Undifferentiated Dyspnoea — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Robert Chen, 72 years old, retired engineer. [1]

Presenting complaint: Two days of worsening breathlessness, a productive cough with yellow sputum, and orthopnoea, presenting to the emergency department. He is now breathless at rest. [1]

Past history: COPD (FEV1 50 per cent predicted, on a dual bronchodilator and an inhaled corticosteroid), ischaemic heart disease (prior NSTEMI five years ago, treated with PCI and a drug-eluting stent; currently on aspirin, atorvastatin, bisoprolol, ramipril), type 2 diabetes (metformin, last HbA1c 58 mmol/mol), hypertension. He smoked 40 pack-years and stopped five years ago. He lives with his wife and is normally independent, walking 200 metres on the flat before stopping with breathlessness. [1]

Examination findings (trainee elicits):

• Respiratory rate 28, SpO2 88 per cent on room air rising to 93 per cent on 4 L via nasal cannulae.
• Temperature 38.2. Heart rate 108 in atrial fibrillation. Blood pressure 144/88.
• JVP raised 4 cm above the sternal angle.
• Bilateral expiratory wheeze and fine basal crackles. Chest expansion reduced bilaterally.
• Peripheral oedema to the mid-shin. [1]

Investigations (available results):

• Chest X-ray: hyperinflated lung fields, increased bronchovascular markings, no focal consolidation.
• ECG: atrial fibrillation at 108 with no acute ischaemic changes.
• NT-proBNP 1800 pg/mL. Troponin 45 ng/L on arrival (upper limit of normal 14); repeat at 3 hours 42 ng/L.
• Haemoglobin 132. Urea 9.2. Creatinine 130 (baseline 110). Potassium 4.4.
• D-dimer 1200 micrograms per litre. CURB-65 is 2 (respiratory rate, urea). [1]

Drug chart (current): aspirin 100 mg daily, atorvastatin 80 mg nocte, bisoprolol 5 mg daily, ramipril 5 mg daily, metformin 1 g twice daily, tiotropium 18 micrograms daily, salmeterol-fluticasone 50/500 twice daily. [1]

Candidate's structured presentation (model)

Opening statement (SASPOP): [1]

"Mr Robert Chen is a 72-year-old retired engineer presenting with two days of worsening breathlessness, a productive cough and orthopnoea, on a background of COPD, ischaemic heart disease, type 2 diabetes and hypertension. He is a 40-pack-year ex-smoker. His main problems are an acute respiratory deterioration that is most likely an infective COPD exacerbation with a coexisting cardiac component suggested by the raised JVP, the fine basal crackles, the new atrial fibrillation and the NT-proBNP of 1800; a type 2 myocardial injury suggested by the raised troponin; and a non-specific D-dimer elevation that does not, by itself, diagnose pulmonary embolism. My immediate priorities are the ABCDE assessment with controlled oxygen targeting 88 to 92 per cent given his COPD, an arterial blood gas, nebulised bronchodilators and corticosteroids, antibiotics, and a careful diuresis, with reassessment at 30 to 60 minutes and a low threshold to reconsider the differential — including pulmonary embolism with a CT pulmonary angiogram — if he does not settle." [1]

Management plan: [1]

