HERMES Adult Respiratory Medicine common mistakes
HERMES Adult Respiratory Medicine · Understand the traps and how to avoid them.
Managing a COPD exacerbation with nebulised bronchodilators and steroids but omitting controlled oxygen targets and a documented reassessment of blood gases after 30–60 minutes, so a rising PaCO2 with acidaemia is recognised too late.
Candidates learn the 'exacerbation bundle' as a list of drugs and treat oxygen as supportive background rather than a titrated therapy; the classic teaching that oxygen can worsen hypercapnia feels old-fashioned, so the Venturi mask target range and repeat gas reassessment get skipped in the rush to write prescriptions.
What to do instead
Write the oxygen prescription explicitly with a target saturation range (88–92% for those at risk of hypercapnia), and state the trigger and timing for repeat arterial or capillary gases (within 30–60 minutes of starting controlled oxygen or if the patient deteriorates). Practise phrasing the escalation pathway: non-invasive ventilation criteria (persistent pH <7.35 with PaCO2 >6.5 kPa despite optimal medical therapy) and when to call critical care.
Labeling every patient with asthma symptoms plus fixed airflow obstruction as COPD, or conversely diagnosing asthma in a 65-year-old smoker without spirometry, bronchodilator reversibility testing, or review of historical records.
The two diseases overlap in older adults and candidates anchor on the demographic (age, smoking) or on a single FEV1/FVC ratio, forgetting that the distinction drives different long-term therapy, exacerbation management, and biologic eligibility; the exam often presents ambiguous histories where the discriminator is serial peak flow or a documented response to treatment.
What to do instead
For any obstructive case, state the objective evidence you would use: post-bronchodilator spirometry, reversibility (≥12% and ≥200 mL), serial peak expiratory flow, FeNO, blood eosinophils, and response to a trial of inhaled corticosteroids. When features overlap, use the label 'asthma–COPD overlap' only with explicit criteria and describe what you would monitor to revise the diagnosis.
Interpreting high-resolution CT patterns of usual interstitial pneumonia (UIP) as diagnostic of idiopathic pulmonary fibrosis without excluding known causes, and failing to check for connective tissue disease, drug exposure, or occupational antigen before starting antifibrotic therapy.
Candidates memorise the UIP pattern (subpleural, basal, honeycombing, traction bronchiectasis) as a terminal answer, but the examination tests the multidisciplinary diagnosis pathway and the secondary causes that change management; the history of rheumatoid arthritis, amiodarone, or bird exposure is deliberately buried in the vignette.
What to do instead
Adopt a fixed checklist for every fibrotic ILD case: full drug and occupational history, autoimmune serology (ANA, rheumatoid factor, anti-CCP, myositis panel), antigen exposure, and review of prior imaging. State when a multidisciplinary team meeting is required and when surgical or transbronchial cryobiopsy is justified. Link the diagnosis explicitly to the treatment decision (antifibrotic versus immunosuppression).
Treating an acute ILD exacerbation or a rapidly progressive interstitial lung disease as infection alone, giving antibiotics and diuretics without considering high-dose corticosteroids, immunosuppression, or urgent transplant referral.
The presentation (fever, bilateral infiltrates, hypoxia) mimics pneumonia, and candidates default to the infection script; they also under-recognise that acute exacerbation of IPF carries very high mortality and that some ILDs (e.g. acute interstitial pneumonia, DAH, eosinophilic pneumonia) respond dramatically to steroids.
What to do instead
In any diffuse bilateral infiltrate with hypoxia, run a parallel differential: infection, acute exacerbation of underlying ILD, alveolar haemorrhage, eosinophilic pneumonia, hypersensitivity pneumonitis, and drug reaction. State the tests that discriminate (bronchoalveolar lavage, eosinophil count, autoimmune serology, echocardiography) and the point at which empirical high-dose corticosteroids and critical care or transplant discussion are indicated.
Assessing a child with recurrent wheeze or chronic cough using adult spirometry criteria and adult drug doses, without adjusting for age, using appropriate reference equations, or considering the age-specific differential (bronchiolitis, foreign body, cystic fibrosis, primary ciliary dyskinesia, aspiration, anatomical airway anomaly).
Adult trainees transfer adult frameworks wholesale; paediatric lung function requires different manoeuvres (tidal breathing, raised-volume rapid thoracoabdominal compression in infants, forced oscillation), different normal values, and different dose calculations by weight or age. Candidates also forget that a 'wheeze' described by parents may be stridor or transmitted noise.
