Lung Function Testing for
Thoracic Surgery

1. The question lung function answers

Pre-operative functional assessment is now framed by NICE NG122 (last updated March 2024), the ERS/ESTS clinical practice guideline on fitness for curative intent treatment of lung cancer (Brunelli, Hardavella, Huber and colleagues 2025) [2], and the ACCP guideline on physiologic evaluation (Brunelli, Kim, Berger and colleagues 2013) [4]. All three documents share an architecture: assess cardiac risk, model operative survival risk, predict post-operative respiratory function. None of them treats any single number as a closed gate. Each measurement is read as one input into the integrated risk picture.

Part 1 — Cardiac risk

The probability that surgery or recovery triggers a cardiac event. History, examination, ECG, and where indicated structured non-invasive cardiac assessment — transthoracic echocardiography, stress echocardiography, myocardial perfusion imaging, stress cardiac MRI, CT coronary angiography, or cardiac-protocol CPET. Established coronary or valvular disease is not in itself a contraindication — the question is whether cardiac function is optimised on contemporary therapy and whether the patient is haemodynamically stable through anticipated peri-operative stresses. Lung resection is not declined on cardiac comorbidity alone — significant cardiac disease is investigated, optimised, and re-stratified before any final decision. Cardiology liaison is integrated into the pathway from the outset where indicated, not deferred. The full assessment framework, including pulmonary hypertension and valvular heart disease, is in section 6.

Part 2 — Operative survival risk

The probability of not surviving the operation and the early peri-operative period. Modelled from large national datasets — the Society for Cardiothoracic Surgery in Great Britain and Ireland (SCTS) National Thoracic Surgery Audit publishes annual benchmark data that informs unit-level performance review and patient-facing risk discussion [9]. National operative survival benchmark for primary lung cancer resection is currently 98.5%; the GSTT 2024–25 figure is 99.59%, audited within the same dataset. These numbers are not abstract — they belong in the consent conversation with named source attribution.

Part 3 — Post-operative respiratory function

The probability of being too breathless after surgery. Predicted post-operative FEV₁ and ppoDLCO are the standard quantitative anchors, supplemented by exercise testing where the resting numbers are borderline and by quantitative ventilation-perfusion imaging where the regional contribution to ventilation and perfusion is non-uniform — as it almost always is in COPD. The 2024 NICE update made an important point explicit: predicted post-operative FEV₁ or transfer factor below 30% does not exclude curative-intent surgery. The decision shifts to a risk-stratified informed consent. The 2025 ERS/ESTS guideline reaches the same conclusion via a different route — categorising ppoDLCO into normal, moderate, and high-risk tiers rather than imposing a binary cutoff.

The shift matters clinically and ethically. Patients told elsewhere that their lung function precludes resection should know that the contemporary frameworks frame the question as a conversation about risk, not a structural exclusion. That conversation is the output of lung function testing. The numbers are inputs; the conversation is the product.

2. Static lung volumes

Static lung volumes describe the total air-holding capacity of the lung partitioned into compartments. Five primary volumes and four derived capacities are clinically relevant.

Volume / Capacity	Definition	Approximate adult value
TLC	Total lung capacity — all air at full inspiration	~6 L
VC	Vital capacity — TLC minus RV; effort-dependent	~4.8 L
FRC	Functional residual capacity — end-tidal resting volume	~2.5 L
TV	Tidal volume — normal breath volume	~0.5 L
ERV	Expiratory reserve volume — FRC minus RV	~1.2 L
IRV	Inspiratory reserve volume — TLC minus end-inspiratory tidal volume	~3 L
RV	Residual volume — air remaining after maximum expiration; not measurable by spirometry	~1.2 L
IC	Inspiratory capacity — TV plus IRV	~3.5 L

RV cannot be measured by spirometry because air remaining after maximum expiration is not exhaled. Two methods are used to derive it.

Helium dilution

A closed-circuit equilibration. The patient breathes from a spirometer of known volume V₁ containing a known concentration of helium C₁. After equilibration the helium concentration falls to C₂ as the gas distributes through the patient’s lung volume. FRC is calculated as V₁ × (C₁ − C₂) / C₂. The method measures only ventilated gas — trapped or non-communicating gas behind closed airways is not detected. The technique is therefore reliable in normal lungs but underestimates true FRC in obstructive disease with significant gas trapping.

Body plethysmography

Boyle’s law applied to intrathoracic gas volume. The patient sits in an airtight box and pants against a closed shutter at FRC. Box pressure and mouth pressure change as lung volume changes with panting. Because Boyle’s law (PV = constant at fixed temperature) relates these measured pressure changes to gas volume, total intrathoracic gas volume can be computed. Plethysmography measures all gas, including non-communicating gas behind closed airways — bullae, hyperinflated trapped lung, and mediastinal gas.

In obstructive disease with gas trapping, the difference between plethysmographic FRC and helium-dilution FRC is itself the trapped-gas volume — a useful clinical signal that ventilatory mechanics are abnormal beyond what spirometry alone reveals.

