Ventilation Strategies

for
ARDS Patients

By

Professor Dr.Tarek Abd El-Gawad

Head of PICU ,Ain Shams University
 Definition
Acute lung injury (ALI) and its
more severe form the acute
respiratory distress syndrome
(ARDS ) are syndromes of acute
respiratory failure that result
from acute pulmonary edema
and inflammation.
 Definition Criteria for
ALI/ARDS
• Onset: Acute
• Oxygenation Index: PaO2/FiO2
<300 (ALI) or <200 (ARDS).
• Chest X-ray: Bilateral pulmonary
infiltrates.
• Pulmonary artery wedge
pressure<18 mm/Hg or no clinical
evidence of left atrial hypertension
(According to the American- European Consensus
Committee(NAECC) on ARDS definition in 1994)
 Incidence:
About 9.9% of mechanically
ventilated children develop ALI

Mortality:
In Europe, the mortality rates ranged from
27-36.5%. In an Asian population it was
double that recorded in Europe (62%).In
Egypt it was 65-73%.
 Clinical disorders
associated with
development of ARDS
Direct lung injury Indirect lung injury
– Pneumonia
– Sepsis
– Aspiration of gastric
contents – Severe trauma
– Pulmonary contusion – Cardiopulmonary
– Fat emboli bypass
– Near drowning – Drug overdose
– Reperfusion edema – Acute pancreatitis
(post transplant)
– Multiple blood
– Inhalational injury
product
transfusions
Pathogenesis of ARDS
(Ware &Matthay,2000)
 Stages of ARDS
Acute, exudative phase
• Rapid onset of respiratory
failure after trigger
• Diffuse alveolar damage
with inflammatory cell
infiltration
• Hyaline membrane
formation
• Capillary injury
• Protein-rich edema fluid in
alveoli
• Disruption of alveolar
epithelium
 Stages of ARDS
Subacute Proliferative
phase

• Persistent hypoxemia
• Development of
hypercarbia
• Fibrosing alveolitis
• Further decrease in
pulmonary compliance
• Pulmonary hypertension
 Stages of ARDS
Chronic, Fibrotic
phase

• Obliteration of
alveolar and
bronchiolar spaces
and pulmonary
capillaries
• Deposition of excess
collagen and
extracellular
matrices and is
associated with
alveolar fibrosis
 Laboratory Studies
To date no lab finding
pathognomonic of ARDS.

-ABG shows:
Early:
hypoxemia
respiratory alkalosis
Late:
respiratory acidosis
 Laboratory Studies
• Leukocytosis,Leukopenia and anemia
are common.

• Renal function abnormalities or liver

function.

• Von willebrand’s factor or complement

in serum may be high.

• Acute phase reactants like

ceruloplasmin or cytokine (TNF,IL-1,IL-
6,IL-8) may be high.
 Laboratory Studies
Bronchoalveolar lavage BAL:

-Increase inflamatory mediators:

cytokines, activated complements,
leukotriens.

-Cellular analysis shows : more than

60% of neutrophils.
 Imaging Studies

X-ray and CAT-scan chest shows

bilateral infiltrates consistent with
pulmonary edema, may be mild or
dense, interstitial or alveolar,
patchy or confluent
Natural History & Fate Of
ALI/ARDS
 ARDS Therapies
Respiratory Mechanical
Innovations: support ventilation
•NO •Low tidal
volume
•Surfactant
•High peep
•Corticosteroid
•Inhaled •Permissive
ARDS
prostacyclines hypercapnia
alternative •Inverse I:E ratio
modalities
Partial High
liquid
ventilation frequency
ventilation
Respiratory Support
 Spontaneously Breathing
Patient
• In the early stages of ARDS the
hypoxia may be corrected by 40 to
60% inspired oxygen with CPAP.

• Peak inspiratory flow rates of more

than 70 liters / min require a tight-
fitting face mask with pretty large
reservoir bag or a high flow generator.
Spontaneously Breathing
Patient

• If the patient is well oxygenated on ≤

60 % inspired oxygen and apparently
stable without CO2 retention, then
ward monitoring may be feasible,
close observation (15 to 30 min), with
continuous oximetry, and regular
ABG is required.
 Indications for
mechanical ventilation:

• Inadequate Oxygenation(PaO2< 80
mmHg on FiO2 ≥ 0.6).

