Respiratory Investigation: PFTs, Bronchoscopy and Thoracoscopy

The answer first

Respiratory investigation is question-driven, not panel-driven. Every test in this topic answers one named question, and the consultant-level skill is stating the question before stating the test: Is this obstruction or restriction? (spirometry plus lung volumes). Is the gas-transfer membrane diseased? (DLCO). Is this asthma with normal spirometry today? (bronchoprovocation). What is this node, nodule or effusion made of? (bronchoscopy, EBUS or pleural biopsy). The examiner's favourite trap is the candidate who orders everything and interprets nothing [1].

Three rules carry you through most DWE questions and every data station [1]:

1. Spirometry diagnoses obstruction; it can only suggest restriction. A low FEV1/FVC ratio (below the lower limit of normal) is obstruction. A low FVC with a preserved ratio is suspected restriction — but restriction is a diagnosis of lung volumes, confirmed only when the total lung capacity is low [1].
2. DLCO is the membrane test — and it lies when haemoglobin is abnormal. Interstitial lung disease, emphysema and pulmonary vascular disease lower it; asthma, obesity and alveolar haemorrhage raise it; and anaemia lowers the measured value without any lung disease at all, which is why haemoglobin adjustment is built into the standard [4].
3. Tissue questions are answered by the least invasive route that reaches the lesion. Mediastinal nodes go to EBUS-TBNA first (not mediastinoscopy), peripheral nodules to navigational or radial-EBUS bronchoscopy, and unexplained exudative pleura to image-guided biopsy or medical thoracoscopy [10] [17].

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Spirometry — the gateway measurement

Spirometry measures forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) during a maximal forced manoeuvre from full inflation. Before any number is interpreted, the manoeuvre must be acceptable and reproducible: a maximal blast without hesitation, no cough in the first second, complete expiration, and repeatability between the two best efforts within about 150 mL — numbers from a badly performed test are worse than no numbers [2].

Obstruction is a low FEV1/FVC ratio — below the lower limit of normal (LLN), conventionally the 5th percentile of the predicted reference distribution. The modern ERS/ATS position is LLN-based interpretation using validated reference equations (the Global Lung Function Initiative set), because a fixed ratio of 0.70 ignores the normal age-related fall in elastic recoil and over-diagnoses obstruction in older adults while under-diagnosing it in the young [1]. Severity is then graded by the FEV1 as a percentage of predicted [3].

Reversibility testing asks whether obstruction improves after a bronchodilator — classically salbutamol 200–400 micrograms by spacer, repeating spirometry after 10–15 minutes. The classic positive response is an increase in FEV1 or FVC of at least 12% of baseline and 200 mL; the 2022 ERS/ATS technical standard expresses it as an increase exceeding 10% of the predicted value. Either way, the physiological claim is the same: a large, immediate improvement supports asthma over fixed airflow limitation — but a negative test does not exclude asthma, because airway calibre in asthma varies over time and with treatment [3] [1].

[1]

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Flow-volume loops — the shape is the diagnosis

Plotting flow against volume through the whole forced manoeuvre turns one number into a picture. The classic patterns were defined by Miller and Hyatt for tracheal and laryngeal lesions, and they remain a favourite DCE data-station gift [8].

The mnemonic that survives exams: the limb that flattens tells you where the pressure works against the airway. Inspiration draws extrathoracic lesions shut (inspiratory plateau); expiration compresses intrathoracic lesions (expiratory plateau); a lesion that cannot move at all flattens both [8].

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Lung volumes — spirometry cannot diagnose restriction

This is the single most examined concept in the whole topic, so say it plainly: restriction is defined by a reduced total lung capacity (TLC), and spirometry does not measure TLC. A low FVC with a preserved or high FEV1/FVC ratio raises the possibility of restriction — the "spirometric restrictive pattern" — but small lungs from a submaximal effort, severe obesity, early neuromuscular disease or true parenchymal restriction can all produce it. Only a measured TLC below the LLN confirms the diagnosis [1] [5].

