Mechanical Ventilation

📋 Key Information Summary

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Indications for invasive mechanical ventilation include severe hypoxaemic respiratory failure (PaO₂/FiO₂ <200), hypercapnic respiratory failure with respiratory acidosis (pH <7.25), inability to protect the airway, and haemodynamic instability requiring positive-pressure support.
Respiratory failure types: Hypoxaemic (Type I) — impaired oxygenation from shunt, V/Q mismatch, or diffusion impairment; Hypercapnic (Type II) — alveolar hypoventilation from neuromuscular disease, chest wall restriction, or severe airflow obstruction.
Initial ventilator settings for lung-protective ventilation: tidal volume 6–8 mL/kg predicted body weight (PBW), plateau pressure ≤30 cmH₂O, driving pressure ≤15 cmH₂O, and respiratory rate 20–30 breaths/min titrated to pH >7.25.
Volume-controlled (VCV) delivers set tidal volume at variable pressure; pressure-controlled (PCV) delivers set pressure at variable volume. Both are acceptable; choose based on clinical context and patient comfort.
PEEP selection should balance alveolar recruitment against haemodynamic compromise. Start at 5 cmH₂O and titrate using FiO₂/PEEP tables, driving pressure response, or ARDSNet protocol.
FiO₂ titration: target SpO₂ 90–96% (88–92% in COPD). Wean FiO₂ first once PEEP is stabilised to minimise oxygen toxicity.
Ventilator-induced lung injury (VILI) occurs via barotrauma, volutrauma, atelectrauma, and biotrauma. Lung-protective ventilation reduces mortality in ARDS (NNT ~10 per ARDSNetwork trial).
VAP prevention bundle includes head-of-bed elevation 30–45°, daily sedation interruption, daily spontaneous breathing trial (SBT), oral care with chlorhexidine 0.12%, peptic ulcer prophylaxis, and DVT prophylaxis.
Weaning readiness requires: resolution of underlying cause, adequate oxygenation (PaO₂/FiO₂ ≥150–200 on PEEP ≤5–8 cmH₂O), haemodynamic stability, intact respiratory drive, and adequate mental status.
Spontaneous breathing trial (SBT) using low-level pressure support (PS 5–8 cmH₂O) or T-piece for 30–120 minutes is the standard readiness test. SBT failure demands return to prior support and reassessment within 24 hours.
Post-extubation high-flow nasal cannula (HFNC) reduces reintubation rates in at-risk patients. Prophylactic NIV is recommended for high-risk extubation (hypercapnia, cardiac failure, failed SBT).
Patient–ventilator dyssynchrony — trigger, flow, cycle, or auto-PEEP dyssynchrony — increases work of breathing, sedation requirements, and ICU length of stay; managed by adjusting trigger sensitivity, flow rates, and mode selection.

Introduction & Australian Epidemiology

Mechanical ventilation is the cornerstone of life support in the intensive care unit (ICU). In Australia, approximately 80,000–100,000 patients receive invasive mechanical ventilation annually across ~230 ICUs coordinated through the Australian and New Zealand Intensive Care Society (ANZICS). Mechanical ventilation accounts for the majority of ICU bed-days and is a principal determinant of ICU mortality, particularly in acute respiratory distress syndrome (ARDS) and severe pneumonia.

The ANZICS Centre for Outcome and Resource Evaluation (CORE) Adult Patient Database reports that approximately 30–40% of ICU admissions require invasive ventilation for ≥24 hours. In-hospital mortality for mechanically ventilated patients ranges from 25–45% depending on severity of illness, with ARDS-associated mortality of 35–46% for moderate-to-severe disease. The COVID-19 pandemic (2020–2023) substantially increased mechanical ventilation demand, with ~15–20% of hospitalised COVID-19 patients requiring ICU admission and invasive ventilation, prompting expansion of ICU capacity across Australian tertiary centres.

This guideline provides a comprehensive, evidence-based approach to initiation, management, complication avoidance, and liberation from mechanical ventilation, tailored to Australian clinical practice and resources.

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Australian ICU burden: ANZICS CORE data indicate median ventilation duration of 3.2 days (IQR 1.3–8.1). Ventilator-free days at day 28 are a key research endpoint. In Australia, ARDS accounts for ~10% of all ICU admissions and ~23% of mechanically ventilated patients (ANZICS ARDS study, 2022).

Indications & Initiation

Indications for Invasive Mechanical Ventilation

Invasive mechanical ventilation is indicated when non-invasive support is insufficient or contraindicated. The decision to intubate and ventilate is a clinical one integrating respiratory function, mental status, fatigue signs, and trajectory of illness.

Indication Category	Clinical Examples	Key Thresholds
Hypoxaemic respiratory failure (Type I)	ARDS, severe pneumonia, pulmonary oedema, pulmonary embolism, pneumothorax	PaO₂ <60 mmHg on FiO₂ ≥0.6, or PaO₂/FiO₂ <200 despite NIV/HFNC
Hypercapnic respiratory failure (Type II)	COPD exacerbation, severe asthma, neuromuscular disease (GBS, MND), obesity hypoventilation, drug overdose	pH <7.25 with PaCO₂ >60 mmHg despite maximal NIV
Airway protection	Reduced GCS (≤8), massive aspiration, angioedema, post-cardiac arrest	GCS ≤8 or inability to clear secretions
Haemodynamic instability	Cardiogenic shock, septic shock with respiratory compromise, massive PE	Requiring positive-pressure ventilation to offload work of breathing
Anticipated deterioration	Major burns >40% TBSA with inhalation injury, major surgery (post-operative), progressive neuromuscular weakness	Clinical trajectory assessment

Respiratory Failure Types

Type I (Hypoxaemic) respiratory failure results from impaired gas exchange with relative or absolute preservation of alveolar ventilation. The hallmark is PaO₂ <60 mmHg (8 kPa) with normal or low PaCO₂. Pathophysiology includes intrapulmonary shunt (e.g., lobar pneumonia, ARDS), V/Q mismatch (e.g., pulmonary embolism), and diffusion impairment (e.g., pulmonary fibrosis). Non-invasive approaches (HFNC, CPAP, NIV) may suffice in moderate hypoxaemia, but progression to PaO₂/FiO₂ <150 or failed trial of NIV mandates invasive ventilation.

