ARDS

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By: doc.mushu (67 month(s) ago)

please allow me to download this ppt as i have to present on ARDS or please mail me at doc.mushu@gmail.com Thanks !

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ARDS:

ARDS Presenter: Lokesh M B Moderator: Dr. B. D. Bande

Case:

Case Malan Shinde 50/F cheif complaints: Cough 1 week Breathlessness 1 week Fever 2 days

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patient was apparently alright one week back, when she developed cough, intermittent, not associated with sputum production Breathlessness since 1 week, gradually progressive, unable to do heavy work due to breathlessness. Fever, intermittent in nature, low grade, not associated with chills and rigors. For the same complaints shown to a local doctor where she was admitted and managed conservatively.

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Shifted to KEMH in view of persistent symptoms. No past history of DM/HTN/IHD

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In Emergency department: CXR bilateral infiltrates ABG: pH 7.39 PaO 2 52 PaCO 2 27 HCO 3 - 16.3 Intubated in view of respiratory failure.

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Commenced on mechanical ventilation: CMV 400/10/0.9 ABG: pH 7.37 PaO2: 66 PaCO2: 43 HCO3: 24.9

investigations:

investigations Hemoglobin: 10.1 TLC: 5900 Platelets: 2.26 lakhs Serum urea: 17mg/dl Serum Creatinine : 0.9 LFT normal Serum electrolytes: 140/3.0

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Widal negative H1N1: negative Weil felix Positive Rikettsial DNA PCR: negative

Treatment chart:

Treatment chart Imipenem+cilastatin 500mgBD Doxycycline 100mg BD Oseltamavir 75mg BD Artesunate 120mg loading f/b 60 mg OD Sedation with midazolam infusion Supportive medications

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Course in hospital: Difficulty weaning Gradual decrease Fio2, PS/PEEP Low grade fevers present Malaria negative – artesunate stopped H1N1 negative, oseltamavir stopped TRAP c/s (13/4): Acientobacter baumani sensitive to Colistin / Tigecycline Started on Colistin 2 MU

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Oxygenation improved gradually.. Date pH PaO2 PaCO2 HCO3 07/04 7.48 56 49 36 08/04 7.47 61 (0.8) 45 32 09/04 7.47 65 42 30 10/04 7.40 60 57 35 11/04 7.45 119 46 32 12/04 7.51 100 47 37 13/04 7.44 65 49 33 14/04 7.51 90 41 32 15/04 7.47 46 43 31

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Developed subcutaneous emphysema 12/04 Plan for trache Trial of extubation 13/04 tolerated. Stop imipenem + cliastatin , entavar , doxycycline Start tigecycline Transferred out 19/04 In wards, stable hemodynamics 24/04 tachypnoea (RR~40)

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Back to ccu : o/e: Conscious oriented HR: 90/min BP 120/70 mmHg RR 40/min RS scattered crepts .

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ABG: pH: 7.51 PaO2: 90 PaCO2: 31 HCO3: 24.7 ABG: bilateral infiltrates. Managed with diuretics and sos NIV

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CT thorax done: Pulmonary thromboembolism Patchy areas of consolidation with few areas ofsacrring and traction broncheactasis in both lungs Pneumomediastinum and pneumopericardium with multiple iternal septae .

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Course: Stabilized with diuretics. SpO2 >95% with 2LO2 by nasal prongs. Shifted out on 27/04 in view of clinical improvement.

Adult Respiratory Distress Syndrome ARDS:

Adult Respiratory Distress Syndrome ARDS

ARDS :

ARDS INTRODUCTION DEFINITION ETIOLOGY EPIDEMIOLOGY PATHOLOGY PATHOPHYSIOLOGY CLINICAL FEATURES PROGNOSIS IMAGING MANAGEMENT SUPPORTIVE MECHANICAL VENTILATION.

INTRODUCTION:

INTRODUCTION 1827 Laennec first scientific description idiopathic anasarca of lungs . 1960- Acute respiratory failure with both lung involvement Shock lung-military hospitals adult respiratory distress syndrome- civilian hospitals. 1967-Ashbaugh lancet-2:319-323 –first description.

AECC 1994:

AECC 1994 ALI ARDS ONSET ACUTE ACUTE OXYGENATION P/F <300mmHg <200mmHg CHEST RADIOGRAPH BILATERAL ALVEOLAR OR INTERSTITIAL INFILTRATES BILATERAL ALVEOLAR OR INTERSTITIAL INFILTRATES ABSENCE OF LA HTN PCWP<18mmHg or NO CLINICAL EVIDENCE OF ELEVATEDLAP PCWP<18mmHg or NO CLINICAL EVIDENCE OF ELEVATEDLAP

LIMITATIONS OF DEFINITION: :

LIMITATIONS OF DEFINITION: No correlation with severity of lung injury ,clinical course, survival. Documentation of low compliance – not necessary Evolves over 4-48 hours:persists for days to weeks. Permeability edema- other structural abnormalities also present.

CRITISICMS AECC1994:

CRITISICMS AECC1994 Hypoxemia – p/f not constant over the range of fio2 and vary according to peep Gowda 1997, Villar 2007 Xrc - Interobserver variability even by experts Wedge pressure - increased in ards either because of transmitted airway pressure or vigorous fluid resuscitation ards net 2006 Perception of ali not as severe ards – underrecognition ferguson 2005. Definitions have to be reviewed ,adjusted to reflect new information and the experience gained since the conception

BERLIN DEFINITION:

BERLIN DEFINITION MILD MODERATE SEVERE TIMING ACUTE ONSET WITHIN 1 WEEK OF A KNOWN CLINICAL INSULT / NEW OR WORSENING RESPIRATORY SYMPTOMS / HYPOXEMIA P/F 201-300 WITH PEEP >5 P/F < 200 WITH PEEP >5 P/F < 100 WITH PEEP >10 ORIGIN OF EDEMA RESPIRATORY FAILURE NOT FULLY EXPLAINED BY CARDIAC FAILURE OR FLUID OVERLOAD XRC BILATERAL OPACITIES BILATERAL OPACITIES OPACITIES INVOLVING ATLEAST 3 QUADRANTS PHYSIOLOGICAL DERANGEMENT N/A N/A VE>10 LITRE/Min

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Clinical Disorders Associated with the Development of the Acute Respiratory Distress Syndrome

INCIDENCE AND MORTALITY:

INCIDENCE AND MORTALITY

RISK FACTORS AND MORTALITY KCLIP DATA :

RISK FACTORS AND MORTALITY KCLIP DATA PATIENT RISK FACTORS SEPSIS PULMONARY 44%:EXTRAPULMONARY 33% ASPIRATION 11% TRAUMA, TRANSFUSION, DRUGS 3% TREATMENT RISK FACTORS MECHANICAL VENTILATION TV,PAP Gajic ICM 2005 :31 ;922 DETERMANN CCM 2010 TRALI/TACO SEPSIS MANAGEMENT DELAYED GOAL DIRECTED RESUCITATION, DELAYED ANTIBIOTICS – INDEPENDENT RISK FACTOR FOR ALI ISCIMEN CCM 2008;1518 MORTALITY ASPIRATION ASSOCIATED 44 % PULMONARY SEPSIS ASOCITED 41% TRAUMA 24% PREHOSPITAL ANTIPLATELET TREATMENT DIABETES – MODULATES RISK Honiden ; DM ,insulin and ALI CCM 2009 ;37;2455 Erlich prehospital antiplatelet treatment Chest 2011 :139

EPIDEMIOLOGY:

EPIDEMIOLOGY Incidence of 17-64/100000 per person years usa 40-43% of ali develop ards . Mortality: Ali 38.5%, Ards 41% rubenfeld nejm:2005:353:1685 Studies in usa - age 49+/- 2 years white:black 2:1 male:female 3:2 non smoker:smoker 2:1. Fatalities- average time from diagnosis to death 16 days. Survivors – average time to discharge 47 days.

TIME COURSE OF ARDS:

TIME COURSE OF ARDS Early exudative – edema, hyaline membrane formation Proliferative – interstitial inflammation, fibrosis, disordered healing .

