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RESPIRATORY FAILURE
AND
ACUTE RESPIRATORY DISTRESS SYNDROME
Fadi J. Zaben RN MSN
IMET2000, Ramallah
RESPIRATORY FAILURE
RESPIRATORY FAILURE:
• Respiratory failure is an alteration in the
function of the respiratory system.
• Partial pressure of arterial oxygen (Pao2) to
fall below 50 mm Hg (hypoxemia).
• And/or the partial pressure of arterial carbon
dioxide (Paco2) to rise above 50 mm Hg
(hypercapnia).
• Respiratory failure is classified as acute,
chronic, or combined acute and chronic.
Classification:
• Acute Respiratory Failure
• Chronic Respiratory Failure.
• Acute and Chronic Respiratory Failure.
Acute Respiratory Failure:
• Characterized by:
Hypoxemia (Pao2 less than 50 mm Hg).
Hypercapnia (Paco2 greater than 50 mm Hg).
Acidemia (pH less than 7.35).
• Occurs rapidly, usually in minutes to hours or
days.
Chronic Respiratory Failure:
• Characterized by:
Hypoxemia (decreased Pao2).
Hypercapnia (increased Paco2).
Normal pH (7.35 to 7.45).
• Occurs over a period of months to years
allows for activation of compensatory
mechanisms.
Acute and Chronic Respiratory Failure:
• Characterized by:
increase in the degree of hypoxemia or
hypercapnia in patients with preexisting chronic
respiratory failure.
• May occur after an acute upper respiratory
infection or pneumonia, or without obvious
cause.
• Extent of deterioration is best assessed by
comparing the patient's present ABG levels
with previous ABG levels.
Pathophysiology and Etiology:
Clinical Manifestations:
• Hypoxemia restlessness, agitation, dyspnea,
disorientation, confusion, delirium, loss of
consciousness.
• Hypercapnia headache, dizziness, and
confusion.
• Tachypnea initially; then when no longer able
to compensate, bradypnea.
• Accessory muscle use.
• Asynchronous respirations.
Diagnostic Evaluation:
• ABG analysis: show changes in Pao2, Paco2, and
pH from patient's normal; or Pao2 less than 50
mm Hg, Paco2 greater than 50 mm Hg, pH less
than 7.35.
• Pulse oximetry: decreasing Sao2.
• End tidal CO2 monitoring: elevated.
• Complete blood count, serum electrolytes,
chest X-ray, urinalysis, electrocardiogram (ECG),
blood and sputum cultures; to determine
underlying cause and patient's condition.
Management:
• Oxygen therapy to correct the hypoxemia.
• Chest physical therapy and hydration to
mobilize secretions.
• Bronchodilators and possibly corticosteroids
to reduce bronchospasm and inflammation.
• Diuretics for pulmonary congestion.
• Mechanical ventilation as indicated.
Noninvasive positive-pressure ventilation
using a face mask may be a successful option
for short-term support of ventilation.
Complications:
• Oxygen toxicity if prolonged high Fio2
required.
• Barotrauma from mechanical ventilation
intervention
Nursing Assessment:
• Note changes suggesting increased work of breathing
(tachypnea, diaphoresis, intercostal muscle retraction,
fatigue) or pulmonary edema.
• Assess breath sounds (diminished or absent sounds,
crackles, wheezing, rhonchi and crackles ).
• Assess level of consciousness (LOC) and ability to
tolerate increased work of breathing.
• Assess for signs of hypoxemia and hypercapnia.
• Analyze ABG and compare with previous values.
• Determine hemodynamic status (blood pressure,
cardiac output)
Nursing Diagnoses:
• Impaired Gas Exchange related to inadequate
respiratory center activity or chest wall
movement, airway obstruction, and/or fluid in
lungs
• Ineffective Airway Clearance related to
increased or tenacious secretions
:Nursing Interventions
• Improving Gas Exchange:
Administer antibiotics, cardiac medications, and
diuretics as ordered for underlying disorder.
Administer oxygen.