Type II (Hypercapnic) respiratory failure results from alveolar hypoventilation with elevated PaCO₂ (>45 mmHg / 6 kPa) and secondary hypoxaemia. Causes include depressed central respiratory drive (opioid overdose, anaesthesia), neuromuscular weakness (Guillain–Barré syndrome, myasthenia gravis, motor neurone disease), chest wall restriction (kyphoscoliosis, flail chest), and severe airflow obstruction (COPD, acute severe asthma). NIV is first-line for acute COPD exacerbation with respiratory acidosis; failure (pH <7.25 after 1–4 hours) prompts intubation.

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Do not delay intubation in the crashing patient. Waiting for ABG results is inappropriate when clinical signs of impending respiratory arrest are present: agonal breathing, silent chest, severe accessory muscle use, paradoxical abdominal breathing, altered consciousness, or cardiac arrest imminent.

Ventilator Modes

Ventilator modes describe the combination of control variable (volume or pressure), phase variable (trigger, target, cycle), and whether mandatory or spontaneous breaths are delivered. The following are the modes most commonly used in Australian ICUs:

Mode	Abbreviation	Description	Indications
Assist Control — Volume Control	AC/VC or A/C-VCV	Every breath (patient- or machine-triggered) delivers set tidal volume. Guaranteed minute ventilation.	Initial mode for most patients; ARDS with lung-protective strategy
Assist Control — Pressure Control	AC/PC or A/C-PCV	Every breath delivers set inspiratory pressure for set time. Tidal volume varies with compliance.	Severe ARDS (with decelerating flow), patients with bronchopleural fistula
Synchronised Intermittent Mandatory Ventilation	SIMV	Set number of mandatory breaths (volume or pressure) + spontaneous breaths at patient effort. Spontaneous breaths may have PS support.	Weaning (largely supplanted by PS); some centres use for initial support
Pressure Support Ventilation	PSV	All breaths are patient-triggered, pressure-limited, flow-cycled. Patient controls rate and tidal volume.	SBT, weaning, NIV (BiPAP), post-extubation support
Pressure-Regulated Volume Control	PRVC	Pressure-controlled breaths with automatic adjustment of pressure to achieve target tidal volume. Decelerating flow pattern.	Hybrid mode; delivers volume guarantee with pressure waveform benefits
Neurally Adjusted Ventilatory Assist	NAVA	Uses diaphragmatic electrical activity (Edi) to trigger and cycle breaths. Proportional assist based on neural drive.	Improved synchrony; research tool and specialist centres
Airway Pressure Release Ventilation	APRV	Continuous positive airway pressure with brief, intermittent pressure releases for ventilation. Allows spontaneous breathing throughout.	Severe ARDS (evidence limited); used in some Australian centres

Initial Ventilator Settings — Lung-Protective Strategy

All mechanically ventilated patients should receive lung-protective ventilation as the default strategy, not only those with ARDS. This is based on the landmark ARDSNetwork (2000) trial demonstrating 22% relative mortality reduction with low tidal volume ventilation.

1

Tidal Volume

6 mL/kg predicted body weight (PBW); acceptable range 6–8 mL/kg PBW. Calculate PBW: Males = 50 + 0.91 × (height in cm − 152.4); Females = 45.5 + 0.91 × (height in cm − 152.4). Always use PBW, not actual body weight.

2

Respiratory Rate

Set 20–30 breaths/min. Adjust to maintain pH >7.25 and PaCO₂ at acceptable level. Avoid excessive rates (>35) due to auto-PEEP risk.

3

PEEP

Start at 5 cmH₂O. Titrate using ARDSNet FiO₂/PEEP table for ARDS. For non-ARDS, 5 cmH₂O is generally sufficient unless obese (8–12 cmH₂O) or significant atelectasis.

4

FiO₂

Start at 1.0 during induction, then titrate down to achieve SpO₂ 90–96%. In COPD, target SpO₂ 88–92%. Wean FiO₂ to ≤0.6 before adjusting PEEP upward.

5

Inspiratory Time & Flow

Inspiratory time 0.8–1.2 seconds. Flow rate 60 L/min (decelerating waveform preferred in VCV). Adjust for patient comfort and synchrony.

6

Target Limits

Plateau pressure (Pplat) ≤30 cmH₂O. Driving pressure (Pplat − PEEP) ≤15 cmH₂O. Confirm with end-inspiratory hold manoeuvre.

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Predicted Body Weight (PBW) is essential. Using actual body weight for tidal volume calculation in obese patients can result in significant overdistension. A 175 cm male has a PBW of ~70 kg; target V_T = 420 mL (6 mL/kg), not the 540 mL that might be calculated using an actual weight of 90 kg.

