Mechanical Ventilation Basics

Mechanical ventilation is the cornerstone of critical-care and intra-operative support, replacing or augmenting the work of breathing while protecting the lung from iatrogenic injury. For NEET PG, the high-yield zone is modes, lung-protective settings, PEEP physiology, auto-PEEP, permissive hypercapnia and weaning — facts that recur almost every year in Anaesthesia and Medicine.

Definitions & basic terminology

A ventilator delivers a breath defined by three things: what triggers it (initiates inspiration), what limits/targets it (the variable held constant during inspiration), and what cycles it (terminates inspiration and begins expiration).

Phase variable	Meaning	Common settings
Trigger	Starts the breath	Time (machine), pressure or flow (patient)
Limit/Target	Variable controlled during inspiration	Volume or pressure
Cycle	Ends inspiration	Volume, time, flow, pressure

Key terms you must define crisply:

• Tidal volume (Vt): volume delivered per breath. Lung-protective target = 6 ml/kg of predicted (ideal) body weight.
• Respiratory rate (RR): breaths/min set on the ventilator.
• Minute ventilation (MV) = Vt × RR — the main determinant of CO₂ clearance (PaCO₂ is inversely proportional to alveolar ventilation).
• FiO₂: fraction of inspired oxygen (0.21–1.0); main determinant of oxygenation along with PEEP.
• PEEP (Positive End-Expiratory Pressure): pressure maintained in the airway at end-expiration; recruits collapsed alveoli, raises FRC and improves oxygenation.
• Plateau pressure (Pplat): alveolar distending pressure measured during an inspiratory hold (no-flow state). Reflects alveolar/lung-and-chest-wall compliance. Target < 30 cm H₂O.
• Peak inspiratory pressure (PIP): maximum pressure during inspiration; includes airway resistance + alveolar pressure.
• Driving pressure = Pplat − PEEP. Strong predictor of mortality in ARDS; keep < 15 cm H₂O.
• I:E ratio: normally 1:2; inverse-ratio ventilation (>1:1) improves oxygenation but risks auto-PEEP.
• Compliance = ΔVolume / ΔPressure = Vt / (Pplat − PEEP).

High-yield: Predicted body weight (not actual) sets the tidal volume. Obese patients have normal-sized lungs — using actual weight over-distends them and causes volutrauma.

Classification of modes

Modes are grouped by what variable the ventilator targets (volume vs pressure) and how much patient effort is allowed (controlled, assisted, spontaneous).

Mode	Control variable	Patient effort	Key point
VCV (Volume-Controlled)	Volume (guaranteed Vt)	Often none/minimal	Constant Vt; pressure varies with compliance — risk of barotrauma
PCV (Pressure-Controlled)	Pressure (set Pinsp)	Variable	Constant pressure; Vt varies with compliance — risk of hypoventilation if compliance falls
A/C (Assist-Control)	Volume or pressure	Patient can trigger	Every triggered breath gets full support; risk of respiratory alkalosis & breath-stacking
SIMV	Volume or pressure	Mandatory + spontaneous breaths	Mandatory breaths synchronised to patient effort; spontaneous breaths between them
PSV (Pressure Support)	Pressure	Fully spontaneous	Patient sets RR & Vt; flow-cycled; used for weaning
CPAP	Constant airway pressure	Fully spontaneous	No inspiratory support beyond continuous pressure; for oxygenation/OSA

Volume-controlled vs pressure-controlled — the classic comparison

• VCV: You set Vt and RR; the machine guarantees the volume. Because volume is fixed, airway pressure rises if compliance falls (e.g. ARDS, pneumothorax) — danger of barotrauma. Flow is typically a constant ("square wave") pattern. Best when guaranteed minute ventilation is essential.
• PCV: You set the inspiratory pressure and time; the machine guarantees the pressure. Flow is decelerating, giving a more even alveolar filling and lower peak pressures. Because pressure is fixed, Vt falls if compliance worsens — danger of hypoventilation/hypercapnia. Decelerating flow improves gas distribution and is preferred in stiff (ARDS) lungs.

