Pulmonology - ARDS - Clinical Practicum II A PDF

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Clinical Practicum II A...

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Pulmonology [ARDS] Pathogenesis and Introduction ARDS is a noncardiogenic pulmonary edema that results from increased permeability of capillaries permitting the transudation of fluid from capillaries into the interstitium. This causes a barrier to diffusion preventing gas exchange resulting in a hypoxemia. It looks and feels like CHF but the cardiovascular function is intact, hydrostatic pressures are normal (meaning that the capillary wedge pressure is normal), and it’s the capillary permeability that drives disease. Too many leaky capillaries then leads to pulmonary edema and alveolar derecruitment.

Normal gas exchange and no leaky capillaries in the normal state

Impaired oxygenation as a product of increased diffusion barrier from leaky capillaries in ARDS

Presentation This is a patient with pulmonary edema (SOB, cough, crackles) and a nasty looking CXR (bilateral white out). The patient is also one without a reason for CHF (MI, HTN, Arrhythmia, Fluid) and has instead a really sick presentation (as in the ICU). To cause capillary permeability to increase so significantly requires GNR septicemia, burns, TRALI, or drowning. These patients usually present to the hospital then crash in the ICU, rather than a person presenting in florid pulmonary edema. Diagnosis A patient with a systemic disease and pulmonary edema (especially someone volume down or hypotensive) is likely enough for the diagnosis. A CXR will show white out bilaterally. However, to definitively diagnose ARDS vs CHF a measurement of capillary-wedge pressures via a Swan-Ganz cath is required. This will show a decreased or normal wedge (no backup of fluid) and an increased or Normal LV function (not heart failure). Both findings are in direct contradiction to CHF. Generally, it’s not done for CHF (patients aren’t sick enough to get a Swan-Ganz), though there are certainly HF patients sick enough to make it to the ICU. A patient with ARDS will be intubated, full of lines, and ripe to do the assessment on. A PaO2 to FiO2 ration will be < 200. Treatment Intubation and Oxygenation are crucial as first line therapy. With intubation, application of PEEP increases the interstitial pressures, forcing the fluid back into the capillaries. The vessels remain leaky and only close once the underlying disease is corrected. Monitoring/Complications When someone’s put on PEEP it’s possible to induce barotrauma or induce pneumothorax. If the patient suddenly presents with worsening SOB after PEEP, suspect barotrauma. However, if a patient becomes hypotensive and has a mediastinal shift (tracheal deviation) a tension pneumo should be suspected. Confirm the diagnosis with a CXR and treat with needle decompression and chest tube.

PEEP provides alveolar recruitment and improves diffusion of oxygen by reducing diffusion barrier

Alveolus

Alveolus Blood

Blood Gas Exchange Ø Impaired

Edema impairs Gas Exchange

J = K [Pcap – Pint ) – (πcap – πint)] Fluid movement across a capillary ARDS causes ↑ in K, fluid leaks out PEEP causes ↑ in Pint, pushes fluid back in

Exacerbating Factors Chest X-Ray Capillary Wedge LV Function Treatment

CHF HTN, MI Fluid Overload Bi Pleural Effusions Bi Hazy Infiltrates ↑ (25) ↓ Diuresis, Control of HTN, PEEP if severe

ARDS Sepsis, Burns, Drowning, TRALI Total White Out Severe Bi Infiltrates Normal (10) Normal PEEP Intubation Tx Underlying Dz

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