ACUTE RESPIRATORY

DISTRESS SYNDROME
(ARDS)
Acute respiratory distress syndrome is a lung
condition that leads to low oxygen levels in the
bloods. It is characterized by the development of
sudden breathlessness within hours to days of an
inciting event.
Inciting events include:

• Trauma
• sepsis (microorganisms growing in a person's
blood),
• drug overdose
• massive transfusion of blood products,
• acute pancreatitis or
• Aspiration (fluid entering the lungs especially
stomach contents).
• ARDS typically develops within 12-48 hours after the
inciting event, although, in rare instances, it may
take up to a few days.
• Persons developing ARDS are critically ill, often with
multisystem organ failure. It is a life-threatening
condition; therefore, hospitalization is required for
prompt management.
• ARDS is associated with severe and diffuse injury to
the alveolar-capillary membrane (the air sacs and
small blood vessels) of the lungs. Fluid accumulates
in some alveoli of the lungs, while some other alveoli
collapse.
• This alveolar damage impedes the exchange of
oxygen and carbon dioxide, which leads to a
reduced concentration of oxygen in the blood.
• Low levels of oxygen in the blood cause damage to
other vital organs of the body such as the kidneys.
ARDS CAUSES
• Sepsis (presence of various pathogenic microorganisms, or
their toxins, in the blood or tissues)
• Severe traumatic injury (especially multiple fractures), severe
head injury, and injury to the chest
• Fracture of the long bones
• Transfusion of multiple units of blood
• Acute pancreatitis
• Drug overdose
• Aspiration of gastric contents.
• Viral pneumonias
• Bacterial and fungal pneumonias
• Near drowning
• Toxic inhalations
ARDS SYMPTOMS
Severe difficulty in breathing
Anxiety
Agitation
Fever
low blood pressure
 confusion,
and extreme tiredness.
PATHOPHYSIOLOGY
The membrane consists of an alveolar epithelial cell,
a capillary endothelial cell and the fused basement
membranes of the two cells
INJURY TO THE ALVEOLI
• "type I epithelial cells“-very thin, which actual gas
exchange takes place.
• Damage to type I cells allows both increased entry of
fluid into the alveoli and decreased clearance of fluid
from the alveolar space.
• "type II alveolar cells". -thicker, square-shaped cells.
Main function of these cells is to produce surfactant
production of surfactant, ion transport, and
proliferation and differentiation into type l cells after
cellular injury.
• Damage to type II cells results in decreased
production of surfactant with resultant decreased
compliance and alveolar collapse.
INJURY TO THE ALVEOLAR CAPILLARIES

• If the original injury is in the alveolar capillaries that

lie just beneath the alveoli, chemical mediators
(usually cytokines) that the immune system releases
in response, rush to the site of the injury, damaging
and causing inflammation to the cells that line the
capillaries (i.e., the capillary endothelium).
• As a result, cells and fluid leak through the
capillaries and into the alveolar spaces; the
capillaries become blocked with cellular debris and
fibrin (i.e., protein that makes up blood clots);
surfactant production ceases; and the alveoli
collapse
STAGES OF ARDS
• Exudative stage: Characterized by accumulation in the
alveoli of excessive fluid, protein and inflammatory cells
that have entered the air spaces from the alveolar
capillaries. The exudative phase unfolds over the first 2
to 4 days after onset of lung injury.

• Fibroproliferative (or proliferative) stage: during this

phase connective tissue and other structural elements
settle in the lung in response to the harmful stimulus and
the lung appears densely cellular when examined
through microscopy. . Also, at this stage, there is a
danger of pneumonia sepsis and rupture of the lungs
causing leakage of air into surrounding areas.
• Resolution and Recovery: During this stage, the
lung reorganizes and recovers. Lung function may
continue to improve for as long as 6-12 months and
sometimes longer, depending on the precipitating
condition and severity of the injury. It is important to
remember that there may be and often are different
levels of pulmonary recovery amongst individuals
who suffer from ARDS.
INVESTIGATION
PHYSICAL EXAMINATION
tachypnea, tachycardia, and the need for high
inspired oxygen concentrations to maintain oxygen
saturation.
patient may be febrile or hypothermic.
Cyanosis of the lips and nail beds may occur.
Examination of the lungs may reveal bilateral rales.
• Arterial blood gas analysis reveals hypoxemia
(reduced levels of oxygen in the blood).
• A complete blood count may be taken. The
number of white blood cells is increased in sepsis.
• Chest x-ray will show bilateral, symmetrical or
asymmetrical, fluffy alveolar infiltrates.
• CT scan of the chest may be required only in
some situations (routine chest x-ray is sufficient in
most cases).
• Echocardiogram may help exclude any heart
problems that can cause fluid build-up in the
lung.
• Bronchoscope may be considered to evaluate the
possibility of lung infection
Anteroposterior (AP) portable chest radiograph in a patient who had
been in respiratory failure for 1 week with the diagnosis of acute
respiratory distress syndrome. This image shows an endotracheal tube,
a left subclavian central venous catheter in the superior vena cava, and
bilateral patchy opacities in mostly the middle and lower lung zones.
Mechanical
 Ventilation
To get more oxygen into your bloodstream, your doctor will likely use
supplemental oxygen and mechanical ventilation.
 In most cases, keeping the patient alive requires mechanical
ventilation. With ARDS, the breathing muscles (i.e., diaphragm and
other muscles in the chest) become fatigued very quickly and can stop
working in their effort to get oxygen into the body.
 The level of oxygen in the blood drops rapidly to dangerously low
levels, causing damage to vital organs and body processes.
 If the oxygen level is not improved quickly and maintained at
adequate levels, damage (including severe brain damage) can be
irreversible. Mechanical ventilation keeps the level of oxygen at life-
sustaining levels..
Positive Pressure Ventilation

