Respiratory and abdominal system

• Introduce yourself, ensure that the patient is sitting comfortably at 45° and then stand back. Placing your hands behind your back is a good way to show you remember the importance of inspection.

• Look around the bedside for metered dose inhalers, nebulisers or sputum pots.

• Note any cachexia.

• Count the respiratory rate (tachypnoea, defined as a respiratory rate > 20 breaths / minute (normal is 12–20 breaths / minute, albeit arbitrary), is often the first sign of respiratory or haemodynamic compromise) and note if the patient is breathless at rest.

Listen

• Listen to the breathing with unaided ears, noting any of the sounds listed in Box 1.1.

Box 1.1 Sounds in respiratory disease you might hear before auscultation

• Expiration longer than inspiration (obstructive airways disease)

• Expiratory wheeze (obstructive airways disease)

• Inspiratory stridor (obstruction of upper airways, e.g. mediastinal mass, bronchial carcinoma)

• Clicks (bronchiectasis)

• Gurgling (airway secretions)

• Look at the size and shape (Box 1.2) of the chest, and note any deformities (e.g. kyphoscoliosis, pectus carinatum, pectus excavatum), thoracotomy scars, radiotherapy field markings, telangiectasia or muscle wasting.

Box 1.2 Big or small chest?

As a simple rule, a ‘big chest’ (with a large anteroposterior diameter, little lateral expansion, and lifting of the rib-cage on inspiration) alerts you to chronic obstructive pulmonary disease, whilst a ‘small chest’ alerts you to possible fibrotic lung disease.

• Look at chest wall movement (upwards in emphysema; asymmetrical in fibrosis, collapse, pleural effusion or pneumothorax).

• Note any use of accessory muscles, including abdominal or scalene muscles, or intercostal indrawing.

Palpation

Neck

• Feel the trachea to determine any mediastinal shift (using the middle finger as the exploring finger and the index and ring fingers resting on the manubriosternum either side; Fig. 1.1) and note the approximate cricoid–suprasternal notch distance, decreased in hyperinflation from the normal three finger-breadths.

Figure 1.1 Determining the position of the trachea.

• Feel for cervical, supraclavicular and axillary lymph nodes, always from behind using flat fingers and not poking with fingertips.

Chest

• Start at the front or back (you are more likely to find signs at the back) but complete all of front or back examination before moving to the other. Remember that the lower lobes occupy most of the posterior chest and the upper lobes the anterior chest (Fig. 1.2).

Figure 1.2 Surface markings of the lobes of the lungs: (A) anterior, (B) posterior, (C) lateral view. (From Douglas, G., Nicol, F., Robertson, C., 2009 Macleod’s Clinical Examination, Twelveth ed. with permission.)

• Examine chest expansion. For the inframammary area and for the back of the chest use a ‘bucket handle’ approach with your fingers in the intercostal spaces either side of the chest and your thumbs floating in the midline (Fig. 1.3). This allows the ribs to move outwards. For the supramammary area, where the ribs move predominantly upwards, place your hands on the chest wall with thumbs meeting.

Figure 1.3 Assessing chest expansion: (A) anterior, (B) posterior. (From Douglas G., Nicol F., Robertson C., 2009. Macleod’s Clinical Examination, Twelveth ed. with permission.)

• Tactile vocal fremitus gives the same information as vocal resonance and may be omitted.

Percussion

Percussion sites

• Percuss the supraclavicular areas, clavicles and chest on both sides (Fig. 1.4). More than four or five levels of percussion is time consuming as a screen but percuss further to delineate any abnormality you find.

Figure 1.4 Percussion sites and technique: (A) anterior, (B) posterior. (From Douglas, G., Nicol, F., Robertson, C., 2009 Macleod’s Clinical Examination, Twelveth ed. with permission.)

Percussion technique

• Compare right with left and superior with inferior (left → right at same level → right inferiorly → left at same level → left inferiorly → right at same level and so on).

• Ensure that the finger applied to the chest (left middle) is applied firmly, and aligning it with the ribs is preferable; the pad of the partly flexed percussing finger (right middle) should tap the middle phalanx of the chest finger lightly, springing away quickly after contact to avoid dampening of the note. This relaxed swinging motion should come from the wrist, not the forearm (Fig. 1.4 inset).

