Physiology: pulmonary blood flow, gas exchange and transport

Question 1

Describe bronchial circulation.

Answer 1

Part of systemic circulation that supplies blood to tissues of lungs. Comprises 2% of left heart output. Drains back into the left side via pulmonary vein (only blood that isn’t oxygenated in this vein).

Question 2

Which vessels carry the cardiac output from the right ventricle?

Answer 2

Right and left pulmonary arteries. This is a high flow, low pressure system (systolic pressure is 25 mmHg and diastolic is 8 mmHg). Has to be low pressure due to the large volumes of blood.

Question 3

What drives gas exchange?

Answer 3

Partial pressure gradients.

Question 4

What is normal cardiac output?

Answer 4

5L.

Question 5

What is systemic venous circulation in equilibrium with?

Answer 5

Peripheral tissues.

Question 6

What is arterial blood in equilibrium with?

Answer 6

Lungs (alveoli).

Question 7

What are PO2 and PCO2 in the alveoli, arteries and veins?

Answer 7

Alveoli: 100 (13.1), 40 (5.3). Arteries: 100, 40. Veins: 40, 46 (6.2) (mirrors peripheral tissues).

Question 8

Why isn’t the rate of diffusion of CO2 as slow as it should be?

Answer 8

Partial pressure gradient is 10 x steeper for O2, however CO2 is a lot more soluble in water than O2.

Question 9

How does emphysema affect gas exchange?

Answer 9

Smaller alveoli merge together into a large alveolus. Reduced surface area for gas exchange. PO2 in alveoli is normal/low and PO2 in capillaries is low. PCO2 increases.

Question 10

How does fibrotic lung disease affect gas exchange?

Answer 10

Thickened alveolar membrane slows gas exchange. PO2 low/normal in alveoli and low in capillaries. PCO2 increases.

Question 11

How does pulmonary oedema affect gas exchange?

Answer 11

Fluid pushes alveoli and capillary apart. PO2 normal in alveoli and low outside. Arterial PCO2 may be normal as it is soluble.

Question 12

How does asthma affect gas exchange?

Answer 12

Low PO2 in alveoli as not as much air getting in. PCO2 increases.

Question 13

What is the ventilation perfusion ration (V/Q)?

Answer 13

Should be 1 as ventilation should match blood flow - ventilation in the alveoli should match perfusion through the pulmonary capillaries.

Question 14

Describe blood flow at the base and apex of the lungs.

Answer 14

Base: highest as arterial pressure exceeds alveolar pressure and vascular resistance is low. Apex: blood flow low as arterial pressure is less than alveolar pressure and vascular resistance is high.

Question 15

What are the 3 types of V/Q ratio?

Answer 15

Matched: V/Q = 1. Mismatch 1: V > Q so > 1. Mismatch 2: V

Question 16

What happens when ventilation is less than blood flow (mismatch 2)?

Answer 16

PCO2 increases and PO2 decreases. Blood passing past this part of the lung does not get oxygenated. Blood is diluted from better oxygenated areas –> shunt. Vessels in lungs constrict in response to hypoxia to try and keep V/Q matched. Increased PCO2 causes mild bronchodilation. Systemic capillaries do the opposite - dilate in response to hypoxia to get more blood to the region.

Question 17

What happens when ventilation is more than blood flow (mismatch 2)?

Answer 17

Opposite to shunt. Increase in alveolar PO2 causes pulmonary vasodilation and decreases in alveolar PCO2 causes bronchial vasoconstriction. Increases perfusion and decreases ventilation slightly - brings ratio back towards 1. If this didn’t happen PE would occur.

Question 18

What is alveolar dead space?

Answer 18

Alveoli that are ventilated but not perfused. Classically seen at the apex of the lung.

Question 19

Define physiological dead space.

Answer 19

Alveolar dead space + anatomical dead space.

Question 20

What would happen if we had no haemoglobin?

