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Acute Respiratory Distress Syndrome

ARDS develops when the capillary membrane in the lungs becomes damaged, allowing fluid to leak into the alveoli sacs. This impairs gas exchange, causing hypoxemia. ARDS progresses through exudative, proliferative, and fibrotic phases. In the exudative phase, pulmonary edema and collapse of alveoli develop within 24 hours. A hyaline membrane forms, further impairing gas exchange. Most ARDS patients require mechanical ventilation with PEEP to maintain respiratory function as the condition causes refractory hypoxemia and decreased lung compliance.
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0% found this document useful (0 votes)
85 views9 pages

Acute Respiratory Distress Syndrome

ARDS develops when the capillary membrane in the lungs becomes damaged, allowing fluid to leak into the alveoli sacs. This impairs gas exchange, causing hypoxemia. ARDS progresses through exudative, proliferative, and fibrotic phases. In the exudative phase, pulmonary edema and collapse of alveoli develop within 24 hours. A hyaline membrane forms, further impairing gas exchange. Most ARDS patients require mechanical ventilation with PEEP to maintain respiratory function as the condition causes refractory hypoxemia and decreased lung compliance.
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ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) Quick Facts about Acute Respiratory Distress

Syndrome (ARDS)
What is ARDS (acute respiratory distress
syndrome)? It’s a type of respiratory failure that  It has a fast onset!
occurs when the capillary membrane that surrounds
 It tends to occur in people who are already sick
the alveoli sac becomes damaged, which causes fluid
(hospitalized) and develops as a complication.
to leak into the alveoli sac.
For example, a patient who has experienced
Result? Impaired gas exchange! Gas exchange severe burns is at risk for ARDS due to the
doesn’t occur properly due to many reasons, such as: systemic inflammation present in the body.
fluid in the alveoli sac, collapsed alveoli sacs, and a
 ARDS has a high mortality rate!
decrease in lung compliance (hence the lungs are
becoming less elastic….”stiff”). What can cause the capillary membrane to become
more permeable and leak fluid? Usually events that
This will lead to oxygen not being able to cross the
lead to major systemic inflammation in the body,
alveolar capillary membrane to go back in the blood
which can be indirectly damage the capillary
to oxygenate it, which will result in hypoxemia. In
membrane or directly damage the capillary
turn, the organs of the body will suffer due to this
membrane.
and death can occur if treatment does not happen. In
majority cases of ARDS, the patient will need Indirect vs. Direct Injury to the Capillary Membrane
respiratory assistance via a ventilator with PEEP Indirect (source isn’t the lungs): the capillary
(discussed in detail below). membrane is INDIRECTLY damaged. There is a
systemic inflammatory response system (SIRS) by the
immune system.
Common Causes: What happens during this phase?
 *Sepsis (most common and there is a very poor  Damage to the capillary membrane that leads
prognosis if the patient has a gram-negative to pulmonary edema. This causes the leaking
bacteria) of fluid, proteins, and other substances into
the interstitium and then into the alveoli sac. It
 Burns
is very important to note this fluid contains a
 Blood transfusion (multiple) LOT of protein. Significance? Remember
 Inflammation of the pancreas (pancreatitis) proteins regulate water pressure, oncotic
pressure! So, if the fluid is high in protein it’s
 Drug overdose going to draw even MORE fluid into the
Direct (source is the lungs)….capillary membrane is interstitium and then the alveoli sac.
DIRECTLY damaged  Cells that produce surfactant become
 Pneumonia overwhelmed and damaged.