• Rising or elevated PaCO2(≥ 60 mmHg).

• Clinical signs of incipient respiratory

failure.
Noninvasive positive
pressure ventilation
(NPPV)
Advantages of NPPV :
1.Reduces the need for endotracheal
intubation.
2.Reduces length of hospital stay .
3.Reduces hospital mortality rate
4.Improves long-term survival
Noninvasive positive
pressure ventilation
(NPPV)
Disadvantages of NPPV:

• Face masks are uncomfortable.

• Skin necrosis and gastric distention.

• Failure and intubation have generally

progressed to a more advanced condition
than if they had been intubated earlier
Conventional mechanical
ventilation
• Development of strategies for
mechanical ventilation in ARDS
needs to take into account a
number of pathophysiologic
concepts :
1. The "baby lung“
2. Cyclical atelectasis
 Baby Lung
• Only a small fraction
of the lung in
(ARDS) participates
in gas exchange, so
that it is functionally
like a "baby lung”.
Much of the lung,
especially in
dependent regions, is
consolidated that
cannot be recruited for
gas exchange.
 Cyclical atelectasis
• Depletion of functional surfactant in
ARDS leads to the development of
wide spread atelectasis.

• Low tidal volume strategies may

exacerbate the atelectasis.

• Some areas of the lung appear to

collapse , expanding on inhalation &
collapsing on exhalation.
Principles of
mechanical
• Low tidal volume
ventilation:
• Permissive hypercapnia

• High PEEP

• Adequate oxygenation

• Inverse I:E ratio

(The Acute Respiratory Distress Syndrome Network, 2004)
 Low Tidal Volume Ventilation
• low tidal volume ventilation is the
only strategy proven to improve
survival in ALI/ARDS patients

• Ideal body weight (IBW) rather than

actual body weight is used to
determine the appropriate tidal
volume for patients with lung disease
receiving mechanical ventilation
 Low Tidal Volume Ventilation

• IBW (kg) Males:

• 50+2.3(height in inches – 60)
Or 50+0.9(height in cm – 152.4)
• IBW (kg) Females:
• 45.5+2.3(height in inches – 60)
Or 45.5+0.9(height in cm – 152.4)
Mechanical Ventilation
Low Tidal volume:
1. Ventilate with low TV (6 ml / kg )
2. The way of ventilation improves the
mortality of ARDS (less mortality
with low tidal volume)

Goal plateau pressure <30 cm H20

Mechanical Ventilation
Hazards:
• Higher respiratory rates.

• Mild hypercapnea and

respiratory acidosis.

• Worsen oxygenation. However,

this effect is tolerable.
 Permissive Hypercapnia:
• Ensure adequate ventilation: goal (pH
≥7.30) (permissive hypercapnea).

• Patients ventilated with low TV often

develops hypercapnea because minute
ventilation is decreased and relative dead
space increased.

• Hypercapnea appears to be an acceptable

side affect of controlled hypoventilation, as
long as adequate oxygenation is assured.
Permissive Hypercapnia:
Contraindications :
• Increased intracranial pressure
• Hemodynamic instability

Precaution:
Most patients require heavy
sedation
 Positive end-expiratory
pressure (PEEP)
• Increases trans-pulmonary
distending pressure
• Displaces edema fluid into
interstitium
• Decreases atelectasis
• Decrease right to left shunt
• Improves compliance
• Improves oxygenation
 Positive end-expiratory
pressure (PEEP)
Hazards :
• Raise airway pressures
alveolar overinflation or
barotrauma
• Decrease venous return
depressing cardiac output (CO) and
oxygen delivery hypotension
• PEEP may cause intra-cardiac
shunting in patients with a
patent foramen ovale
 Oxygenation:
∀ ↓ FiO2 < 50% if possible.
• O2 is a toxic medicine ( produce
oxygen radicals which is harmful
• It can be calculated according to
Fio2:PEEP ratio

F i O 20
20 .30
.3 0 .40
.4 0 .40
.4 0 .50
.5 0 .50
.5 0 .60
.6 0 .70
.7 0 .70
.7 0 .70
.7 0 .80
.8 0 .90
.9 0 .90
.9 0 .91
.9 1 .0
P E E P5 5 8 8 1 0 1 0 1 0 1 2 1 4 1 4 1 4 1 6 1 8 2 0-2
 Inverse I:E ratio
I:E (2:1 to 3:1)
• Longer inspiratory time.