Lung volumes are measured by body plethysmography or gas-dilution techniques, and the numbers that matter are TLC, residual volume (RV) and the RV/TLC ratio [5]:

• TLC below LLN — true restriction. Now use DLCO to split parenchymal from extrapulmonary causes [1].
• TLC normal or high with a low FVC — not restriction; think obstruction with air trapping, poor effort, or a mixed picture.
• Raised RV and RV/TLC — air trapping; supports obstructive disease, especially emphysema.
• Discrepancy between plethysmographic and gas-dilution volumes — trapped, non-communicating gas (bullous emphysema) is seen by the box but missed by dilution [5].

The neuromuscular pattern deserves its own paragraph because it is a DWE staple: respiratory muscle weakness (motor neurone disease/ALS, myasthenia, myopathy, phrenic nerve palsy) gives a low FVC, a low TLC, a normal DLCO and a normal or raised KCO — the alveolar-capillary membrane is intact, and the ventilated units are simply underfilled. The supporting clues are orthopnoea (the diaphragm works hardest lying flat), a weak cough, and low maximal inspiratory and expiratory pressures (MIP, MEP) or a low sniff nasal inspiratory pressure; a meaningful drop in FVC from sitting to supine points specifically at the diaphragm [1].

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DLCO and KCO — the gas-transfer test

DLCO (transfer factor for carbon monoxide) measures how much CO crosses from alveolus to capillary blood in a single breath-hold. It integrates membrane thickness, capillary blood volume, haemoglobin availability and the alveolar volume actually ventilated — which is why it must be read with the haemoglobin and with KCO, the transfer coefficient per unit alveolar volume [4].

The two exam-critical subtleties: first, anaemia lowers measured DLCO artefactually because CO uptake depends on haemoglobin binding, and polycythaemia raises it — the 2017 ERS/ATS standard includes haemoglobin-adjustment equations and expects them to be applied before interpretation [4]. Second, alveolar haemorrhage can raise DLCO dramatically because free haemoglobin within alveoli binds the test CO directly — a classic DWE discriminator in the dyspnoea-plus-falling-haemoglobin vignette, and the reason DLCO is sometimes used to track pulmonary capillaritis activity [3].

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Bronchoprovocation — answering "is this asthma?" when spirometry is normal

Asthma is variable airflow obstruction, so a normal spirometry result on a single day proves nothing. Bronchial challenge testing provokes the airway with a controlled stimulus and measures the fall in FEV1: methacholine (a direct muscarinic agonist) and mannitol (an indirect osmotic stimulus that triggers mast-cell mediator release) are the two in routine use, with exercise and eucapnic voluntary hyperpnoea as the physiological alternatives [6] [7].

Practical rules the exam expects [6] [7]:

• A negative challenge has a high negative predictive value — it makes current, untreated asthma unlikely, which is the main clinical use of the test [6].
• A positive challenge does not diagnose asthma by itself — airway hyperresponsiveness occurs in rhinitis, post-viral states, COPD and cystic fibrosis; the result only counts when it fits the clinical picture [7].
• Preparation matters: withhold short-acting bronchodilators for at least 6–8 hours, long-acting agents and leukotriene antagonists for longer, avoid caffeine on the day, and do not test within weeks of a respiratory infection — all of these blunt or exaggerate the response [6].
• The endpoint is the provocative dose or concentration causing a 20% fall in FEV1 (PD20/PC20 for methacholine; PD15 for mannitol) — the lower the dose needed, the more hyperresponsive the airway [7].

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Reading PFTs as one physiological statement

The DCE data station gives you all four datasets at once — spirometry, the loop, lung volumes and DLCO — and the pass-level answer is one integrated sentence per dataset, then a synthesis and the next test [1].

[1]

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Bronchoscopy — match the tool to the question

Flexible bronchoscopy is not one test but a delivery platform, and the yield depends entirely on matching the sampling tool to the question [9].

EBUS-TBNA changed mediastinal diagnosis. In a prospective controlled trial against mediastinoscopy for lung-cancer staging, EBUS-TBNA achieved equivalent sensitivity for nodal disease with a fraction of the invasiveness — which is why guidelines place endosonography first and keep mediastinoscopy for the EBUS-negative high-suspicion case [10]. For sarcoidosis, the GRANULOMA randomised trial showed endosonography roughly doubled the granuloma-detection yield of conventional bronchoscopic biopsy — making EBUS-TBNA the standard first tissue test for bilateral hilar lymphadenopathy [11].

