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Level 2 of 6Must-remember

COPD exacerbation and respiratory failure

Assess, manage and stay safe — enough on its own

The card — assess, manage, caution

Assessment— look, ask, measure

  • Ask what has changed against this patient's own baseline: an exacerbation is an episodic worsening of increased dyspnoea, increased cough and a change in the volume or character of sputum beyond that individual's day-to-day variation, usually evolving over less than fourteen days and requiring a change in therapy — what matters is deviation from their own baseline, not the absolute level of breathlessness.
  • Seek the three cardinal symptoms, because they guide the antibiotic decision: increased breathlessness, increased sputum volume, and increased sputum purulence.
  • Take the background functional history before deterioration: what the patient could do a week ago, home oxygen or nocturnal ventilation, previous admissions and intubations, smoking history (COPD is unusual with fewer than 10 pack-years), and in advanced disease ask specifically about peripheral oedema and morning headache (suggesting nocturnal hypercapnia).
  • Assess the conscious level and, critically, the ability to cough — a patient who cannot cough cannot clear secretions or protect the airway, and this observation determines whether non-invasive ventilation is feasible.
  • Look for carbon dioxide retention: warm peripheries, bounding pulses with a wide pulse pressure, and a flapping tremor (asterixis) sought with arms outstretched and wrists extended for 30 seconds; headache, confusion and drowsiness follow, and coma is late.
  • Look for airflow obstruction: wheeze, prolonged expiration, hyperinflation, intercostal indrawing and pursed-lip breathing — breath sounds are characteristically quiet, and scanty bilateral breath sounds in a tiring patient are more ominous than loud wheeze.
  • Look for cor pulmonale: peripheral oedema, raised jugular venous pressure, hepatomegaly and ascites.
  • The critically ill patient may not appear distressed — a patient in carbon dioxide narcosis is warm, quiet and sleepy, and drowsiness in a breathless COPD patient is deterioration, not settling.
  • Danger signs: a reduced or falling conscious level; a falling respiratory rate, particularly with a rising saturation (the signature of impending narcosis); feeble respiratory effort, a silent chest, or paradoxical inward movement of the abdominal wall on inspiration (diaphragmatic failure); cyanosis, new peripheral oedema or altered consciousness (the three features mandating hospital assessment rather than home treatment); and haemodynamic instability.
  • The arterial blood gas is the defining investigation — record the inspired oxygen concentration and device at the moment of sampling, and read four numbers in order: PaO₂; pH (below 7.35 defines acute respiratory acidosis); PaCO₂ (above 6.5 kPa / 49 mmHg with pH below 7.35 defines decompensated failure); and bicarbonate with base excess, the chronicity marker.Not available at your setup — Arterial blood gas.
  • Know the gas thresholds: PaO₂ above 8 kPa (60 mmHg) is the target; PaO₂ above 7 kPa (52 mmHg) is the minimum safe value accepted while treatment is titrated; PaO₂ below 5 kPa (37 mmHg) is dangerous and demands an immediate increase in inspired oxygen; PaCO₂ above 8 kPa (60 mmHg) and rising with exhaustion or drowsiness is an indication for urgent mechanical ventilation.Not available at your setup — Arterial blood gas.
  • It is the pH, not the PaCO₂, that tells you whether ventilatory failure is acute: pH at or above 7.35 with a high PaCO₂ and a high bicarbonate is a compensated chronic retainer at baseline; the same PaCO₂ with pH below 7.35 is an emergency; pH below 7.25 and falling with a rising PaCO₂ carries a high risk of NIV failure.Not available at your setup — Arterial blood gas.
  • Name the type of failure: type I (acute hypoxaemic) is a low PaO₂ with a normal or low PaCO₂ from ventilation–perfusion mismatch or shunt; type II (ventilatory) is a low PaO₂ with a high PaCO₂, of which COPD is by far the commonest cause — and respiratory failure in practice means a PaO₂ below 8 kPa (60 mmHg) or a PaCO₂ above 7 kPa (55 mmHg), with hypercapnia conventionally defined above 6.0 kPa (45 mmHg).Not available at your setup — Arterial blood gas.
  • Always hunt the precipitant, because none of them respond to bronchodilators: pneumonia, pneumothorax (common in bullous lungs), pulmonary embolism, decompensated left ventricular failure, acute coronary syndrome, arrhythmia, sedative or opioid administration, non-adherence or an empty inhaler, deteriorating air quality, and surgery, rib fracture or any pain preventing deep breathing and coughing.
  • Certain findings forbid the label "exacerbation" alone: finger clubbing is never a feature of COPD and should trigger investigation for lung cancer, pulmonary fibrosis or bronchiectasis; persistent crackles raise bronchiectasis; haemoptysis must never be attributed to COPD without investigation; weight loss and anorexia are how lung cancer and tuberculosis present; and asymmetry on chest examination suggests large airway obstruction or a pneumothorax mimicking an exacerbation.
  • COPD does not occur in children: a child with airflow obstruction and a rising PaCO₂ has another disease, and adult COPD reasoning — including the 88–92% oxygen target — must not be transposed onto them.