High-yield: In VCV → volume constant, pressure variable. In PCV → pressure constant, volume variable. This single dichotomy is the most repeated MCQ in ventilation.

SIMV and CPAP

• SIMV (Synchronised Intermittent Mandatory Ventilation): delivers a set number of mandatory breaths synchronised with patient effort; between mandatory breaths the patient breathes spontaneously (often supported by PSV). Historically used for weaning, though pure PSV/spontaneous-breathing trials are now preferred.
• CPAP: a single continuous pressure throughout the respiratory cycle in a spontaneously breathing patient. No tidal cycling support is added. Used in obstructive sleep apnoea, cardiogenic pulmonary oedema, and as a weaning/oxygenation tool. BiPAP = two levels (IPAP > EPAP) and is essentially CPAP + pressure support — first-line non-invasive ventilation for COPD exacerbation with hypercapnia.

Indications for mechanical ventilation

1. Hypoxaemic respiratory failure (Type I) — PaO₂ < 60 mm Hg on high FiO₂ (ARDS, pneumonia, pulmonary oedema).
2. Hypercapnic respiratory failure (Type II) — rising PaCO₂ with acidosis (COPD, neuromuscular disease, drug overdose).
3. Airway protection — GCS ≤ 8, loss of gag, severe secretions.
4. Increased work of breathing / fatigue — RR > 35, accessory muscle use.
5. Apnoea, peri-operative paralysis, raised ICP requiring controlled PaCO₂.

Lung-protective ventilation (ARDSNet strategy)

The landmark ARMA / ARDSNet trial (NEJM 2000) showed that low-tidal-volume ventilation reduces mortality in ARDS. This is the single most testable "management" fact in ICU ventilation.

Stepwise approach (ARDSNet):

1. Set initial Vt = 6 ml/kg predicted body weight (range 4–8).
2. Maintain Pplat < 30 cm H₂O → if exceeded, reduce Vt in steps of 1 ml/kg (minimum 4 ml/kg).
3. Keep driving pressure (Pplat − PEEP) < 15 cm H₂O.
4. Use a PEEP–FiO₂ table to titrate oxygenation; target SpO₂ 88–95% or PaO₂ 55–80 mm Hg.
5. Permit permissive hypercapnia — allow PaCO₂ to rise as long as pH stays ≥ 7.20–7.25.
6. RR up to 35/min to compensate for the small Vt.

High-yield: ARDSNet trio → Vt 6 ml/kg PBW, Pplat < 30, SpO₂ 88–95%. Low Vt reduces volutrauma and is proven to lower mortality in ARDS.

Severe ARDS adjuncts (PaO₂/FiO₂ < 150): prone positioning (PROSEVA trial — mortality benefit, prone ≥ 16 h/day), neuromuscular blockade (early, short course), high PEEP, and ECMO as rescue (CESAR/EOLIA). Recruitment manoeuvres are used cautiously.

The Berlin definition grades ARDS by PaO₂/FiO₂ ratio on PEEP ≥ 5: mild 200–300, moderate 100–200, severe < 100.

PEEP — physiology and pitfalls

PEEP keeps alveoli open at end-expiration, increasing functional residual capacity (FRC) and recruiting atelectatic lung, thereby improving the shunt fraction and oxygenation. Standard "physiological" PEEP is 5 cm H₂O.

Benefits: ↑ oxygenation, ↓ shunt, prevents atelectrauma (cyclic alveolar collapse/reopening), reduces work of breathing in cardiogenic oedema by lowering LV preload/afterload.

Harms of excessive PEEP:

• ↓ Venous return → ↓ cardiac output and hypotension.
• Barotrauma/volutrauma → pneumothorax.
• Over-distension increasing dead space and ↑ pulmonary vascular resistance (RV strain).
• Falsely elevated CVP/PCWP readings; raised ICP.