• Remember that the upper level of liver dullness is around the sixth rib in the right mid-clavicular line. Resonance below this level is a sign of hyperinflation. Cardiac dullness may also be elicited.

Auscultation

Auscultation is traditionally with the diaphragm, but the bell may not provoke as much extraneous sound from hairy chests and is able to get into the supraclavicular areas. The patient should breathe comfortably with the mouth open.

• Auscultate, as for percussion, the supraclavicular areas, axillae and upper, middle and lower chest for breath sounds, added sounds and vocal resonance.

Breath sounds and added sounds

These are described in Table 1.1.

Table 1.1

Breath sounds and added sounds

Vocal resonance

• Vocal resonance, like tactile vocal fremitus, represents transmission of sound from the central airways to the chest wall. Sound transmission is enhanced through solid tissue (consolidation) provided the airways are patent and attenuated through fluid (pleural effusion) compared with transmission through air (normal). The principles are as for bronchial breathing in consolidation and reduced breath sounds in a pleural effusion. Enhanced sound transmission in consolidation is analogous to the vibration of an earthquake that can be felt through the ground before it can be heard through the air. Attenuated sound in a pleural effusion is analogous to diving underwater, the sound of people on land suddenly muffled. ‘Ninety-nine’ is the conventional sound used to assess vocal resonance, but the intended nasal ‘oi’ is better demonstrated by ‘neun-und-neuzig’.

• Whispering pectoriloquy, when whispered sounds are heard clearly, confirms consolidation because a whispered voice is clearly audible through solid lung. Aegophony is an unusual sign in which compressed lung above a pleural effusion creates a high-pitched bleat from conducted voice.

Additional ward tests

• Mention that you would perform ward spirometry and pulse oximetry as part of your examination.

Integration

Some patterns of important focal abnormalities are shown in Figure 1.5.

Figure 1.5 Patterns of important focal abnormalities.

Summary

A summary of the respiratory system examination sequence is given in the Summary box.

Summary box – respiratory system examination sequence

From a distance look for bedside clues, look for cachexia and count the respiratory rate.

Look at the hands for clubbing, cyanosis or wasting.

Look at the face for pursed lip breathing or Horner’s syndrome.

Look at the JVP.

Look at the shape of the chest and chest wall movement and note any use of accessory muscles.

Feel for tracheal deviation and feel for any lymphadenopathy.

Assess chest expansion.

Percuss for areas of dullness (consolidation, collapse, pleural effusion) or hyper-resonance (hyperinflation, pneumothorax).

Listen to breath sound quality (normal or vesicular) and intensity (reduced in consolidation, collapse, pleural effusion, hyperinflation, pneumothorax).

Listen for added sounds (crackles, wheeze).

Listen to vocal resonance (increased in consolidation, decreased in pleural effusion).

Cases

Case 1.1 Chronic obstructive pulmonary disease

Instruction

This 67-year-old woman has been troubled with cough, wheeze and shortness of breath. Please examine her chest and discuss your findings.

Recognition

There may be tar-stained fingers (Fig. 1.6), central cyanosis (Box 1.3), pursed lip breathing and a generally plethoric appearance. A bounding pulse and flapping tremor suggest CO₂ retention.

Box 1.3 Cyanosis

Cyanosis refers to blue discoloration of skin and mucous membranes and requires a deoxygenated haemoglobin concentration of > 5 g/dl. Thus it does not occur in anaemia. Central cyanosis (blue and warm) is seen at the lips and tongue and occurs in hypoventilation (e.g. chronic obstructive pulmonary disease, neuromuscular disease), V / Q mismatch, impaired gas transfer (e.g. pulmonary oedema) and right-to-left cardiac shunts. Peripheral cyanosis (pink lips, cool peripheries) is the result of local vascular effects and occurs in shock and peripheral vascular disease.

Figure 1.6 Tar staining.

Chest

There are signs of hyperinflation (Box 1.4, Fig. 1.7), but many patients have a degree of cachexia from chronic disease (Fig. 1.8). There may be an expiratory wheeze. Inspiratory crackles suggest superimposed infection.

