Session 7: Hypoxia & Respiratory Failure

Question 1

Steps of the oxygen supply chain.

Answer 1

Air -> Airways -> Alveolar gas -> Alveolar membrane -> Arterial blood -> Regional arteries -> Capillaries -> Tissues

Question 2

Define hypoxia.

Answer 2

Reduced oxygen at tissue level. This can be abnormalities of any point of the oxygen supply chain which can lead to hypoxia.

Question 3

Define hypoxaemia.

Answer 3

Decrease in pO2 in the blood.

Question 4

Is it possible to be hypoxic without hypoxaemia?

Answer 4

Yes.

Question 5

Explain how it is possible to be hypoxic without being hypoxaemic.

Answer 5

E.g. severe anaemia where there is reduced oxygen carrying capacity due to low Hb levels. This leads to hypoxia but not reduced pO2 in arteries.

Also poor perfusion which can lead to hypoxia of the affected tissue like in an MI despite having normal gas exchange in lungs and normal pO2 in arteries.

Question 6

What is respiratory failure defined as?

Answer 6

When arterial pO2 falls below 8kPa or 60 mmHg when breathing air at sea level.

Question 7

Define Type 1 Respiratory failure

Answer 7

A pO2 below 8kPa

Normal or low pCO2

Question 8

Define type 2 respiratory failure.

Answer 8

A pO2 below 8kPa

High pCO2 of above 6.7 kPa

Question 9

Effects of hypoxia.

Answer 9

Impaired CNS function

Central cyanosis

Cardiac arrhythmias

Hypoxic vasoconstriction of the pulmonary vessels

Question 10

Effects of hypercapnia.

Answer 10

Respiratory acidosis

Impaired CNS functions like drowsiness, confusion, coma and tremors.

Peripheral vasodilation leading to warm hands and bounding pulse.

Cerebral vasodilation leading to headache.

Question 11

What is needed to maintain arterial pO2 at a normal level?

Answer 11

Normal inspired pO2

Normal alveolar ventilation

Matching V/Q

Normal alveolar capillary membrane (no thickening)

No right to left shunts.

Question 12

Why is it important to not have a right to left shunt to maintain arterial pO2?

Answer 12

CO from right heart needs to pass through gas exchanging alveoli

Question 13

Considering the factors needed to maintain normal arterial pO2.

Why might hypoxaemia arise?

Answer 13

Low inspired pO2 at e.g. high altitude.

Hypoventilation

V/Q mismatch

Diffusion impairment

Right to left shunts.

Intra-lung shunt like ARDS

Question 14

What type of respiratory failure is hypoventilation?

Answer 14

Type 2 resp

Question 15

What type of respiratory failure is V/Q mismatch?

Answer 15

Type 1 resp failure

Question 16

What type of resp failure is diffusion impairment?

Answer 16

Type 1 resp failure

Question 17

Explain hypoxaemia due to high altitude.

Answer 17

High altitude means lower atmospheric pressure. This leads to lower arterial and alveolar pO2.

This leads to stimulation of peripheral chemoreceptors and causes hyperventilation. The end result is low pO2 and low pCO2.

Question 18

Physiological adaptations to survive in high altitudes for a long time.

Answer 18

Polycythaemia (increased Hb) by EPO

Increased 2-3 DPG

Increased capillary density at tissue level

Question 19

At what O2 sat and pO2 does tissue damage start to occur

Answer 19

<90%

<8kPa

Question 20

What does chronic hypoxic vasoconstriction of pulmonary vessels result in?

Answer 20

Pulmonary hypertension

Right heart failure

Cor pulmonale

Question 21

Give causes of hypoventilation.

Answer 21

Head injury, drug overdose

Resp muscle weakness (damage to muscles or nerves)

Mechanical problems of the chest wall like scoliosis, kyphosis, morbid obesity or rib fractures.

Lung fibrosis

Airway obstructions like in severe asthma or late stages of COPD.

Question 22

Explain the compensatory effects of chronic hypoxia.

Answer 22

Polycythaemia by increased EPO by kidneys leading to increased Hb levels.

Increased 2,3 DPG to better unload O2

Hypoxia induced vasoconstriction which will lead to pulmonary hypertension and eventually right ventricular hypertrophy and right heart failure.

