Hypoxaemia and Respiratory Failure

Question 1

What is the difference between hypoxaemia and hypoxia?

Answer 1

Hypoxaemia = low pOxygen in the blood
Hypoxia = Oxygen deficiency at tissue level. 

Tissues can be hypoxic without hypoxaemia (e.g. anaemia, poor circulation)

Question 2

What is the range of hypoxaemia?

Answer 2

Anything below 94% Oxygen sats or pO2 below 9.3kPa.

But, tissue damage is more likely when oxygen sats are below 90% and pO2 is below 8kPa so this is what we use to diagnose respiratory failure.

Question 3

What is respiratory failure?

Answer 3

An impairment in gas exchange causing hypoxia with to without hypercapnia.

Question 4

What is the difference between type 1 and type 2 respiratory failure?

Answer 4

Type 1 = only oxygen affected without carbon dioxide levels changing.

Type 2 = Low pO2 and high pCO2

Question 5

What things can cause hypoxia?

Answer 5

• Low inspired pO2
• Hypoventilation (respiratory pump failure)
• Ventilation / Perfusion mismatch
• Diffusion defect-problems of the alveolar capillary membrane
• Right to left shunt (cyanotic heart disease)

Question 6

How much air is moved in and out of the lungs per minute?

Answer 6

Roughly 5L (5250ml).

This is the same as the amount of blood going through the lungs in a minute.

This means the V/Q ratio is about 1 which i optimal for gas exchange.

Question 7

What is hypoventilation?

Answer 7

This is a situation when the entire lung is poorly ventilated.

Alveolar ventilation (minute volume) is reduced.

Amount of oxygen entering the blood and CO2 entering the alveolus per minute remains the same as metabolic rate is the same.

This means alveolar pO2 falls so arterial pO2 falls leading to hypoxaemia.

Also, alveolar pCO2 rises which causes arterial pCO2 to increase resulting in hypercapnia.

HYPERVENTILATION ALWAYS CAUSES HYPERCAPNIA - TYPE 2 RESPIRATORY FAILURE. (Can see this on an ABG)

Question 8

In what situation do you get acute hypoventilation?

Answer 8

Opiate overdose
Head injury
Very severe asthma

Question 9

How do you treat acute hypoventilation?

Answer 9

Need urgent treatment including (maybe) artificial ventilation

Question 10

In what situations do you get chronic hypoventilation?

Answer 10

Severe COPD.
This is the most common cause of chronic type 2 respiratory failure.
Acute exacerbations may occur due to LRT infection

Question 11

How would a patient with chronic hypoventilation present?

Answer 11

Chronic hypoxia and hypercapnia 
Slow onset and progression 
Time for compensation
Therefore better tolerated. 
if chest infection, can cause acute on chronic respiratory failure which requires urgent treatment.

Question 12

What are some possible causes of hypoventilation?

Answer 12

Brainstem - narcotics, stokes

Cervical spine - Trauma to cervical spine (C3,4,5 as damage to phrenic nerve)

Phrenic nerve and intercostal nerves - Guillain-Barre syndrome,

Neuromuscular junctions - Myasthenia Gravis

Muscles of respiration - Myopathy, MND

Chest wall - severe obesity, Kyphoscoliosis

Pleural cavity - pneumothorax, large pleural effusion

Poor lung compliance)stiff lungs) - Respiratory distress syndrome, lung fibrosis

High airway resistance - severe acute asthma, late stage COPD

Upper airway construction - Laryngeal oedema, foreign body

Question 13

What are the effects of hypoxaemia?

Answer 13

Imapired CNS fiction, confusion, irritability

Cyanosis

Cardiac arrhythmias

Hypoxic vasoconstriction of pulmonary vessels.

Question 14

What is cyanosis?

Answer 14

Blueish discolouration of the skin due to the presence of over 50mg/L of unsaturated Hb in the blood.

It can be peripheral (fingers, toes) or central (oral mucosa, tongue lips). Central indicates hypoxaemia.

Question 15

What are the compensatory mechanisms of a patient id chronically hypoxic?

Answer 15

Increased EPO secreted by kidney - raised Hb

Increased 2,3-BPG

Hypoxic vasoconstriction of pulmonary vessels - BUT causes pulmonary hypertension which results in right heart failure (Cor pulmonale)

Question 16

What are the effects of hypercapnia?

