The acute respiratory distress syndrome (ARDS)

The Acute Respiratory Distress Syndrome (ARDS) J Christopher Farmer A bad day in the ICU…now what? FIO2 = 1.0, PEEP = 15 cm H2O, SpO2 = 85% What is ARDS?    Definition Clinical criteria for diagnosis pathophysiology Clinical diagnostic criteria for ARDS    Diffuse bilateral infiltrates (> of quadrants) P/F ratio < 200 Absence of heart failure/pulmonary edema ALI versus ARDS Onset PaO2/FIO2 CXR Cause ALI Acute ≤ 300 diffuse infiltrates No LA HTN PAWP ≤ 18* * Flash pulmonary edema; LV dysfunction in ARDS ARDS Acute ≤ 200 diffuse infiltrates No LA HTN PAWP ≤ 18* Acute Lung Injury  VILI  Ventilator-induced lung injury  Barotrauma, biotrauma  Over-distention, recruitment/de-recruitment, immune injury  VALI  Ventilator-associated lung injury  Underlying injury made worse by mechanical (mainly) effects of MV  VASI  Ventilator-associated systemic inflammation  Biotrauma The continuum of ARDS V/Q mismatch ALI shunt ARDS inflammation VALI VILI fibrosis & alveolar destruction VASI ARDS histopathology Typical histological findings of ARDS include alveolar inflammation, thickened septae and protein leak (pink), hyaline membranes, congestion and decreased alveolar volume Risk Factors for ARDS Pulmonary  Aspiration pneumonia  Infectious pneumonia  Smoke or toxic gas inhalation  Trauma with lung contusion  Near drowning  Acute eosinophilic pneumonia  BOOP Risk Factors for ARDS Extra-pulmonary  Acute pancreatitis  Cardiopulmonary bypass  Drug overdose  Surface burns  Lung and bone marrow transplantation  Venous air embolism  Neurogenic  Fulminant hepatic failure  Multiple bone fractures with fat     emboli syndrome Blood transfusion Sepsis Post upper airway obstruction Drugs (bleomycin) Oxygenation with HFOV Machine adjustable parameters: FIO2 Paw TI% Ventilation during HFOV CV (“bulk flow”) VE = f x VT HFOV (“facilitated diffusion”) VE = f x VT2 small changes in TV have greater effect during HFOV Ventilation during HFOV To ↓ PaCO2 ↑∆P ↓Hz Cuff leak ↑ET size ↑I-Time % When should HFOV be initiated? If FIO2 > 60% and unable to maintain Pplat < 30 cmH20 ? If mPaw on CV is > 20 cmH2O and high FIO2 > 60% ? (or PEEP > 15?) If patient requiring paralysis for oxygenation Earlier intervention better How should HFOV be initiated? Adequate sedation, analgesia (paralysis during transition?) Set mPaw 3-5 cm H2O> mPaw on CV (initial cm H2O ETT cuff-leak) Set ∆P at @ “20 + PaCO2” (range 55-90) Set Hz at (unless compartment syndromes, obesity, etc) (range - Hz) Set TI% at 33% and bias flow @ 30 lpm Unresolved Issues in HFOV  At what severity threshold should HFOV be tried?  How to best predict responders or failures to HFOV?  Does HFOV cause less VALI in adults than conventional “protective lung” ventilation?  Does HFOV “rescue” patients who would have died?  How does HFOV compare with “best” lung protective CV or other “open lung” approaches (e.g APRV, HFPV/VDR)?  Larger “protocol-driven” trial needed to definitively prove lower mortality and ventilator-free days Inhaled Vasodilators in ARDS         Inhaled NO and prostacyclin – no outcome benefit Dose 1.5 to 40 ppm Abrupt interruption worsens oxygenation and pulmonary HTN It does not help all patients Less effective in sepsis Toxic substances – NO2 and methemoglobin Potential for immunosuppression and mutagenesis Inhaled prostacyclin – no sophisticated equipment required Other Therapies in ARDS  Corticosteroids, inhaled and intravenous PGE1, ketoconazole, ibuprofen have been tried in RCT with negative results  A small recent small study for late ARDS showed survival benefit for steroids Prognosis in ARDS    Improvement in survival from 67% in 1983 to 40% in 1990 Cause of death Respiratory failure is unusual (16%)  In the first three days, the underlying disease  Later, nosocomial infections and sepsis account for most of the deaths  Long term survivors have mild pulmonary abnormalities and usually asymptomatic Poor Prognostic Factors in ARDS  Advanced age  Sepsis  Multiple organ dysfunction  Underlying disease  Persistent neutrophils in BAL  Persistent pro-inflammatory cytokines (TNF, IL-1, IL-8)  Lower anti-inflammatory cytokines (IL-10, IL-1 receptor antagonist) Case study #1 A 60 year old man (70 kg IBW) was admitted for RML pneumonia and has required mechanical ventilation for 24 hours His most recent ABG shows pH 7.33, PaCO2 48 torr, and PaO2 48 torr on FIO2 = 1.0 His ventilator is set to CMV with VT 0.6, f 16, PEEP 5, and I:E 1:3 His CXR now shows infiltrates in of quadrants Your next steps are… Problem(s) Goals Approach Case study #2 A 60 year old man is admitted to the ICU for severe respiratory distress that developed during a blood transfusion His SpO2 is 85% despite CFM O2 Your next steps are… Problem(s) Goals Approach Case study #3 A 60 year old man (70 kg IBW) has been in the ICU with severe ARDS for days His current ventilator setting are FIO2 1.0, PEEP 15 cm H2O, and SIMV 16/min Despite this support, his ABG shows pH 7.33, PaCO2 48 torr, PaO2 48 torr Your next steps are… Problem(s) Goals Approach Case study #4 A 60 year old man has been in the ICU with severe ARDS for 10 days His current ventilator setting are FIO2 1.0, PEEP 15 cm H2O, and SIMV 16/min Despite this support, his ABG shows pH 7.33, PaCO 48 torr, PaO2 48 torr Your next steps are… Problem(s) Goals Approach Case study #5 A 60 year old man has been in the ICU with severe ARDS for weeks His current ventilator setting are FIO2 1.0, PEEP 15 cm H2O, and SIMV 16/min Despite this support, his ABG shows pH 7.33, PaCO 48 torr, PaO2 48 torr Your next steps are… Problem(s) Goals Approach