Acute Respiratory Distress Syndrome

(ARDS)

Dr.Loai Tawalbeh

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 (ARDS)
Represent a complex clinical syndrome
Acute in onset, symptoms develop over 4-48hr
after insult

It is acute rather than adult

All patients have ARDS have (Acute Lung

Injury) ALI, but not all patients have ALI, have
ARDS

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 Causes
Direct lung injuries:
- Aspiration
- Pneumonia
- Lung contusions with trauma
- Toxic inhalation
- Airway obstruction
- Pulmonary oedema

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 Causes
Indirect pulmonary injuries:
- Sepsis
- Burns
- Trauma
- Blood transfusion
- Drug or alcohol overdose
- Drug rxn
- Acute pancreatitis
- Air embolism
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 pathophysiology
increased lung oedema and impaired gas exchange are the
hallmarks

the pathogeneses of ARDS occur over phases:

Phase 1:
Injury reduce normal blood flow to the lung. PLT aggregate
and mediators released. (PGs, Histamin, bradykinin)

Phase 2:
These inflammation (Vasodilation) and damage the alveolar-
capillary membrane  inc capillary permeability  fluids
shift into interstitial space
Release of IL-1 and TNF-----fever

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 pathophysiology
Phase 3:
As permeability increases, protein and fluids leak
out  inc osmotic pressure and causing
pulmonary oedema.

Phase 4:
Dec blood flow and fluids in the alveoli damage
surfactant and impair the cell ability to produce
more  alveoli collapse  impeding gas
exchange and decrease lung compliance.

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 pathophysiology
Phase 5:
Gases cannot cross the alveolar-capillary
membrane.

Phase 6:
Pulmonary oedema worsens, inflammation leads
to fibrosis, and gas exchange further impeded.

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 Stages of ARDS
• The pathologic changes associated with ARDS
start with increasing pulmonary edema and
progress to inflammation, fibrosis, and
impaired healing in the later stages
 stage 1
• diagnosis is difficult because the signs of
impending ARDS are subtle

• Clinically, the patient exhibits increased dyspnea

and tachypnea, but there are few radiographic
changes

• At this point, neutrophils are sequestering;

however, there is no evidence of cellular damage.
• Within 24 hours (a critical time for early
treatment), the symptoms of respiratory
distress increase in severity, with cyanosis,
coarse bilateral crackles on auscultation, and
radiographic changes consistent with patchy
infiltrates.
 Stage 1 (first 12 h):
• X-ray: Normal chest x-ray
• S/S: Dyspnea, tachypnea
• Neutrophil sequestration, no evidence of
cellular damage
 stage 2
• A dry cough or chest pain may be present.

• the mediator-induced disruption of the

vascular bed results in increased interstitial
and alveolar edema.

• The endothelial and epithelial beds are

increasingly permeable to proteins.
• This is referred to as the “exudative” stage.

• The hypoxemia is resistant to supplemental

oxygen administration, and mechanical
ventilation is required for worsening ratio of
arterial oxygen to fraction of inspired oxygen
(PaO2:FiO2 ratio).
 Stage 2—Exudative (24 h):
• X-ray:Patchy alveolar infiltrate, primarily in
dependent lung areas; normal heart size

• S/S: Dyspnea, tachypnea, cyanosis,

tachycardia, coarse crackles, hypoxemia

• Neutrophil infiltration, vascular congestion,

fibrin strands, increased interstitial and
alveolar edema
 Stage 3
• The “proliferative” stage, develops from the 2nd
to the 10th day after injury.

• Evidence of SIRS is now present, with

hemodynamic instability, generalized edema,
increased hypoxemia, and lung involvement.

• Air bronchograms may be evident on chest

radiography as well as decreased lung volumes
and diffuse interstitial markings.
 Stage 4
• The “fibrotic” stage, develops after 10 days
and is typified by few additional radiographic
changes.

