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An arterial blood gas, or ABG, is a blood sample taken from an artery — usually at the wrist — that measures how much oxygen and carbon dioxide are in the blood and how acidic the blood has become. It answers two questions a finger probe cannot: whether enough oxygen is getting in, and whether enough carbon dioxide is being blown out. Because it is a needle into an artery it is not done casually, but when someone is very breathless or drowsy it is often the test that decides what happens next. This page explains what the numbers mean, how they are read in order, and how they change physiotherapy treatment.
What an ABG measures
An arterial sample is analysed within minutes for pH, partial pressures of carbon dioxide and oxygen, bicarbonate and base excess, with lactate, haemoglobin, electrolytes and glucose usually reported alongside. Together these separate three questions that bedside observation blurs: oxygenation (is oxygen reaching the blood), ventilation (is carbon dioxide being cleared), and acid–base balance (what the body is doing about it, and for how long).
Reference ranges
| Value | Normal range | What it tells you |
|---|---|---|
| pH | 7.35–7.45 | Net acid–base state — the direction of the primary problem |
| PaCO2 | 35–45 mmHg (4.7–6.0 kPa) | Alveolar ventilation — the respiratory component |
| PaO2 | 80–100 mmHg (10.7–13.3 kPa) on room air | Oxygenation — interpret against inspired oxygen |
| HCO3− | 22–26 mmol/L | Metabolic component — slower to move, so it dates the problem |
| Base excess | −2 to +2 mmol/L | Metabolic acid or base load |
| Lactate | < 2 mmol/L | Tissue perfusion — a rising lactate is a warning independent of the gas |
Australian laboratories report in mmHg or kPa depending on the centre — check the units before interpreting, and note that a venous gas is not interchangeable (venous pH and bicarbonate approximate arterial values, but venous PO2 is meaningless and venous PCO2 runs higher).
A five-step interpretation
- Look at oxygenation first. What is the PaO2, and on how much inspired oxygen? A PaO2 of 75 mmHg on room air is mild; the same value on 60% oxygen is severe. As a rough bedside check, PaO2 should be somewhere near five times the inspired oxygen percentage.
- Read the pH. Below 7.35 is acidaemia, above 7.45 alkalaemia. This tells you which way the primary disturbance is pushing.
- Read the PaCO2. If it moves in the opposite direction to the pH (high CO2 with low pH), the problem is respiratory. If it moves in the same direction, the respiratory system is compensating for something else.
- Read the bicarbonate. If it moves in the same direction as the pH (low bicarbonate with low pH), the problem is metabolic.
- Assess compensation and time course. No compensation means acute; full or partial compensation with a near-normal pH means the process has been present for hours to days. A normal pH with abnormal CO2 and bicarbonate is a chronic, compensated picture — the classic stable hypercapnic COPD gas.
The four primary patterns, and how each compensates
| Pattern | pH | PaCO2 | PaO2 | HCO3− | BE | Typical cause |
|---|---|---|---|---|---|---|
| Respiratory acidosis | ↓ | ↑ primary | ↓ or normal | normal, then ↑ compensating | normal, then ↑ compensating | COPD exacerbation, opioid or sedative excess, neuromuscular weakness, exhaustion |
| Respiratory alkalosis | ↑ | ↓ primary | normal or ↓ | normal, then ↓ compensating | normal, then ↓ compensating | Hyperventilation, pain, anxiety, early pulmonary embolism, sepsis |
| Metabolic acidosis | ↓ | ↓ compensating | usually normal | ↓ primary | ↓ primary (below −2) | Sepsis and lactate, renal failure, diabetic ketoacidosis, diarrhoea |
| Metabolic alkalosis | ↑ | ↑ compensating | usually normal | ↑ primary | ↑ primary (above +2) | Vomiting, diuretics, prolonged nasogastric drainage |
In each row one value is the primary defect and the other is the body compensating for it — marked primary and compensating above. Respiratory compensation is fast (minutes to hours); renal compensation is slow (hours to days), which is why the respiratory rows read normal when acute and shifted when chronic. Compensation moves the pH back toward normal but never overshoots it, so a pH on the wrong side of 7.40 still points at the primary problem.
PaO2 does not classify the disturbance — the pattern is set by pH, PaCO2 and bicarbonate. Oxygenation is assessed separately and always against the inspired oxygen, which is why it is step one of the interpretation above. It is shown here because the two are read off the same gas and the combination is what determines the response.
Oxygenation versus ventilation
This is the distinction that matters most at the bedside, because the two failures need opposite responses. Type 1 (hypoxaemic) failure is a low PaO2 with a normal or low PaCO2 — a gas-exchange problem from shunt or ventilation–perfusion mismatch, seen in pneumonia, pulmonary oedema, atelectasis and ARDS. It responds to oxygen, positioning and recruitment.