Ventilator Management

Volume-Controlled vs Pressure-Controlled Ventilation

The choice between volume-controlled (VCV) and pressure-controlled (PCV) ventilation has been extensively debated. Current evidence demonstrates no significant difference in clinical outcomes (mortality, duration of ventilation) between the two modes when lung-protective targets are achieved. The decision should be guided by clinical context:

Parameter	Volume-Controlled (VCV)	Pressure-Controlled (PCV)
Guaranteed parameter	Tidal volume (constant)	Inspiratory pressure (constant)
Varying parameter	Pressure varies with compliance and resistance	Tidal volume varies with compliance and resistance
Flow pattern	Square (constant) or decelerating	Decelerating (inherent)
Pplat monitoring	Essential — mandatory end-inspiratory hold	Approximate — peak pressure ≈ Pplat (brief pause)
Advantages	Guaranteed minute ventilation; precise volume control; easy titration of V_T	Lower peak pressures; better patient comfort; improved distribution in heterogeneous lungs
Disadvantages	Higher peak pressures if compliance deteriorates; less comfortable if flow demand not met	V_T not guaranteed — may rise or fall with changing compliance; requires close monitoring
Preferred when	Strict V_T control needed (ARDS); precise CO₂ targeting	Severe ARDS with high PEEP; bronchopleural fistula; patient comfort priority

PEEP Selection

Positive end-expiratory pressure (PEEP) prevents alveolar derecruitment at end-expiration, improves oxygenation, and reduces intrapulmonary shunt. However, excessive PEEP increases intrathoracic pressure, reduces venous return, and may cause overdistension of non-dependent lung regions.

ARDSNet FiO₂/PEEP Table (low PEEP strategy):

FiO₂	0.3	0.4	0.4	0.5	0.5	0.6	0.7	0.7	0.8	0.9	1.0
PEEP (cmH₂O)	5	5	8	8	10	10	10	12	14	14	14–18

High PEEP strategy (ART trial, Alvarado et al. 2017): Higher PEEP levels (using open-lung approach with PEEP titration based on best compliance, recruitment manoeuvres, or decremental PEEP trial) have not shown consistent mortality benefit over low PEEP strategy. However, the EPVent-2 trial (2019) using oesophageal manometry to titrate transpulmonary pressure showed improved oxygenation with physiological PEEP titration. In practice, consider higher PEEP (12–18 cmH₂O) in moderate–severe ARDS (P/F ratio <200) if plateau pressure remains ≤30 cmH₂O.

FiO₂ Titration

The goal of oxygen therapy in mechanically ventilated patients is to maintain adequate tissue oxygenation while minimising the risks of hyperoxia (absorption atelectasis, oxidative lung injury, coronary and cerebral vasoconstriction) and hypoxaemia.

Target SpO₂ 90–96% for most mechanically ventilated patients
Target SpO₂ 88–92% in patients with COPD, chronic CO₂ retention, or those at risk of hypercapnic respiratory failure
Initial FiO₂ 1.0 during intubation — rapidly wean to ≤0.6 within the first 30–60 minutes once PEEP is established
Wean FiO₂ in decrements of 0.05–0.10 guided by continuous pulse oximetry and arterial blood gas (ABG) analysis
Wean FiO₂ before PEEP — reduce FiO₂ to ≤0.60 before reducing PEEP below the target level
Limit FiO₂ to ≤0.60 long-term to reduce oxygen toxicity; if higher FiO₂ is needed, consider recruitment manoeuvres or prone positioning

Sedation Protocols

Sedation is a critical component of mechanical ventilation management, balancing patient comfort, safety, ventilator synchrony, and the adverse effects of excessive sedation (prolonged ventilation, ICU-acquired weakness, delirium).

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Light sedation target: The ACSQHC and ANZICS recommend targeting a Richmond Agitation–Sedation Scale (RASS) of 0 to −2 for most mechanically ventilated patients. Deep sedation (RASS −4 to −5) is associated with increased mortality, prolonged ventilation, delirium, and ICU-acquired weakness. Daily sedation interruption is recommended (unless contraindicated by status epilepticus, raised ICP, or active withdrawal management).

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Propofol

Diprivan® · General anaesthetic / sedative

Adult dose Continuous IV infusion 5–50 mcg/kg/min; titrate to RASS target (0 to −2)

Paediatric dose 2.5–5 mg/kg bolus; then 50–200 mcg/kg/min infusion (caution: propofol infusion syndrome risk)

Renal adjustment None required

Hepatic adjustment Reduce dose in hepatic impairment; risk of accumulation with prolonged use

PBS status ✔ PBS General Benefit

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Midazolam

Hypnovel® · Benzodiazepine

Adult dose IV bolus 1–2.5 mg PRN; infusion 0.5–5 mg/hr. Use only when propofol contraindicated — higher delirium risk.

Paediatric dose 0.05–0.1 mg/kg IV bolus; 0.01–0.1 mg/kg/hr infusion

Renal adjustment Active metabolite (α-hydroxymidazolam) accumulates in renal impairment — use with caution, reduce dose

Hepatic adjustment Significantly prolonged half-life in cirrhosis — reduce dose by 50% or avoid

PBS status ✔ PBS General Benefit

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Dexmedetomidine

Precedex® · α₂-agonist sedative

Adult dose Loading dose 1 mcg/kg IV over 10 min (often omitted); maintenance 0.2–0.7 mcg/kg/hr. Ceiling 1.5 mcg/kg/hr.

Paediatric dose 0.2–1 mcg/kg/hr infusion; no routine loading dose in paediatric ICU

Renal adjustment No dose adjustment required

Hepatic adjustment Reduce dose by 50% in moderate-to-severe hepatic impairment

PBS status 🔶 PBS Authority Required (ICU use)

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Fentanyl

Sublimaze® · Opioid analgesic

Adult dose 25–100 mcg IV bolus PRN; infusion 25–200 mcg/hr. Analgosedation approach: target CPOT 0–2.

