Oxygen therapy, non-invasive and invasive ventilation

• Oxygen is a drug with a target saturation, not a reflex for breathlessness. Give it to correct hypoxaemia, titrate it, and stop it when it is no longer needed.
• Most acutely unwell adults without risk factors for carbon dioxide retention should be kept at an oxygen saturation of about 94 to 98 percent; adults at risk of hypercapnia (chronic lung disease, obesity hypoventilation, neuromuscular and chest wall disease) should be kept at about 88 to 92 percent.
• Non-invasive ventilation is first-line for acute hypercapnic respiratory failure from COPD and for cardiogenic pulmonary oedema, provided the patient is breathing, can protect the airway and is not in shock.
• Intubation is indicated by failure of non-invasive support, exhaustion, worsening acidosis, impaired airway protection, haemodynamic instability, or a physiology that makes delay dangerous.
• Invasive ventilation should use a lung-protective strategy: low tidal volumes, a plateau pressure under 30 cm water, and enough positive end-expiratory pressure to keep alveoli open. ^[6]

By the end of this page you should be able to:

1. Prescribe oxygen with the correct target saturation for a given patient and escalation need.
2. Choose between nasal cannula, mask, high-flow nasal oxygen, CPAP and BiPAP, and describe their initial settings.
3. Decide when non-invasive ventilation is likely to help, when it is contraindicated, and how to titrate and wean it.
4. List the indications for endotracheal intubation and invasive mechanical ventilation.
5. Set up a lung-protective ventilation strategy and state the rationale behind each setting.
6. Plan liberation (weaning) from invasive and non-invasive support.

This page is a bedside procedure reference. It covers oxygen therapy, high-flow nasal oxygen, CPAP and BiPAP, intubation and mechanical ventilation, and weaning in adults. It is written for a medical student meeting the topic for the first time. Doses are typical adult values; check your local formulary and the patient before every intervention. Low-resource notes are included because oxygen and ventilation are often scarce where they matter most.

The editions named below are the sources of the specific numbers used here: the British Thoracic Society guideline for oxygen use in adults in healthcare and emergency settings (O'Driscoll and colleagues, 2017), the European Respiratory Society and American Thoracic Society clinical practice guidelines on non-invasive ventilation for acute respiratory failure (Rochwerg and colleagues, 2017) and on high-flow nasal cannula (Oczkowski and colleagues, 2022), the Chest 2024 interprofessional algorithm for non-invasive ventilation in COPD (Farmer and colleagues, 2024), Lagina and Valley (2024) on diagnosis and management of acute respiratory failure, and Poole and colleagues (2017) on tidal volume use in lung-protective ventilation.

This procedure topic applies when a patient has actual or threatened hypoxaemia or hypercapnia, increased work of breathing, or a need to secure and control the airway. Indications fall into four groups:

• Hypoxaemia (defined as a partial pressure of oxygen in arterial blood under 60 mmHg, or an arterial oxygen saturation under 88 percent) that persists despite treatment of the cause. ^[2]
• Hypercapnic respiratory failure (partial pressure of carbon dioxide at least 45 mmHg with pH under 7.35) where non-invasive support can avert intubation. ^[2]
• Increased work of breathing that threatens exhaustion or lung injury, even if blood gases are not yet critical.
• Airway protection or control needs: reduced consciousness, inability to clear secretions, impending obstruction, or the need for a protected airway during a procedure.

Oxygen itself has few absolute contraindications, but its unnecessary use is harmful: it can worsen carbon dioxide retention, cause absorption atelectasis and free-radical injury, and mask clinical deterioration. Non-invasive ventilation has absolute and relative contraindications, which are set out in the table below. Invasive ventilation is a life-support intervention, not a drug; the real contraindications are patient preference (for example a known do-not-intubate decision) and futility in the face of irreversible organ failure. Delayed escalation, not intubation itself, is the common harm.

