PNEUMONIA

Pneumonia has been estimated to account for 20% of presentations requiring mechanical ventilation.¹³ It is most commonly caused by S. pneumoniae and H. influenzae but Mycoplasma, Legionella, enteric Gram-negatives and viruses are occasional causes.

LEFT VENTRICULAR FAILURE

Left ventricular (LV) systolic failure may result from coexisting ischaemic heart disease, fluid overload, tachyarrhythmias or biventricular failure secondary to cor pulmonale. LV diastolic failure occurs commonly and is precipitated by hypoxaemia, tachycardia,¹⁴ pericardial constraint due to intrinsic positive end-expiratory pressure (PEEP_i) or right ventricular (RV) dilation. Increased work of breathing related to COPD will also increase by up to 10-fold the amount of blood flow to the respiratory pump muscles,¹⁵ thereby causing an increased demand upon the overall cardiac output. In patients with borderline cardiac status, this may precipitate heart failure. The components of right and LV failure can be accurately distinguished by Doppler echocardiography. Pulmonary congestion can be difficult to diagnose because of the abnormal breath sounds and chest X-ray appearance which are commonly present in COPD. In a recent publication, 51% of patients with acute exacerbation of COPD had echocardiographic evidence of left heart failure (systolic 11%, diastolic 32%, systolic and diastolic 7%).¹⁶

UNCONTROLLED OXYGEN ADMINISTRATION

This may precipitate acute hypercapnia in patients with more severe COPD, due to: (1) shunting blood to low-V/Q lung units and increasing dead space; (2) loss of hypoxic drive; (3) dissociation of CO₂ from Hb molecule (Haldane effect); and (4) anxiolysis and reduction in tachypnoea.

DIAGNOSIS

The clinical examination findings of COPD depend upon severity.

In mild stable disease (e.g. forced expiratory volume in 1 second (FEV₁) 50–70% predicted normal), an expiratory wheeze on forced expiration and mild exertional dyspnoea may be the only symptoms.

In moderate-severity COPD (e.g. FEV₁ 30–50% predicted normal), modest to severe exertional dyspnoea is associated with clinical signs of hyperinflation (ptosed upper border of liver beyond the level of nipple and loss of cardiac percussion) and signs of increased work of breathing (use of accessory muscles and tracheal tug).

In severe stable COPD (e.g. FEV₁ < 30% predicted normal), marked accessory muscle use is associated with tachypnoea at rest, pursed-lip breathing, hypoxaemia and signs of pulmonary hypertension (RV heave, loud and palpable pulmonary second sound and elevated a-wave in jugular venous pressure (JVP)) and cor pulmonale (elevated JVP, hepatomegaly, ankle swelling).

In severe unstable COPD, there is marked tachypnoea at rest, hypoxaemia and tachycardia, and, in some, signs of hypercapnia (dilated cutaneous veins, blurred vision, headaches, obtunded mentation, confusion).

Clinical examination may also identify associated medical conditions that might have precipitated the exacerbation such as crackles and bronchial breathing due to infection, crackles and cardiomegaly related to heart failure or mediastinal shift related to a pneumothorax.

Basic investigations such as spirometry are very useful in confirming a clinical diagnosis and determining severity of disease. The severity of COPD may be best judged by the reduction in FEV₁ compared with predicted values. Vital capacity (VC) is initially normal and decreases later in the course of the disease, but to a lesser degree than the FEV₁.

An FEV₁/VC ratio < 70% with an FEV₁ of 50–80% predicted normal without a bronchodilator response usually indicates mild COPD. A significant bronchodilator response, which implies asthma, is regarded as a 12% or greater increase and 200 ml increase in either FEV₁ or VC. An FEV₁ 30–50% predicted normal indicates moderately severe COPD and FEV₁ < 30% predicted normal indicates severe COPD.

Although the diagnosis may be based on spirometry alone, further lung function testing may be useful to characterise the disease. Flow–volume curves demonstrate reduced expiratory flow rates at various lung volumes and show the characteristic concave expiratory flow pattern. Lung volumes measured by either helium dilution or plethysmography show elevated total lung capacity, FRC and residual volume. Characteristically, the residual volume/total lung capacity ratio is > 40% in COPD and represents intrathoracic gas trapping. The total lung carbon monoxide (TLCO) uptake is a measurement of alveolar surface area and its reduction approximates the amount of emphysema present (usually < 80% predicted normal).

A chest X-ray will commonly show hyperinflated lung fields, as suggested by 10 ribs visible posteriorly, six ribs visible anteriorly or large airspace anterior to heart (> 1/3 of the length of the sternum), flattened diaphragms (best seen on lateral chest X-ray) and a paucity of lung markings. Pulmonary hypertension is manifest by enlarged proximal and attenuated distal vascular markings and by RV and atrial enlargement. Lung bullae may be evident.

A high-resolution computed tomographic (CT) scan of the chest (1–2-mm slices) can demonstrate characteristic appearance and regional distribution of emphysema. It can also assess for coexistent bronchiectasis, LV failure¹⁷ and pulmonary fibrosis. Such scans are less sensitive than standard chest CT scans (1-cm slice) for detecting pulmonary lesions (e.g. neoplasms). Nuclear ventilation perfusion scans can also provide a characteristic appearance of COPD.