Surgical relevance: TLC and RV inform whether reduced FVC reflects true restriction (proportional fall in TLC and RV) or obstruction with hyperinflation (TLC normal or raised, RV markedly raised). The distinction changes operative risk assessment, anaesthetic planning, and post-operative pulmonary rehabilitation strategy.

3. Ventilatory tests — obstruction and restriction

Tests of ventilatory capacity quantify how much air the patient can move and how fast. They are the entry point to the assessment.

Spirometry — FEV₁, FVC, and the ratio

FEV₁ — forced expiratory volume in the first second of forced expiration from TLC. Reflects airway resistance and effort-dependent lung mechanics. FVC — total volume exhaled with maximal effort from TLC to RV. Reflects accessible lung capacity. FEV₁/FVC ratio — the principal differentiator of obstructive from restrictive physiology. Both measurements are mandatory in every candidate for major thoracic surgery.

Pattern recognition is the first interpretive step:

Pattern	FEV1	FVC	FEV1/FVC
Normal	≥ 80%	≥ 80%	≥ 0.7
Obstructive	↓	↓ or N	< 0.7
Restrictive	↓	↓↓	N or ↑
Mixed	↓↓	↓↓	< 0.7

The ratio is the single most reliable discriminator. A reduced FEV₁/FVC ratio defines obstruction; a preserved or raised ratio with reduced absolute volumes signals restriction. Mixed disease — obstructive plus restrictive — is not uncommon in patients with cancer who have both COPD and lobar collapse or tumour-related volume loss.

Forced expiratory flow (FEF_25–75%)

Mean expiratory flow over the middle 50% of the FVC manoeuvre. More sensitive than FEV₁ for early small airway disease — the territory of early COPD, asthma, and the asymptomatic smokers in whom FEV₁ is still preserved. Effort-independent over its measurement range, though dependent on previously achieving a complete TLC inflation. A reduced FEF_25–75% with normal FEV₁ is a soft signal that operative reserve may be lower than the headline number suggests.

Factors reducing ventilatory capacity

A simple driving-pressure-versus-resistance model organises the differential:

Reduced driving pressure or lung volume: kyphoscoliosis, interstitial lung disease, neuromuscular disease (poliomyelitis, muscular dystrophy, phrenic nerve palsy), pleural disease (effusion, fibrothorax, pneumothorax), obesity, prior major resection, large mediastinal mass.

Increased airway resistance: COPD, asthma, bronchiectasis, post-tracheostomy or post-intubation tracheal stenosis, central airway obstruction (extrinsic compression, intraluminal tumour, tracheomalacia), foreign body.

Flow-volume curves and dynamic compression

During forced expiration, pleural pressure exceeds airway pressure downstream of the equal pressure point. Airways collapse at this point, limiting flow rate independent of effort. The flow-volume loop captures this: in normal lungs the descending limb is convex (high peak flow, smooth decline). In COPD the descending limb is concave or scooped (effort-independent flow limitation across most of the FVC manoeuvre, reflecting small airway closure at high lung volumes).

The inspiratory limb adds diagnostic value. Fixed upper airway obstruction (tracheal stenosis after intubation or tracheostomy, malignant central airway compression) flattens both inspiratory and expiratory limbs. Variable extrathoracic obstruction (vocal cord dysfunction, laryngomalacia) flattens the inspiratory limb only. Variable intrathoracic obstruction (intrathoracic tracheomalacia, central airway tumour) flattens the expiratory limb only. The pattern is read in seconds and changes the diagnostic and surgical pathway. Central airway interventions — clinician reference →

4. Gas exchange and DLCO

Spirometry tests airflow. Diffusion testing tests gas transfer across the alveolar-capillary membrane. Both are required — some patients have entirely normal FEV₁ but a markedly reduced DLCO, especially in emphysema and pulmonary vascular disease.

Arterial blood gases

Arterial PO₂ reflects oxygenation. Arterial PCO₂ reflects alveolar ventilation. pH reflects acid-base status — respiratory or metabolic. The alveolar gas equation, PAO₂ = FiO₂ × (P_B − P_H2O) − PaCO₂/R, anchors the alveolar-arterial (A–a) gradient calculation. A normal A–a gradient with hypoxaemia points to hypoventilation or low FiO₂. A widened A–a gradient indicates V/Q mismatch, diffusion impairment, or shunt.

Five mechanisms of hypoxaemia

1. Hypoventilation: raised PaCO₂ is the hallmark. A–a gradient normal. Causes — CNS depression, neuromuscular weakness, chest wall disease (kyphoscoliosis, severe obesity), upper airway obstruction.

2. V/Q mismatch: the most common mechanism in lung disease. Widened A–a gradient. Largely correctable with supplemental oxygen because the abnormal areas still receive some ventilation.

3. Diffusion impairment: thickened alveolar-capillary membrane (ILD, emphysema with destroyed surface area, pulmonary vascular disease). Normal at rest with reserve, becomes apparent on exercise as cardiac output rises and pulmonary capillary transit time falls below the time required for equilibration. Largely correctable with supplemental oxygen.

4. Intrapulmonary shunt: blood traverses the pulmonary circulation without contacting ventilated alveoli. Definition: PO₂ of shunted blood equals mixed venous PO₂ (~40 mmHg). The 100% O₂ test discriminates shunt from V/Q mismatch — true shunt does not correct. Causes: collapse, consolidation, AVMs, intracardiac right-to-left shunt.