Box 1.4 Signs of hyperinflation

• Increased anteroposterior chest diameter (‘barrel chest’)

• Indrawing of the intercostal muscles and supraclavicular fossae

• Flattening of the subcostal angle

• A shortened cricoid–notch distance (normally greater than three finger-breadths)

• Decreased chest expansion

• Attenuation of heart and liver dullness (with diminished heart sounds)

• Hyperresonance

Figure 1.7 ‘Barrel chest’ and intercostal indrawing of chronic obstructive pulmonary disease.

Figure 1.8 Chronic obstructive pulmonary disease cachexia.

Interpretation

Confirm the diagnosis

Tell the examiners you would perform spirometry. National Institute for Health and Clinical Excellence (NICE) recommendations for diagnosing chronic obstructive pulmonary disease (COPD) are as follows:

• COPD should be considered in patients aged over 35 years with a risk factor (generally smoking) and exertional breathlessness, chronic cough, regular sputum production, frequent winter ‘bronchitis’ or wheeze (without features of asthma – unproductive cough, nocturnal / diurnal or variable symptoms).

• Post-bronchodilator spirometry should be measured to confirm the diagnosis of COPD.

• Alternative diagnoses or investigations should be considered in older people without typical symptoms of COPD where the ratio of forced expiratory volume in 1 second (FEV₁) to forced vital capacity (FVC) is < 0.7 or in younger people with symptoms of COPD where the FEV₁ / FVC ratio is ≥ 0.7.

What to do next – consider causes

Smoking is by far the commonest cause, confirmed by tar staining; α-antitrypsin deficiency causes lower zone emphysema.

Consider severity / decompensation / complications

Tell the examiners that you would be alert to cor pulmonale (right-sided heart failure due to pulmonary hypertension in chronic lung disease) and CO₂ retention (type 2 respiratory failure). Extrapulmonary complications of COPD are given in Box 1.5, and adversely affect health status, functional capacity and survival.

Box 1.5 Extrapulmonary complications of chronic obstructive pulmonary disease

• Skeletal muscle dysfunction due to reduced physical activity, hypoxia, inflammation and smoking (cachexia in advanced disease, but may also be due to malignancy)

• Osteoporosis due to reduced physical activity, inflammation, smoking and corticosteroids

• Cardiovascular disease due to smoking, vascular dysfunction, neurohumeral activation and hyperinflation

• Cognitive dysfunction due to hypoxia, systemic inflammation, smoking and depression

Consider function

Disability in COPD can be poorly reflected in the FEV₁. A more comprehensive assessment of severity includes the degree of air-flow obstruction and disability, the frequency of exacerbations, and the following known prognostic factors: breathlessness (Medical Research Council dyspnoea scale, Box 1.6), health status, body mass index, cor pulmonale, FEV₁, exercise capacity (for example, 6-minute walking test), transfer factor for carbon monoxide and partial pressure of oxygen in arterial blood.

Box 1.6 Functional scale for breathlessness

• I only get breathless with strenuous exercise

• I get short of breath when hurrying on the level or walking up a slight hill

• I walk slower than people of the same age on the level because of breathlessness or have to stop for breath when walking at my own pace on the level

• I stop for breath after walking about 100 yards or after a few minutes on the level

• I am too breathless to leave the house or breathless when dressing or undressing

Discussion

What do you understand by the term chronic obstructive pulmonary disease (COPD)?

COPD is a chronic, progressive disease characterised by signs of air-flow obstruction and obstructive lung disease on spirometry. There is minimal reversibility with bronchodilators. The terms chronic bronchitis and emphysema are sometimes used synonymously. Over 3 million people in the UK are estimated to have COPD, the majority still undiagnosed.

Chronic bronchitis

This is defined clinically (UK Medical Research Council) as chronic, productive cough for at least 3 months of two consecutive years in the absence of other diseases causing sputum production. Mucus hypersecretion results from gland hypertrophy and increased goblet cell numbers. Large airways (bronchitis) and small airways (bronchiolitis) are affected in continuum.

Emphysema

This is defined pathologically as permanent enlargement of airways distal to the terminal bronchiole. There is destruction of their walls without obvious fibrosis. It may be predominantly centriacinar (destruction of alveoli at the centre of the acini, especially associated with smoking and affecting upper lobes), panacinar, paraseptal or localised around scars. Bullae are large emphysematous spaces > 1 cm in diameter.