• There is increasing multiorgan involvement,

SIRS, and increases in the arterial carbon
dioxide tension (PaCO2) as progressive lung
fibrosis and emphysematous changes result in
increased dead space.
 Pathophysiology
• Injury----Inflammation------vasodilation------
increase capillary permeability------P.E-------
Decrease surfactant------alveolar collapse-------
V-P mismatch----Refractory hypoxemia-------
shunt------inflammation------scare tissues-----
decrease compliance

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 Criteria
• 1-Acute onset

• 2-Bilateral infiltrate

• 3-PAWP less than 19mmhg

• 4-PaO2/FiO2 less than 200

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 Assessment
History:
Past hx
Past relevant incidents (meds, blood transfusion,
radiograph contrast)
Use of medical therapies
Social factors
Risk factors

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 Assessment
Diagnostic studies:
ABGs:
Hypoxemia (PaO2<60mmhg), refractory hypoxemia
At early stages: resp alkalosis (rapid resp  low
PaCO2)
Later stages: Respiratory acidosis

Radiographic:
Early: patchy bilateral infiltrate  diffuse infiltrate
 consolidation
Daily x-ray to evaluate progression

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 S/S
• 1-Tachypnea, dyspnea, nasal flaring and
respiratory alkalosis, cyanosis, moist skin

• 2-Tachycardia

• 3-Hemoptysis, crackles

• 4-Agitation, lethargy, L.O.C

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 Intrapulmonary Shunt Measurement
• An intrapulmonary shunt is a type of ventilation–
perfusion mismatch defined as the percentage of C.O
that is not oxygenated owing to pulmonary blood
flowing past collapsed or fluid-filled and
nonventilated alveoli (a physiologic shunt)

• absence of blood flow to ventilated alveoli (alveolar

dead space), or a combination of both of these
conditions (silent unit [alveoli with no ventilation and
no perfusion]
• An intrapulmonary shunt of 3% to 5% is
present in all people;

• however, advanced respiratory failure and

ARDS are associated with a shunt of 15% or
more due to changes in blood flow, endothelial
disruption, and alveolar collapse.
• As the intrapulmonary shunt increases to 15%
and greater, more aggressive interventions,
including mechanical ventilation, are required
because this level of shunt is associated with
profound hypoxemia.
• Measurement of intrapulmonary shunt requires
the use of a pulmonary artery catheter, which
may be used in more severe cases.

• The intrapulmonary shunt fraction (Qs/Qt) is

calculated using the arterial oxygen content
(CaO2), the mixed venous oxygen content
(CvO2), and the capillary oxygen content
(CcO2).
• Oxygen content is determined by Hgb, oxygen
saturation (SO2), and partial pressure of
oxygen, measured by calculating the oxygen
content in the pulmonary capillary bed, in the
systemic arterial system, and in the mixed
venous blood from the pulmonary artery
• The intrapulmonary shunt fraction may also be
estimated using the ratio of arterial oxygen to
inspired oxygen (ie, PaO2:FiO2 ratio).

• In general, a PaO2:FiO2 ratio greater than 300

is normal.
• Values less than 200 are associated with an
intrapulmonary shunt of 15% to 20%, and a
value of 100 or less is associated with an
intrapulmonary shunt of more than 20%.
 Management
1-Supportive treatment
Oxygenation and ventilation
O2 delivery:
Refractory hypoxemia
DaO2: amount of O2 delivered to the tissues and
organs every minutes.
Parameters that determine DaO2 are: Hb, arterial
oxygenation, C.O

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 Management
1-Hb: sufficient amount of it. 8mg/dl sufficient,
below need transfusion.

2-C.O: it is altered due to the affect of hypoxemia on

the myocardium.