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Exudative phase: <1 week Epithelial and endothelial cell death Neutrophil sequestration Platelet fibrin thrombi Interstitial edema Exudates in airspaces – compact into hyaline membranes

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Proliferative phase: Second week Organisation of exudates Proliferation of type II alveolar cells, fibroblasts. Areas of squamous metaplasia , granulation tissue occluding alveolar ducts.

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Fibrotic phase (3-4 weeks) Usually start with proliferative phase – fibroproliferative phase Alveolar septa expanded, airspaces filled with connective tissue Airspace: resolve / fibrosis

pathogenesis:

pathogenesis Alveolar fluid clearance Type II pneumocytes By active sodium transport (Na-K ATPase ) Though disrupted in ARDS, some areas have preserved AFC Protein resorption – may take longer. Neutrophils : not essential for development of ARDS but may affect the severity

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Leucocytes and coagulation: Dysregulated coagulation Alveolar macrophages – tissue factor- FVII PAI-1 (inhibit fibrinolysis ) Presence of microthrombi

Pathophysiology :

Pathophysiology Refractory hypoxemia Decreased respiratory compliance Propensity for alveolar closure

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Refractory hypoxemia: Alveolar fluid- physiologic shunt Scattered microthrombi – more to well perfused ‘normal’ areas of lung So increase in both shunt and dead space. Pumlonary hypertension: hypoxia/thrombotic ? Can aggravate pulmonary edema

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Decreased compliance: Decreased lung compliance Inc surface tension, alveolar edema Baby lung: Fluid filled areas remain collapsed throughout tidal volume, hence inc compliance Complaince is a direct measure of areated lung So, normal lung receive more tidal volume – overdistension

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Propensity for alveolar closure Surfactant: inhibitory binding of plasma proteins and cholesterol Decreased production by type II pneumocytes Mechanical ventilation

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FEATURE CAUSE(S) HYPOXEMIA TRUE SHUNT IMPAIRED HPV V/Q MISMATCH-MINOR COMPONENT inc DEPENDENT DENSITIES CT SURFACTANT DYSFUNCTION ALVEOLAR INSTABILITY COLLAPSE/ CONSOLIDATION EXAGERRATION OF NORMAL COMPRESSION OF DEPENDENT LUNG DUE TO inc WEIGHT(LUNG WATER, INFLAMMATION) inc ELASTANCE(dec COMPLIANCE) SURFACTANT DYSFUNCTION BABY LUNG INCREASED CHEST WALL ELASTANCE FIBROSING ALVEOLITIS inc MINUTE VOLUME REQUIREMENT INCREASED ALVEOLAR DEAD SPACE INCREASED VCO2 inc WORK OF BREATHING inc ELASTANCE AND MV REQUIREMENT PULMONARY HYPERTENSION PULMONARY VASOCONSTRICTION PULMONARY MICROVASCULAR THROMBOSIS PEEP

CONSEQUENCES:

CONSEQUENCES IMPAIRED GAS EXCHANGE – SHUNT V/Q MISMATCH. DECREASED COMPLIANCE PULMONARY HYPERTENSION 25% OF ARDS PATIENTS HYPOXIC VASOCONSTRICTION VASCULAR COMPRESSION BY POSITIVE AIRWAY PRESSURE LUNG PARENCHYMAL DESTRUCTION AIRWAY COLLAPSE PULMONARY VASOCONSTRICTORS.

PROTECTIVE MECHANISMS AGAINST PULMONARY EDEMA:

PROTECTIVE MECHANISMS AGAINST PULMONARY EDEMA OSMOTIC GRADIENT- RETENSION OF PROTEINS IN ITRAVASCULAR SPACE ARROWS –LYMPHATIC MOVEMENT CIRCLE- PROTEIN

EVOLUTION OF EDEMA :

EVOLUTION OF EDEMA ENDOTHELIAL BREACH LEAKAGE OF PROTIENS INTO INTERSTITIUM OVERWHELMED INTERSTITIUM AND LYMPHATICS ALVEOLAR EDEMA

Mechanical ventilation:

Mechanical ventilation Barotrauma Volutrauma Atelectrauma biotrauma

ATELECTRAUMA:

ATELECTRAUMA When lung units collapse, they may stretch adjacent, non- atelectatic lung units and create damaging shear forces

BIOTRAUMA:

BIOTRAUMA BIOTRAUMA IS THE MISSING LINK BETWEEN THE PATHOPHYSIOLOGY OF ARDS AND THE PATHOBIOLOGY OF MODS

Mechanisms responsible for resolution of ALI/ARDS:

Mechanisms responsible for resolution of ALI/ARDS

CLINICAL FEATURES:

CLINICAL FEATURES EARLY REFLECT PRECIPITANT OF ARDS, EFECTS OF DAD FEVER,HYPOTENSION IN SEPTIC SHOCK ABDOMINAL PAIN OF ACUTE PANCREATITIS PULMONARY DYSFUNCTION – 24 TO 48 HRS OF INCITING EVENT RAPIDLY WORSENING TACHYPNEA, HYPOXEMIA, INCREASED OXYGEN REQUIREMENT EXAMINATION- CYANOSIS,TACHYCARDIA,RALES ON CHEST

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MECHANICALVENTILATION UNIVERSALLY REQUIRED ABG - ALKALOSIS,INCREASED A-a gradient, SEVERE HYPOXEMIA. SUBSEQUENT COURSE OXYGENATION IMPROVES WITH RESOLUTION OF PULMONARY EDEMA VENTILATOR DEPENDENCY COMLICATIONS- VALI,INFECTION, MODS LATE EXUDATIVE PHASE- INCREASED DEAD SPACE ORGANISATION OF FIBROSIS- INCREASED AIRWAY PRESSURE, PHTn

XRAY CHEST:

XRAY CHEST BILATERAL INFILTRATES OF ANY SEVERITY. STAGE 1 0-24 HRS- NORMAL STAGE 2 24-36 HRS AIR SPACE INFILTRATIONION . STAGE 3 3-14 DAYS PATHOLOGICAL RADIOLOGICAL RESOLUTION. RADIOLOGICAL RESOLUTION SLOWER THAN PULMONARY EDEMA – PROTEINACEOUS EDEMA

CT CHEST:

CT CHEST Pulmonary asymmetrical,mix of consolidation and ground glass appearance. Extrapulmonary symmetrical groundglass appearance. Anterior reticular pattern – ards survivors. Identificatio of complications of barotrauma – ct .

HRCT GRADING (HRCT CHEST-W.RICHARD WEBB 4 EDITION):

HRCT GRADING ( HRCT CHEST-W.RICHARD WEBB 4 EDITION ) GRADE 1 - NORMAL ATTENUATION GRADE 2 - GROUNDGLASS OPACITY GRADE 3 - CONSOLIDATION GRADE 4 - GGO WITH TRACTION BRONCHIECTASIS GRADE 5 - CONSOLIDATION WITH TRACTION BRONCHIECTASIS. GRADE 6 - HONEY COMBING. LOWER SCORE ASSOCIATED WITH GREATER NUMBER OF VENTILATOR FREE DAYS ( P=<0.018), LOWER INCIDENCE OF BAROTRAUMA ( P<0.013)

PROGNOSIS:

PROGNOSIS Mortality- respiratory-16% ;non respiratory-30-50%. Leading cause of death –sepsis Sepsis precedes ards - abdomen predominant source. Sepsis occuring after onset of ards - pulmonary source. VAP- 55% with ards vs 28% non ards ajrccm 98 age >75 mortalityPredictors of poor outcome 60% vs <45 age 20% underlying cause of ards - trauma related – lower likelihood of death Apache score prbc transfusion alcoholism- nonpulmonary organ dysfunction after ali .

