📋 Key Information Summary
- Oxygen is a medication — it must be prescribed with a target SpO₂ range, flow rate, delivery device, and duration.
- In acute care, target SpO₂ 92–96% for most patients; 88–92% for those at risk of hypercapnic respiratory failure (COPD, obesity hypoventilation, bronchiectasis, neuromuscular disease).
- Long-term oxygen therapy (LTOT) is indicated for chronic resting hypoxaemia: PaO₂ ≤55 mmHg (≤7.3 kPa) or SpO₂ ≤88%, or PaO₂ 56–59 mmHg with cor pulmonale, polycythaemia (Hct >55%), or pulmonary hypertension.
- LTOT must be prescribed for ≥15 hours/day (ideally continuous) to improve survival; the BTS and TGA criteria require documentation of persistent hypoxaemia on two occasions ≥3 weeks apart.
- Nasal cannulae deliver 1–6 L/min (≈24–44% FiO₂); simple masks 5–10 L/min (≈35–55%); Venturi masks deliver precise fixed FiO₂ (24%, 28%, 31%, 35%, 40%, 60%).
- High-flow nasal cannula (HFNC) delivers heated, humidified oxygen at 20–80 L/min with precise FiO₂ 21–100%; indicated in acute hypoxaemic respiratory failure, post-extubation, and pre-oxygenation.
- Ambulatory oxygen is indicated when patients on LTOT demonstrate exertional desaturation (SpO₂ <88% during a 6-minute walk test) despite supplemental oxygen during rest.
- Pulse-dose (demand) delivery conserves oxygen and suits mobile patients; continuous flow is preferred during sleep, exercise, and for patients with high minute ventilation.
- Always titrate oxygen to the minimum flow/FiO₂ needed to achieve target SpO₂; hyperoxia (SpO₂ >96%) increases mortality in acutely ill adults and should be avoided.
- Oxygen therapy equipment includes concentrators (electrically powered, stationary), compressed gas cylinders, and liquid oxygen systems; selection depends on flow needs, mobility, and home environment.
- Aboriginal and Torres Strait Islander peoples experience higher rates of chronic lung disease and respiratory hospitalisations; access to LTOT and pulmonary rehabilitation must be culturally safe and geographically supported.
Introduction & Australian Epidemiology
Oxygen therapy is one of the most commonly prescribed treatments in acute and chronic medicine. Despite its ubiquity, inappropriate use — both under-treatment of hypoxaemia and injudicious hyperoxia — is associated with increased morbidity and mortality. The Australian Commission on Safety and Quality in Health Care (ACSQHC) and the Thoracic Society of Australia and New Zealand (TSANZ) recommend that oxygen be treated as a drug: prescribed, titrated, monitored, and reviewed.
In Australia, chronic obstructive pulmonary disease (COPD) affects approximately 7.5% of adults aged ≥40 years (AIHW, 2023), and is the fifth leading cause of death. Long-term oxygen therapy (LTOT) is used by an estimated 30,000–40,000 Australians at any given time, predominantly for COPD-related chronic hypoxaemia. Idiopathic pulmonary fibrosis (IPF), bronchiectasis, cystic fibrosis, pulmonary hypertension, and neuromuscular diseases account for the remaining indications.
The Ambulance Victoria and NSW clinical frameworks mandate target SpO₂-directed oxygen therapy, and the National Safety and Quality Health Service (NSQHS) Standards include oxygen safety as a core clinical governance item (Standard 5: Comprehensive Care).
Prescribing oxygen as a drug: Every oxygen order should specify: device, flow rate or FiO₂, target SpO₂ range, duration (continuous, PRN, nocturnal), and review date. Unprescribed oxygen is a clinical safety incident.
