ACUTE RESPIRATORY DISTRESS SYNDROME

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ACUTE RESPIRATORY DISTRESS SYNDROME:

ACUTE RESPIRATORY DISTRESS SYNDROME R.SIVA PRASAD

Acute Respiratory Failure:

Acute Respiratory Failure Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. Furthermore, respiratory failure may be acute or chronic. While acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent. Failure in one or both gas exchange functions: oxygenation and carbon dioxide elimination. In practice: PaO2<60mmHg or PaCO2>46mmHg. Derangements in ABGs and acid-base status.

Acute Respiratory Failure:

Acute Respiratory Failure Hypercapnic v Hypoxemic respiratory failure ARDS and ALI

ARDS Definition:

ARDS Definition Severe, acute lung injury involving diffuse alveolar damage, increased microvascular permeability and non cardiogenic pulmonary edema. Acute refractory hypoxemia. Annual incidence 75/100,000 in the US. High mortality- 40%-60%. First described in 1967.

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The AECC (American European conference) later defined two subsets in their consensus conference “a direct ("primary" or "pulmonary") insult, that directly affects lung parenchyma, and an indirect ("secondary" or "extra-pulmonary") insult, that results from an acute systemic inflammatory response”

ARDS Criteria:

ARDS Criteria Acute onset of respiratory failure. Bilateral infiltrate on CXR(some cases do present unilaterally or with pleural effusion. PCWP <18 or absence of left atrial htn, PaO2/FiO2 < 200 .

ARDS:

ARDS Develops ~4-48h Persists days-wks Diagnosis: Distinguish from cardiogenic edema History and risk factors

ARDS:

ARDS pulmonary oedema normal vascular pedicle no cardiomegaly or upper lobe blood diversion when pulmonary vessels can be distinguished they are often constricted septal lines usually absent because capillary leak occurs directly into alveolar spaces (cf cardiogenic pulmonary oedema) progressive lung destruction and transition from alveolar to interstitial opacities Chronic phase

Acute Respiratory Distress Syndrome :

Acute Respiratory Distress Syndrome Severe ALI B/L radiographic infiltrates PaO2/FiO2 <200mmHg (ALI 201-300mmHg) No e/o L Atrial P; PCWP<18

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pulmonary oedema normal vascular pedicle no cardiomegaly or upper lobe blood diversion

ARDS mechanism of lung injury :

ARDS mechanism of lung injury Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant

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Inflammatory Alveolar Injury

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Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells. Increased permeability of alveolar capillary membrane. Influx of protein rich edema fluid and inflammatory cells into air spaces. Dysfunction of surfactant.

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Inflammatory Alveolar Injury Pro-inflmm cytokines (TNF, IL1,6,8)

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Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces

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Inflammatory Alveolar Injury Pro-inflmm cytokines (TNF, IL1,6,8) Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium

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Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactan t

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Inflammatory Alveolar Injury Fluid in interstitium and alveoli Pro-inflmm cytokines (TNF, IL1,6,8) Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium

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Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant

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Inflammatory Alveolar Injury Fluid in interstitium and alveoli Impaired gas exchange  Compliance  PAP Pro-inflmm cytokines (TNF, IL1,6,8) Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium

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Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces

ARDS causes:

ARDS causes Direct Lung Injury : a) PNA and aspiration of gastric contents or other causes of chemical pneumonitis b) pulmonary contusion, penetrating lung injury c) fat emboli d) near drowning e) inhalation injury f) reperfusion pulm edema after lung transplant

ARDS causes:

ARDS causes Indirect lung injury a) sepsis b) severe trauma w/ shock hypoperfusion c) drug over dose d) cardiopulmonary bypass e) acute pancreatitis f) transfusion of multp blood products

Stages of ARDS :

Stages of ARDS 1. Exudative (acute) phase - 0- 4 days 2. Proliferative phase - 4- 8 days 3. Fibrotic phase - >8 days 4. Recovery

Hypoxemic Respiratory Failure:

Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome Exudative phase Fibrotic phase Proliferative phase Diffuse alveolar damage

Permissive Hypercapnia :

Permissive Hypercapnia Low Vt (6ml/kg) to prevent over-distention increase respiratory rate to avoid very high level of hypercapnia PaCO 2 allowed to rise Usually well tolerated May be beneficial Potential Problems: tissue acidosis, autonomic dysregulation, CNS effect, and circulatory effects

ARDS Treatment:

ARDS Treatment Ventilator-induced lung injury: it was previously thought that oxygen toxicity was one of the most important factors in the progression of ARDS and resultant mortality. Recently, it was found that high volume(volutrauma) and high press(barotrauma) are equally if not more detrimental to these pts Treatment strategy is one of low volume and high frequency ventilation(ARDSNet protocol) Search for and treat the underlying cause Treat abdominal infx promptly w/ abx and surgery Ensure adequate nutrition and place on GI/DVT prophylaxis Prevent and treat nosocomial infx Consider short course of high dose steroids in pts w/ severe dz that is not resolving .

