01Purpose and principlesWhat the treatment does and how it fits into care.
Invasive ventilation is not simply the next oxygen device. It transfers control of the airway and much of breathing to a high-risk system that can cause hypotension, ventilator-induced lung injury, infection, delirium and weakness. Its benefit is greatest when the underlying process is reversible or bridgeable and escalation occurs before arrest. The critical-care conversation therefore combines immediacy, reversibility, baseline function, frailty, wishes and the probability that ventilation can achieve an outcome the person would value.
Respiratory failure can demand intubation through several mechanisms. Hypoxaemic failure may remain severe despite optimised oxygen, recruitment and positioning. Ventilatory failure may produce worsening carbon dioxide and acidaemia despite treatment and NIV. Airway failure arises from obstruction, coma or aspiration risk even if the first blood gas is tolerable. Neuromuscular weakness and secretion retention may cause sudden decompensation with little visible distress, so preserved oxygen saturation must not falsely reassure.
The first ventilator prescription is a monitored hypothesis. Use predicted rather than actual body weight when selecting protective tidal volume, avoid excessive plateau and driving pressures, titrate inspired oxygen away from unnecessary hyperoxia, and match PEEP to recruitability and haemodynamics. Disease-specific priorities differ: longer expiration in severe airflow obstruction, careful pressure limitation in injured lungs, and reliable backup rate plus secretion support in neuromuscular disease.
Key points
- Escalate on clinical trajectory, work of breathing, consciousness, haemodynamics, gas exchange and response to treatment rather than one numerical threshold in isolation.
- Call critical care early when NIV or high-flow support is being considered in a patient who could require intubation; rescue referral after collapse is preventable harm.
- Common indications include threatened airway, respiratory arrest, refractory oxygenation failure, progressive hypercapnic acidosis, severe fatigue, secretion failure and need for deep sedation or controlled ventilation.
- NIV failure is a diagnosis made actively: mask leak, synchrony, settings and reversible disease must be corrected, but prolonged ineffective NIV must not postpone intubation in an escalation candidate.
- Agree and document treatment ceilings before deterioration where possible; a decision against intubation should trigger an explicit alternative symptom and NIV plan, not therapeutic abandonment.
- Tracheal intubation in critical illness is a high-risk team procedure requiring pre-oxygenation, checklist, haemodynamic preparation, backup airway plans and waveform capnography.
- After intubation, immediately confirm ventilation, secure tube depth, institute analgesia and sedation, and treat hypotension and the precipitating disease.
- Use lung-protective ventilation where lung injury is present, then individualise PEEP, oxygen, respiratory rate and inspiratory flow to mechanics and gas-exchange goals.
- In obstructive disease, allow enough expiratory time and look for dynamic hyperinflation; worsening hypotension after ventilation may be caused by excessive intrinsic PEEP.
- Reassess every intervention through waveforms, pressures, blood gases and the patient; the ventilator supports physiology while sepsis, bronchospasm, oedema, weakness or another cause is treated.
02Indications, selection and cautionsWho may benefit, who needs urgent treatment and important alternatives.
Progressive upper-airway obstruction, recurrent aspiration, copious bleeding, seizures or reduced consciousness with inadequate airway reflexes requires expert airway control before oxygenation and access become impossible.
Persistent hypoxaemia despite appropriately delivered oxygen and non-invasive support, especially with increasing work, diffuse lung injury or haemodynamic compromise, requires immediate critical-care evaluation for invasive support and adjuncts.
Rising PaCO2 with worsening pH, somnolence, fatigue or reduced chest movement despite optimised cause-specific care and NIV signals inadequate alveolar ventilation and possible need for intubation.
Deteriorating pH, respiratory rate, consciousness or oxygenation after competent interface and setting optimisation means NIV is not achieving its goal; escalation status determines urgent intubation versus revised ceiling care.
Hypotension, rising airway pressures and incomplete expiratory flow return in severe asthma or COPD suggests breath stacking and intrinsic PEEP; disconnecting briefly and correcting expiratory time may be lifesaving.
03Assessment before treatmentTests and checks that guide safe selection.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Continuous ABCDE assessment and physiological trendFirst step - Why
- Identify immediate danger and response to respiratory support.