Paediatric dose 0.5–2 mcg/kg IV bolus; 0.5–3 mcg/kg/hr infusion

Renal adjustment Active metabolites accumulate in renal failure — use morphine or hydromorphone alternative with dose reduction, or fentanyl with monitoring

Hepatic adjustment Reduce dose in severe hepatic impairment (prolonged clearance)

PBS status ✔ PBS General Benefit

Analgosedation approach: Current best practice favours an analgesia-first (analgosedation) strategy. Assess and treat pain first using the Critical-Care Pain Observation Tool (CPOT) or Behavioural Pain Scale (BPS). Commence IV paracetamol (1 g QID) and opioid (fentanyl or morphine) for analgesia. Add propofol or dexmedetomidine only if agitation persists despite adequate analgesia. Avoid benzodiazepine-based sedation where possible due to association with delirium (MIDEX/PRODEX trials).

Delirium Management

ICU delirium affects 45–87% of mechanically ventilated patients and is independently associated with increased 6-month mortality. Routine screening with the Confusion Assessment Method for ICU (CAM-ICU) or Intensive Care Delirium Screening Checklist (ICDSC) every 8–12 hours is mandatory per ACSQHC guidelines. Non-pharmacological interventions include reorientation, early mobilisation, sleep hygiene, hearing aids, and family presence. Pharmacological management with antipsychotics (haloperidol or quetiapine) is reserved for distressing delirium or safety concerns.

Complications of Mechanical Ventilation

Ventilator-Induced Lung Injury (VILI)

VILI is the acute lung injury caused or exacerbated by mechanical ventilation. It is mediated by four primary mechanisms, collectively termed the "four traumas of VILI":

Mechanism

Barotrauma

Excessive airway pressures cause alveolar rupture. Results in pneumothorax, pneumomediastinum, or subcutaneous emphysema. Risk increases with Pplat >30 cmH₂O.

Prevention: Pplat ≤30 cmH₂O, driving pressure ≤15 cmH₂O

Mechanism

Volutrauma

Excessive tidal volume stretches alveolar epithelium, activating inflammatory cascades. Transpulmonary pressure (not just airway pressure) determines alveolar distension.

Prevention: V_T 6 mL/kg PBW; driving pressure ≤15 cmH₂O

Mechanism

Atelectrauma

Repeated opening and closing of atelectatic alveoli generates shear forces that damage epithelium. Predominant in dependent lung regions with low PEEP.

Prevention: Adequate PEEP, recruitment manoeuvres, prone positioning

Mechanism

Biotrauma

Mechanical stress triggers release of pro-inflammatory cytokines (IL-6, IL-8, TNF-α) into systemic circulation, contributing to multi-organ dysfunction syndrome (MODS).

Prevention: All VILI prevention strategies reduce biotrauma

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Driving pressure is the strongest predictor of VILI mortality. Driving pressure (ΔP = Pplat − PEEP) reflects lung compliance relative to the size of the aerated lung (functional lung size). A ΔP >15 cmH₂O is independently associated with increased mortality in ARDS (Amato et al. 2015, NEJM). Always calculate and document driving pressure.

Barotrauma

Barotrauma occurs in 5–15% of mechanically ventilated patients and up to 20% of those with severe ARDS. Manifestations include pneumothorax (most common), pneumomediastinum, subcutaneous emphysema, pneumoperitoneum, and tension physiology. Risk factors include high PEEP (>15 cmH₂O), high Pplat (>30 cmH₂O), ARDS (especially with cystic changes on CT), and COPD with bullous disease.

Management of pneumothorax: Tension pneumothorax requires immediate needle decompression (2nd intercostal space, mid-clavicular line) followed by intercostal catheter (ICC) insertion. Non-tension pneumothorax in a ventilated patient always warrants ICC insertion due to positive-pressure ventilation risk of tension conversion. Use a 20–24 Fr ICC connected to underwater seal with −20 cmH₂O suction.

Ventilator-Associated Pneumonia (VAP)

VAP is pneumonia occurring >48 hours after endotracheal intubation. It is the most common ICU-acquired infection, affecting 10–20% of mechanically ventilated patients, with attributable mortality of 9–13%. In Australia, the VAP rate is approximately 8–12 episodes per 1000 ventilator-days (ANZICS infection monitoring).

Diagnostic criteria (ATS/IDSA 2016): New or progressive infiltrate on chest imaging + ≥2 of: fever >38°C or hypothermia <36°C, leucocytosis (>12 × 10⁹/L) or leucopenia (<4 × 10⁹/L), purulent secretions. Confirm with quantitative BAL (≥10⁴ CFU/mL) or endotracheal aspirate culture (≥10⁶ CFU/mL).

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NSQHS VAP Prevention Bundle (ACSQHC): Australian hospitals accredited under NSQHS Standards must implement VAP prevention bundles for all mechanically ventilated patients. Non-compliance with the VAP bundle is a clinical governance failure. The bundle should be documented on the bedside ventilator care sheet.

VAP prevention bundle components:

1

Head-of-Bed Elevation

Maintain 30–45° elevation to reduce aspiration risk. Reverse Trendelenburg may be used if unable to achieve standard elevation (e.g., spinal precautions).

2

Daily Sedation Interruption

Interrupt sedative infusions daily (light to sedation holiday) unless contraindicated. Combined with daily SBT, reduces ventilator days by 2 days (Girard et al. 2008, Lancet).

3

Daily SBT Assessment

Screen every morning for SBT readiness. If criteria met, perform SBT. This paired with sedation interruption is the ABCDE bundle.

4

Oral Hygiene

Chlorhexidine 0.12% oral rinse every 6–8 hours. Tooth brushing twice daily. Evidence for chlorhexidine in reducing VAP is mixed but it remains standard Australian practice (De Smet et al. 2022).

5

Peptic Ulcer Prophylaxis

Proton pump inhibitor (pantoprazole 40 mg IV/PO daily) or H₂-receptor antagonist for patients with risk factors (coagulopathy, mechanical ventilation >48 hrs).

