[Physiopathology of chronic bronchitis].
The physiopathology of chronic bronchitis consists of sequential reactions which progressively result in respiratory failure, blood gas abnormalities and finally, post-hypoxia cor pulmonale. Airway obstruction produces maldistribution of inspired gas and starts off a series of compensatory mechanisms with increased resting lung volume and prolonged expiration time resulting in diminution of tidal volume. Abnormal ventilation/perfusion ratios result in shunt and dead space effects, determine blood gas disorders and hypoxia due to reflex vasoconstriction and ultimately lead to pulmonary arterial hypertension with elevated cardiac output and increased vascular resistances. These physiopathological chain-mechanisms account for the clinical symptoms observed, including dyspnoea, episodes of acute bronchitis and in the end, signs of chronic cor pulmonale. They also indicate that the primary objective of treatment is to correct hypoxaemia. This can be achieved by continuous low flow rate oxygen therapy, by drugs capable of redistributing more evenly the ventilation/perfusion ratios and, accessorily, by respiratory analeptic agents. As regards the treatment of pulmonary arterial hypertension, one must admit that many uncertainties are still surrounding the use of vasodilators.
D001991:Bronchitis / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D000697:Central Nervous System Stimulants / Q000627:therapeutic use; D002908:Chronic Disease; D006801:Humans; D006976:Hypertension, Pulmonary / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology / Q000628:therapy; D008168:Lung / Q000503:physiopathology; D008173:Lung Diseases, Obstructive / Q000503:physiopathology; D012119:Respiration; D014692:Ventilation-Perfusion Ratio
D000697:Central Nervous System Stimulants
Physiopathologie de la bronchite chronique.