ARDS

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ARDS

• Ian B. Hoffman, MD, FCCP
• Pulmonary Critical Care Medicine

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Respiratory Failure

• Any disruption of function of respiratory system
  CNS, nerves, muscles, pleura, lungs
• Any process resulting in low pO2 or high pCO2
  arbitrarily 50/50
• Acute respiratory failure can be exacerbation of
  chronic disease or acute process in previously
  healthy lungs

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History

• 1940s polio, barbiturate OD
• 1960s blood gas analysis readily available,
  aware of hypoxemia
• 1970s decreased hypoxic mortality, increased
  multiorgan failure (living longer)
• 1973 relationship between resp muscle fatigue
  and resp failure

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Types of Respiratory Failure

• Type 1 (nonventilatory) hypoxemia with or
  without hypercapnia disease involves lung
  itself (i.e, ARDS)
• Type 2 failure of alveolar ventilation
  decrease in minute ventilation or increase in
  dead space (i.e. COPD, drug OD)

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Goals of Treatment

• Correct hypoxemia or hypercapnia without causing
  additional complications
• Nonivasive ventilation vs. intubation and
  mechanical ventilation
• Goal of mechanical ventilation is NOT necessarily
  to normalize ABGs

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Ventilatory Failure

• Failure of respiratory pump to adequately
  eliminate CO2
• pCO2 CO2 production
  alveolar ventilation

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V/Q Relationships and Hypercapnia

• Healthy humans have V/Q matching
• High V/Q areas well ventilated but poorly
  perfused wasted ventilation increased dead
  space
• Low V/Q areas can cause hypercapnia if large
  amount of venous blood flows through

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To intubate or not

• Decision to mechanically ventilate is clinical
• Some criteria
• Decreased level of consciousness
• Vital capacity lt15 ml/kg
• Severe hypoxemia
• Hypercarbia
• Vd/Vt gt0.60
• NIF lt -25 cm H20

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ARDS Acute Respiratory Distress
Syndrome
(formerly Adult Respiratory Distress Syndrome)
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ARDS - Definition

• Severe end of the spectrum of acute lung injury
• Acute and persistent lung inflammation with
  increased vascular permeability
• Diffuse infiltrates
• Hypoxemia paO2/FiO2 lt200
• (i.e. pO2 70 / FiO2 0.5 140)
• No clinical evidence of elevated left atrial
  pressure (PCWP lt18 if measured)

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ARDS History/Definitions

• 1967 Ashbaugh described 12 pts with acute
  respiratory distress, refractory cyanosis,
  decreased lung compliance, diffuse infiltrates
• 1988 4 point lung injury score (level of PEEP,
  pO2/FiO2, lung compliance, degree of infiltrates)
• 1994 acute onset, bilat infiltrates, no direct
  or clinical evidence of LV failure, pO2/FiO2)

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ARDS - Incidence

• Annual incidence 75 per 100,000
• 9 of American critical care beds occupied by
  patients with ARDS

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ARDS - Diagnosis

• Clinically and radiographically resembles
  cardiogenic pulmonary edema
• PCWP can be misleading high or low
• 20 of pts with ARDS may have LV dysfunction

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ARDS - Causes

• Direct injury to the lung
• Indirect injury to the lung in setting of a
  systemic process
• Multiple predisposing disorders substantially
  increase risk
• Increased risk with alcohol abuse, chronic lung
  disease, acidemia

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ARDS - Causes

• Direct Lung Injury
• Pneumonia
• Gastric aspiration
• Lung contusion
• Fat emboli
• Near drowning
• Inhalation injury
• Reperfusion injury

• Indirect Lung Injury
• Sepsis
• Multiple trauma
• Cardiopulmonary bypass
• Drug overdose
• Acute pancreatitis
• Blood transfusion

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ARDS - Physiologic Derangements

• Inflammatory injury to alveoli producing diffuse
  alveolar damage
• Proinflammatory cytokines (TNF, IL-1, IL-8)
• Neutrophils recruited release toxic mediators
• Normal barriers to alveolar edema are lost,
  protein and fluid flow into air spaces,
  surfactant lost, alveoli collapse
• Impaired gas exchange
• Impaired compliance
• Pulmonary hypertension

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ARDS Features

• Severe initial hypoxemia
• Prolonged need for mechanical ventilation
• Initial exudative stage
• Proliferative stage
• resolution of edema, proliferation of type II
  pneumocytes, squamous metaplasia, collagen
  deposition
• Fibrotic stage

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ARDS Course

• Early
• Inciting event, pulmonary dysfunction (worsening
  tachypnea, dyspnea, hypoxemia)
• Nonspecific labs
• CXR diffuse alveolar infiltrates
• Subsequent
• Improvement in oxygenation
• Continued ventilator dependence
• Complications
• Large dead space, high minute ventilation
  requirement
• Organization and fibrosis in proliferative phase