Management— do this, in order

  • Sit the patient upright, which reduces the work of breathing in hyperinflation, and run five things in parallel: controlled oxygen to a defined target, relief of airflow obstruction, suppression of airway inflammation, treatment of the precipitant, and ventilatory support if the acidosis does not resolve. The bronchodilator and the corticosteroid do not wait for the blood gas or the radiograph.
  • Controlled oxygen by Venturi mask at 24% or 28%, aiming to maintain SaO₂ 88–92% or PaO₂ above 8 kPa (60 mmHg) without worsening acidosis — a Venturi mask is a fixed-performance device, whereas nasal cannulae and simple masks are variable-performance and unsuitable as the primary device where hypercapnia is a risk. Venturi valve flows: 24% at 2 L/min, 28% at 4, 31% at 6, 35% at 8, 40% at 10 and 60% at 15 L/min.
  • Titrate the oxygen by measurement: start at 24%; if SpO₂ remains below 88%, step up through 28% and 35% repeating the gas after each change; if SpO₂ exceeds 92%, step down — most patients need no more than 24–28%. Where hypercapnic failure has not been documented, the standard adult target of 94–98% applies.Not available at your setup — Arterial blood gas.
  • If the patient is peri-arrest, unconscious, or the saturation unrecordable, give high-concentration oxygen by reservoir mask at 15 L/min and correct the target once a gas is available — hypoxaemia kills in minutes, hypercapnia in hours, and oxygen must not be withheld for fear of worsening acidaemia.
  • Nebulised salbutamol 5 mg with ipratropium bromide 500 micrograms in the same chamber, repeated 4–6 hourly, and every 20–30 minutes in the first hour if severe.
  • Drive the nebuliser with compressed air in adults with COPD, giving oxygen concurrently by nasal cannula at 1–2 L/min — an oxygen-driven nebuliser at 6–8 L/min delivers roughly 60% oxygen throughout the treatment; where only oxygen is available, keep the run short and restore the controlled-oxygen device immediately.
  • If no nebuliser exists: salbutamol 100 micrograms by metered-dose inhaler through a large-volume spacer — 4–10 puffs one at a time with five tidal breaths each, up to three times in the first hour — is equivalent in mild to moderate exacerbation.
  • Oral prednisolone 30 mg daily for 5 days is the currently recommended dose (some sources use 40–60 mg, with no evidence that higher doses or longer courses improve outcome); a five-day course needs no taper, and weaning is required only after a recent corticosteroid course or the equivalent of more than 7.5 mg prednisolone daily for a prolonged period.
  • If swallowing is unsafe: hydrocortisone 100–200 mg intravenously then 100 mg 6-hourly, converting to oral prednisolone when safe.Doctor / Nurse
  • Give an antibiotic where there is purulent sputum, increased sputum volume, fever, radiographic consolidation, or a raised CRP or white cell count, and record the reason: amoxicillin 500 mg orally three times daily for 5–7 days first line; co-amoxiclav 625 mg orally 8-hourly (or 1.2 g intravenously 8-hourly if unable to swallow); doxycycline 200 mg orally on day 1 then 100 mg once daily in penicillin allergy (avoid in pregnancy); clarithromycin 500 mg orally twice daily; or azithromycin 500 mg orally daily for 3 days.
