Lung-protective ventilation strategy in acute respiratory distress syndrome: a critical reappraisal of current practice

Why This Article Matters

For more than 20 years, lung-protective ventilation has been synonymous with a single number: 6 mL/kg predicted body weight (PBW).

This target has been taught, audited, benchmarked, and enforced across ICUs worldwide. Yet despite near-universal endorsement, real-world adherence remains inconsistent—and outcomes have plateaued.

This 2025 review asks an uncomfortable but necessary question:

Have we transformed a physiologic principle into a rigid rule—and lost nuance along the way?

Rather than rejecting lung protection, Park argues that tidal volume alone is an incomplete and sometimes misleading surrogate for lung injury, and that modern ARDS care must move beyond fixed formulas toward physiology-driven ventilation.


Historical Context: How 6 mL/kg Became Dogma

The foundation of low tidal volume ventilation rests on five landmark randomized trials conducted between 1998 and 2006. Of these:

  • Only two trials demonstrated a mortality benefit, most notably the ARDSNet trial.
  • The ARDSNet comparison was 6 mL/kg vs ~12 mL/kg, not against intermediate volumes.
  • High-VT arms often permitted very high plateau pressures, magnifying harm.

Importantly, no randomized trial has directly compared 6 mL/kg with 7–9 mL/kg, leaving a large evidence gap in the range most clinicians actually use.

The review emphasizes a critical distinction:

The strongest signal in the literature may reflect harm from excessively high tidal volumes, rather than proof that 6 mL/kg is universally optimal.


The “Baby Lung” Concept—and Its Consequences

ARDS does not reduce lung size uniformly. Instead, it creates a small, heterogeneously aerated “baby lung.”

Key implications:

  • VT is distributed across functional lung units, not total lung volume.
  • Two patients with identical PBW may have vastly different recruitable lung volumes.
  • Applying the same VT can produce very different local strain.

This explains why a “safe” VT in one patient may cause overdistension in another—and why PBW alone cannot reflect mechanical risk.


Why Fixed VT Targets Can Become Harmful

1. Compliance and dead space are ignored

Many ARDS patients develop:

  • Low respiratory system compliance
  • High physiologic dead space
  • Severe ventilation-perfusion mismatch

Aggressive VT reduction in these patients often leads to:

  • Profound hypercapnia
  • Respiratory acidosis
  • Escalating respiratory rates
  • Increased mechanical power

In practice, clinicians compensate by raising RR, which may increase VILI risk despite lower VT.


2. Strict VT reduction may worsen patient–ventilator interaction

Low VT strategies frequently require:

  • Deep sedation
  • Neuromuscular blockade
  • Suppression of spontaneous effort

These interventions carry downstream consequences:

  • Diaphragm atrophy
  • Prolonged ventilation
  • ICU-acquired weakness

The review highlights that ventilation strategies that worsen synchrony and drive may not be lung-protective in a holistic sense.


3. Real-world data do not confirm a sharp VT threshold

Observational studies and post-hoc analyses suggest:

  • Mortality curves flatten between ~6.5 and 9–10 mL/kg PBW
  • No consistent harm signal until VT exceeds ~10–12 mL/kg
  • Clinicians frequently individualize VT based on gas exchange and mechanics—often appropriately

This challenges the notion of a single “correct” VT for all ARDS patients.


What Actually Causes Ventilator-Induced Lung Injury (VILI)?

The review reinforces that VILI is not caused by VT alone. It emerges from the interaction of:

  • Stress (transpulmonary pressure)
  • Strain (VT relative to lung size)
  • Driving pressure
  • Mechanical power
  • Heterogeneous regional ventilation

Focusing narrowly on VT risks ignoring the true injurious forces applied to lung tissue.


Driving Pressure: A More Informative Signal

Multiple analyses show that driving pressure (ΔP) correlates more closely with outcomes than VT or PEEP alone.

Key concept:

  • A lower VT that raises ΔP may be more injurious than a slightly higher VT that lowers ΔP through recruitment.

Thus, VT should be interpreted in context, not in isolation.


Toward a Physiology-Based Approach

Park does not advocate abandoning low VT ventilation. Instead, the review calls for a balanced, patient-specific strategy, incorporating:

  • Lung compliance
  • Dead space fraction
  • Acid–base status
  • Patient effort and synchrony
  • Disease phase (early vs late ARDS)

In this framework:

  • 6 mL/kg is a starting point, not an endpoint
  • Deviations should be intentional, reasoned, and reassessed frequently

Implications for Practice and Guidelines

This review highlights a growing tension in critical care:

  • Guidelines favor simplicity and standardization
  • Physiology demands flexibility and nuance

As monitoring tools improve (EIT, esophageal pressure, advanced waveform analysis), reliance on a single numeric target becomes increasingly difficult to justify.


Bottom Line

Lung protection is not a tidal volume—it is a strategy.

Low VT ventilation remains foundational, but rigid adherence to 6 mL/kg without regard for lung mechanics, dead space, or patient response risks replacing precision with protocolism.

The future of ARDS ventilation lies in individualized, physiology-driven care, not in one-size-fits-all thresholds.


Discussion Question

Have we reached a point where strict VT targets limit our ability to deliver truly lung-protective ventilation?

We look forward to hearing how you individualize VT at the bedside.

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