Acute Respiratory
Distress
Syndrome
Objectiv
es
• Review the causes and differentials for
ARDS
• Briefly discuss the pathophysiology
• Discuss the clinical manifestations of
ARDS
• Understand evidence based treatment
options
Statisti
• Epidemiology
cs
—Annual incidence: 60/100,000
—200/«ICU patients meet criteria for ARDS
• Morbidity / Mortality
—26-44%, most (80 /o)deaths attributed to non-pulmonary
0
organ failure or sepsis
• Risk Factors
— Advanced age, pre-existing organ dysfunction or chronic
medical illness
— Patient with ARDS from direct lung injury has higher incidence
of death than those from non-pulmonary injury
Definiti
on
1) Acute onset
2) Bilateral infiltrates
3) No clinical evidence of
left heart failure
PaO2:FiO2 s 300 (or PCW_P < = 1 8 ) PaO2:FiO2 <
200
SaO2:FiO2 s 315 SaO2:PiO2 s 235
Acute Lung Injury Acute Respiratory
Distress Syndrome
Bernard et al. AJRCCIVi 1994; 149.81B
Rice et al. Chest 2007. 132. 410
Table 3. The Berlin Definition of Acute Respiratory Distress Syndrome
Acute Respiratory Distress Syndrome
Wrthin 1 week of a known clinical insult or new or worsening
respiratory symptoms
Chest Bilateral opacities— not fully explained by effusions, IobarJung
imaginga collapse, or nodules
Origin of Respiratory failure not fully explained by cardiac failure or fluid
edema overload Need objective assessment (eg, echocardiography) to
exclude hydrostatic
Oxygenatio edema iT no risk factor present
nb Mild
Moderat 200 mm Hg < Pao,/FiO, 300 mm Hg with PEEP or CPAP 5
e cm H,OC
Severe Pao,/Fa, 100 mm Hg with PEEP
5 cm HCOCPAP, continuous
Abbreviations: 100 mm Hg <:
posilive Pap/FIO,
airway 200F mm
pressure: Hg with
c2. traction of PEEPS
inspiredcm H2 Pan,
oxygen:
partial pressure of
oxygen; PEEP, positive end- expiratory
b
pressure.
If altitude radiograph
is higler or compr‹ted
the 1000 m, the correction factor shoed be cdculated as follows: (PacJFi 2 X
tomography
ometric pres iW scan.
Causes of
ARDS
Other: drowning,
pancreatitis,
reperfusion,
salicylate and
narcotic OD,
fat/amniotic
embolism,
smoke/chemical
inhalation.
Differenti
•
als
Left ventricular failure/volume overload
• Mitral stenosis
• Pulmonary veno-occlusive disease
• Lymphangitic spread of malignancy
• Interstitial and/or airway disease
—Hypersensitivity pneumonia
—Acute eosinophilic pneumonia
—Acute interstitial pneumonitis
Injured Alveolus during the
Acute Phase
_ - Sloughing of broochi eI epirhe
Direct or indirect injury
lium
to the alveolus causes
alveolar macrophages to
release pro-
inflammatory cytokines
Wid en
ed,
M|
F
Fibr obja
Ware et al. NEJM 2000:
st 342:1334
Pathophysiol
ogy
2. Cytokines attract
neutrophils into the
alveolus and interstitum,
where they damage the
alveolar-capillary
membrane (ACM).
Ware et al. NEJM 2000; 342:1234
Injured Alveofusduringthe Aeute Pathophysiology
Phase
3. ACM integrity is lost,
Slo‹tghing of bronchi al epi \helium
interstitial and alveolus fills
with proteinaceous fluid,
surfactant can no longer
support alveolus
Migrati ng neutrophil
,Widened,
edematou
Endot
heT‹at
Wave et at. NEJN\ 2000; 342:1334
Pathophysiol
• ogy
Consequences of lung injury
include:
—Impaired gas exchange
—Decreased compliance
—Increased pulmonary arterial pressure
Impaired Gas Exchange
• V/Q mismatch
—Related to filling of alveoli
—Shunting causes hypoxemia
• Increased dead space
—Related to capillary dead space and V/Q mismatch
—Impairs carbon dioxide elimination
—Results in high minute ventilation
Decreased Compliance
• Hallmark of ARDS
• Consequence of the stiffness of poorly or
nonaerated lung
• Fluid filled lung becomes stiff/boggy
• Requires increased pressure to deliver Vt
Increased Pulmonary Arterial
Pressure
• Occurs in up to 25% of ARDS patients
• Results from hypoxic vasoconstriction
• Positive airway pressure causing vascular
compression
• Can result in right ventricular failure
• Not a practice we routinely measure
Evidence based management
of
•ARDS
Treat the underlying cause
• Low tidal volume ventilation
• Use PEEP
• Monitor Airway pressures
• Conservative fluid management
• Reduce potential complications
Low Tidal Volume Ventilation
• When compared to larger tidal volumes, Vt of 6mI/kg of
ideal body weight:
• Decreased mortality
• Increased number of ventilator free days
• Decreased extrapulmonary organ failure
• Mortality is decreased in the low tidal volume group
despite these patients having:
• Worse oxygenation
• Increased pCO2 (permissive hypercapnia)
• Lower pH
ARDSnet. NEJM 2000; 342: 1301
Low Tidal Volume
Ventilation
ARDS affects the lung
in a heterogeneous
fashion
Normal alveoli
Iniured alveoli can
potentially participate
in gas exchange,
susceptible to damage
from opening and
• Dama ed alveoli
filled with fluid, do not
participate in gas
exchange
Low Tidal Volume Ventilation
• Protective measure to avoid over distention of
normal alveoli
• Uses low (normal) tidal volumes
• Minimizes airway pressures
• Uses Positive end-expiratory pressure (PEEP)
PEEP
• Higher levels of PEEP/FiO2 does not
improve outcomes
—may negatively impact outcomes:
• Causing increased airway pressure
• Increase dead space
• Decreased venous return
° Barotrauma
PEEP
• Positive End Expiratory Pressure
• Every ARDS patient needs it
• Goal is to maximize alveolar recruitment and
prevent cycles of recruitment/derecruitment
PEEP
• As FiO2 increases, PEEP should also increase
Lower PEEP/higher FiO2
FiO 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7
PEEP 5 5 8 8 10 10 10 12
FiOz 0.7 0.8 0.9 0.9 0.9 1.0
PEEP 14 14 14 16 18 18-24
ARDSnet. NEJM 2004; 351,
Airway Pressures in ARDS
• Plateau pressure is most predictive of lung injury
• Goal plateau pressure < 30, the lower the better
• Decreases alveolar over-distention and reduces risk of
lung strain
• Adjust tidal volume to ensure plateau pressure at goal
• It may be permissible to have plateau pressure > 30
in some cases
• Obesity
• Pregnancy
• Ascites
Terragni et al. Am J Resp Crit Care Med.
