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Most cardiorespiratory patients arrive with a page of blood results already taken. This guide covers the handful that genuinely alter management — the inflammatory markers, the cardiac markers, the clotting marker used to exclude clot, and the everyday chemistry that decides whether a session is safe to run — and, just as usefully, which results do not mean what they are often taken to mean.
Full blood count
The FBC is ordered on almost everyone and read closely on almost no one. Four values matter in cardiorespiratory practice.
| Value | What it changes |
|---|---|
| Haemoglobin | Anaemia is one of the most commonly missed causes of exertional breathlessness, and it is correctable. It also caps what exercise training can achieve — a patient plateauing in rehabilitation with an unexplained ceiling deserves an FBC before the programme is blamed. Conversely, a raised haemoglobin and haematocrit in a chronically hypoxaemic patient (secondary erythrocytosis) is a marker of sustained desaturation and should prompt oximetry, including overnight and on exertion. |
| White cell count | Useful mainly for its trend. A normal WCC does not exclude infection in the frail or the immunosuppressed, and a raised WCC with a neutrophilia is entirely expected for 24–48 hours after surgery or a course of oral corticosteroids. |
| Eosinophils | The single most actionable line on the FBC in airways disease — it now guides inhaled corticosteroid decisions in COPD and biologic eligibility in asthma. Covered in full on the allergy and eosinophil testing page. |
| Platelets | Relevant before manual techniques and before mobilising a patient on therapeutic anticoagulation. Thrombocytopenia is common in critical illness and in liver disease; check local thresholds before percussion, vigorous manual techniques or resisted exercise. |
Inflammatory markers
CRP rises within 6–8 hours of an inflammatory stimulus and peaks around 48 hours, which makes the trajectory more informative than any single value. It is exquisitely sensitive and entirely non-specific: surgery, exacerbation, infection, infarction, malignancy and autoimmune disease all raise it. A falling CRP during an admission is reassuring; a CRP that plateaus or climbs on day 3–4 post-operatively is a genuine prompt to look for a complication — and retained secretions with lobar collapse is one of them.
ESR moves slowly and is now rarely more useful than CRP, with the exception of some connective tissue disease and vasculitis.
Procalcitonin rises more specifically with bacterial infection and is used in some services to shorten antibiotic courses in respiratory infection; a Cochrane review found this reduces antibiotic exposure without increasing mortality.1 It is not a physiotherapy decision, but a falling procalcitonin explains why antibiotics were stopped while the patient still sounds wet.
Natriuretic peptides — BNP and NT-proBNP
These are the most useful blood tests in the differential of breathlessness, because they are far better at excluding heart failure than at confirming it.2,3 In an untreated patient with a normal level, chronic heart failure is very unlikely and another explanation should be sought.
| Context | Threshold | Action |
|---|---|---|
| Rule out chronic HF (ESC, non-acute) | NT-proBNP <125 pg/mL; BNP <35 pg/mL | Heart failure unlikely — look elsewhere3 |
| Suspected HF (NICE) | NT-proBNP 400–2000 ng/L | Specialist assessment and echocardiography within 6 weeks2 |
| Suspected HF (NICE) | NT-proBNP >2000 ng/L | Urgent — within 2 weeks; higher levels carry a worse prognosis2 |
What raises it other than heart failure: age, atrial fibrillation, renal impairment, pulmonary embolism, pulmonary hypertension, sepsis and right heart strain from any cause. What lowers it: obesity — a substantial effect, so a mid-range result in a patient with a high BMI should be treated with more suspicion, not less.3
Levels also fall with effective treatment, which is why a rising NT-proBNP in a known heart failure patient is a decompensation signal worth acting on before the weight chart moves.
Troponin
High-sensitivity troponin is a marker of myocardial injury, not of myocardial infarction. Infarction requires a rise and/or fall around the 99th percentile upper reference limit together with clinical evidence of ischaemia.4 Contemporary assays permit rapid 0/1-hour rule-out and rule-in algorithms in the emergency department.5
The practical point for physiotherapy is the long list of non-coronary causes: pulmonary embolism, heart failure, myocarditis, sepsis, renal impairment, arrhythmia, and prolonged strenuous exercise. A mildly raised troponin in an unwell inpatient usually reflects demand ischaemia or strain rather than a blocked artery — but the distinction is a medical one, and any new or unexplained rise means the session waits until it has been reviewed.
