Shanholtz – Acute Respiratory Distress Syndrome




Maryland CC Project show

Summary: <br> <br> @import url('https://fonts.googleapis.com/css?family=Merriweather&amp;display=swap');<br> p, li, h1, h2, h3, h4 {font-family: 'Merriweather', serif;font-size:18px; color:black;}<br> <br> <br> <br> <br> Carl Shanholtz, MD, Professor of Medicine in the Division of Pulmonary and Critical Care and Director of the Medical ICU at the University of Maryland presents the multi-departmental critical care curriculum lecture on ARDS.<br> <br> <br> <br> <br> <br> <br> <br> <br> <br> Lecture Summary by Dr. Jason Nam<br> <br> <br> <br> Introduction<br> <br> <br> <br> * ARDS is a common disorder of acute injury to<br> lungs. It can occur in children. Lack of standard definition prior to 1994. * Why use P/F ratio in the definition? It is a<br> surrogate measure of shunt. Shunt fraction needs to be done with Swann-Ganz. * Consensus Conference definitions- between<br> American and European<br> <br> <br> <br> <br> Characteristic<br> <br> AECC Definition 1994 <br> <br> Berlin Definition 2012<br> <br> Timing<br> <br> Acute, without any specification<br> <br> Maximum within a week after a trigger insult<br> <br> Imaging<br> <br> Chest X-ray with bilateral infiltrates<br> <br> Chest X-ray or CT scan with bilateral infiltrates, not fully<br> explained by effusion, lung collapse or nodules<br> <br> Non-cardiogenic source of edema<br> <br> Confirmation of non-elevated left atrial pressure<br> <br> Respiratory failure not completely explained by excessive<br> volume loading or cardiac failure<br> <br> Classification<br> <br> Based on PaO2/FiO2<br> Based on PaO2/FiO2 calculated with PEEP &gt;5 cmH2O <br>  <br> Acute lung injury:&lt;300 Mild: 201-300 <br>  <br> ARDS:&lt;200 Moderate: 101-200 <br>  <br>  – Severe: &lt;100 <br> Predisposing condition<br> <br> Not specified<br> <br> If none identified, then need to rule out cardiogenic edema<br> with additional data<br> <br> <br> <br> <br> Pathophysiology<br> <br> <br> <br> * Active exudative phase. Leads to the pulmonary<br> edema (non-cardiogenic). Loss of compliance and hypoxemia refractory to supplemental<br> oxygen. Loss of capillary surface area and increase in dead space. We get “baby<br> lungs.”* When we try to ventilate, we get VILI. <br> <br> <br> <br> Lung protection strategies<br> <br> <br> <br> * <a href="https://www.nejm.org/doi/full/10.1056/NEJM200005043421801">ARMA Trial</a> – mortality was lower, and ventilator-free days higher in the group treated with lower tidal volumes * Improvement in oxygenation doesn’t seem to predict outcome of ARDS. Oxygenation was a bad surrogate for outcome. * Is there a safe plateau pressure? At any quartile. The lower TV patients had an improved mortality. * Is higher PEEP protective? It was thought that moderate-to-severe ARDS patients would benefit from higher alveolar recruitment. Gattinoti, et al, found that moderate-to-severe ARDS patients had more atelectatic and thereby more recruitable lung. * What about driving pressure? driving pressure is directly proportional to mortality regardless of driving pressure and PEEP. No one yet knows how to titrate driving pressures as there is current evidence and interest in closed-lung strategies.* Does lung prevention ventilation strategies prevent ARDS? PReVENT trial. Multicenter RCT in Netherlands. A low tidal volume strategy did not result in a greater number of ventilator-free days than an intermediate tidal volume strategy<br> <br> <br> <br> Fluid Management and ARDS<br> <br> <br> <br> * <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa062200">Fluid and Catheter<br> Treatment Trial</a> – Fluid conservative vs.