DECLINING TRENDS IN MORTALITY IN ARDS:

DECLINING TRENDS IN MORTALITY IN ARDS Data from the University of Washington demonstrating decreasing mortality among ARDS patients during the early 1990's. Redrawn from Milberg, JA, Davis, DR, Steinberg, KP, et al. JAMA 1995; 273:306. IMPROVED SUPPORTIVE CARE AND THOUGHTFUL MECHANICAL VENTILATION

SEQUELE OF ARDS:

SEQUELE OF ARDS ¼ No impairement at 1 year ¼ Moderate impairement , ½ mild impairement . Exertional dyspnea –most common Mc pulmonary abnormality- decreased single breath co diffusing capacity. Spirometry - mixed restrictive and obstructive abnormalities. Functional recovery- Respiratory factors Decreased static compliance Peep level Non pulmonary sequele : Impairement in neurocognitive skills Protracted perception of a poor quality of life.

MANAGEMENT:

MANAGEMENT Mechanical ventilation Low tidal volume Peep Other strategies Fluid management Pharmacological interventions: Steroids Surfactant Beta agonists anticoagulants

INITIAL MANAGEMENT OF ARDS:

INITIAL MANAGEMENT OF ARDS Initiate volume / pressure –controlled ventilation Tv <6ml/kg PBW PLATEAU< 30 cm water RR< 35 bpm Oxygnate fio2<0.6 PEEP<10 cmh20 SPO2 88- 95% MINIMISE ACIDOSIS ph>7.30 RR< 35 bpm DIURESIS map>65mmhg HYPOPERFUSION

GOALS:

GOALS Maintain acceptable gas exchange, minimise vali . Open lung strategy - targeting airway pressures Peep- alveolar recruitment Map- alveolar recruitment,predictor of hemodynamic effects Plateu pressure – best predictor of alveolar overdistension

LOW TIDAL VOLUME:

LOW TIDAL VOLUME Ards - heterogenous disease with patchy lung involvement. Rationale LTV less alveolar distension- less VALI. Benefit – improves mortality Evidence- arma 31% vs 40%, more ventilator free days :12 vs 10 days. Consequence - hypercapnic respiratory acidosis.

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Permissive hypercapnia - ventilatory strategy that accepts alveolar hypoventilation in order to maintain a low alveolar pressure and minimise alveolar overdistension . Minimise hypercarbia - decrease deadspace –vent tubings , hme - heated humidifier.

PERMISSIVE HYPERCAPNIA:

PERMISSIVE HYPERCAPNIA Reduction of minute volume: ↑ PaCO2, ↓ pH (6.8-7.3), resp rate 35 to achieve low tidal volume and airway pressure (plateau <30cmH2O) Safety profile not established Acceptable when necessary to limit tidal volume Limited use in preexisting metabolic acidosis and ↑ ICP Hickling et al, Crit Care Med 1994.

PRIORITISATION SCHEMES OF TRADITIONAL VS LOW TIDAL VOLUME VENTILATION IN ALI/ARDS:

PRIORITISATION SCHEMES OF TRADITIONAL VS LOW TIDAL VOLUME VENTILATION IN ALI/ARDS Traditional TV strategy Lower TV strategy Higher priority Normal arterial PaCO2, pH Lowest possible FIO2, PEEP to maintain acceptable oxygenation Higher priority avoid overdistension Lower priority avoid overdistension LOWER PRIORITY Normal arterial PaCO2, pH Lowest possible FIO2, PEEP to maintain acceptable oxygenation

TV USED IN TRIALS OF LUNG PROTECTIVE STRATEGIES:

TV USED IN TRIALS OF LUNG PROTECTIVE STRATEGIES TRIAL TRADITIONAL TV LOWER TV TRADITIONAL TV MORTALITY LOWER TV MORTALITY AMATO et al C24/T29 12ml/kg MESURED BODY WEIGHT <6ml/kg MEASURED BODY WEIGHT 71% 38% P<.001 NIH ARDS NET C429/T432 11.8 ml/kg of PBW 6.2 ml/kg PBW 40% 31% P .007 BROCHARD et al C58/T58 10.3 ml/kg of dry body weight 7.1 ml/kg PBW 38% 47% STEWERT et alC60/T 60 10.8 7.2 47% 50% BROWES et alC26/T26 10.2 ml/kg PBW 7.3 ml/kg PBW 46% 50%

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INCLUSION CRITERIA: Acute onset of 1. PaO 2 /FiO 2 ≤ 300 (corrected for altitude) 2. Bilateral (patchy, diffuse, or homogeneous) infiltrates consistent with pulmonary edema 3. No clinical evidence of left atrial hypertension

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PART I: VENTILATOR SETUP AND ADJUSTMENT 1. Calculate predicted body weight (PBW) Males = 50 + 2.3 [height (inches) - 60] Females = 45.5 + 2.3 [height (inches) -60] 2. Select any ventilator mode 3. Set ventilator settings to achieve initial V T = 8 ml/kg PBW 4. Reduce V T by 1 ml/kg at intervals ≤ 2 hours until V T = 6ml/kg PBW. 5. Set initial rate to approximate baseline minute ventilation (not > 35 bpm ). 6. Adjust V T and RR to achieve pH and plateau pressure goals below.

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OXYGENATION GOAL: PaO 2 55-80 mmHg or SpO 2 88-95% Use a minimum PEEP of 5 cm H 2 O. Consider use of incremental FiO 2 /PEEP combinations such as shown below (not required) to achieve goal.

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PLATEAU PRESSURE GOAL: ≤ 30 cm H 2 O Check Pplat (0.5 second inspiratory pause), at least q 4h and after each change in PEEP or V T . If Pplat > 30 cm H 2 O: decrease V T by 1ml/kg steps (minimum = 4 ml/kg). If Pplat < 25 cm H 2 O and V T < 6 ml/kg, increase V T by 1 ml/kg until Pplat > 25 cm H 2 O or V T = 6 ml/kg. If Pplat < 30 and breath stacking or dys -synchrony occurs: may increase V T in 1ml/kg increments to 7 or 8 ml/kg if Pplat remains < 30 cm H 2 O.

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pH GOAL: 7.30-7.45 Acidosis Management: (pH < 7.30) If pH 7.15-7.30: Increase RR until pH > 7.30 or PaCO 2 < 25 (Maximum set RR = 35). . If pH < 7.15: Increase RR to 35. If pH remains < 7.15, V T may be increased in 1 ml/kg steps until pH > 7.15 ( Pplat target of 30 may be exceeded). May give NaHCO 3 Alkalosis Management: (pH > 7.45) Decrease vent rate if possible. I: E RATIO GOAL: Recommend that duration of inspiration be < duration of expiration.

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PART II: WEANING A. Conduct a SPONTANEOUS BREATHING TRIAL daily when: 1. FiO 2 ≤ 0.40 and PEEP ≤ 8. 2. PEEP and FiO 2 ≤ values of previous day. 3. Patient has acceptable spontaneous breathing efforts. (May decrease vent rate by 50% for 5 minutes to detect effort.) 4. Systolic BP ≥ 90 mmHg without vasopressor support. 5. No neuromuscular blocking agents or blockade.

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SPONTANEOUS BREATHING TRIAL (SBT): If all above criteria are met and subject has been in the study for at least 12 hours, initiate a trial of UP TO 120 minutes of spontaneous breathing with FiO2 < 0.5 and PEEP < 5: 1. Place on T-piece, trach collar, or CPAP ≤ 5 cm H 2 O with PS < 5 2. Assess for tolerance as below for up to two hours. a. SpO 2 ≥ 90: and/or PaO 2 ≥ 60 mmHg b. Spontaneous V T ≥ 4 ml/kg PBW c. RR ≤ 35/min d. pH ≥ 7.3 e. No respiratory distress (distress= 2 or more) HR > 120% of baseline Marked accessory muscle use Abdominal paradox Diaphoresis Marked dyspnea 3. If tolerated for at least 30 minutes, consider extubation . 4. If not tolerated resume pre-weaning settings.

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Definition of UNASSISTED BREATHING (Different from the spontaneous breathing criteria as PS is not allowed) 1. Extubated with face mask, nasal prong oxygen, or room air, OR 2. T-tube breathing, OR 3. Tracheostomy mask breathing, OR 4. CPAP less than or equal to 5 cm H 2 0 without pressure support or IMV assistance.