- Interpretation and limitations
- Respiratory rate, effort, mental state, SpO2, haemodynamics and urine output may deteriorate before a scheduled gas. Clinical concern itself should trigger response under NICE CG50.
- 02
Arterial blood gas with documented oxygen or support - Why
- Quantify oxygenation, ventilation, acid-base state and lactate.
- Interpretation and limitations
- Trend pH and PaCO2 after treatment; interpret PaO2 against FiO2 and device. A normal saturation on substantial oxygen can conceal severe gas-exchange failure, while weakness may cause hypercapnia before hypoxaemia.
- 03
Chest imaging and bedside lung assessment - Why
- Identify cause and reversible procedural complications.
- Interpretation and limitations
- Radiograph, ultrasound or CT may show oedema, consolidation, collapse, effusion or pneumothorax. Imaging must not delay decompression of suspected tension pneumothorax or control of a failing airway.
- 04
Ventilator waveforms, airway pressures and expiratory flow - Why
- Detect resistance, poor compliance, dyssynchrony and intrinsic PEEP.
- Interpretation and limitations
- High peak with preserved plateau suggests resistance; both high suggests reduced compliance or overdistension. Expiratory flow not returning to baseline before the next breath indicates gas trapping.
- 05
Waveform capnography after tracheal intubation - Why
- Confirm ongoing tracheal placement and monitor ventilation changes.
- Interpretation and limitations
- A sustained appropriate waveform supports tracheal placement in a perfusing patient. Sudden loss prompts immediate tube, circuit and circulation assessment; chest rise alone is insufficient confirmation.
- 06
Cause-directed microbiology, ECG and laboratory profile - Why
- Find reversible disease and anticipate induction risk.
- Interpretation and limitations
- Culture, viral testing, electrolytes, renal function, blood count, troponin or other tests follow the syndrome. Treat sepsis, hyperkalaemia or shock without waiting for all results.
04Treatment approachPreparation, options, escalation and aftercare.
01EscalateRecognise support failure earlyFirst stepEscalationRespiratory distress, gas-exchange failure or reduced consciousness is worsening despite initial treatment.+
- 1Call senior respiratory, anaesthetic and critical-care help while continuing ABCDE, target oxygen, monitoring and cause-specific emergency treatment.
- 2Assess airway protection, work and fatigue, consciousness, haemodynamics, secretions and serial gas trajectory; state what current support is failing to achieve.
- 3EscalationCorrect quickly reversible NIV problems such as interface leak, synchrony and settings only while an intubation-capable team prepares if escalation is appropriate.
- 4Confirm the treatment ceiling and communicate it to the patient or surrogate where feasible; document the plan for deterioration and symptom care.
02IntubatePrepare a high-risk airwayThe team decides invasive ventilation is necessary and consistent with the person's goals.+
- 1Allocate roles, use the local intubation checklist, optimise position and pre-oxygenation, and prepare primary, rescue and front-of-neck airway plans.
- 2Anticipate cardiovascular collapse with suitable access, vasopressor and fluid strategy; choose induction and neuromuscular medicines for physiology and allergy risk.
- 3The most experienced available operator performs the procedure with continuous monitoring and immediate waveform capnography, minimising repeated attempts and hypoxaemia.
- 4Secure and record tube position, start appropriate ventilation and sedation, obtain post-procedure assessment, and actively treat hypotension, pneumothorax or other complication.
03VentilateSet a protective first prescriptionA tracheal tube is confirmed and mechanical ventilation begins.+
- 1Select a controlled mode familiar to the unit and base tidal volume on predicted body weight, with pressure limits appropriate to lung injury risk.
- 2Titrate FiO2 to the clinical saturation target, choose PEEP from oxygenation, recruitability and haemodynamics, and set a rate that avoids harmful gas trapping.
- 3Check exhaled volume, plateau or equivalent pressure, waveforms, synchrony and blood gas; change one variable with a stated physiological goal.
- 4Use early prone positioning through the trained critical-care protocol when severe ARDS criteria and timing support it, alongside ongoing lung-protective ventilation.
04DeteriorateTroubleshoot sudden ventilator collapseA ventilated patient acutely desaturates, becomes hypotensive or develops high pressures.+
- 1Call for help, give high inspired oxygen and hand-ventilate if necessary while checking tube depth, patency, circuit disconnection and capnography.
