Session 7: Hypoxia & Respiratory Failure Flashcards
Steps of the oxygen supply chain.
Air -> Airways -> Alveolar gas -> Alveolar membrane -> Arterial blood -> Regional arteries -> Capillaries -> Tissues
Define hypoxia.
Reduced oxygen at tissue level. This can be abnormalities of any point of the oxygen supply chain which can lead to hypoxia.
Define hypoxaemia.
Decrease in pO2 in the blood.
Is it possible to be hypoxic without hypoxaemia?
Yes.
Explain how it is possible to be hypoxic without being hypoxaemic.
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.
What is respiratory failure defined as?
When arterial pO2 falls below 8kPa or 60 mmHg when breathing air at sea level.
Define Type 1 Respiratory failure
A pO2 below 8kPa
Normal or low pCO2
Define type 2 respiratory failure.
A pO2 below 8kPa
High pCO2 of above 6.7 kPa
Effects of hypoxia.
Impaired CNS function
Central cyanosis
Cardiac arrhythmias
Hypoxic vasoconstriction of the pulmonary vessels
Effects of hypercapnia.
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.
What is needed to maintain arterial pO2 at a normal level?
Normal inspired pO2
Normal alveolar ventilation
Matching V/Q
Normal alveolar capillary membrane (no thickening)
No right to left shunts.
Why is it important to not have a right to left shunt to maintain arterial pO2?
CO from right heart needs to pass through gas exchanging alveoli
Considering the factors needed to maintain normal arterial pO2.
Why might hypoxaemia arise?
Low inspired pO2 at e.g. high altitude.
Hypoventilation
V/Q mismatch
Diffusion impairment
Right to left shunts.
Intra-lung shunt like ARDS
What type of respiratory failure is hypoventilation?
Type 2 resp
What type of respiratory failure is V/Q mismatch?
Type 1 resp failure
What type of resp failure is diffusion impairment?
Type 1 resp failure
Explain hypoxaemia due to high altitude.
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.
Physiological adaptations to survive in high altitudes for a long time.
Polycythaemia (increased Hb) by EPO
Increased 2-3 DPG
Increased capillary density at tissue level
At what O2 sat and pO2 does tissue damage start to occur
<90%
<8kPa
What does chronic hypoxic vasoconstriction of pulmonary vessels result in?
Pulmonary hypertension
Right heart failure
Cor pulmonale
Give causes of hypoventilation.
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.
Explain the compensatory effects of chronic hypoxia.
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.
Effects of chronic hypercapnia.
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’
What is the most common cause of hypoxaemia?
V/Q mismatch
What causes V/Q mismatch?
Usually reduced ventilation
Give examples of conditions leading to reduced ventilation and V/Q mismatch.
Pneumonia
Asthma
COPD
Respiratory distress syndrome
Give another examples of V/Q mismatch not due to poor ventilation.
Pulmonary embolism.
Explain V/Q mismatch due to pulmonary embolism.
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.
Explain why hyperventilation cannot correct the hypoxaemia due to V/Q mismatch.
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.
Explain why diffusion may be impaired.
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.
Explain why pCO2 can be normal or low in diffusion problems and not as affected as O2.
Because CO2 much more readily than O2. This means that O2 is the main gas that is affected and not CO2.
Can type 1 resp failure lead to type 2?
Yes
Give an example of a disease where type 1 resp failure leads to type 2.
Asthma from being in its early stages to leading to a more severe form of it.
How would you treat a patient with chronic type 2 respiratory failure?
By controlled oxygen therapy with 24% or 28% with a target SaO2 of 88 to 92%.
Why is it important to treat chronic type 2 resp failure with controlled oxygen therapy?
Because uncontrolled O2 therapy to correct the hypoxia of chronic type 2 resp failure can lead to worsening hypercapnia.
Explain the two mechanisms that lead to severe hypercapnia due to uncontrolled O2 therapy of chronic type 2 respiratory failure.
- 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.