5. Low inspired oxygen: altitude, equipment failure. A–a gradient normal.

Diffusing capacity for carbon monoxide (DLCO / TLCO)

The single-breath DLCO method is standardised by the 2017 ATS/ERS technical statement (Graham and colleagues) [8]. The patient inhales a gas mixture containing 10% helium (tracer) and 0.3% carbon monoxide (low concentration, safe at single-breath dose) from RV to TLC, breath-holds for 10 seconds, and exhales. Carbon monoxide diffuses across the alveolar-capillary membrane during the breath-hold; the rate of CO uptake reflects gas transfer capacity. Helium dilution corrects for distribution volume.

DLCO is reduced by any process that destroys or thickens the alveolar-capillary interface: emphysema (destroyed alveolar surface area), interstitial lung disease (thickened membrane), pulmonary vascular disease (reduced capillary blood volume), pulmonary embolism (acute reduction in perfused capillary bed), anaemia (reduced haemoglobin available to bind CO), and prior lung resection (reduced absolute lung tissue).

The DLCO/V_A ratio (also called K_CO) partitions parenchymal disease from volume reduction. A reduced DLCO with proportionately reduced V_A and preserved K_CO suggests volume loss without parenchymal disease — consistent with prior resection or chest wall restriction. A reduced DLCO with reduced K_CO indicates parenchymal pathology — emphysema, ILD, or pulmonary vascular disease.

In the 2025 ERS/ESTS framework [2], ppoDLCO is categorised into three risk tiers:

ppoDLCO category	Pre-operative risk profile
≥ 60%	Normal risk — mortality and morbidity baseline
40 – 59%	Moderate risk — warrants integrated functional assessment, low-tech exercise testing or CPET, MDT review
< 40%	High risk — informed consent conversation about increased mortality and morbidity; quantitative VQ SPECT often refines the picture; sublobar resection considered where oncologically appropriate

The 2025 panel notes that evidence on the clinical relevance of specific ppoFEV₁ thresholds remains limited, and warns explicitly against using ppoFEV₁ as the sole stratifier of operative risk — particularly in COPD, where simple segment-counting overestimates the functional cost of resection. ppoDLCO carries more discriminative weight than ppoFEV₁ in this group.

5. The functional algorithm — three-framework convergence

The historical approach was a stepwise algorithm with binary cutoffs — if ppoFEV₁ below threshold A, do test B; if test B below threshold C, surgery contraindicated. The contemporary approach reads the same data as a constellation. The thresholds are still useful as anchors, but they identify risk categories rather than fitness or unfitness.

Quantitative ventilation-perfusion SPECT

Quantitative VQ SPECT measures the actual perfusion contribution of each lobe and segment, derived from regional tracer uptake. The corrected ppoFEV₁ and ppoDLCO calculated from SPECT-derived perfusion fractions are routinely higher than segment-counting estimates in heterogeneous emphysema, because the destroyed lobes contribute far less than their segment count would predict. In selected patients, quantitative VQ SPECT shifts a borderline candidate from the "unfit" to the "fit" category — without changing any underlying physiology, simply by reading the data accurately.

In our practice this is the imaging that anchors the combined cancer-and-LVRS pathway described in section 7. Without quantitative perfusion mapping, segment-counting will routinely deny surgery to patients in whom the operation will, in fact, improve their breathing. With it, the calculation can be done properly.

The low-technology exercise battery (2025 update)

The 2025 ERS/ESTS guideline formalises a battery of low-technology exercise tests as legitimate stratification tools alongside CPET: 6-minute walk test, incremental shuttle walk test, stair climbing test, and the BODE composite score. The panel notes that evidence is too limited to recommend specific cutoffs across all tests, but proposes anchors: 6MWT distance below 400 m, ISWT distance below 400 m, and stair climb below 12 metres of vertical climb (typically ~3–4 standard storeys, depending on storey height) all signal increased peri-operative risk and warrant escalated assessment. The combined picture — not any single test — is the basis for stratification.

6. Cardiac assessment for thoracic surgery

Clinical history and red flags

The pre-operative cardiac history is not a checklist exercise. The questions earn their place because each finding shifts the assessment pathway and, in some cases, the surgical timing.

Ischaemic heart disease: stable angina (Canadian Cardiovascular Society I–IV classification frames severity); unstable symptoms or recent acute coronary syndrome (within 60 days defers elective surgery in 2024 AHA/ACC); previous percutaneous coronary intervention (timing of stent — bare-metal versus drug-eluting — drives dual antiplatelet therapy duration and the safe peri-operative window); prior coronary artery bypass surgery (graft patency relevant if symptoms have returned). Heart failure: HFrEF, HFpEF, or HFmrEF — distinct entities with distinct optimisation; recent decompensation is the strongest non-procedural predictor of peri-operative cardiac events. Arrhythmia: atrial fibrillation (rate or rhythm controlled, anticoagulation status), high-grade AV block, ventricular ectopy, prior implantable cardioverter-defibrillator or pacemaker. Valvular signs: exertional syncope, classical aortic stenosis murmur, pansystolic mitral regurgitation murmur, peripheral oedema with raised jugular venous pressure. Functional capacity: not what the patient says — what the patient does. Climbing stairs, household activity, breathlessness threshold; supplemented by structured measures where doubt exists.