Question 23

Effects of chronic hypercapnia.

Answer 23

Respiratory acidosis is compensated by retention of HCO3- by the kidneys to restore CO2/HCO3- ratio.

Central chemoreceptors in persisent hypercapnia leads to choroid plexus secreting HCO3- into CSF to restore the CO2/HCO3- ratio in the CSF. This resets the central chemoreceptors to higher CO2 levels.

Peripheral chemoreceptors lead the hyperventilation after this.

‘Pink puffers’

Question 24

What is the most common cause of hypoxaemia?

Answer 24

V/Q mismatch

Question 25

What causes V/Q mismatch?

Answer 25

Usually reduced ventilation

Question 26

Give examples of conditions leading to reduced ventilation and V/Q mismatch.

Answer 26

Pneumonia

Asthma

COPD

Respiratory distress syndrome

Question 27

Give another examples of V/Q mismatch not due to poor ventilation.

Answer 27

Pulmonary embolism.

Question 28

Explain V/Q mismatch due to pulmonary embolism.

Answer 28

PE leads to obstruction of a branch of the pulmonary artery. No blood will go to that area of the lung and will instead be redirected.

The ventilation of the un-perfused alveoli is now wasted as no blood reaches.

The diversion of the blood results in increased perfusion of the parts of the lung that are still being supplied by blood for gas exchange.

If hyperventilation is not sufficient to match the increased perfusion of the healthy alveoli the V/Q ratio will drop <1 and lead to hypoxia.

Question 29

Explain why hyperventilation cannot correct the hypoxaemia due to V/Q mismatch.

Answer 29

Alveolar units with a V/Q ratio of >1 cannot compensate for hypoxia arising in alveolia with a V/Q ratio <1.

This is because Hb is already fully saturated in the alveolar units with V/Q ratio of >1. Any further increase in ventilation will increase alveolar pO2 but this can only increase the amount of dissolved oxygen in the blood and not the amount of O2 carried by Hb. This means that it is insufficient to correct the hypoxia arising from alveoli with a low V/Q <1.

Question 30

Explain why diffusion may be impaired.

Answer 30

Thickened barrier as in lung fibrosis.

Diffusion pathway lengthened in pulmonary oedema -> extra layer fluid increases the distance across which gases have to diffuse.

If total area available for diffusion is reduced like in emphysema.

Question 31

Explain why pCO2 can be normal or low in diffusion problems and not as affected as O2.

Answer 31

Because CO2 much more readily than O2. This means that O2 is the main gas that is affected and not CO2.

Question 32

Can type 1 resp failure lead to type 2?

Answer 32

Yes

Question 33

Give an example of a disease where type 1 resp failure leads to type 2.

Answer 33

Asthma from being in its early stages to leading to a more severe form of it.

Question 34

How would you treat a patient with chronic type 2 respiratory failure?

Answer 34

By controlled oxygen therapy with 24% or 28% with a target SaO2 of 88 to 92%.

Question 35

Why is it important to treat chronic type 2 resp failure with controlled oxygen therapy?

Answer 35

Because uncontrolled O2 therapy to correct the hypoxia of chronic type 2 resp failure can lead to worsening hypercapnia.

Question 36

Explain the two mechanisms that lead to severe hypercapnia due to uncontrolled O2 therapy of chronic type 2 respiratory failure.

Answer 36

• Choroid plexus imports HCO3- into the CSF to restore the CO2/HCO3- ratio in the CSF. This leads to recalibration of the central chemoreceptors to a higher pCO2. The peripheral chemoreceptors will now be responsible for hyperventilation to decrease pCO2. The peripheral chemoreceptors mainly respond to low pO2 which is the case in type 2 resp failure. When you give pO2 the patient will stop to hyperventilate because the peripheral chemoreceptors thinks that everything’s okay. This leads to an increase in pCO2 further.
• O2 therapy can lead to worsening V/Q mismatch in poorly ventilated alveoli. This is because the hypoxia causes vasconstriction to divert blood to healthy alveoli. When the hypoxia is treated the vasoconstriction will cease. This leads to increased perfusion of the poorly ventilated alveoli and diverts blood away from better ventilated alveoli.