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Ian B. Hoffman, MD, FCCPPulmonary & Critical Care Medicine
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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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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
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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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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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Failure of respiratory pump to adequately eliminate CO2
pCO2 : CO2 production alveolar ventilation
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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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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
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(formerly Adult Respiratory Distress Syndrome)
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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)
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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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Annual incidence 75 per 100,000 9% of American critical care beds occupied by
patients with ARDS
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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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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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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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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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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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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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Ventilator induced lung injury Sedation and neuromuscular blockade Nosocomial infection Pulmonary emboli Multiple organ dysfunction
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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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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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Provide adequate oxygenation without causing damage related to: Oxygen toxicity Hemodynamic compromise Barotrauma Alveolar overdistension
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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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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
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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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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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Increases FRC – recruits “recruitable” alveoli Decreases shunt, improves V/Q matching No consensus on optimal level of PEEP
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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%)
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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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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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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
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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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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
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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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