Chronic Obstructive Pulmonary Disease
Chronic obstructive pulmonary disease (COPD) is characterized by irreversible expiratory airfl w obstruction, hyperinflation mucus hypersecretion and increased work of breathing. COPD encompasses chronic bronchitis and emphysema, which often present together but reflec different underlying processes. Typically, smoking and other risk factors (Fig. 26a) accelerate the normal age-related decline in lung function (Chapter 22), and cause chronic respiratory symptoms interposed with intermittent acute exacerbations, eventually leading to disability and respiratory failure (Chapter 23). Chronic hypoxaemia in COPD can lead to pulmonary hypertension (Chapter 27). Asthma is not classifie as COPD as it is reversible (Chapters 24 and 25).
Diagnosis and pathophysiology
COPD is diagnosed by airfl w obstruction indicated by a reduced FEVl/FVC ratio of less than 0.7, which is irreversible (<l5% increase in FEVl) with bronchodilator or steroid therapy (Fig. 26c; Chapter 20). Restrictive lung disease (e.g. fibrosis should be excluded. Patients with COPD have symptoms of dyspnoea (breathlessness) at rest or on exertion. Many asymptomatic smokers have lung function abnormalities that predate symptoms, which may be prevented by early smoking cessation. Although chronic bronchitis and emphysema most often coexist, they reflec different underlying processes (Fig. 26b) with differing signs and symptoms (Fig. 26d).
Chronic bronchitis is associated with airways obstruction caused by chronic mucosal inﬂammation, mucous gland hypertrophy and mucus hypersecretion, coupled with bronchospasm (Fig. 26b). It is define by daily morning of cough and excessive mucus production for 3 months in 2 successive years, in the absence of airway tumour, acute/chronic infection or uncontrolled cardiac disease. Most patients have normal total lung capacity (TLC), functional residual capacity (FRC), residual volume (RV), DLco (diffusing capacity) and static lung compliance (Chapter 20). Patients with advanced chronic bron- chitis have reduced respiratory drive and CO2 retention, which is associated with bounding pulse, vasodilatation, confusion, headache, flappin tremor and papilloedema. Hypoxaemia is mostly due to VA/Q mismatch (Fig. 26b; Chapter l4), and leads to polycythaemia (increased red cells) and increased pulmonary artery pressure (pulmonary hypertension) due to hypoxic pulmonary vasoconstriction. The resulting impairment of the right side of the heart function leads to renal f uid retention, raised central venous pressure and peripheral oedema, subsequently leading to cor pulmonale (flui retention/heart failure secondary to lung disease). Pulmonary hypertension is potentiated by extensive capillary loss in late disease. There are no radiographical signs, diagnostic of chronic bronchitis.
Emphysema is caused by progressive destruction of alveolar septa and capillaries, leading to development of enlarged airways and airspaces (bullae), decreased lung elastic recoil and increased air- way collapsibility. Airway obstruction is caused by collapse of distal airways during expiration due to loss of elastic radial traction present in the normal lung (Fig. 26b). The resulting hyperinﬂation enhances expiratory airflow, but inspiratory muscles work at a mechanical disadvantage. The pathophysiology of emphysema may involve an imbalance between inflammator cell proteases and antiprotease defences ntrilobular emphysema is associated with cigarette smoking and predominantly involves the upper lung zones. Panacinar emphysema is associated with α1-antitrypsin deﬁciency (Chapter l8) and predominantly involves the lower lung zones. Patients with emphysema typically have airfl w obstruction with elevated TLC, FRC and RV, reduced DLco and increased static lung compliance. Such patients tend to be breathless and tachypnoeic (fast respiratory rate) at rest, with signs of hyperinflatio and malnutrition including barrel chest and thin body, use of accessory respiratory muscles and purse-lipped breath- ing. The latter increases pressure in the upper airways and thus limits distal airway collapse. Auscultation reveals distant breath sounds with a prolonged expiratory wheeze. Blood gases are normal at rest, with marked O2 desaturation during exertion. Radiographically, emphysema may appear as hyperinflate lungs with a large retrosternal airspace and fla diaphragms. When the condition is advanced, there may be areas with a lack of vascularity or visualization of bullae. High-resolution computed tomography (CT) is useful to demonstrate enlarged airspaces and air trapping.
No specifi therapy reverses COPD, but treatment can slow disease progression, ease chronic symptoms and prevent acute exacerbations. Smoking cessation is critical. Pharmacological therapy has similarities to that of asthma (Chapter 25).
Inhaled β2-agonists (e.g. salbutamol) and anticholinergics may improve symptoms and lung function, and have additive effects when combined. Xanthines have negligible effects on spirometry, yet may improve exercise performance and blood gases. Patients producing large amounts of sputum may benefi from mucolytics. Inhaled cor- ticosteroids are recommended in severe disease (FEVl < 50% predicted). Long-term oral corticosteroids (to reduce inflammation are best avoided as they improve function in less than 25% of COPD patients but cause significan side effects. Pulmonary rehabilitation strengthens respiratory muscles and improves quality of life and ex- ercise tolerance while reducing hospitalizations but has no effect on lung function. O2 therapy prolongs life in patients with resting day-time hypoxaemia by slowing progression of cor pulmonale. O2 should be utilized as much as possible, as benefi increases with use. Patients with nocturnal or exercise desaturation benefi from supplemental O2 at night or during exercise. In αl-antitrypsin deﬁciency, replacement therapy can increase plasma and lung antiprotease levels; however, the benefit on lung function and survival are controversial. Surgical lung volume reduction or transplantation may be indicated in advanced COPD for carefully selected patients.
Prevention of acute COPD exacerbations includes pneumococcal and influenz vaccination. Patients with any combination of increased dyspnoea, increased sputum or purulent sputum benefi from antibiotics targeted against common respiratory pathogens (e.g. Haemophilus in- ﬂuenzae). Short courses of oral corticosteroids improve lung function and hasten recovery in patients with acute exacerbations.
Overall prognosis for COPD patients is dependent on the severity of airfl w obstruction. Patients with a FEVl less than 0.8 L have a yearly mortality of approximately 25%. Patients with cor pulmonale, hypercapnia, ongoing cigarette smoking and weight loss have a worse prognosis. Death usually occurs from infection, acute respiratory failary embolus or cardiac arrhythmia.
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