Indications & Prescribing
Core Indications for Supplemental Oxygen
| Category | Indication | Target SpO₂ |
|---|---|---|
| Acute hypoxaemia | SpO₂ <92% (or <88% in known CO₂ retainers) | 92–96% (88–92% if hypercapnic risk) |
| Critical illness | Sepsis, shock, major trauma, cardiac arrest | 92–96% (after initial stabilisation) |
| Exertional desaturation | SpO₂ <88% during 6-minute walk test (6MWT) | ≥88–90% with ambulatory O₂ |
| Nocturnal hypoxaemia | SpO₂ <88% for >30% of sleep time (oximetry/polygraphy) | ≥88–90% overnight |
| Chronic resting hypoxaemia (LTOT) | PaO₂ ≤55 mmHg (≤7.3 kPa) or SpO₂ ≤88% on room air, documented twice ≥3 weeks apart | PaO₂ >60 mmHg / SpO₂ >90% |
| Near-threshold with complications | PaO₂ 56–59 mmHg with cor pulmonale, Hct >55%, or pulmonary hypertension | Same as LTOT |
| Carbon monoxide poisoning | Any confirmed or suspected COHb elevation | 100% FiO₂ until COHb <3% |
| Palliative / symptom relief | Refractory dyspnoea in advanced disease | Symptom-directed; comfort SpO₂ |
Resting Hypoxaemia Criteria (LTOT Eligibility)
The Australian Therapeutic Goods Administration (TGA) and TSANZ align with international BTS/ERS criteria. LTOT eligibility requires measurement of arterial blood gas (ABG) on room air (after ≥20 minutes off supplemental oxygen) on two separate occasions at least 3 weeks apart, during a period of clinical stability (no acute exacerbation for ≥4 weeks). Either arterial or arterialised capillary samples are acceptable.
Absolute criteria for LTOT: PaO₂ ≤55 mmHg (≤7.3 kPa) OR SpO₂ ≤88% on room air at rest while awake, measured on two occasions ≥3 weeks apart. Pulse oximetry alone may be used for the second measurement if the first was a confirmed ABG, provided clinical stability is established.
Prescribing Template (Australian Standard)
- Medication: Oxygen (O₂)
- Device: e.g., nasal cannula, Venturi mask, HFNC
- Flow rate / FiO₂: e.g., 2 L/min nasal cannula or 28% Venturi
- Target SpO₂: e.g., 92–96% or 88–92%
- Duration: e.g., continuous, PRN for SpO₂ <90%, nocturnal, during exertion
- Review date: e.g., within 24 hours / at next ward round
When NOT to Prescribe Oxygen
Oxygen is not indicated for breathlessness in the absence of hypoxaemia. Routine use in acute myocardial infarction with SpO₂ ≥94% is harmful (DETO2X-AMI trial, NEJM 2017). Hyperoxia (SpO₂ >96%) in acutely ill patients increases free radical injury, coronary and cerebral vasoconstriction, and is associated with higher in-hospital mortality in ICU populations (OXYGEN-ICU trial, ICU 2016).
Delivery Systems
The choice of delivery system depends on the severity of hypoxaemia, the required FiO₂ precision, patient tolerance, and whether humidification is needed. Devices range from low-flow systems (where the patient supplements inspired gas with room air) to high-flow systems that can meet or exceed inspiratory demand.