D-dimer
D-dimer is a rule-out test and nothing else. Its value lies in a high negative predictive value when combined with a validated clinical probability score (Wells, revised Geneva) in patients assessed as non-high probability — in whom a negative result safely excludes pulmonary embolism without imaging.6
An age-adjusted threshold (age × 10 µg/L FEU in patients over 50) increases specificity without increasing missed events, and reduces the number of patients sent for CTPA.7
It rises with almost anything: surgery, trauma, pregnancy, infection, malignancy, age, and any recent inflammatory event. A positive D-dimer in a post-operative patient is close to uninformative — which is precisely why it should not be ordered in a patient with a high pre-test probability, where imaging is indicated regardless.
Everyday chemistry that changes a session
- Potassium. Beta-2 agonists drive potassium intracellularly; combined with diuretics, hypokalaemia is common and arrhythmogenic. Check it before a supervised exercise test in a diuretic-treated heart failure patient.
- Sodium. Hyponatraemia in heart failure is a marker of severity and of poor prognosis, and it causes fatigue and confusion that will be blamed on deconditioning.
- Urea and creatinine. Rising values during diuresis change the fluid plan, and they change what a natriuretic peptide means.
- Magnesium and phosphate. Both are needed for respiratory muscle function; low phosphate in the refed or critically ill patient contributes directly to weaning failure.
- Glucose and HbA1c. Relevant to exercise prescription, to wound healing after thoracic surgery, and to infection risk.
Alpha-1 antitrypsin — the one-off test that is still missed
GOLD recommends that every patient with a diagnosis of COPD is tested once for alpha-1 antitrypsin deficiency.8 It remains substantially under-diagnosed, and the diagnosis changes family screening, occupational counselling and, in selected patients, access to augmentation therapy. Suspect it particularly with early-onset disease, basal-predominant emphysema, minimal smoking history, a family history, or unexplained liver disease. See alpha-1 antitrypsin deficiency.
Reference ranges at a glance
Consolidating the values discussed above. Ranges are laboratory-specific — the interval printed on the report by the reporting laboratory always takes precedence over any table, including this one. Adult values; paediatric and pregnancy ranges differ throughout.
| Test | Typical adult range | Reading it in practice |
|---|---|---|
| Full blood count | ||
| Haemoglobin | Male 130–180 g/L Female 115–165 g/L | Low: a correctable cause of exertional breathlessness and a ceiling on training gains. High: consider secondary erythrocytosis from sustained hypoxaemia. |
| White cell count | 4.0–11.0 ×109/L | Read the trend, not the single value. Normal does not exclude infection in the frail or immunosuppressed. |
| Neutrophils | 2.0–7.5 ×109/L | Expected to rise for 24–48 hours after surgery or oral corticosteroids. |
| Eosinophils | 0.0–0.5 ×109/L | Guides inhaled corticosteroid decisions in COPD and biologic eligibility in asthma. The thresholds used are disease-specific, not the reference interval. |
| Platelets | 150–400 ×109/L | Marked thrombocytopenia is a caution for vigorous manual techniques; check local policy. |
| Inflammatory markers | ||
| CRP | <5 mg/L | Rises and falls within hours; the most useful single marker of treatment response. |
| ESR | Age-dependent, broadly <20 mm/h | Slow to move in both directions — a poor guide to today’s state. |
| Procalcitonin | <0.5 µg/L | Where available, supports antibiotic decisions rather than physiotherapy ones. |
| Cardiac markers | ||
| BNP | <100 ng/L makes heart failure unlikely | A rule-out test. Raised values have many causes besides heart failure, including age, renal impairment and atrial fibrillation. |
| NT-proBNP | <125 ng/L rules out chronic heart failure; acute thresholds are age-banded | Use the age band the laboratory reports against, not a single cut-off. |
