Respiratory Examination — Written Clinical Reasoning

SAQ 1 — The Systematic Respiratory Examination (20 marks, 30 minutes)

Prompt: Outline your systematic approach to the respiratory short case, addressing: (a) the eleven-step examination routine; (b) the four cardinal chest sign patterns; (c) the physiological basis and lung causes of clubbing; (d) fine versus coarse crackles; (e) the model presentation template; and (f) the three most common errors. [1]

Model Answer

(a) The eleven-step examination routine (4 marks): [1]

The routine follows an invariant sequence: end of bed, hands, face, neck, anterior chest (IPAA), posterior chest (IPAA), legs, and additional bedside tests. [1]

At the end of the bed, I take five seconds to observe: breathlessness, use of accessory muscles, pursed-lip breathing, barrel chest, cachexia, cyanosis (central versus peripheral), oxygen tubing, an inhaler or spacer on the bedside table, the patient's position, and the respiratory rate and pattern. This observation often reveals the diagnosis before I touch the patient. [1]

In the hands, I assess clubbing (and its lung causes — lung cancer, bronchiectasis, pulmonary fibrosis, mesothelioma, but NOT uncomplicated asthma or COPD), peripheral cyanosis, a fine tremor from beta-agonist use, asterixis from CO2 retention, tar staining from smoking, and the peripheral stigmata of endocarditis and connective tissue disease. [1]

In the face, I look for a plethoric facies (polycythaemia), Horner syndrome (an apical lung tumour or Pancoast tumour — ptosis, miosis, anhidrosis), nasal polyps (cystic fibrosis, allergy), central cyanosis, and oral candidiasis (inhaled corticosteroid use). [1]

In the neck, I assess the JVP (elevated in cor pulmonale), the tracheal position (central; deviated away from a space-occupying lesion, towards a volume-loss lesion), the cricosternal distance (reduced in hyperinflation), and the cervical and supraclavicular lymph nodes. [1]

On the anterior chest, I perform the IPAA sequence: Inspection (shape, symmetry, scars), Palpation (expansion and tactile vocal fremitus), Percussion (resonant, dull, stony dull, hyperresonant), and Auscultation (breath sounds, added sounds, vocal resonance). I compare symmetrical areas at each step. [1]

On the posterior chest, I repeat the IPAA sequence, which provides the best acoustic window to the lower lobes, and I check for sacral oedema. [1]

In the legs, I look for DVT signs (calf swelling and tenderness — the source of a pulmonary embolism) and peripheral oedema (right heart failure, cor pulmonale). [1]

Finally, I offer the additional bedside tests: pulse oximetry, peak flow, the sputum pot, the inhaler technique check, spirometry, and a chest X-ray. [1]

(b) The four cardinal chest sign patterns (4 marks): [1]

The principle is that each pathological process produces a signature combination of percussion, breath sounds, vocal resonance, and expansion. Consolidation conducts sound better (bronchial breathing, increased vocal resonance) and is dull to percussion. Pleural fluid blocks all sound transmission (absent breath sounds, reduced vocal resonance, stony dull). Pleural air blocks sound and adds resonance (absent breath sounds, reduced vocal resonance, hyperresonant). Volume loss pulls the trachea towards the lesion and reduces all findings on the affected side [1][2][3].

(c) Clubbing — physiological basis and lung causes (3 marks): [1]

Clubbing is the selective enlargement of the distal segments of the fingers caused by connective tissue proliferation between the nail matrix and the distal phalanx. The pathophysiology involves the failure of the pulmonary circulation to filter megakaryocyte fragments and platelet-derived growth factors (PDGF, VEGF), which then lodge in the digital capillary beds and stimulate fibroblast proliferation and angiogenesis [4].

The lung causes of clubbing are: lung cancer (especially non-small cell), bronchiectasis, pulmonary fibrosis (idiopathic pulmonary fibrosis, asbestosis [5]), mesothelioma, and lung abscess or empyema. Clubbing does NOT occur in uncomplicated asthma or COPD — if the COPD patient has clubbing, there is a complication (lung cancer, bronchiectasis, or coexisting pulmonary fibrosis).

(d) Fine versus coarse crackles (3 marks): [1]

Fine crackles are late-inspiratory, high-pitched, and Velcro-like. They are produced by the sudden opening of small airways and alveoli that have collapsed during expiration. They do NOT clear with coughing. They indicate interstitial lung disease (especially idiopathic pulmonary fibrosis) or early pulmonary oedema. [1]

Coarse crackles are mid-inspiratory, low-pitched, and bubbling. They are produced by air bubbling through secretions in the medium and large airways. They MAY clear with coughing. They indicate pneumonia, bronchiectasis, or chronic bronchitis. [1]

The teaching point: the crackles that clear with coughing are secretions; the crackles that persist are parenchymal. The candidate who describes crackles without specifying fine or coarse has not completed the examination [1].

