SIGNS AND SYMPTOMS RATIONALE

1. Tachypnea Due to impaired gas exchange, the body

tissue will have insufficient oxygen, as a
response it will attempt to aid the body
system by breathing faster to inspire
more oxygen.
2. Tachycardia When the alveoli collapse, the oxygen
won’t be able to diffuse in the
bloodstream leading insufficient oxygen in
the tissue, that’s when the heart pumps
rapidly to speed up the circulation as a
compensation for lack of oxygen in the
tissues
3. Dyspnea As the disease progresses, fibrotic tissue
will form in the pulmonary causing the
alveolar wall to become stiff and thick
therefore decreasing compliance and
impairing elasticity leading to shortness of
breath
4. Crackles Due to the infiltration of inflammatory
cells, the alveolar wall will be impaired
causing an increasing permeability and
allowing protein-rich fluids to enter the
alveoli and interstitium of the lung.
Crackles is heard upon auscultation.
5. Hypoxemia As the alveoli collapse, gas exchange will
be impaired causing retention of CO2 and
deprivation of O2
6. Cough It is a body’s response when something
irritates the throat or airways, when the
cell wall of alveoli is damaged its debris
will be engulfed by the pulmonary
macrophages out from the lungs causing
a cough mechanism.
7. Nail clubbing Clubbing occurs when there is an
increased fluid pooled at the ends of soft
tissue in the fingers. Though the exact
reason for this is unknown, clubbing is
directly associated with insufficient
oxygen in the blood.
8. Cyanosis As the alveoli collapse, gas exchange will
be impaired causing retention of CO2 and
deprivation of O2 resulting to bluish
discoloration of the fingers or mucous
membrane
b. Symptomatology
c. ANATOMY AND PHYSIOLOGY OF THE ALVEOLI

 Alveoli
- The functional unit of
the lungs, it
responsible for
diffusion of oxygen and
carbon dioxide in the
blood

 Type I alveolar cell

- The cell in the alveoli
that processes gas
exchange

 Type II alveolar cell

- A type of alveolar cell
that is responsible for
the synthesis and
release of surfactant

 Surfactant
- It is responsible for reducing the surface tension therefore keeping the alveoli
open

 Pulmonary Interstitium
- It provides fibers to support the intralobular air-exchanging portion of the lung
- Fibers - is responsible for the property of passive tissue recoil, which is
necessary for expiration and proper ventilation.

 Alveolar capillary membrane

- It is a membrane of the lungs where gas exchange between blood and
alveolar air occur

 Neutrophils
- In the airways, neutrophils fulfill an important role such as maintaining sterility.
And as a major effector cell in innate immunity, neutrophils act as a double-
edged sword.

 Alveolar Macrophages
- Alveolar macrophages are critical for tissue homeostasis, host defense,
clearance of surfactant and cell debris, pathogen recognition, initiation and
resolution of lung inflammation, and repair of damaged tissue
 Fibroblast
- Lung fibroblasts are crucial for maintaining the integrity of the alveolar
structure by proliferating and repairing injured areas

 Bronchial epithelium
- It is composed club cells that can help the regeneration and replacement of
injured pneumocytes

 Compliance
- Is a measure of lung
expandability

 Elasticity
- Is responsible for the passive
recoil of the lungs to exhale
the air out.

 Tnf, IL-1 Cytokines

- are cytokines required for
activating the innate immune
response

 Chemokines
- are a family of
chemoattractant
cytokines which play a vital
role in cell migration through venules from blood into tissue and vice versa
d. Disease Process

Predisposing Factors Precipitating Factors

1. Genetics 1.Sepsis (ILI)
2.Aspiration (DLI)
3.Pneumonia (DLI)
4.Severe Trauma (ILI)
5.Massive Transfusion
6.Transfusion-related Acute lung
injury
7.Lung and hematopoietic stem cell
transplantation
8.Drugs and Alcohol
9.Near drowning
10. Pancreatitis
11. Smoke Inhalation

Release of cytokines
TNF, IL -1

Activates the innate immune

response, mediating the recruitment
and adherence of circulating
phagocytic cells

A
 Migration of Neutrophils in Exudative
the lungs Phase

Pulmonary endothelial
damage and pulmonary
endothelial activation

Activated endothelial cells

expresses adhesion
molecules, and chemokines

Further attracts phagocytic

cell neutrophils into the alveoli
and interstitium
 A

Neutrophils degranulate and release

inflammatory mediators in the alveoli
1. Proteases
2. Reactive oxygen species
3. Cytokines
4. Macrophage migration
inhibitory factor

Increased recruitment &

adhesion of neutrophils

More endothelial Pneumocyte damage

damage Type I, Type II

Pulmonary capillary Type I – less gas exchange

leak
Type II – less surfactant

S/S: Fluid enters the alveoli

causing pulmonary Alveolar Inspissated protein,
- Crackles Collapse fluid rich edema, cell
upon edema
debris organize
auscultation
- Pulmonary
bilateral
infiltration
Impairs Gas
exchange Hyaline membrane
formation
Reduced
S/S: Ventilation with
normal perfusion
- Hypoxemia This will provide
- Cyanosis structural framework
- Tachypnea
- Tachycardia
for future fibrosis

7 days and
beyond, the body
Proliferative attempts to heal
Phase the damage B
B
 Macrophages removes
S/S: cellular debris and
releases fibro genetic
- Cough
cytokines such as TGF
beta & PDGF

