Mechanical Ventilation in the ICU — Complete Structured Guide

🫁 1 · Overview & Goals

What mechanical ventilation is — and is not

"Mechanical ventilation supports gas exchange while the cause of respiratory failure is treated — it is a form of life support, not a cure. Because positive pressure can itself injure the lung, the modern goal is not to normalise the blood gases but to keep the patient alive with the least possible harm: 'less is better'."

Summarised from Marino's The ICU Book; Irwin & Rippe's Intensive Care Medicine; Oh's Intensive Care Manual.

The four things a ventilator is asked to do

Goal	What it means	Set mainly by
Oxygenation	Raise/maintain arterial O₂	FiO₂ and mean airway pressure (PEEP, I:E)
Ventilation (CO₂)	Clear CO₂, control pH	Minute ventilation = tidal volume × respiratory rate
Reduce work of breathing	Rest fatigued muscles, cut myocardial O₂ demand	Level of support (control vs assist)
Buy time / protect the airway	Bridge while the disease is treated; secure the airway	The decision to intubate itself

Golden rule: oxygenation and ventilation are controlled by different knobs. Hypoxaemia → think FiO₂ and PEEP. Hypercapnia/acidosis → think tidal volume and rate. Confusing the two is the commonest bedside error.

📋 2 · Indications

When to start invasive ventilation

Category	Trigger	Typical causes
Airway protection	GCS ≤8, lost gag/cough, cannot clear secretions	Coma, TBI, stroke, seizures, poisoning
Hypoxaemic failure (Type 1)	PaO₂ <60 mmHg or SpO₂ <90% despite high-flow O₂; P/F falling on HFNO/NIV	ARDS, pneumonia, cardiogenic oedema
Hypercapnic failure (Type 2)	Rising PaCO₂ with pH <7.25, fatigue, rising work of breathing	COPD, asthma, neuromuscular weakness, sedative overdose
Haemodynamic / metabolic	Offload the work of breathing; secure ventilation for shock or high CO₂ production	Cardiogenic shock, post-arrest, severe sepsis, DKA with exhaustion
Peri-procedural	Controlled ventilation for surgery/transport/imaging	Theatre, agitated transfers, status epilepticus

Ventilation is a clinical decision, not a number. A tiring patient with a "reassuring" gas still needs support — trajectory and work of breathing matter more than a single value.

📐 3 · Respiratory Mechanics & the Pressures

The one equation that explains the ventilator

The equation of motion

P_applied = (Flow × Resistance) + (Volume ÷ Compliance) + PEEP

Every pressure the ventilator shows is a mix of a resistive part (moving gas through the tube and airways) and an elastic part (stretching the lung and chest wall). Separating the two is the whole art of reading a ventilated patient — and you separate them with a hold.

Peak, plateau and the inspiratory hold

A brief (~0.5 s) inspiratory hold stops flow. With no flow, the resistive component vanishes and the pressure falls from peak to the plateau — which equals alveolar pressure.

Pressure / measure	What it is	How to get it	Target / normal
Peak pressure (Ppeak)	Resistive + elastic pressure at end-inspiration	Read off the ventilator	Context-dependent
Plateau pressure (Pplat)	Alveolar pressure = elastic recoil only	Inspiratory hold ~0.5 s, passive patient	≤30 cmH₂O
Ppeak − Pplat	Airway resistance pressure	Subtract	Small; ↑ = obstruction/secretions/kink
PEEP (applied)	Pressure held in alveoli at end-expiration	Set on ventilator	≥5 cmH₂O usual
Auto-PEEP (occult/intrinsic)	Trapped end-expiratory pressure from incomplete emptying	Expiratory hold, passive patient	Ideally 0; treat if >5
Driving pressure (ΔP)	Tidal stretch of the lung = Pplat − total PEEP	Calculate	<14–15 cmH₂O
Mean airway pressure	Average airway pressure per cycle — drives oxygenation & haemodynamics	Displayed	↑ improves oxygenation, ↓ preload
Static compliance	Vt ÷ (Pplat − total PEEP)	Calculate	Normal 50–80; ARDS <25 mL/cmH₂O
Mechanical power	Total energy delivered/min (Vt, ΔP, rate, flow, PEEP)	Ventilator/derived	Lower is safer (emerging)

Read Pplat and ΔP with every big change. Peak pressure alone misleads — a high peak with a normal plateau is a resistance problem (suction, bronchodilate), while a high plateau is a lung/chest-wall problem (reduce Vt, treat the cause).