What to do instead
For every paediatric respiratory vignette, state the child's age and weight, use age-appropriate reference values and dosing (mg/kg with maximum caps), and list the age-specific differential before committing to asthma. Describe the first-line investigation for each alternative (sweat test, nasal nitric oxide, immunoglobulins, barium swallow, bronchoscopy) and when to refer to a paediatric respiratory centre.
Diagnosing pulmonary embolism or pulmonary hypertension on clinical impression alone, ordering CT pulmonary angiography without checking renal function or considering the D-dimer and clinical probability pathway, and failing to risk-stratify before choosing anticoagulation, thrombolysis, or referral.
Candidates want to jump to the definitive imaging answer and skip the probability assessment that determines whether imaging is even indicated; in pulmonary hypertension they may accept echocardiographic estimates of systolic pressure as diagnostic without right heart catheterisation, missing the classification that dictates therapy.
What to do instead
For suspected PE, explicitly apply a validated clinical probability score, state D-dimer interpretation by age and probability, and describe risk stratification (haemodynamic instability, right ventricular strain, troponin, sPESI) to choose between anticoagulation, systemic thrombolysis, catheter-directed therapy, and embolectomy. For pulmonary hypertension, state that right heart catheterisation is required for diagnosis and classification, and name the WHO group before proposing therapy.
In respiratory critical care scenarios, adjusting ventilator settings without stating the target and the reason - for example increasing tidal volume or FiO2 in ARDS without applying lung-protective limits, or failing to recognise patient–ventilator dyssynchrony and auto-PEEP in obstructive airflow limitation.
Candidates memorise numbers (6 mL/kg predicted body weight, plateau <30 cmH2O) but do not connect them to the physiological problem in the stem, so they fail to notice when the scenario demands permissive hypercapnia, prolonged expiratory time, or prone positioning. The predicted-body-weight calculation from height is often skipped.
What to do instead
Structure every ventilation answer as target, current setting, and adjustment with justification: tidal volume by predicted body weight, plateau pressure and driving pressure limits, PEEP titration, permissive hypercapnia, and recruitment or prone positioning criteria for severe ARDS. For obstructive disease, name the interventions that reduce dynamic hyperinflation (lower respiratory rate, higher inspiratory flow, longer expiratory time) and how to detect auto-PEEP.
Choosing empirical antibiotics for community-acquired pneumonia without assessing severity (CURB-65 or PSI), without documenting allergy and recent antibiotic exposure, and without deciding the site of care; or treating a pleural effusion complicating pneumonia as simple parapneumonic effusion without thoracentesis and pH analysis.
Candidates focus on the drug name and forget that severity scoring, local resistance patterns, and the presence of a complicated effusion drive mortality; they also under-use pleural fluid analysis (pH <7.20, glucose, Gram stain, culture) to decide on chest drainage.
What to do instead
For every pneumonia case, state the severity score, the site-of-care decision, the empirical regimen with dose and route justified by allergy and prior antibiotics, and the review point at 48–72 hours. If a parapneumonic effusion is present, state that diagnostic thoracentesis is indicated and list the criteria for chest tube drainage (pH <7.20, loculation, positive Gram stain or culture, empyema).
Diagnosing obstructive sleep apnoea from symptoms alone or from a home oximetry trace without interpreting the apnoea–hypopnoea index in context, and prescribing CPAP without addressing the driving factors, adherence plan, or the safety-critical question of fitness to drive.
Candidates treat the sleep study as a formality and the AHI as a binary result; they miss that severity depends on the index plus symptoms plus comorbidity, that central and obstructive events require different management, and that the driver-licensing and occupational-safety implications must be documented.
What to do instead
For each sleep case, state the diagnostic test used and its limitations, report AHI with oxygen desaturation index and symptoms, classify severity, and name the treatment with a plan for titration and adherence review. Explicitly address obesity and alcohol, alternative therapies (mandibular advancement, positional therapy, surgery), and the advice given about driving and notifying the licensing authority until control is demonstrated.
Staging a lung cancer case without documenting the full TNM stage, performance status, and molecular and immunological markers before proposing treatment, or presenting a solitary pulmonary nodule without a validated risk assessment and a clear management pathway.
Candidates jump to 'chemotherapy' or 'surgery' from the histology alone; the examination tests that treatment depends on stage, performance status, PD-L1 expression, EGFR and ALK status, and patient preference, and that a nodule's probability of malignancy determines surveillance versus biopsy versus resection.
What to do instead
For every thoracic oncology case, write the stage explicitly (T, N, M and overall stage), performance status, pulmonary function if resection is considered, and the biomarker results that determine systemic therapy. For a solitary nodule, apply a validated malignancy probability model, state the Brock or equivalent risk factors, and describe the multidisciplinary decision between CT surveillance, PET-CT, biopsy, and surgical resection.