PULMONARY CAUSES
Type 1 (hypoxaemic)
Recap that type 1 is the failure to oxygenate arterial blood due to V/Q
mismatches or shunts and hence any disease that damages the lung tissues
can be a cause. Causes include:
o Asthma
o Emphysema
o Interstitial lung diseases
o Pneumonia
o Pulmonary embolism
o Pulmonary oedema
Asthma
Characterised by:
o Increased responsiveness of the tracheobronchial tree to a range of
stimuli
o Bronchi inflammation with eosinophil recruitment and resultant mucus
gland hypertrophy
o Limited airflow which is usually reversible with or without medication
Emphysema
Emphysema itself is the enlarged distension of the air sacs distal to the
terminal bronchiole and accompanied with alveolar wall damage. Also, alveoli
elastic recoil is absent and this collapses the airways in expiration. V/Q
defects and hyperinflated lungs filled with trapped air are therefore seen.
Symptoms include progressive dyspnoea, cough with sputum and wheeze
Interstitial lung diseases
This covers a range of restrictive lung diseases (e.g. extrinsic allergic
alveolitis, cryptogenic fibrosing alveolitis, sarcoidosis, pneumoconiosis), which
are caused by inflammatory insults that lead to cell recruitment and
consequent scarring. Overall, lung function is decreased.
Symptoms vary but usually include a dry cough and progressive dyspnoea
Pneumonia
Infection of the pulmonary parenchyma by a variety of micro-organisms (e.g.
streptococcus pneumoniae, staphylococcus aureus)
Symptoms include sudden onset fever, tachypnoea, cough with purulent
sputum and dyspnoea
Pulmonary embolism
The obstruction of the pulmonary arteries from a thrombus in the venous
circulation (e.g. from DVT)
Symptoms include sudden onset dyspnoea, pleuritic chest pain, haemoptysis,
and syncope
Pulmonary oedema
The accumulation of excessive fluid in the air spaces of the lungs.
Generalised pulmonary oedema only occurs in ARDS (adult respiratory
distress syndrome) and factors that disturb the Starling equilibrium such as
left ventricular failure, renal failure (volume overload) and liver failure
(hypoalbuminaemia).
Type 2 (hypercapnic)
Recap type 2 is due to alveolar hypoventilation and the consequent build up
of CO2. Causes include:
o Chest wall defects
o Respiratory muscle weakness
o Reduced respiratory centre drive
o Severe pulmonary disease
Chest wall defects
These include flail chest and kyphoscoliosis
Flail chest is due to trauma causing fracture of three or more ribs in at least
two areas. The flail piece moves paradoxically during inspiration and
expiration and therefore alters the normal movement of the ventilation
apparatus to induce RF.
Kyphoscoliosis is the posterolateral curvature of the spine that can be
congenital or affected by diseases of the vertebrae and surrounding muscles.
This curvature of the spine may eventually cause restrictive ventilatory failure
because total lung volumes, FEV1 and FVC are all reduced, and the work of
breathing is increased to try to ventilate the lungs.
Respiratory muscle weakness
These can affect the muscles of inspiration and active expiration.
Can occur with:
o Myasthenia gravis
o Muscular dystrophy
or
May be a result of neurological diseases:
o Phrenic nerve paralysis
o Lesions in the cervical spine
o Guillain-Barré syndrome
Reduced respiratory centre drive
Causes include:
o Drugs that act as a sedative such as opiates
o Trauma to the brainstem
Severe pulmonary disease
These include COPD, asthma, pulmonary fibrosis, and pneumonia, which can
induce either type 1 or type 2 patterns of RF, and not affect the ventilatory
apparatus. If these induce type 2 then it suggests ventilation is completely
inadequate to compensate for the hypoxaemia and implicates most, if not all,
the lung is damaged.
Severe chronic obstructive pulmonary disease (COPD) is the most common
cause of type 2 RF.
COPD
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A progressive disorder where there is an increased resistance to
airflow with limited reversibility
FEV1 <80% and FEV1:FVC ratio <70%
Cigarette smoking is the main aetiological factor
Two diseases comprise COPD: emphysema (previously mentioned)
and chronic bronchitis
Chronic bronchitis is defined clinically as cough with sputum for at least 3
months in 2 successive years. Pathologically, it consists of hypertrophic
mucus secreting glands in cartilaginous airways, and inflammatory cells and
intraluminal mucus plugs in smaller airways. All these contribute to a
significant obstruction to the airflow.
There are two groups of patients that present with COPD but these are NOT
strictly distinct from each other - it just makes understanding easier:
Pink puffers
Blue bloaters
Typical
Thin and not cyanosed
Overweight and cyanosed
Appearance
(central and peripheral)
Clinical
Dyspnoea +/- cough
Cough with sputum,
symptoms
exacerbated by infections
Blood gases
PaO2 : low
PaO2 : low
(ABGs)
PaCO2 : low or normal
PaCO2 : high
Physiology
Attempts to maintain normal
Fails to increase respiratory
ABGs by increasing the effort effort thus CO2 levels rise to
for respiration
drive respiration
Predominate Emphysema
Chronic bronchitis
disease
Respiratory
Failure
Typically type 1
Typically type 2
In the long-term, the COPD of ‘blue bloaters’ become severe in that they
depend upon hypoxaemic levels of oxygen to stimulate ventilation, and the
normal CO2 drive is loss. This makes oxygen therapy for their type 2 RF
limited, as too much O2 would cause their respiratory drive to shut down.
Be aware that although the paragraph above is usually taught in clinical medicine, there is
actually little experimental evidence to support the dependency on hypoxic drive and there
are alternative factors that may contribute, e.g. administration of oxygen may result in hypoxic
vasoconstriction such that the V/Q mismatch worsens and results in hypercapnia.