Oxygenation and ventilation depend on the airway, the lung units and the bellows. Know the upper airway from lips to carina, because a mask seal, an oral airway or a tracheal tube all interact with the same anatomy. The alveoli provide a large surface area for gas exchange; the physics that matter here are the inspired oxygen concentration, alveolar ventilation (tidal volume multiplied by rate minus dead space), and ventilation-perfusion matching. The diaphragm and intercostals generate the pressure that moves gas; in hypercapnic failure it is this pump that has failed, so oxygen alone will not fix the problem unless ventilation is supported.

• Oxygen source and delivery devices: nasal cannula, simple face mask, Venturi mask, reservoir mask, high-flow nasal cannula, and non-invasive ventilator.
• Pulse oximetry in every location where oxygen is given, and arterial blood gas sampling.
• Non-invasive ventilator capable of CPAP or BiPAP with back-up rate, its alarms, and a compatible interface (full-face mask first, then nasal pillows if needed).
• For invasive ventilation: appropriate tracheal tube, suction, capnography, ventilator with multiple modes, monitoring (ECG, blood pressure, pulse oximetry, end-tidal carbon dioxide).
• Rescue airway equipment and a trained team; the full algorithm for difficult intubation sits with the separate topic on general anaesthesia and airway management.

Explain the plan to the patient and family, including the possibility of escalation to intubation. Confirm oxygen device and flow suit the target. For non-invasive ventilation, ensure the mask fits, alarms are connected, and the patient is in a monitored bed with head of bed raised to at least 30 degrees. Infrastructurally, ensure nursing and respiratory therapist staffing, and that the patient can remove the mask if they vomit. For invasive ventilation, follow the pre-induction checklist used locally: large-bore intravenous access, preoxygenation, airway assessment and a declared failed-intubation plan. ^[5]

The correct target saturation depends on the risk of carbon dioxide retention. These two values are guideline-backed and differ between UK and international sources: the British Thoracic Society target for most patients is 94 to 98 percent, while several other guidelines quote 92 to 96 percent. Both are correct. The safe approach is to know which your local protocol uses and stay inside a single chosen band rather than chasing a number, and to review early. ^[1][2]

• Standard risk (no risk of hypercapnia): target about 92 to 98 percent. If your local protocol is BTS-based, use 94 to 98; if it follows TSANZ or the German S3 guideline, use 92 to 96. ^[1][2]
• High risk of hypercapnia (COPD, obesity hypoventilation, neuromuscular or chest wall disease): 88 to 92 percent. ^[1][2]
• Critical illness and resuscitation: the highest feasible inspired oxygen during resuscitation, then a target of 94 to 98 percent until stabilised; shock, sepsis, trauma, drowning and anaphylaxis need high-concentration oxygen initially. ^[1]
• Intubated and invasively ventilated: a conservative range (arterial partial pressure of oxygen roughly 55 to 80 mmHg, or saturation about 90 to 98 percent) is likely safe, although prolonged hyperoxia should be avoided. ^[2]
• Darker skin tones: where arterial blood cannot be sampled, consider the more liberal end of the target range (about 92 to 98 percent), because pulse oximetry can overestimate saturation. ^[2]
• Tail (paraquat or bleomycin): oxygen should be avoided unless the patient is hypoxaemic, with a lower target of about 85 to 88 percent. ^[1]

Conventional devices deliver an approximate (not exact) inspired oxygen concentration that falls when the patient's own minute ventilation rises above the device flow. Escalate when conventional delivery cannot hold the target without more than about 6 L per minute or an inspired fraction of roughly 40 percent. ^[2]

Practical points: start with the least invasive device that meets the target; raise the flow in single-litre steps and reassess breathing and blood gases within 30 to 60 minutes. In a hypoxaemic patient at risk of hypercapnia, use a controlled device (Venturi) at a known concentration and recheck an arterial blood gas. ^[1]

High-flow nasal oxygen delivers heated, humidified oxygen at flow rates up to 60 L per minute, with an inspired fraction from about 21 to 100 percent. ^[2] It washes dead space out of the upper airway, creates a small positive pharyngeal pressure (especially when the mouth is closed), and is usually better tolerated than a mask. Initiate it at roughly 40 to 60 L per minute, 100 percent inspired oxygen and 37 degrees Celsius temperature, then titrate the fraction down to keep the saturation in target. Lower flow rates around 35 to 40 L per minute often improve comfort at the start. ^{[2] [7]} (Current devices can deliver more than 60 L per minute in selected studies, but 60 L per minute is the limit most units use.) ^[2]

