David W. Chang, EdD, RRT University of South Alabama

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

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

Definition of ALI and ARDS (1994 AECC)  Acute onset  Hypoxemia (PaO 2 /F I O 2 = 200 or 300 mm Hg)  Bilateral infiltrates  PCWP <18 mm Hg

1. Definitions of ALI and ARDS

Definition of ARDS (2011 Berlin)  P/F index  mild ARDS: mmHg (≤ 39.9 kPa)  moderate ARDS: mmHg (≤ 26.6 kPa)  severe ARDS: ≤ 100 mmHg (≤ 13.3 kPa)  Radiographic severity  Respiratory compliance ≤ 40 mL/cm H 2 O  PEEP ≥ 10 cm H 2 O  Corrected minute ventilation ≥ 10 L/min

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

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)

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)

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

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)

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

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

Pathophysiology Indirect injury may 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

Pathophysiology Indirect injury may 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 Transudate is caused by disturbance of hydrostatic pressure and colloid osmotic pressure

Pathophysiology Indirect injury may 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

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

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 overdistended at high pressures (video)  Barotrauma or volutrauma is more likely to occur in normal lung units

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

Clinical presentations (ventilation & oxygenation)  Tachypnea  Rapid shallow breathing (↑f/V T ) ↑V D /V T ↓V A (V A = V T – V D ) ↑V/Q mismatch  ↑Intrapulmonary Shunting  ↓PaO 2 /F I O 2 (P/F) index  ↑PaCO 2 due to fatigue of respiratory muscles  Impending ventilatory failure  Acute ventilatory failure

Clinical presentations (radiographic)  Bilateral infiltrates  No signs of large pleural effusion (normal costophrenic angles)  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)

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

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

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

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

Management Strategies  Mechanical ventilation (volume-controlled or pressure-controlled) to reduce work of breathing  Keep airway pressures below thresholds PIP < 50 cm H 2 O Plateau pressure < 35 cm H 2 O (ARDSNet recommends < 30 cm H2O) Mean airway pressure < 30 cm H 2 O PEEP < 10 cm H 2 O

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  mPaw may be used to monitor hemodynamic effects  plateau pressure may be used to monitor overdistention Recommended F I O 2 /PEEP combinations (Table) Recruitment maneuver to determine optimal PEEP (Video)

Management Strategies Low V T and Permissive Hypercapnia to minimize lung injury (Table)  6 mL/Kg  as low as 4 mL/Kg to keep P PLAT < 30 cm H 2 O  permit PaCO 2 to rise  acidosis is managed by bicarbonate or tromethamine

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

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

Management Strategies Inverse ratio ventilation (IRV)  Facilitate gas exchange (esp. O 2 )  Reduce F I O 2 and PEEP requirement  Require sedation and neuromuscular blockade  Monitor for improvement & hemodynamic effects

Management Strategies Prone positioning  Lung zones  Lung volume distribution * Improvement in oxygenation is temporary

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

Complications  Ventilator-associated pneumonia  Prevention and intervention  Hypoxic-ischemic encephalopathy  Brain (2% body weight, 15% energy consumption, cannot hold or store energy in the form of glycogen, cannot utilize fatty acids, depends on a constant supply of oxygen and glucose)  CPP = MAP – ICP (normal 70 to 80 mm Hg)

 Early intervention  Team approach  Tailor management strategies to patient’s need  Prevent complications