• Breath starts before expiratory flow

from prior breath reaches baseline →
auto-PEEP with recruitment of alveoli

• Lower inflating pressures.

• Potential for decrease in cardiac output

due to increase in MAP.
 Start Calculate predicted body weight

CMV (A/C), VCV, Vt 8 mL/kg, then 7 mL/kg after 1 hr, then 6 mL/kg
after next 1 hr, increase inspiratory rate to maintain minute ventilation,
I:E ratio 1:2, PEEP and FiO2 per FiO2/PEEP table

Pplat < no no
↑ VT by 1 mL/kg VT 5 mL/kg VT 4 mL/kg
30 cm H2O

yes yes yes

yes Pplat <

VT <6 mL/kg
25 cm H2O

yes
↑ VT to 7-8 mL/kg Severe dyspnea
no

PaO2 55-80 no Adjust FiO2 or PEEP

SpO2 88-95 Per FiO2/PEEP table

yes
↑ rate yes <7.30 >7.45 FiO2 ≤ 0.4 no
Consider HCO3 pH < 7.15 pH ↓ rate
↑ VT PEEP= 8
no
7.30-7.45 yes
↑ rate
Evaluate for weaning
Positioning
 Positioning
“PRONING”
1-Improved gas exchange
2-More uniform alveolar ventilation
3-Recruitment of atelectasis in dorsal
regions
4-Improved postural drainage.
5-Redistribution of perfusion away from
edematous, dependent regions.
 Positioning
“PRONING”
HOW?

• Place head at right of the bed to monitor

ETT
• All lines over shoulder, chest tube along
side of body
• Place dependent arm under the hip.
• Small pillow under chest/clavicles and
hip.
• Check ABG within 30minutes.
• Provide range of motion every 2 hours
Positioning
“PRONING”
Contraindications:

– Spine instability
– Hemo-dynamic instability
– Arrhythmias
– Thoracic and abdominal surgeries
– Increased intracranial pressure
Positioning
“PRONING”
Complications:
- Extubation
- ETT obstruction
- Dislodging CVCs
- Hemo-dynamic instability
- Facial edema
- Pressure sores
Alternative Therapies
for ARDS
Partial liquid ventilation PLV:

• Reduces surface tension

• Alveolar recruitment – liquid
PEEP.
• Increases surfactant
phospholipid synthesis and
secretion.
• Anti Inflamatory Properties
High Frequency Ventilation:
• Raise MAP
• Recruit lung volume
• Small changes in tidal volume
• Impedes venous return
necessitating intravascular
volume expansion and/ or
pressors
 Surfactant
• Prevention of alveolar collapse
• Maintenance of pulmonary compliance
• Optimization of oxygenation
• Enhancement of ciliary function and
bacterial killing

No effect on mortality or duration of

mechanical ventilation.
 Anti-inflammatory
Strategies
Steroids:
Early ARDS not beneficial.
Late ARDS : remains contraversial
Possible mechanisms:
Improves oxygenation
More ventilator-free & shock-free days
More re-intubations
More neuromuscular weakness
Steroids remain controversial
Anti-inflammatory Strategies
LISOPHYLLINE AND PENTOXIFYLINE:

•PDE-I
•Inhibit neutrophil chemostaxis and
activation.
•Lisophylline inhibit release of FF
from cell memb. under oxidative
stress
•TNF : IL-1 ; IL-6
•No evidence suggestive of any
benefit.
 Selective Pulmonary
Vasodilators
Nitric oxide:
1-Improves Oxygenation.

2-Selective vasodilatation of vessel a/w better

ventilation → (decrease shunt)Improves v/q
mismatch.
3-Reduction in pulmonary artery pressure
-Improves oxygen.
-direct smooth muscle relaxation.
-improved RV Fn.
-reduced capillary leak.
-Inhibit platelet aggregation & neutrophil
adhesion.

4-Mortality Benefits – None

 Inhaled Aerosolized
Prostacyclin (IAP)
• Potent selective pulmonary vasodilator
• Effective for pulmonary hypertension
• Short half-life ( 2-3 min) with rapid
clearance
• Little or no hemodynamic effect
• Randomized clinical trials have not
been done