Risk calculators and functional capacity

Two risk calculators are routinely used. The Revised Cardiac Risk Index (Lee 1999) — six clinical variables, decades of validation. The American College of Surgeons NSQIP MICA calculator (Gupta 2011) — incorporates surgery type, age, ASA status, and creatinine, with more contemporary validation. Both are recommended; neither alone is sufficient. Both should inform the integrated risk picture.

Functional capacity is the single most important non-cardiac variable. The threshold is 4 metabolic equivalents (METs) — the energy cost of light housework or climbing one flight of stairs. Above 4 METs and asymptomatic, peri-operative cardiac risk is generally low even with structural disease. Below 4 METs, or where capacity cannot be assessed, the test choice escalates. Self-reported METs are unreliable: the METS-CABG study (Wijeysundera, Lancet 2018) demonstrated poor correlation between subjective MET estimates and measured peak VO₂. The Duke Activity Status Index (DASI) outperformed self-reported METs and correlates with peak VO₂; a DASI score ≤34 identifies poor functional capacity warranting further investigation.

Non-invasive cardiac investigations

Each investigation answers a specific question. Tests are ordered in sequence, not in parallel — each only earns its place if the result will change management. The 2024 AHA/ACC and 2022 ESC perioperative guidelines are explicit on this: tests judiciously, only when results inform decisions.

Investigation	What it answers	Notes and limitations
Transthoracic echo (TTE)	LV systolic and diastolic function, valvular disease, estimated pulmonary pressures, RV function	First-line; operator-dependent; image quality limited in obese or hyperinflated chests
Stress echo (dobutamine or exercise)	Inducible regional wall motion abnormality, territorial localisation	Useful where exercise is feasible; limited in three-vessel disease (balanced ischaemia) and left bundle branch block
Myocardial perfusion scan (MPS / SPECT)	Reversible perfusion defects, attenuation-corrected territorial assessment	Most validated test for peri-operative risk; vasodilator stress where exercise infeasible; radiation; attenuation artefact in obesity and breast tissue
Stress cardiac MRI with gadolinium	Inducible perfusion defects, late gadolinium enhancement (scar), RV function, valvular morphology — integrated in a single study	Increasingly first-line in UK tertiary centres; no ionising radiation; gadolinium considerations in renal impairment; pacemaker compatibility
CT coronary angiography (CTCA)	Anatomical coronary assessment with high negative predictive value	Role expanded in 2022 ESC and 2024 AHA/ACC for selected patients with suspected coronary artery disease; iodinated contrast and radiation; image quality limited by heavy calcification
Coronary calcium score (CACS)	Calcified plaque burden as risk marker	Adjunct to CTCA or stand-alone risk reclassification; not a substitute for ischaemia testing
Cardiac-protocol CPET	Integrated cardiopulmonary fitness with continuous twelve-lead ECG (and sometimes echocardiographic) monitoring during exercise	Specialist test for established cardiac disease being considered for major surgery; arranged in collaboration with cardiology; not a substitute for dedicated stress imaging

When invasive coronary angiography is indicated

A positive ischaemia test does not automatically lead to invasive coronary angiography. The trigger is clinically significant inducible ischaemia — defined by extent (large or multi-territorial defect), severity (low-threshold ischaemia, reduced LV ejection fraction, transient cavity dilatation), or symptomatic correlation (typical angina or breathlessness reproduced at low workload). Small, unifocal reversible defects in asymptomatic patients with preserved LV function may not change management for the planned surgery and do not necessarily warrant invasive workup pre-operatively.

Where the ischaemia signal does meet the trigger, the conversation is heart-team — interventional cardiology, surgical cardiology, thoracic surgery, anaesthesia. Two principles set by the 2022 ESC and 2024 AHA/ACC guidelines apply. First, pre-operative coronary revascularisation is indicated only where it is independently indicated by the cardiac findings — not as a peri-operative protective intervention alone. The CARP and DECREASE-V trials demonstrated no survival benefit from prophylactic pre-NCS revascularisation in stable coronary disease without independent indication. Second, surgical urgency frames the decision: a small lung nodule on surveillance can wait for revascularisation and antiplatelet stabilisation; an aggressive locally-advanced cancer cannot, and the timing trade-off is taken at the heart-team and chest MDT together. Recent stenting drives antiplatelet duration: dual antiplatelet therapy is generally continued for at least one month after bare-metal stent and at least three to six months after drug-eluting stent in the contemporary literature, with elective surgery deferred where feasible.