| Troponin | Assay-specific — use the reporting laboratory’s 99th-centile cut-off | High-sensitivity assays differ by manufacturer and by sex. No universal number exists; the change between serial samples matters more than one value. |
| D-dimer | <500 µg/L FEU, age-adjusted (age × 10) above 50 years | A rule-out test in low pre-test probability only. Raised after surgery, in infection, pregnancy and malignancy. |
| Everyday chemistry | ||
| Sodium | 135–145 mmol/L | Hyponatraemia causes confusion, unsteadiness and falls — relevant before mobilising. |
| Potassium | 3.5–5.2 mmol/L | Both extremes cause weakness and arrhythmia. A common consequence of diuretics. |
| Urea | 3.0–8.0 mmol/L | Rises with dehydration and with gastrointestinal bleeding. |
| Creatinine | Male 60–110 µmol/L Female 45–90 µmol/L | Interpret alongside eGFR and muscle mass — a normal creatinine in a very frail patient can conceal poor function. |
| eGFR | >90 mL/min/1.73m2 | Affects drug clearance, including some antibiotics and contrast decisions. |
| Magnesium | 0.70–1.10 mmol/L | Low magnesium contributes to weakness, cramps and arrhythmia, and blocks potassium correction. |
| Phosphate | 0.75–1.50 mmol/L | Low phosphate directly weakens the diaphragm — check it in failure to wean. |
| Corrected calcium | 2.10–2.60 mmol/L | Both extremes affect neuromuscular function; correct for albumin. |
| Albumin | 35–50 g/L | A marker of nutritional and inflammatory state; low values track with poorer rehabilitation outcomes. |
| Lactate | 0.5–2.2 mmol/L | A rising lactate is a reason to defer exercise and escalate, not to push on. |
| HbA1c | <42 mmol/mol (<6.0%) | Diabetes affects wound healing, infection risk and exercise response. |
| TSH | 0.4–4.0 mIU/L | Both hypo- and hyperthyroidism present as fatigue and exertional breathlessness. |
| Ferritin | Male 30–300 µg/L Female 15–200 µg/L | An acute-phase reactant — a normal value does not exclude iron deficiency during inflammation. |
Two values in this table have no universal range at all. Troponin is assay-specific and NT-proBNP is age-banded, so both must be read against the cut-offs the reporting laboratory prints. Quoting a single number for either is the most common way these tests are misread.
What this means for physiotherapy
- Read haemoglobin before concluding a rehabilitation plateau is effort or motivation.
- Read eosinophils before assuming inhaled therapy is optimised.
- Read the CRP trend, not the CRP, when deciding whether a post-operative chest is deteriorating.
- Read potassium before a maximal test in anyone on a diuretic and a beta-agonist.
- Treat a new troponin or an unexplained natriuretic peptide rise as a reason to pause and ask, not to push on.
References & evidence base
- Schuetz P, Wirz Y, Sager R, et al. Procalcitonin to initiate or discontinue antibiotics in acute respiratory tract infections. Cochrane Database Syst Rev. 2017;10:CD007498.
- National Institute for Health and Care Excellence. Chronic heart failure in adults: diagnosis and management. NICE guideline NG106. London: NICE; 2018 (updated 2024).
- McDonagh TA, Metra M, Adamo M, et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2021;42(36):3599–3726.
- Thygesen K, Alpert JS, Jaffe AS, et al. Fourth Universal Definition of Myocardial Infarction (2018). Eur Heart J. 2019;40(3):237–269.
- Byrne RA, Rossello X, Coughlan JJ, et al. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J. 2023;44(38):3720–3826.
- Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2020;41(4):543–603.
- Righini M, Van Es J, Den Exter PL, et al. Age-adjusted D-dimer cutoff levels to rule out pulmonary embolism: the ADJUST-PE study. JAMA. 2014;311(11):1117–1124.
- Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management and prevention of COPD: 2026 report. GOLD; 2026. Available at: goldcopd.org
References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.
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