 Aspiration  Role of surfactant: decreases surface


tension in the lungs. In other words, the
 Inhaling a toxic substance
alveoli sacs stay stable. Therefore, when
 Significant drowning event a person exhales the sac
does NOT collapse. 
 Embolism
 A decrease in surfactant creates
How it happens? Pathophysiology: Phases (varies on
an unpredictable alveoli sac that
severity…this is worst case scenario)
can easily collapse. This leads to:
Exudative Phase: occurs about 24 hours after injury
 ATELETASIS will occur
to the lung (directly or indirectly)
(collapse of the lung tissue)
 To make matters worse: a Early: Due to all this the patient will experience an
membrane that is made up of increase in breathing (still have hypoxemia). WHY?
dead cells and other substances The body is trying to increase the oxygen level, but it
start to collect on the alveoli. This won’t be able to! This will cause the patient to blow
is called a hyaline membrane. This off too much carbon dioxide (CO2 can still cross the
membrane will continue to membrane but O2 can’t)….respiratory ALKALOSIS will
develop in the next phase and will develop BUT in the late phase (as the patient
cause the lungs to become LESS progresses to the 2nd and 3rd phases (late), carbon
elastic and can further impair gas dioxide levels start to rise. This is because the hyaline
exchange! membrane continues to develop leading to carbon
dioxide not being able to cross over to be exhaled,
End Result? With all the fluid in the alveoli sac
and the patient will no longer be able to maintain
(pulmonary edema), development of a hyaline
breathing due to weak respiratory
membrane, collapsing of the sacs, and decreased
muscles. Respiratory acidosis will start to develop
surfactant = inadequate ventilation where alveoli
later on.
sacs are NOT getting enough air (leading to V/Q
mismatch) AND a hallmark sign and Proliferative Phase: occurs about 14 days after the
symptom: REFRACTORY HYPOXEMIA injury (grow or reproduce new cells quickly)
Refractory hypoxemia is where the patient will  repair structures, fluid in the sac is reabsorbed,
maintain a low blood oxygen level even though they but lung tissue becomes very dense and
are receiving high amounts of oxygen! fibrous….lung compliance and hypoxemia
becomes even worse
Fibrotic Phase: occurs about 3 weeks after
injury….major fibrosis of the lung tissue, decreases
lung compliance and hypoxemia with dead space Then as time goes on:
filling the lungs.
 Symptoms of full respiratory failure:
Patients who enter the fibrotic phase will have major tachypnea, difficulty breathing, major
lung damage and poor recovery. hypoxemia even though receiving a high about
of oxygen (refractory hypoxemia), cyanosis,
Pathophysiology of ARDS in a Nutshell
low oxygen saturation, mental status change
Atelectasis (alveolar sac fill with fluid and collapse… (tired, confused), tachycardia, chest
pulmonary edeam) retractions, decrease lung compliance, lung
Refractory Hypoxemia sound: crackles throughout, low Pao2, high
PaCo2 x-ray with white-out of bilateral lung
Decrease in lung compliance (lung aren’t as elastic or infiltrates.
stretchable….hyaline membrane develops)
Nursing Interventions for ARDS (acute
Surfactant cell damaged (decrease in surfactant respiratory distress syndrome)
production)
Maintain airway/respiratory function:
Signs and Symptoms of ARDS
Most patients with ARDS will need: mechanical
In the very early phase: sign and symptoms are hard ventilation with PEEP (positive end-expiratory
to detect. At first the fluid is leaking in the interstitum pressure)
so lung sounds may be normal or random a crackle
here or there. But as it progresses the patient will  The patient will need high amounts of PEEP
have difficulty breathing and be “air hunger”. There because of the collapsed sacs, stiffening of the
will be an increased respiratory rate, low oxygen in lung, and pulmonary edema. Usually the
the blood and respiratory alkalosis. pressure is anywhere from 10 to 20 cm of
water. This high amount of pressure will open
the sacs, improve gas exchange, and help keep  Help with perfusion and ventilation
them clear of fluid. (helping with correcting the V/Q
mismatch)
 Nurse: high PEEP can cause issues
with intrathoracic pressure and  Help move secretions from other areas
decrease cardiac output (watch out for a that were fluid filled and couldn’t move
low blood pressure) along with in the supine position
hyperinflation of the lungs (possible
 Help improve atelectasis.
pneumothorax or subq emphysema…this
is where air escapes into skin from a lung How does the MD know if this is pulmonary
leaking air) edema caused by a cardiac issue like heart
failure or due to a leaking capillary
Monitoring ABGs
membrane? A pulmonary artery wedge
Positioning to help with respiratory function: pressure can help with that!
Prone Positioning: turning the patient from  This is where a pulmonary catheter with a
supine to prone (putting the patient on their balloon is inserted into the pulmonary arterial
belly) branch
 This helps improve oxygen levels without  If the reading is less than 18 mmHg it
actually giving the patient a high concentration indicates ARDS, but if it’s greater than
of oxygen! Remember in this position the heart this number it indicates a cardiac
will shift forward and not compress the back of problem.
the lungs and it will help drain areas of the
Assessing other systems of the body to make