OPEN LUNG VENTILATION:

OPEN LUNG VENTILATION STRATEGY THAT COMBINES LTV AND PEEP TO MAXIMISE ALVEOLAR RECRUITEMENT & DECREASE VALI. LTV- LESS ALVEOLAR DISTENSION PEEP – MINIMISES CYCLIC ATELACTASIS. BENEFIT- MAY IMPROVE MORTALITY/OXYGENATION/OUTCOMES. EVIDENCE- AMATO et al NEJM 1998 5,338(6),347-54 MORTALITY BENEFIT, LESS INCIDENCE OF BAROTRAUMA ARIES ESPANA STUDY:CCM 2006 MAY :34(5):1311 DECREASED ICU,HOSPITAL MORTALITY,VENTILATOR FREE DAYS.

ARIES ESPANA STUDY LIMITATION- HIGHER TIDAL VOLUME IN CONTROL GROUP:

ARIES ESPANA STUDY LIMITATION- HIGHER TIDAL VOLUME IN CONTROL GROUP CONTROL PFLEX/LTV P VALUE ICU MORTALITY 24/45(53.3%) 16/50(32%) P 0.04 HOSPITAL MORTALITY 25/45(55.5%) 17/50(34%) P 0.04 VENT FREE DAYS 6.02+/_7.95 10.90 <0.008

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EVIDENCE BASED RECOMMENDATIONS FOR ARDS THERAPIES LTV A High PEEP or open lung C Prone position C Recruitment maneuvers C HFO and ECMO D Steroids C Surfactant / iNO D A- BASED ON RCTS-RECOMMENDED B- BASED ON SUPPORTIVE LIMITED CLINICAL DATA C- INDERMINATE EVIDENCE- ALTERNATIVE THERAPY D- NOT RECOMMENDED – CLINICAL EVIDENCE AGAINST THERAPY.

PRESSURE VOLUME CURVE IN ARDS:

PRESSURE VOLUME CURVE IN ARDS The slope of the curve is flat at low and high airway In these areas, increases in airway pressure produce minimal increases in lung volume. Compliance is maximized on the straight part of the curve. The deflection point is defined as the level at which the curve begins to divert from a straight line. Above this threshold, the lung is likely to begin to become overdistended . Mechanical ventilation is considered optimal when it takes place on the straight part of the curve between the inflection and deflection points. Redrawn from Brunet, F, Jeanbourquin , D, Monchi , M, et al, Am J Respir Crit Care Med 1995; 152:524.

PEEP:

PEEP OPENS COLLAPSED ALVEOLI, REDUCES CYCLIC ATELECTASIS. OPTIMUM PEEP JAMA 2008 PEEP IN ARDS FEB13:299(6):646-55 PEEP AIMED AT INCREASING ALVEOLAR RECRUITEMENT VS MINIMISING ALVEOLAR DISTENSION – NO SURVIVAL BENEFIT: DID IMPROVE LUNG FUNCTION, DURATION OF MV, DURATION OF ORGAN FAILURE. Minimal distension 382 Increased recruitment385 28 mortality 31.2% 27.8% p<.31 Hospital mortality 39% 35% p<0.3 Ventilator free days 3 7 p<0.04 Organ failure days 2 6 p<0.04

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HIGH VS LOWER PEEP IN ARDS- CLINICAL OUTCOMES WERE SIMILAR. ALVEOLI STUDY NEJM 2004:351:327-36. LIMITATION- HIGH PEEP – OLDER AGE GROUP, LOW PAO2/FI02 AT BASELINE, CARE GIVERS WERE UNBLINDED.

RECRUITMENT MANEUVERS :

RECRUITMENT MANEUVERS Brief application of a high level of continuous positive airway pressure 35-40 cmH2O for 40 sec. Purpose- open the alveoli that have collapsed. LTVV –reduced VALI– decruitment . RM- with peep prevent derecruitment . Shear forces due to cyclic opening and closing – biotrauma , VALI. RM – balance the high pressure –VALI / low pressure- derecruitment .

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No consensus on duration/frequency of RM. Techniques- high pressure sigh breaths inspiratory hold. Monitoring of efficacy- gas exchange, lower chest wall elastance Prone ventilation- makes lungs topographically more favorable for rm. Predictors of recuitability . P/f ,compliance, reduced pco2—sesitivity 71%,specificity 59%. Rescue therapy in refractory hypoxia.

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Improves oxygenation- magnitude of increase is greatest when RM is followed by high levels of peep. Trasport /tube changings - derecruitment Sigh breaths – prone ventilation, extra pulmonary causes of ards . RM – improve oxygenation, reduce shunt, increase compliance RM – works early in ards , and in patients without impaired chest wall compliance.

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More effective in extrapulmonary than pulmonary cause of ards . A RM without adequate peep – unstable alveoli and VALI. Recruitable lung units - < 10% densities on CT. Unanswered questions- is it important to recuit 10%???? Should the lungs be always open????

PRONE VENTILATION:

PRONE VENTILATION

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Improves oxygenation Mechanisms - Improve V/Q matching Decreases shunt flow Gravitational distribution of blood flow. Changes the regional diaphragm motion Less compression from heart (1-4% in pv vs 16-42% in sv ajrccm ;161;1660-1665, 2000 . Dorsal to ventral orientation of major airways- more efficient drainage of secretions, higher fFRC Effect of RM – incresed prolonged. Vali - reduction. Extrapulmonary - better response to PPV.

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Effect of ppv on the survival of patients with ARF Gattinoni - nejm-2001. 304 patients. 6/ more hours /day for 10 days. Pf ratio 63+/- 66.8 vs 44.6 +/- 68.2 p <0.02. Responders - 73% ppv pf increased by 10 and 70% within an hour. Each maneuver – mean 10+/- 12 mnts : mean of 4.6+/- 0.9 persons. Post hoc analysis - lower 10 day mortality : 162 patients 83 vs 79 (20.5% vs40%) patients with pfr < 88 (23 vs 47%) apache ii >49 (19.4% vs 48.5%) HTV>12 ml/kg PBW.

MULTICENTRE TRIAL OF PROLONGED PPV IN SEVERE ARDS MANCEBO etal AJRCCM-2006, 173:1233.:

MULTICENTRE TRIAL OF PROLONGED PPV IN SEVERE ARDS MANCEBO etal AJRCCM-2006, 173:1233. Targetted 20 hrs of proning vs 7 hrs in gattinoni . Pa02/fio2 161 (s) vs 132 (p). Multi logistic regression - supine independent predictor of death. 15% absolute and 25% relative reduction in icu mortality. Prone ventilation- safe,feasible and reduces mortality in patients with severe ards,when it is initiated early and applied for most of the day. Downside of proning pao2 may drop labor intensive loss of airway compression injury to soft tissues Lines / tubes

META ANALYSIS OF PPV CCM 2008.:

META ANALYSIS OF PPV CCM 2008. 5 RCTS No difference in icu / 28 day mortality/ 90 day mortality. Significant reduction in mortality in higher illness severity. Significant and persistent improvement in PFR in early,intermediate , late period. No difference in ventilator free days/ VAP.

HFOV:

HFOV ventilator strategy – small vts 1 ml/kg @ high frequencies 1-15 hz Gas is actively pushed in and actively withdrawn. Vt is less than the dead space Mechanisms of gas exchange bulk flow- convection- direct flow of inspired gas delivered to alveoli close to tracheobronchial tree. Taylor dispersion -mixing of residual with fresh gas at airway interface Pendular effect of mixing gases bet lung regions of different impedance Coaxial flow with net center inflow and net peripheral outflow Molecular diffusion thru relatively still air

EVIDENCE FOR HFV IN ADULT ARDS:

EVIDENCE FOR HFV IN ADULT ARDS Derdak et al ajrccm 2002, 166 :801-808 rct , 148 ards patients early improvement in pfr <16 hours. 30 day mortality 37% with hfov vs 52% with cmv p(0.102). No difference in hemodynamic variables,oxygenation , barotraumas. Fort et al CCM :1997:25:937-947.Prospective observational 17 ards adult patients. Reduction in the OI (p <0.01), fio2(p<0.02) 12,24,48 hrs after hfov .

