Undifferentiated Dyspnoea — Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Robert Chen is a 72-year-old retired engineer presenting with two days of worsening breathlessness, a productive purulent cough and orthopnoea, on a background of COPD with an FEV1 of 50 per cent predicted, ischaemic heart disease with a prior NSTEMI, type 2 diabetes and hypertension. He is a 40-pack-year ex-smoker who stopped five years ago and is normally independent, walking 200 metres before stopping. [1]

His main problems are:

1. An acute respiratory deterioration that is most likely an infective COPD exacerbation, with a coexisting cardiac component suggested by the orthopnoea, the raised JVP, the fine basal crackles and the NT-proBNP of 1800.
2. New atrial fibrillation at 108, almost certainly secondary to the acute illness, requiring rate control rather than rhythm control in the first instance.
3. A raised troponin of 45 that is most consistent with a type 2 myocardial injury from the tachyarrhythmia and the respiratory distress, rather than an acute coronary syndrome.
4. A raised D-dimer that is non-specific in this context and does not, by itself, diagnose pulmonary embolism.
5. Multimorbidity and polypharmacy — the bisoprolol may be contributing to the COPD exacerbation and requires review. [1]

My immediate priorities are the ABCDE assessment with controlled oxygen targeting 88 to 92 per cent given his COPD, an arterial blood gas to assess for hypercapnia and acidosis, nebulised bronchodilators and systemic corticosteroids for the COPD exacerbation, antibiotics for the suspected infection, and a careful intravenous diuresis for the cardiac component. I will reassess at 30 to 60 minutes — if he is not settling, I will reconsider the differential and, in particular, the question of pulmonary embolism with a CT pulmonary angiogram." [1]

Examiner probing questions and model answers

Q1: "His NT-proBNP is 1800. How does that change 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 acute dyspnoea [2]. But I interpret it in the clinical context — he has COPD, atrial fibrillation and an acute infection, all of which can elevate the peptide, and the value does not by itself quantify how much of his dyspnoea is heart failure and how much is COPD. The value confirms that there is a cardiac component, and it shifts my management towards a cautious diuresis alongside the bronchodilator and the corticosteroid therapy [1]. The trap to avoid is treating the number rather than the patient — the diuresis is titrated to the clinical response, not to a target NT-proBNP. The other trap is the false positive — an elevated peptide in renal failure, atrial fibrillation, PE or sepsis does not diagnose heart failure, and I weigh the value with the JVP, the crackles and the chest X-ray."

Q2: "How do you decide how much of his breathlessness is COPD and how much is heart failure?" [1]

"I do not try to separate them at the first assessment — I treat both in parallel and I reassess. The COPD component is addressed with the controlled oxygen, the nebulised bronchodilators and the systemic corticosteroids. The cardiac component is addressed with the cautious intravenous diuresis. The reassessment at 30 to 60 minutes tells me which is responding — if the wheeze improves and the saturations rise with the bronchodilator, the COPD component was dominant; if the JVP falls and the crackles reduce with the diuresis, the cardiac component was significant. In the patient with COPD and heart failure, the two are often coexistent and mutually exacerbating, and the integrated management is safer than forcing a single diagnosis at the cost of missing the other." [1]

Q3: "He is in atrial fibrillation at 108. Do you cardiovert?" [1]

"No. The AF is almost certainly secondary to the acute illness — the infection, the hypoxia, the sympathetic surge, the electrolyte disturbance — and it will usually settle as the acute illness is treated. He is haemodynamically stable, so there is no indication for synchronised DC cardioversion. My approach is rate control with a drug that does not worsen the COPD — a beta-blocker is relatively contraindicated in the exacerbation, so I would use 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 would anticoagulate him once the acute phase is resolving, because the new AF carries a stroke risk and his CHA2DS2-VASc is high. The teaching point is the order: treat the cause of the AF, not the AF itself." [1]

Q4: "His troponin is 45. Is this an acute coronary syndrome?" [1]

"Not necessarily. The troponin is elevated, which indicates myocardial injury — but the injury may be type 2 (demand ischaemia from the tachyarrhythmia, the hypoxia, the respiratory distress, and the sympathetic surge) rather than type 1 (a plaque rupture with thrombosis). The supporting evidence for the type 2 interpretation is the static trend on the repeat (45 to 42 ng/L), the absence of chest pain, and the absence of ischaemic ECG changes. I manage the underlying illness and monitor the trend. If the troponin were rising dynamically with chest pain or ischaemic ECG changes, I would investigate for an acute coronary syndrome. The trap is interpreting a single elevated troponin in a breathless, tachycardic patient as an acute coronary syndrome and activating the catheter lab without weighing the type 2 alternative." [1]

Q5: "How would you investigate him for pulmonary embolism?" [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: does he have pleuritic chest pain, leg swelling, immobility, or a history of VTE? If the clinical picture is consistent with PE, I proceed to CTPA. If the clinical picture is not consistent and the patient is settling with the above therapy, I do not pursue PE. If the patient is not settling — if the hypoxaemia or the tachycardia persists despite the bronchodilators, the corticosteroids, the antibiotics and the diuresis — 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]."