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ABJUNCTS IN TREATMENT OF ARDS Ventilatory Strategies other than Lung Protective Strategy. - Prone Ventilation - Liquid Ventilation - High Frequency Ventilation - Tracheal Gas Insufflation - Extracorporeal Gas Exchange Hemodynamic Management – Fluids, Vasopressors. Selective Pulmonary vasodilators. Surfactant replacement therapy. Anti-inflammatory Strategies. a) Corticosteroids. b) Cycloxygenase & lipoxygenase inhibitors. c) Lisofylline and pentoxifylline. Antioxidants – NAC : Procysteine Anticoagulants.

When all else fails..:

When all else fails.. Recruitment maneuvers Prone Inhaled nitric oxide High frequency oscillation

PRONE VENTILATION :

PRONE VENTILATION Effect on gas exchange Improves oxygenation – allows decrease Fio 2 ; PEEP - Variable - not predictable response rate – 50-70% Proposed mechanism – how it improves oxygenation 1) Increase in FRC 2) Improved ventilation of previously dependent regions. (a) Difference in diaphragmatic movement - supine : dorsal and ventral portion move symmetrically - prone : dorsal > ventral

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P PL at dorsal Higher Less TP pressure Lower More Result Atelactasis opening Decrease chest wall compliance in p.p Redistribution of tidal volume to atelactatic dorsal region. Weight of heart may affect ventilation. Improvement in Cardiac output Better clearance of secretions Improved lymphatic damage PP L -3.0 +2.8 P PL -1.0 +1.0 Supine prone

CONTRAINDICATION :

CONTRAINDICATION Unresponsive cerebral hypertension - Unstable bone fractures - Left heart failure - Hemodynamic instability - Active intra abdominal pathology TIMING ARDS > 24 hrs./ 2 nd day FREQUENCY Usually one time per day DURATION 2 to 20 hrs /day. OUTCOME Improvement in oxygenation No improvement in survival POSITIONING ACHIEVED BY Circ Olectric , bed (Late 1970s). Manual 2 step Light weight portable support frame ( Vollman prone positioner)

PARTIAL LIQUID VENTILATION :

PARTIAL LIQUID VENTILATION In ARDs there is increased surface tension which can be eliminated by filling the lungs with liquid (PFC). Perflurocarbon : Colourless , clear, odourless , inert, high vapour pressure Insoluble in water or lipids MC used – perflubron ( Perfluoro octy bromide ) ( Liquivent ) Bromide  radiopaque ANIMAL EXPERIENCE Improved - Compliance - Gas exchange (dose dependent) - lung function - Survival Anti- inflam . properties Decrease risk of nosocomial pneumonia. Reduces pulm . vascular resistance. Little effect on central hemodynamics.

Mechanism of action :

Mechanism of action Reduces surface tension Alveolar recruitment – liquid PEEP. Selective distribution to dependent regions. Increases surfactant phospholipid synthesis and secretion. Anti Inflam . Properties A. Indirect Mitigation of VILI B. Direct a) decrease endotoxin stimulated release of TNF; IL-1; IL-8. b) decrease production of reactive oxygen species. c) Inhibit neutrophil activation and chemostaxis . d) Lavage of cellular debris.

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Technique of PFC Ventilation : Total liquid ventilation Partial liquid ventilation TLV PLV 1. Ventilator Liquid Conventional 2. Tidal volume delivered of Oxygenated PFC Gas 3. Lungs are filled Completely by PFC Filled till FRC by PFC 4. Feasibility Expt. Yes 5. Disadvantage Loss of gas by evap., cost.

TRACHEAL GAS INSUFFLATION (TGI):

TRACHEAL GAS INSUFFLATION (TGI) In ARDS/ALI Increase physiological dead space OLS / permissive hypercapnia DURING CONVENTIONAL VENTILATION : Bronchi and trachea are filled with alveolar gas at end exhalation which is forced back into the alveoli during next inspiration. IN TGI Stream of fresh air (4 to 8 L/min) insufflated thr. – small cath. or through small channel in wall of ET into lower trachea flushing Co2 laden gas.

HIGH FREQUENCY VENTILATION:

HIGH FREQUENCY VENTILATION Utilizes small volume (<V D ) and high RR (100 b/min) Avoids over distention ( Vili ). Alveolar recruitment. Enhances gas mixing, improves V/Q. APPLIC. Neonatal RDS. ARDS. BPF. COMPLIC. Necrotizing trachebronchitis . Shear at interface of lung. Air trapping.