Type 2 (hypercapnic) failure is a raised PaCO2, with or without hypoxaemia — a pump problem from inadequate alveolar ventilation, seen in severe COPD, obesity hypoventilation, neuromuscular disease, chest-wall restriction, sedation and respiratory-muscle fatigue. Oxygen alone does not fix it and may worsen it; the treatment is ventilation, which is why NIV exists.
A patient becoming less tachypnoeic while looking worse is not improving. In a tiring patient a falling respiratory rate with a rising PaCO2 and falling pH is impending ventilatory failure. Stop the session, sit them upright, get help — do not reassure yourself with a saturation reading, which can stay acceptable on supplemental oxygen while the CO2 climbs.
Venous blood gases
Venous blood gases (VBGs) have become the default first sample in many emergency departments and wards. They are drawn from an ordinary peripheral cannula or venepuncture, so there is no arterial puncture, no pain, no radial artery risk and no need for a specific credential — and on a point-of-care analyser the result is back in minutes. The clinical question is not whether a VBG is easier, but which numbers on it can be trusted.
What agrees, and what does not
| Value | Agreement with arterial | Use it? |
|---|---|---|
| pH | Very close — venous runs about 0.03–0.04 lower, with tight limits of agreement1 | Yes. Reliable for acidosis and alkalosis |
| Bicarbonate / base excess | Close — venous about 1–2 mmol/L higher | Yes. Reliable for the metabolic picture and for trends |
| Lactate | Good agreement at normal and moderately raised values | Yes for screening; confirm a high value if it will change management |
| Potassium, sodium, glucose, haemoglobin | Clinically usable on a point-of-care analyser | Yes |
| PCO2 | Venous averages roughly 4–6 mmHg higher, but the limits of agreement are wide — an individual value can be several mmHg out in either direction1,2 | Screening only — see below |
| PO2 | No useful relationship to arterial oxygenation whatsoever | No. A venous PO2 says nothing about how well the lung is oxygenating |
The screening rule for CO2
The most useful role of a VBG is to exclude hypercapnia. A venous PCO2 below about 45 mmHg (6 kPa) makes arterial hypercapnia very unlikely — the test is highly sensitive, so a normal venous CO2 is a reasonable rule-out and an arterial sample can often be avoided.3,4
The reverse does not hold. A raised venous PCO2 tells you hypercapnia is possible, not that it is present, and it does not tell you by how much. Where the actual number will drive a decision — starting or titrating NIV, judging whether an acute-on-chronic picture is worsening — take an arterial sample.
There is no venous equivalent of PaO2, and no way to calculate a P/F ratio from a venous sample. If the question is how well is this lung oxygenating, a VBG cannot answer it — use oximetry for a trend and an arterial gas when the number matters. Reading a low venous PO2 as hypoxaemia is a genuine and recurring error.
When an arterial sample is still required
- Assessing oxygenation — any question of hypoxaemic failure, shunt, or a P/F ratio.
- Titrating NIV in acute hypercapnic failure, where the CO2 trend guides the pressures.
- Suspected acute-on-chronic hypercapnia, where the degree of respiratory acidosis determines escalation.
- Critical illness and shock, where precision matters and an arterial line is usually already in place.
- Carbon monoxide poisoning or suspected methaemoglobinaemia — co-oximetry on an arterial sample.
Central and mixed venous samples are a different test
A central venous gas from a jugular or subclavian line agrees more closely with arterial values than a peripheral one, and its oxygen saturation (ScvO2) is used as a marker of the balance between oxygen delivery and consumption. A mixed venous sample from a pulmonary artery catheter (SvO2) does the same more accurately. Neither is a substitute for an arterial gas — they answer a question about perfusion and oxygen extraction, not about lung function.
Pulse oximetry, and where it stops
Oximetry is continuous, painless and repeatable, and it should remain the physiotherapist's routine monitor. But it measures saturation, not partial pressure or ventilation — so it cannot detect hypercapnia at all, it flattens out at the top of the oxyhaemoglobin dissociation curve (a fall from 100 to 95% may represent a large fall in PaO2), and it is unreliable with poor perfusion, movement, dark nail polish, and in carbon monoxide poisoning. Accuracy is also reduced in patients with darker skin pigmentation, with occult hypoxaemia more likely to be missed — a reason to correlate with clinical state rather than trust the number alone.5,6
What an ABG changes in physiotherapy
- It sets the oxygen target. In patients at risk of hypercapnic failure, the target saturation range is 88–92% rather than the usual 92–96%, and an ABG is what confirms which group the patient is in.7
- It identifies the patient for whom NIV is indicated — a respiratory acidosis with pH below 7.35 and a raised PaCO2 in an exacerbation of COPD is the strongest single indication in respiratory medicine.8
- It tells you whether treatment worked. A repeat gas after an hour of NIV, positioning or clearance is objective evidence in a way that the patient's appearance is not.
