Transcript A R D S.ppt

ARDS
Jhansi Nalamati MD FCCP
Asst. Prof. Of Medicine, AECOM
BRONX NY
Definition
 Acute Respiratory Distress Syndrome
 First described in 1967 in Lancet as Adult
Respiratory Distress Syndrome by Asbaugh
et.al.
 12 pts. had developed acute respiratory
distress, cyanosis , diffuse pulmonary infiltrates
decreased lung compliance and was refractory
to Oxygen therapy
 Also called as “wet lung”, “shock lung” and “Da
Nang lung”
Incidence
 Crude estimates of 78.9/100,000 person
years
 In patient mortality 38.5%
 190,600 cases/year in the US with
74,500 deaths and 3.6 million hospital
days
ARDS and ALI (Acute Lung
Injury) in 1992
 Defined by American European
Consensus
 “Acute Lung Injury” is an umbrella term
for “ Hypoxemia Respiratory Failure” , a
severe version of which is “ARDS”.
 Bilateral Infiltrates
 PCWP< 18mm Hg
 PaO2/FiO2< 300 = ALI
 PaO2/FiO2<200 =ARDS
ALI/ARDS ( Addl. Features)
 Bilateral widespread infiltrates on CXR
 Airway collapse ( low lung Volumes)
 Surfactant deficiency
 Reduced lung compliance
Etiology
 Direct insult to the lungs- bacterial, viral,
fungal agents, lung contusion, Fat
embolism
 Systemic medical and surgical
conditions- trauma, shock, sepsis, burns,
pancreatitis
 Noxious agents- exposure to smoke ,
aspiration
PATHOPHYSIOLOGY
 Altered Pulmonary Capillary
Permeability secondary to endothelial
injury
 Altered alveolar diffusion capacity
 Increased intrapulmonary shunt
 Degree of epithelial injury can predict
outcome
Patho-physiology(contd.)
 Loss of epithelial integrity and injury to
type II alveolar cells can disrupt fluid
transport thereby leading to impairing the
removal of fluid from alveolar space
 Injury to type II pneumocytes can reduce
the production of surfactant which leads
to worsening atelectasis and gas
exchange
Histo-pathological phases
 1) Exudative Phase: 1-3 days- diffuse
alveolar damage ( DAD) with majority of
type I pneumocyte necrosis, diffuse
microvascular injury and influx of
inflammatory cells and proteinaceous
fluid into the interstitium
Fibroproliferative phase
 Day 3-7- repair manifested by type I
pneumocyte hyperplasia and
proliferation of fibroblasts
Treatment of ARDS
 Corner stone of treatment is to keep
PaO2 >60mm Hg, without causing injury
to lung with excessive O2 or excessive
TV ( FiO2 < 60% and TV of 6ml/kg)
 Plateau pressure should not exceed
30mmHg and minimal TV should be at
least 4ml/kg ( irrespective of MAP or
plateau pressure)
 “Avoid Volutrauma and Barotrauma”
ATS recommendations
 Minimize O2 toxicity
 Recruit alveoli
 Minimize high airway pressures
 Prevent atelectasis
 Use sedation and paralysis judiciously
Tx of ARDS/ALI
 “SUPPORTIVE CARE”
 “SUPPORTIVE CARE”
 “SUPPORTIVE CARE”
Low Tidal Volume Ventilation
with or without High PEEP
 Minimizes the amount of phasic stretch
of lung units in inspiration to prevent
VILI( Ventilator Induced Lung Injury)
 Proven to be effective in an NIH
coordinated multi center trial( NEJM ),
patients ventilated with TV of 6ml/kg had
a 22% reduction in mortality compared to
patients ventilated with TV of 10-12ml/kg
Open Lung approach
 Attempts to optimize lung mechanics
and minimize phasic damage by
strategically placing PEEP above Pflex.
 Quasi- Static Volume Pressure curvethe lungs are said to be most compliant
between the lower inflection point and
the upper inflection point, beyond which
over distension occurs
PCV( Pressure Controlled
ventilation)
 Better gas distribution than volume
control ventilation by avoiding over
distension of low complaint units
 Plateau pressure not to exceed 30mm of
Hg
 Reverse I:E Ratio
APRV ( Airway pressure
release ventilation)
 Sets pressure high and pressure low and
time high and time low
 Patient can spontaneously breathe
within these limits, minimizing sedation
requirements
 Unclear what is the PEEP ( ? Pressure
high, ? Pressure low, ? Mean)
HFV ( High frequency
ventilation)
 Reduces barotrauma and improves VQ
mismatch
 Potential complications- inspication of
mucus, airway damage due to high gas
velocities and over distension causing
alveolar injury and worsening ALI
Tx ( contd.)
 Prone Positioning
 Permissive Hypercapnia ( potential
complications include pulmonary
vasoconstriction, pulmonary HTN,
proarrhythmic effects, cerebral
vasodilatation, increasing ICP)
 Prophylactic Bil. chest tubes
Inhaled Nitric Oxide
 Improves oxygenation and decreases





Pulmonary Vascular Resistance
Dose varies from 1.25 to 40ppm
NO clear benefit in limited randomized
controlled trials
Needs to be given for days to weeks
Sensitization can occur
Can cause renal dysfunction,
immunosuppression, potentially mutagenic ,
can cause methhemoglobinemia and NO2
concentration
Steroids in ARDS
 Controversial
 Cytokines decline over the first week in
survivors of ARDS, but persist in non
survivors
Steroid regimen( Prednisone)
 2mg/kg day 1-14
 1mgkg day 15-21
 0.5mg/kg day 22-28
 0.25mg/kg day 29-30
 0.125mg/kg day 31-32
 Not to be started before 7days of ALI or
admission or beyond 28days of ALI or
admission
Novel therapies for ARDS
 Albuterol
 Salmetrol
 Surfactant
 Pentoxyfylline
 Cyclooxygenase inhibitors
 Antioxidants
 TNF antibodies infusion
 PAF inhibitors and receptor antagonists
 Antiproteases
Cause of death
 Underlying cause
 Secondary complications- sepsis from
ventilator associated pneumonia, GI
bleed, multi organ failure
Management of secondary
effects
 Judicious use of sedation and
neuromuscular blockade
 Hemodynamic management
 Nutritional support
 Glucose control
 Nosocomial pneumonia prevention and
Tx
 GI and DVT prophylaxis
Nosocomial Pneumonia
 60% of pts with ARDS in 30days
 Can occur as early as 10days
 Prevention strategies include-continuous
subglottic aspiration of secretions,
selective GI tract decontamination ( does
not prevent pseudomonas) elevation of
head 30 degrees, mouth care, avoiding
vent. Circuit changes or clearing the
condensate
Nosocomial pneumonia
(contd.)
 Closed suction is of no benefit
 Avoid unnecessary antibiotics
 No use of antibiotic or silver impregnated
ETT tubes