Presentation is loading. Please wait.

Presentation is loading. Please wait.


Similar presentations

Presentation on theme: "RESPIRATORY FAILURE AND ACUTE RESPIRATORY DISTRESS SYNDROME Fadi J. Zaben RN MSN IMET2000, Ramallah."— Presentation transcript:



3 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.

4 Classification: Acute Respiratory Failure Chronic Respiratory Failure. Acute and Chronic Respiratory Failure.

5 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.

6 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.

7 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.

8 Pathophysiology and Etiology:

9 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.

10 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.

11 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.

12 Complications: Oxygen toxicity if prolonged high Fio2 required. Barotrauma from mechanical ventilation intervention

13 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)

14 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

15 :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.

16 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.


18 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.

19 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.

20 ……. 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.

21 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.

22 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.

23 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.

24 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.

25 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.

26 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.

27 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.

28 Nursing Interventions: Nursing Care is similar to patient with respiratory failure.


Similar presentations

Ads by Google