Development of pulmonary hypertension

Chronic bronchitis and emphysema overlap and pulmonary vasculature changes – intimal and medial thickening, smooth muscle proliferation and inflammatory cell infiltration – with hypoxaemia and vasoconstriction lead to pulmonary vascular remodelling and ultimately sustained pulmonary hypertension.

What is the pathogenesis of COPD?

What is one smoking pack year?

One pack year is equivalent to smoking 20 cigarettes a day for 1 year.

List some causes of COPD other than smoking

• α₁-antitrypsin deficiency

• Environmental (short-term exposure to high-level particulate air pollution correlates with exacerbations)

• Occupational, e.g. coal workers, cadmium workers

• Genetic polymorphisms (probably determine susceptibility to environmental causes)

What is α₁-antitrypsin deficiency?

α₁-antitrypsin is a protease inhibitor (Pi) enzyme, synthesised in the liver during the acute-phase response, which inhibits neutrophil elastase. Low levels of the enzyme, determined by various genotypes (PiZZ the most severe with enzyme levels < 10% of those with normal M alleles), fail to protect the lung from proteolytic attack, resulting in destruction of alveolar walls, particularly in times of infection when vigorous elasteolytic activity is unopposed. This ultimately results in basal, panlobular emphysema, accelerated in smokers, and cirrhosis. Patients typically present in the fourth or fifth decades.

How may the diagnosis of COPD be confirmed?

A post-bronchodilator FEV₁ < 80% of the predicted value with a ratio of FEV₁ : FVC < 70% that is not fully reversible is consistent with COPD.

List some other tests that you might consider in assessing a patient with COPD

• Full blood picture (polycythaemia)

• Arterial blood gases (ABGs)

• Chest X-ray (hyperinflation, bullae, prominent pulmonary vessels)

• Electrocardiogram (p pulmonale, right axis deviation, right bundle branch block)

How might you grade COPD severity?

The Global Initiative for Chronic Obstructive Lung Disease classification and NICE staging based on FEV₁ (Table 1.2) align with international guidelines and are prognostically informative.

Table 1.2

The Global Initiative for Chronic Obstructive Lung Disease and National Institute for Health and Clinical Excellence classification of chronic obstructive pulmonary disease (COPD) (when the post-bronchodilator ratio of forced expiratory volume in 1 second (FEV₁) to forced vital capacity (FVC) is < 0.7)

LTOT, long-term oxygen therapy. *Symptoms should be present to diagnose COPD in people with mild air-flow obstruction. **Or when FEV₁ < 50% is accompanied by respiratory failure.

What management options are there in stable COPD?

Specialist referral

This may be appropriate at all stages of the disease. Indications include diagnostic uncertainty, rapidly changing disease (both on spirometry and in symptoms) and onset of complications such as cor pulmonale.

Smoking cessation

All patients should be encouraged to stop smoking. Unless contraindicated, nicotine replacement therapy (varenicline or bupropion) should be offered, together with a support programme.

Inhaled therapy

A NICE clinical algorithm provides an evidence-based rationale for the sequencing of inhaled drugs used singly and in combination according to persistence of symptoms, exacerbations, and severity of air-flow obstruction (Fig. 1.9) and clarifies options for escalating inhaled treatment according to whether FEV₁ is above or below 50%.

Figure 1.9 Inhaled therapy in chronic obstructive pulmonary disease. Inhaled corticosteroid (ICS) is recommended only in a combination inhaler. The evidence for a long-acting beta agonist (LABA) plus ICS over LABA is strong in severe or very severe air-flow obstruction (forced expiratory volume in 1 second (FEV₁) < 50%) but weaker with mild or moderate air-flow obstruction (FEV₁ ≥ 50) with recommendation for LABA + ICS treatment only if symptoms persist with LABA alone. Limited evidence for adding LABA plus ICS in those still symptomatic despite LAMA led to a recommendation for triple therapy only in this situation. Adding LAMA to LABA plus ICS (triple therapy) to people who remain breathless or have exacerbations despite taking LABA plus ICS irrespective of FEV₁, is based on stronger evidence. LAMA, long-acting muscarinic antagonist; SABA, short-acting beta-agonist; SAMA; short-acting muscarinic antagonist. (From NICE 2010 Chronic Obstructive Pulmonary Disease (partial update), replacing NICE clinical guideline 12, with permission.)