  • Reassess at 30–60 minutes, recording conscious level, respiratory rate, SpO₂ with device and flow, pulse and blood pressure, and repeat the gas. If pH is 7.35 or above with PaCO₂ 6.5 kPa or below, continue controlled oxygen, nebulisers and corticosteroid and treat the precipitant; most such patients settle.Not available at your setup — Arterial blood gas.
  • If pH is below 7.35 with PaCO₂ above 6.5 kPa, the next hour is active treatment, not observation: controlled oxygen at the right concentration, repeated bronchodilators, corticosteroid and antibiotic given, precipitant treated, patient upright, secretions cleared, and every sedating drug stopped.Not available at your setup — Arterial blood gas.
  • If the acidosis has not corrected after that hour, start non-invasive ventilation — it reduces mortality and the rate of invasive ventilation in exacerbations complicated by mild to moderate respiratory acidosis (pH below 7.35, PaCO₂ above 6.5 kPa); begin modestly, commonly IPAP 12–15 cmH₂O and EPAP 4–5 cmH₂O, increasing IPAP against tolerance, chest expansion and the repeat gas, with entrained oxygen titrated to the same 88–92% target. The gas one hour after NIV begins is the decisive measurement.DoctorNot available at your setup — Mechanical ventilator, Arterial blood gas.
  • Supportive care: furosemide 20–40 mg intravenously for peripheral oedema repeated by response, urine output and renal function with potassium monitored; frequent physiotherapy with or without pharyngeal suction; correction of hypokalaemia, hypophosphataemia, hypomagnesaemia, anaemia, hyperglycaemia and dehydration; and venous thromboembolism prophylaxis unless contraindicated. Do not stop maintenance inhalers.Doctor / NurseNot available at your setup — Serum electrolytes.
  • Children — the 88–92% target does not apply: there is no hypoxic-drive concern in children, so give oxygen freely and target SpO₂ 94–98% (the sole exception being a child with established chronic hypercapnia and a documented individual target). Estimate weight as (age in years + 4) × 2 kg for children aged 1–10 years.
  • Paediatric drug doses: salbutamol nebulised 2.5 mg under 5 years and 5 mg from 5 years, oxygen-driven, every 20–30 minutes in the first hour; ipratropium nebulised 250 micrograms under 12 years and 500 micrograms from 12 years; prednisolone 1–2 mg/kg once daily to a maximum of 40 mg for 3–5 days; hydrocortisone 4 mg/kg intravenously 6-hourly to a maximum of 100 mg per dose; magnesium sulphate 40 mg/kg intravenously over 20 minutes to a maximum of 2 g; amoxicillin 15–30 mg/kg orally 8-hourly; co-amoxiclav 30 mg/kg 8-hourly; azithromycin 10 mg/kg daily or clarithromycin 7.5 mg/kg twice daily (maximum 500 mg per dose) in penicillin allergy — with adult doses if over 40 kg.Doctor / Nurse
  • Escalate to invasive ventilation where acidosis deteriorates despite optimal NIV settings, where the interface cannot be tolerated, where the airway cannot be protected, for severe distress persisting despite maximal therapy (respiratory rate above 40/min, inability to speak, exhaustion), for declining consciousness, for a rising PaCO₂ above 8 kPa (60 mmHg), or for extreme hypoxaemia below 8 kPa despite oxygen.DoctorNot available at your setup — Mechanical ventilator, Endotracheal intubation kit, ICU / HDU bed, Arterial blood gas.

