Systmes Pathology: Respiratory Failure Flashcards
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
Tachyopnea
Use of accessory muscles
Nasal flaring
Intercostal, suprasternal or supraclavicular recession
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
Chronic
-type 1-> increased Hb and pulmonary hypertension due to vasoconstriction
-type 2-> metabolic compensation
Resp failure investigations
Physical examination Chest imagine Atrial blood gas analysis Urea and electrolytes FBC
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
Shunting
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
Emphysema
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
Hypoxia
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
Pneumoconiosis
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