Acute Respiratory Distress Syndrome

Write about Acute Respiratory Distress Syndrome here.

• A form of acute respiratory failure due to permeability pulmonary oedema resulting from endothelial damage developing in response to an initiating injury or illness

• Lung damage and release of inflammatory mediators cause increased capillary permeability and non-cardiogenic pulmonary oedema often accompanied by multi-organ failure

Pressure Pulmonary Oedema (NOT ARDS)

Permeability Pulmonary Oedema - ARDS

The characteristic feature of permeability pulmonary oedema in ARDS is that the Pulmonary Capillary Wedge Pressure (PCWP) is not elevated


ARDS develops in response to injury or illness to the lungs -> direct (pneumonia etc) or indirect (pancreatitis)

• 12-48 hours later patient develops respiratory distress with increasing dyspnoea and tachypnoea

• ABG show deteriorating hypoxaemia, poorly responsive to O2 therapy

• CXR => Diffuse bilateral infiltrates in the absence of CARDIOGENIC pulmonary oedema

• Spectrum of ARDS - Full Blown ARDS:

• Hx of initiating injury or illness

• Hypoxaemia , refractory to O2 therapy (e.g. Po2<8 kPa or 60 mmHg on 40% O2)

• This is due to shunting of blood through areas of lung not being ventilated due to alveoli filled with exudate and undergoing atelectasis

• PO2/FiO2 <26 (FiO2:100% O2 = FiO2 of 1 = fractional inspired O2 concentration... FiO2:50% O2 = 0.5)

• Bilateral diffuse infiltrates on CXR

• No evidence of cardiogenic pulmonary oedema (e.g. PCWP < 18 mmHg)


• Initiating injury treatment and optimisation

Respiratory Support 

• CPAP can prevent alveolar atelectasis - V/Q mismatch reduced

• ET intubation and mechanical ventilation necessary in most - indications = PO2 <8.3 despite 60% O2, PCO2 >6

• => ITU

• Conventional ventilation & reduced lung compliance may lead to high peak airway pressure ± pneuomthorax

• PEEP increases oxygenation but reduces venous return, cardiac output and kidney and liver perfusion

• High pressure + high O2 concentration may -> microvascular damage perpetuating initial permeability problems (ventilator lung/oxgen toxicity)

• Techniques to overcome this

• Inverse ratio ventilation (inspiration longer than expiration, but may cause progressive air trapping)

• High-frequency jet ventilation (small volumes often)

Circulatory Support:

• Invasive haemodynamic monitoring allows guidance of use of diuretic and vasodilators (of pulmonary arteries)

• Balance between low pulmonary artery pressure (reduce fluid leak) and adequate system blood pressure (to maintain perfusion)

• Most drugs used to vasodilate the pulmonary arteries (nitrates, Ca antagonists) also cause systemic vasodilation, with hypotension and impaired organ perfusion

• Inotropes and vasopressor agents, such as dobutamine and noradrenaline may be needed to maintain systemic BP and CO particularly in patients with sepsis syndrome - sepsis with systemic vasodilation

• Inhaled NO can be used as a selective pulmonary vasodilator (rapidly inactivated by haemoglobin)

General Management:

• Correction of anaemia

• Nutritional support

• Steroids don't help in acute phase but may help >7 days


• Overall mortality = 50 - 75%

• Varies with:

• age

• cause of ARDS (pneumonia = 86%, trauma = 38%)

• Number of organs involved (3 organs involved for > 1/52 => invariably fatal)