🎛 4 · Modes of Ventilation

Modes without the jargon

"There are said to be well over a hundred named modes, yet only a handful are needed to ventilate almost every patient safely. A mode is just two choices: what the ventilator controls during the breath, and who decides when breaths happen."

Summarised from Marino's The ICU Book; Oh's Intensive Care Manual.

Choice 1 — what the ventilator controls

Control variable	You set	What varies	Where it shines
Volume control (VC)	Tidal volume + flow	Pressure varies with mechanics	Guarantees lung-protective Vt — the ICU default
Pressure control (PC)	Inspiratory pressure + time	Volume varies with compliance	Comfort, decelerating flow, leaks; poor lungs
Dual / adaptive (PRVC, VC⁺, AutoFlow)	Target Vt, capped pressure	Ventilator adjusts pressure breath-to-breath	Volume guarantee + pressure limit combined

Choice 2 — who triggers the breaths

Breath sequence	How it behaves	Best used for
Assist–Control (AC / CMV)	Every breath (patient- or timer-triggered) gets the full set breath	Full support; the standard starting mode
SIMV	Set mandatory breaths synchronised with the patient; extra breaths are spontaneous (± pressure support)	Largely historical for weaning; mixed breaths
Pressure Support (PSV) / spontaneous	Patient triggers every breath; ventilator adds a set pressure boost. No backup rate	Spontaneous breathing & weaning trials
APRV	Prolonged high CPAP with brief releases; spontaneous breathing throughout	Rescue oxygenation in selected ARDS
CPAP	Constant pressure, all breaths spontaneous, no inspiratory boost	Oxygenation support, SBTs, NIV

The pragmatic takeaway

Volume-Control Assist–Control (VC-AC) is the safe default for almost every newly-intubated ICU patient because it guarantees a lung-protective tidal volume. Switch to Pressure Support when the patient is waking and you are weaning. The head-to-head differences are tabulated in §14.

💊 5 · Initial Settings & Targets

Setting up the ventilator

Default starting point — Volume-Control Assist–Control

Mode: VC-AC (guarantees tidal volume)
Tidal volume: 6–8 mL/kg predicted body weight (start 8, fall to 6)
Rate: 12–16/min, titrated to pH 7.35–7.45
FiO₂: start 1.0, wean fast to the SpO₂ target
PEEP: 5 cmH₂O (higher in ARDS by table)
Flow: 60 L/min (80–100 in obstruction)
I:E: 1:2 (1:3–1:4 in COPD/asthma)
Trigger: flow 1–2 L/min or −1 to −2 cmH₂O

Predicted body weight (PBW) — always dose Vt on this, never actual weight

The formula

Male: PBW = 50 + 2.3 × (height in inches − 60)
Female: PBW = 45.5 + 2.3 × (height in inches − 60)
PBW depends on height only — the lungs of a tall thin person and an obese person of the same height are the same size.

Height (cm)	PBW male (kg)	PBW female (kg)	Vt 6 mL/kg (M/F)	Vt 8 mL/kg (M/F)
155	55.5	51.0	333 / 306 mL	444 / 408 mL
160	57.7	53.2	346 / 319 mL	462 / 426 mL
165	62.2	57.7	373 / 346 mL	498 / 462 mL
170	66.8	62.3	401 / 374 mL	534 / 498 mL
175	71.3	66.8	428 / 401 mL	570 / 534 mL

Targets to defend at the bedside

Parameter	Target	If out of range
Plateau pressure	≤30 cmH₂O	Reduce Vt by 1 mL/kg (down to 4); raise rate to hold minute ventilation
Driving pressure (ΔP)	<14–15 cmH₂O	Lower Vt or re-titrate PEEP to the lowest ΔP
Auto-PEEP	≈0	Lengthen expiration: ↓ rate, ↑ flow, ↓ I:E; treat obstruction
SpO₂	88–95% (ARDS); 92–96% others	Low → ↑ PEEP/FiO₂; high → wean FiO₂ (toxicity)
pH	7.35–7.45 (accept 7.25–7.30 permissive)	Acidaemia → ↑ rate if Pplat allows; alkalaemia → ↓ rate

🫁 6 · Lung-Protective Ventilation & ARDS

Why the ventilator can injure the lung

"The discovery that the ventilator can produce a lung injury indistinguishable from ARDS changed everything. Every setting is now chosen to limit stretch, cyclic collapse and the energy delivered to the lung. The only ventilator strategy that has ever improved survival in ARDS is the one that limits this injury."

