Acute Respiratory Distress Syndrome – ARDS - Clinical Cheat Sheet

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Overview

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● An acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, lung congestion with hypoxemia and bilateral radigraphic opacities, associated with decreased lung compliance.

Berlin criteria (2013)

● Acute onset over 1 week or less● Bilateral opacities consistent with pulmonary edema must be present; they may be detected on CT or CXR● PaO2/FiO2 ratio <300mmHg with a minimum of 5 cmH20 PEEP● Volume overload with heart failure should be ruled out either subjectively or an “objective assessment“ (e.g. echo cardiogram) should be performed in most cases if there is no clear cause such as trauma or sepsis.

Radiographic assessment

Acute pulmonary edema Pulmonary hemorrhage

● CXR findings of ARDS are non-specific and resemble those of typical pulmnary edema or pulmonary hemorrhage.● Develop 12-24 hours after initial lung insult as a result of proteinaceous interstitial edema.● In contrast to cardiogenic pulmonary edema, which responds to diuretic therapy, ARDS persists for days to weeks.● Clues to ARDS: normal heart size, absent pleural effusions, absent Kerley B lines, and the presence of air bronchograms (relatively uncommon in cardiogenic pulmonary edema).

Severity categories

ARDSseverity PaO2/FiO2 Mortality

Mild

Moderate

Severe

200 – 300

100 – 200

< 100

27%

32%

45%

Early-phase CT scan features

● Pulmonary opacification: anteroposterior density gradient within the lung, with dense consolidation in the most dependent regions, merging into a background of widespread ground-glass attenuation and then normal or hyperexpanded lung in the non-dependent region.● Ground-glass opacification: a non-specific sign that reflects an overall reduction in the air content of the affected lung. In acute ARDS likely represent edema and protein within the interstitial and alveolar spaces.● Bronchial dilatation within areas of ground-glass opacification

Causes

Management

Dense dependant consolidation

● Calculate predicted body weight ● Select any ventilator mode● Set ventilator settings to achieve initial VT = 8 ml/kg PBW● ↓ VT by 1 ml/kg at intervals ≤ 2 hours until VT = 6ml/kg PBW.● Set initial rate to ~ baseline min ventilation (not > 35 bpm).● Adjust VT and RR to achieve pH and plateau pressure goals as shown in table:

Oxygenationgoal

Plateaupressure goal

pH goal

Inspiration:expiration goal

PaO2 55-80 or SpO2 88-95%

7.30-7.45

≤ 30 cm H2O

I:E < 1

Mechanical Ventilation

Weaning

● Conduct spontaneous breathing trial daily when FiO2 ≤ 0.40 and PEEP ≤ 8 OR FiO2 < 0.50 and PEEP < 5, patient has acceptable spontaneous breathing efforts, SBP ≥ 90 mmHg without pressors, No neuromuscular blocking agents.● Assess for tolerance as below of SBT for up to two hours: a. SpO2 ≥ 90: and/or PaO2 ≥ 60 mmHg b. Spontaneous VT ≥ 4 ml/kg PBW c. RR ≤ 35/min d. pH ≥ 7.3 e. No respiratory distress● Extubate if tolerate for > 30 min

● Use a minimum PEEP of 5 cm H2O. Consider use of incremental FiO2/PEEP combinations.

Other techniques

● Prone posture: ↓ mortality, improves oxygenation● inhaled iNO, inhaled prostacycline● VV-ECMO

● Early resuscitation, appropriate antibiotic agents, and source control if sepsis-associated ARDS.● Conservative fluid-management● Supportive management with early enteral nutrition● Treat the underlying cause● Glucortecoids may improve oxygenation in pneumonia and are harmful if started >14 days after dx of ARDS

Direct lunginjury

Indirect lunginjury

pneumonia, bacterial, viral including COVID19!, fungal, aspiration,

contusion, inhalational, near drowning

Sepsis, hemorrhagic shock, pancreatitis,major burn, drug overdose, transfusion

references are available on the website