Answer 20

Arterial O2 content is 3ml/L and CO is 5L = it would taken 15 mins for O2 to reach tissues.

Question 21

What is the O2 demand of resting tissues?

Answer 21

250 ml/min.

Question 22

How does the addition of haemoglobin increase O2 delivery?

Answer 22

200ml/L plasma x CO 5L = 1000 ml/min. This has a huge safety margin as only 250 ml is needed at rest. The other 75% goes back to the heart and is termed deoxygenated.

Question 23

Which % of O2 in the blood is bound to HbA?

Answer 23

98%.

Question 24

Which factor is the major determinant of how saturated haemoglobin is with O2?

Answer 24

PaO2 of the blood. Saturation is complete after 0.25 seconds contact time with alveoli.

Question 25

Define anaemia.

Answer 25

Any condition in which the O2 carrying capacity of blood is compromised, eg. Fe deficiency, vitamin B12 deficiency or haemorrhage.

Question 26

What happens to the PaO2 in anaemia?

Answer 26

Normal. It is possible to have a normal PaO2 while total blood O2 is low, but not possible to have low PaO2 and normal blood O2 content.

Question 27

Is it possible for RBC’s to be fully saturated with O2 in anaemia?

Answer 27

Yes. Only caveat is Fe deficiency where the number of binding sites would be reduced.

Question 28

Which chemical factors decrease the affinity of haemoglobin for O2?

Answer 28

Decrease in pH, increase in PCO2 or increase in temperature - all occur in exercising muscle. Conditions that exist locally in actively metabolising tissues and facilitate the dissociation of O2 from haemoglobin.

Question 29

Which chemical factors increase the affinity of haemoglobin for O2?

Answer 29

A rise in pH, fall in PCO2, fall in temperature - makes O2 unloading more difficult.

Question 30

What is the effect of DPG on O2 affinity for haemoglobin?

Answer 30

DPG is made by RBC’s. Itspresence decreases the affinity of O2 for haemoglobin. DPG increases/is synthesised in conditions where there is low O2 - heart/lung disease, high altitude etc to make O2 unloading easier.

Question 31

Why is CO a problem once dissolved in circulation?

Answer 31

It has an affinity 250 X greater for haemoglobin than O2 and so it binds readily to form carboxyhaemoglobin and dissociates very slowly.

Question 32

What are the symptoms of CO poisoning?

Answer 32

Hypoxia, nausea, anaemia, headaches, red skin and mucous membranes, normal respiration rate (normal arterial PCO2), potential brain damage and death.

Question 33

What is the main treatment for CO poisoning?

Answer 33

100% O2 to increase PaO2.

Question 34

What are the 5 main types of hypoxia (inadequate supply of O2 to tissues)?

Answer 34

1) Hypoxic: most common, reduction in O2 diffusion at lungs due to decreased atmospheric O2 or pathology, 2) Anaemic: reduction in O2 carrying capacity in blood, 3) Ischaemic (stagnant): heart disease results in inefficient pumping of blood to lungs/around body, 4) Histotoxic: poisioning - cells can’t use O2 delivered to them, 5) Metabolic: O2 delivery does not meet increased demand.

Question 35

What happens when CO2 molecules diffuse from tissues into the blood?

Answer 35

7% remains dissolved in plasma and RBC’s, 23% combines in RBC’s with deoxyhaemoglobin to form carbamino compounds, and 70% combines with RBC’s and water to form carbonic acid.

Question 36

What happens to carbonic acid?

Answer 36

It dissociates to yield bicarbonate and protons, then moves out of RBC’s to plasma in exchange for chloride ions (chloride shift). Excess protons bind to deoxyhaemoglobin.

Question 37

What happens in pulmonary capillaries?

Answer 37

CO2 moves down its concentration gradient from blood to alveoli.

Question 38

How can CO2 change ECF pH?

Answer 38

Hypoventilation: causes CO2 retention which causes respiratory acidosis. Hyperventilation: blows off more CO2 which leads to respiratory alkalosis.