Summarised from Marino's The ICU Book; Irwin & Rippe's Intensive Care Medicine; Oh's Intensive Care Manual.

Ventilator-induced lung injury (VILI) — the four mechanisms

Mechanism	Cause	Prevented by
Volutrauma	Over-distension from large tidal volumes into small ARDS lungs ("baby lung")	Low Vt (6 mL/kg PBW), Pplat ≤30, low ΔP
Atelectrauma	Repeated opening/closing (shear) of unstable alveoli	Adequate PEEP to keep alveoli open
Barotrauma	Air leak — pneumothorax, pneumomediastinum — from high alveolar pressure	Limit Pplat, low Vt
Biotrauma	Mechanical stress → cytokine release → systemic inflammation & multi-organ failure	All of the above (limit stress/strain & power)

The ARDSNet lung-protective protocol

Set volume & oxygenation

PBW → Vt 8 mL/kg, PEEP 5, lowest FiO₂ for SpO₂ 88–95%. Then reduce Vt by 1 mL/kg every ~2 h to 6 mL/kg.

Protect the alveoli

Measure Pplat. If >30 → drop Vt in 1 mL/kg steps (to a floor of 4 mL/kg). Keep ΔP <14–15.

Titrate PEEP to FiO₂

Use a PEEP/FiO₂ table; higher PEEP for moderate–severe ARDS. Optimise for lowest ΔP and best oxygenation without over-distension.

Accept permissive hypercapnia

Low Vt raises CO₂ — tolerate pH down to ~7.25–7.30 provided no contraindication (raised ICP, severe pulmonary hypertension).

Rescue for refractory hypoxaemia (P/F <150)

Prone ≥16 h/day (PROSEVA); neuromuscular blockade in early severe ARDS; consider recruitment cautiously; ECMO (EOLIA/veno-venous) if still failing.

ARDS adjuncts — evidence at a glance

Intervention	When	Evidence
Low Vt (6 mL/kg)	All ARDS	ARDSNet — absolute mortality ↓ ~9%; the foundation
Low driving pressure	All ARDS	ΔP is the variable most strongly linked to survival (Amato)
Prone positioning	P/F <150, moderate–severe	PROSEVA — significant mortality reduction with ≥16 h/day
Neuromuscular blockade	Early severe ARDS, dyssynchrony	Improves oxygenation; use short course (ACURASYS/ROSE)
Higher PEEP	Moderate–severe, PEEP-responsive	Benefit in more severe disease; individualise
Veno-venous ECMO	Refractory despite the above	Rescue in expert centres (EOLIA + meta-analysis)

🌀 7 · Obstructive Disease & Auto-PEEP

The opposite problem — the lung that won't empty

"In severe airflow obstruction, exhalation is not finished before the next breath begins. Gas is trapped, the lung hyperinflates, and end-expiratory pressure builds up unseen. It raises the trigger threshold, impedes venous return, and can collapse the circulation."

Summarised from Marino's The ICU Book; Oh's Intensive Care Manual.

Aspect	Detail
Where	Asthma, COPD — high airway resistance, slow emptying
Consequences	Dynamic hyperinflation → ↑ intrathoracic pressure → ↓ venous return → hypotension; missed triggers & extra work; barotrauma risk
Detect	Expiratory flow does not return to zero before the next breath (flow waveform)
Measure	Expiratory-hold manoeuvre (passive patient) reveals the trapped pressure
Treat	Lengthen expiration: ↓ rate, ↑ inspiratory flow, ↓ I:E (1:3–1:4), smaller Vt; treat bronchospasm; suction. Match a modest applied PEEP to reduce trigger work
Emergency	Sudden hypotension on the ventilator in an asthmatic → disconnect and let the chest deflate (and exclude pneumothorax)

Permissive hypercapnia is deliberate here too. In severe asthma, accept a high CO₂ and low-ish pH to avoid the lethal spiral of fast rates and gas-trapping.

