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ARDS Old Problem Current strategies november 4, 2013

ARDS Old Problem Current strategies november 4, 2013. David W. Chang, EdD , RRT University of South Alabama. Outline. 1. Definition 2. History 3. Pathophysiology 4. Mechanical Stress 5. Clinical presentations 6. Management Strategies 7. Complications. Outline. 1. Definition

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ARDS Old Problem Current strategies november 4, 2013

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  1. ARDSOld ProblemCurrent strategiesnovember 4, 2013 David W. Chang, EdD, RRT University of South Alabama

  2. Outline 1. Definition 2. History 3. Pathophysiology 4. Mechanical Stress 5. Clinical presentations 6. Management Strategies 7. Complications

  3. Outline 1. Definition 2. History 3. Pathophysiology 4. Mechanical Stress 5. Clinical presentations 6. Management Strategies 7. Complications

  4. Definition of ALI and ARDS (1994 AECC) • Acute onset • Hypoxemia (PaO2/FIO2 = 200 or 300 mm Hg) • Bilateral infiltrates • PCWP <18 mm Hg

  5. Outline 1. Definitions of ALI and ARDS

  6. Definition of ARDS (2011 Berlin) • P/F index • mild ARDS: 201 - 300 mmHg (≤ 39.9 kPa) • moderate ARDS: 101 - 200 mmHg (≤ 26.6 kPa) • severe ARDS: ≤ 100 mmHg (≤ 13.3 kPa) • Radiographic severity • Respiratory compliance ≤ 40 mL/cm H2O • PEEP ≥ 10 cm H2O • Corrected minute ventilation ≥ 10 L/min

  7. Outline 1. Definition 2. History 3. Pathophysiology 4. Mechanical Stress 5. Clinical presentations 6. Management Strategies 7. Complications

  8. History • 1950’s – Pulmonary edema (respirator lung, DaNang lung, shock lung, post-traumatic lung, wet lung) • 1959 – Neonatal RDS (Avery and Mead) • 1967 – ARDS (Ashbaugh et al)

  9. History • Late 1960s – intensive care units became common in the U.S. • 1930s to 1950s – Drinker respirator (negative pressure ventilation, iron lung, chest cuirass) • 1950s to present – manual ventilation, positive pressure breathing, mechanical ventilator, microprocessor controlled ventilator Mortality ranges from 90% (untreated) to 25% (treated aggressively)

  10. Outline 1. Definition 2. History 3. Pathophysiology 4. Mechanical Stress 5. Clinical presentations 6. Management Strategies 7. Complications

  11. Pathophysiology • Direct injury (e.g., pneumonia, aspiration, inhalation of toxins, near drowning, pulmonary contusion, fat embolism) • Indirect injury (e.g., sepsis, severe trauma, acute pancreatitis, cardiopulmonary bypass, transfusion of blood products, drug overdose)

  12. Pathophysiology Direct injury may lead to (A) activation of alveolar macrophages (B) development of inflammatory response within the lungs (C) alveolar epithelial damage (D) alveolar walls are thickened due to acute distention of capillaries and interstitial edema

  13. Pathophysiology Direct injury may lead to (E) pathological abnormality in the intra-alveolar space (F) alveolar filling by edema, fibrin, collagen, neutrophilicaggregates or blood (G) V/Q mismatch and intrapulmonary shunting

  14. Pathophysiology Indirect injurymay lead to (A) Inflammatory mediators released from the extrapulmonary foci into the systemic circulation (B) target of damage is the pulmonary vascular endothelial cell (C) Endothelial dysfunction causes fluid extravasation from the capillaries and impaired drainage of fluid from the lungs

  15. Pathophysiology Indirect injurymay lead to (D) Dysfunction of type II pulmonary epithelial cells leads to reduction of surfactant (E) Increase of vascular permeability (transudate – a pale esinophilic finely granular, replaces the air) *Exudate is caused by inflammation Transudateis caused by disturbance of hydrostatic pressure and colloid osmotic pressure

  16. Pathophysiology Indirect injurymay lead to (F) Recruitment of monocytes, polymorphonuclear leukocytes, platelets, and other abnormal cells (G) Primary pathological alteration is microvascular congestion and interstitial edema (H) V/Q mismatch and intrapulmonary shunting