(e) The model presentation template (3 marks): [1]

The presentation follows a fixed structure: summary statement, positive findings by system, relevant negatives, differential diagnosis, and proposed investigation plan. The model: [1]

"On general inspection, the patient is [breathless or comfortable] at rest, with [notable features: accessory muscle use, barrel chest, cachexia, oxygen, inhaler]. In the hands, there is [clubbing and grade, or no clubbing], [cyanosis or no cyanosis], [tremor or asterixis or neither]. In the face, there is [Horner syndrome or no Horner syndrome], [central cyanosis or no central cyanosis]. In the neck, the JVP is [elevated or not elevated], and the trachea is [central or deviated]. On examination of the chest, there is [reduced expansion on one side or bilaterally], [percussion finding], [breath sound quality], [added sounds], and [vocal resonance finding]. Posteriorly, [confirmation or additional findings]. In the legs, [oedema or DVT signs or neither]. These findings are consistent with [the diagnosis]. My differential diagnosis includes [the ranked list]. I would like to [the proposed investigations]." [1]

(f) The three most common errors (3 marks): [1]

1. Omitting the end-of-bed inspection. The five-second observation reveals the diagnosis in a significant proportion of cases. The candidate who walks straight to the chest has demonstrated a failure of the systematic approach. [1]

2. Auscultating only the anterior chest. The posterior chest provides the best acoustic window to the lower lobes, and the candidate who does not examine the back has missed the consolidation, the effusion, the fibrosis, and the pulmonary oedema that are most often basal. [1]

3. Failing to compare symmetrical areas. The single most useful finding in the respiratory examination is asymmetry, and this can only be detected by comparing right with left at each level. The candidate who percusses the right base then the right mid-zone then the left base has lost the comparison. [1]

SAQ 2 — Interpreting a Complex Respiratory Short Case (10 marks)

Prompt: A 66-year-old woman, a 50-pack-year ex-smoker, is examined in the DCE short case. Findings: cachectic, breathless at rest, barrel chest, pursed-lip breathing, oxygen at 2 L via nasal cannulae, grade 3 clubbing, no asterixis, JVP elevated 4 cm, trachea central, reduced expansion bilaterally, hyperresonant percussion, globally reduced breath sounds with expiratory wheeze, no crackles anteriorly, but bilateral coarse crackles at the bases posteriorly, and peripheral oedema to the mid-shin. (a) Interpret the constellation of findings and give the primary diagnosis. (b) What is the significance of the clubbing? (c) What investigation does the coarse crackle finding prompt? (d) What is the significance of the raised JVP and the peripheral oedema? [1]

Model Answer

(a) Primary diagnosis (3 marks): [1]

The constellation of barrel chest, pursed-lip breathing, reduced expansion bilaterally, hyperresonant percussion, globally reduced breath sounds with expiratory wheeze, and the inhaler and oxygen is consistent with severe COPD. The bilateral coarse crackles at the bases suggest a coexisting infective exacerbation (bronchitis or early pneumonia). The cachexia reflects the systemic inflammation and the increased work of breathing of advanced COPD. [1]

(b) Significance of clubbing (2 marks): [1]

Clubbing does NOT occur in uncomplicated COPD. In this patient with known COPD, the grade 3 clubbing signals a complication: lung cancer (the most likely, given the heavy smoking history and the cachexia), bronchiectasis (given the basal crackles and the productive cough that would accompany it), or coexisting pulmonary fibrosis (the combined pulmonary fibrosis and emphysema syndrome). I would investigate with a chest X-ray and a CT chest to look for a mass, bronchiectasis, or interstitial changes [4].

(c) Investigation prompted by the coarse crackles (2 marks): [1]

The bilateral basal coarse crackles suggest infection (bronchitis or pneumonia). I would order a chest X-ray to look for consolidation, sputum for culture and sensitivity, and blood cultures if the patient is febrile. I would treat with antibiotics guided by the local COPD exacerbation guideline (amoxicillin-clavulanate or doxycycline). If the crackles do not resolve with treatment, I would reconsider bronchiectasis (a CT chest would confirm dilated bronchi with a signet-ring appearance). [1]

(d) Significance of the raised JVP and peripheral oedema (3 marks): [1]

The raised JVP and the peripheral oedema indicate cor pulmonale — the right heart failure of chronic lung disease. The mechanism is pulmonary hypertension: the chronic hypoxaemia of COPD causes pulmonary vasoconstriction, and the destruction of the pulmonary vascular bed in emphysema increases the pulmonary vascular resistance, leading to right ventricular hypertrophy and eventually right ventricular failure. I would confirm with an echocardiogram (right ventricular hypertrophy, elevated pulmonary artery systolic pressure, tricuspid regurgitation). The management includes optimising the COPD (to reduce the hypoxaemia), long-term oxygen therapy if chronically hypoxaemic, and diuretics for the fluid overload. The prognosis of COPD with cor pulmonale is worse than COPD alone. [1]