1. ABCDE with controlled oxygen. Target SpO2 88 to 92 per cent with a Venturi 24 to 28 per cent mask, given the COPD and the risk of hypercapnia. Sit him upright. Check an arterial blood gas within 30 to 60 minutes for hypercapnia and acidosis; if the pH is below 7.35 with a PaCO2 above 6, start non-invasive ventilation (bilevel positive airway pressure).
2. Bronchodilators and corticosteroids. Salbutamol 5 mg and ipratropium 500 micrograms nebulised, repeated as needed. Prednisone 50 mg daily for five days (or hydrocortisone 100 mg intravenously if he cannot take oral).
3. Antibiotics. Amoxicillin-clavulanate 875/125 mg twice daily (or doxycycline 100 mg daily if penicillin-allergic), guided by the local guideline and the sputum culture. Send blood cultures before the first antibiotic dose.
4. Diuresis for the cardiac component. Furosemide 40 mg intravenously, with reassessment of the JVP, the crackles and the oxygenation. Cautious, given the COPD (over-diuresis dries the secretions) and the renal function.
5. Rate control for the atrial fibrillation. Digoxin or diltiazem, avoiding a beta-blocker during the COPD exacerbation. Anticoagulate once the acute phase is resolving, weighing the CHA2DS2-VASc and the HAS-BLED.
6. Monitor the troponin. Repeat at intervals; the static trend supports the type 2 myocardial injury interpretation. Do not activate the catheter lab unless the dynamic trend, the chest pain or the ECG changes suggest an acute coronary syndrome.
7. Review the drug chart. The bisoprolol may be reduced or held during the exacerbation, with a plan to reintroduce. The ramipril is continued unless the renal function or the potassium contraindicate it. The metformin is continued unless he becomes hypoxic or the renal function deteriorates.
8. Reassess the PE question. If the clinical picture is consistent with PE (pleuritic chest pain, leg swelling, immobility) or if he does not settle with the above therapy, proceed to CTPA. [1]

Communication and shared decision-making: Explain to Mr Chen and his wife that he has a flare of his lung disease with an infection, and that the heart is also under strain. Explain that the immediate priorities are the breathing, the infection and the heart, and that the next 24 to 48 hours will tell whether the treatment is working. Surface the advance care planning — a patient with COPD and heart failure should have an early conversation about the goals of care and the ceiling of treatment, so that the next deterioration is met with a plan. [1]

Examiner discussion questions

Q1: "His NT-proBNP is 1800 and his troponin is 45. Walk me through your interpretation of each and how each changes your management." [1]

"The NT-proBNP of 1800 is above the PRIDE age-stratified rule-in cutpoint of 900 pg/mL for a patient over 50, which supports a cardiac contribution to this dyspnoea [2]. But I interpret it in context — he has COPD, atrial fibrillation and an acute infection, all of which elevate the peptide, and the value does not by itself quantify the cardiac contribution [1]. The value confirms a cardiac component and shifts my management towards a cautious diuresis alongside the respiratory therapy. The troponin of 45, static on the repeat, is most consistent with a type 2 myocardial injury from the tachyarrhythmia and the respiratory distress rather than a type 1 infarction. The static trend, the absence of chest pain and the absence of ischaemic ECG changes support the type 2 interpretation. I do not activate the catheter lab; I manage the underlying illness and monitor the trend. The teaching point is that both biomarkers answer different questions — the NT-proBNP asks 'is there a cardiac component?' and the troponin asks 'is there myocardial injury?' — and both are interpreted in the clinical context, not in isolation."

Q2: "How do you balance the COPD and the heart failure in his oxygen and diuretic strategy?" [1]

"For the oxygen, I use controlled oxygen (Venturi 24 to 28 per cent, target SpO2 88 to 92 per cent) because of the COPD and the risk of hypercapnia, and I check a blood gas within 30 to 60 minutes. If the gas shows an acidic hypercapnia (pH below 7.35, PaCO2 above 6), I start non-invasive ventilation — the indication is the acidotic hypercapnic respiratory failure, not the absolute CO2. For the diuresis, I give furosemide 40 mg intravenously and reassess the JVP, the crackles and the oxygenation; I am cautious because over-diuresis dries the secretions and worsens the work of breathing in COPD, and because his renal function is already mildly impaired. The integrated approach — controlled oxygen, bronchodilators, corticosteroids, antibiotics, and a cautious diuresis — addresses both the COPD and the heart failure in parallel, and the reassessment at 30 to 60 minutes tells me which is responding." [1]