An electrocardiogram (ECG) is commonly normal but may show features of right atrial or RV hypertrophy and RV strain, including P pulmonale, right-axis deviation, dominant R-waves in V1–2, right bundle-branch block, ST depression and T-wave flattening or inversion in V1–3. These changes may be chronic or may develop acutely if there is significant increase in pulmonary vascular resistance during the illness. The ECG may also show coexistent ischaemic heart disease, tachycardia and atrial fibrillation. Occasionally, continuous ECG monitoring is required to identify transient arrhythmias, which may also precipitate acute deterioration. Plasma brain natriuretic peptide (BNP) levels may also assist in the diagnosis of heart failure (elevated BNP) from pulmonary causes (low BNP) in patients under 70 years free of renal impairment.

DIFFERENTIAL DIAGNOSIS

The history of chronic asthma is one of long-term dyspnoea, wheeze and cough, usually at night or upon exercise, beginning in childhood with clear-cut precipitating agents (e.g. weather, dust, pets, drugs) and a favourable response to either steroids or inhaled β₂-agonists. Late-onset asthma (> 40 years of age) is not uncommon and is often associated with recurrent gastro-oesophageal reflux. In both forms of asthma, TLCO is normal. There is usually a bronchodilator response in the FEV₁ if the patient has unstable asthma. In patients in whom asthma is considered but lung function tests are normal, the FEV₁ response to an inhalational challenge (e.g. methacholine or hypertonic saline) may assist in discriminating asthma from other causes of dyspnoea.

Bronchiolitis obliterans is a condition which presents as a fixed airflow obstruction following a viral illness, inhalation of toxic fumes, following bone marrow or heart/lung transplantation, or related to drugs (e.g. penicillamine). It generally begins as a cough some weeks after insult and insidious onset of dyspnoea. There is a broad spectrum of radiological appearances from normal to reticulonodular to diffuse nodular. Lung tissue via bronchoscopy or by thoracoscopy is required for diagnosis. Histologically, there is a characteristic chronic bronchiolar inflammation appearance, and if granulation tissue extends into the alveoli, it is referred to as bronchiolitis obliterans or organising pneumonia. Removal of the offending agent and instigation of steroids are generally associated with a favourable prognosis.

Bronchiectasis is often associated with fixed mild to moderate airflow obstruction. A chronic productive cough (daily for 2 consecutive years) is characteristic. Clinical features such as clubbing, localised pulmonary crackles and a characteristic appearance on high-resolution CT, with dilated or plugged small airways at least twice the size of accompanying blood vessel, assist in the diagnosis.

Chronic heart failure (CHF) may be a differential diagnosis of COPD, or simply coexist, as both disorders are common in smokers.^14,16 Orthopnoea and paroxysmal nocturnal dyspnoea are features which correlate with heart failure severity. A past history of myocardial ischaemia or atrial fibrillation should alert one to the possibility of heart failure. An echocardiogram and high-resolution CT (looking for shift in interstitial oedema with changes in posture from supine to prone)¹⁷ are sensitive markers of CHF.

DIAGNOSIS OF RESPIRATORY FAILURE

An exacerbation of COPD is usually clinically obvious. However, it is important to diagnose the extent of deterioration. The following may be useful.

OXYGEN THERAPY

Oxygen given by low-flow intranasal cannulae or 24–35% Venturi mask should be titrated to achieve a saturation (SpO₂) of 90 ± 2% as these levels will avoid significant increases in PaCO₂ in the majority of COPD patients with ARF. Increases in PaCO₂ are most common in patients with initial PaCO₂ > 50 mmHg and pH < 7.35.¹⁸ If the rise in PaCO₂ is excessive (> 10 mmHg or 1.33 kPa), then FiO₂ should be reduced, titrating SpO₂ to 2–3% below the previous value, and arterial blood gases should be repeated. If no PaCO₂ rise occurs with oxygen therapy, then a higher SpO₂ may be targeted with repeat blood gases.

Inadequate reversal of hypoxia (e.g. SpO₂ < 85%) is suggestive of an additional problem such as pneumonia, pulmonary oedema or embolus, or a pneumothorax. Investigation of this should commence and a higher O₂ delivery system should be used (see Chapter 24). Although high levels of O₂ should be avoided, reversal of hypoxia is important and O₂ should not be withheld in the presence of hypercapnia, or withdrawn if it worsens.

BRONCHODILATORS

Bronchodilators are routinely given in all acute exacerbations of COPD because a small reversible component of airflow obstruction is common, and bronchodilators improve mucociliary clearance of secretions.¹⁹ However, a large meta-analysis of 22 large randomised controlled long-term trials of ambulatory COPD patients involving either anticholinergics and/or β₂ agonists (short- and long-acting) over 3–60 months indicates that anticholinergics are more favourable than placebo in terms of acute exacerbations, hospitalisations and respiratory deaths.²⁰ There were no favourable advantages with β₂-agonists compared with placebo for acute exacerbations or hospitalisations, and placebo was better than β₂-agonists in terms of respiratory death.²⁰