Answer 16

Respiratory acidosis (compensated by retention of HCO3- by kidney)

Impaired CNS function: drowsiness, confusion, coma. flapping tremors.

Peripheral vasodilation - warm hands, bounding pulse.

Question 17

What is the effect of chronic CO2 retention on central chemoreceptors?

Answer 17

CO2 diffuses into CSF - CSF pH drops - stimulates central chemoreceptors

Persistant CSF acidity is harmful to neurones

Low CSH pH corrected by choroid plexus cells which secrete [HCO3-] into CSF

The CSF pH returns to normal; central chemoreceptors are no longer stimulated by low pH / high CO2 in the blood

Persistant hypoxia stimulates peripheral chemoreceptors - respiratory drive now driven by hypoxia.

Question 18

Why could treatment of hypoxia worsen the hypercapnia?

Answer 18

Oxygen removes stimulus for the hypoxic respiratory drive - alveolar ventilation drops causing worsening hypercapnia.

Correction of hypoxia removes pulmonary hypoxic vasoconstriction leading to increased perfusion of the poorly ventilated alveoli, diverting blood away from better ventilated alveoli.

• Give oxygen of lifesaving but monitor pCO2
• Controlled oxygen therapy with target sats of 88-92%
• If risen pCO2, ventilatory support

Question 19

What happens when the V/Q ratio is less than 1?

Answer 19

Alveolar pO2 falls and pCO2 rises

-As if in hypoventilation

Question 20

What happens when the V/Q ratio is more than 1?

Answer 20

pO2 rises and pCO2 falls.

Question 21

In what conditions do you get a V/Q ratio of less than 1?

Answer 21

Asthma (variable airway narrowing)

Pneumonia (exudate in affected alveoli)

Question 22

Why does V/Q mismatch cause hyperventilation and what effect does this have?

Answer 22

Hyperventilation occurs due to stimulation of chemoreceptors. But, the alveoli are still poorly ventilated due to pathology. The unaffected segments have increased ventilation (V/Q > 1) as pO2 rises and pCO2 falls.

• Rise in pO2 leads to an increase in dissolved oxygen.
• But, Hb is fully saturated above 10kPa so further increases in pO2 have no effect on Hb so the oxygen content in not significantly increased (only tiny amount of extra dissolved O2).
• This extra is insufficient to compensate for low pO2 from the segments with V/Q < 1.
• Drop in pCO2 accompanied by reduction in total CO2 content in blood.
• Sufficient to compensate for CO2 retention from segments with V/Q < 1.

Results in type 1 respiratory failure.

Question 23

What can cause V/Q mismatch?

Answer 23

Asthma (variable airway narrowing)
Pneumonia (exudate in affected alveoli)
RDS in newborns (some alveoli not expanded)
Pulmonary oedema (fluid in alveoli)
Pulmonary embolism

Question 24

How does a diffusion defect cause type 1 respiratory failure?

Answer 24

CO2 is more soluble so CO2 diffusion is less affected than diffusion of oxygen

Results in low pO2 and normal PCO2.

Question 25

What conditions can cause a diffusion defect?

Answer 25

Fibrotic lung disease (thickened alveolar membrane slows gas exchange)

Pulmonary oedema (fluid in interstitial space)

Question 26

What are some possible causes of diffuse lung fibrosis?

Answer 26

Idiopathic fibrosing alveolitis
Asbestos
Extrinsic allergic alveolitis
Pneumoconiosis

Question 27

How does a pulmonary embolism cause V/Q mismatch?

Answer 27

The embolus results in redistribution of pulmonary blood flow

The blood is diverted to unaffected areas of the pulmonary circulation

Leads to V/Q ratio < 1 if hyperventilation cannot match the increased perfusion

Causes hypoxaemia
Hyperventilation sufficient to get rid of CO2

Question 28

What is the ABG in hypoventilation?

Answer 28

Respiratory acidosis
pO2: Low 
pCO2: high 
pH: low 
HCO3-: depends on if corrected

Question 29

What is the ABG in diffusion impairment?

Answer 29

pO2: Low
pCO2: normal
pH: normal

Question 30

What is the ABG in ventilation-perfusion mismatch?

Answer 30

Respiratory acidosis
pO2: Low
pCO2: normal
pH: normal