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High-Frequency Oscillation in Early Acute Respiratory Distress Syndrome Niall D. Ferguson , M.D., Deborah J. Cook, M.D., Gordon H. Guyatt , M.D., Sangeeta Mehta, M.D., Lori Hand, R.R.T., Peggy Austin, C.C.R.A., Qi Zhou, Ph.D., Andrea Matte, R.R.T., Stephen D. Walter, Ph.D., Francois Lamontagne , M.D., John T. Granton , M.D., Yaseen M. Arabi , M.D., Alejandro C. Arroliga , M.D., Thomas E. Stew art, M.D., Arthur S. Slutsky , M.D., and Maureen O. Meade, M.D. for the OSCILLATE Trial Investigators and the Canadian Critical Care Trials Group N Engl J Med 2013; 368:795-805 February 28, 2013 DOI: 10.1056/NEJMoa1215554 In adults with moderate-to-severe ARDS, early application of HFOV, as compared with a ventilation strategy of low tidal volume and high positive end-expiratory pressure, does not reduce , and may increase,in -hospital mortality .

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High-Frequency Oscillation for Acute Respiratory DistressSyndrome Duncan Young, D.M., Sarah E. Lamb, D.Phil., Sanjoy Shah, M.D., Iain MacKenzie , M.D., William Tunnicliffe , M.Sc., RanjitLall , Ph.D., Kathy Row an, D.Phil., and Brian H. Cuthbertson , M.D. for the OSCAR Study Group N Engl J Med 2013; 368:806-813 February 28, 2013 DOI: 10.1056/NEJMoa1215716 Conclusions: The use of HFOV had no significant effect on 30-day mortality in patients undergoing mechanical ventilation for ARDS.

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Findings for patients after day 14 randomisation substantial and significant positive results for secondary variables portrayed as negative- increased mortality in subgroup of patients. Treated group- older,low compliance, higher LIS. Effect on mortality with prolonged glucocortcoid treatment. Initiation before 14 days- mortality decreased 24% vs 40% :p<0.01 Conclusion - prolonged glucocorticoid treatment substantially and significantly improves meaningful patient centered outcome variables and has a distinct survival benefit when initiated before day 14 of ards .

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Critical care medicine 2004; 32;1

NOVEL THERAPIES:

NOVEL THERAPIES BETA AGONISTS INTRAVENOUS ALBUTEROL – LESS LUNG WATER, LESS MEAN AIRWAY PRESSURE. SURFACTANT MODULATES ALVEOLAR SURFACE TENSION ,PREVENTS ATELECTASIS, FACILITATES MUCUS CLEARENCE, SCAVENGES OXYGEN RADICALS, SUPRESSES INFLAMATION. PEDIATRIC MORTALITY BENEFIT. INHALED VASODILATORS ECMO ANTIINFLAMMATORY ANTIOXIDANTS.

FLUID MANAGEMENT:

FLUID MANAGEMENT FACTT NEJM 2006;354:2564-75 wiederman Diuresis – may improve lung function ,but could jeopardise extrapulmonary organ function Conservative vs liberal Rct ; 1000 patients Primary end point – death at 60 days Secondary end points ventilatory free days organ failure free days Measures of lung physiology

FLUID STRATEGY IN ARF WEIDEMANN NEJM 2006:354:2564-75.:

FLUID STRATEGY IN ARF WEIDEMANN NEJM 2006:354:2564-75. Conservative group- CVP<4 mmhg : PAOP<8mmhg LIBERAL CVP 10-14 mmhg : PAOP 14-18mmhg. Conservative strategy: improvement in lung function shortened duration of mv , icu stay without increasing nonpulmonary organ failure. CONSERVATIVE LIBERAL P DEATH AT 60 DAYS 25% 28.4% 0.030 VENTILATOR FREEDAYS 14.6 12.1 <0.001 DAYS NOT SPENT IN ICU 13.4+/-0.4 11.2+/-0.4 <0.001

OTHER FLUID MANAGEMENT STRATEGIES:

OTHER FLUID MANAGEMENT STRATEGIES HYPOPROTEINEMIA RISK FACTOR IN ALI Albumin and furosemide therapy in hypoproteinemic patients with acute lung injury MARTIN CCM 2002 Oct;30(10):2175-82 37 PATIENTS WITH ALI AND ALBUMIN < 5mg/dl FRUSEMIDE AND ALBUMIN 8 TH HOURLY FOR 5 DAYS IMPROVED FLUID BALANCE, OXYGENATION, HEMODYNAMICS NO SURVIVAL BENEFIT STATISTICALLY NOT POWERED A randomized, controlled trial of furosemide with or without albumin in hypoproteinemic patients with acute lung injury. CCM 2005 Aug;33(8):1681-7 CONCLUSIONS: The addition of albumin to furosemide therapy in hypoproteinemic patients with acute lung injury/acute respiratory distress syndrome significantly improves oxygenation, with greater net negative fluid balance and better maintenance of hemodynamic stability. Additional randomized clinical trials are necessary to examine mechanisms and determine the effect on important clinical outcomes, such as the duration of mechanical ventilation

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OTHER FLUID MANAGEMENT STRATEGIES Crit Care Med. 2002 Oct;30(10):2175-82. Albumin and furosemide therapy in hypoproteinemic patients with acute lung injury. Martin GS , Mangialardi RJ , Wheeler AP , Dupont WD , Morris JA , Bernard GR . . OBJECTIVE: Hypoproteinemia , fluid retention, and weight gain are associated with development of acute lung injury and mortality in critically ill patients, without proof of cause and effect. We designed a clinical trial to determine whether diuresis and colloid replacement in hypoproteinemic patients with acute lung injury would improve pulmonary physiology. DESIGN: Prospective, randomized, double-blind, placebo-controlled trial. SETTING: All adult intensive care units from two university hospitals. PATIENTS: Thirty-seven mechanically-ventilated patients with acute lung injury and serum total protein </=5.0 g/ dL . INTERVENTIONS: Five-day protocolized regimen of 25 g of human serum albumin every 8 hrs with continuous infusion furosemide , or dual placebo, targeted to diuresis , weight loss, and serum total protein. MEASUREMENTS AND MAIN RESULTS: Measured outcomes included change in weight, serum total protein, fluid balance, hemodynamics , respiratory system compliance, and oxygenation. Baseline characteristics were similar between groups (treatment, n = 19; control, n = 18), with trauma being the major cause of acute lung injury. Diuresis and weight loss over 5 days (5.3 kg more in the treatment group, p =.04) was accompanied by improvements in the Pao2/Fio2 ratio in the treatment group within 24 hrs (from 171 to 236, p =.02). Respiratory mechanics were unchanged. Mean arterial pressure increased from 80 to 88 mm Hg (p =.10), and heart rate decreased from 110 to 95 beats/min (p =.008) over time in the treatment group. No difference in mortality was observed, with favorable trends in measures of intensive care. CONCLUSIONS: Albumin and furosemide therapy improves fluid balance, oxygenation, and hemodynamics in hypoproteinemic patients with acute lung injury. Determining the effect of this simple therapy on cost, outcomes, and other patient populations requires further study.