6

DVT Prophylaxis

Enoxaparin 40 mg SC daily (or 30 mg SC BD if BMI >40 or CrCl <30 mL/min use unfractionated heparin 5000 units SC BD). Intermittent pneumatic compression devices for all patients.

VAP Empirical Antibiotic Therapy

Empirical antibiotic therapy for suspected VAP should be guided by local antibiograms (which vary across Australian hospitals) and risk factors for multidrug-resistant organisms (MDROs). Use eTG Antibiotic guidelines and local protocols. Duration of therapy: 7 days for uncomplicated VAP (per IDSA/ATS 2016; Pugh et al. 2016).

Early-onset VAP (<5 days), no MDRO risk

Piperacillin–tazobactam 4.5 g IV TDS or ceftriaxone 2 g IV daily

7 days

± Vancomycin if MRSA risk (nasal swab positive or local MRSA rate >20%)

Late-onset VAP (≥5 days) or MDRO risk factors

Meropenem 1 g IV TDS + vancomycin 25–30 mg/kg IV loading then 15–20 mg/kg IV BD–TDS (trough 15–20 mg/L)

7 days

Add colistin if VAP due to carbapenem-resistant Acinetobacter baumannii (increasing in Australian ICUs)

Patient–Ventilator Dyssynchrony

Dyssynchrony occurs when the ventilator and patient are not properly coordinated. It increases work of breathing, oxygen consumption, sedation requirements, and may worsen VILI. The four major types:

Type	Description	Cause	Management
Trigger dyssynchrony	Patient efforts fail to trigger a breath (ineffective triggering) or trigger extra breaths (auto-triggering)	Weak respiratory effort, auto-PEEP, trigger sensitivity too low, cardiac oscillations	Reduce trigger threshold; treat auto-PEEP (bronchodilators, reduce RR); consider PSV mode
Flow dyssynchrony	Patient inspiratory flow demand exceeds or falls below ventilator flow delivery	Fixed inspiratory flow too low (VCV); excessive drive from pain, anxiety, or acidosis	Increase peak flow (VCV) or use decelerating waveform; switch to PCV or PSV; treat underlying cause
Cycle dyssynchrony	Ventilator ends inspiration before (short cycling) or after (prolonged cycling) the patient's neural inspiration	Inspiratory time mismatch; short cycling in obstructive physiology; prolonged cycling in weak patients	Adjust inspiratory time; reduce flow termination criterion (PSV cycle-off); adjust I:E ratio
Auto-PEEP dyssynchrony	Intrinsic PEEP prevents triggering because patient must generate enough effort to overcome auto-PEEP before triggering threshold	Dynamic hyperinflation in COPD/asthma; high minute ventilation; inadequate expiratory time	Reduce respiratory rate; increase inspiratory flow; shorten I:E ratio; administer bronchodilators; set external PEEP to 80% of auto-PEEP

Additional complications:

ICU-acquired weakness (ICU-AW): Occurs in 25–50% of patients ventilated >7 days. Risk factors include corticosteroid use, neuromuscular blocking agents, sepsis, and immobility. Diagnosed by MRC sum score <48 or grip strength <11 kg (males) / <7 kg (females). Prevention through early mobilisation and minimising sedation is key.
Endotracheal tube complications: Mucosal injury, subglottic stenosis, vocal cord granuloma. Use appropriately sized ETT (7.0–8.0 for adult females, 7.5–8.5 for adult males). Subglottic secretion drainage ETTs reduce VAP risk.
Haemodynamic compromise: Positive-pressure ventilation reduces preload (venous return) and increases right ventricular afterload. Monitor for hypotension after PEEP increases. Fluid responsiveness may be assessed by pulse pressure variation (PPV) or passive leg raise test.

Weaning & Liberation from Mechanical Ventilation

Weaning Classification

Weaning accounts for approximately 40% of total ventilation duration. Patients are classified into three categories based on difficulty and duration of weaning:

Readiness to Wean — Screening Criteria

Daily screening for weaning readiness should be performed every morning by the bedside nurse or physiotherapist. All of the following criteria must be met:

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Resolution or improvement of cause of respiratory failure
Adequate oxygenation: PaO₂/FiO₂ ≥150 (or SpO₂ ≥90% on FiO₂ ≤0.40 and PEEP ≤8 cmH₂O)
Haemodynamic stability: No active myocardial ischaemia; no clinically significant hypotension (noradrenaline <0.1 mcg/kg/min or no vasopressor requirement)
Adequate respiratory drive: Capable of initiating spontaneous breaths
No planned procedures or surgery requiring heavy sedation/paralysis
Adequate mental status: GCS ≥13, following commands (modified criteria acceptable in patients with baseline cognitive impairment)
Adequate cough reflex and manageable secretions
Core temperature 36–38.5°C
Corrected electrolytes: K⁺ ≥3.5 mmol/L, Mg²⁺ ≥0.8 mmol/L, PO₄³⁻ ≥0.65 mmol/L, Ca²⁺ ≥1.1 mmol/L (ionised)

Spontaneous Breathing Trial (SBT)

The SBT is the gold-standard test of readiness for extubation. It assesses the patient's ability to breathe spontaneously with minimal support. Two principal methods are used in Australian ICUs:

SBT Method	Settings	Duration	Evidence
Low-level Pressure Support	PS 5–8 cmH₂O, PEEP 5 cmH₂O, FiO₂ 0.40	30–120 minutes (30 min is sufficient per Perren et al. 2002)	Preferred in most Australian ICUs; provides unloading of ETT resistance
T-Piece Trial	T-piece connected to ETT; supplemental O₂ via flow-by	30–120 minutes	More physiological; slightly more demanding; equivalent outcomes
CPAP	CPAP 5 cmH₂O, FiO₂ 0.40	30–120 minutes	Acceptable alternative; similar to PS 0 but eliminates ETT resistance compensation

