Acute exacerbation of COPD

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Exacerbations are heterogeneous: viral or bacterial infection, pollution and non-adherence can trigger them, while major mimics produce the same symptom triad. The first management branch is therefore severity and respiratory failure, followed by bronchodilation/steroid, then selective antimicrobial and ventilatory treatment.

Controlled oxygen and NIV are complementary. Oxygen treats hypoxaemia; NIV treats failing ventilation and work of breathing. Reducing oxygen alone cannot correct dangerous alveolar hypoventilation, and excessive uncontrolled oxygen can worsen hypercapnia.

Recovery begins before discharge. Each attack should trigger review of diagnosis, exacerbation phenotype, inhalers, vaccination, rehabilitation and advance/escalation planning where disease is advanced.

Key points

An exacerbation is sustained worsening beyond normal day-to-day variation—typically breathlessness, cough and/or sputum—that requires treatment change; it remains a diagnosis after assessing alternatives.
Actively exclude pneumonia, pulmonary embolism, pneumothorax, acute heart failure, ACS/arrhythmia and sedative/opioid effects when features are atypical or severe.
Give controlled oxygen to SpO2 88-92% pending blood gases in COPD at risk of hypercapnic respiratory failure; do not withhold oxygen from hypoxaemia.
Increase short-acting bronchodilation: salbutamol 2.5-5 mg nebulised or repeated pMDI/spacer; add ipratropium 500 micrograms nebulised in more severe attacks.
Give prednisolone 30 mg orally once daily for 5 days when breathlessness significantly increases and interferes with daily activities; do not prolong routinely.
Antibiotics are not automatic. Consider them with sputum purulence plus increased volume or breathlessness, severe illness, ventilation need or high complication risk.
First-choice oral antibiotic options for 5 days are amoxicillin 500 mg three times daily, doxycycline 200 mg day 1 then 100 mg daily, or clarithromycin 500 mg twice daily; use microbiology history and allergy.
If pH remains below 7.35 and PaCO2 above 6.5 kPa after about 1 hour of optimal treatment, start NIV promptly when appropriate with a documented escalation plan.
Repeat gases after oxygen/ventilation changes; improvement in pH, respiratory rate and consciousness is more important than normalising chronic PaCO2.
Before discharge optimise inhalers, check technique, establish rescue/self-management advice, arrange follow-up and assess rehabilitation, smoking treatment and home-support needs.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Respiratory infection

Viral infection and bacterial infection or overgrowth commonly increase airway inflammation, sputum volume or purulence and breathlessness beyond normal day-to-day variation.

Environmental exposure

Air pollution, smoke, cold conditions and poor indoor air quality can provoke airway inflammation without a proven infective cause.

Treatment disruption

Missed inhaled therapy, poor device technique or loss of home support may contribute to deterioration and should be sought alongside acute triggers.

Alternative acute disease

Pneumonia, pulmonary embolism, pneumothorax, heart failure or arrhythmia may mimic or coexist with an exacerbation and frequently change immediate management.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Inflammatory surge
An acute trigger increases bronchial inflammation, mucus production and airway wall swelling on a background of fixed expiratory flow limitation.
2
Worsening gas trapping
Narrower airways prolong expiration and increase dynamic hyperinflation, raising inspiratory workload and generating severe breathlessness, contributing to the resulting loss of respiratory reserve.
3
Ventilation-perfusion mismatch
Uneven ventilation worsens relative to perfusion, causing hypoxaemia while poorly ventilated alveoli contribute to carbon dioxide retention.
4
Pump failure
Respiratory muscle fatigue and reduced effective alveolar ventilation can produce acute or acute-on-chronic hypercapnic acidosis and impaired consciousness.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Moderate exacerbationRed flag

Worsened breathlessness/cough/sputum requiring short-acting bronchodilator increase and often oral steroid or antibiotic, without life-threatening physiological disturbance.

Acute hypercapnic respiratory failureRed flag

pH below 7.35 with PaCO2 above 6.5 kPa after initial treatment, often with tachypnoea, fatigue or drowsiness. This is a ventilatory emergency and usually an NIV pathway.