- It flags who should not be exercised. An uncompensated acidosis, a rising lactate or a rapidly worsening gas is a reason to defer mobilisation and escalate.
- It contextualises exertional desaturation in chronic disease, where a baseline gas explains why a patient sits at 90% and why that is not an emergency.
Practical points and pitfalls
- Always record the inspired oxygen with the result. A gas without an FiO2 is close to uninterpretable.
- Sampling errors are common: air bubbles raise PaO2 and lower PaCO2, delay before analysis lowers PaO2, and excess heparin dilutes the sample. A result that does not fit the patient should be repeated, not acted on.
- Allow equilibration time. After an oxygen change, wait around 20–30 minutes before sampling in chronic lung disease, or the gas reflects the previous state.
- Arterial puncture is painful and briefly raises minute ventilation; a gas taken during distress may show a spuriously low CO2.
- Capillary and venous gases are reasonable for pH and bicarbonate trends, and are widely used in paediatrics, but do not assess oxygenation.
- Arterial lines allow repeated sampling in critical care; check the local scope-of-practice position on who samples and who interprets.
Worked examples
| Gas | Interpretation | Physiotherapy response |
|---|---|---|
| pH 7.21 · PaCO2 78 · HCO3 30 · PaO2 52 on 28% | Acute-on-chronic respiratory acidosis with hypoxaemia | Escalate for NIV; upright positioning; defer exertion; treat sputum load if genuinely present |
| pH 7.47 · PaCO2 28 · HCO3 22 · PaO2 65 on room air | Acute respiratory alkalosis with hypoxaemia | Look for embolism, pain or sepsis before attributing to anxiety; do not coach breathing until a cause is excluded |
| pH 7.38 · PaCO2 58 · HCO3 34 · PaO2 60 on room air | Chronic compensated respiratory acidosis | Stable baseline — target SpO2 88–92%, rehabilitate normally, do not over-oxygenate |
| pH 7.28 · PaCO2 30 · HCO3 14 · lactate 4.5 | Metabolic acidosis with respiratory compensation | Not a physiotherapy problem — the tachypnoea is compensatory; escalate for the underlying cause |
Role of the physiotherapist
Physiotherapists are not usually the ones taking the sample, but in acute cardiorespiratory practice they are frequently the ones reading it before the next treatment decision. Competent interpretation changes three decisions: whether to treat at all, what to treat, and when to stop and call for help. It distinguishes a patient who needs recruitment and positioning from one who needs ventilation, it prevents the two commonest errors — over-oxygenating a chronic retainer and mobilising a patient in decompensating ventilatory failure — and it makes handover precise. Interpretation should always be paired with the clinical picture: the gas describes a moment, while the patient's trajectory, work of breathing and conscious state describe the direction.
Evidence summary
Framing. An arterial blood gas is a snapshot of three separable physiological questions — oxygenation, alveolar ventilation and acid–base status — and its clinical value in physiotherapy lies almost entirely in the second. Pulse oximetry covers oxygenation adequately in most situations but is blind to hypercapnia, so the ABG is what identifies the patient in whom the correct intervention is ventilatory support rather than oxygen, clearance or exercise.5,7
Oxygen targeting- Titrated oxygen saves lives in COPD. A cluster-randomised prehospital trial found titrated oxygen to a target of 88–92% reduced mortality by 58% compared with high-flow oxygen in acute exacerbations, with less hypercapnia and acidosis.9
- Guideline targets are 92–96% for most acutely unwell adults and 88–92% for those at risk of hypercapnic failure, with an ABG to confirm risk status and monitor response.7
- Liberal oxygen is not benign — systematic review in acutely ill adults found higher mortality with liberal versus conservative oxygen strategies.10
- NIV in acute hypercapnic exacerbation of COPD reduces intubation and mortality, with the strongest benefit where pH is 7.25–7.35; the decision rests on the gas, not on appearance.8,11
- Failure to improve pH and PaCO2 within 1–2 hours of adequate NIV predicts failure and should prompt escalation review rather than persistence.11
- In obesity hypoventilation, a raised serum bicarbonate is a validated screening surrogate for chronic hypercapnia in patients with sleep-disordered breathing — a cheap, accessible prompt to refer.12
- Pulse oximetry over-estimates arterial saturation more often in patients with darker skin pigmentation, with an increased frequency of occult hypoxaemia — correlate with clinical state and consider a gas where the picture does not fit.6
- Venous gases correlate acceptably with arterial pH and bicarbonate but not PCO2 at the extremes, and not at all for oxygenation; they screen rather than confirm.1
- Pre-analytical error — air bubbles, delayed analysis, excess heparin, sampling during distress — is a common cause of results that do not fit the patient.13
- Read the FiO2 with every gas. A PaO2/FiO2 ratio, even estimated, is far more informative than an isolated PaO2, and it trends usefully across a shift.