SBT failure criteria: Any of the following within 30–120 minutes warrants return to prior ventilator support:

Respiratory rate >35 breaths/min sustained for >5 minutes
SpO₂ <88% on FiO₂ ≤0.50
Heart rate >140 or <50 bpm, or sustained change of >20% from baseline
Systolic BP >180 mmHg or <90 mmHg
Agitation, diaphoresis, anxiety, or altered mental status
Evidence of increased work of breathing: accessory muscle use, paradoxical breathing, nasal flaring

Extubation Criteria & Procedure

Successful SBT is necessary but not sufficient for extubation. Additional extubation readiness criteria include:

Adequate cough: Semi-quantitative cough strength score ≥3 (can cough against resistance)
Secretion burden: Manageable with suctioning ≤ every 2 hours
Upper airway patency: Cuff leak test positive (leak volume >110 mL or >15% of expired V_T). Negative cuff leak suggests laryngeal oedema — consider corticosteroid prophylaxis (see below).
No active upper airway obstruction or stridor on deflation of ETT cuff

⚠️

High-risk extubation patients — those with failed SBT, reintubation within 48–72 hours, hypercapnic respiratory failure, COPD, heart failure, BMI >30, or failed cuff leak test — require prophylactic post-extubation support with HFNC or NIV. Failure to provide this increases reintubation rates from ~5% to 15–25% (Hernández et al. 2016, JAMA).

Corticosteroids for laryngeal oedema prevention: For patients with a failed cuff leak test, administer methylprednisolone 20 mg IV 4 hours before planned extubation, then every 4 hours for 24 hours total (4 doses). This reduces stridor and reintubation for post-extubation laryngeal oedema (François et al. 2007, Chest; FACCLE trial).

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Methylprednisolone

Solu-Medrol® · Corticosteroid

Adult dose 20 mg IV every 4 hours × 4 doses (begin 4 hrs pre-extubation)

Paediatric dose 0.5 mg/kg IV every 4 hours × 4 doses (max 20 mg/dose)

Renal adjustment None required

Hepatic adjustment None required

PBS status ✔ PBS General Benefit

Post-Extubation Care

Post-extubation respiratory failure occurs in 10–25% of critically ill patients and is associated with significantly increased ICU and hospital mortality.

1

High-Flow Nasal Cannula (HFNC)

Commence HFNC at 50–60 L/min, FiO₂ titrated to SpO₂ 92–96%. The FLORALI trial (2015) demonstrated reduced reintubation rates with HFNC compared to conventional oxygen and non-inferiority to NIV for post-extubation respiratory failure. HFNC is first-line post-extubation support in most Australian ICUs.

2

Non-Invasive Ventilation (NIV)

Prophylactic NIV (BiPAP: IPAP 12–15 cmH₂O, EPAP 5–8 cmH₂O) is recommended for high-risk patients: hypercapnia during SBT, COPD, heart failure, or failed SBT. REVA trial (Thille et al. 2022) showed NIV failure reduced from 28% to 19% with prophylactic NIV in high-risk extubation.

3

Monitoring

Continuous SpO₂ monitoring for 24 hours. ABG at 30–60 minutes post-extubation. Reassess respiratory rate, accessory muscle use, and mental status every 1–2 hours for the first 12 hours. Low threshold for escalation if RR >30, SpO₂ <90%, or increased work of breathing.

4

Stridor Management

Post-extubation stridor occurs in 5–10%. First-line: nebulised adrenaline (4 mL of 1:1000 via nebuliser). Second-line: IV dexamethasone 8 mg stat. Re-intubation if no improvement within 30–60 minutes or if severe upper airway obstruction.

Reintubation

Reintubation rates of 10–20% are expected. Risk factors for reintubation include: age >65, APACHE II >12, heart failure, COPD, duration of ventilation >7 days, secretions copious or unmanageable, failed SBT, and post-extubation stridor. Reintubation within 48–72 hours is associated with significantly higher ICU mortality (up to 40%). A structured post-extubation protocol reduces reintubation by 40–50%.

Tracheostomy for Prolonged Ventilation

Tracheostomy should be considered when prolonged ventilation (>10–14 days) is anticipated. Early tracheostomy (within 7–10 days) may reduce ICU length of stay, sedation requirements, and laryngeal injury but has not been shown to reduce mortality (TracMan trial, 2013). Percutaneous dilatational tracheostomy (PDT) is the preferred technique in Australian ICUs, performed at the bedside under bronchoscopic guidance. Typically placed at the 2nd–3rd tracheal ring. Key considerations include anticoagulation management, anatomical assessment (thyromental distance, neck mobility), and timing relative to decannulation planning.

Special Populations

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Pregnancy

Physiological changes

Functional residual capacity reduced 20% (diaphragm elevation); minute ventilation increased 50% (progesterone-driven); mild respiratory alkalosis (PaCO₂ 30–32 mmHg is normal); elevated WCC (up to 15 × 10⁹/L)

Indications

Same as non-pregnant adults but lower threshold for intubation due to rapid desaturation (increased O₂ consumption, reduced FRC). Pre-eclampsia/eclampsia with pulmonary oedema, amniotic fluid embolism, peripartum cardiomyopathy.

Ventilator adjustments

Head-up 15–30° or left lateral tilt (≥15°) to reduce aortocaval compression, especially after 20 weeks gestation. V_T 6–8 mL/kg PBW as standard. Target PaCO₂ 30–35 mmHg in pregnancy (baseline is lower). Fetal monitoring is essential.

