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Flashcards in Systmes Pathology: Respiratory Failure Deck (15)

Respiratory failure definition

Sydrome where one or both gases exchange functions fail
PaO2 < 8kpa type 1
PaCO2 > 6.7kpa type 2
Acute-> happens fast no compensation
-type 1-> increased Hb and pulmonary hypertension due to vasoconstriction
-type 2-> metabolic compensation


Clinical features of resp failure

Signs of resp compensation
Increase sympathetic tone-> tachycardia, hypertension, sweating
End organ hypoxia-> altered mental state, bradycardia, hypertension
Haemoglobin desaturation-> cyanosis
Use of accessory muscles
Nasal flaring
Intercostal, suprasternal or supraclavicular recession


Resp failure investigations

Physical examination
Chest imagine
Atrial blood gas analysis
Urea and electrolytes


Resp failure may occur in 3 places

1) transfer of O2 across alveolus
2) transport of O2 to tissue
3) removal of CO2 from blood into the alveolus and then into the exhaled breath


Resp failure classification

Resp pump failure-> ventilation failure
Lung failure-> oxygenation failure
Hypoxaemic (type 1) hypercapnic (type 2)
Acute or chronic


V/Q mismatch

Even in normal lung there isn't perfect matching of ventilation and perfusion
-> ventilated alveoli not perfused
-> perfused alveoli not ventilated
Low V/Q most common cause of hypoxaemia and hypercapnia -> corrected by 100% O2
As hypoxaemia increases resp rate via resp stimulation-> CO2 not related
High V/Q don't effect gaseous exchange unless severe


Diffusion problems

Physical separation of gas and blood-> scarring in disease
Shortened time of RBCs through capillaries-> emphysema with capillary bed loss



Persistence of hypoxaemia despite 100% O2
Deoxygenated blood bypasses the ventilated alveoli and mixes with oxygenated blood-> reduce O2
-> pneumonia
-> lung collapse
-> severe pulmonary oedema
Large shunt produces hypercapnia


Type 1 respiratory failure

PaO2 < 8 and normal paCO2
Most common
Virtually all acute lung diseases which involve fluid filling or alveolar collapse-> chronic bronchitis, emphysema, pneumonia, pulmonary oedema, pulmonary fibrosis, asthma, pneumothorax, embolism, pneumoconiosis, bronchiastasis, ARDS



Permanent dilation of air spaces distal to terminal bronchiole with destruction of their walls in the absence of scarring via protease destruction-> smoking causes elastase release
-> decreased area for gaseous exchange
Breathlessness on slight exertion
Cyanosis, hypercapnia and cor pulmonale develop late in disease


Chronic bronchitis

Hyperplasia of mucous glands in bronchial wall
Smooth muscle hyperplasia
Predispose to secondary bacterial infections-> acute bronchitis and pneumonia



Disease caused by inhalation of non organic mineral dust
-> coal, asbestos, silicosis
Inflammatory reaction and scarring


Extrinsic allergic alveolitis

Inhalation of organic ducts with local allergic reaction in lungs
Inflammation leads to fibrosis


Type 2 failure

Hypercapnia resp failure
PaCO2 > 6.7
Hypoxaemia common if breathing normal air
Blood pH depends on bicarbonate, which is dependent on duration of hypercapnia
-> chronic bronchitis, emphysema, severe asthma, poisoning, neuropathies, primary muscle disorder, head and spinal chord damage, primary alveolar hypoventilation, obesity hypo ventilation syndrome, pulmonary oedema


Pulmonary hypertension

Often present in resp failure
Alveolar hypoxaemia potentiated by hypercapnia-> pulmonary arteriolar constriction
-> chronic also-> Hypertrophy and hyperplasia of pulmonary arterial smooth muscle
-> increased vascular resistance-> increase RV pressure-> RV failure-> enlargement of liver and peripheral oedema -> cor pulmonale

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