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Expiration Passive Active Passive Potentiation of intrinsic PEEP 3+ 2+ 1+ VT x f product for effective V A >> Conv >> Conv P PK < Conv < Conv P mean <or> conv <or> conv JET Oscillator Conventional Freq avail upto 600 b/min 300-3000 b/min 2-60 b/min Tidal volume delivered <or> V D < V D >> V D Comparison of HFV Vs Conv. Ventil.

EXTRACORPOREAL MEMBRANE OXYGENATION :

EXTRACORPOREAL MEMBRANE OXYGENATION Adaptation of conventional cardiopulmonary bypass technique. Oxygenate blood and remove CO 2 extracorporally . TYPES High-flow venoarterial bypass system. Low-flow venovenous bypass system. Criteria for treatment with extracorporeal gas exchange Fast entry criteria PaO 2 <50 mmHg for >2 h at FiO 2 1.0; PEEP > 5 cmH 2 O Slow entry criteria PaO 2 <50 mmHg for >12 h at FiO 2 0.6; PEEP > 5 cmH 2 O maximal medical therapy >48 h Q s / Q t > 30%; CTstat <30 ml/cmH 2 O

Complication:

Complication Mechanical Patient related Problem Oxygenator failure Bleeding Circuit disruption Neurological complications Pump or heat exchanger Additional organ failure mal functioning. Cannula placement/removal Barotrauma, infection, metabolic

HEMODYNAMIC MANAGEMENT :

HEMODYNAMIC MANAGEMENT Controversial Restriction of Fluid Benefit Obs. Studies Show  pulm . edema formation  compliance, lungs fn. Improved survival Negative fluid balance is associated with improved survival Humphrey et al., 1990 Chest 97 ; 1176-80. Net positive balance <1 lt. in first 36 hrs. a/w improved survival decrease length of ventilation, ICU stay and hospitalization.

Goal :

Goal Correct Volume deficit Guidelines for management of tissue hypoxia International consensus conference (AJRCCM- 1996) Promote oxygen delivery Adequate volume CVP – 8-12 mmHg PAOP-14-16 mmHg (Optimal co; less risk of Edema) Crystalloids vs Colloids Transfuse < 10 gm /dl Reduce oxygen demand : a) Sedation : Analgesia, NMBA b) Treat Hyperpyrexia c) Early institution of mech. vent. (shock). No role of supraphysiol . oxygen delivery

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Vasopressors Following fluid resuscitation Norepinephrine vs Dopamine GOAL to achieve MAP 55 to 65 mmHg Inotropes Co. is low

PULMONARY VASCULAR CHANGES IN ARDS/ALI:

PULMONARY VASCULAR CHANGES IN ARDS/ALI Reduced pulmonary vasoconstriction in hypoxic shunt areas, along with vasoconstriction in well ventilated areas. PAH ( Pulm . Vasoconst . ; Thromboembolism; Interstitial edema) - PAH aggravates edema by increasing inflow pressure. - So role of pulm . vasodilators .

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Selective Pulmonary Vasodilators : Inhaled Nitric oxide ( iNo ) iv almitrine with/without iNo . Aerosolized prostacyclins . Inhibition of cyclic nucleotide phosphodiesterase . Inhalation of Endothelin receptor antagonists.

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1. Inhaled Nitric Oxide How it is beneficial in ARDs Improves Oxygenation - Selective vasodilatation of vessel a/w better ventilation  (decrease shunt) - Improves v/q mismatch. Reduction in pulmonary artery pressure - Improves oxygen - direct smooth muscle relaxation - improved RV Fn. - reduced capillary leak. Inhibit platelet aggregation and neutrophil adhesion. Selectivity of iNO Rapid inactivation on contact with hemoglobin. 60 % of pat respond to iNo by increase in PO2 >20%.

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DOSAGE Effect Dose Increase PaO 2 1-2 ppm to <10 ppm decrease PAP 10-40 ppm Time of Response <10 min to several hours. Response to iNo is not static phenomenon. Intra-individual variation in response : - lung recruitment - Coexistent pathology - resolution of inflammation Mortality Benefits – None

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Almitrine iv : low dose Potentates hypoxic vasoconstriction Decrease shunt, improved oxygenation Has additive effect with iNo iNo + prone position

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Aerosolized Prostacyclin iv prostacyclin decrease pulm. a. pressure (non selective vasodilatation) can increase shunt; worsen oxygenation. Inhaled prostacyclin selectively vasodilates the well perfused areas Selectivity in dose of 17-50 ng/kg/min. PGI 2 - Not metabolized in lung so selectively lost at higher doses. PGE 1 - 70-80% is metabolized in lung. Inhibition of cyclic nucleotide phosphodiesterases No  increase CGMP  Protein G-Kinase Calcium gated potassium Channels  Vasodilatation PDE prevent degradation of CGMP (PDE-5) PDE –5 Inhibitors Dipyridamole ; Sildenafil