Oral therapies

Maintenance oral corticosteroid therapy in COPD is not normally recommended. Theophylline may be offered only after trials of short- and long-acting bronchodilators or to people who cannot use inhaled therapy. It can be used in combination with β₂-agonists and muscarinic antagonists. Dose reduction is needed with macrolide or fluroquinolone antibiotics. Mucolytic therapy may be used for chronic productive cough if symptoms improve, but not routinely to prevent exacerbations.

Pulmonary rehabilitation

This should be offered to all patients who consider themselves functionally disabled by COPD, including following admission for an acute exacerbation, but is not suitable for patients who are unable to walk, have unstable angina, or had a recent myocardial infarction.

Vaccination

Annual influenza vaccination and 5- to 10-year pneumococcal vaccination are important.

How can treatment response be assessed in stable COPD?

There is often minimal improvement in spirometry. Short-term changes in FEV₁ in response to bronchodilators or steroids are poor predictors of symptomatic benefit in moderate to severe COPD. Symptomatic improvement is more useful, e.g. reduced breathlessness, increased exercise capacity and improved sleep.

Is there a role for surgery in COPD?

Lung volume reduction surgery may increase exercise capacity by reducing dynamic hyperinflation, improving diaphragmatic function and improving elastic recoil and may be useful for large bullae, especially upper lobe disease. Surgery is contraindicated with FEV₁ < 20% or if emphysema is homogeneous.

What are the indications for long-term oxygen therapy (LTOT), ambulatory oxygen therapy and short-burst oxygen therapy?

COPD

LTOT is indicated for managing respiratory failure in stable COPD and is one of few interventions shown to improve survival in COPD. Oxygen is administered via nasal cannulae at 2–4 l / min via a concentrator for at least 15 hours a day, aiming for paO₂ > 8 kPa. Patients must not smoke! Eligibility criteria are shown in Box 1.7.

Box 1.7 Indications for long-term oxygen therapy

• p_aO₂ < 7.3 kPa (55 mmHg) on air

• p_aO₂ 7.3–8.0 kPa (55–60 mmHg) if there is pulmonary hypertension or nocturnal hypoxaemia

• FEV₁ < 1.5 litres

Arterial blood gases should be measured when clinically stable and on two occasions at least 3 weeks apart (PO₂ should rise with treatment above 8 kPa without unacceptable hypercapnia).

Those on ambulatory oxygen may be classified into those with low activity who are usually immobile and require the same flow rate as their LTOT and those who are active who desaturate on exercise, some of whom are on LTOT. Short-burst oxygen therapy for breathless patients is not evidence based.

Other conditions

Conditions other than COPD considered suitable for LTOT and ambulatory oxygen therapy include severe chronic asthma, interstitial lung disease (ILD), cystic fibrosis (CF) and pulmonary vascular disease. Conditions suitable for LTOT but not ambulatory oxygen therapy include bronchiectasis, pulmonary malignancy and heart failure. Conditions of hypoventilation are better managed with non-invasive ventilation.

How do acute exacerbations of COPD arise?

Most exacerbations are triggered by tracheobronchial infection with viruses (rhinovirus, coronavirus, adenovirus, respiratory syncytial virus, influenza) or bacteria (Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, Pseudomonas aeruginosa, Chlamydia pneumoniae). Some pollutants are triggers. Triggers activate transcription factor NF-KB in airway epithelial cells and macrophages. These cells release inflammatory cytokines both within the airway and systemically including the neutrophil chemoattractant interleukin (IL)-8 (CXCL-8), and tumour necrosis factor-α and interleukin-6 (IL-6), which amplify inflammation. C-reactive protein (CRP) rises are often sensitive markers of COPD exacerbations.

How does an acute exacerbation of COPD (AECOPD) lead to type 2 respiratory failure?