Safety is part of the exam answer. Diagnostic bronchoscopy is usually done under topical lignocaine plus conscious sedation (midazolam, with or without an opioid), with continuous oximetry and supplemental oxygen. The BTS guideline's anticoagulation rules are a recurring DWE item [9]:

• Aspirin: continue, including for biopsy [9].
• Clopidogrel and other P2Y12 inhibitors: withhold (typically 5 days) before biopsy — simple inspection and BAL carry lower bleeding concern than forceps sampling [9].
• Warfarin: withhold and confirm a safe INR before biopsy; DOACs: omit doses around the procedure per renal function and bleeding risk [9].
• Transbronchial biopsy, not forceps biopsy of a visible lesion, is the manoeuvre that carries the pneumothorax risk — arrange imaging after transbronchial parenchymal sampling in symptomatic or higher-risk patients [9].

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Thoracoscopy and the pleural space

Every pleural effusion workup begins with the same two questions: is it an exudate, and does it need a drain? Both are answered by the fluid, not the scan — and the fluid should be obtained under ultrasound guidance, which BTS pleural guidance ties to fewer failed taps and fewer pneumothoraces [18].

The diuretic trap. Diuresis concentrates a heart-failure transudate: protein and LDH rise in the pleural space faster than in serum, and Light's criteria flip the fluid to "exudate" — the pseudoexudate. When the clinical picture says transudate but Light's criteria say exudate, the corrective move is a serum-to-pleural-fluid protein gradient above 3.1 g/dL (31 g/L) (or an albumin gradient above 1.2 g/dL), which pulls the fluid back to transudate [15] [14].

pH guides drainage in parapneumonic effusion. Meta-analysis of parapneumonic chemistry shows that a pleural pH at or below 7.2 (with low glucose and high LDH as concordant markers) identifies effusions that will not resolve with antibiotics alone — they need tube drainage. A pH above that threshold, with a non-purulent fluid and no organisms, supports antibiotics and observation [16].

The randomised comparison by Metintas and colleagues found both CT-guided Abram's biopsy and medical thoracoscopy highly sensitive, with image-guided biopsy performing best where CT shows focal pleural disease and thoracoscopy adding value through vision, larger samples and same-session pleurodesis — so the modern answer is not "which is better" but "which suits this pleura and this question" [17].

Pneumothorax, briefly. The investigative overlap is small but examinable: recurrent spontaneous pneumothorax is the setting where VATS (surgical) rather than medical thoracoscopy is the intervention — for bullectomy and pleurodesis — while the physician's procedures (aspiration, intercostal drainage) remain ultrasound-and-safety governed by the same pleural guidance [18].

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Choosing the test — the question-first framework

The whole topic compresses into one discipline: state the question, choose the least invasive test that answers it, and know in advance what each possible result will change [1].

[9]

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The DCE angles

Short case — the PFT data station. This is the classic data-driven viva: you are handed spirometry, a loop, volumes and DLCO for a patient with dyspnoea, and examined on the read. The winning structure is the six-step sequence above — quality, ratio, volumes, gas transfer, synthesis, next test — delivered in about ninety seconds, ending with the single investigation that changes management. The three station archetypes to rehearse: ILD (restrictive with low DLCO → HRCT), obesity (low FVC, normal TLC, normal DLCO → no lung disease, deconditioning workup) and ALS/neuromuscular (low TLC, normal DLCO, high KCO → MIP/MEP and sniff pressures) [1] [4].

Long case — the ILD workup. Progressive dyspnoea with Velcro crackles integrates everything in this topic: HRCT pattern first (UIP versus non-UIP changes the whole pathway), PFTs to quantify the restrictive defect and the gas-transfer impairment (and to follow progression or treatment response), serology and exposure history to hunt a cause, and then the multidisciplinary question of whether tissue is needed at all — BAL cellularity in selected phenotypes, cryobiopsy or surgical biopsy only when the result would change treatment, weighed against procedural risk in a fibrotic lung [1] [9]. The examiner is listening for the discipline: the test is chosen because its answer changes management, and deferred when it does not.

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Exam traps, collected

References

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