - sigma (c-i)]
sigma = reflection coefficient 
Kf = Hydraulic conductivity (permeability)
38
Q

Summarise pulmonary fluid balance

A

 There are 4 balancing forces involved but interstitial hydrostatic plays a very small role.
 In healthy individuals, the 1mmHg out is cleared by functional lymphatics  no oedema.

Plasma hydrostatic - 9mmHg out
Interstitial hydrostatic- nothing in
Plasma oncotic- 25 mmHg in
Interstitial oncotic - 17mmHg out

net 1mmHg out- cleared and returned by lymphatics

39
Q

What are the consequences of mitral valve stenosis

A

plasma hydrostatic pressure increases because pressures back up through pulmonary circulation, increasing pressure; causes net accumulation of fluid that exceeds lymphatic capacity leading to oedema and SOB on exertion

40
Q

What are the consequences of liver failure

A

Plasma oncotic pressure reduced

Less fluid drawn into capillary

Fluid accumulates in interstitium

Lymph clearance exceeded

OEDEMA develops

41
Q

What are the consequences of metastatic breast cancer

A

Cancerous cells spread to nearby thoracic lymph nodes/ducts

Tumours obstruct lymphatic drainage

Lymph clearance compromised

OEDEMA develops

42
Q

In real terms, why may blood flow in the pulmonary circulation be slightly less than Q

A

Proportion of the coronary circulation from the aorta drains directly into the left ventricle and the bronchial circulation from the aorta drains into pulmonary veins, thus bypassing the lungs- more blood returns to left ventricle

43
Q

What is the roles of the vessels in the low resistance in the pulmonary circulation

A

Large number of resistance vessels (which are dilated- increasing total area for flow)
small muscular arteries- less smooth muscle- more easily distended