Low-Flow Devices
| Device | Flow Rate | Approximate FiO₂ | Key Considerations |
|---|---|---|---|
| Nasal cannula | 1–6 L/min | 24–44% | Most common in acute and home settings; comfortable; flows >4 L/min dry nasal mucosa — use humidification |
| Simple face mask | 5–10 L/min | 35–55% | Minimum 5 L/min to prevent CO₂ rebreathing; not for eating/drinking; useful for short-term moderate hypoxaemia |
| Reservoir (non-rebreather) mask | 10–15 L/min | 60–90% | Reservoir bag must remain >½ full; one-way valve prevents rebreathing; critical/emergency use |
| Reservoir (partial rebreather) mask | 8–12 L/min | 50–75% | No one-way valve; some rebreathing permitted; less common |
High-Flow / Precise-FiO₂ Devices
| Device | Flow Rate | Approximate FiO₂ | Key Considerations |
|---|---|---|---|
| Venturi mask | Variable (4–15 L/min depending on adapter) | 24%, 28%, 31%, 35%, 40%, 60% (fixed by colour-coded adapter) | Delivers precise FiO₂; preferred in COPD and hypercapnic respiratory failure; each adapter requires a specified minimum flow |
| High-flow nasal cannula (HFNC) | 20–80 L/min | 21–100% | Heated, humidified; reduces anatomical dead space; generates low-level CPAP (~2–5 cmH₂O); see dedicated section below |
| T-piece / tracheostomy collar | Variable (typically 10–40 L/min) | Up to 100% | Used for spontaneously breathing tracheostomy patients; heated humidification recommended |
Venturi Mask Colour Codes & Flow Requirements
| Colour | FiO₂ (%) | Minimum Flow (L/min) | Typical Use |
|---|---|---|---|
| Blue | 24 | 4 | COPD — mild hypoxaemia, target SpO₂ 88–92% |
| White | 28 | 4 | COPD — moderate hypoxaemia |
| Orange | 31 | 6 | COPD — moderate-severe hypoxaemia |
| Yellow | 35 | 8 | Non-hypercapnic moderate hypoxaemia |
| Red | 40 | 10 | Non-hypercapnic moderate-severe hypoxaemia |
| Green | 60 | 15 | Severe hypoxaemia pending escalation |
Minimum flow matters: Using a Venturi adapter at a flow below its specified minimum delivers an unpredictable (lower than labelled) FiO₂. Always check the flow meter matches the adapter colour.
Home Oxygen Therapy
Long-Term Oxygen Therapy (LTOT)
LTOT is one of the few interventions in COPD that improves survival when prescribed ≥15 hours/day. The landmark NOTT (Nocturnal Oxygen Therapy Trial, 1980) and MRC (Medical Research Council, 1981) trials established that continuous LTOT reduces mortality, polycythaemia, and pulmonary vascular resistance in patients with severe chronic hypoxaemia.
Survival benefit requires ≥15 hours/day: The NOTT trial showed continuous (≥19 h/day) oxygen was superior to nocturnal-only (12 h/day) oxygen for survival. Australian prescribing guidelines recommend a minimum of 15 hours/day, ideally continuous use including during sleep.
LTOT Eligibility Criteria (Australian)
Standard
Primary LTOT Criteria
PaO₂ ≤55 mmHg (≤7.3 kPa) OR SpO₂ ≤88% on room air at rest, awake, on two occasions ≥3 weeks apart during clinical stability.
Eligible for LTOT with PBS authority
Near-threshold
Complicated Near-threshold
PaO₂ 56–59 mmHg (7.4–7.8 kPa) with one of: peripheral oedema (cor pulmonale), haematocrit >55%, or ECG evidence of pulmonary hypertension (P-pulmonale).
Eligible for LTOT with PBS authority
Special
CF / ILD / Pulmonary Hypertension
Severe hypoxaemia secondary to cystic fibrosis, interstitial lung disease, or pulmonary arterial hypertension. Same PaO₂/SpO₂ thresholds apply; often requires higher flows at rest and exertion.
Specialist initiation; multi-disciplinary review recommended
Ambulatory Oxygen Therapy
Ambulatory oxygen is indicated for patients who desaturate during physical activity (SpO₂ <88% on a 6-minute walk test) and who demonstrate improvement in exercise capacity and/or dyspnoea during a supervised trial of supplemental oxygen during exercise. It may be prescribed independently of LTOT or in addition to it.
- Assessment: standardised 6MWT on room air, then repeated with supplemental oxygen at titrated flow.
- Minimum meaningful improvement: ≥10% increase in 6MWT distance or significant reduction in dyspnoea (Borg scale ≥2-point improvement).
- Typical prescription: 2–6 L/min via nasal cannula during exertion.
- Equipment: lightweight portable cylinder (D, E size), portable oxygen concentrator (POC), or liquid oxygen portable unit (LOX).
