Chapter 26 Acute respiratory failure in chronic obstructive pulmonary disease

The terms ‘chronic obstructive pulmonary or airways disease’ (COPD or COAD) are applied to patients with chronic bronchitis and/or emphysema. COPD affects 5% of the adult population, is the fifth most common cause of death worldwide and is the only major cause of death that is increasing in prevalence.¹ Despite this, when an acute deterioration occurs, most precipitating factors are reversible and the outcome is usually good.² This justifies aggressive management in the majority of patients.

AETIOLOGY

The causes of COPD can be divided into environmental and host factors. Environmental factors include tobacco smoke, air pollution, indoor fumes (e.g. indoor cooking with solid biomass fuel) and poor socioeconomic status. The biggest single factor in over 95% of patients with COPD is tobacco smoking (Figure 26.1). However, only approximately 15% of smokers develop COPD. Marijuana smoking may cause premature and quite advanced bullous emphysema compared with tobacco smokers due to extremely hot and toxic inhaled smoke held at peak inspiration for prolonged periods of time.³ Host factors are the balance between circulating proteases and antiproteases (e.g. alpha-1 antitrypsin deficiency) and the intake of antioxidant vitamins (A, C, E).⁴

Figure 26.1 Decline in lung function with age in different smoking categories. FEV₁, forced expiratory volume in 1 second; COPD, chronic obstructive pulmonary disease.

PATHOPHYSIOLOGY

Reduced expiratory airflow in COPD is due to both increased airway resistance and reduced lung elastic recoil. Airway resistance is increased by mucosal oedema and hypertrophy, secretions, bronchospasm, airway tortuosity and airflow turbulence and loss of lung parenchymal elastic tissues that normally support the small airways. Loss of lung elastic recoil pressure is due both to loss of lung elastin and loss of alveolar surface tension from alveolar wall destruction.

Reduced lung elastic recoil decreases expiratory airflow by reducing the alveolar pressure driving expiratory airflow and by reducing the intraluminal airway pressure, which normally distends small airways during expiration. Forced expiration increases alveolar driving pressure but also causes dynamic airway compression resulting in no improvement or sometimes reduction in expiratory airflow. These factors are present in varying proportions, depending on the degree of chronic bronchitis and emphysema and the individual patient.

Airflow limitation results in prolonged expiration, pulmonary hyperinflation, inspiratory muscle disadvantage, increased work of breathing and the sensation of dyspnoea. All these factors are worsened during an exacerbation of COPD.

Pulmonary hyperinflation has both static and dynamic components. The static component remains at the end of an expiratory period long enough for all expiratory airflow to cease (30–120 s), enabling the lungs and chest wall to reach their static functional residual capacity (FRC). This component of hyperinflation is due to loss of parenchymal elastic recoil, chest wall adaptation ⁵ and airway closure that occurs throughout expiration. Dynamic pulmonary hyperinflation is the further increase in hyperinflation due to slow expiratory airflow not allowing completion of expiration before the arrival of the next breath. The extent of dynamic hyperinflation depends on the severity of airflow obstruction, the amount inspired (tidal volume) and the expiratory time.⁶ Thus, the degree of hyperinflation may vary in a patient with changes in minute ventilation due to changes in CO₂ production (depending on exercise, diet or the metabolic response to illness) or dead space, as well as with changes in airflow obstruction during an exacerbation.

Chest wall hyperinflation leads to suboptimal muscle length–tension relationships and mechanical disadvantage, thereby predisposing patients to respiratory muscle fatigue, as the work of breathing increases, particularly if associated with myopathic situations (steroids, electrolyte disturbances). Minor reductions in lung function due to infection, mild cardiac failure or atelectasis increase the work of breathing, due to both increases in respiratory impedance and increases in dead space. With acute changes in workload, rapid decompensation with ventilatory failure and acute hypercapnia may occur.

Central respiratory drive may also be impaired, or poorly responsive to physiological triggers – hypoxaemia or hypercapnia – and lead to chronic hypercapnia. This may occur in the setting of sleep (i.e. obstructive sleep apnoea), obesity or drugs (sedatives, antiepileptics, alcohol).

Hypoxia and vascular wall changes lead to pulmonary vasoconstriction, pulmonary hypertension, cor pulmonale, V/Q mismatching and the development of shunts.

CHRONIC BRONCHITIS OR EMPHYSEMA?

