Tuesday, February 3, 2009

PULMONARY EDEMA






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Pulmonary Edema



PULMONARY EDEMA

  • Pulmonary Edema is caused by an abnormal accumulation of fluid in the lung, in both the interstitial and alveolar spaces.
  1. Origin is most often cardiac: Pulmonary congestion occurs when the pulmonary vascular bed receives more blood from the right side of the heart (venous return) than the left side of the heart (cardiac output) can accommodate.
  2. Pulmonary edema results from severe impairment in the ability of the heart to maintain cardiac output, thereby causing an engorgement of the pulmonary vascular bed.
Assessment
  1. Risk factors/etiology.
    1. Hypertention
    2. Aortic valva problems, CHF.
    3. Cardiac myopathy.
    4. Overhydration.
  1. Clinical manifestations: hypoxia
    1. Problem may occur at night or in clients for whom bed rest has been prescribed. The supine position increases venous return and promotes reabsorption of edema from the legs, thus precipitating an increase in cardiac workload and an increase in circulating volume.
    2. Sudden onset of dyspnea.
    3. Severe anxiety, restlessness, irritability.
    4. Cool, moist skin.
    5. Tachycardia (S3, S4 gallop)’tachypnes.
    6. Jugular vein distention
    7. Severe coughing
    8. Noisy, wet respirations that do not clear with coughing.
    9. Frothy, blood-tinge sputum.
*GERIATRIC PRIOT|RITY: Pulmonary edema can occur very rapidly and become a medical emergency.
  1. Diagnostics.
    1. Clinical manifestations.
    2. Predisposing condition.
    3. BNP (B-type natriuretic peptide) levels measured to assess for CHF (<100 pg/ml rules out CHF).
Treatment
Condition demands immediate attention; medications are administered intravenously.
  1. O2 high in concentration.
  2. Sedation (morphine) to allow controlled ventilation: decreases preload/vasoconstriction, as well as decreasing anxiety and pain.
  3. Diuretics to reduce the myocardial workload.
  4. Dopamine to facilitate myocardial contractility.
  5. Medications to increase cardiac contractility and cardiac output
  6. Vasodilators to decrease afterload.
Nursing Intervention
*GOAL: To assess and decrease hypoxia
*GOAL: To improve ventilation.
  1. Place in high-Fowler’s position with the legs dependent.
  2. Administer high levels of O2.
  3. Evaluate level of hypoxia and dyspnea; may need endotracheal tube intubation and mechanical ventilation.
  4. I.V. sedatives/narcotics.
    1. To decrease anxiety and dyspnea and to decrease pressure in pulmonary capillary bed.
    2. Closely observe for respiratory depression.
*ALERT: Pulmonary edema is one of the few circumstances in which a client with respiratory distress may be given a narcotic. The fear of not being able to breath is so strong that the client cannot cooperate. When a sedative/narcotic is administered, the nurse must be ready to support ventilation if respirations become severely depressed.
  1. Administer bronchodilators and evaluate clieant’esponse and common side effects.
*GOAL: To reduce circulating volume and cardiac workload.
  1. Diuretics.
  2. Medications to decrease afterload and increase cardiac output.
  3. Carefully monitor all I.V. fluids and evaluate overall hydration status.
  4. Do not elevate the client’s legs because this will rapidly increase the venous return and the circulating volume.
*GOAL: To provide psychological support and decrease anxiety.
A. Approach client in a calm manner.
B. Explain procedures.
C. Administer sedatives.
D. Remain with the client in acute respiratory distress.
*GOAL: To prevent recurrence of problem.
  1. Recognize early stages.
  2. Maintain client in semi-Fowler’ position.
  3. Decrease levels of activity.
  4. Use extreme caution in administration of fluids and transfusions.

comments:



  1. New York City Man
    said...



    This is very informative.

    Thanx!!!



  2. VMUF College of Nursing
    said...



    WOW!!! Very nice informative site for nurses!!! This would be a great help for our student nurses
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