Pulmonary Vascular Physiology Flashcards

1
Q

There are 2 types of circulation

A

Pulmonary circulation and Bronchial circulation

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2
Q

Pulmonary circulation

A

From Right Ventricle

Receives 100% of cardiac output (4.5-8L/min)

Red cell transit time ≈5 seconds.

280 billion capillaries & 300 million alveoli.

Surface area for gas exchange 50 – 100 m2

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3
Q

Bronchial circulation

A

2% of Left Ventricular Output

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4
Q

Vessel wall of pulmonary arteries is thin

A

Vessel wall of systemic arteries is thick

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5
Q

Muscularization of pulmonary arteries is minor

A

Muscularization of systemic arteries is major

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6
Q

There is no Need for redistribution in pulmonary artery in normal state

A

There is Need for redistribution in systemic arteries

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7
Q

What is the pressure in the RA? (MmHg)

A

5

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8
Q

What is the pressure in the RV? (MmHg)

A

25/0

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9
Q

What is the pressure in the PA? (MmHg)

A

25/8

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10
Q

What is the pressure in the LA? (MmHg)

A

5

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11
Q

What is the pressure in the LV? (MmHg)

A

120/0

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12
Q

What is the pressure in the aorta? (MmHg)

A

120/80

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13
Q

Left ventricle is larger than hothead right ventricle as

A

The left ventricle sees higher pressure than the right ventricle

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14
Q

Pouiseuille’s Law

A

Resistance= (8 x L x viscosity) / (pi x r^4)

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15
Q

Effect of Transmural Pressure on Pulmonary Vessels During Inspiration

A
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16
Q

Ohms law

A

V= IR

17
Q

Pressure across circuit =

A

Cardiac output x Resistance

18
Q

Pressure across pulmonary circulation=

A

mPAP – Left Atrial Pressure x Pulmonary Vascular Resistance

19
Q

Pressure across pulmonary circulation

A

mPAP – PAWP = CO x PVR

mPAP (mean pulmonary arterial pressure),
PAWP (pulmonary arterial wedge pressure left atrial pressure),
CO (cardiac output), PVR (pulmonary vascular resistance)

20
Q

What happens to mPAP on exercise?

A

On exercise mPAP remains stable in normal subjects but CO increases significantly

21
Q

How is this possible?

A

Recruitment and Distention in Response to Increased Pulmonary Artery Pressure

22
Q

Two types of respiratory failure

A

Type I
Type II

23
Q

Type 1 Respiratory Failure

A

pO2 < 8 kPA
pCO2 <6 kPA

24
Q

Type II respiratory failure

A

pO2 < 8 kPA
pCO2 >6 kPA

25
Q

Causes of Hypoxaemia

A

Hypoventilation
Diffusion Impairment
Shunting
V/Q mismatch

26
Q

Hypoventilation causes type II Respiratory failure as

A

Slide 33

27
Q

Diffusion Impairment

A

Gaseous diffusion impairment due to pulmonary oedema

Blood diffusion impairment due to anaemia due to less haemoglobin being present for O2 to then diffuse into

Membrane diffusion due to interstitial fibrosis- membrane can thicken

28
Q

Physiologic V/Q mismatch

A

V= ventilation (air going into the alveoli)
Q= Perfusion (amount of blood flow to the alveoli)

The lung is divided into 3 zones- the Ventilation: Perfusion ratio is higher at the apex of the lung. Towards the base of the lung the ventilation perfusion ratio is decreased

Average Ventilation: Perfusion ratio is 0.8. This means there is more perfusion to the lungs and alveoli than there is ventilation. This differs through different parts of the lung and with diseases of the lung.

In zone 1- apex of lung- the blood travelling to here will be decreased because of gravity- decreased perfusion at apex
So In zone 3- increased perfusion

Therefore, at the apex of the lung we have wasted ventilation as all the gas that goes to the alveoli is not exchanged efficiently because theres less perfusion

At the base of the lung there is wasted perfusion as there is too much perfusion relative to ventilation

Ventilation and perfusion is overall higher at the base of the lungs than the apex of the lungs

The part of the lung Above the heart has larger alveoli. There’s reduced pulmonary intravascular pressure because of less blood flow to this area and so less perfusion.
Because of the larger alveoli there’s also lower rates of ventilation. Despite the reduced ventilation the perfusion is much more lower so there’s wasted ventilation
As you go to the the base of the lungs the alveoli becomes smaller because of the difference in intrapleural plush pressure
More perfusion and more ventilation as the smaller alveoli are able to expand more. But ventilation increase isn’t as much as the increase in perfusion so the V:Q is lower here

In zone 1: alveolar pressure is highest
Pulmonary artery pressure is next highest
Pulmonary vein pressure is lowest

In zone 2: Pulmonary artery pressure exceeds alveolar pressure which then exceeds pulmonary ventilation

In zone 3: alveolar pressure exceeds pulmonary ventricular pressure which exceeds pulmonary artery pressure

In summary-
The ventilation increases from the apex of the lung to the base of the lung
But perfusion to the lungs and alveoli increases a lot more from the apex of the lung to the base of the lung

29
Q

Shunt v V/Q mismatch

A

V/Q=0 This is termed absolute pulmonary shunt
No oxygen is coming into the alveoli, so overall low oxygen levels leaving the system but there is still a large build up of CO2 as it cannot be breathed out

30
Q

What is a shunt?

A

Blood going through the lung but not taking part in gas transfers
Perfusion without ventilation

Slide 43

31
Q

Causes of shunt- blood going through lung/part of lung but not taking part in any gas transfer

A

Physiological
Bronchial arteries
Thesebian veins

Intracardiac
Eg VSD - R-L Shunt (Eisenmenger’s Syndrome)

Pulmonary
ArterioVenous Malformation (AVM)
Complete Lobar Collapse

32
Q

Eisenmenger’s Syndrome

A

Ventricular Septum defect (VSV)- Hole in septum

When baby is born, blood will be higher in the left ventricle. So if this VSV is not closed then the net direction of flow will be left to right so there will be more blood than normal going through the arteries under higher pressure
The pulmonary arteries, especially small pulmonary arteries, are not designed to cope with this, resulting in damage to them. The pulmonary arteries respond by narrowing down, increasing pressure and increasing resistance
Once the resistance and pressure gets above a certain limit, then the pressure in the right ventricle is similar and sometimes higher than the left ventricle so there is now right to left movement.
So there begins to be deoxygenated blood coming from the SBC into the right atrium and right ventricle and then it starts going from right to left

So the deoxygenated blood is going straight into systemic circulation and is no longer taking part in just transfer

Patients with this syndrome have low oxygen levels

33
Q

V/Q Mismatch

A

Physiological

Pulmonary Embolism: a clot occludes the pulmonary capillary pr artery causing reduced perfusion which will subsequently increase the perfusion rate causing a mismatch

Asthma

Pneumonia

Pulmonary Oedema

34
Q

Hypoxia Pulmonary Vasocontstriction

A

At high altitude all the vessels narrow down so one of the ventricles has a high pressure

35
Q

Hypoxic Pulmonary Vasoconstriction

A

Poorly understood
Local action of hypoxia on pulmonary artery wall
Weak response as little muscle
Aims to improve V/Q matching
Local hypoxia (eg peanut)
Generalised hypoxia (eg altitude)

36
Q

Diseases of the Pulmonary Circulation

A

Pulmonary Embolism caused by VQ mismatch

Pulmonary Hypertension caused by increased PVR

Pulmonary AVMs caused by shunt