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Crit Care Med. 2005 Aug;33(8):1681-7. A randomized, controlled trial of furosemide with or without albumin in hypoproteinemic patients with acute lung injury. Martin GS , Moss M , Wheeler AP , Mealer M , Morris JA , Bernard GR . Abstract OBJECTIVE: Hypoproteinemia is a common condition in critically ill patients, associated with the development of acute lung injury and acute respiratory distress syndrome and subsequent worse clinical outcomes. Albumin with furosemide benefits lung physiology in hypoproteinemic patients with acute lung injury/acute respiratory distress syndrome, but the independent pharmacologic effects of these drugs are unknown. DESIGN: Randomized, double-blinded, placebo-controlled multicentered trial. SETTING: Eleven medical, surgical, and trauma intensive care units including 190 beds within two university hospital systems. PATIENTS: Forty mechanically ventilated patients with acute lung injury/acute respiratory distress syndrome, whose serum total protein concentrations were <6.0 g/ dL were included. Patients were excluded for hemodynamic instability or significant renal or hepatic failure. INTERVENTIONS: Subjects were equally randomly allocated to receive furosemide with albumin or furosemide with placebo for 72 hrs, titrated to fluid loss and normalization of serum total protein concentration. MEASUREMENTS AND MAIN RESULTS: The primary outcome was change in oxygenation from baseline to day 1, with secondary physiologic and clinical outcomes. There were no differences in baseline characteristics of the subjects in relation to group assignment. Albumin-treated patients had greater increases in oxygenation (mean change in Pao2/Fio2: +43 vs. -24 mm Hg at 24 hrs and +49 vs. -13 mm Hg at day 3), serum total protein (1.5 vs. 0.5 g/ dL at day 3), and net fluid loss (-5480 vs. -1490 mL at day 3) throughout the study period (all p < .05). Fluid bolus administration to control patients reduced net negative fluid balance; control patients more frequently developed hypotension and had fewer shock-free days, which translated to differences in organ failure at study end. CONCLUSIONS: The addition of albumin to furosemide therapy in hypoproteinemic patients with acute lung injury/acute respiratory distress syndrome significantly improves oxygenation , with greater net negative fluid balance and better maintenance of hemodynamic stability . Additional randomized clinical trials are necessary to examine mechanisms and determine the effect on important clinical outcomes, such as the duration of mechanical ventilation.

PHARMACOTHERAPY:

PHARMACOTHERAPY SURFACTANT INHALED NITRIC OXIDE BETA AGONISTS STEROIDS NMBS NUTRITION INHALED NITRIC OXIDE SELECTIVE PULMONARY VASODIALATATION IMPROVE V/Q MISMATCH TRIALS – IMPROVEMENT IN OXYGENATION PULMONARY HEMODYNAMICS CONSISTENT LACK OF MORTALITY BENEFIT SHORT LIVED < 24-48 HOURS. RESCUE THERAPY –NO ROLE IN STANDARD THERAPY. ACURACY S N Engl J Med 2010; 363 :1107-1116 PAPAZIAN 340 PATIENTS SEVERE ARDS P/F<150 CISATRACURIUM WITHIN 48 HOURS 90 DAY SURVIVAL, TIME OFF VENTILATOR IN TX GROUP ICU AQUIRED PARESIS SIMILAR

SURFACTANT :

SURFACTANT

EVIDENCE :

EVIDENCE Paediatic Exogenous surfactant standard life saving intervention in prevention and treatment of neonatal RDS Rcts upto 21 years survival in direct pulmonary forms of rds . Adults - current evidence less compelling than pediatric Aerosolised surfactant in adults with sepsis induced ards antonio nejm 1996 ;334;1417 no effect on 30 day survival ,length of stay in icu , duration of mechanical ventilation or physiologic function.

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Pulmonary vasodliators : iNO Useful in neonatal RDS In ARDS benefit transient, no survival benefit Some benefit seen in patient receiving 5ppm iNO Dillinger et al CCJM 1998

BALTI GAVIN AJRCCM :173:2006:281-287:

BALTI GAVIN AJRCCM :173:2006:281-287 RESOLUTION OF ALVEOLAR SPACE EDEMA -CRITICAL TO RECOVERY FROM ALI. DEPENDENT ON ACTIVE TRANSPORT OF SODIUM . BETA AGONISTS AUGMENTS SODIUM TRANSPORT – CAMP REDUCE ALVEO-CAPILLARY PERMEABILITY. HAPE SALMETROL REDUCED INCIDENCE OF HAPE NEJM 2002 ;346; 1631-1636 . BALTI RATIONALE MANIPULATION OF ALVEOLAR FLUID CLEARENCE WITH BETA AGONISTS -ACCELERATES RESOLUTION OF ALVEOLAR EDEMA. SINGLE CENTERED DOUBLE BLIDED RCT . 40 PATIENTS ;IV SALBUTAMOL 15 mcg /kg/h for 7 days EVLW AT 7 DAY BY Picco TX PLACEBO EVLW 9.2 13.2 P-0.038 PLATEU 23.9 29.5 P-0.04 TREND TOWARD LOWER LIS

NUTRTION:

NUTRTION

STEROIDS IN ARDS:

STEROIDS IN ARDS Experimental and clinical evidence – strong cause –effect – relationship persistent systemic inflammation and progression of ards . Prolonged immune dysregulation even after clinical recovery Circi unresolving ards : Inadequate gc mediated down regulation of NF-kb despite elevated cortisol Activated NF kb –ongoing tissue injury intra and extravascular coagulation maladaptive lung repair endorgan dysfunction and failure. 80 s – high dose pulse steroids in early ards – no benefit. 90s - fibroproliferative stage - beneficial.

EFFECT OF PROLONGED METHYLPREDNISOLONE IN UNRESOLVING ARDS G UMBERTO MEDURI JAMA:1998:280:159-165.:

EFFECT OF PROLONGED METHYLPREDNISOLONE IN UNRESOLVING ARDS G UMBERTO MEDURI JAMA:1998:280:159-165. 24 PATIENTS RCT .FAILED LIS IMPROVEMENT BY 7 DAY. INTERVENTIONS -16 RECEIVED MP / 8 PLACEBO. PROTOCOL 2mg/KG 1-14 DAYS. 1mg/KG 15 – 21 DAY S. 0.5 mg/KG 22-28 DAYS. 0.25mg/KG 29& 30 DAY. 0.125mg/KG 31 & 32 DAY. MP Placebo P P/F 262 148 <0.001 LIS 1.7 3 <0.001 MODS score 0.7 (mean) 1.8 <0.001 ICU mortality 0 5/8 (62%) <0.02 Hospital mortality 2/16 (12%) 5/8 (62%) <0.03

EFFICACY AND SAFETY OF STEROIDS IN PERSISTENT ARDS ARDS NET NEJM 2006/354 La SRS:

EFFICACY AND SAFETY OF STEROIDS IN PERSISTENT ARDS ARDS NET NEJM 2006/354 La SRS Rct : 180 patients. Ards patients of at least 7 days. Hospital mortality at 60 days mp 29.2 vs 28.6 in placebo hospital mortality at 180 days 31.5 vs 31.9 ventilator free days 11.2 vs 6.8 p <0.001. Mp for persistent ards improves cardiopulmonary physiology Mp after 2 weeks increases death. Pro steroids - better oxygenation, better compliance, less septic shock. Pro placebo - less neuromyopathy , less hyperglycemia.

STEROID TREATMENT IN ARDS :CRITICAL APPRAISAL OF THE ARDS NET TRIAL AND THE RECENT LITERATURE. MEDURI :ICM:2008:34:61-69.:

STEROID TREATMENT IN ARDS :CRITICAL APPRAISAL OF THE ARDS NET TRIAL AND THE RECENT LITERATURE. MEDURI :ICM:2008:34:61-69. 5 rcts:518 patients. Findings during treatment Improvement in p/f Reduction in markers of systemic inflammation Duration of mv / icu stay. Ventilator free days - far greater than ltvv / conservative fluid management.(12+/_ 11 vs 10+/_ ;p<0.007 and 14.6+/-0.5 vs 12.1+/- 0.5 ;p<0.001. Findings after rapid tapering of treatment Ards net steroid was removed within 3-4 days of extubation . Ards - systemic and pulmonary inflammation continue for weeks and extend well beyond extubation Rapid tapering- rebound inflammation/proliferation

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Corticosteroids in the prevention and treatment of acute respiratory distress syndrome (ARDS) in adults: meta-analysis BMJ 2008:JOHN PETER BMJ 2008:PETER Conclusions A definitive role of corticosteroids in the treatment of ARDS in adults is not established. A possibility of reduced mortality and increased ventilator free days with steroids started after the onset of ARDS was suggested. Preventive steroids possibly increase the incidence of ARDS in critically ill adults.

