Acute Respiratory Distress Syndrome ARDS

  • There is lung injury manifested as increased perme­ability of alveolar capillary membrane, diffuse alveo­lar damage, proteinaceous pulmonary edema.
  • Age: ARDS or Acute Respiratory Distress Syndrome may occur in children or adults.
  • Syndrome characterized by abrupt onset of diffuse lung injury with severe hypoxemia and bilateral pulmonary infiltrates
  • Absence of left atrial hypertensiom (HTN)
  • By consensus, PaO2/FiO2 <200
  • Most severe form of acute lung injury
  • System(s) affected: Pulmonary; Cardiovascular
  • Synonym(s): Shock lung; Wet lung; Noncardiac pulmonary edema
  • Acute respiratory distress syndrome (ARDS) develops rapidly and includes severe dyspnea and hypoxemia;
  • it typically causes respiratory failure.
  • Key diagnostic criteria for ARDS include  diffuse bilateral pulmonary infiltrates on chest x-ray (CXR);   PaO2 (arterial partial pressure of oxygen in mmHg)
Acute Respiratory Distress Syndrome (ARDS)

Acute Respiratory Distress Syndrome (ARDS) Causes Clinical feature Treatment

Criteria of ARDS

  • Severe hypoxemia
  • Decreased pulmonary compliance
  • Diffuse pulmonary infiltrates on chest X-ray.
  • It is a form of noncardiogenic pulmonary edema. Acute Lung Injury (ALI) is a less severe form of ARDS.

All criteria

  • Acute onset
  • PaO2/FI02 < 300mg Hg
  • Chest X-ray – Bilateral infiltrates.
  • PAP –< 18 mmHg (Pulmonary artery pressure is less than 18mmHg).
  • No clinical evidence of left atrial hypertension.

ARDS criteria

  • Acute onset
  • PaO2/FI02 < 200mg Hg
  • Bilateral infiltrates.
  • PCWP ~ 18 mmHg (Pulmonary capillary wedge pres­sure is less than 18mmHg).
  • No clinical evidence of increased LA pressure.

 Predisposing factors

  • Severe sepsis, trauma, aspiration of gastric contents. 40% of these will develop ARDS.
  •  A H/O chronic alcohol abuse increases risk of ARDS.
  • ARDS occurs within 5 days of the precipitating event.
  •   50% develop within 1 day.
Risk Factorsfor Acute Respiratory Distress Syndrome (ARDS)
  • Severe infection (localized or systemic ) most common
  • Aspiration of gastric contents
  • Shock
  • Infection
  • Lung contusion
  • Nonthoracic trauma
  • Toxic inhalation
  • Near drowning
  • Multiple blood transfusions

Clinical feature of ARDS

  • There is : Increased respiratory rate
  • Dyspnoea
  • In sepsis there is increased ne.
  • In pancreatitis, there is increased serum amylase level.

Physical Exam in ARDS

  • Flat neck veins
  • Hyperdynamic pulses
  • Physiologic gallop
  • Absence of edema
  • Tachypnea and tachycardia during the 1st 12– 24 h; respiratory distress
  • Lethargy, obtundation
  • Moist, cyanotic skin: Manifestations of underlying disease


  • diffuse infiltrates with heterogenous pattern – more in dependent lung.

Pathophysiology of Acute Respiratory Distress Syndrome (ARDS)

  • 3 phases:
    • Acute exudative phase: Characterized by profound hypoxia and associated with inflammation with infiltration of inflammatory and proinflammatory mediators and diffuse alveolar damage
    • Fibrosing alveolitis phase: Coincides with recovery or after ~1–2 weeks; patients continue to be hypoxic and have increased dead space and decreased compliance.
    • Resolution may require 6–12 months.
  • Heightened inflammatory response Initiation
  • Acceleration
  •   Injury.

Causes of Acute Respiratory Distress Syndrome (ARDS)

  • Trauma
  • Aspiration of gastric contents –
  • Drowning
  • Contusion to lungs
  • Toxin inhalation
  • Sepsis syndrome
  • Non-thoracic trauma
  • Pancreatitis
  • CABG.
  • There is mediator and cytokine-release like TNF alpha interleukin-
  • 1. Neutrophils cause acceleration of rseponse
  • Release of oxygen, metabolites and proteases causes injury leading to MODS (Multiple Organ Dysfunction, Syndrome).
  • Pulmonary edema
  • Bronchial wall edema
  • Narrowing of bronchi leading to :
  • Bronchospasm
  • High pulmonary vascular resistance
  • High pulmonary arteriolar pressure due to
  • release of thromboxane A2 and leukotrines.
  • There may be recovery or chronic pulmonary disease. Chronic changes in lung often leads to death.

Treatment of Acute Respiratory Distress Syndrome (ARDS)

  • No single drug or combination of drugs prevents or treats full-blown ARDS. Treatment is supportive while addressing the underlying cause.
  • Supplemental oxygen
  • Ventilatory support most often requires endotracheal intubation with emphasis on lower tidal volumes per weight and optimization of positive end-expiratory pressure (PEEP).
  • 02 inhalation is not effective.
  • Mechanical ventilation should be instituted. Mechanical ventilation can lead to 02 toxicity, barotrauma, pneumothorax, pneumo-mediasti­num, SIC emphysema.
  • Tidal volume of 10 ml/Kg can lead to barotrauma. Maximum inflation pressure < 35cm H20.
  • Tidal volume should be <6 ml/kg.
  • FI02 is kept < .6
  • Pa02 maintained at 60 mmHg.
  • PEEP added 5 cm H20 up to 20 cm H20. Restriction of fluids.
  • Inotropic agents: Dobutamine to maintain adequate cardiac output after appropriate fluid resuscitation fails to restore perfusion
  • Deep vein thrombosis (DVT) prophylaxis
  • Ulcer prophylaxis
  • Inhaled B2 agonists may be helpful during the resolution phase.
  • Maintain lowest possible intravascular hydrostatic pressure.
  • Hypercapnia, respiratory acidosis occurs with mechanical ventilation called permissive hyper­capnia.
  • Steroids may be given. Give surfactants, nitric oxide inhalation to reduce pulmonary arterial pressure.
  • Mortality 50% to 70% Early mortality <3 days Late mortality >3 days


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