ARDS Flashcards
1
Q
ARDS Berlin definition (4)
A
- Respiratory symptoms within 1 week of known clinical insult
- Bilateral opacities consistent with pulmonary oedema on chest radiograph (CXR) or computed
tomography (CT) - Respiratory failure must not be fully explained by cardiac failure or fluid overload. Echo may be
required to exclude hydrostatic pulmonary oedema - Oxygenation impairment, defined by PaO2/FiO2 ratio at least ≤300 mmHg (40 kPa) despite positive
end-expiratory pressure (PEEP) ≥5 cmH2O
2
Q
ARDS severity classifications (3)
A
- Mild ARDS—PaO2/FiO2 >200 mmHg (27 kPa)
- Moderate ARDS—PaO2/FiO2 >100 mmHg (13 kPa)
- Severe ARDS—PaO2/FiO2 ≤100 mmHg (13 kPa)
3
Q
ARDS pathophysiology
A
- Inflammatory damage to the alveoli, by pro-inflammatory mediators either locally produced pro-or remotely produced and arriving via the pulmonary artery.
- These mediators recruit neutrophils, which release proteases and reactive oxygen species causing capillary and alveolar damage.
- Changes in pulmonary capillary permeability allow fluid and protein leakage into the alveolar spaces with pulmonary infiltrates.
- The alveolar surfactant is diluted with loss of its stabilizing effect, resulting in diffuse alveolar collapse and stiff lungs. This leads to:
a. Gross impairment of ventilation-perfusion (V/Q) matching with shunting, causing arterial hypoxia and very large A–a gradients. There are usually enough remaining functioning alveoli such that hyperventilation maintains CO2 clearance; thus, hypercapnia is infrequently a problem.
b. Pulmonary hypertension (PHT) will develop 2° to the hypoxia, but this may be helpful (aids V/Q matching), rather than deleterious.
c. Reduced compliance (stiff lungs) due to loss of functioning alveoli (alveolar collapse, filled with fluid and protein) and hyperinflation of remaining alveoli to their limits of distension.
4
Q
ARDS common causes (3)
A
- sepsis/ pneumonia (increased risk with alcoholism and smoking)
- gastric aspiration
- trauma/ burns
4
Q
ARDS less common causes (7)
A
- Acute pancreatitis
- TRALI
- Lung transplant
- Bone marrow transplant
- Drug overdose e.g. tricyclic antidepressants, opiates, cocaine, aspirin
- Near drowning
- Following upper airway obstruction
4
Q
What are the 3 phases of ARDS (3)
A
- early period of diffuse alveolar damage and hypoxaemia with pulmonary infiltration
- fibroproliferative - develops after a week or so as the pulmonary infiltrates resolve and, on histology, seems to be associated with an increase in type II pneumocytes (surfactant producers), myofibroblasts, and early collagen formation.
- fibrotic - fibrotic stage that leaves the lung with cysts, deranged micro-architecture and much fibrosis on histology.
5
Q
ARDS clinical features
A
- ARDS should be considered in any patient with a predisposing risk factor who develops severe hypoxaemia and a widespread diffuse pulmonary infiltrate.
- Approximately 1–2 days following the clinical presentation of the precipitating cause (sepsis, aspiration, etc.), there is rapidly worsening dyspnoea (± a dry cough) and hypoxaemia, requiring rapidly escalating amounts of supplemental O2 up to 100% via a non-rebreathe system (see p. 788). Coarse crackles in the chest.
- Intubation and ventilation are nearly always required, although initiating HFNO or continuous positive airway pressure (CPAP) via a face mask at 5–10 cmH2O with 100% O2 can improve oxygenation temporarily.
6
Q
ARDS alternative differentials (5)
A
- Left ventricular failure - check echo
- Diffuse alveolar haemmorhage e.g. goodpastures, sle
- ILD
- acute eosinophilic pneumonia
- cancer
7
Q
ARDS Mx (4)
A
- Treat precipitating cause
- Adequate oxygenation
- Avoid further damage from barotrauma, hyperoxia and nosocomial infections
- Can try low total volumes and prone positioning
8
Q
ARDS complications (4)
A
- high ventilation pressures lead to barotrauma - pneumothorax, surgical emphysema and pneumomediastinum.
- nosocomial infections
- myopathy
- VTE, GI haemmorhage, inadequate nutrition
