ARDS for student

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

17.  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

18.  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

19.  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

21.  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

22.  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

24.  Ventilator induced lung injury
 Sedation and neuromuscular blockade
 Nosocomial infection
 Pulmonary emboli
 Multiple organ dysfunction

25.  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

26.  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

27.  Provide adequate oxygenation without causing
damage related to:
 Oxygen toxicity
 Hemodynamic compromise
 Barotrauma
 Alveolar overdistension

28.  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

29.  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

30.  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

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

33.  Increases FRC – recruits “recruitable” alveoli
 Decreases shunt, improves V/Q matching
 No consensus on optimal level of PEEP

34.  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%)

36.  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)

37.  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

38.  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

39.  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

40.  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

41.  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