Use high-flow nasal oxygen for hypoxaemia above the capacity of conventional devices, for dyspnoea with elevated work of breathing, and in acute hypoxaemic respiratory failure. Many clinicians start HFNO when a patient needs more than about six L per minute of conventional oxygen (about 40 percent inspired). The ERS 2022 guideline suggests HFNO over conventional oxygen in adults with acute hypoxaemic respiratory failure, conditional on a trial; it also suggests a trial of non-invasive ventilation before HFNO in COPD with acute hypercapnic failure. ^[4] HFNO is now an acceptable alternative to non-invasive ventilation in COPD exacerbation, although guideline bodies still prefer BiPAP. ^[5]

Society for Airway Management guidance recommends preoxygenation for at least 3 minutes before intubation, delivered by high-flow nasal oxygen or non-invasive ventilation, to build a large alveolar reserve. ^[2] A common trap is to leave a patient on high flows for many days. Although HFNO use beyond 48 hours has been associated with higher mortality in observational data, there is no single safe time limit; reassess daily and intubate early if the work of breathing or acidosis worsens. ^[2]

Continuous positive airway pressure (CPAP) is continuous positive pressure during both inspiration and expiration delivered via a tight-fitting mask. It splints the airway open and increases functional residual capacity, so it improves oxygenation but provides essentially no ventilatory support. It is first-line in cardiogenic pulmonary oedema, and useful for obesity hypoventilation with CO2 retention once a BiPAP has corrected ventilation. ^[2]

Bilevel positive airway pressure (BiPAP) is CPAP plus an additional inspiratory pressure support. It lowers the work of breathing, increases tidal volume and minute ventilation, and so treats hypercapnia. Typical home or sleep apnoea BiPAP pressures are much lower than the acute values set out below.

CPAP for acute cardiogenic pulmonary oedema. Continuous positive pressure via tight-fitting mask reduces preload and afterload and markedly lowers the work of breathing; many units start at a low level (for example 5 to 8 cm water) and titrate to effect. Use and titration follow local critical care practice, since the open comparative studies do not define a single starting pressure. ^{[2] [5]}

BiPAP starter settings in acute hypercapnic failure (COPD). ^[5]

• Mode: spontaneous/timed, with a back-up rate of 8 to 12 breaths per minute. ^[5]
• Rise time: 0.2 seconds. ^[5]
• Inspiratory positive airway pressure (IPAP): 8 to 12 cm water (10 most common).
• Expiratory positive airway pressure (EPAP): 3 to 5 cm water (5 most common).
• Inspired oxygen: as needed, titrated to an oxygen saturation of 88 to 92 percent.
• Head of bed raised at least 30 degrees; patient seated if possible.
• Titrating the IPAP up by 2 cm water at a time, to a maximum of 20 to 30 cm water, over 10 to 30 minutes; EPAP can be increased to 8 to 10 cm water if oxygenation remains inadequate on 3 to 5. ^[5]

Do not begin with the highest inspiratory pressures: that can worsen hyperinflation, increase intrinsic positive end-expiratory pressure and promote asynchrony in COPD. ^[5] If oxygenation remains poor on EPAP of 3 to 5 cm water, increase EPAP toward 8 to 10 and raise IPAP in parallel so the pressure support (IPAP minus EPAP, i.e. the delivered tidal volume) is not lost.

The ERS and ATS 2017 guideline makes a strong, high-certainty recommendation for bilevel non-invasive ventilation in acute respiratory failure leading to acute or acute-on-chronic hypercapnic respiratory acidosis (pH 7.35 or lower, partial pressure of carbon dioxide above 45 mmHg) attributable to COPD. Non-invasive ventilation is also appropriate in acute cardiogenic pulmonary oedema, in immunocompromised patients, after extubation in high-risk patients, in chest trauma and in selected palliative situations. ^{[3][2] [5]}

Non-invasive ventilation is used as first-line for hypercapnic failure provided all of these criteria are met ^[2]:

• the patient is breathing spontaneously;
• the patient can protect the airway and remove the mask if they vomit;
• there is no immediate deterioration requiring intubation;
• staffing and equipment are adequate for close monitoring.