Monitor fluid balance by intake and output
measurement, urine specific gravity, daily weight to
detect presence of hypovolemia or hypervolemia.
Provide measures to prevent atelectasis and
promote chest expansion and secretion clearance,
as ordered (incentive spirometer, nebulization, head
of bed elevated 30 degrees, turn frequently, out of
bed).
Monitor ABG levels.
Patient Education and Health Maintenance:
Instruct patient with preexisting pulmonary
disease to seek early intervention for infections
to prevent acute respiratory failure.
Teach patient about medication regimen:
1. Proper technique for inhaler use.
2. Dosage and timing of medications.
3. Monitoring for adverse effects of corticosteroids:
weight gain due to fluid retention, polyuria and
polydipsia due to hyperglycemia, mood changes.
Acute Respiratory Distress Syndrome:
ARDS is a clinical syndrome also called
noncardiogenic pulmonary edema.
It is a life-threatening lung condition that
prevents enough oxygen from getting into the
blood.
It is severe hypoxemia and decreased
compliance of the lungs.
It leads to both oxygenation and ventilatory
failure.
Mortality is 50% to 60% but is improved with
early intervention.
Pathophysiology and Etiology:
• Pulmonary and/or nonpulmonary insult to the
alveolar-capillary membrane causing fluid
leakage into interstitial spaces.
• Ventilation-perfusion mismatch caused by
shunting of blood.
……. Continue
• Etiologies are numerous and can be
pulmonary or nonpulmonary. These include:
1) Pneumonia, sepsis, aspiration.
2) Shock (any cause), trauma.
3) Metabolic, hematologic, and immunologic
disorders.
4) Inhaled agents smoke, high concentration of
oxygen, corrosive substances.
5) Major surgery, fat or air embolism.
Clinical Manifestations:
Symptoms usually develop within 24 to 48
hours of the original injury or illness.
Severe dyspnea, use of accessory muscles.
Increasing requirements of oxygen therapy.
Hypoxemia refractory to supplemental oxygen
therapy.
Severe crackles and rhonchi heard on
auscultation.
Diagnostic Evaluation:
• The hallmark sign for ARDS is a shunt;
hypoxemia remains despite increasing oxygen
therapy.
• Decreased lung compliance; increasing
pressure required to ventilate patient on
mechanical ventilation.
• Chest X-ray exhibits bilateral infiltrates.
Treatment:
• The treatment for ARDS is aimed at symptom
management, but the underlying cause must be
treated or the ARDS will not resolve.
• Supportive measures will assist the patient while
the underlying cause is being treated.
• The underlying cause for ARDS must be
determined so appropriate treatment can be
initiated.
Continue………
• Ventilatory support and low oxygen therapy
concentration.
• Fluid management must be maintained.
• Medications are aimed at treating the
underlying cause.
• Corticosteroids are used infrequently due to
the controversy regarding benefits of usage.
• Adequate nutrition should be initiated early
and maintained.
Complications:
• Infections, such as pneumonia, sepsis.
• Respiratory complications, such as pulmonary
emboli, barotrauma, oxygen toxicity,
subcutaneous emphysema, or pulmonary
fibrosis.
• GI complications, such as stress ulcer, ileus.
• Cardiac complications, such as decreased
cardiac output and dysrhythmias.
• Renal failure, disseminated intravascular
coagulation.
Prognosis:
1. A third of people with ARDS die from the
disease.
2. Many people have permanent (usually mild)
lung damage.
3. Many people who survive ARDS have
memory loss or other quality-of-life problems
after they recover.
Prevention:
• The only way to prevent ARDS is to avoid those
diseases and harmful conditions that damage the
lung.
• For instance, the danger of aspirating stomach
contents into the lungs can be avoided by making
sure a patient does not eat shortly before
receiving general anesthesia.
• If a patient needs oxygen therapy, as low a level
as possible should be given.
• Any form of lung infection, or infection anywhere
in the body that gets into the blood, must be
treated promptly to avoid the lung injury that
causes ARDS.
Nursing Interventions:
Nursing Care is similar to patient with
respiratory failure.