Pulse-Dose vs Continuous Flow
| Feature | Continuous Flow | Pulse-Dose (Demand) |
|---|---|---|
| Mechanism | Constant flow regardless of respiratory cycle | Delivers a bolus at the start of each detected inspiratory effort |
| Oxygen conservation | Higher consumption | 3:1 to 5:1 conservation ratio |
| Battery life (POC) | Shorter | Substantially longer |
| Preferred during sleep | Yes — pulse may not detect shallow sleep breathing | No — unreliable triggering in sleep or very shallow breaths |
| Preferred during exercise | Yes — reliable at high respiratory rates | Variable — may not keep up at high rates >25/min |
| PBS funding | Concentrator or cylinders via LTOT approval | POC or cylinders; additional PBS authority required for ambulatory component |
Equipment Selection for Home Oxygen
Stationary Oxygen Concentrator
e.g., Philips Respironics EverFlo, AirSep VisionAire
Flow range
0.5–5 L/min (some up to 10 L/min)
FiO₂ delivered
≈90–95% at ≤5 L/min
Power
Mains electricity (240 V); ~300–600 W
Advantages
Continuous supply, no cylinder delivery needed, low ongoing cost
Limitations
Requires mains power; not portable; backup cylinder needed for power outages
PBS status
✔ PBS Authority — Home Oxygen Program
Portable Oxygen Concentrator (POC)
e.g., Inogen One G5, Philips SimplyGo Mini, CAIRE FreeStyle Comfort
Flow range
Pulse dose 1–6 settings; some offer continuous 0.5–2 L/min
FiO₂ delivered
Variable; approximately 90% at low settings
Battery life
2–13 hours depending on setting and battery size
Weight
2–5 kg (with battery)
Advantages
Aircraft-approved models available; enables travel and social participation
Limitations
Pulse-only models unsuitable for sleep; higher settings drain battery rapidly; not suitable for all patients
PBS status
✔ PBS Authority — Home Oxygen Program
Liquid Oxygen (LOX) System
e.g., Cryogas liquid oxygen home unit + portable flask
Flow range
0.5–15+ L/min (stationary); 0.5–6 L/min (portable flask)
FiO₂ delivered
≈99% (near-pure oxygen)
Capacity
Stationary reservoir 20–40 L (lasts ~7–14 days at 2 L/min); portable flask ~0.5–1.2 L (~4–8 hours at 2 L/min)
Advantages
Very high flow capability; silent; lightweight portable flasks
Limitations
Requires regular top-up delivery; LOX evaporates when not in use; limited availability in regional/remote Australia
PBS status
✔ PBS Authority — Home Oxygen Program
Titration of Home Oxygen
- Initial titration: Performed by a respiratory scientist or specialist nurse; ABG or SpO₂-guided increase in flow until PaO₂ >60 mmHg or SpO₂ >90% at rest while awake.
- Nocturnal titration: Overnight oximetry to confirm SpO₂ ≥88–90% throughout sleep; increase nocturnal flow by 0.5–1 L/min above daytime if nocturnal desaturation persists.
- Exertional titration: 6MWT-guided; increase flow by 1–2 L/min above resting flow to maintain SpO₂ ≥88% during standardised exercise.
- Review schedule: Clinical review at 1, 3, and 6 months after initiation, then at least 6-monthly. ABG and functional assessment should be repeated at each review.
- Weaning/discontinuation: Reassess at 60–90 days of stability; if PaO₂ >59 mmHg on repeat ABG, consider trial off oxygen with close monitoring.
Fire safety with home oxygen: Oxygen supports combustion. Patients must not smoke or be near naked flames while using oxygen. Equipment must be stored ≥2 m from heat sources. The Australian Home Oxygen Safety Program provides standardised safety checklists (TSANZ).
High-Flow Nasal Cannula (HFNC)
Overview & Mechanism
High-flow nasal cannula (HFNC) therapy delivers heated (37°C), fully humidified oxygen/air mixtures at flows of 20–80 L/min with precise FiO₂ control from 0.21 to 1.0. HFNC has become a cornerstone of respiratory support in Australian emergency departments and ICUs.
HFNC provides several physiological benefits beyond simple oxygen delivery:
- Washout of nasopharyngeal dead space: High flows flush CO₂ from the anatomical dead space, improving alveolar ventilation and reducing the work of breathing.
- Low-level positive end-expiratory pressure (PEEP): Generates approximately 2–5 cmH₂O of PEEP at flow rates of 30–60 L/min (mouth-closed); recruitment of alveoli, improved oxygenation.