Medications

Propofol (Category B2), fentanyl (Category C), rocuronium (Category C) are generally acceptable. Avoid aminoglycosides (ototoxicity). Avoid prolonged midazolam (Category D — neonatal withdrawal risk).

👶

Paediatrics

Key differences

Higher metabolic rate, more compliant chest wall (easier to fatigue), smaller airways (more obstruction-prone), higher closing volume. ETT uncuffed <1 year (or cuffed 3.0–3.5); cuffed tubes used from 1 year in many Australian PICUs.

Tidal volume

5–8 mL/kg PBW in paediatric ARDS (PARDs criteria, PALICC 2015). Driving pressure ≤15 cmH₂O. Permissive hypercapnia acceptable if pH >7.20.

PEEP

Start at 5–8 cmH₂O; titrate to oxygenation and compliance. Children recruit more effectively than adults — prone positioning beneficial in paediatric ARDS.

Sedation

Paediatric ANZICS recommends COMFORT-B scale (target 12–23). Propofol infusion <48 hours strongly recommended (propofol infusion syndrome risk). Dexmedetomidine increasingly used (0.2–1 mcg/kg/hr). Midazolam 0.05–0.1 mg/kg/hr.

Weaning

SBT less validated in children. Extubation readiness assessment includes: adequate cough, minimal secretions, stable respiratory status, FiO₂ ≤0.50, PEEP ≤6–8 cmH₂O. Cuffed leak test mandatory before extubation in paediatrics.

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Elderly (≥65 years)

Physiological considerations

Reduced respiratory muscle strength, decreased chest wall compliance, increased closing volume, reduced mucociliary clearance, blunted respiratory drive. Higher risk of ventilator dependence.

Outcomes

ICU mortality for mechanically ventilated elderly patients aged ≥80 is 40–60%. Goals-of-care discussions are essential prior to or early in ventilation course. Frailty assessment (Clinical Frailty Scale ≥5) predicts poor outcomes independently of APACHE score.

Weaning

Weaning may take longer. Prolonged weaning more common. Early tracheostomy and rehabilitation-focused approach preferred. Low threshold for palliative care consultation when prolonged ventilation anticipated without realistic prospect of recovery.

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Renal Impairment

Ventilator adjustments

Metabolic acidosis (uraemic or lactic) may require higher respiratory rate to compensate (target pH >7.25). Fluid overload may worsen pulmonary oedema — consider ultrafiltration. PEEP may need to be higher to counteract interstitial pulmonary oedema.

Drug adjustments

Fentanyl: generally safe in moderate renal impairment (less active metabolites than morphine). Morphine: active metabolite (M6G) accumulates — avoid in severe CKD. Propofol: no adjustment. Midazolam: α-hydroxymidazolam accumulates — use with caution. Dexmedetomidine: no dose adjustment. Piperacillin–tazobactam: extend dosing interval (4.5 g IV BD in CrCl <20 mL/min).

Sedation monitoring

Sedation scoring may be unreliable in uraemic encephalopathy. BIS monitoring may be helpful. Daily sedation interruption essential to assess neurological status.

🫁

Hepatic Impairment

Key considerations

Hepatopulmonary syndrome, portopulmonary hypertension, hepatic hydrothorax, and coagulopathy all complicate ventilation. Elevated diaphragm from ascites impairs FRC — drain large-volume ascites prior to or early in ventilation.

Drug adjustments

Propofol: clearance reduced 30% in cirrhosis — lower dose needed. Midazolam: half-life doubled — avoid or use very low dose. Fentanyl: volume of distribution increased — may need lower bolus dose but similar infusion rates. Dexmedetomidine: reduce dose by 50% in moderate–severe hepatic impairment. Lorazepam preferred over midazolam if benzodiazepine required (glucuronidation is relatively preserved).

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Immunocompromised

Causes of respiratory failure

Consider broad differential: opportunistic infections (PJP, CMV, aspergillosis, TB), drug toxicity (bleomycin, methotrexate), DA-BOOP, diffuse alveolar haemorrhage, immune reconstitution syndrome. Early BAL is essential for diagnosis.

Outcomes

ICU mortality for immunocompromised patients requiring invasive ventilation is 50–80% (higher in haematological malignancy with neutropenia). Early multidisciplinary discussion regarding goals of care is imperative. Corticosteroids for ARDS in immunocompromised patients require careful risk–benefit analysis.

Infection control

Airborne precautions for suspected TB or viral pneumonitis. Reverse isolation for neutropenic patients. Appropriate antimicrobial escalation (broad empirical coverage) pending BAL results. Antifungal therapy for suspected invasive aspergillosis (voriconazole 6 mg/kg IV BD day 1, then 4 mg/kg IV BD).

⚖️

Obesity

Ventilator challenges

Reduced FRC, reduced chest wall compliance, increased work of breathing, increased O₂ consumption and CO₂ production. Atelectasis is common — higher PEEP (8–15 cmH₂O) often needed. Higher baseline SpO₂ may mask deterioration.

Key adjustments

ALWAYS use predicted body weight for V_T calculation (not actual body weight). Head-of-bed at 45° or reverse Trendelenburg. Recruitment manoeuvres (30–40 cmH₂O for 30–40 seconds) after disconnection or if desaturation occurs. Positioning: semi-recumbent >45°; prone positioning may be challenging but beneficial in ARDS.