Valvular heart disease

The 2021 ESC/EACTS guidelines for the management of valvular heart disease [12] anchor pre-operative valvular assessment, with a dedicated algorithm for severe aortic stenosis and non-cardiac surgery. Severe aortic stenosis is the highest-risk valvular lesion in non-cardiac surgery; symptomatic severe AS unaccompanied by valve intervention substantially increases peri-operative mortality and morbidity. Where severe AS is identified pre-operatively in a patient otherwise fit for lung resection, the heart-team discussion considers transcatheter aortic valve implantation (TAVI) or surgical aortic valve replacement before lung surgery, or balloon aortic valvuloplasty as a bridge in time-critical cancer surgery. Severe primary mitral regurgitation, severe aortic regurgitation, and clinically significant rheumatic mitral stenosis carry their own peri-operative profiles and management algorithms; the principle is consistent — valvular disease is identified, classified, and integrated into the heart-team plan rather than discovered intraoperatively.

Patients with mechanical heart valves require structured anticoagulation bridging, balanced against bleeding risk. Bioprosthetic valves and patients with atrial fibrillation on direct oral anticoagulants follow distinct peri-operative algorithms that are best agreed in advance with the cardiology and anaesthetic teams.

Pulmonary hypertension

Pulmonary hypertension is the cardiopulmonary diagnosis at which respiratory and cardiac assessment converge most tightly. The 2022 ESC/ERS pulmonary hypertension guidelines (Humbert, Kovacs, Hoeper) [13] redefined PH as mean pulmonary arterial pressure (mPAP) >20 mmHg at rest, measured at right heart catheterisation — a threshold lowered from the previous ≥25 mmHg. Pre-capillary PH is now defined by mPAP >20 mmHg with pulmonary vascular resistance >2 Wood units (also lowered from >3) and pulmonary arterial wedge pressure ≤15 mmHg.

The five clinical groups remain: (1) pulmonary arterial hypertension; (2) PH associated with left heart disease; (3) PH associated with lung diseases or hypoxia; (4) PH due to pulmonary artery obstructions, including chronic thromboembolic pulmonary hypertension (CTEPH); (5) unclear or multifactorial. Group 3 PH — the cohort thoracic surgeons see most — is largely driven by COPD, interstitial lung disease, and combined pulmonary fibrosis-emphysema. Right heart catheterisation is the diagnostic gold standard; transthoracic echocardiography provides screening estimates of pulmonary artery systolic pressure (PASP).

The American Heart Association Scientific Statement on PH in non-cardiac surgery [14] provides the contemporary peri-operative framework. Risk markers specifically validated in the lung-resection literature:

Marker	Adverse threshold	Source
PASP on TTE	>40 mmHg	ACOSOG Z4032 / Z4033 lung cancer trials
mPAP at right heart catheterisation	>35 mmHg, particularly >40 mmHg	ESC/ERS 2022 risk stratification
6-minute walk distance	<400 m	British Journal of Anaesthesia expert consensus 2021
Serum NT-proBNP / BNP	Elevated, with risk-table-defined cut-offs	ESC/ERS 2022
Right ventricular function (TAPSE on TTE)	<17 mm	ESC/ERS 2022
Right atrial pressure (RHC)	>7 mmHg	ESC/ERS 2022
CMR-derived RV ejection fraction	<35%	Increasing prognostic literature; integrated in 2022 ESC/ERS risk table

Group 3 PH does not preclude lung resection but stratifies risk meaningfully. Patients with established PH on targeted therapy (prostacyclins, phosphodiesterase-5 inhibitors, endothelin receptor antagonists) are managed in coordination with the pulmonary hypertension service; therapy is generally continued through the peri-operative period. Sublobar resection is considered over lobectomy where oncologically appropriate, to limit the post-operative pulmonary vascular load. Anaesthetic strategy includes avoidance of hypoxaemia and hypercapnia (both raise pulmonary vascular resistance), careful fluid management, and contingency planning for inhaled pulmonary vasodilator (nitric oxide, iloprost) escalation. CTEPH — group 4 PH — warrants pulmonary endarterectomy assessment via the national CTEPH service at the Royal Papworth Hospital before elective non-cardiac surgery is undertaken.

Optimisation and the multidisciplinary decision

The closing step is integration. Significant cardiac disease is optimised on contemporary therapy first — guideline-directed medical therapy for heart failure, anti-anginal therapy, anticoagulation review, blood pressure control, statin and SGLT2 inhibitor where indicated. Re-stratification follows optimisation. The lung-cancer surgical decision is then taken at the chest multidisciplinary team meeting with cardiology input — formally for patients with significant cardiac comorbidity, informally as a heart-team-and-chest-MDT integration where the disease and timing demand it. Lung resection is not declined on cardiac comorbidity alone. The integrated pre-operative pathway in section 9 describes how this works in private practice and at GSTT.

7. Cardiopulmonary exercise testing (CPET)

CPET is the integrated test. It measures cardiac, pulmonary, and peripheral oxygen utilisation simultaneously during graduated exercise on a cycle ergometer, with continuous breath-by-breath gas analysis and ECG. No other test in the pre-operative battery interrogates cardiopulmonary fitness as a unified physiology.

The Fick principle

The fundamental equation is VO₂ = cardiac output × (CaO₂ − CvO₂), equivalent to VO₂ = HR × SV × O₂ extraction. Maximal oxygen uptake (VO₂ max) thus integrates heart rate response, stroke volume, peripheral oxygen extraction, and gas exchange capacity into one number. A reduced VO₂ max can be due to any limb of this equation — which is why CPET also resolves the question of which limb is the limiter.