High-yield: The chief haemodynamic complication of high PEEP is reduced venous return → hypotension. Treat with fluids and reduce PEEP if needed.

Auto-PEEP (intrinsic PEEP / breath-stacking)

Auto-PEEP is air trapping when the patient cannot fully exhale before the next breath, so gas accumulates and end-expiratory alveolar pressure exceeds the set PEEP.

Causes: high RR, prolonged expiration disorders (COPD, asthma), inadequate expiratory time, inverse-ratio ventilation, high minute ventilation.

Consequences: dynamic hyperinflation → ↓ venous return → hypotension and pulseless electrical activity (PEA) / cardiac arrest; difficulty triggering the ventilator; barotrauma.

Detection: end-expiratory hold manoeuvre; expiratory flow not returning to zero on the flow–time waveform.

Management — flow: Recognise auto-PEEP → disconnect the circuit (allow full exhalation) if haemodynamically unstable → reduce RR, shorten inspiratory time / increase expiratory time (lower I:E), treat bronchospasm, reduce Vt; apply modest extrinsic PEEP (~80% of auto-PEEP) to ease triggering.

High-yield: A ventilated asthmatic who suddenly becomes hypotensive → think auto-PEEP / dynamic hyperinflation (and exclude tension pneumothorax). First step: disconnect from ventilator and allow exhalation.

Permissive hypercapnia

Deliberately accepting an elevated PaCO₂ (and mild respiratory acidosis) to keep tidal volumes and pressures low — protecting the lung in ARDS and severe asthma.

• Acceptable down to pH ≈ 7.20–7.25; below this, increase RR or give sodium bicarbonate cautiously.
• Contraindicated in raised intracranial pressure (CO₂ → cerebral vasodilation → ↑ ICP), and used cautiously in pulmonary hypertension/RV failure (hypercapnia raises PVR).

Ventilator-induced lung injury (VILI)

Four overlapping mechanisms — mnemonic "Bad Vibes Are Bio":

Type	Mechanism	Prevented by
Barotrauma	High airway pressures → alveolar rupture, pneumothorax, pneumomediastinum	Pplat < 30
Volutrauma	Over-distension by large Vt	Vt 6 ml/kg PBW
Atelectrauma	Repeated collapse–reopening (shear)	Adequate PEEP
Biotrauma	Cytokine release → systemic inflammation, MODS	Overall lung-protective strategy

High-yield: Volutrauma (over-distension by volume), not pressure per se, is now regarded as the principal driver of VILI — hence low-Vt ventilation.

Monitoring & investigations

• Arterial blood gas (ABG): the investigation of choice to titrate ventilation — guides FiO₂/PEEP (oxygenation) and RR/Vt (PaCO₂/pH).
• Capnography (EtCO₂): confirms tube placement, monitors ventilation continuously; sudden loss of EtCO₂ = displaced tube/circuit disconnection/cardiac arrest.
• Pressure–volume and flow–time loops: detect auto-PEEP, over-distension ("beaking"), and patient–ventilator dyssynchrony.
• Chest X-ray / lung ultrasound: tube position and complications (pneumothorax).

Weaning from mechanical ventilation

Weaning begins once the cause of respiratory failure is improving. Readiness is assessed daily.

Readiness (objective) criteria:

• Underlying illness resolving; haemodynamically stable, minimal/no vasopressors.
• Adequate oxygenation: PaO₂/FiO₂ > 150–200, FiO₂ ≤ 0.4, PEEP ≤ 5–8.
• pH > 7.25, intact respiratory drive, adequate cough.

Spontaneous breathing trial (SBT): T-piece or low-level PSV (5–8) / CPAP for 30–120 min — the gold-standard weaning test.

Rapid Shallow Breathing Index (RSBI) = RR / Vt (in litres).

• RSBI < 105 → likely to wean successfully.
• RSBI > 105 → likely to fail (rapid, shallow breathing).

High-yield: RSBI = f/Vt; < 105 predicts successful extubation. This exact cut-off is a perennial MCQ.

