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ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
ARDS from the Pulmonologists Perspective - Hoffman 2009
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ARDS from the Pulmonologists Perspective - Hoffman 2009

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  • 1. Ian B. Hoffman, MD, FCCP Pulmonary & Critical Care Medicine
  • 2.  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
  • 3.  1940’s – polio, barbiturate OD  1960’s – blood gas analysis readily available, aware of hypoxemia  1970’s – decreased hypoxic mortality, increased multiorgan failure (living longer)  1973 – relationship between resp muscle fatigue and resp failure
  • 4.  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)
  • 5.  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
  • 6.  Failure of respiratory pump to adequately eliminate CO2  pCO2 : CO2 production alveolar ventilation
  • 7.  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
  • 8.  Decision to mechanically ventilate is clinical  Some criteria  Decreased level of consciousness  Vital capacity <15 ml/kg  Severe hypoxemia  Hypercarbia  Vd/Vt >0.60  NIF < -25 cm H20
  • 9. (formerly Adult Respiratory Distress Syndrome)
  • 10.  Severe end of the spectrum of acute lung injury  Acute and persistent lung inflammation with increased vascular permeability  Diffuse infiltrates  Hypoxemia – paO2/FiO2 <200  (i.e. pO2 70 / FiO2 0.5 = 140)  No clinical evidence of elevated left atrial pressure (PCWP <18 if measured)
  • 11.  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)
  • 12.  Annual incidence 75 per 100,000  9% of American critical care beds occupied by patients with ARDS
  • 13.  Clinically and radiographically resembles cardiogenic pulmonary edema  PCWP can be misleading – high or low  20% of pts with ARDS may have LV dysfunction
  • 14.  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
  • 15.  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
  • 16.  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
  • 17.  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
  • 18.  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
  • 19.  Ventilator induced lung injury  Sedation and neuromuscular blockade  Nosocomial infection  Pulmonary emboli  Multiple organ dysfunction
  • 20.  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
  • 21.  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
  • 22.  Provide adequate oxygenation without causing damage related to:  Oxygen toxicity  Hemodynamic compromise  Barotrauma  Alveolar overdistension
  • 23.  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
  • 24.  Low tidal volume, plateau pressure <30 (less alveolar overdistension)  PEEP – enough, not too much  Pressure controlled vs. volume cycled  Open lung strategy  PC-IRV ventilation  Vt < 6ml/kg, PEEP 16, RR <30, Peak pressure <40
  • 25.  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
  • 26.  Decreases peak airway pressure  Improves alveolar recruitment  Increases ventilation of dependent lung zones  Improves oxygenation  BUT – no evidence yet of improved outcome
  • 27.  Increases FRC – recruits “recruitable” alveoli  Decreases shunt, improves V/Q matching  No consensus on optimal level of PEEP
  • 28.  Initial tidal volume of 6 ml/kg IBW and plateau pressure <30 vs.  Initial tidal volume of 12 ml/kg IBW and plateau pressure <50  Reduction in mortality of 22% (31% vs 40%)
  • 29.  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)
  • 30.  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
  • 31.  Known for decades that high levels of positive pressure ventilation can rupture alveolar units  In 1950’s became apparent that high FiO2 can produce lung injury
  • 32.  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
  • 33.  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 <30) – lower mortality
  • 34.  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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