Bacterial signal

New sputum purulence, particularly with increased volume and breathlessness, supports antibiotic consideration. Fever/focal signs may indicate pneumonia rather than uncomplicated exacerbation.

Pneumonia or pneumothoraxRed flag

Focal crackles/bronchial breathing, pleuritic pain/fever or sudden unilateral reduced air entry redirects imaging and management; do not intensify nebulisers alone.

Unsafe home situationRed flag

Severe baseline disease, rapid onset, poor response, inability to eat/sleep/walk, frailty, inadequate support or diagnostic uncertainty lowers the admission threshold even if initial observations are borderline.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
ABCDE, NEWS2 scale 2, SpO2 and baseline functionFirst step
Why
Grade immediate risk and decide location of care.
Interpretation and limitations
Use scale 2 in known hypercapnic respiratory failure where appropriate. Compare mobility, cognition and oxygen requirement with baseline; one normal observation does not offset fatigue or confusion.
02
Venous gas screen followed by ABG/arterialised capillary gas when indicated
Why
Detect acidosis/hypercapnia and guide oxygen/NIV.
Interpretation and limitations
A venous pH below 7.35 should prompt an arterial/capillary gas within the acute pathway. Persistent arterial pH below 7.35 with PaCO2 above 6.5 kPa after optimal therapy supports NIV.
03
CXR
Why
Identify pneumonia, pneumothorax, oedema or another structural cause.
Interpretation and limitations
Obtain in hospital and whenever focal signs, severe illness or diagnostic uncertainty exist; hyperinflation alone does not explain an acute change.
04
FBC, U&E, CRP, glucose and ECG
Why
Assess infection, anaemia, renal/electrolyte risk and cardiac mimics/treatment safety.
Interpretation and limitations
CRP does not independently prove bacterial infection. Potassium and rhythm matter with repeated beta2 agonist; renal function affects antibiotics and fluid strategy.
05
Sputum culture
Why
Guide therapy in recurrent, resistant, severe or non-responding infection.
Interpretation and limitations
Send when sputum is purulent in hospital, prior resistant organisms/bronchiectasis exist, ventilation is needed or response fails; use previous cultures when choosing empiric therapy.
06
Targeted troponin, BNP/echo, D-dimer/CTPA or viral testing
Why
Investigate mimics and infection-control implications.
Interpretation and limitations
Choose according to pre-test probability. Troponin can rise in physiological stress; interpret with symptoms/ECG and serial change rather than ignoring or overcalling it.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Pneumonia

Focal chest signs, fever, new consolidation or systemic inflammatory features support pneumonia, which can also trigger a genuine COPD exacerbation.

Acute heart failure

Orthopnoea, oedema, raised venous pressure, cardiac biomarkers or pulmonary congestion suggest fluid overload rather than airway inflammation alone.

Pulmonary embolism

Pleuritic pain, haemoptysis, venous thromboembolism risk or unexplained hypoxaemia should prompt probability-led investigation because symptoms overlap substantially.

Pneumothorax

Sudden unilateral pain, asymmetric breath sounds or unexpected deterioration indicates pleural air, especially in emphysematous disease.

Medicine-related hypoventilation

Opioids, sedatives or excess oxygen in a susceptible patient may worsen ventilation and consciousness without the expected increase in cough or sputum.

Additional chapter-specific clues

Cardiac or thromboembolic mimicRed flag

Chest pain, syncope, disproportionate hypoxaemia, calf symptoms, raised JVP/oedema, new arrhythmia or troponin/BNP context suggests PE, ACS or heart failure.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01ImmediateFirst-hour treatmentFirst stepHospital-level exacerbation or significant physiological disturbance.

