Acute Respiratory Distress Syndrome = non-cardiogenic pulmonary edema
—Syndrome — one disease, many causes;
–Secondary disease! It’s always ARDS secondary to another diagnosis. It’s a complication, not a primary illness, but the treatment of ARDS is actually separate from the treatment of the underlying disease.
–Disease of inflammation, and prone to happen in high-inflammation states:
- Trauma (not just pulmonary trauma!) Early onset in trauma (< 48 hrs) is usually capillary leakage; late onset (> 48 hrs) is usually PNA or MODS/MOF.
- Smoke inhalation
- Shock of any kind
- Narcotics use
—Often a byproduct of bad vent settings! High tidal volumes during vent can cause injury ==> ARDS.
–SEVERE dyspnea REQUIRING intubation — ARF ==> ALI ==> ARDS
Diagnostics: Requires ABGs (maybe not, but this is gonna be a long admission anyway). Hypoxemia; “Ground glass” / diffuse patchy infiltrates on CXR; PaO2 / FiO2 (.21 to 1.0) < 200. **
Differentiation With P:F Ratios: Acute Respiratory Failure (>300) ==> ALI (200-300) ==> ARDS (<200) ; PETAL is the new ARDSNet trying to get a focus on prevention of ARDS and “catch it in the act” in ALI.
- Exudative (leaking)
- Capillary damage – capillary leakage
- Diffuse endothelial injury due to micro / macro thrombi formation. Can lead to defects in peripheral pulmonary vasculature.
- Can cause pulmonary HTN, RV dilation, & therefore cor pulmonale
- Atelectasis (alveolar collapse)
- Proliferative (fibroproliferative; stiff lung, “shock lung”) – This is the most dangerous phase in terms of ventilation, because the lung tissues are developing fibrotic scar tissue. Also prone to PNA, sepsis, MODS/MOF at this stage. Typically lasts 3-10 weeks.
- Fibrotic stage / repair and recovery stage. In terms of mortality, this is the “out of the woods” phase. Inflammation starts to resolve. Extubation becomes possible. Recovery and improvement can last as long as 6 months.
- MODS/MOF – Hypoxemia is bad for organs, and these patients often will have poor systemic oxygenation. That leads to organ failure in various systems depending on the individual’s base health and what the inciting disease is that prompted development of ARDS.
- Pulmonary HTN & Cor Pulmonale – vascular damage causes blood backup in the PA, which in turn causes RV dilation and “D”ing of the septal wall – the intraventricular septum buckles into the left ventricle during contraction. Of the Cor Pulmonale patients, it gets worse—25% have a PFO with right-to-left shunting, causing deoxygenated blood to enter systemic circulation. That PFO is exacerbated by high PEEP, which is too bad, because that’s one of the main treatments for ARDS.
Next Time, On PIG-ICC, ARDS PART TWO! Treatment, vent management, and what doesn’t work (but should).