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SURFACTANT REPLACEMENT THERAPY In ARDs there is deficiency and fn abn. of surfactant Decrease production (injury to type-2 pneumocytes) Abn. composition (decrease phosphatidyl choline, phosphotidylglycerol, Sp.A & Sp. B) Inhibitors of surfactant fn (TNF- a, reactive oxygen sp. Peroxynitrite, neutrophil elastases) Conversion of large to small surfactant aggregates Alteration/Destruction caused by substances in alveolar space (plasma, fibrinogen, fibrin, alb; Hb) Impaired surfactant fn  1) Atelactasis / collapse 2) Increase edema formation In experimental ALI models surfactant replacement. Improved lungs fn., compliance, oxygenation.

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Surfactant of possible therapeutic use : Class Origin Example Natural Amniotic Human amniotic fluid surfactant Modified - Bovine Infasurf, alveofact Natural BLESS, Survanta - Procine Curosurf Synthetic Exosurf, ALEC, KL 4 Surfactant, Venticute DOSE Sufficient dose should reach alveolar environment TIMING As early as possible [<48 hr] Little benefit at 3 to 5 days [Fibrosis already set]

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Surfactant Delivery Techniques Instillation Lavage Aerosolization Rapid Can deliver large volume Homogenous distribution Efficacious in clinical trials May remove toxic subst. Can deliver large vol. Homogenous distrib. Lab studies suggest efficacy Continuous smaller vol. Non uniform distribution. Lab. Studies show efficacy Techn. Not standardized Short term impairment in ventilation Vol. recover can be poor Short term impairment in ventil. Slow, no optimal device, Filters may plug.

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HOW STEROIDS ARE BENEFICIAL : Inhibit transcriptional activation of various cytokines. Inhibit synthesis of phospholipase A 2 : cycloxygenase . Reduced prod. of prostanoids , PAF, No.  fibrinogenesis LISOPHYLLINE AND PENTOXIFYLINE PDE-I Inhibit neutrophil chemostaxis and activation. Lisophylline inhibit release of FF from cell memb . under oxidative stress TNF : IL-1 ; IL-6 NIH ARDS trial no benefit.

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CYCLOOXYGENASE INHIBITORS TxA 2 and Prostaglandin produced from AA by Cyclooxygenase pathway. Cause Neutrophil chemostaxis and adhesion Broncho constriction  vascular permeability platelet aggregation Animal studies shown that C.I Attenuate lung injury Improve pulm . hypertension and hypoxia

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KETOCONAZOLE TxA 2 Pulmonary vasoconstriction Platelet and neutrophil aggregation Blockade of Tx synthesis or receptor antagonism ameliorates experimental lung injury Ketoconazole Specific inhibitor of thromboxane synthetase Inhibits 5 – Lipoxygenase [LTB 4 & procoag activity]

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ANTIOXIDANTS Reactive oxygen metabolites derived from neutrophils, macrophages and endothelial cells OXIDANTS INCLUDE Super oxide ion (02-), hydrogen peroxide (H2O2) hypochlorous acid ( Hocl ), hydroxyl radical (OH..) Interact with proteins, lipid and DNA ENDOGENOUS ANTIOXIDANTS Superoxide dismutase, Glutathione, Catalase Vit E & Vit C Sulfhydryls

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ANTICOAGULANT THERAPY IN ALI/ARDS In ARDS – Fibrin deposition intra-alveolar and interstitial. Local procoagulant activity and reduced fibrinolysis.  Procoagulant  Fibrinolysis  TF (VII a ) Fibrinolytic inhibitors  PAI–1 ; PAI-2, 2 antiplasmin  urokinase and tPA  Fibrin Inhibit surfactant  atelactasis + Fibrinonectin  Matrix on which fibroblast aggregate + N Fibroblast proliferation Potent chemotactic (Neutrophil recruitment) Lung vasculature  PAH

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PROTEIN- C Inactivates Va & VIIa – limit thrombin generation. Inhibit PAI-1 activity -  fibrinolysis. Anti- inflam . -  cytokines, inhibit apoptosis. In the PROWESS study APC administ . Improved survival. 28 days absolute risk reduction in mortality – 6.1%. 19.4% reduction in relative risk. Risk of bleeding (3.5% vs 2.0%) Faster resolution of respiratory dysfun . ventilatory free days (14.3 vs 13.2 days) Bernad GR ; NEJM 2001; 344; 699-709

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ENHANCED RESOLUTION OF ALVEOLAR EDEMA Alveolar clearance of edema depends on active sodium transport across the alveolar epithelium b 2 adrenergic stimulation : Salmetrol Dopamine Dobutamine ENHANCED REPAIR : Mitogen for type-II pneumatocyte : Hepatocyte growth factor Keratinocyte growth facto r.

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