1Use ABCDE, controlled oxygen to 88-92%, monitoring and early blood gas. Call senior help for confusion, exhaustion, severe acidosis or haemodynamic instability.
2Give salbutamol 2.5-5 mg nebulised and ipratropium 500 micrograms nebulised, or repeated pMDI/spacer if suitable; use an air-driven nebuliser with separately titrated oxygen in hypercapnic-risk patients where available.
3Give prednisolone 30 mg orally and assess antibiotic indication. Obtain CXR, ECG, bloods and targeted microbiology/mimic testing without delaying respiratory support.
4EscalationReassess within 1 hour: symptoms, RR, consciousness, SpO2/device, pH/PaCO2 and ability to eat/mobilise; define escalation ceiling and involve respiratory/critical care early if high risk.

02NIVAcidotic hypercapnic failureAfter about 1 hour of optimal therapy, pH remains below 7.35 with PaCO2 above 6.5 kPa.

1Confirm potentially reversible acute hypercapnic respiratory failure, exclude/resolve an undrained pneumothorax and discuss goals/ceiling with the patient and senior respiratory/critical-care team.
2Start NIV in an experienced monitored area, commonly IPAP 10-15 and EPAP about 4 cmH2O, then increase pressure support over 10-30 minutes to improve ventilation and comfort under the local protocol.
3Repeat gas and clinical assessment after about 1 hour. Improving pH, RR and consciousness supports continuation; pH below 7.25, worsening hypoxaemia, mask intolerance or failure to improve needs immediate critical-care/intubation or ceiling-of-care review.
4Continue controlled oxygen, bronchodilator, steroid and cause treatment; NIV is not a replacement for them.

03AntibioticUse bacterial likelihood and riskPurulent sputum with increased volume/breathlessness, severe illness, ventilation or high complication risk.

1Review current sputum change, previous cultures/resistance, recent antibiotics, allergy, renal function and pneumonia/bronchiectasis possibility.
2Use a 5-day first-choice course: amoxicillin 500 mg TDS, doxycycline 200 mg day 1 then 100 mg OD, or clarithromycin 500 mg BD. Choose rather than combine for uncomplicated exacerbation.
3If high risk of failure, culture-guided options include co-amoxiclav 500/125 mg TDS or co-trimoxazole 960 mg BD for 5 days. Use levofloxacin 500 mg OD only with specialist advice when other recommended antibiotics are inappropriate under MHRA restrictions.
4EscalationReview response and culture. Escalate diagnosis rather than automatically extending/switching antibiotics if not improving.

04DischargeSafe recovery planPhysiology and function have returned sufficiently towards baseline.

1Confirm stable oxygen requirement/mental state, safe mobility/intake, bronchodilator plan and home support; reconcile and demonstrate maintenance inhalers.
2Complete 5-day steroid/antibiotic courses where indicated, provide written exacerbation advice and explain red flags. Do not start routine home nebulisers solely because they were used in hospital.
3Arrange timely primary/community respiratory follow-up, pulmonary rehabilitation after admission where suitable, smoking treatment and review of repeated attacks/advanced-care planning.

Key medicines and prescribing safety5 treatments · regimens, roles and cautions

Treats hypoxaemia while reducing excessive oxygen exposure.

Controlled oxygen

24% Venturi at 2-3 L/min or 28% Venturi at 4 L/min (or nasal cannulae 1-2 L/min) initially, titrated to SpO2 88-92% pending gases unless an individual alert-card target applies.

Repeat gases 30-60 minutes after change; increase support if hypoxaemia persists rather than accepting dangerous saturation. Critical illness may require initial high-concentration oxygen before rapid titration.

Rapid relief of acute airflow obstruction.

Salbutamol plus ipratropium

Salbutamol 2.5-5 mg nebulised plus ipratropium 500 micrograms nebulised; repeat bronchodilator according to response and monitored protocol.

Monitor pulse, rhythm, potassium and lactate; ipratropium can worsen glaucoma if aerosol reaches eyes. Transition to hand-held inhalers as recovery permits.

Shortens recovery and improves lung function in a significant exacerbation.

Prednisolone

30 mg orally once daily for 5 days.

Avoid routine extension; review glucose, mood, infection and repeated-course bone/adrenal risk. If already steroid dependent, return to the maintenance regimen under clinician guidance.