lungs that normally can’t be drained in the
sure they are getting enough oxygen: mental
supine position. So, this will:
status, urine output, heart (blood pressure and QUIZ
cardiac output with PEEP)
Preventing complications: pressure injury, 1.) You're providing care to a patient who is being
blood clots, infection related to ventilator, treated for aspiration pneumonia. The patient is on a
nutrition, pneumothorax 100% non-rebreather mask. Which finding below is a
HALLMARK sign and symptom that the patient is
Administering drugs: corticosteroids (help with developing acute respiratory distress syndrome
inflammation), antibiotics (preventing and (ARDS)?*
treating infection), fluids colloids or crystalloids A. The patient is experiencing bradypnea.
solutions if cardiac output decreased along
B. The patient is tired and confused.
with drugs like that have an inotropic effect
(helps with heart muscle contraction), GI drugs C. The patient's PaO2 remains at 45 mmHg.
for stress ulcers D. The patient's blood pressure is 180/96.
2. You're teaching a class on critical care concepts to a
group of new nurses. You're discussing the topic of
acute respiratory distress syndrome (ARDS). At the
beginning of the lecture, you assess the new nurses
understanding about this condition. Which statement
by a new nurse demonstrates he understands the
condition?*
A. "This condition develops because the exocrine
glands start to work incorrectly leading to thick,
copious mucous to collect in the alveoli sacs."
B. "ARDS is a pulmonary disease that gradually causes
chronic obstruction of airflow from the lungs."
C. "Acute respiratory distress syndrome occurs due to C. white-out infiltrates bilaterally
the collapsing of a lung because air has accumulated in
D. normal chest x-ray
the pleural space."
5. You're providing care to a patient who was just
D. "This condition develops because alveolar capillary
transferred to your unit for the treatment of ARDS.
membrane permeability has changed leading to fluid
The patient is in the exudative phase. The patient is
collecting in the alveoli sacs."
ordered arterial blood gases. The results are back.
3. During the exudative phase of acute respiratory Which results are expected during this early phase of
distress syndrome (ARDS), the patient's lung cells that acute respiratory distress syndrome that correlates
produce surfactant have become damaged. As the with this diagnosis?*
nurse you know this will lead to?*
A. PaO2 40, pH 7.59, PaCO2 30, HCO3 23
A. bronchoconstriction
B. PaO2 85, pH 7.42, PaCO2 37, HCO3 26
B. atelectasis
C. PaO2 50, pH 7.20, PaCO2 48, HCO3 29
C. upper airway blockage
D. PaO2 55, pH 7.26, PaCO2 58, HCO3 19
D. pulmonary edema
6. Which patient below is at MOST risk for developing
4. A patient has been hospitalized in the ICU for a ARDS and has the worst prognosis?*
near drowning event. The patient's respiratory
A. A 52-year-old male patient with a pneumothorax.
function has been deteriorating over the last 24
hours. The physician suspects acute respiratory B. A 48-year-old male being treated for diabetic
distress syndrome. A STAT chest x-ray is ordered. ketoacidosis.
What finding on the chest x-ray is indicative of ARDS?
C. A 69-year-old female with sepsis caused by a gram-
*
negative bacterial infection.
A. infiltrates only on the upper lobes
D. A 30-year-old female with cystic fibrosis.
B. enlargement of the heart with bilateral lower lobe
7. As the nurse you know that acute respiratory
infiltrates
distress syndrome (ARDS) can be caused by direct or
indirect lung injury. Select below all the INDIRECT this condition. Which findings below indicate this
causes of ARDS:* type of positioning was beneficial for your patient
with ARDS?*
A. Drowning
A. Improvement in lung sounds
B. Aspiration
B. Development of a V/Q mismatch
C. Sepsis
C. PaO2 increased from 59 mmHg to 82 mmHg
D. Blood transfusion
D. PEEP needs to be titrated to 15 mmHg of water
E. Pneumonia
10. A patient is experiencing respiratory failure due to
F. Pancreatitis
pulmonary edema. The physician suspects ARDS but
wants to rule out a cardiac cause. A pulmonary artery
wedge pressure is obtained. As the nurse you know
that what measurement reading obtained indicates
8. A patient is on mechanical ventilation with PEEP that this type of respiratory failure is NOT cardiac
(positive end-expiratory pressure). Which finding related?*
below indicates the patient is developing a
A. >25 mmHg
complication related to their therapy and requires
immediate treatment?* B. <10 mmHg

A. HCO3 26 mmHg C. >50 mmHg

B. Blood pressure 70/45 D. <18 mmHg

C. PaO2 80 mmHg 11. You’re precepting a nursing student who is


assisting you care for a patient on mechanical
D. PaCO2 38 mmHg
ventilation with PEEP for treatment of ARDS. The
9. You are caring for a patient with acute respiratory student asks you why the PEEP setting is at 10 mmHg.
distress syndrome. As the nurse you know that prone Your response is:*
positioning can be beneficial for some patients with
A. "This pressure setting assists the patient with
breathing in and out and helps improve air flow."
B. "This pressure setting will help prevent a decrease
in cardiac output and hyperinflation of the lungs."
C. "This pressure setting helps prevent fluid from filling
the alveoli sacs."
D. "This pressure setting helps open the alveoli sacs
that are collapsed during exhalation."

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