Thresholds for major lung resection

VO2 max	Risk profile and surgical implication
> 20 mL/kg/min	Low risk — suitable for major resection including pneumonectomy
15–20 mL/kg/min	Low-to-intermediate risk — lobectomy generally appropriate; further stratification by VE/VCO2 slope
10–15 mL/kg/min	Intermediate risk — sublobar resection considered over lobectomy. NICE NG122 places this group in the lobectomy-with-caution band
< 10 mL/kg/min	High risk — alternative therapies (SBRT, ablation, systemic) usually appropriate; surgery only after very explicit consent and MDT consensus

VE/VCO₂ slope — the additional discriminator

The minute ventilation to carbon dioxide output relationship reflects ventilatory efficiency. A high VE/VCO₂ slope — specifically above 35 — identifies patients with impaired ventilatory efficiency and is now recognised as an independent predictor of peri-operative mortality and morbidity that adds discriminative power in the 10–20 mL/kg/min VO₂ max range. Where VO₂ max alone places a patient in an intermediate band, VE/VCO₂ slope sub-stratifies: above 35 indicates intermediate-high risk, below 35 indicates intermediate-low risk. The 2025 ERS/ESTS framework integrates this measurement explicitly.

Cardiac versus pulmonary limit identification

CPET also discriminates the cause of exercise limitation. Reaching the predicted heart rate with reserve in pulmonary parameters and a high respiratory exchange ratio (RER > 1.05) suggests cardiac limitation. Reaching the ventilatory limit (breathing reserve below 30%) with heart rate reserve and a normal RER suggests pulmonary limitation. Where both limits are reached simultaneously, the limit is the lower of the two reserves. A patient assumed to have pulmonary-limited exercise tolerance who shows clear cardiac limitation on CPET requires cardiology liaison before any final surgical decision — the calculation changes once the limiting organ is identified accurately.

Cardiac-protocol CPET

For patients with established coronary or valvular disease, CPET can be conducted with continuous twelve-lead ECG monitoring and combined echocardiographic surveillance, providing simultaneous functional capacity and dynamic cardiac assessment. This is the appropriate test in patients where stress echocardiography or myocardial perfusion imaging has identified inducible ischaemia or moderate valvular disease and the question is whether the patient’s integrated cardiopulmonary reserve permits surgery. CPET in these patients is arranged in collaboration with the cardiology service.

8. Disease-specific assessment — severe COPD and IPF

Severe COPD — GOLD III/IV with cancer

Patients with FEV₁ below 50% predicted (GOLD III), and especially those below 30% (GOLD IV), have for decades been routinely declined surgical resection by units reading lung function in isolation. The contemporary frameworks reject this. Three physiological features of severe COPD invalidate simple segment-counting approaches.

Dynamic hyperinflation: in severe COPD, expiratory flow limitation prevents complete exhalation between breaths. End-expiratory lung volume rises, intrinsic PEEP develops, and the diaphragm becomes flat and mechanically disadvantaged. Resting FEV₁ measured in the laboratory captures this state; the patient cannot relieve it, but the operation can — if the resected lobe is contributing primarily to hyperinflation rather than to gas exchange.

Heterogeneous destruction: emphysematous destruction is rarely uniform across the lung. Heavily destroyed lobes contribute little to ventilation or perfusion. Segment-counting treats every segment as equivalent — in heterogeneous disease this is wrong.

Reduced diaphragmatic excursion: hyperinflated lung pushes the diaphragm down and flat. Mechanical efficiency falls; the work of breathing rises. Removing destroyed lung allows the remaining diaphragm to recover normal curvature, with disproportionate functional improvement.

The combined cancer-and-LVRS pathway

Where a lung cancer is located within heavily destroyed emphysematous lung, the surgical resection performed for cancer cure delivers a lung volume reduction effect simultaneously. This is not theoretical. It was first described by Cooper and colleagues in 1998 (Journal of Thoracic and Cardiovascular Surgery), built on Cooper’s foundational 1996 series of 150 consecutive bilateral lung volume reduction procedures [5], and formally established in a 21-patient series by Choong, Meyers, Battafarano, Guthrie, Davis, Patterson, and Cooper in 2004 [6]. That series reported no hospital deaths, 100% one-year survival, and improved lung function in every patient measured at follow-up. Subsequent series have replicated these findings.

Patient selection rests on three imaging-led decisions:

1. High-resolution CT of the chest — mapping the distribution of emphysematous destruction. The pattern must be heterogeneous — concentrated in one or two zones rather than uniform across all lobes. Predominantly upper-lobe disease is the classical NETT-validated pattern; lower-lobe-predominant disease has been reported but is less common.

2. Quantitative ventilation-perfusion SPECT — confirming which lobes contribute meaningfully to gas exchange and which are functional dead space. The cancer should be located in lung that is already poorly perfused; the remaining lobes should hold sufficient functional reserve to support post-operative respiration.

3. Pulmonary function and exercise testing — spirometry, DLCO, lung volumes, and where indicated CPET, to anchor the predicted post-operative function calculation against quantitative perfusion data rather than segment counting.

