Acute Respiratory Distress Syndrome

Prof. Manal Ismail

Head of Critical Care and Emergency Nursing
 Outlines
• Introduction
• Definition of acute respiratory distress syndrome
• Criteria of acute respiratory distress syndrome
• Causes of acute respiratory distress syndrome
• Pathophysiology of acute respiratory distress syndrome
• Stages of acute respiratory distress syndrome
• Clinical features of acute respiratory distress syndrome
• Medical and Nursing management of acute respiratory
distress syndrome
 Acute Respiratory Distress
Syndrome
Acute respiratory distress syndrome (ARDS) is a

breathing failure that can occur in critically ill

persons with underlying illnesses. It is not a

specific disease. Instead, it is a life-threatening

condition that occurs when there is severe fluid

buildup in both lungs

Acute Respiratory Distress Syndrome
•The fluid buildup prevents the lungs from

working properly ( allowing the transfer of

oxygen from the air into the body and

carbon dioxide out of the body into the air).

 Definition

ARDS is defined as an acute condition

characterized by bilateral pulmonary infiltrates
and severe hypoxemia in the absence of evidence
for cardiogenic pulmonary edema cellular
function.
 Criteria of ARDS

• According to the Berlin definition of ARDS, there

are three distinct categories of ARDS (mild,

moderate, and severe) based on the severity of

hypoxemia. The criteria of ARDS is as follows:

 Criteria of ARDS
Timing: within 1 week of known clinical insult or new
or worsening respiratory symptoms.
Chest imaging: bilateral opacities not fully explained
by effusions, lobar/lung collapse, or nodules.
Origin of edema: respiratory failure not fully
explained by heart failure or fluid overload; need
objective assessment to exclude hydrostatic edema
if no risk factor present.
 Criteria of ARDS
Oxygenation

ARDS Severity PaO2/FiO2* Mortality**

Mild 200 – 300 27%

Moderate 100 – 200 32%

Severe < 100 45%

 Causes of ARDS
A. Direct lung injury (pulmonary ARDS):
Direct injuries are those in which the lung epithelium
sustains a direct insult as
Aspiration of gastric content or other toxic substance.
Infectious pneumonia.
Trauma: lung contusion, penetrating chest injury.
 Near drowning.
Fat embolism.
Oxygen toxicity
 Causes of ARDS
B. Indirect injury (non pulmonary ARDS)
Indirect injuries are those in which the insult occurs
elsewhere in the body and mediators are transmitted
via the bloodstream to the lungs as:
- Sepsis especially gram negative.
-Acute pancreatitis
-Multiple traumas, burns.
-Shock states.
-Multiple blood transfusions.
- Cardiopulmonary bypass.
- Narcotic drugs abuse.
- Disseminated intravascular coagulation (DIC).
 Pathophysiology of ARDS

• Acute respiratory distress syndrome (ARDS): is a life-

threatening condition that causes lung swelling and

fluid build up in the air sacs.

 Pathophysiology of ARDS
• The fluid buildup also makes the lungs heavy and stiff,

and the lungs' ability to expand is severely decreased.

Blood concentration of oxygen (Pa02) can remain

dangerously low in spite of supplemental oxygen

delivered by a mechanical ventilator through the

endotracheal tube.
 Pathophysiology of ARDS

ARDS occurs when the permeability of the alveolar-

capillary membrane increases leading to leak and
accumulation of protein-rich fluid in interstitial and intra
alveolar spaces.

Decrease Surfactant activity and alveoli collapse and resist

re-expansion. Eventually the interstitium, alveoli, and
terminal airways fill with fluid, blood, and protein.
 Pathophysiology of ARDS
• Gas exchange no longer occurs, resulting in edema,
hemorrhage, and focal atelectasis.

• V/Q mismatching occurs as lung areas are perfused but not

ventilated.

• Pa02 falls and there is an increase in shunt fraction (amount of

blood returning to the arterial system without passing through
ventilated lung) and physiologic dead space.

• Fatigue occurs as increase WOB, and respiratory failure

ensues
 Phases of ARDS
(Pathogenesis of ARDS)

Phase 1: injury reduces the blood flow to the

lungs, platelets aggregates and release histamine
(H), serotonin(S) and bradykinine (B)
 Phases of ARDS
(Pathogenesis of ARDS)

Phase 2: those substances especially histamine

inflame and damage the alveolar capillary membrane
increasing capillary permeability of fluid then shift
into interstitial space.
 Phases of ARDS
(Pathogenesis of ARDS)

Phase 3: capillary permeability increase protein and

fluid leak out, increasing interstitial osmotic pressure
and causing pulmonary edema
 Phases of ARDS
(Pathogenesis of ARDS)

Phase 4: decrease blood flow and fluids in alveoli,

damage surfactant and impair cell ability to produce
more as result alveoli collapse, impending gas
exchange and decrease lung compliance.
 Phases of ARDS
(Pathogenesis of ARDS)

Phase 5: sufficient oxygen can not across the alveolar

capillary membrane but CO2 can and is lost with
every exhalation, O2 and CO2 level decreased in the
blood.
 Phases of ARDS
(Pathogenesis of ARDS)

Phase 6: pulmonary edema worsens,

inflammation leads to fibrosis and gas exchange
is further impeded.
 Stages of ARDS

ARDS has generally been characterized into three

stages. In full-blown cases, these three stages occurs

over a period of several weeks to several months.

 Stages of ARDS
1. Exudative stage: the mediators cause injury to the
pulmonary capillaries → increased capillary
membrane permeability → leakage of fluid(filled
with protein, blood cells, fibrin, and activated
cellular and humoral mediators )in the alveoli →
entered the air spaces from the alveolar capillaries.