Alveolar ventilation (i.e. the volume of useful air exchanged) refers to minute ventilation (the total volume of air moving in and out of the lungs per minute, given by tidal volume × respiratory rate) minus the dead space (the proportion of minute ventilation trapped in the lungs). Dead space is increased in COPD because of expiratory air-flow obstruction that is only partially compensated for by increased expiratory time, leading to hyperinflation. This ultimately leads to decreased muscle function, flattening of the diaphragm from its optimum dome shape and failure of the intercostal muscles to exert adequate upward pull. This leads to intrinsic positive end expiratory pressure (PEEP); normally, resting pressure is atmospheric but in COPD it is always greater, causing positive airway pressure, a situation demanding extra work to get air into the lungs. Tidal volume ultimately decreases and the respiratory rate must increase to compensate, creating a vicious cycle because an increased respiratory rate exacerbates gas trapping with worsening type 2 respiratory failure.

How would you manage acute respiratory failure in COPD?

Controlled oxygen therapy and supportive ventilation (non-invasive ventilation or invasive mechanical ventilation) aim to prevent tissue hypoxia and control acidosis and hypercapnia while medical therapy maximises lung function and reverses any precipitating cause. Antibiotics have a role in acute exacerbations of COPD but not stable COPD, as do nebulisers.

Intravenous aminophylline fell from favour following a Cochrane review demonstrating its failure to increase FEV₁ or shorten hospital admission, while at the same time increasing adverse effects. Oral prednisolone 30 mg is generally given for 7–14 days and then stopped. Assessment for LTOT should occur 6 weeks after an exacerbation.

The best marker of severity is pH; it reflects acute deterioration in alveolar hypoventilation (acute rise in p_aCO₂) compared with the chronic stable state. A pH of < 7.26 is associated with 30% mortality.

Increases in p_aCO₂ are associated with significant mortality but the absolute p_aCO₂ and p_aO₂ are less significant than pH; for example, a p_aCO₂ of 8.5 kPa associated with a bicarbonate of 35 mmol / l and a normal pH might merely reflect chronic respiratory acidosis with metabolic compensation whereas a p_aCO₂ of 9 kPa with a normal bicarbonate and low pH more likely reflects acute decompensation.

Some typical ABG results are shown in Table 1.3.

Table 1.3

Typical arterial blood gas (ABG) results and action needed

Oxygen therapy

Oxygen delivery vital for organ function relies upon adequate total blood oxygen content, adequate haemoglobin to carry it, and cardiac output. Because of the steep slope of the oxyhaemoglobin dissociation curve at tissues, falls in oxygen delivery are offset by increased oxygen extraction. Normal p_aO₂ is 10–13kPa and oxygen delivery cannot be significantly enhanced by increasing p_aO₂ above 16 kPa where haemoglobin is fully saturated. Maximising oxygen saturation not only fails to optimise tissue oxygenation but also may cause adverse physiological effects. The best example of this is in AECOPD in which p_aO₂ above 10 kPa is associated with respiratory acidosis and CO₂ narcosis and worse outcomes; the mechanisms are likely decreased hypoxic drive, absorption atelectasis, the Haldane effect (decreased CO₂ buffering by oxyhaemoglobin) and, probably the greatest contributor, release of hypoxic pulmonary vasoconstriction promoting worsening ventilation–perfusion mismatch – usually alveolar hypoxia due to poor ventilation causes vasoconstriction and so deoxygenated pulmonary artery blood is diverted from diseased lung but with hyperoxia these alveoli are re-oxygenated and re-perfused but remain poorly ventilated and cannot clear CO₂. In relatively healthy lungs, regional hypoventilation may be compensated for by overall increased ventilation, but this is not possible in COPD. Other adverse effects of hyperoxia include coronary vasoconstriction and neuronal injury (especially damaging in stroke).

Guidelines for oxygen therapy in acute situations recommend high-concentration oxygen when monitoring is unavailable (pre-hospital) and in critical illness, but oxygen only to maintain normal oxygen saturations in most monitored situations. This means:

• In those at risk of hypercapnic respiratory failure, starting with a 24% or 28% Venturi mask and aiming for oxygen saturation 88–92%

• In those not at risk of hypercapnic respiratory failure with saturations ≥ 85% starting with nasal cannulae (2–6 l / min) or face mask (5–10 l / min) and aiming for oxygen saturation 94–98%

• In those not at risk of hypercapnic respiratory failure with saturations < 85% using a reservoir or bag–valve mask.

Non-invasive positive pressure ventilation (NIV)

NIV in COPD is outlined in Box 1.8.