Caution— what harms

  • Never withhold oxygen for fear of respiratory acidaemia: the two rules of oxygen are not in conflict — give no more than is needed and never less than is needed. A patient at 85% is under-treated as surely as a patient at 99% is over-treated, and hypoxaemia is more detrimental than hypercapnia.
  • Never sedate a hypercapnic, agitated COPD patient: benzodiazepines, opioids and sedating anti-emetics reduce central respiratory drive, and agitation in a hypercapnic patient is hypoxaemia and hypercapnia until proved otherwise.
  • Do not treat drowsiness as settling — it is a vital sign in this condition. The deterioration to be caught is not a falling saturation but a patient who has become quiet, warm and easy to look after; a falling respiratory rate with a rising saturation is the signature of impending narcosis.
  • Do not mistake a large bulla for a pneumothorax on the plain film — a bulla usually shows a concave inner margin with vessels traceable beyond it, a pneumothorax a convex lung edge with no markings beyond; where there is clinical tension, decompression precedes imaging.
  • Do not ventilate a COPD patient rapidly by bag: breath-stacking causes dynamic hyperinflation with intrinsic PEEP and abrupt hypotension — the correct response is to disconnect the circuit for 20–30 seconds and allow full exhalation, while excluding tension pneumothorax.
  • Do not use pulse oximetry as a substitute for an arterial gas here: a saturation of 90% carries no information about the PaCO₂, and it is the PaCO₂ and pH that determine management.Not available at your setup — Arterial blood gas.
  • Do not send a gas without recording the inspired oxygen concentration and device — a gas without an FiO₂ attached cannot be interpreted or compared with the next.
  • Do not start non-invasive ventilation in the wrong patient: it requires a patient who is conscious, cooperative, able to protect the airway and able to expectorate. Contraindications are respiratory arrest or agonal breathing, inability to protect the airway or remove the mask, vomiting or high aspiration risk, unclearable secretions (retained sputum is a leading cause of failure), haemodynamic instability, facial trauma, burns or recent facial surgery, and an undrained pneumothorax.Not available at your setup — Mechanical ventilator.
  • Do not attribute clubbing, persistent crackles, haemoptysis, weight loss or chest asymmetry to COPD — each demands investigation for lung cancer, fibrosis, bronchiectasis, tuberculosis, large airway obstruction or pneumothorax.
  • Do not over-read the chest film: the baseline appearances are over-inflation with low flattened diaphragms, an increased retrosternal air space, sometimes large bullae, and pruned pulmonary vessels — and the film is often normal even in advanced disease.
  • Do not use theophylline routinely — it is recommended only where other long-acting bronchodilators are unavailable, and is limited by side effects, unpredictable metabolism and interactions requiring level monitoring; and β-blockers are generally avoided in severe COPD without a compelling cardiac indication.
  • Do not cardiovert multifocal atrial tachycardia — it is treated by treating the underlying condition, though verapamil 240–480 mg orally daily in divided doses helps some patients.
  • Do not prescribe long-term oxygen therapy from an acute gas, and do not attempt a reversibility trial acutely — spirometry and gas transfer belong to the stable clinic.
  • Do not transpose adult COPD reasoning onto a child: the 88–92% target does not apply, oxygen is given freely to target SpO₂ 94–98%, and in a distressed child a normal or rising PaCO₂ signals impending respiratory failure, not improvement.

Refer / escalate

Escalate urgently for a reduced or falling conscious level, feeble or paradoxical respiratory effort, a falling respiratory rate with a rising saturation, shock, PaO₂ below 5 kPa (37 mmHg), pH below 7.25 and falling, PaCO₂ above 8 kPa (60 mmHg) and rising with exhaustion or drowsiness, or failure of non-invasive ventilation after one hour — and because mortality is high, consider the ceiling of care early, ideally before critical illness, informed by pre-admission function, previous ventilatory episodes, reversibility of the precipitant, comorbidity and the patient's own wishes.

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