Other indices (less used): negative inspiratory force (NIF) more negative than −20 to −30 cm H₂O; vital capacity > 10–15 ml/kg; minute ventilation < 10 L/min.

Weaning flow: Treat cause → daily sedation interruption + readiness screen → SBT (30–120 min) → assess RSBI/tolerance → extubate (ensure cuff-leak, adequate cough, GCS) → consider NIV to prevent re-intubation in high-risk (COPD).

Complications of mechanical ventilation

• Ventilator-associated pneumonia (VAP): pneumonia > 48 h after intubation; prevent with the VAP bundle — head elevation 30–45°, daily sedation breaks + spontaneous breathing trials, DVT and peptic-ulcer prophylaxis, oral chlorhexidine, subglottic suction.
• VILI (as above), barotrauma → tension pneumothorax.
• Auto-PEEP, haemodynamic compromise from positive intrathoracic pressure.
• Oxygen toxicity (prolonged FiO₂ > 0.6 → absorption atelectasis, free-radical injury).
• Tracheal injury, sinusitis, ICU-acquired weakness, delirium, stress ulceration.

Key differentials & decision points

• VCV vs PCV: stable compliance / need guaranteed MV → VCV; stiff lungs, high pressures, paediatrics → PCV.
• NIV vs invasive: COPD exacerbation/cardiogenic oedema with intact airway and consciousness → trial NIV (BiPAP) first; failure or airway compromise → intubate.
• Hypoxia not improving on FiO₂ → it's a shunt → raise PEEP (FiO₂ alone won't fix true shunt).
• Sudden desaturation/high pressure alarm — DOPE: Displacement of tube, Obstruction/secretions, Pneumothorax, Equipment failure.

Recently asked / exam angle

• ARDSNet tidal volume = 6 ml/kg predicted body weight and Pplat < 30 cm H₂O (repeatedly tested as the protective ventilation combo).
• RSBI < 105 predicts successful weaning — direct one-liner MCQ.
• Difference between VCV (volume fixed, pressure varies) and PCV (pressure fixed, volume varies).
• Berlin definition PaO₂/FiO₂ cut-offs for mild/moderate/severe ARDS.
• Auto-PEEP in a ventilated asthmatic/COPD presenting as hypotension; first step = disconnect circuit.
• Driving pressure < 15 as a mortality predictor — newer favourite.
• High PEEP complication → decreased venous return / hypotension.
• Prone positioning improves mortality in severe ARDS (PROSEVA).
• Permissive hypercapnia is contraindicated in raised ICP.
• Decelerating flow waveform is characteristic of pressure-controlled ventilation.

Rapid revision

1. MV = Vt × RR; PaCO₂ is inversely proportional to alveolar ventilation.
2. VCV → volume constant, pressure variable; PCV → pressure constant, volume variable (decelerating flow).
3. Lung-protective ventilation: Vt 6 ml/kg PBW, Pplat < 30, driving pressure < 15, SpO₂ 88–95%.
4. PEEP ↑ FRC and recruits alveoli; main harm = ↓ venous return → hypotension.
5. Auto-PEEP = air trapping in COPD/asthma; sudden hypotension → disconnect circuit + lower RR + ↑ expiratory time.
6. Permissive hypercapnia acceptable to pH ~7.20; contraindicated in raised ICP.
7. VILI = Barotrauma, Volutrauma, Atelectrauma, Biotrauma; volutrauma is the key driver.
8. RSBI = RR/Vt; < 105 predicts successful weaning; SBT is the gold-standard test.
9. ABG is the investigation of choice for titrating the ventilator.
10. Berlin ARDS: PaO₂/FiO₂ mild 200–300, moderate 100–200, severe < 100 (on PEEP ≥ 5).
11. Prone positioning (≥16 h) lowers mortality in severe ARDS (PROSEVA); ECMO is rescue.
12. Sudden ventilator desaturation → DOPE (Displacement, Obstruction, Pneumothorax, Equipment).