Q3: "He is in atrial fibrillation. How do you manage the rate and the anticoagulation?" [1]

"The AF is almost certainly secondary to the acute illness and will usually settle as the underlying cause is treated. I would not give a beta-blocker during the COPD exacerbation. My options for rate control are digoxin or a rate-limiting calcium-channel blocker such as diltiazem, with the recognition that the rate will often settle as the underlying illness improves. I anticoagulate him once the acute phase is resolving, because the new AF carries a stroke risk and his CHA2DS2-VASc is high (age, hypertension, diabetes, prior vascular disease, heart failure). I weigh the HAS-BLED against the CHA2DS2-VASc, and I favour a direct oral anticoagulant unless there is a contraindication. The teaching point is the order: treat the cause of the AF, rate-control if the rate is symptomatic, and anticoagulate once the acute phase is resolving." [1]

Q4: "How would you investigate him for pulmonary embolism, given the raised D-dimer?" [1]

"The D-dimer is unhelpful here — it is elevated by the infection, the COPD and the atrial fibrillation, and it cannot exclude PE [4]. I use the clinical assessment and the Wells score. If the Wells score classifies him as PE likely, or if the clinical picture is consistent with PE, I proceed to CTPA. If the clinical picture is not consistent and he is settling with the above therapy, I do not pursue PE. If he is not settling — if the hypoxaemia or the tachycardia persists despite the therapy — I reconsider PE and proceed to CTPA. The Wells score is a guide, not a substitute for clinical judgement, and the PE-is-the-most-likely-diagnosis item is the one I weigh most heavily [3]."

Q5: "What is your plan for his long-term management after this admission?" [1]

"The admission is an opportunity to optimise both the COPD and the heart failure, guided by the 2021 ESC Heart Failure Guidelines [5]. For the COPD, I confirm the inhaler technique and the adherence, I optimise the dual bronchodilation, I enrol him in pulmonary rehabilitation, I check his vaccination status, and I assess him for long-term oxygen therapy. For the heart failure, I optimise the four pillars of therapy if his echo shows a reduced ejection fraction — the beta-blocker, the ACE inhibitor or ARNI, the mineralocorticoid receptor antagonist, and the SGLT2 inhibitor. For the atrial fibrillation, I formalise the anticoagulation and the rate or rhythm strategy. And I address the advance care planning — the goals of care and the ceiling of treatment — so that the next deterioration is met with a plan, not a crisis."

Q6: "What is the single most important lesson from this case for a registrar managing undifferentiated dyspnoea?" [1]

"The single most important lesson is to resist the anchoring error. Mr Chen has COPD, and the easy diagnosis is an exacerbation — but the actual picture is a COPD exacerbation with a coexisting heart failure component, a new atrial fibrillation, a type 2 myocardial injury, and a possible PE that the D-dimer cannot exclude. The registrar who stops at 'exacerbation' and treats only with bronchodilators and corticosteroids has missed the cardiac component, the AF, the troponin rise and the PE question. The integrated approach — the time-course framework, the focused history, the systematic examination, the first-tier investigations interpreted together, and the parallel management of the competing diagnoses — is what keeps the complex dyspnoeic patient safe. The corollary is the reassessment: the patient who is not settling at 30 to 60 minutes is telling the registrar that the working diagnosis is incomplete." [1]

DCE Short Case — The Systematic Respiratory Examination in the Breathless Patient

Instruction

"You are the medical registrar assessing a 68-year-old woman on the ward with progressive exertional dyspnoea over three months and a recent worsening over one week. Examine her respiratory system, present your findings, and offer a differential diagnosis. You have 5 minutes to outline your examination approach and 5 minutes for discussion." [1]

Provided data: The patient is a 68-year-old woman, a lifelong non-smoker, with progressive exertional dyspnoea over three months and orthopnoea. On examination: respiratory rate 24, SpO2 93 per cent on room air. Fine bilateral basal crackles (Velcro quality). Finger clubbing present. JVP raised 3 cm. No peripheral oedema. Chest X-ray (shown) shows bilateral basal reticulonodular change. [1]