Box 1.8 Non-invasive ventilation (NIV) in chronic obstructive pulmonary disease (COPD)

NIV is indicated for acute exacerbations of COPD with respiratory failure, and also other conditions including chest wall disease and obesity hypoventilation syndrome.

Patient selection

NIV should be considered in an acute exacerbation of COPD where respiratory acidosis (pH < 7.35, pCO₂ > 6 kPa) persists despite immediate maximum standard medical treatment (nebulised salbutamol 2.5–5 mg and ipratropium 500 µg, prednisolone 30 mg, antibiotics if appropriate) on controlled oxygen for no more than 1 hour. Acidosis is the key determinant of NIV. Based on pre-morbid state, severity, reversibility, the presence of relative contra-indications and patient wishes where possible, patients should be stratified into:

1. Requiring immediate intubation and ventilation and intensive care

2. Suitable for NIV and for escalation to 1

3. Suitable for NIV but not suitable for 1

4. Not suitable for NIV but suitable for full active medical management

5. Palliative care agreed as most appropriate.

Absolute contraindications to NIV include fixed upper airway obstruction, facial trauma or burns, and vomiting. Most other contraindications such as secretions, impaired consciousness, pneumothorax and haemodynamic instability are relative.

Early studies demonstrated that in sicker patients with pH < 7.25 NIV was not a substitute for intubation, ventilation and intensive care because mortality was around 30%; however, the greater usage and experience with NIV has lowered this threshold to < 7.25 in the eyes of many experts. Of course, not all NIV environments, expertise, and equipment are the same.

How NIV works

NIV is delivered via a tightly fitting face-mask with humidifier and a bi-level positive airway pressure (BIPAP) box with or without oxygen. NIV overcomes auto-positive end-expiratory pressure (auto-PEEP) and reduces inspiratory effort. It is patient triggered. The patient initiates a breath and the box kicks in to raise inspiratory positive airway pressure (IPAP) to a set reading. The patient learns to ‘relax’ into what at first may be an uncomfortable apparatus. Expiratory positive airway pressure (EPAP) = PEEP and IPAP can be balanced with a small amount of PEEP. Oxygen can be entrained to maintain saturations between 85% and 92%. BIPAP is different to continuous positive airway pressure (CPAP), which delivers 5–10 cmH₂O throughout the breathing cycle. IPAP, by providing positive airway pressure, assists ventilation, while EPAP recruits underventilated lung and improves the ventilation–perfusion ratio as well as reducing rebreathed air by eliminating exhaled air via the expiratory port.

Set-up

Patients should be capable of protecting their airway and cooperative, sitting or semi-recumbent. The following are recommended:

• A full-face mask for the first 24 hours followed by a switch to a nasal mask if preferred by the patient

• Initial IPAP of 10 cmH₂O and EPAP of 4–5 cmH₂O, tolerated by most patients

• IPAP increased by 2–5 cm increments at a rate of 5 cmH₂O every 10 minutes with a target of 20 cmH₂O or until therapeutic response; EPAP generally unaltered as higher pressures are rarely tolerated

• Oxygen when needed entrained into the circuit and flow adjusted to achieve target saturation, usually 88–92%

• Bronchodilators preferably administered off NIV.

Monitoring and escalation

• Baseline arterial blood gas (ABG) analysis, respiratory rate and heart rate

• Continuous pulse oximetry

• Repeated ABGs at 1 hour and 1 hour after every subsequent change in settings

• Frequent clinical monitoring of acutely ill patients – respiratory rate, heart rate, conscious level, chest wall movement, ventilator synchrony, accessory muscle use – every 15 minutes in the first hour, every 30 minutes in the 1–4-hour period and hourly in the 4–12-hour period

As a very general rule, pH < 7.3 should provoke an adjustment in NIV settings and consideration of intensive care if the patient is suitable (a decision for intensive care involvement should usually be within the first few hours), pH 7.30–7.35 suggests continuing NIV (80% chance of improvement) and pH > 7.35 suggests improvement and provokes consideration of stopping NIV.

Duration

Patients who benefit from NIV in the first 4 hours should receive it for as long as possible (minimum of 6 hours) in the first 24 hours.

Weaning

Weaning should be in daytime hours, and the following is recommended: NIV for 16 hours on day 2; NIV for 12 hours on day 3 including 6–8 hours overnight; NIV discontinued on day 4.