Enhancing preload and contractility

3-Fluid management (preload): to manage edema

Positive inotropes e.g: dopamine or dobutamine

(contractility).
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 Management
4- Mechanical ventilation:
Goal is to improve tissue oxygenation and
ventilation

Lung protective ventilation strategies, which

limits ventilator associated lung injury:

- Low Tv (<6 ml/kg): to minimize airway

pressure  preventing or reducing lung damage
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 Management
• Use of adequate PEEP to reduce the risk of
using a high FiO2: 10-20 cm H2O: to maintain
adequate oxygenation.

• Using lowest FiO2 to achieve adequate

oxygenation

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 Management
• Mode of Ventilations
• 1-Pressure Controlled ventilation:Measured
airway plateau pressure below 30 cm H2O

• 2-Inverse ratio ventilation inverse the I/E ratio

to 2:1 or 3:1 to prolong inspiration

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• Permissive hypercapnia is a strategy that
allows the PaCO2 to rise slowly above normal
through reduction of tidal volume, therefore
limiting the plateau and peak airway pressures.

• A PaCO2 between 55 and 60 mm Hg and a pH

of 7.25 to 7.35 are tolerated when achieved
gradually
• High-frequency oscillatory ventilation
(HFOV) uses very low tidal volumes (1 to 4
mL/kg) delivered at rates of 3 to 15 Hz or
cycles/s rather than breaths/min, resulting in
lower airway pressures and reduced
volutrauma.
• Deleterious effects of HFOV include increased
trapping of air in the alveoli (auto-PEEP) and
increased mean airway pressures to high levels
in some patients.

• HFOV requires sedation and paralysis as any

change in airway pressure will cause
oscillation to cease.
 Extracorporeal Therapie
• Extracorporeal lung support (ECLS)
technology involves the use of large vascular
cannulas to remove blood from the patient.

• A pumping device and circuit circulate the

blood, and one or two “artificial lungs” remove
carbon dioxide and oxygenate the blood.
• These highly invasive, high-risk technologies
allow the lungs to “rest,” because near-apneic
ventilation or ventilation with small tidal
volumes and slow respiratory rates greatly
reduce air-way pressures while gas exchange
takes place in the artificial membrane lungs.
 Bundle
• Prevention or reduction in the incidence of
VAP can be accomplished by using in-line
suction catheters.

• The use of endotracheal tubes that allow for

the removal of pooled sub-glottic secretions
has been shown to reduce VAP.

• Sinusitis is also associated with VAP

 Bundle
• The critical care nurse needs to monitor for
nasal secretions and ensure that devices such
as nasotracheal or feeding tubes are removed
from the nose when these occur.

• Oral care is an essential component in the

prevention of VAP, as it decreases the amount
of organisms in the mouth, which may migrate
to the lungs
 Bundle
• Elevating the head of the bed 30 degrees and
feeding the critically ill patient with a
postpyloric feeding tube have been shown to
reduce microaspiration and VAP
 Bundle
• Immobility caused by bed rest, sedation, or
pharmacologic paralysis has multisystem
effects.

• frequent repositioning
 Management
Positioning:
Prevent and reverse atelectasis and facilitate
removal of secretion from airways.

Prone position: improve gas exchange, facilitate

pulmonary drainage

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 Management
Pharmacological therapy:
Supportive

If infections  AB

Bronchodilator and mucolytic  airway patency,

reduce inflammatory process

Surfactant: useful, but, still under-research

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 Management
• Corticosteroids: anti-inflamatory

• Anti-inflamatory mediators.

• Sedation:

• To promote comfort, reduce resp effort  dec O2

demands

• e.g: propofol
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 Management
Nutritional support:

for 2 reasons:
-1-Mediators stimulate release of proteolytic
enzymes that stimulate protein catabolism from
skeletal muscle.