Q6: "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, and to address the precipitants. 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 if he is chronically hypoxaemic. For the heart failure, I optimise the four pillars of therapy if his echo shows a reduced ejection fraction — the bisoprolol, the ramipril or an ARNI, a mineralocorticoid receptor antagonist, and an SGLT2 inhibitor — guided by the 2021 ESC Heart Failure Guidelines [5]. For the atrial fibrillation, I formalise the anticoagulation and the rate or rhythm strategy. And I address 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, not a crisis."

Short Case Discussion

The systematic respiratory examination

Examiner instruction: "Examine this patient's respiratory system. Present your findings and offer a differential diagnosis." [1]

Candidate's model answer: [1]

*"My routine is hands, face, neck, chest, back, legs — the integrated examination that does not stop at the stethoscope. Before I touch the patient, I take five seconds at the end of the bed: is he in distress, is he breathing comfortably, is the colour normal, is the conscious level appropriate? The respiratory rate and the effort are the first observations I record — the respiratory rate is the most informative and the most neglected vital sign. [1]

Hands. I look for clubbing (lung cancer, pulmonary fibrosis, bronchiectasis, infective endocarditis), peripheral cyanosis, a fine tremor (beta-agonist), asterixis (CO2 retention), and the peripheral stigmata of endocarditis and connective tissue disease. [1]

Face. I look for Horner syndrome (an apical lung tumour, Pancoast), plethoric facies (polycythaemia), parotid enlargement, nasal polyps, and central cyanosis. [1]

Neck. I assess the JVP (elevated in heart failure, cor pulmonale, pulmonary embolism, tamponade), the tracheal position (central; deviated away from a pneumothorax or effusion; deviated towards a collapse or fibrosis), the cricosternal distance (reduced in hyperinflation), and the cervical and supraclavicular nodes. [1]

Chest. I inspect for symmetry, scars, deformity (pectus, kyphoscoliosis), paradoxical breathing (diaphragmatic weakness). I measure the expansion anteriorly and posteriorly — reduced bilaterally in COPD and restrictive disease, unilaterally in effusion, consolidation and pneumothorax. I percuss — dull in effusion and consolidation, hyper-resonant in pneumothorax and hyperinflation. I auscultate — the breath sounds, the added sounds (wheeze, crackles fine versus coarse, a pleural rub), and the vocal resonance. [1]

Back. I repeat the percussion and the auscultation posteriorly, and I check for sacral oedema. [1]

Legs. I check for peripheral oedema (right heart failure, cor pulmonale), the deep vein thrombosis signs (calf swelling, tenderness, warmth — the source of the PE), and the peripheral pulses. [1]

The examination does not stop at the respiratory system if the findings suggest a cardiac cause — I extend it to the cardiovascular system, examining the apex, the murmurs and the heart sounds, because dyspnoea is often multifactorial and the integrated assessment is what keeps the patient safe."* [1]

Examiner: "What is the significance of the fine versus the coarse crackles?" [1]

"The fine, late-inspiratory, Velcro-like crackles suggest interstitial lung disease or early pulmonary oedema — the opening of small airways and alveoli that have been stuck together. The coarse, bubbling, mid-inspiratory crackles suggest pneumonia or bronchiectasis — the movement of secretions in the larger airways. The crackles that clear with coughing are secretions; the crackles that persist are parenchymal. In a patient with COPD and heart failure, the fine basal crackles are more consistent with the pulmonary oedema than with the COPD itself, which is why they shift my differential towards the cardiac component." [1]

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

"The single most important lesson is that the examination does not stop at the respiratory system — it extends to the cardiovascular system whenever the findings suggest a cardiac cause, because dyspnoea is multifactorial and the missed cardiac component is the commonest error in the COPD patient. The registrar who examines only the chest in a breathless patient has examined only half the patient. The corollary is the integration of the findings: the respiratory rate, the JVP, the crackles, the wheeze, the murmurs and the oedema are not isolated observations but a single picture that, read together, discriminates the cardiac from the respiratory cause and frames the first-tier investigations." [1]