- 2Consider displacement, obstruction, pneumothorax, equipment failure and severe bronchospasm; use rapid examination and ultrasound without delaying decompression when tension is likely.
- 3In obstructive gas trapping, allow full expiration by reducing rate or disconnecting briefly while treating bronchospasm and haemodynamic compromise.
- 4EscalationRepeat gas and imaging after stabilisation, identify the precipitant and document the revised ventilator and escalation plan.
05Regimens, contraindications and interactionsTreatment details and the circumstances that modify them.
Rapid-sequence induction agent selected for physiology
Use the anaesthetist-selected intravenous, weight-based dose from the current local critical-care intubation protocol, reducing it when shock or frailty requires.No induction agent is haemodynamically neutral. Prepare vasopressor support and a failed-airway plan; awareness can occur if dosing is inadequate, while full routine dosing in profound shock may cause cardiovascular collapse.
Rocuronium for rapid neuromuscular blockade
Give the protocol-specified rapid-sequence intravenous dose based on appropriate body-weight calculation, with immediate post-intubation sedation already prepared.Paralysis provides neither unconsciousness nor analgesia and can outlast a short induction drug. Maintain sedation, monitor neuromuscular recovery when continued, and anticipate difficult ventilation before administering any blocker.
Analgesia-first post-intubation sedation
Start a locally approved opioid and sedative infusion titrated to a documented sedation target, pain, haemodynamics and ventilator synchrony.Deep sedation prolongs ventilation and delirium unless specifically needed for paralysis, severe dyssynchrony or intracranial and respiratory goals. Review accumulation, hypotension, ileus, withdrawal and renal or hepatic clearance daily.
06Complications, monitoring and follow-upAdverse effects, response and longer-term review.
- Continuously monitor ECG, oxygen saturation, blood pressure and waveform capnography after intubation, with invasive pressure monitoring according to instability.
- Trend blood gas after material ventilator changes and clinical deterioration, interpreting pH, PaCO2 and oxygenation beside waveforms and mechanics.
- Record exhaled tidal volume, FiO2, PEEP, plateau or relevant pressure, compliance, secretions and synchrony on every critical-care review.
- Assess analgesia, sedation depth, delirium, neuromuscular blockade, pressure areas, eye care, thrombosis risk and readiness to lighten sedation each day.
- Review the invasive-ventilation indication, reversibility, liberation potential and treatment ceiling daily with the multidisciplinary team and family communication.
07Special situationsVariants, exceptions and circumstances that change the usual approach.
Intubation is haemodynamic therapy
Positive intrathoracic pressure reduces venous return and induction removes sympathetic drive. A marginal circulation can collapse even after technically perfect tube placement unless anticipated.
Peak is not plateau
A high peak pressure with a lower plateau points toward airway resistance or tube obstruction; a high plateau points toward compliance, volume or chest-wall problems.
The silent weak patient
Neuromuscular failure may present without dramatic accessory-muscle use. Falling vital capacity, weak cough, bulbar dysfunction and rising CO2 can be more informative than apparent calm.
NIV needs an exit
Every NIV trial should state success measures, review time and the response to failure. Without an exit plan, a helpful therapy becomes a mechanism for delayed intubation.
Permissive is not neglect
Accepting some hypercapnia can reduce ventilator injury, but only with deliberate pH, intracranial, pregnancy and haemodynamic assessment rather than failure to achieve ventilation.
08Common pitfallsFrequent interpretation and management errors.
- 01
Waiting for respiratory arrest before contacting critical care because one oxygen saturation appears acceptable.
- 02
Continuing ineffective NIV despite worsening acidosis and fatigue in a patient intended for invasive escalation.
- 03
Administering induction and paralysis without cardiovascular optimisation, post-intubation sedation or a failed-airway plan.
- 04
Using actual body weight to prescribe large protective tidal volumes in obesity.
- 05
Responding to high airway pressure without distinguishing resistance, compliance, pneumothorax and dynamic hyperinflation.
- 06
Treating the ventilator number while losing sight of sepsis, pulmonary oedema, obstruction, weakness or another reversible cause.