Where all three converge, the pathway delivers curative cancer surgery and improvement in measured lung function. Selected patients leave the operation with better FEV₁ than they had before. The operation is performed by robotic or VATS keyhole approach to preserve chest wall function and minimise the additional respiratory cost of thoracotomy. In selected cases, a combined cancer resection plus additional lung volume reduction in a separate, more destroyed lobe is performed at the same operation.

At GSTT, this is the pathway Mr Okiror leads as the Trust’s sole designated lung volume reduction surgery and endobronchial valve operator. The Advanced Emphysema multidisciplinary team meeting reviews these cases monthly. The same pathway is available privately at London Bridge Hospital. Emphysema surgery in 2026 — clinician reference →

Idiopathic pulmonary fibrosis — the reverse trap

IPF and the broader UIP pattern present the inverse problem to severe COPD. Spirometry can be deceptively preserved in early disease — the FVC/TLC may be reduced in proportion, but the FEV₁/FVC ratio remains normal or raised because there is no airflow obstruction. Reading spirometry alone, an IPF patient can appear "well preserved." DLCO tells the truer story.

In IPF, DLCO is markedly and disproportionately reduced — often the earliest and most severely affected functional parameter, falling below 40% predicted while FVC remains in the 70–80% range. The reverse trap is the patient with apparently preserved FVC and a DLCO below 40%. Operative risk in this group is substantially higher than the FVC alone would suggest, and the consent conversation must be explicit.

The peri-operative concern in IPF is not solely the immediate surgical mortality — it is the recognised risk of acute exacerbation of IPF following thoracic surgery. Published series report acute exacerbation incidence of 5–15% in the first month following lobectomy in patients with established IPF, with case fatality of 50–100% when exacerbation occurs. The cumulative published mortality attributable to peri-operative IPF exacerbation is 10–30%, depending on the cohort and the resection extent. Sublobar resection — segmentectomy or wedge — appears to carry lower exacerbation risk than lobectomy and is generally preferred where oncologically appropriate.

Where surgery is offered, the decision is taken jointly with the interstitial lung disease team. Anti-fibrotic therapy (pirfenidone or nintedanib) is reviewed at consultation; in some series, perioperative anti-fibrotic continuation has been associated with lower exacerbation rates, though high-quality randomised evidence is limited. Anaesthetic strategy includes lung-protective ventilation and avoidance of high inspired oxygen concentrations where possible. The MDT discussion is the substrate for the consent conversation, not a substitute for it.

9. The integrated pre-operative pathway

The tests do not exist in isolation. They are sequenced into a workflow whose purpose is to deliver a clear surgical recommendation to the patient and the multidisciplinary team within a clinically appropriate timeframe.

Sequence at first consultation

At first attendance, the candidate’s scans, prior lung function, and clinical letters are reviewed. Spirometry and DLCO are organised the same day if not already performed within the past three months. The clinical examination includes resting oxygen saturation, a short walk test where appropriate, and a focused respiratory and cardiac history. A surgical recommendation is given at this consultation where the data are sufficient. Where additional testing is required, the next decision point is scheduled, typically within two weeks for self-pay or insured patients.

Reflex CPET

CPET is reflex-ordered when initial spirometry or DLCO is borderline (typically when ppoFEV₁ or ppoDLCO falls below 60% predicted), when the limit on exercise tolerance cannot be attributed clearly to a cardiac or pulmonary cause, or when established cardiac disease requires cardiac-protocol CPET in collaboration with cardiology. CPET is organised at London Bridge Hospital where indicated, with results typically available within one to two weeks of the first consultation.

Quantitative VQ SPECT

Quantitative VQ SPECT is added when the patient has significant COPD or emphysema, when the cancer is located in heavily destroyed lung on HRCT, or when standard ppoFEV₁ calculation places the patient in a marginal category and segment-counting may be misrepresenting the real functional cost of resection. The output is a corrected ppoFEV₁ and ppoDLCO calculated from regional perfusion data — routinely higher than segment-counting estimates in heterogeneous disease.

Cardiology liaison

Cardiology liaison is integrated where indicated by history, ECG, or echocardiography — the structured framework for this assessment is in section 6. The high-risk multidisciplinary team coordinates the liaison as part of the pre-operative pathway. Patients with significant cardiac comorbidity proceed to lung cancer surgery once the cardiac assessment is optimised and re-stratified.

Prehabilitation

Pre-operative optimisation runs in parallel where indicated. The framework is set by the Centre for Perioperative Care POPS guideline (2021) and the Manchester Prehab4Cancer programme (Bradley and colleagues 2022). Standard window is two to six weeks for elective surgery. Patients receiving chemoimmunotherapy before surgery are referred for prehab in parallel with the oncology pathway, so surgery is not delayed. Patient-facing fitness page covers this in detail →

Multidisciplinary review

Every cancer case is discussed at the chest multidisciplinary team meeting before any operation proceeds — the GSTT chest MDT for NHS patients, the London Bridge Hospital chest MDT for private patients. No treatment plan is made by a single doctor. The MDT discussion is the substrate for the consent conversation, where the integrated risk picture is presented and the patient’s preference, expectation, and acceptance of risk shape the final decision.