Fibroblast growth
Collagen deposition
Fibrotic
Fibrosis of Alveolar Phase
S/S:
wall - ↓ Compliance
- ↑ Elasticity Fibroblast activity
- Dyspnea leads to deposition
- Tachypnea
of collagen in alveoli
Bronchiolar stem Uninjured capillary and alveolar
cell proliferate to endothelium capillaries
replace proliferate to restore
pneumocyte endothelium

Pulmonary Intrapulmonary
Fibrosis Atelectasis shunting
Increased useful Functional
surface area for epithelium is able
gas exchange to absorb fluid
back into Impairment of gas
circulation exchange
S/S:
- Increased PaO2 & SpO2
- Decreased CO2
(Impaired Oxygenation)
Constricting the
- Clearing of Chest radio graph
endothelium

Results in Increased
greater pressure in Refractory
resistance of lungs Pulmonary Hypoxemia
blood Hypertension S/S:
- Cyanosis
COMPLICATION
- Nail Clubbing
ACUTE
Increase work from Eventually thickens RESPIRATORY
the rise to push and enlarge the DISTRESS
blood through right side of the SYNDROME
pulmonary artery heart

Right sided heart C

failure
 IF TREATED C IF NOT TREATED

4 Key Criteria for the diagnosis:

As impairment The underlying
- Acute Onset progresses, severe condition that
- Diffuse bilateral pulmonary infiltrates hypoxemia triggered ARDS
- PaO2/FiO2 ≤ 200mg develops becomes severe
- Absence of elevated left atrial pressure throughout the
(Pulmonary capillary wedge pressure ≤18 mmHg body
Diagnostic tests:
Severe sepsis
- CBC develops
- Liver function test Deprivation of Oxygen in
- Renal function test the tissue and major
- ABG organs
- Bronchoscopy
Decrease in blood
- BNP
pressure,
- Chest x-ray Resulting to Organ weakening of the
- Echocardiography dysfunction heart
- CT SCAN
Medical management:
- Aggressive, supportive care must be provided Resulting to Organ
 Endotracheal intubation dysfunction
 Mechanical Ventilation
 Adequate fluid volume and nutritional support Failing multiple organs
- ABG monitoring including lungs,
- Pulse oximetry monitoring kidneys and liver
- Provide ventilator PEEP
Pharmacologic Therapy
- Neuromuscular block agents, sedatives, and
Septic shock
analgesics may be use.
- Inhalation of nitric oxide
Nutritional Therapy
- Patient with ARDS require 35 to 45kcal/kg/day DEATH
- Enteral feeding is the first consideration however
parenteral nutrition may also be required
- Limit the intake of carbohydrates if patient is able
to eat orally
Nursing management
- Frequent assessment of patient status
- Proper positioning or turning the patient every 2
hours
- Prone position can improve oxygenation
- Closely monitor patient for deterioration in
oxygenation with changes in position
- Allow the patient to rest to limit oxygen PROGNOSIS:
consumption Fair
B. NARRATIVE
Acute Respiratory Distress Syndrome (ARDS) is a disease that forms from an acute
lung injury to a severe form, life-threatening ARDS. Acute lung injury could be direct or
indirect. Any insult to the lungs that causes TFN and IL-1 cytokines release can be the
root of ARDS development. When TFN and IL-1 cytokines are released, it will trigger a
migration of neutrophils in the lungs damaging the pulmonary endothelial wall and at the
same time activating the pulmonary endothelial cell, which then expresses and
adhesion of molecules and chemokines. Chemokines play a vital role in cell migration;
this mechanism further attracts neutrophils into the alveoli and interstitium. Neutrophils
will release inflammatory mediators that increase the recruitment and adhesion of
phagocytic cells. From this point, neutrophils will further damage the endothelial cell
lining, causing a capillary leak and pulmonary edema. Also, neutrophils will disrupt the
lining of pneumocytes, resulting in less surfactant and less gas exchange. The fluid-rich
edema, inspissated protein, and cell debris will then organize, forming a hyaline
membrane that will be a structure for the formation of future fibrosis. As surfactant
decreases and fluid in the alveoli increases, the alveolar system will collapse, worsening
the impairment of gas exchange and reducing ventilation while having normal perfusion.
After seven days or more, the body will attempt to heal the damage, and macrophages
will remove cellular debris and releases fibrogenic cytokines that facilitate fibroblast
growth and collagen deposition, causing fibrosis in the alveolar wall. Bronchial stem
cells will proliferate to replace damaged pneumocytes, thus increasing functional
surface area for gas exchange. Also, intact capillary endothelium will proliferate to
restore the loss of endothelium, and functional endothelium will now absorb the fluid
back into the circulation, decreasing pulmonary edema. In rare cases, fibroblast activity
leads to collagen deposition in the alveoli and alveolar capillaries, causing pulmonary
fibrosis (which could develop into right-sided heart failure), atelectasis, and pulmonary
shunting, further disrupting gas exchange and increases oxygen deprivation of the
tissue increases resulting refractory hypoxemia and ARDS.

To treat ARDS, the underlying cause must be treated first to stop the inflammatory
response that initiates ARDS. With proper management in terms of nursing, medical,
pharmacological, and nutritional prognosis can be fair. Since ARDS can cause
permanent scarring in the pulmonary tissue depending on the severity of the disease, it
may cause life-threatening concern to the person or no harm at all. But if ARDS is left
untreated, severe sepsis may develop, causing multiple organ dysfunction, septic
shock, and even death.