1/26/16. Prone Position How does asynchrony impact LPV and how should it be managed? Is there a role for NIV and HFNC in ARDS?

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1 What is ARDS?: how our understanding changed over time What are the risk factors and major etiologies? How does MV exacerbate or attenuate lung injury? Ventilator managment of ARDS Rich Kallet MS RRT FAARC FCCM Director of Quality Assurance Respiratory Care Services UCSF at San Francisco General Hospital Prone Position How does asynchrony impact LPV and how should it be managed? Is there a role for NIV and HFNC in ARDS? 1821: Rene Laennec: idiopathic anasarca of the lungs w/o heart failure. Universally fatal Double PNA 1900: Osler: uncontrolled septicemia leads to frothy pulmonary edema that resembles serum, not the sanguinous transudative edema seen in congestive heart failure. 1918: Phosgene gas poisoning / Spanish Influenza WWII: Brewer/Burford: persistent wet lung of trauma in battle casualties w/ severe brain, thoracic, abdominal & extremity trauma..most difficult to resuscitate, highest mortality. 1948: Moon: shock lung following hemorrhage 1959: Petersdorf: Asian influenza pandemic of : Vietnam War: wet lung ; Da Nang Lung 1

2 Sudden onset of respiratory distress w/o hx of pulm disease. Variety of insults (7 (~60%) Trauma, pancreatitis, viral PNA, Drug OD, Aspiration) Non-cardiogenic pulmonary edema* Diffuse opacities on CXR Diffuse inflammation interstitial fibrosis (late ARDS autopsy) Low compliance Hypoxemia refractory to high FI O2 Responsiveness to PEEP * 7/12 pts had evidence of fluid overload LIS (1988) AECC (1994) Berlin (2012) 5 pt scoring system (0-4) 4 categories CXR (0-4 quadrants) PaO2/FiO2* (> 300: 0; < 100: 4) Crs (> 80: 0; < 20: 4) PEEP (< 5: 0; > 15:4) ARDS > 2.50 Acute Onset Bilateral Opacities (Diffuse or patchy) Not explained by atelectasis, pleural effusions P/F < 300: ALI P/F < 200: ARDS Absence of LA HTN or Fluid Overload PAOP < 18 mmhg Onset: < 7 days from insult. Bilateral Opacities (Diffuse or patchy) Not fully explained by atelectasis, pleural effusions, Origin of Edema: Not fully explained by cardiac, fluids Minimal PEEP > 5 Mild: Mod: Severe: < 100 Major Causes Pneumonia Sepsis Aspiration Trauma Lesser Causes Transfusions (TRALI) Pancreatitis Hemorrhagic Shock Inhalation Injury IV Drug Fat Embolism Near Drowning Exotic / Unusual Protozoan: Malaria Fungal: Coccidiomycosis Hemorrhagic Fevers: Marburg, Ebola Eclampsia Amniotic fluid embolism Inhalation of Fumes Reaction to Contrast Reaction to drugs (Amantadine, Bleomycin, Amiodarone) Annual Incidence USA: 190,000 adult cases Overall Mortality: ~40% ( s > 60%) Clinical Trials (ARDS Net): 39% to 22% Berlin Definition: Mild: 27% [24-30] Moderate: 32% [29-34] Severe: 45% [42-48] Impact of Comorbidities ESLD, BMTransplant: ~70% ARDS + Renal Failure (dialysis): ~67% SFGH Presence of Comorbidities (pre/post LPV): 78% vs. 48% 2

3 Berlin Definition Mild: 5 days [2-11] Moderate: 7 days [4-11] Severe: 9 days [5-17] Attraction /migration/ activation of macrophages, platelets, neutrophils. Stimulation & Release of ROS, Hyaline membrane formationactivation of fibrin,leakage of plasma proteins, cellular debris (necrosis / apoptosis) Necrosis: Inability to reabsorb edema fluid via active ion pumps Lymphatic drainage capacity exceeded Volutrauma Overdistension: Excessive Strain V Atelectrauma Shearing P 3

4 1/26/16 Estimated Strain of a 6 vs. 12 ml/kg VT as FRC Decreases In severe ARDS ~ 1/3 of lung appears to be normally aerated ~ 300g of tissue =lung size of a 5 yo child (Vt ~ 150 ml) Traditional VT ventilation ml/kg 68 kg adult ml Functionally: ml/kg VT 6 ml/kg VT 40 ml/kg VT 1.8 Strain 6 ml/kg 0.6 Strain 12 ml/kg Note: Strain-stress plays out in alveolar regions of different gas volumes: Stress Raisers amplifiers CT HU Color Coding Red: Hyperiflated, Blue Normal, Yellow Poorly Aerated, Green Non Aerated N = 30, ARDS Net Protocol: 6 ml/kg & Pplat < 30 cmh2o PCV 35 PCV 15 Control Injury Gajic et al Am J Respir Crit Care Med More Protected: 53% normal aerated tissue 26% non-aerated tissue Pplat 26 cmh2o Crs: 26 ml/cmh2o Less Protected: 53% normal aerated tissue 49% non-aerated tissue Pplat 29 cmh2o Crs: 26 ml/cmh2o IL-6 TNFα stat sig only for hyperinflated tissue 4