  17. Outline 1. Definition 2. History 3. Pathophysiology 4. Mechanical Stress 5. Clinical presentations 6. Management Strategies 7. Complications

  18. Mechanical Stress • In ARDS, lung structure and function are not homogenous (i.e., healthy and sick lung units are mingled) • Collapsed lung units require higher positive pressure • Normal lung units become overdistendedat high pressures (video) • Barotrauma or volutraumais more likely to occur in normal lung units

  19. Outline 1. Definition 2. History 3. Pathophysiology 4. Mechanical Stress 5. Clinical presentations 6. Management Strategies 7. Complications

  20. Clinical presentations (ventilation & oxygenation) • Tachypnea • Rapid shallow breathing (↑f/VT) ↑VD/VT ↓VA (VA = VT– VD) ↑V/Q mismatch • ↑Intrapulmonary Shunting • ↓PaO2/FIO2 (P/F) index • ↑PaCO2 due to fatigue of respiratory muscles • Impending ventilatoryfailure • Acute ventilatoryfailure

  21. Clinical presentations (radiographic) • Bilateral infiltrates • No signs of large pleural effusion (normal costophrenicangles) • No signs of atrial enlargement • No signs of heart failure (e.g., PCWP >18 mm Hg) or volume overload (high systemic blood pressure, peripheral edema)

  22. Outline 1. Definition 2. History 3. Pathophysiology 4. Mechanical Stress 5. Clinical presentations 6. Management Strategies 7. Complications

  23. Management Strategies (ineffective, controversial, transient positive effects or not validated in large studies) • Drugs • Inhaled synthetic surfactant, IV antibody to endotoxin, ketoconazole (anti-fungal), ibuprofen (NSAID), simvastatin (cholesterol reduction), and inhaled nitric oxide (pulmonary vasodilator) • Nutritional support and supplement • Devices • ECMO, HFOV

  24. Management Strategies (reasonable and potentially useful) • Fluid management • Infection control (early intervention) • Prevention of VAP • Noninvasive ventilation (early intervention) • Nutritional support (enteral feeding tube) • Frequent position changes and range of motion

  25. Management Strategies (current practice) • Mechanical ventilation with PEEP • Decramental recruitment maneuver for optimal PEEP • Low VT and permissive hypercapnia • Airway pressure release ventilaiton • Inverse ratio ventilation • Prone positioning

  26. Management Strategies • Mechanical ventilation(volume-controlled or pressure-controlled) to reduce work of breathing • Keep airway pressures below thresholds PIP < 50 cm H2O Plateau pressure < 35 cm H2O (ARDSNet recommends < 30 cm H2O) Mean airway pressure < 30 cm H2O PEEP < 10 cm H2O

  27. Management Strategies Oxygen and PEEP to provide oxygenation • Note effects of PEEP and other factors on airway pressures (Figure) • mPaw= (f x I time / 60) x (PIP – PEEP) + PEEP • mPawmay be used to monitor hemodynamic effects • plateau pressure may be used to monitor overdistention Recommended FIO2/PEEP combinations (Table) Recruitment maneuver to determine optimal PEEP (Video)

  28. Management Strategies Low VT and Permissive Hypercapniato minimize lung injury (Table) • 6 mL/Kg • as low as 4 mL/Kg to keep PPLAT < 30 cm H2O • permit PaCO2 to rise • acidosis is managed by bicarbonate or tromethamine

  29. Management Strategies Airway Pressure Release Ventilation (APRV) (Figure) ↓decreased airway pressure requirement ↓ minute ventilation ↓ dead-space ventilation promote spontaneous breathing ↓ use of sedation & neuromuscular blockade optimized ABG results ↑ FRC ↑ cardiac output

  30. Management Strategies Inverse ratio ventilation (IRV) Pressure-Controlled + IRV (pressure titrated to low VT 4 to 7 mL/kg) Long inspiratory time (inspiratory flow titrated to desired inverse ratio)

  31. Management Strategies Inverse ratio ventilation (IRV) • Facilitate gas exchange (esp. O2) • Reduce FIO2 and PEEP requirement • Require sedation and neuromuscular blockade • Monitor for improvement & hemodynamic effects

  32. Management Strategies Prone positioning • Lung zones • Lung volume distribution * Improvement in oxygenation is temporary

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