The value of labelling patients as chronic bronchitis or emphysema is uncertain as the two disease processes usually coexist and the principles of management are similar. Five pathophysiologic processes may be present to varying degrees in each patient with COPD: (1) inflammatory airway narrowing (bronchiolitis); (2) loss of connective tissues tethering airways; (3) loss of alveoli and capillaries; (4) hyperinflation; and (5) increased pulmonary vascular resistance. Early/mild COPD tends to be dominated by bronchiolitis with a minimal component of emphysema (Figure 26.2), whereas when COPD becomes severe, the reverse is true. However, recognition that COPD is dominated by one of these patterns is helpful with regard to clinical pattern and prognosis.

Figure 26.2 Proportional contributions of bronchiolitis and emphysema at different levels of severity of lung disease.

CLINICAL FEATURES OF ACUTE RESPIRATORY FAILURE IN COPD

Acute respiratory failure (ARF) in COPD can present with two distinct clinical patterns ⁷ (Table 26.1).

Table 26.1 Clinical differences between normocapnic and hypercapnic chronic obstructive pulmonary disease

Normocapnic (PaCO₂ 35–45 mmHg)	Hypercapnic (PaCO₂ > 45 mmHg)
Emphysema > chronic bronchitis	Chronic bronchitis > emphysema
Thin	Obese
Pursed-lip breathing	Central nervous system depression: consider the role of oxygen therapy
Accessory muscle use	Alcohol, sedatives, analgesics
Hyperinflated	Sleep-related hypoventilation
Right heart failure late	Right heart failure early

PRECIPITANTS OF ACUTE RESPIRATORY FAILURE

In approximately 50% of patients, there is an infective cause, in 25% heart failure and in the remaining 25% retained secretions, air pollution, coexistent medical problems (e.g. pulmonary embolus, medication compliance or side-effects) or no cause can be identified ⁸ (Table 26.2).

Table 26.2 Precipitants of acute respiratory failure in chronic obstructive pulmonary disease

Infective (including aspiration)

Left ventricular failure (systolic and diastolic failure)

Sputum retention (postoperative, traumatic)

Pulmonary embolism

Pneumothoraces and bullae

Uncontrolled oxygen

Sedation

Medication – non-compliance or side-effects

Nutritional (K, PO₄, Mg deficiency, CHO excess)

Sleep apnoea

The most common bacterial isolates are Streptococcus pneumoniae and Haemophilus influenzae in 80% of exacerbations.⁹S. viridans,¹⁰Moraxella (previously Branhamella) catarrhalis,¹¹Mycoplasma pneumoniae¹² and Pseudomonas aeruginosa may also be found. Viruses can be isolated in 20–30% of exacerbations¹³ and include rhinovirus, influenza and parainfluenza viruses, coronaviruses and occasionally adenovirus, and respiratory syncytial virus. Whether these organisms are pathogens or colonisers is often unclear.

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 AND ASSESSMENT

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 failure ¹⁷ 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.

BLOOD GASES

Blood gases are mandatory to assess hypoxia, hypercapnia and acid–base status. Chronic hypercapnia may be recognised by a bicarbonate level > 30 mmol/l and a base excess > 4 mmol/l indicating renal compensation. However, other causes of a high serum bicarbonate need to be excluded (e.g. diuretic therapy, high-dose steroids or high-volume gastric fluid loss) or chronic hypercapnia may be incorrectly assumed and the severity of COPD overestimated. Renal compensation for chronic hypercapnia will increase the serum bicarbonate by approximately 4 mmol/l for each 10 mmHg (1.33 kPa) of chronic PaCO₂ rise above 40 mmHg (5.3 kPa), in order to return pH to the low-normal range. Irrespective of the COPD patient’s usual PaCO₂ level, an acute increase in PaCO₂ leads to a decreased arterial pH. This indicates that compensatory mechanisms are exhausted and there is an increased risk of respiratory collapse.

NON-VENTILATORY MANAGEMENT

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

ANTICHOLINERGIC AGENTS

Anticholinergic agents, such as ipratropium bromide, have been shown to have a similar or greater bronchodilator action than β-agonists in COPD,^1,^21,²² and also to have fewer side-effects and no tachyphylaxis. Anticholinergic agents should be used routinely in COPD with ARF and many now believe them to be the agent of first choice.¹ An ipratropium bromide nebule of 0.5 mg in 2 ml should be nebulised initially 2-hourly, then every 4–6 hours. Long-term use of ipratropium bromide has been shown to reduce the incidence of exacerbations²³ and is therefore recommended for chronic use in ambulatory COPD. Long-acting anticholinergics (e.g. tiotropium) offer potential of once-daily dosing.

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