GENERAL PRINCIPLES:

GENERAL PRINCIPLES SUPPORTIVE CARE Recognition and treatment of underlying medical and surgical disorders Minimizing procedures and their complications Prophylaxis against venous thrombo-embolism, GI bleeding, CVC infections Prompt recognition and treatment of nosocomial infections Provision of adequate nutrition

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Intervention Year Study No. of Pt Findings Reference High levels of PEEP 1975 Observational 28 High incidence of pneumothorax Kirby et al. [307] Extra corporeal membrane oxygenation 1979 Phase 3 multicenter 90 No benefit Zapol et al. [308] High-frequency ventilation 1983 Phase 3 multicenter 309 No benefit Carlon et al. [309] Preventive PEEP (8 cm H 2 O) 1984 Phase3 single center 92 No benefit in patients at risk of ALI/ARDS Pepe et al. [310] Glucocorticoids (during acute phase) 1987 Phase 3 87 No benefit Bernard et al. [284] Results of RCT of Treatments and Ventilation Strategies for ALI and ARDS

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Glucocorticoids (during acute phase) 1988 Phase 3 59 No benefit Luce et al. [283] Alprostadil Intravenous 1989 Phase 3 100 No benefit Bone et al. [311] Liposomal 1999 Phase 3 350 Stopped for lack of efficacy Abraham et al. [312] Surfactant (aerosolized) 1996 Phase 3 725 No benefit Anzueto et al. [268] Open-lung approach (recruitment maneuver and ideal PEEP) 1998 Phase 3 single center 53 Decreased 28-day but not in-hospital mortality (compared to conventional ventilation) Amato et al. [2] Low tidal volume ventilation (7 vs. 11 ml/kg) 1998 Phase 3 120 No benefit in patients at risk for ALI/ARDS Stewart et al. [147]

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Low tidal volume ventilation (7 vs. 10 ml/kg) 1998 Phase 3 116 No benefit Brochard et al. [145] Glucocorticoids during late fibrosing alveolitis phase 1998 Phase 3 24 Decreased mortality, but study small Meduri et al. [288] Inhaled nitric oxide 1998 Phase 2 177 No benefit Dillinger et al. [253] Inhaled nitric oxide 1999 Phase 3 203 No benefit Payen et al. [314]

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Ketoconazole 2000 Phase 2 234 No benefit NIH ARDS Network Low tidal volumes (6 vs. 12 ml/kg) 2000 Phase 3, multicenter 861 Decreased mortality from 40% to 30% (compared to traditional tidal volumes) NIH ARDS Network Prone-positioning during mechanical ventilation 2001 Phase 3, multicenter 304 Improved oxygenation but no benefit in mortality Gattinoni et al. Partial-liquid ventilation 2002 Phase 3, multicenter 90 Lower progression to ARDS, but no benefit in mortality Hirschl et al.

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Recombinant surfactant protein C-based surfactant 2004 Phase 3, multicenter 448 Improved oxygenation at 24 hours but no benefit in mortality Spragg et al. Prone-positioning for hypoxemic acute respiratory failure 2004 Phase 3, multicenter 791 No benefit in 28- or 90-day mortality and some safety concerns Guerin et al. Higher vs. lower PEEP during low tidal volume ventilation 2004 Phase 3, multicenter 549 No benefit in mortality or days with ventilator support Brower et al. Low- and high-dose partial liquid ventilation 2006 Phase 3, multicenter 311 No benefit in mortality and some safety concerns Kacmerek et al. Glucocorticoids for late/persistent ARDS 2006 Phase 3, multicenter 180 No benefit in mortality; ↑ mortality when started more than 2 weeks after onset NIH ARDS Network Glucocorticoids for ARDS, a meta analysis 2008 Lower mortality rates with use of corticosteroids Tang et al

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MECHANICAL VENTILATION:

MECHANICAL VENTILATION

VENTILATOR INDUCED LUNG INJURY:

VENTILATOR INDUCED LUNG INJURY ARDS- heterogeneous- dependent > apex Attempts to fully inflate consolidated lung – over distension of normal lung – injury VILI by repeated over distension and recurrent alveolar collapse

VENTILATOR STRATEGY:

VENTILATOR STRATEGY Goal: optimize oxygen delivery and hemodynamic function. Permissive hypercapnia Hickling et al intensive care med 1990 Open lung protective strategy: low tidal volumes recruitment maneuver optimal PEEP Amato et al 1998

Optimal Ventilator Strategy in ARDS: What is Still Unclear:

Optimal Ventilator Strategy in ARDS: What is Still Unclear Mode of Ventilation Method of Setting PEEP PEEP Level Need for Lung Recruitment High Frequency Ventilation Prone Positioning Liquid Ventilation Bob Kacmarek MIH

LOW TIDAL VOLUME:

LOW TIDAL VOLUME In ALI can prevent progression to ARDS 6ml/kg ideal body weight Ideal body weight: NIH-ARDS 2000 Men [ 50 + 0.91 (Ht in cm) – 152.4] Women [ 45.5 + 0.91 (Ht in cm) - 152.4 ] Target: maintain plateau pressure Only intervention till date to reduce mortality from 40% (conventional) to 31% Mechanism: reduced activation of inflammatory cascade lower levels of soluble TNFRI, ↓ in IL-6, IL-8.

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A.No PEEP B.With PEEP C.With PEEP + low tidal volume D.With PEEP and normal tidal volume AAFP 2002 RECRUITMENT

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Sustained deep inflations with the intention of reopening collapsed regions of the lung. Benefit often transient if not followed by high levels of PEEP Extra pulmonary : more greater degree of edema and alveolar collapse. More amenable to recruitment Benefits negligible or short lived Oczenski Anesthesiology, 2004.

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Strategies: Richards et al Johannesburg 1999 Incremental increases in PEEP High-Frequency Oscillatory Ventilation Prone Position Spontaneous Breathing Pressure controlled ventilation with elevated cumulative product of pressure and inflation time Sustained inflations with peak inflation pressure limited to bet 30-40cm H2O Sigh

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CXR before and after recruitment maneuver Richards et al Johannesburg 1999

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Advantages: Minimize atelectasis Prevent over distension of normal alveoli Disadvantages: Worsen oxygenation by shunting blood flow to poorly aerated areas, barotrauma . Impair cardiac output – limit venous return and cardiac preload Hemodynamic compromise – hypotension Excessive over distension or repeated opening of atelectatic alveoli – injury Fujino et al, Bond et al CCM 2003

Positive end expiratory pressure PEEP:

Positive end expiratory pressure PEEP High or low PEEP? Can’t recruit collapsed alveoli Modulate effect of RM Optimal PEEP? Doesn’t reduce edema or force fluid back to interstitium Cause redistribution of fluid within alveoli Considered when P/F ratio <150 or shunt fraction (on pulm artery catheter) >20%

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Contraindications: Absolute – presence of undrained pneumothorax Relative – ↑ ICP Hypovolemia Marginal CVS function Emphysema Cavitatory pneumonias Unilateral lung disease u/l lung ds – PEEP causes compliant lung to ↑ more than stiff lung. Selective bronchial intubation with double lumen tube and differential PEEP.