- Use the gas to choose the intervention: type 1 failure → positioning, recruitment, oxygen, treat the parenchymal cause; type 2 failure → ventilatory support, and clearance only where secretions are genuinely contributing.
- Do not mobilise into a deteriorating gas. A falling pH with a rising PaCO2, an uncompensated metabolic acidosis or a rising lactate are reasons to defer and escalate.
- Do not over-oxygenate the chronic retainer during or after treatment, and hand over the target range explicitly at the end of the session.7,9
- Use serial gases as outcome data for NIV, positioning and clearance, and document them — they are the most persuasive evidence of physiotherapy effect available in the acute setting.
- A normal pH with abnormal CO2 and bicarbonate is chronic and usually stable; a normal CO2 in a severely breathless asthmatic is ominous, not reassuring, because it signals fatigue.
- Compensation never over-corrects. A pH on the acidaemic side of normal with mixed abnormalities identifies which disturbance is primary.
- Tachypnoea with a metabolic acidosis is compensation, not a respiratory problem — suppressing it with breathing retraining is harmful.
- Match the gas to the trajectory: one abnormal gas describes a moment, two describe a direction, and the direction determines urgency.
- No study has evaluated whether physiotherapist ABG interpretation changes patient outcomes, despite it being an expected competency in acute practice.
- Optimal oxygen targets during physiotherapy treatment and exercise in hypercapnic patients are undefined.7
- Thresholds at which a deteriorating gas should stop mobilisation in critical care are consensus-based.
- Transcutaneous CO2 monitoring is promising as a non-invasive alternative during treatment but is not yet validated for this use.1
References & evidence base
- Byrne AL, Bennett M, Chatterji R, Symons R, Pace NL, Thomas PS. Peripheral venous and arterial blood gas analysis in adults: are they comparable? A systematic review and meta-analysis. Respirology 2014;19(2):168–175.
- Kelly AM. Review article: can venous blood gas analysis replace arterial in emergency medical care? Emerg Med Australas 2010;22(6):493–498.
- Bloom BM, Grundlingh J, Bestwick JP, Harris T. The role of venous blood gas in the emergency department: a systematic review and meta-analysis. Eur J Emerg Med 2014;21(2):81–88.
- McCanny P, Bennett K, Staunton P, McMahon G. Venous vs arterial blood gases in the assessment of patients presenting with an exacerbation of chronic obstructive pulmonary disease. Am J Emerg Med 2012;30(6):896–900.
- Nickson C, Cadogan M. Arterial blood gas interpretation. In: Oh's Intensive Care Manual. 8th ed. Sydney: Elsevier; 2019.
- Sjoding MW, Dickson RP, Iwashyna TJ, Gay SE, Valley TS. Racial bias in pulse oximetry measurement. N Engl J Med 2020;383(25):2477–2478.
- O'Driscoll BR, Howard LS, Earis J, Mak V. BTS guideline for oxygen use in adults in healthcare and emergency settings. Thorax 2017;72(Suppl 1):ii1–ii90.
- Osadnik CR, Tee VS, Carson-Chahhoud KV, Picot J, Wedzicha JA, Smith BJ. Non-invasive ventilation for the management of acute hypercapnic respiratory failure due to exacerbation of chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2017;(7):CD004104.
- Austin MA, Wills KE, Blizzard L, Walters EH, Wood-Baker R. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial. BMJ 2010;341:c5462.
- Chu DK, Kim LHY, Young PJ, et al. Mortality and morbidity in acutely ill adults treated with liberal versus conservative oxygen therapy (IOTA): a systematic review and meta-analysis. Lancet 2018;391(10131):1693–1705.
- Rochwerg B, Brochard L, Elliott MW, et al. Official ERS/ATS clinical practice guidelines: noninvasive ventilation for acute respiratory failure. Eur Respir J 2017;50(2):1602426.
- Mokhlesi B, Masa JF, Brozek JL, et al. Evaluation and management of obesity hypoventilation syndrome: an official American Thoracic Society clinical practice guideline. Am J Respir Crit Care Med 2019;200(3):e6–e24.
- Baird G. Preanalytical considerations in blood gas analysis. Biochem Med 2013;23(1):19–27.
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.
Corrections: If something on this page is wrong, out of date or unclear, we want to know. Email reception@inspireclinic.au with the page name and what you believe is incorrect. Substantive corrections are made promptly, and the guide’s version and last-updated date are changed to reflect it.