The absolute and relative contraindications are summarised in the contraindications table above.

Improvement is judged at the bedside and with blood gases:

• Anticipated predictors of success: improvement in pH and carbon dioxide, and a fall in respiratory rate, within the first one to two hours. ^[5]
• Obtain an arterial blood gas every 30 to 60 minutes after starting support, and check mental status, respiratory rate, accessory muscle use, mask leak and asynchrony. ^[5]
• Markers of asynchrony include double triggering, auto-triggering, premature or delayed cycling and flow mismatch; correct leaks, rise time and trigger sensitivity first. ^[5]
• If the pH does not normalise, carbon dioxide does not fall, or clinical status worsens within a four-hour trial, intubate. ^[2] Benefit in COPD is usually apparent within one to four hours. ^[2]

Non-invasive ventilation fails most often because of poor patient selection, an inappropriate interface, high leak, inappropriate settings or lack of experience at the bedside; each of these is correctable.

After at least 24 hours of successful non-invasive ventilation for hypercapnic failure, discontinuation can be planned; success is defined as pH at least 7.35, normalisation of respiratory rate, and resolution of the precipitating cause and symptoms. Parameters suggesting readiness to wean are set out in the table. ^[5]

Weaning may be abrupt or gradual; protocol-directed discontinuation shortens non-invasive duration and hospital stay compared with physician-driven weaning. High-flow nasal oxygen is useful as a bridge during breaks off the mask, particularly in COPD. Prolonged non-invasive use risks skin breakdown and infection, so wean as soon as the primary problem is corrected.

There is no universal oxygen or carbon dioxide threshold that dictates intubation. The decision is made on clinical grounds: failure of non-invasive support, tissue hypoperfusion, haemodynamic instability, or loss of airway protection. ^[2]

Strong clinical indications include:

• failure of high-flow nasal oxygen or non-invasive ventilation with persistent hypoxaemia, rising carbon dioxide or worsening acidosis;
• inability to protect the airway (impaired consciousness, absent gag, uncontrolled vomiting or bleeding);
• haemodynamic instability with respiratory failure;
• shock with aspiration risk;
• exhaustion, falling tidal volumes or dropping mental status;
• anticipated prolonged or worsening course, severe acidemia (pH 7.25 or lower in COPD), or a "physiologically difficult airway" where delay is dangerous. ^[5]

Preoxygenate for at least 3 minutes before rapid sequence induction, using high-flow nasal oxygen or non-invasive ventilation, and consider apnoeic oxygenation by bag-valve mask during the apnoeic period (mixed trial evidence, but little harm). Video laryngoscopy increases first-pass success over direct laryngoscopy. In refractory hypoxaemia consider awake fibre-optic intubation. ^[2]

In hypercapnic failure, intubation corrects acidosis rapidly because alveolar ventilation is restored. Apnoea during the induction can worsen acidemia, so avoid a long apnoeic period: continue ventilation with non-invasive ventilation or bag-valve mask during the apnoeic interval, and consider awake fibre-optic intubation in selected cases. The decision to restrict a non-invasive trial to four hours before intubation, which is the approach taken in many units, should be discussed and agreed locally. ^[2]

Initial settings are chosen to be "normal" and then adjusted to the patient. The principles, and the evidence behind them, are:

• Mode. Start with a controlled (assist-control) mode so that minute ventilation is guaranteed; move to spontaneous (pressure support) as sedation lightens and the patient triggers.
• Tidal volume. Use the patient's predicted body weight, not actual weight. Current guidelines recommend 6 to 8 mL per kilogram of predicted body weight, particularly for ARDS. ^[6]
• Plateau pressure. Keep the plateau pressure (the pressure in the airways at end-inspiration, measured during a short inspiratory hold) under 30 cm water. ^[6]
• Positive end-expiratory pressure (PEEP). Use enough to keep recruited alveoli open, generally starting with a low level and titrating up in injurious lung disease alongside the inspired oxygen. The ARDSNet low-tidal-volume protocol table of PEEP and inspired-oxygen combinations remains a common reference; PEEP choices should be titrated to lung mechanics, oxygenation and haemodynamics. (No single starting value is mandated by the sources used here.)
• Respiratory rate. Titrate to keep the partial pressure of carbon dioxide normal or at the patient's chronic baseline.
• Inspired oxygen (FiO2). Titrate to the oxygen targets above (about 90 to 98 percent invasively ventilated), using the lowest concentration that achieves them. Avoid prolonged hyperoxia.
• Inspiratory (I:E) ratio. Use a conventional pattern with longer expiration; lengthen inspiration only in severe ARDS under deep sedation.
• Trigger sensitivity. Set to detect patient effort reliably.
• Plateau pressure limit and driving pressure (plateau pressure minus PEEP) are monitored; higher driving pressures are associated with worse outcomes in ARDS.

Sedate to a documented target (usually Richmond Agitation-Sedation Scale minus 2 to 0 in mechanically ventilated adults) and keep the patient calm enough to tolerate the tube but no deeper. Use continuous analgesia. Avoid unnecessary neuromuscular blockade; if prone positioning, severe patient-ventilator asynchrony or highly unstable oxygenation demands it, use the shortest effective paralysis and document the rationale. Delirium prevention, early mobilisation and reorientation shorten ventilation time and improve outcomes.

• Ventilator-induced lung injury: barotrauma (pneumothorax), volutrauma, atelectrauma, biotrauma.
• Ventilator-associated pneumonia and sinusitis.
• Cardiovascular effects: positive pressure reduces venous return and can cause hypotension.
• Critical illness weakness and ICU-acquired weakness.
• Sedation-related delirium, withdrawal and post-traumatic stress.
• Airway injury: endotracheal tube damage, tracheal stenosis, vocal cord injury.
• Adverse effects of any intervention are heightened in prolonged or overly deep ventilation.

Weaning has three parts: readiness assessment, a spontaneous breathing trial, and extubation.

Readiness markers (general critical care practice) include reversal of the precipitating cause, acceptable oxygenation on low-to-moderate inspired oxygen, haemodynamic stability, adequate cough and consciousness, manageable secretions, and no excess sedation.

A spontaneous breathing trial uses a low level of pressure support or a T-piece trial for a predefined period. Success is judged by the respiratory rate, tidal volume, oxygenation, carbon dioxide, haemodynamics and patient comfort. A rapid shallow breathing index (respiratory rate divided by tidal volume in litres) is often used as a screening test, but it should be interpreted in context rather than relied on alone.

After extubation, consider prophylactic high-flow nasal oxygen or non-invasive ventilation in high-risk patients (obesity, hypercapnia, previous failed extubation) to reduce reintubation. A patient who fails a spontaneous breathing trial or extubation needs a clear plan: more time, better clearance of the cause, or a tracheostomy in prolonged failure.

A tracheostomy is considered when prolonged ventilation is anticipated, or when the patient has severe upper airway obstruction or needs improved comfort and secretion clearance. It reduces sedation needs and may shorten weaning, but adds stoma infection and tracheal stenosis risks.

After any oxygen or ventilation intervention, reassess: saturation and blood gas, work of breathing, consciousness, haemodynamics, and the patient's goals. Write the target saturation on the chart and leave it there. De-escalate as the patient improves. Oxygen should be reduced once saturations are adequate and discontinued when air breathing maintains target, leaving the prescription in place for future deterioration. Non-invasive settings should be rechecked at every shift. Teach the clinical team and document clearly.

• Hyperoxia: absorption atelectasis, oxidative stress, coronary and cerebral vasoconstriction, and higher mortality with liberal oxygen strategies in some trials.
• Oxygen-induced hypercapnia in chronic lung disease, through removal of hypoxic vasoconstriction and the Haldane effect.
• Oxygen toxicity in premature infants (retinopathy) and prolonged high concentrations in adults.
• Interface trauma: dry nose, sinus pain, skin breakdown from masks and tubing.
• False reassurance from a normal saturation in carbon monoxide poisoning, dark skin, low perfusion or methaemoglobinaemia.
• Fire risk with high-flow oxygen.