📈 8 · Monitoring, Waveforms & DOPE

Reading the ventilated patient

Clue	Interpretation	Action
↑ Peak, normal Plateau	Airway resistance problem	Suction, bronchodilators, check tube/kink
↑ Peak, ↑ Plateau	Lung/chest-wall compliance problem	↓ Vt; treat oedema/ARDS/pneumothorax/abdomen
Expiratory flow not to zero	Auto-PEEP / gas trapping	Lengthen expiration (§7)
Pressure–time "scooping"	Flow starvation (air hunger)	↑ flow, switch to decelerating flow/PC
Double-triggering / missed triggers	Patient–ventilator dyssynchrony	Adjust trigger, Ti, flow, sedation; treat auto-PEEP

🚨 Sudden deterioration on the ventilator — DOPE

D — Displacement: tube in the oesophagus, right main bronchus, or out — check ETCO₂, position, air entry
O — Obstruction: secretions/mucus plug, biting, kink → suction, pass a catheter
P — Pneumothorax: tension — unilateral silent chest, tracheal shift, collapse → decompress
E — Equipment: circuit/O₂/ventilator failure → disconnect and hand-bag with 100% O₂ — this both rescues and diagnoses

⚠️ 9 · Complications of Mechanical Ventilation

What positive pressure costs

Complication	Mechanism	Prevention / management
VILI (volu-/atelec-/baro-/biotrauma)	Excess stretch, cyclic collapse, air leak, inflammation	Lung-protective settings; limit Pplat, ΔP, power
Haemodynamic compromise	↑ intrathoracic pressure → ↓ venous return & RV afterload	Volume, lower mean airway pressure, treat auto-PEEP
Ventilator-associated pneumonia	Micro-aspiration past the cuff	Ventilator bundle: head-up 30–45°, oral care, sedation holds, subglottic suction
Oxygen toxicity	Sustained high FiO₂ → free-radical lung injury	Wean FiO₂ to the lowest that meets the SpO₂ target
Auto-PEEP / dynamic hyperinflation	Incomplete emptying	Prolong expiration (§7)
Diaphragm dysfunction (VIDD)	Disuse atrophy from over-assist/over-sedation	Allow spontaneous effort, avoid deep sedation, wean early
Patient–ventilator dyssynchrony	Mistimed support	Tune trigger/flow/Ti; analgo-sedation; treat cause
ICU-acquired weakness & delirium	Immobility, sedation	ABCDEF bundle: daily SAT/SBT, early mobilisation

🎯 10 · Weaning & Extubation

Getting the patient off the ventilator

"Weaning should begin the day intubation begins. The evidence is consistent: a daily paired sedation-and-breathing trial liberates patients sooner than any gradual 'wind-down' of support. Most patients do not need to be weaned — they need to be recognised as ready."

Summarised from Marino's The ICU Book; Irwin & Rippe's Intensive Care Medicine; Oh's Intensive Care Manual.

Step 1 — daily readiness screen

Domain	Ready when…
Cause	Reason for ventilation improving/resolved
Oxygenation	P/F ≥150; PEEP ≤8; FiO₂ ≤0.5
Haemodynamics	No/low vasopressor, stable
Neurology & airway	Awake, following commands, good cough, manageable secretions

SAT then SBT (paired)

Pass a spontaneous awakening trial (sedation off), then a spontaneous breathing trial: PS 5–8 + PEEP 5 (or T-piece) for 30–120 min.

Judge the SBT

Pass: SpO₂ ≥90%, RR <35, HR/BP stable, comfortable. RSBI = RR ÷ Vt(L); <105 predicts success. Fail: distress, tachypnoea, desaturation → rest 24 h, find why.

Extubate

Do a cuff-leak test if prolonged/traumatic intubation or high stridor risk; treat a low leak with steroids before extubation. Have re-intubation kit ready.

Support after extubation

HFNO and/or prophylactic NIV reduce re-intubation in high-risk patients (hypercapnia, obesity, cardiac, COPD). Consider tracheostomy if weaning is prolonged.

😮‍💨 11 · NIV & High-Flow Nasal Oxygen

Support without a tube

Where the evidence is strongest for NIV

Indication	Strength	Note
COPD exacerbation with respiratory acidosis (pH <7.35)	Strong — first line	Reduces intubation and mortality
Cardiogenic pulmonary oedema	Strong	CPAP or NIV; rapid improvement
Immunocompromised hypoxaemia	Reasonable (early)	Avoid intubation-related infection
Post-extubation (high-risk / COPD)	Preventive	Prophylactic NIV/HFNO cut re-intubation
De novo hypoxaemic failure / ARDS	Cautious	Watch closely; late failure is dangerous — don't delay intubation

HFNO — how it helps & when to worry

High-flow nasal oxygen

Warmed, humidified O₂ up to 60 L/min delivering a stable high FiO₂, some PEEP effect, dead-space washout and comfort. Track the ROX index = (SpO₂/FiO₂) ÷ RR — a low or falling ROX (roughly <4.88 at 2–12 h) flags likely failure and the need to escalate.