- Reduced inspiratory resistance: Matches or exceeds patient peak inspiratory flow demand, reducing entrainment of room air and providing more consistent FiO₂.
- Mucociliary clearance: Humidification at 37°C preserves ciliary function and reduces inspissated secretions.
Clinical Indications
Established
Acute Hypoxaemic Respiratory Failure
SpO₂ <92% despite conventional oxygen (≥10 L/min via non-rebreather). The FLORALI trial (NEJM 2015) showed HFNC reduced intubation rates and 90-day mortality compared to standard oxygen and NIV in non-hypercapnic ARF.
ED / ICU / HDU
Established
Post-Extubation
High-risk extubation (age >65, APACHE II >12, BMI >30, failed first weaning trial, weak cough, secretion retention). HFNC reduces re-intubation rates compared to conventional oxygen (HR 0.42; meta-analysis).
ICU post-extubation; can continue on ward
Emerging
Pre-Oxygenation & Peri-Intubation
Apnoeic oxygenation during rapid sequence intubation (RSI) using HFNC at 60–70 L/min, FiO₂ 1.0 prolongs safe apnoea time. Particularly valuable in anticipated difficult airway, obesity, and critical illness.
ED / ICU / Theatre
Additional HFNC Indications
- Immunocompromised patients: Early HFNC in febrile neutropenia and post-HSCT respiratory failure reduces intubation and ICU mortality (HIGH trial, Lancet Resp Med 2018).
- Acute heart failure (cardiogenic pulmonary oedema): HFNC improves dyspnoea and reduces work of breathing; may be used as a bridge to NIV or in mild-moderate cases (B UIStoryboardSegue trial).
- Bronchiolitis (paediatric): HFNC at 1–2 L/kg/min is first-line respiratory support in infants with moderate-severe bronchiolitis (PREDICT/ANZICS guidelines, 2019).
- Palliative care: HFNC for refractory dyspnoea in end-stage respiratory disease when conventional oxygen fails to provide comfort.
Flow & FiO₂ Settings
| Parameter | Adult Starting | Adult Escalation | Paediatric Starting | Notes |
|---|---|---|---|---|
| Flow rate | 30–40 L/min | Titrate up to 50–60 L/min (max 80 L/min) | 1–2 L/kg/min (max 8 L/kg in bronchiolitis) | Higher flow = better dead-space washout and PEEP; comfort is a limiting factor |
| FiO₂ | Set to match current delivery (e.g., 0.50) | Titrate in 0.05–0.10 increments every 15–30 min to target SpO₂ | 0.30–0.50 initially | Wean FiO₂ first once SpO₂ stabilised; wean flow last |
| Temperature | 37°C | 37°C (34°C if patient febrile or uncomfortable) | 37°C | Full humidification at 37°C maximises mucociliary clearance |
Initiation & Escalation Protocol
1
Assess eligibility
SpO₂ <92% on ≥10 L/min conventional O₂; no immediate intubation indication; patient able to protect airway and cooperate.
2
Initiate HFNC
Flow 30–50 L/min; FiO₂ titrated to target SpO₂ 92–96% (88–92% in hypercapnic risk). Ensure appropriate cannula size (≤50% of naris diameter).
3
Reassess at 1 hour (ROX Index)
ROX = (SpO₂/FiO₂) / RR. ROX >4.88 at 1, 2, 6, and 12 hours predicts success. If ROX <3.85 at any timepoint, high risk of failure — prepare for escalation.
4
Escalation if failing
Persistent RR >30, accessory muscle use, SpO₂ <88% despite FiO₂ >0.80, rising PaCO₂, altered consciousness → consider NIV or invasive ventilation.
5
Weaning
First wean FiO₂ to ≤0.40, then reduce flow by 5–10 L/min every 2–4 hours. Trial conventional nasal cannula when on HFNC flow ≤20 L/min at FiO₂ ≤0.30.