• The exudative phase unfolds over the first 2 to 4 days

after onset of lung injury.
 Stages of ARDS

2. Fibroproliferative: (or proliferative) stage

 Connective tissue and other structural elements in the
lungs proliferate in response to the initial injury.
Cellular granulation and collagen deposition occur
within the alveolar-capillary membrane.
 Stages of ARDS
2. Fibroproliferative: (or proliferative) stage
The alveoli become enlarged and irregularly shaped
(fibrotic), and the pulmonary capillaries become
scarred. → stiffening of the lungs, increasing
pulmonary hypertension, and continued hypoxemia

There is a danger of pneumonia sepsis and rupture

of the lungs causing leakage of air into surrounding
areas.
 Stages of ARDS
3.Resolution and Recovery
During this stage, the lung reorganizes and recovers. structural and
vascular remodeling take place to re-establish the alveolar-capillary
membrane.
The intra- alveolar fluid is transported out of the alveolus into the
interstitium.
Lung function may continue to improve over several weeks to
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 different levels of pulmonary recovery
amongest individuals who suffer from ARDS.
 Clinical features of ARDS

Initially the patient with ARDS may be seen with a

variety of clinical manifestations, depending on the
precipitating event. As the disorder progresses, the
patient’s signs and symptoms can be associated with
the phase of ARDS that he or she is experiencing.
 Clinical features of ARDS

• During the exudative phase: tachypnea,

restlessness, apprehension, and moderate increase in
accessory muscle use.

• During the fibroproliferative phase: the patient’s

signs and symptoms progress to agitation, dyspnea,
fatigue, excessive accessory muscle use, and fine
crackles as respiratory failure develops.
 Laboratory Studies

Arterial blood-gas analysis reveals

• a low PaO2, despite increases in supplemental
oxygen administration (refractory hypoxemia).
• Initially the PaCO2 is low as a result of hyper-
ventilation, but eventually the PaCO2 increases as
the patient fatigues.
• The pH is high initially but decreases as respiratory
acidosis develops.
 Chest x-ray film

• Initially may be normal because changes in the lungs do

not become evident for up to 24 hours.

• As the pulmonary edema becomes apparent, diffuse,

patchy interstitial and alveolar infiltrates appear.

• This progresses to multifocal consolidation of the lungs,

which appears as a “whiteout” on the chest x-ray film.
 Medical management of ARDS

• No specific therapy for ARDS exists, treatment of the

underlying condition is essential
• Mechanical ventilation with low tidal volume
ventilation
• Because infection is often the underlying cause of
ARDS: careful assessment of the patient for infected
sites and appropriate antibiotic therapy are essential
• Promoting gas exchange
• Oxygen is administered at the lowest level possible to
support tissue oxygenation
• Administer bronchodilators and mucolytics.
• Preventing complications.
 Nursing diagnosis of ARDS

• Impaired Gas Exchange related to ventilation/perfusion

mismatching or intrapulmonary shunting

• Decreased Cardiac Output related to alterations in preload

• Imbalanced Nutrition( Less Than Body Requirements) related to

lack of exogenous nutrients or increased metabolic demand

• Risk for Infection

 Nursing management of ARDS
A. Oxygenation and ventilation
• Auscultate breath sounds every 2 to 4 hs and as required.
• Suction endotracheal airway when appropriate.
• Monitor airway pressures every 2 hours.
• Turn side-to-side every 2 hours.
• Perform chest physiotherapy every 4 hours, if tolerated
• Consider prone positioning.
• Monitor pulse oximetry and end-tidal carbon dioxide.
• Monitor arterial blood gases as indicated by changes in
noninvasive parameters.
 B. Circulation/Perfusion
• Assess hemodynamic effects of initiation of MV
(decreased venous return and cardiac output).
• Monitor ECG for dysrhythmias related to hypoxemia.
• Assess effects of ventilator setting changes on cardiac
output and oxygen delivery.
• Administer intravascular volume to maintain preload.
• Monitor vital signs every 1 to 2 hours.
• Monitor pulmonary artery pressures every hour
• Administer red blood cells and colloid infusion as ordered
to increase oxygen delivery
 C. Fluids/Electrolytes
• Monitor hydration status to reduce viscosity of lung
secretions.
• Monitor intake and output.
• Administer fluids and diuretics to maintain intravascular
volume and renal function.
• Replace electrolytes as ordered.
• Monitor blood urea nitrogen (BUN), and creatinine as
required.
 D. Mobility/Safety

• Initiate deep venous thrombosis (DVT) prophylaxis.

• Reposition frequently.
• Consult physiotherapist.
• Conduct range-of-motion and strengthening exercises
when able.
• Use strict aseptic technique during procedures, and
monitor others.
• Change chest tube and other dressings and invasive
catheters.
• Culture blood and other fluids and line tips when they are
changed
 References

• Aitken, L., Marshall, A., & Chaboyer, W. (2016). ACCCN's

Critical Care Nursing. Elsevier Health Sciences.

• Matthay, M. A., Zemans, R. L., Zimmerman, G. A., Arabi, Y.

M., Beitler, J. R., Mercat, A., ... & Calfee, C. S. (2019). Acute
respiratory distress syndrome. Nature Reviews Disease
Primers, 5(1), 18.

• Morton, P. G.& Fontaine, D.K.(2018). Critical Care Nursing A

Holistic Approach (11th edition).Walters, Iipincotin.357