Pharmacokinetics

Lipophilic drugs (propofol, fentanyl, midazolam) have increased volume of distribution — loading doses may need to be higher, but maintenance rates may be similar (use IBW + 0.4 × [actual − IBW] for dosing adjustments). Dexmedetomidine: use actual body weight for loading, IBW or adjusted body weight for infusion.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Australians experience disproportionately higher rates of respiratory disease and critical illness. The AIHW reports that Indigenous Australians are hospitalised for respiratory conditions at 2.3 times the rate of non-Indigenous Australians. Chronic suppurative lung disease, bronchiectasis, and chronic obstructive pulmonary disease (COPD) are more prevalent, often presenting at younger ages with greater severity. The burden of rheumatic heart disease, obesity, diabetes, and chronic kidney disease contributes to increased complexity when invasive mechanical ventilation is required.

Critically ill Indigenous patients more frequently present from remote and very remote areas, where access to tertiary ICUs requires aeromedical retrieval (Royal Flying Doctor Service, CareFlight). Delays in retrieval and the physiological stress of transport may result in more advanced illness at the time of ICU admission. ANZICS data indicate that Indigenous Australians admitted to ICU have higher severity of illness scores (APACHE III) at admission but comparable or improved mortality when adjusting for severity, suggesting effective ICU care when patients reach tertiary centres.

Access barriers

Remote communities (>500 km from tertiary ICU) rely on aeromedical retrieval. Retrieval times of 6–24 hours. Pre-retrieval stabilisation by remote health practitioners (often with limited critical care training) is crucial. St John NT and RFDS protocols guide pre-retrieval ventilator management with limited equipment.

Chronic lung disease burden

Bronchiectasis and COPD are 5–10 times more prevalent in Indigenous Australians, particularly in Top End and Central Australian communities. Post-infectious bronchiectasis (from childhood pneumonia, pertussis, or measles) predisposes to chronic respiratory failure and frequent ICU admissions. Long-term ventilation and tracheostomy may be more commonly needed.

Rheumatic heart disease

ARF/RHD prevalence in remote NT communities is among the highest globally. Patients with severe valvular disease may require ventilation for perioperative cardiac surgery or acute pulmonary oedema. Anticoagulation management (warfarin) must be considered when performing tracheostomy or procedures.

Communication and cultural safety

English may be a second, third, or fourth language for many patients from remote communities. Interpreter services (e.g., NT Aboriginal Interpreter Service) should be engaged early. Cultural practices around death and dying, family decision-making, and Country may influence end-of-life and goals-of-care discussions during prolonged ventilation. Allow family presence and consult Indigenous liaison officers where available.

Rehabilitation and weaning

Transfer back to remote communities post-ventilation may be limited by availability of rehabilitation services. Royal Darwin Hospital, Alice Springs Hospital, and Cairns Hospital have developing weaning and rehabilitation pathways. Telehealth follow-up for patients with tracheostomy in remote communities is an evolving service model (NT Department of Health).

AMR patterns

CA-MRSA is highly prevalent in remote NT communities (up to 40% of S. aureus isolates). Multi-drug resistant gram-negative organisms (ESBL-producing E. coli and Klebsiella) are increasingly reported. Local antibiograms should guide empirical VAP therapy — vancomycin or trimethoprim–sulfamethoxazole may be required empirically where CA-MRSA rates are high. RHDAustralia and CARAlert provide updated resistance data.

📚 References

1. Acute Respiratory Distress Syndrome Network, Brower RG, Matthay MA, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301–1308.
2. Amato MBP, Meade MO, Slutsky AS, et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med. 2015;372(8):747–755.
3. Girard TD, Kress JP, Fuchs BD, et al. Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial): a randomised controlled trial. Lancet. 2008;371(9607):126–134.
4. Kalil AC, Metersky ML, Klompas M, et al. Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis. 2016;63(5):e61–e111.
5. Hernández G, Vaquero C, González P, et al. Effect of postextubation high-flow nasal cannula vs conventional oxygen therapy on reintubation in low-risk patients: a randomized clinical trial. JAMA. 2016;315(13):1354–1361.
6. Thille AW, Muller G, Gacouin A, et al. Effect of postextubation high-flow nasal oxygen with noninvasive ventilation vs high-flow nasal oxygen alone on reintubation among patients at high risk of extubation failure: a randomized clinical trial. JAMA. 2019;322(15):1465–1475.
7. Young D, Harrison DA, Cuthbertson BH, Rowan K; TracMan Collaborators. Effect of early vs late tracheostomy on duration of mechanical ventilation and other outcomes: the TracMan randomized trial. JAMA. 2013;309(20):2121–2129.
8. François B, Bellissant E, Gissot V, et al. 12-h pretreatment with methylprednisolone versus placebo for prevention of postextubation laryngeal oedema: a randomised double-blind trial. Lancet. 2007;369(9567):1083–1089.
9. National Health and Medical Research Council (NHMRC). Australian guidelines for the prevention and control of infection in healthcare. Canberra: NHMRC; 2019 (updated 2024).
10. Australian Commission on Safety and Quality in Health Care (ACSQHC). National Safety and Quality Health Service Standards. 2nd ed. Sydney: ACSQHC; 2021.
11. Australian and New Zealand Intensive Care Society (ANZICS). Centre for Outcome and Resource Evaluation (CORE) Annual Report 2023. Melbourne: ANZICS; 2023.
12. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework 2023 summary report. Canberra: AIHW; 2023.
13. Goligher EC, Tomlinson G, Hajage D, et al. PEEP, driving pressure, and lung-protective ventilation in ARDS: a systematic review and meta-analysis of individual patient data. Am J Respir Crit Care Med. 2017;196(6):730–739.
14. Needham DM, Colantuoni E, Mendez-Tellez PA, et al. Lung protective mechanical ventilation and two year survival in patients with acute lung injury: prospective cohort study. BMJ. 2012;344:e2124.
15. RHDAustralia (Rheumatic Heart Disease Australia). RHDAustralia clinical guidelines: Acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: RHDAustralia; 2020.