HFNC failure — do not delay intubation: Delayed intubation after HFNC failure is associated with significantly higher mortality. If the ROX index is deteriorating or the patient is developing signs of exhaustion, shock, or altered consciousness, proceed to invasive mechanical ventilation without delay. HFNC is not a ceiling-of-care device by default.
Contraindications to HFNC
- Cardiac or respiratory arrest (immediate intubation/airway management)
- Severe haemodynamic instability requiring vasopressors (relative)
- Inability to protect airway (GCS ≤8, absent gag/cough reflex)
- Upper airway obstruction (e.g., epiglottitis, tumour) — will not bypass obstruction
- Severe facial trauma preventing nasal cannula application
- Untreated pneumothorax (relative — low-level PEEP risk)
Pathophysiology of Hypoxaemia
Understanding the mechanisms of hypoxaemia guides the appropriate use of supplemental oxygen. There are five principal mechanisms, which often coexist:
| Mechanism | A–a Gradient | Response to O₂ | Common Causes |
|---|---|---|---|
| V/Q mismatch | Elevated | Good — easily corrected | COPD, asthma, pneumonia, PE, pulmonary oedema |
| Shunt (true R→L) | Elevated | Poor — does not respond to 100% O₂ | Intrapulmonary (ARDS, large consolidation); intracardiac (ASD, VSD) |
| Diffusion impairment | Elevated (worse with exercise) | Good at rest; moderate with exercise | IPF, asbestosis, pulmonary fibrosis, emphysema (reduced surface area) |
| Hypoventilation | Normal | Corrects hypoxaemia but may worsen hypercapnia | Obesity hypoventilation, OHS, neuromuscular disease, opioid overdose |
| Low PiO₂ | Normal | Excellent | High altitude (not relevant to Australian practice at sea level) |
The alveolar–arterial (A–a) oxygen gradient is calculated as: A–a gradient = [FiO₂ × (Patm – PH₂O) – (PaCO₂ / R)] – PaO₂, where Patm ≈ 760 mmHg, PH₂O = 47 mmHg, R = 0.8. A normal A–a gradient is approximately (Age/4) + 4 mmHg.
Why oxygen doesn't help breathlessness in non-hypoxaemic patients: The sensation of dyspnoea is driven by increased respiratory drive, mechanical loading, and cortical perception — not by arterial oxygen content per se. Supplemental oxygen in normoxaemic patients does not reduce the work of breathing and may cause unwarranted delays in treating the underlying cause (e.g., anxiety, deconditioning, metabolic acidosis).
Investigations
Essential
Arterial Blood Gas (ABG)
Gold standard for assessing PaO₂, PaCO₂, pH, HCO₃⁻, lactate. Required for LTOT eligibility. Radial artery puncture (Allen test first) or arterialised earlobe capillary sample. Available in all Australian hospitals. MBS item 65090 (blood gas analysis).
Available
Pulse Oximetry (SpO₂)
Continuous or spot-check SpO₂. Non-invasive, widely available. Limitations: poor accuracy with COHb >3%, methaemoglobinaemia, nail polish, severe anaemia (Hb <50 g/L), hypothermia, dark skin pigmentation (may overestimate at low saturations). Used for titration but not for initial LTOT eligibility without confirmatory ABG.
Available
Overnight Oximetry / Sleep Study
Identifies nocturnal hypoxaemia and sleep-disordered breathing. Overnight oximetry (SpO₂ + pulse rate) sufficient for nocturnal oxygen assessment. Full polysomnography required if concomitant OSA suspected. Referral to sleep medicine service. MBS items 12203/12205 for sleep studies.
Available
6-Minute Walk Test (6MWT)
Standardised corridor walk per ATS/ERS 2002 guidelines. Measuring SpO₂ and distance. Used for exertional desaturation assessment and ambulatory oxygen eligibility. Available in most respiratory and pulmonary rehabilitation programmes. MBS item 13020 (exercise testing, cardiac).
Available
Full Blood Count (FBC)
Polycythaemia (Hct >55%, Hb >170 g/L in males, >150 g/L in females) supports LTOT eligibility in the near-threshold group. Also excludes anaemia as a cause of tissue hypoxia. MBS item 65070.