Positive pressure ventilation does two things:

It pushes air into the lungs, relieving fatigued,
nonfunctioning breathing muscles.
It creates positive pressure in the alveoli, keeping
them from collapsing and pushing fluid out of the
alveolar spaces.
Noninvasive positive pressure
ventilation (NIPPV)
Positive pressure ventilation is sometimes accomplished
with a facemask that forms a tight seal around the
mouth and nose or just the nose in patients who have
ARDS.
Since ventilation via an endotracheal tube is more
efficient, NIPPV is usually used on a temporary basis
and for milder cases.
Continous positive airway
pressure (CPAP)

CPAP may be used temporarily in patients who can

maintain breathing but cannot oxygenate adequately.
CPAP is applied through a mask, in this instance usually
over both the nose and mouth, that forms a tight seal.
Positive pressure is applied by a machine with inspiration
and expiration, causing fluid to be pushed out of the
alveolar space and opening alveoli or preventing them
from collapsing.
Positioning.

Sometimes, putting a patient into the prone position

(on their stomach) helps positive pressure get oxygen
into the bloodstream easier. Lying on the stomach
increases gas exchange in the alveoli.
Fluids control
given to improve the flow of blood through your body and to
provide nutrition.
Too much fluid can fill the lungs, making it harder to get the
oxygen you need.
Not enough fluid can limit blood and oxygen flow to the body's
organs.
Fluids usually are given through an IV line inserted in one of
your blood vessels. Intravenous fluids are given to provide
nutrition and prevent dehydration, and are carefully monitored
to prevent fluid from accumulating in the lungs (pulmonary
edema).
closely monitor the amount of fluids to get just the right
balance to regain lung function but protect other organs.
Medication
1) Anti-inflammatory drugs, such as corticosteroids, to
reduce inflammation in the lungs in the late phase of
ARDS or sometimes if the person is in septic shock
corticosteroids have no proven benefit for early ARDS, they
may be beneficial 7 to 10 days following mechanical
ventilation.
2) Sedating or muscle-paralyzing drugs are used during
mechanical ventilation to prevent resistance to the forced
movement of air.
3) Antibiotics to fight infection
4) Pain relievers
5) Drugs to relieve anxiety and keep the patient calm
and from "fighting" the breathing machine. Anti-
anxiety drugs to relieve anxiety
6)Drugs to raise blood pressure or stimulate the heart.
Drugs to counteract low blood pressure that may be
caused by shock
7) Diuretics to eliminate fluid from the lungs
8) Inhaled drugs administered by respiratory therapists to open up the
airways (bronchodilators)
9)Sometimes it is necessary to paralyze the skeletal muscles to relax
them and prevent them from "fighting" the respirator.
10) anticoagulant to prevent blood clots (deep venous thrombosis) and
pulmonary embolism.
11) Nitric oxide (Vasodilator)
- inhaled nitric oxide (40 ppm in air) reduces pulmonary hypertension
and in concentrations of 15-20 ppm decreases shunting and improves
gas exchange in ARDS by preferentially increasing blood flow to
ventilated areas of the lung
- no systemic effects because nitric oxide scavenged rapidly by Hb
COMPLICATION
 Infections.
 Being in the hospital and lying down for a long time prone to
infections, such as pneumonia.
 Being on a ventilator higher risk for infections.
 Pneumothorax.
 condition in which air or gas collects in the space around the lungs,
which can cause one or both lungs to collapse.
 The pressure of the air from a ventilator can cause this condition.
Leaks of air through holes in the lungs are caused by pressure from
the breathing machine that is needed to be sure the patient gets
enough air, and from the very stiff lungs. Air from the injured lungs
may enter the space between the lungs and the lining around the
lungs (the pleura)
 Air may also enter the space between the membranes that line the
abdomen (pneumoperitoneum) or the soft tissue under the skin
(subcutaneous emphysema)
 Lung scarring(Pulmonary fibrosis)
ARDS causes the lungs to become stiff (scarred) and makes it hard for
them to expand and fill with air.
Scarring and thickening of the tissue between the air sacs (interstitium)
can occur within a few weeks of the onset of ARDS. This stiffens your
lungs, making it even more difficult for oxygen to flow from the air
sacs into your bloodstream.
Being on a ventilator also can cause lung scarring.
 Blood clots.
Lying down for long periods can cause blood clots to form in your body.
A blood clot that forms in a vein deep is called a deep vein thrombosis.
This type of blood clot can break off, travel through the bloodstream
to the lungs, and block blood flow. This is called pulmonary
embolism.
tracheal injury/stenosis (result of intubation and/or
irritation by endotracheal tube.
Nutritional: malnutrition (catabolic state), electrolyte
deficiency.
Muscle wasting and weakness. use a ventilator for
longer than a week, it can begin weakening the muscles
because of nutritional deficiency.
Memory, cognitive and emotional problems. Sedatives
and low levels of oxygen in the blood can lead to memory
loss and cognitive problems after ARDS. In some cases, the
effects may lessen over time, but in others, the damage
may be permanent
Depression
 Most ARDS survivors also report going through a
period of depression, which for some people is quite
severe.