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ARDS - Complications

• Ventilator induced lung injury
• Sedation and neuromuscular blockade
• Nosocomial infection
• Pulmonary emboli
• Multiple organ dysfunction

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ARDS - Prognosis

• Improved survival in recent years mortality was
  50-60 for many years, now 25-40
• Improvements in supportive care, newer
  ventilatory strategies
• Early deaths (3 days) usually from underlying
  cause of ARDS
• Later deaths from nosocomial infections, sepsis,
  MOSF
• Severity of gas exchange at admission does not
  correlate with mortality
• Respiratory failure only responsible for 16 of
  fatalities
• Long-term survivors usually show mild
  abnormalities in pulmonary function (DLCO),
  impaired neurocognitive function

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Poor Prognostic Factors

• Failure to improve over 1st few days
• Initially increased dead space
• Advanced age
• Sepsis
• Multiple organ dysfunction (higher APACHE)
• Steroids given prior to onset of ARDS
• Blood transfusion
• Not managed by Intensivist

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Ventilatory Goals in ARDS

• Provide adequate oxygenation without causing
  damage related to
• Oxygen toxicity
• Hemodynamic compromise
• Barotrauma
• Alveolar overdistension

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Mechanical Ventilation in ARDS

• Reliable oxygen supplementation
• Decrease work of breathing
• Increased due to high ventilatory requirements,
  increased dead space, and decreased compliance
• Recruit atelectatic lung units
• Decreased venous return can help decrease fluid
  movement into alveolar spaces

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Ventilatory Strategies

• Low tidal volume, plateau pressure lt30 (less
  alveolar overdistension)
• PEEP enough, not too much
• Pressure controlled vs. volume cycled
• Open lung strategy
• PC-IRV ventilation
• Vt lt 6ml/kg, PEEP 16, RR lt30, Peak pressure lt40

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Ventilatory Strategies

• Prolong inspiratory time (increase mean airway
  pressure and improve oxygenation)
• Permissive hypercapnia
• Secondary effect of low tidal volumes
• Maintain adequate oxygenation with less risk of
  barotrauma
• Sedation/paralysis usually necessary

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APRV

• Decreases peak airway pressure
• Improves alveolar recruitment
• Increases ventilation of dependent lung zones
• Improves oxygenation
• BUT no evidence yet of improved outcome

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PEEP in ARDS

• Increases FRC recruits recruitable alveoli
• Decreases shunt, improves V/Q matching
• No consensus on optimal level of PEEP

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ARDS Network Trial

• Initial tidal volume of 6 ml/kg IBW and plateau
  pressure lt30
  vs.
• Initial tidal volume of 12 ml/kg IBW and plateau
  pressure lt50
• Reduction in mortality of 22 (31 vs 40)

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Other modalities without definite benefit

• APRV
• High-frequency ventilation
• ECMO
• Beta agonists
• Nitric Oxide
• Surfactant
• Steroids (possible benefit if given early -or- in
  late fibroproliferative phase)
• ?benefit from tube feeds containing combination
  of eicosapentaenoic acid and gamma-linolenic acid
  (?antiinflammatory effects)

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Nitric Oxide

• Selectively dilates vessels that perfuse better
  ventilated lung zones, resulting in improved V/Q
  matching, improved oxygenation, reduction of
  pulmonary hypertension
• Less benefit in septic patients
• No clear improvement in mortality

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Ventilator Induced Lung Injury

• Known for decades that high levels of positive
  pressure ventilation can rupture alveolar units
• In 1950s became apparent that high FiO2 can
  produce lung injury

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Ventilator Induced Lung Injury

• Macrobarotrauma
• Pneumothorax, interstitial emphysema,
  pneumomediastinum, SQ emphysema,
  pneumoperitoneum, air embolism
• ? resulting from high airway pressures, or just a
  marker of severe lung injury
• Higher PEEP predicts barotrauma

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Ventilator Induced Lung lnjury

• Microbarotrauma
• Alveolar overinflation exacerbating and
  perpetuating lung injury edema, surfactant
  abnormalities, inflammation, hemorrhage
• Less affected lung accommodates most of tidal
  volume regional overinflation
• Cyclical atelectasis (shear) adds to injury
• Low tidal volume strategy (initial tidal volume
  6 ml/kg IBW, plateau pressure lt30) lower
  mortality

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Supportive Care

• Prophylaxis for DVT
• Prophylaxis for GI bleeding
• Measures to avoid nosocomial pneumonia
• Treat nosocomial pneumonia
• Nutritional support
• Sedation and paralysis
• Treating hypoxemia
• Diuresis
• Prone positioning
• Decrease oxygen consumption

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The End