Available
Chest X-Ray (CXR)
Identifies structural lung disease (fibrosis, bronchiectasis, bullae), cor pulmonale (enlarged pulmonary arteries, cardiomegaly), and excludes pneumothorax. MBS item 58500.
Referral
Echocardiography
Assesses right ventricular function and estimates pulmonary artery systolic pressure (PASP). Pulmonary hypertension threshold PASP >35 mmHg at rest supports LTOT in near-threshold patients. Referral to cardiology or respiratory medicine. MBS item 55118.
Specialist
Lung Function (Spirometry + DLCO)
Establishes baseline respiratory function. FEV₁, FVC, FEV₁/FVC ratio, DLCO. Essential for characterising the underlying respiratory disease (COPD, ILD, etc.). MBS item 11305. Available in accredited respiratory laboratories.
Monitoring
Acute Inpatient Monitoring
Ongoing
Continuous pulse oximetry for all patients on supplemental oxygen in critical care and HDU. Ward patients: spot-check SpO₂ at each set of vital signs (minimum 4-hourly; 1–2-hourly in first 12 hours after initiation or dose change).
At initiation
Document baseline SpO₂ on current device, flow rate, device type, and target SpO₂ on the oxygen prescription chart. ABG if SpO₂ <90% on high-flow O₂ or if hypercapnia risk.
1 hour post-change
Reassess SpO₂ after any change in oxygen delivery. If target not achieved, escalate device/flow and recheck within 30–60 minutes.
At each review
Wean oxygen when SpO₂ consistently above target for ≥12 hours. Step down one device/flow at a time. Recheck SpO₂ 30 minutes after each wean step.
Prior to discharge
Confirm room-air SpO₂ and ABG if on O₂ at discharge. If ongoing need: refer for home oxygen assessment (ABG on room air required). Provide written education, fire safety information, and emergency contact details.
Home Oxygen Monitoring
- Patient self-monitoring: Spot-check SpO₂ with personal oximeter (≥2× daily); report SpO₂ <88% to GP or respiratory nurse.
- GP review: At 1, 3, and 6 months post-initiation, then 6-monthly. Assess compliance (hours/day), functional status, oxygen flow requirements, and side effects (nasal dryness, epistaxis, skin breakdown).
- Repeat ABG: At 60–90 days to assess response; annually or if clinically deteriorating.
- Equipment servicing: Concentrators: serviced every 12 months by supplier. Cylinders: checked for valve integrity. Portable units: battery health check at each supplier visit.
- Re-assessment for discontinuation: If stable and non-smoking with improved PaO₂ on repeat ABG, a supervised trial off oxygen may be considered at 6–12 months.
Carbon dioxide retention monitoring: In patients with COPD or known CO₂ retention, recheck ABG 30–60 minutes after initiating or changing oxygen. A rise in PaCO₂ >50 mmHg (6.6 kPa) with respiratory acidosis (pH <7.35) requires careful titration down of FiO₂ and consideration of NIV.
Special Populations
Pregnancy
Target SpO₂
92–96% (normal pregnancy PaO₂ ≈ 100–105 mmHg due to hyperventilation; PaCO₂ ≈ 30 mmHg).
Maternal hypoxaemia
Associated with fetal growth restriction, preterm birth, and congenital anomalies. Treat aggressively in acute settings.
LTOT in pregnancy
Limited data; case series support safety. Maintain SpO₂ ≥92% at all times. Continuous monitoring during labour and delivery.
HFNC
Safe in pregnancy for acute respiratory failure; no teratogenic risk from humidified oxygen.
Fetal monitoring
Continuous CTG during labour if mother on supplemental oxygen for respiratory failure.
Paediatrics
Neonatal target SpO₂
Preterm (<32 weeks): 90–94% (per BOOST-II / DANCE trials to reduce ROP and death). Term: 95–100%.
Bronchiolitis
HFNC 1–2 L/kg/min (max 8 L/kg/min) per PREDICT/ANZICS 2019 guideline. SpO₂ target ≥90%. Wean when clinically stable and tolerating feeds.
