COPD is characterized by reduced maximum expiratory flow and slow forced emptying of the lungs, not reversible by bronchodilators. Most patients with COPD have features of both emphysema and chronic bronchitis.
Emphysema is a pathologic definition - permanent destructive enlargement of the airspaces distal to the terminal bronchioles, without fibrosis.
Inflammatory cells in the lung release elastase, a proteolytic enzyme. Elastase digests the elastin of the lung. Normally there is a protection of the lung by the elastase inhibitor alpha-1 antitrypsin (AAT). Expansion of the alveolar air spaced (the work of breathing) occurs by creating negative pressure in the chest. Normal elastin in the lung causes the alveoli to contract.Approximately 50-100K Americans have an inherited deficiency in AAT - causing a congenital form of emphysema.
Chronic bronchitis is a clinical definition - productive cough (from bronchial secretions) on most days for 3 months/year for 2 consecutive years. The mucus hypersecretion is from hypertrophy of the bronchial glands.
FVC - Forced Vital CapacityFEV1 - Forced Expiratory Volume, .percentage of total volume exhaled in the first second of a forced expiration..Normal FEV1 to FVC ratio is > 75%
Restrictive Disease represents failure of lung expansion, causing a drop in Vital Capacity, without changing the FEV1 : FVC.
Obstructive disease, from airway obstruction, reduces the FEV1 and the FEV1 : FVC ration. Vital capacity may/may not be decreased.
The clinical picture of COPD include signs of hyperinflation:barrel chest ( large sagittal diameter)accessory muscles of respirationreduced cricosternal distancetracheal tugparadoxical retraction of lower ribs (Hoover’s sign)pursed lip breathing
Right ventricular decompensation from chronic hypoxemia and hypercapnea. Peripheral edema, increased jugular venous pressure (distention), liver congestion, flapping tremor.These may be due to renal dysfunction, and not direct cardiac dysfunction. Renal dysfunction causing salt and water retention.