• Pregnancy: maternal and fetal oxygenation must both be maintained; prevent hypoxia early, as the mother's tolerance of hypoxaemia is the safety margin for the fetus. Standard targets do not change much, but resuscitation targets higher saturations.
• Older adults: hypoxaemia may present as delirium or a fall; drug sensitivity demands lower sedation doses and slower titration.
• Children: lower saturation thresholds and different causes (bronchiolitis, congenital heart disease) apply; use paediatric oxygen and ventilation protocols.
• Immunocompromised patients: atypical progression and low thresholds for imaging and arterial blood gas sampling.

Oxygen is an essential medicine and often the single most useful therapy available. Concentrators that extract oxygen from room air are the preferred source in rural and low-resource hospitals and in home care; cylinders are expensive to transport and refill. Power reliability matters, and units should have a back-up oxygen source and a plan for filter maintenance and repair. Pulse oximetry is the key triage tool everywhere oxygen is given; where arterial blood gas testing is unavailable, clinical judgement and close observation carry the burden. Non-invasive ventilation requires a mask, a ventilator and trained staff; if these are absent, correct the treatable cause, give controlled oxygen and transfer.

Cross-checking with emergency medicine practice matters in three situations: oxygen prescribing, escalation speed and peri-intubation safety.

• Oxygen is a drug. In the emergency department, aim for the same target bands and record the device and flow on the observation chart. ^[1]
• Escalation is time-sensitive. A non-invasive trial should be reviewed within one to four hours and stopped promptly if there is no benefit. ^[2]
• Peri-intubation. Preoxygenate for at least 3 minutes, use apnoeic oxygenation where available, and treat hypoxaemia as a physiologically difficult airway. ^[2]
• Airway rescue algorithms (DAS 2015, ASA 2022) sit with the separate topic on general anaesthesia and airway management, which this page does not duplicate; the principle shared by both is that oxygenation takes priority over everything else, including the attempt to intubate. If intubation fails but oxygenation continues, oxygenation is not a failure.
• Cardiogenic pulmonary oedema in the emergency setting responds well to CPAP or BiPAP plus disease-directed therapy, with oxygen saturations kept at 92 to 98 percent when there is no hypercapnic risk. ^[2]

• Prescribe oxygen to a target saturation and monitor to keep within it; oxygen treats hypoxaemia, not breathlessness.
• Most acutely unwell adults need about 94 to 98 (or 92 to 96) percent; those at risk of hypercapnia need 88 to 92 percent.
• Escalate from cannula to face mask, reservoir mask, high-flow nasal oxygen and then non-invasive or invasive ventilation, using the least invasive device that works.
• High-flow nasal oxygen delivers up to 60 L per minute; start around 40 to 60 L per minute and titrate the oxygen fraction.
• Non-invasive ventilation is first-line for acute or acute-on-chronic hypercapnic respiratory failure and cardiogenic pulmonary oedema, with bilevel starter settings around 8 to 12 over 3 to 5 cm water.
• Intubate when non-invasive support fails, when the airway is unsafe, when haemodynamics are failing, or when exhaustion is impending; there is no single blood-gas threshold.
• Keep invasive ventilation lung-protective: 6 to 8 mL/kg predicted body weight, plateau pressure under 30 cm water, PEEP titrated, lowest tolerated inspired oxygen.
• Wean only after the cause reverses; use spontaneous breathing trials and prophylactic high-flow nasal oxygen after extubation in high-risk patients.
• Watch for hyperoxia, oxygen-induced hypercapnia, occult hypoxaemia in dark skin, and the limits of the oxygen saturation reading.
• In low-resource settings, concentrators, pulse oximetry and trained staff matter as much as the devices.

Oxygen targets and respiratory failure diagnosis; Acute respiratory distress syndrome; Chronic obstructive pulmonary disease; Asthma; Cardiogenic shock and acute heart failure; Pulmonary embolism; General anaesthesia and airway management; Pneumonia; Guillain-Barre syndrome and other neuromuscular causes of ventilatory failure. These are plain-text pointers; links will be added once the corresponding topics are verified.