STEPS TO INSTITUTE PEEP TRIAL:

STEPS TO INSTITUTE PEEP TRIAL Establish baseline values ↑ PEEP by 2.5 – 5 increments. Observe for immediate effects Allow 15 min for stabilization. Repeat measurements Analyze If PaO2 ↑ – reduce FiO2 (up to < 0.5) If PaO2 ↓ – reduce PEEP to original level SpO2 ↓(10%), CO ↓ (20%) – reduce PEEP PEEP can be increased till SpO2 >88% with FiO2 <0.5, or shunt fraction <20% or complications develop. ASCCA

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Guidelines for PEEP reduction: ASSCA Patient no longer have sepsis Patient on stable clinical course for at least 12 hours (PaO 2 of 80mmHg or more on FiO 2 of 0.4 or less) Close monitoring after trial

HIGH FREQUENCY VENTILATION:

HIGH FREQUENCY VENTILATION Very small tidal volumes (less than or equal to dead space) delivered at a very high rate. No survival benefit Mechanisms: Exact mech not known Pendular effect of mixing gases bet lung regions of different impedance Coaxial flow with net center flow and net peripheral flow Augmented dispersion producing mixing of fresh and residual air along leading edge Molecular diffusion thru relatively still air

NON INVASIVE AND PARTIAL SUPPORT:

NON INVASIVE AND PARTIAL SUPPORT Patient participation in triggering breaths - spontaneous breathing Improve aeration and V/Q mismatch within dependent regions d/t ↑ trans pulmonary pressure by actively moving diaphragm Advantages: Patient ventilator synchrony Lower sedation requirements Improved hemodynamics V/Q matching Non-invasive face mask- reduction of infectious complications, can safely be used Atonelli et al NEJM 1998

PARTIAL LIQUID VENTILATION:

PARTIAL LIQUID VENTILATION Filling the lung close to FRC with PFC Perfluorocarbons: ↑ O2 carrying capacity ↓ surface tension Improved alveolar recruitment Intrinsic anti-inflammatory properties Direct attenuation of lung injury and VILI

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Success in animal models and neonatal RDS leech et al NEJM 1996 High density – settle in dependent regions – overdistension. So PFC vapour or aerosol – more homogenous distribution. Kandler et al AJCC 2001 Not proved

PRONE POSITION VENTILATION:

PRONE POSITION VENTILATION

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Improve oxygenation and ventilation Douglas et al 1997 Mechanisms Improved ventilation of dorsal regions. Reduction of dependent lung compression by weight of heart or mediastinum Regional changes in chest wall mechanics Disadvantages: safety concern ET tube obstruction Accidental extubation ↑ pressure sores

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NEJM 2006

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No survival benefit Guerin et al JAMA 2004 Length of time prone 7 + 4.8 hours/day Ventilator strategy V T 10.3 + 2.8 ml/kg PEEP 9.6 + 30 cmH 2 O Rate 17.2 + 5.1/min Gattinoni NEJM 2001:345;568

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Critical care medicine 2004; 32;1

FLUID MANAGEMENT:

FLUID MANAGEMENT Topic of controversy Prevent pulmonary edema vs adequate perfusion Conservative fluid management reduces duration of mech ventilation or ICU stay FACTT study NEMJ 2006 Maintain adequate fluid balance BP maintained by vasopressors than IV fluids Duiretics can be used to reduce fluid load Colloid vs crystalloid? Controversy Am society of Cr care an Use of pulmonary artery catheter is not indicated in routine management FACTT study

DRUGS :

DRUGS Pulmonary vasodliators : iNO Useful in neonatal RDS In ARDS benefit transient, no survival benefit Some benefit seen in patient receiving 5ppm iNO Dillinger et al CCJM 1998 Corticosteroids: Potential to reduce inflammation No benefit in acute Bernard NEJM 87, Luce 88 or late ARDS NIH2006 Significant reduction in mortality in early ARDS tang et al 2007 meta analysis

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Surfactant replacement Large proteins: lamellar structure, tubular myelin – surfactant property Small proteins: limited surface activity ↑ small proteins in ARDS Useful in neonatal RDS No survival benefit Reasons: ? inactivated by plasma proteins Insufficient quantity delivered Distributed preferentially only to well ventilated lung

PROSPECTIVE FUTURE THERAPY:

PROSPECTIVE FUTURE THERAPY Beta agonists: Improve alveolar fluid clearance McCauley et al CCJM 2004 Reduced no of ICU days but no reduction in mortality Anticoagulation/fibrinolysis: Fibrin in alveoli binds with and inhibit surfactant Beneficial effect of activated protein C Bernard et al NEJM 2004 Micro vascular occlusion and thrombosis – wasted ventilation

PROGNOSIS :

PROGNOSIS Mortality rate 35-50% Milberg et al JAMA 1995 Risk factors for ↑ mortality ALI secondary to sepsis Male sex African-American race Advanced age Alcoholism Malignancy Liver disease Chronic steroid use HIV infection Diabetics have reduced risk

OUTCOME :

OUTCOME Survivors suffer from prolonged disturbance in lung function Impairment in neorucognitive skills Protracted perception of poor quality of life Majority recover in lung function by 1 year. Few also suffer from depression, anxiety, decreased quality of life, Post traumatic stress disorder.

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Intervention Year Study No. of Pt Findings Reference High levels of PEEP 1975 Observational 28 High incidence of pneumothorax Kirby et al. [307] Extra corporeal membrane oxygenation 1979 Phase 3 multicenter 90 No benefit Zapol et al. [308] High-frequency ventilation 1983 Phase 3 multicenter 309 No benefit Carlon et al. [309] Preventive PEEP (8 cm H 2 O) 1984 Phase3 single center 92 No benefit in patients at risk of ALI/ARDS Pepe et al. [310] Glucocorticoids (during acute phase) 1987 Phase 3 87 No benefit Bernard et al. [284] Results of RCT of Treatments and Ventilation Strategies for ALI and ARDS

PowerPoint Presentation:

Glucocorticoids (during acute phase) 1988 Phase 3 59 No benefit Luce et al. [283] Alprostadil Intravenous 1989 Phase 3 100 No benefit Bone et al. [311] Liposomal 1999 Phase 3 350 Stopped for lack of efficacy Abraham et al. [312] Surfactant (aerosolized) 1996 Phase 3 725 No benefit Anzueto et al. [268] Open-lung approach (recruitment maneuver and ideal PEEP) 1998 Phase 3 single center 53 Decreased 28-day but not in-hospital mortality (compared to conventional ventilation) Amato et al. [2] Low tidal volume ventilation (7 vs. 11 ml/kg) 1998 Phase 3 120 No benefit in patients at risk for ALI/ARDS Stewart et al. [147]

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Low tidal volume ventilation (7 vs. 10 ml/kg) 1998 Phase 3 116 No benefit Brochard et al. [145] Glucocorticoids during late fibrosing alveolitis phase 1998 Phase 3 24 Decreased mortality, but study small Meduri et al. [288] Inhaled nitric oxide 1998 Phase 2 177 No benefit Dillinger et al. [253] Inhaled nitric oxide 1999 Phase 3 203 No benefit Payen et al. [314] Ketoconazole 2000 Phase 2 234 No benefit NIH ARDS Network Low tidal volumes (6 vs. 12 ml/kg) 2000 Phase 3, multicenter 861 Decreased mortality from 40% to 30% (compared to traditional tidal volumes) NIH ARDS Network Prone-positioning during mechanical ventilation 2001 Phase 3, multicenter 304 Improved oxygenation but no benefit in mortality Gattinoni et al. Partial-liquid ventilation 2002 Phase 3, multicenter 90 Lower progression to ARDS, but no benefit in mortality Hirschl et al.

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Recombinant surfactant protein C-based surfactant 2004 Phase 3, multicenter 448 Improved oxygenation at 24 hours but no benefit in mortality Spragg et al. Prone-positioning for hypoxemic acute respiratory failure 2004 Phase 3, multicenter 791 No benefit in 28- or 90-day mortality and some safety concerns Guerin et al. Higher vs. lower PEEP during low tidal volume ventilation 2004 Phase 3, multicenter 549 No benefit in mortality or days with ventilator support Brower et al. Low- and high-dose partial liquid ventilation 2006 Phase 3, multicenter 311 No benefit in mortality and some safety concerns Kacmerek et al. Glucocorticoids for late/persistent ARDS 2006 Phase 3, multicenter 180 No benefit in mortality; ↑ mortality when started more than 2 weeks after onset NIH ARDS Network Glucocorticoids for ARDS, a meta analysis 2008 Lower mortality rates with use of corticosteroids Tang et al

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