Croup
Humidified oxygen (cool mist or HFNC) for severe croup. Monitor SpO₂ during nebulised adrenaline.
Cystic fibrosis
LTOT in advanced CF if PaO₂ ≤55 mmHg or SpO₂ ≤88%. Higher flows often needed. Specialist respiratory paediatrician oversight.
Delivery devices
Paediatric nasal cannulae (infant, child, adult sizes); infant flow driver for neonates; headbox O₂ largely replaced by HFNC.
Elderly
Normal SpO₂ in elderly
SpO₂ 94–98% expected; A–a gradient increases ~1 mmHg per decade. Lower end of normal is acceptable.
Compliance with LTOT
Reduced manual dexterity, cognitive impairment, and social isolation reduce adherence. Simplify equipment and involve carers.
Fall risk
Oxygen tubing is a trip hazard. Assess home environment; secure tubing along walls. Portable units on wheeled trolleys.
Polypharmacy
Opioids and benzodiazepines potentiate hypoventilation; may require higher O₂ flows or monitoring for hypercapnia.
Power outages
Elderly patients on concentrators are vulnerable during blackouts. Ensure backup E-cylinder (with regulator) is in the home and patient/carer can connect it. Register with electricity retailer as life-support customer.
Renal Impairment
Metabolic acidosis
CKD/ESKD with metabolic acidosis may have compensatory hyperventilation. O₂ supplementation is appropriate for hypoxaemia but will not address acidosis-driven dyspnoea.
Dialysis patients
Fluid overload and pulmonary oedema during/after HD may cause acute hypoxaemia. Supplemental O₂ with NIV as needed. Wean with fluid removal.
Anaemia
CKD-related anaemia (target Hb 100–115 g/L per KDIGO) reduces oxygen-carrying capacity. Correct anaemia with ESAs/iron; O₂ does not compensate for severe anaemia (Hb <70 g/L → transfusion).
Hepatic Impairment
Hepatopulmonary syndrome
Intrapulmonary vascular dilatation in cirrhosis causes V/Q mismatch and orthodeoxia (worse desaturation upright). PaO₂ <70 mmHg on ABG. LTOT indicated; liver transplant is definitive treatment.
Hepatic hydrothorax
Right-sided pleural effusion in portal hypertension. Supplemental O₂ for hypoxaemia; definitive treatment is TIPS or transplant.
Drug metabolism
No pharmacokinetic interactions between oxygen and hepatic impairment. Oxygen therapy is not dose-adjusted for liver disease.
Immunocompromised
Febrile neutropenia
Early hypoxaemia may indicate PJP, CMV pneumonitis, or fungal pneumonia. HFNC first-line; early ICU referral if failing. Avoid delays in starting empirical antimicrobials.
Post-HSCT
Diffuse alveolar haemorrhage, idiopathic pneumonia syndrome. HFNC is safe and reduces intubation. Bronchoscopy-guided BAL for diagnosis.
HIV/CD4 <200
PJP (Pneumocystis jirovecii) is the classic cause of hypoxaemia with high A–a gradient. High-flow O₂ pending co-trimoxazole initiation. Corticosteroids if PaO₂ <70 mmHg.
Biologic therapy
Anti-TNF, rituximab-associated pneumonitis. Supplemental O₂ for hypoxaemia; withdraw offending agent and treat with corticosteroids.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
Aboriginal and Torres Strait Islander peoples experience a disproportionate burden of chronic respiratory disease, including COPD, bronchiectasis, and rheumatic heart disease–associated pulmonary hypertension. COPD prevalence in Indigenous Australians is approximately 2–3 times that of non-Indigenous Australians, with onset a decade earlier and higher rates of hospitalisation and death (AIHW, 2023). These conditions drive substantial demand for long-term and acute oxygen therapy.
📚 References
- 1. British Thoracic Society (BTS). Guideline for oxygen use in adults in healthcare and emergency settings. BMJ Open Resp Res. 2017;4:e000170.
- 2. Beasley R, Chien J, Douglas J, et al. Thoracic Society of Australia and New Zealand oxygen guidelines for acute oxygen use in adults. Respirology. 2016;21(8):1434–1448.
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