Treat likely bacterial exacerbation when clinical criteria and risk support antibiotics.

First-choice oral antibiotics

Amoxicillin 500 mg TDS for 5 days; or doxycycline 200 mg on day 1 then 100 mg OD to complete 5 days; or clarithromycin 500 mg BD for 5 days.

Check allergy, renal/hepatic function, pregnancy, QT/interactions and previous cultures. Doxycycline administration reduces oesophagitis risk; macrolides interact with several QT/statin medicines.

For higher treatment-failure risk guided by prior cultures and clinical context.

Higher-risk alternative antibiotics

Co-amoxiclav 500/125 mg TDS for 5 days or co-trimoxazole 960 mg BD for 5 days; levofloxacin 500 mg OD for 5 days only if other alternatives are inappropriate and with specialist advice.

Use co-trimoxazole only when culture and susceptibility support it; check sulfonamide/trimethoprim allergy, renal function and dose adjustment, potassium, full blood count, pregnancy, marrow suppression risk and warfarin interaction. Fluoroquinolones can cause disabling, long-lasting tendon, nerve, psychiatric and other reactions and must be reserved under MHRA rules; avoid concurrent corticosteroid where possible and adjust for renal function.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Acute respiratory failure

Severe ventilation-perfusion mismatch or pump fatigue causes dangerous hypoxaemia, hypercapnia and acidosis requiring closely monitored ventilatory support.

Cardiovascular stress

Hypoxaemia, inflammation and sympathetic activation can precipitate arrhythmia, myocardial injury or decompensated right or left heart disease.

Delirium and functional loss

Acidosis, infection, medicines and hospitalisation can cause delirium, deconditioning and loss of independence, particularly in frail patients.

Recurrent exacerbation

An exacerbation increases near-term vulnerability to another event, further hospitalisation and cumulative decline in exercise tolerance and quality of life.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Reassess within 1 hour in high-risk disease: RR, work, consciousness, SpO2/oxygen, haemodynamics and repeat gas where acidotic/hypercapnic.
On NIV, monitor mask fit, synchrony, pressure tolerance, leaks, pH/PaCO2 and a documented failure/escalation plan in an experienced area.
With repeated beta2 agonist check pulse/rhythm, potassium, glucose and lactate; interpret tachypnoea with airflow response.
Review antibiotic response, cultures and adverse effects at 48-72 hours or earlier if worsening; reconsider pneumonia/PE/heart failure rather than simply broadening.
Before discharge compare mobility, oxygen and cognition with baseline and document inhalers, course stop dates, action plan and follow-up.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Oxygen and ventilation are different prescriptions

A saturation in range can coexist with worsening CO2 and pH. NIV treats ventilatory failure while oxygen is titrated through the circuit.

One in five may improve before NIV

Optimal initial medical therapy and controlled oxygen deserve rapid delivery and reassessment, but persistent acidosis at the 1-hour point should trigger NIV—not repeated waiting.

Purulence is useful but imperfect

It raises bacterial probability; imaging, severity, culture history and bronchiectasis determine whether this is uncomplicated exacerbation, pneumonia or chronic infection.

A low pH is a trajectory marker

The absolute value matters, but a falling pH with fatigue or reduced consciousness is even more urgent than a stable chronic PaCO2 number.

The discharge bundle prevents the next admission

Inhaler error, smoking, absent action plan and missed rehabilitation are modifiable; treating only the five inpatient days forfeits that opportunity.

11Common pitfallsFrequent interpretation and management errors.

01
Giving uncontrolled high-flow oxygen until saturation is 100% in a hypercapnic-risk patient.
02
Stopping oxygen instead of supporting ventilation when CO2 rises.
03
Giving antibiotics for every exacerbation without purulence/risk assessment.
04
Missing pneumonia, PE, pneumothorax, heart failure or ACS.
05
Delaying NIV beyond persistent acidotic hypercapnia or starting it without a failure/escalation plan.
06
Extending prednisolone beyond 5 days by routine rather than indication.