Presentation template

"I have examined this woman's respiratory system. At the end of the bed she is comfortable at rest but breathless on minimal exertion. Her respiratory rate is 24, her oxygen saturation is 93 per cent on room air. Her hands show finger clubbing, grade 3, with no cyanosis and no asterixis. The JVP is raised 3 cm. The trachea is central. The chest expansion is reduced at the bases bilaterally. Percussion is resonant. Auscultation reveals fine, late-inspiratory, Velcro-quality crackles at both bases, with no wheeze. There is no peripheral oedema. My findings are most consistent with an interstitial lung disease — the fine Velcro crackles, the finger clubbing, and the bilateral basal reticulonodular change on the chest X-ray — and I would confirm this with a high-resolution CT chest and pulmonary function tests. The raised JVP raises the question of cor pulmonale, and I would arrange an echocardiogram to assess the right heart." [1]

Discussion

Examiner: "What is your differential diagnosis, and how would you discriminate?" [1]

"My leading diagnosis is an interstitial lung disease — the fine Velcro crackles, the clubbing and the basal reticulonodular change are the classic triad. The differential within the interstitial lung diseases includes idiopathic pulmonary fibrosis (the usual interstitial pneumonia pattern on the high-resolution CT, with basal and subpleural honeycombing), the connective tissue disease-associated interstitial lung diseases (systemic sclerosis, rheumatoid arthritis, the antisynthetase syndrome — I would examine for the extrapulmonary signs), the hypersensitivity pneumonitides (the occupational and environmental history is critical — bird exposure, mouldy hay), the drug-induced pneumonitides (amiodarone, methotrexate, nitrofurantoin, bleomycin), and the sarcoidoses. The high-resolution CT and the pulmonary function tests discriminate these, and the bronchoalveolar lavage or the surgical lung biopsy may be needed for the atypical cases. The raised JVP raises cor pulmonale, which complicates advanced interstitial lung disease, and the echocardiogram assesses the right heart." [1]

Examiner: "She is orthopnoeic. Does this not indicate heart failure?" [1]

"Orthopnoea classically indicates left heart failure, but it also occurs in diaphragmatic weakness and in advanced bilateral lung disease — the supine position reduces the functional residual capacity and worsens the dyspnoea. The discriminator is the rest of the picture: this woman has fine Velcro crackles, clubbing and a reticulonodular chest X-ray, which point to an interstitial lung disease rather than heart failure. Heart failure would give a raised JVP with a third heart sound, bibasal crackles that are typically finer and more diffuse, and often a murmur or a displaced apex; and the chest X-ray would show cardiomegaly, upper lobe diversion and pleural effusions rather than reticulonodular change. The NT-proBNP would be the discriminator biomarker — a value below 300 pg/mL would exclude acute heart failure and confirm that the orthopnoea is from the lung disease. The teaching point is that orthopnoea is not pathognomonic of heart failure; the registrar weighs it with the rest of the examination." [1]

Examiner: "What is the lesson about the missed diagnoses in chronic dyspnoea?" [1]

"The lesson is that the missed diagnoses in chronic dyspnoea are pulmonary hypertension and the interstitial lung diseases, both of which may have a near-normal chest X-ray in the early stage and both of which require a high-resolution CT, pulmonary function tests and an echocardiogram for the diagnosis. The registrar who evaluates chronic dyspnoea with a chest X-ray and a spirometry alone, and concludes 'no cause found,' has not excluded pulmonary hypertension (which needs an echocardiogram) or interstitial lung disease (which needs a high-resolution CT). The corollary is that chronic dyspnoea with a normal chest X-ray and a normal spirometry is an indication for an echocardiogram and a high-resolution CT, not a conclusion." [1]