– Clinical Definition: hypersecretion of mucus sufficient to cause cough and mucous expectoration and / or daily Mucopurulent at least 3 consecutive months a year, and that for at least two years following.
– There are 2 groups of chronic bronchitis:
* Simple chronic bronchitis marked by a expecto
ration -> no obstructive spirometry syndrome; histologically was hyperplasia of the bronchial glands in the large and medium bronchi.
* Chronic obstructive bronchitis: obstructive lung disease detected by the decrease in FEV. Histologically, there is a goblet cell hyperplasia, inflammation and sclerosis of the small airways with a caliber <2 mm.
– The airway obstruction is due 6 mechanisms:
* Luminal obliteration by a build up of mucus and pus
* Change parietal: increased height of the epithelium, mucosal edema, inflammatory cell infiltration; muscle hypertrophy.
* Loss intrinsic stiffness of the airway, which tend to be collapsed at the end
* Decreased lung elastic recoil forces associated emphysema
* Fibrosis scarring as a result of inflammatory destruction, infectious and degenerative
* Bronchiolar obliteration and destruction of the center of the acinus (centrilobular emphysema) => shunt effect (areas still perfused but poorly ventilated).
– The obstructive ventilatory disorders (TVO) is defined by increased resistance to gas flow expiratory airway. Decreased FEV, FEV / CV (report Tiffeneau) and FVC. It appears when there is at least 75% obstruction of small airways. Typically no reversibility in beta-2-agonists.
– TVO with thoracic distension: increased lung compliance with elevated non-marketable volumes (CPT, RV, FRC). Flattening of the diaphragm (potential fatigue); inspiratory time and decrease time expiratory increase. The result is fatigue of the respiratory muscles.
– Disruption haematosis: report ventilation / perfusion (Va / Q) decreased => shunt effect.
– Consequence of the shunt effect => hypoxia -> hyperventilation (hypocapnia initially); polycythemia; reflex vasoconstriction => PAH. Hypercapnia is late => offset acidosis.
– Hemodynamic Effects: PAH precapillary vasoconstriction by constrictive. => IVD => diastolic LV dysfunction.
– Sleep apnea syndrome (nocturnal oxygen desaturation) in stage IV COPD (resting hypoxemia)
– Clinical signs (BCO): exertional dyspnea and rest; thoracic distension; Hoover sign (paradoxical inspiratory decrease in the base of the thorax diameter => flattening of the diaphragm). Sign Campbell (decrease the distance between thyroid cartilage and the manubrium). Expiration of pursed lips. Rating Decrease inspiratory time and increasing expiratory time; thoracoabdominal asynchrony.
– Radiological signs: diaphragmatic flattening, widening of the intercostal spaces; horizontalisation coast: scalloped cupolas (insertion sites visible). Opening the sternodiaphragmatique angle; increase in the retrosternal clear space and retrocardiac. Opacities rails. At the advanced stage -> lesions of centrilobular emphysema.
– NB: RV (residual volume) is measured by dilution with helium or better plethysmography (also CPT and CRF).
– EFR: FEV <80%; FEV / CV <70%; increase in RV and FRC; crushing of the flow-volume curve. CPT> 120% => stage emphysema (distention is increased). ; static compliance and increased dynamics.
– Fiberoptic bronchoscopy is not systematic
– The factors triggering the IRA:
* Bronchial Superinfection (pneumococcus, Haemophilus influenzae, Moraxella)
* Sedatives; taking beta blocker
* Taking diuretics of Henle (inhibition of breathing reflex by central metabolic alkalosis).
* Pulmonary embolism
* Chest trauma
* Oxygen therapy (either decrease or increase in flow)
* Atelectasis by obstruction by a mucus plug favored by intracellular dehydration
* Left ventricular failure
– Almitrine (Vectarion) -> improvement in the ratio Va / Q by increasing the hypoxic pulmonary vasoconstriction (risk increase PAH). It is not used in case of basic PAH.
– Are cons-indicated: sedatives, sleeping pills, cough and thinners.