Contraindications / cautions to NIV
Cardiac/respiratory arrest · unprotected airway, coma, high aspiration risk · facial trauma/surgery · haemodynamic instability or arrhythmia · undrained pneumothorax · copious secretions · agitation/non-cooperation · rapidly deteriorating gas exchange (needs intubation)

The cardinal NIV error is persisting with a failing trial. Reassess within 1–2 h — if pH, CO₂, work of breathing or consciousness are not improving, intubate rather than "give it longer".

🚫 12 · Common Mistakes

Common mistakes

❌ 1 — Dosing tidal volume on actual (not predicted) body weight

An obese patient's lungs are sized to height, not weight. Using actual weight delivers huge volumes into small lungs = volutrauma. Always calculate PBW before connecting the ventilator.

❌ 2 — Watching peak pressure and ignoring plateau

Peak pressure is not alveolar pressure. In bronchospasm the peak may be high while the plateau is safe; in ARDS a "modest" peak can hide a dangerous plateau. Measure Pplat and ΔP.

❌ 3 — Fast rates in asthma/COPD

Short expiration → gas trapping → auto-PEEP → hypotension. Use low rates, high flow and long expiratory time; tolerate the CO₂.

❌ 4 — Leaving FiO₂ at 1.0

Sustained hyperoxia injures the lung. Wean FiO₂ quickly to the lowest that meets the SpO₂ target (88–95% in ARDS).

❌ 5 — No daily SAT + SBT

Gradual "weaning modes" prolong ventilation. A daily paired awakening + breathing trial liberates patients sooner and improves outcomes — document why if skipped.

❌ 6 — Flogging a failing NIV trial

Delayed intubation after NIV failure worsens outcomes. Set a clear 1–2 h reassessment and escalate decisively.

🎓 13 · Exam Pearls — DrNB / PDCC / IDCCM / IFCCM

Exam pearls

Q: Why 6 mL/kg and why predicted body weight?
Low tidal volume limits volutrauma/biotrauma; PBW (height-based) matches lung size — the ARDSNet strategy is the only ventilator setting shown to improve ARDS survival.

Q: How do you measure the plateau pressure and what is it?
A ~0.5 s inspiratory hold in a passive patient; with no flow the pressure equals alveolar pressure (elastic recoil). Target ≤30. Ppeak − Pplat = airway resistance pressure.

Q: What is driving pressure and its target?
ΔP = Pplat − total PEEP = the tidal strain on the lung. It is the parameter most strongly associated with mortality; keep <14–15 cmH₂O.

Q: How do you detect and treat auto-PEEP?
Detect: expiratory flow not returning to zero. Measure: expiratory-hold manoeuvre. Treat: prolong expiration (↓ rate, ↑ flow, ↓ I:E) and relieve obstruction; disconnect if it causes shock.

Q: RSBI — definition and cut-off?
Rapid Shallow Breathing Index = respiratory rate ÷ tidal volume in litres, measured on minimal support. <105 predicts a successful breathing trial/extubation.

Q: Rescue options for refractory ARDS (P/F <150)?
Prone ≥16 h/day, neuromuscular blockade in early severe disease, individualised higher PEEP, and veno-venous ECMO when these fail.

Q: DOPE?
Displacement, Obstruction, Pneumothorax, Equipment — and the first move for sudden deterioration is to disconnect and hand-bag with 100% O₂.

⭐ 14 · Key Differences — Comparison Tables

All the head-to-head comparisons in one place

The distinctions people confuse most, collected at the end for quick revision. Learn these as pairs — most viva questions and bedside decisions are a choice between two of them.

Volume Control vs Pressure Control

Feature	Volume Control (VC)	Pressure Control (PC)
You set	Tidal volume + flow	Inspiratory pressure + time
Guaranteed	Tidal volume	Airway pressure
What varies	Airway pressure (with mechanics)	Tidal volume (with compliance)
Flow pattern	Constant (square)	Decelerating
Main strength	Lung-protective Vt guaranteed	Comfort, leak tolerance, less dyssynchrony
Main risk	High pressures if lungs stiffen	Volutrauma if compliance suddenly improves

Assist–Control vs SIMV vs Pressure Support

Feature	AC / CMV	SIMV	PSV (spontaneous)
Every breath supported?	Yes — full set breath	Only the mandatory ones	Yes, but patient-triggered
Backup rate	Yes	Yes	No
Work of breathing	Lowest	Intermediate/variable	Patient does most
Best use	Full support, sick lungs	Largely historical	Weaning / SBT