5 Hyperoxic Acute Lung Injury: 240 years of research Tissue injury & aging occurs through generation ROS RNS Breathing a F IO2 > 0.80 for approximately 3-6 days typically is fatal to most animals Pretreatment w/ hyperoxia prior to, or combining hyperoxia with high-stretch ventilation significantly magnifies VILI. LPV + prolonged (17hrs) needless exposure to high F IO2 (> 0.70) worsening oxygenation index at 48h & longer duration of MV. Dose dependent effect (i.e. still seen at F IO2 > 0.55 Alveolar epithelial cell cultures exposed to both 48h of hyperoxia ( ). Hyperoxia stiffens the cell membrane; increases its resistance to stretch. Alveolar cell cultures attached to an artificial basement membrane that was stretched resulted in substantial detachment of alveolar cells from its supporting matrix. Oxidative stress induced a loss of pliability within the alveolar epithelial cell membrane (relative to the basement membrane) inducing shear-injury that enhances stretch-induced injury. Number of Patients LIP (cm H2O) Frequency distribution of 197 discreet measurements of lower inflection points from 16 clinical studies. 5

6 Balance: severity of lung injury vs. deleterious effects sedation /paralytics Mild Moderate Severe V T : 6-8 ml/kg FiO 2 < 0.60 PEEP: 5-10 Pplat: < 26 Pplat-PEEP: < 15 V T : < 6 ml/kg FiO 2 < 0.60 PEEP: Pplat: 26 Pplat-PEEP: < 15 Prone? V T : < 6 ml/kg FiO 2 < 0.60 PEEP: Pplat:? Pplat-PEEP: < 15 Prone 18% 30% 52% Gattinoni Anesthesiology

7 PP Pa O2 / Fi O2 SP Qs/Qt PP PP SP Multi-center RCT N = 466: 90 Day mortality 41 to 24% Adjusted RR for mortality 0.48 (SOFA); VFD 4 & 14 (D-28,D-90) No difference in complication rates N Engl J Med

8 1/26/ VT Global Inspiratory Muscle Shortening Peak Flow/ Flow Pattern Velocity of Contraction Respiratory Drive Corollary Discharge to Sensory WOB vent (Joules/L) % VT Demand C MV Dyspnea: Efferent impulse/muscle tension > speed & magnitude of chest/lung displacement. Breathlessness: Unpleasent urge to breathe (excessive drive related in part to PCO2 Pain & Dyspnea are processed in the same ancient brain structures Sim ulate d VT De m and VC-DF PCV 2.5 WOB sim (Joules/L) 200 VC-CF UB Sim ulated VT Dem and VC-CF 50 0 VC-DF PCV 8

9 Pmus: average in AMV ~ 15 cmh 2 O Distress: Pmus cmh 2 O (PAOP 18-29) Magnifies hydrostatic ΔP capillary interstitium edema formation ( cardiac function) O 2 cost of breathing PVO2 magnifies Qs/Qt Note: survival from ARDS depends upon the ability to clear pulmonary edema Loaded muscles instinct full relaxation force of contraction Forced expiration: Counteracts PEEP ΔP needed to keep V T ~ 6-7 ml/kg Peak Flow Capacity WOB V T V T mismatching cannot be treated without either matching V T or sedation ~ sec on CPAP = PEEP on CMV Evaluate V T, peak flow, Ti: variability Compare to LPV goals vs. Sedation goals Severe, early ARDS: sedation,? NMBA Milder ARDS: liberalize V T goals Trifecta of ARDS: shock, hypoxemia, acidosis! Pay attention to PAIN & ACIDOSIS NIV: ARDS is not short-term condition like COPD exacerbation / cardiogenic edema (5-7 vs days) ~ 50-70% of ARDS patients fail a trial of NIV (related to presence of shock, acidosis Failed NIV + Delayed Intubation mortality 68 vs. 39% predicted High-Flow Nasal O2 (FLORALI Study): need for MV compared to standard suppl O 2 Rx for PNA- ARDS Contraindicated if Pa CO2 > 45 mmhg, hemodynamic instability. Poor methods prevent assessing efficacy to NIV (8hrs/d) Abandon w/in 30min if respiratory distress persists 9

10 190,000 cases/yr, Overall mortality ~ 40% New Berlin Definition Mild, Moderate & Severe based on P/F (27, 32, 45% Mortality). 3 Injuries: strain, shear, O 2 toxicity Better P targets: Pplat 26, Pplat-PEEP < 15 Better PEEP: (Mil) 5-10, (Mod) 10-15, (Sev): Avoid prolonged exposure FiO 2 >.80 (Goal < 0.60) Prone YES for severe ARDS (P/F < 150) Diagnostic CPAP to evaluate asynchrony Very cautious use of NIV, HFNC 10

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