2007;
Permissible Plateau
Pressures
• Assess cause of high Plateau Pressures
• Always represents some pathology:
— Stiff, non-compliant lung: ARDS, heart failure
— Pneumothorax
— Auto-peeping
— Mucus Plug
— Right main stem intubation
— Compartment syndrome
— Chest wall fat / Obesity
Airway Pressures
Peak Inspiratory
Airway Pressure
Pressures
Plateau Pressure
PEEP
Time
Fluid Mana
ement
Increased lung water is
the underlying cause of
many of the clinical
abnormalities in ARDS
(decreased compliance,
poor gas exchange,
atelectasis)
• After resolution of shock,
effort
should be made to
axempt diuresis
• CVP used as guide,
goal <4
• Shortens time on vent
and ICUARDSnet.
length of2006;
NUM stay (13
354:
11 days)
days vs2564
Weaning
• Daily CPAP breathing trial
— FiO2 <.40 and PEEP <8
— Patient has acceptable spontaneous breathing efforts
— No vasopressor requirements, use judgement
• Pressure support weaning
— PEEP 5, PS at Scm H2O if RR <25
— If not tolerated, Vt — return to
IRR, A/C
• Unassisted breathing
— T-piece,
— Assess trach
for 30minutes-2 hours
collar
Weaning
• Tolerating Breathing Trial?
— SpO2 190
— Spontaneous Vt a4mI/kg PBW
— RR s3S
— pH 17.3
— Pass Spontaneous Awakening Trial (SAT)
— No Respiratory Distress ( 2 or more)
• HR > 1200/ baseline
• Accessory muscle use
• Abdominal Paradox
• Diaphoresis
• Marked Dyspnea
— If tolerated, consider extubation
Putting it all
together
1) Calculate patient's predicted body weight:
• Men (kg) 50 + 2.3(height in inches —
60)
• Females (kg) 45.5 + 2.3(height in inches
— 60)
2) Set Vt = predicted body weight x 6cc
3) Set initial rate to approximate baseline
minute ventilation (RR x Vt)
4) Set FiO2 and PEEP to obtain SaO2 goal of >—
&8Oo
Common Problems
Plateau pressure > 30 •Decrease Vt by 1cc/kg to as low as 4cc/kg IBW
mm Hg •Ensure no pneumothoraX, auto-PEEP or
other reason for acute change in compliance
Breath stacking / •If Pplat < 30, increase Vt by 1cc/kg to as high
Dyssynchrony as 8cc/kg ensuring Pplat < 30
•Increase inspiratory flow rate (watch Pplat)
•Sedation / paralytics if needed for hypoxia
Hypotension •Give volume
•Ensure no pneumothorax
•EvaIuate for auto-PEEP
•Minimize sedation (if possible)
pH < •Increase minute ventilation (up to RR 35)
7.30 •Increase minute ventilation (up to RR 35)
pH < •Consider sodium bicarbonate
Refractory Hypoxia
• Mechanical Trouble (tubing, ventilator, ptx, plugging)
• Neuromuscular blockade
• Recruitment maneuvers — positioning, “good lung
down” optimizes V/Q mismatch
• Increase PEEP
• Inhaled epoprostenol sodium (Flolan)
— When inhaled, the vasodilator reaches the normal lung, is
concentrated in normal lung segments and recruits blood flow to
functional alveoli where it is oxygenated. This decreases shunting
and hypoxemia
• High frequency ventilation
Supportive Therapies
• Treat underlying infection
• DVT prophylaxis / stress ulcer
prevention
• HOB 30°
• Hand washing
• Use full barriers with chlorhexadine
• Sedation / analgesia
• Feeding protocol
• Avoid contrast nephropathy
• Pressure ulcer prevention, turning Q2h
• Avoid steroid use
Conclusion
• Recovery dependent on health prior to onset
• Within 6 months, will have reached max recovery
• At 1 year post-extubation, >1/3 have normal spirometry
• Significant burden of emotional and depressive
symptoms with increased depression and PTSD in
ARDS survivors
• Survivor clinic catches symptoms early by screening patients
• New treatment modalities, lung protective ventilation
Levy BD, & Choi AM, Harrison's Principles of Internal Medicine, 2012