Peak vs Plateau pressure

Pattern	Meaning	Do
↑ Peak, normal Plateau	Resistance problem (secretions, bronchospasm, kink)	Suction, bronchodilate, check tube
↑ Peak, ↑ Plateau	Compliance problem (ARDS, oedema, pneumothorax, tight abdomen)	↓ Vt, treat the cause

The VILI mechanisms

Term	Injury from	Fixed by
Volutrauma	Over-distension (big volumes)	Low Vt
Barotrauma	High pressure → air leak	Limit Pplat
Atelectrauma	Cyclic open/close (shear)	Adequate PEEP
Biotrauma	Inflammatory cascade	Limit stress/strain & power

Applied PEEP vs Auto-PEEP

Feature	Applied (extrinsic) PEEP	Auto (intrinsic/occult) PEEP
Origin	Set by you on the ventilator	Trapped gas, incomplete emptying
Visible?	Yes, on the display	Hidden — needs an expiratory hold
Purpose/effect	Keeps alveoli open (good)	Hyperinflation, hypotension, extra work (bad)
Management	Titrate to oxygenation/ΔP	Prolong expiration, treat obstruction

Restrictive (ARDS) vs Obstructive (COPD/asthma) ventilator strategy

Setting	ARDS (stiff lungs)	COPD / Asthma (obstructed)
Core danger	Over-distension of small lung	Gas trapping / auto-PEEP
Tidal volume	Low (6 mL/kg)	Low–normal
Rate	Higher (compensate low Vt)	Low (allow full exhalation)
I:E	1:1–1:2	1:3–1:4
Flow	Moderate	High (shorten inspiration)
PEEP	Higher (recruit)	Low/matched to auto-PEEP
Key rescue	Prone, NMBA, ECMO	Bronchodilators; disconnect if shocked

CPAP vs BiPAP (NIV) vs HFNO

Feature	CPAP	BiPAP / NIV	HFNO
Pressures	One constant pressure	Two levels (IPAP + EPAP)	Flow-based, small PEEP effect
Helps mainly	Oxygenation	Ventilation (IPAP−EPAP boosts Vt) + oxygenation	Oxygenation + comfort/washout
Best for	Cardiogenic oedema, OSA	COPD with hypercapnic acidosis	Hypoxaemic failure, post-extubation
Interface	Mask	Mask	Nasal cannula (well tolerated)

NIV vs Invasive ventilation

Feature	Non-invasive (NIV)	Invasive (via ETT/tracheostomy)
Airway protection	None	Yes (cuffed tube)
Best candidates	Awake, cooperative, reversible cause (COPD, oedema)	Coma, shock, secretions, failed/failing NIV
Key risks	Aspiration, delay to intubation, mask injury	VILI, VAP, sedation, weaning, tube trauma
Escalation	Reassess in 1–2 h — intubate if not improving	De-escalate via weaning & SBT

SBT pass vs fail

Sign	Pass (extubate)	Fail (rest & reassess)
RSBI	<105	>105
Respiratory rate	<35	>35, accessory muscles
SpO₂	≥90% on low FiO₂	Desaturation
Haemodynamics	Stable	Tachycardia, hypertension, agitation

📚 15 · References

References

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Irwin RS, Lilly CM, Mayo PH, Rippe JM (eds). Irwin & Rippe's Intensive Care Medicine. 9th ed. Philadelphia: Wolters Kluwer; 2023.
Bersten AD, Handy JM (eds). Oh's Intensive Care Manual. Elsevier; 2026.
Acute Respiratory Distress Syndrome Network (ARDSNet). Ventilation with lower tidal volumes for acute lung injury and ARDS. N Engl J Med. 2000;342:1301–1308.
Amato MBP, Meade MO, Slutsky AS, et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med. 2015;372:747–755.
Guérin C, Reignier J, Richard JC, et al. (PROSEVA). Prone positioning in severe acute respiratory distress syndrome. N Engl J Med. 2013;368:2159–2168.
Papazian L, Forel JM, Gacouin A, et al. (ACURASYS). Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med. 2010;363:1107–1116.
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Girard TD, Kress JP, Fuchs BD, et al. (ABC trial). Paired sedation and ventilator weaning protocol. Lancet. 2008;371:126–134.
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Roca O, Caralt B, Messika J, et al. The ROX index to predict outcome of high-flow nasal oxygen. Am J Respir Crit Care Med. 2019;199:1368–1376.