ARDS

Question 1

Definition

Answer 1

=>Acute respiratory distress syndrome (ARDS) is the rapid and catastrophic response of the lung to injury that results in severe hypoxemic respiratory failure.

=>The current Berlin definition defines ARDS as a process that:
* Occurs within 7 days of a known clinical insult.
* Presents with bilateral opacities on chest imaging not fully explained by effusions, collapse, or nodules.
* Manifests with hypoxemia defined by the ratio of PaO₂/FiO₂ ≤ 300 mm Hg with PEEP ≥ 5 cm H₂O.

Question 2

Ventilator-Induced Lung Injury (VILI) – Mechanisms

Answer 2

3 major mechanisms:
* Volutrauma
* Atelectrauma
* SILI

Question 3

1). Volutrauma

Answer 3

=>Definition: **Alveolar over-distension **due to excessive tidal volumes or high inflation pressures.

=>Mechanism:
* Occurs from cyclic over-stretching of alveoli during inspiration.
* Injury is related to transpulmonary pressure (alveolar − pleural pressure), not absolute airway pressure.
* “Baby lung” concept: Only a small fraction of lung is aerated and compliant in ARDS; therefore, this segment receives most of the delivered volume and pressure, increasing stress and strain.

=>Clinical implication: Use low-tidal-volume ventilation (6 mL/kg PBW) and limit plateau pressure < 30 cm H₂O.

Question 4

2). Atelectrauma

Answer 4

=>Definition: Injury from repetitive opening and closing of atelectatic alveoli during tidal ventilation.
=>Mechanism:
->Collapsed alveoli reopen with each breath → high shear stress on epithelial surfaces.
increases inflammation and potentiates volutrauma reduces effective “baby lung” size).
=>Prevention: **Use optimal PEEP **to keep alveoli recruited and minimize cyclic collapse.

Question 5

3). Patient Self-Inflicted Lung Injury (P-SILI)

Answer 5

=>Definition: VILI caused by the patient’s own spontaneous respiratory efforts during mechanical ventilation or non-invasive support.
=>Mechanisms:
1). Strong inspiratory efforts → markedly negative pleural pressure → ↑ transpulmonary pressure → alveolar overdistension.
2). Ventilator asynchrony: Spontaneous breaths may coincide with ventilator cycles → excessive tidal volume and high transpulmonary pressure.

3). ->Pendelluft phenomenon: Air shifts between lung regions due to regional pressure differences; causes local overdistension and shear stress.
=>Risk: Heterogeneous lungs (as in ARDS) make regional pressure changes uneven, amplifying injury.

=>Clinical implication: Control respiratory drive (sedation, neuromuscular blockade if needed) and monitor transpulmonary pressures.

Question 6

Lung Protective Ventilation

Answer 6

🫁 Lung-Protective Ventilation (LPV)

=>Definition:
Refers to limiting tidal volume (VT) and inspiratory pressures to minimize VILI.

=>Key Evidence – ARMA Trial (NEJM 2000):
* Compared low VT (4-8mL/kg PBW) vs traditional VT (12 mL/kg PBW).
* Plateau pressure (Pplat) maintained < 30 cm H₂O in the LPV group.
* Results:
* Mortality reduced from 39.8% → 31% (absolute risk reduction 8.8%; NNT = 11).
* Lower barotrauma and shorter duration of ventilation.

=>Key Concept:
* Mortality correlates with plateau pressure: the higher the Pplat, the greater the risk of death.
* No single “safe” upper threshold exists, but risk increases progressively > 30 cm H₂O.
* Further reduction of VT (< 6 mL/kg) may reduce strain but can risk hypercapnia and acidosis (“ultra-protective ventilation” sometimes combined with ECMO).

Predicted BW - usually used over IBW in critical care settings.
Men: 0.7x {height in cm-80} Women: 0.6x{height in cm-80}

Question 7

Open lung ventilation

Answer 7

=>Ventilation strategy where lung is maximally recruited through application of a higher PEEP and an effort is made to minimise derecruitment

=> * Aim: To reduce cyclic collapse and re-inflation of alveoli (i.e., cyclic atelectasis).

=>Concept of Optimal PEEP
* Based on the PEEP above critical opening pressure, where FRC is raised above the critical closing volume.
* The goal is to keep alveoli open at end-expiration without causing overdistension.

=>Critical Opening Pressure- Pressure at which most alveoli remain open at end expiration.

=>Critical closing volume is the lung volume at which small airways close,
->”closing capacity” is the sum of this volume plus the residual volume ((CC=CV+RV) –>significant concept in respiratory physiology because if the closing capacity is greater than the functional residual capacity (FRC), airways will close during a normal breath, leading to atelectasis.

Question 8

PEEP Evidence

Answer 8

=>Amato et al: High vs lower PEEP- Higher PEEP asso with lower mortality esp. in Moderate- Severe ARDS- findings confounded by use of higher TV with Lower PEEP
=>ALVEOLI- High PEEP/FiO2 ratio vs Low PEEP/FiO2 ratio, all recieved LTV. No mortality difference, study stopped early due to futility.
=>EXPRESS
No difference in mortality but ↑ ventilator-free days in high-PEEP group.
=>LOVS
High PEEP + RM vs low PEEP
No mortality difference; trend toward benefit in moderate–severe ARDS.
=>ART
RM + incremental PEEP up to 45 cm H₂O vs lower PEEP
↑ 28-day mortality (55.3% vs 49.3%); more barotrauma and hypotension → trial stopped early.
=> Meta-analyses: of ALVEOLI, LVOS and EXPRESS:
* High PEEP beneficial only in moderate–severe ARDS (PaO₂/FiO₂ ≤ 200).
* In patients with higher inflammatory phenotype (“recruitable” ARDS), high PEEP improved outcomes; non-recruitable phenotypes may worsen with overdistension.

Question 9

Best PEEP

Answer 9

Individualization of PEEP
* Appropriate PEEP must be individualized based on the potential recruitability of the lung.

• Empirically applied high PEEP is unlikely to benefit in non-recruitable lungs.

* Improved compliance and reduction of driving pressure are clinically useful indicators of recruitability.