Non-surgical alternatives

Where the integrated assessment places the patient in the highest peri-operative risk band, or where surgery is declined after risk-stratified informed consent, the non-surgical pathway is structured rather than residual. Stereotactic ablative body radiotherapy (SABR/SBRT) for stage I peripheral disease, percutaneous ablation (radiofrequency, microwave, or cryoablation) for selected small tumours, and systemic therapy where stage or biology dictates — these are valid curative-intent or disease-modifying options, not consolation prizes. The MDT discussion identifies which alternative is appropriate; the assessment that delivered the surgical "no" is not redundant — it informs the choice of the next pathway.

References

1. National Institute for Health and Care Excellence. Lung cancer: diagnosis and management. NICE guideline NG122. Last updated 8 March 2024. https://www.nice.org.uk/guidance/ng122
2. Brunelli A, Hardavella G, Huber RM, et al. European Respiratory Society and European Society of Thoracic Surgeons clinical practice guideline on fitness for curative intent treatment of lung cancer. Eur Respir J 2025;66(5):2500156. DOI: 10.1183/13993003.00156-2025. Concurrent publication: Eur J Cardiothorac Surg 2025;67(11):ezaf329.
3. Brunelli A, Charloux A, Bolliger CT, et al; European Respiratory Society and European Society of Thoracic Surgeons joint task force on fitness for radical therapy. ERS/ESTS clinical guidelines on fitness for radical therapy in lung cancer patients (surgery and chemo-radiotherapy). Eur Respir J 2009;34(1):17–41. PMID 19567600. (Foundational 2009 guideline; superseded by reference 2.)
4. Brunelli A, Kim AW, Berger KI, Addrizzo-Harris DJ. Physiologic evaluation of the patient with lung cancer being considered for resectional surgery: diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest 2013;143(5 Suppl):e166S–e190S. DOI: 10.1378/chest.12-2395.
5. Cooper JD, Patterson GA, Sundaresan RS, Trulock EP, Yusen RD, Pohl MS, Lefrak SS. Results of 150 consecutive bilateral lung volume reduction procedures in patients with severe emphysema. J Thorac Cardiovasc Surg 1996;112(5):1319–30. PMID 8911330. (Foundational LVRS series; combined LVRS-and-cancer practice subsequently described by Cooper and colleagues 1998.)
6. Choong CK, Meyers BF, Battafarano RJ, Guthrie TJ, Davis GE, Patterson GA, Cooper JD. Lung cancer resection combined with lung volume reduction in patients with severe emphysema. J Thorac Cardiovasc Surg 2004;127(5):1323–31. PMID 15115988.
7. Batchelor TJP, Rasburn NJ, Abdelnour-Berchtold E, Brunelli A, Cerfolio RJ, Gonzalez M, et al. Guidelines for enhanced recovery after lung surgery: recommendations of the Enhanced Recovery After Surgery (ERAS) Society and the European Society of Thoracic Surgeons (ESTS). Eur J Cardiothorac Surg 2019;55(1):91–115. PMID 30304509.
8. Graham BL, Brusasco V, Burgos F, Cooper BG, Jensen R, Kendrick A, et al. 2017 ERS/ATS standards for single-breath carbon monoxide uptake in the lung. Eur Respir J 2017;49(1):1600016. PMID 28049168.
9. Society for Cardiothoracic Surgery in Great Britain and Ireland. SCTS National Thoracic Surgery Audit 2024–25. Operative outcomes data including Guy’s and St Thomas’ NHS Foundation Trust.
10. Thompson A, Fleisher LA, Beckman JA, et al. 2024 AHA/ACC/ACS/ASNC/HRS/SCA/SCCT/SCMR/SVM Guideline for Perioperative Cardiovascular Management for Noncardiac Surgery: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 2024;150(19):e351–e442. PMID 39316661. (Multi-society perioperative cardiac assessment guideline; supersedes 2014 ACC/AHA.)
11. Halvorsen S, Mehilli J, Cassese S, Hall TS, Abdelhamid M, Barbato E, et al. 2022 ESC Guidelines on cardiovascular assessment and management of patients undergoing non-cardiac surgery. Eur Heart J 2022;43(39):3826–3924. DOI: 10.1093/eurheartj/ehac270. PMID 36017553.
12. Vahanian A, Beyersdorf F, Praz F, Milojevic M, Baldus S, Bauersachs J, et al. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J 2022;43(7):561–632. DOI: 10.1093/eurheartj/ehab395. PMID 34453165.
13. Humbert M, Kovacs G, Hoeper MM, Badagliacca R, Berger RMF, Brida M, et al. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart J 2022;43(38):3618–3731. DOI: 10.1093/eurheartj/ehac237. PMID 36017548. (mPAP >20 mmHg threshold; PVR >2 Wood units; five-group classification preserved.)
14. American Heart Association. Evaluation and Management of Pulmonary Hypertension in Noncardiac Surgery: A Scientific Statement From the American Heart Association. Circulation 2023. (Contemporary peri-operative framework for PH in NCS; risk markers and group-specific management.)

Frequently asked questions