-2-Protein leak by interstitial loss

Diet balanced with caloric, protein, carbohydrate,
and fat intake calculated based on metabolic needs.
Enteral nutrition to Prevent infection
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 Bundle to prevent VAP
• Elevate the head of the bed 30 to 45 degrees
• Weaning protocol
• Deep vein thrombosis (DVT) prophylaxis
• Peptic ulcer prophylaxis
• Suction

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 Prevention of complications
1-VAP
2-Sepsis
3-High level of PEEP  volutrauma and
barotraumas  pneumothorax, emphysema  chest
tube

Immobility  accumulation of secretion,

pneumonia

 DVT low dose heparin, elastic Stocking,

external pneumoatic compression, freq
mobilization,

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• Barotrauma: is physical damage to body tissues
caused by a difference in pressure between an air
space inside or beside the body and the surrounding
fluid

• Volutauma: damage to the lung caused by

overdistention by a mechanical ventilator set for an
excessively high tidal volume

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 Acute respiratory failure
Sudden and life threatening deterioration in gas
exchange, resulting in Co2 retention and
inadequate oxygenation.

MR: 44%

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 Pathophysiology
PaCo2> 50 mmhg
PaO2 <50 mmhg
pH < 7.25

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 causes
Malfunction of resp centres, abnormal respiratory
neuromuscular system, chest wall diseases, airway obstruction

this hypoxemia-hypercapnia resulted from:

V-Q mismatch

Alveolar hypoventilation

Impairment of diffusion

Rt-lt shunt

Reduce O2 in mixed venous blood.

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 Classifications
1- Type I (acute hypoxemic respiratory failure):
Abnormal O2 transport, with increased
alveolar ventilation resulting in a low PaCo2

Cause: v-q mismatch, rt-to-lt shunt and alveolar

hypoventilation.

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 Causes of hypoxemia:

• A-O2 delivery to alveoli:

• 1-O2 of the FiO2
• 2-VentilaTION OF THE ALVEOLI

• B-Diffusion of O2 from alveoli to blood:

• 1-balance between alveolar ventilation and
perfusion
• 2-diffusion of O2 across alvocapillary membrane
• 3-Perfusion capillary membrane
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 Classifications
2- Type II (Acute Hypercapnic Failure)
Inadequate alveolar ventilation, elevation of CO2

three factors contribute to type II failure:

-1-Dec ventilator drive: meds, brainstem lesions,
hypothyroidism, morbid obesity, sleep apnea

-2-Respiratory muscle fatigue or failure: neuro

muscular dysfunction

- 3-Inc. work of breathing: COPD, asthma,

pneumotorax, pleural effusion.
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 Classifications
3- Combined hypoxemic and hypercapnic
respiratory failure:
Combined inadequate ventilation and abnormal
gas transport
e.g: asthma exacerbation, emphysema,
pulmonary edema, PE.

Any cause of type I failure may lead to combined

failure, especially if increased work of breathing
and hypercapnia involved.
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 Assessment
History:
Baseline resp status, S&S

PHYSICAL FINDINGS:
Determine if intubation and ventilation required

Determine Mental status (headache, confucion

and LOC)

Presence of hypoxemia, cyanosis, hypercapnia

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 Assessment
Dx studies:
ABGs
To detect cause: CXR, sputum examination, PFT,
angiography, CT, CBC, bronchoscopy,
thoracentesis.

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 Acute Respiratory Failure
• Clinical Manifestations
1.Impaired oxygenation & restlessness
2.Fatigue & headache
3.Dyspnea & air hunger
4.Tachycardia & hypertension
5.Confusion & lethargy
6.Diaphoresis & Uses of accessory muscles
7.Decrease breath sound Respiratory Arrest

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 Management
Correcting the cause and alleviating hypoxia and
hypercapnea

-ETT & MV

To inc PaO2 by inc Fio2

- Continuous pulse oximeter monitoring until

saO2 of 90% or higher achieved
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 Acute Respiratory Failure
• Nursing management:
1.Monitoring patient responses and arterial blood
gases
2.Monitoring vital sign
3.turning ,mouth care , skin care , and rang of
motion .
4.Teaching about the underlying disorders
5.Assists in intubations procedure

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September 2011 Dr. Ahmad Tubaishat 69