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570 Pulmonary Edema, Acute

Pulmonary Edema, Acute

Pulmonary edema is the abnormal accumulation of fluid in the
interstitial spaces of the lungs that diffuses into the alveoli.
Pulmonary edema is an acute event that results from left ven-
tricular failure. With increased resistance to left ventricular
filling, blood backs up into the pulmonary circulation. The
patient quickly develops pulmonary edema, sometimes called
“flash pulmonary edema,” from the blood volume overload in
the lungs. Pulmonary edema can also be caused by noncardiac
disorders, such as renal failure and other conditions that cause
the body to retain fluid. The pathophysiology is similar to that
seen in HF, in that the left ventricle cannot handle the volume
overload and blood volume and pressure build up in the left
atrium. The rapid increase in atrial pressure results in an acute
increase in pulmonary venous pressure, which produces an
increase in hydrostatic pressure that forces fluid out of the pul-
monary capillaries into the interstitial spaces and alveoli.
Lymphatic drainage of the excess fluid is ineffective.

Clinical Manifestations
• As a result of decreased cerebral oxygenation, the patient
becomes increasingly restless and anxious.
P • Along with a sudden onset of breathlessness and a sense of
suffocation, the patient’s hands become cold and moist, the
nail beds become cyanotic (bluish), and the skin turns ashen
(gray).
• The pulse is weak and rapid, and the neck veins are dis-
tended.
• Incessant coughing may occur, producing increasing quanti-
ties of foamy sputum.
• As pulmonary edema progresses, the patient’s anxiety and
restlessness increase; the patient becomes confused, then
stuporous.
• Breathing is rapid, noisy, and moist-sounding; the patient’s
oxygen saturation is significantly decreased.
• The patient, nearly suffocated by the blood-tinged, frothy
fluid filling the alveoli, is literally drowning in secretions.
The situation demands emergent action.
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Pulmonary Edema, Acute 571

Assessment and Diagnostic Methods

• Diagnosis is made by evaluating the clinical manifestations
resulting from pulmonary congestion.
• Abrupt onset of signs of left-sided HF (eg, crackles on auscul-
tation of the lungs) may occur without evidence of right-sided
HF (eg, no jugular venous distention [JVD], no dependent
edema).
• Chest x-ray reveals increased interstitial markings.
• Pulse oximetry to assess ABG levels.
Medical Management
Goals of medical management are to reduce volume overload,
improve ventricular function, and increase respiratory exchange
using a combination of oxygen and medication therapies.
Oxygenation
• Oxygen in concentrations adequate to relieve hypoxia and
dyspnea
• Oxygen by intermittent or continuous positive pressure, if
signs of hypoxemia persist
• Endotracheal intubation and mechanical ventilation, if res-
piratory failure occurs
• Positive end-expiratory pressure (PEEP)
• Monitoring of pulse oximetry and ABGs
P
Pharmacologic Therapy
• Morphine given intravenously in small doses to reduce anx-
iety and dyspnea; contraindicated in cerebral vascular acci-
dent, chronic pulmonary disease, or cardiogenic shock; have
naloxone hydrochloride (Narcan) available for excessive
respiratory depression
• Diuretics (eg, furosemide) to produce a rapid diuretic effect
• Vasodilators such as IV nitroglycerin or nitroprusside
(Nipride) may enhance symptom relief
Nursing Management
• Assist with administration of oxygen and intubation and
mechanical ventilation.
• Position patient upright (in bed if necessary) or with legs
and feet down to promote circulation. Preferably position
patient with legs dangling over the side of bed.
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572 Pulmonary Embolism

• Provide psychological support by reassuring patient. Use

touch to convey a sense of concrete reality. Maximize time
at the bedside.
• Give frequent, simple, concise information about what is
being done to treat the condition and what the responses to
treatment mean.
• Monitor effects of medications. Observe patient for exces-
sive respiratory depression, hypotension, and vomiting. Keep
a morphine antagonist available (eg, naloxone hydrochlo-
ride). Insert and maintain an indwelling catheter if ordered
or provide bedside commode.
• The patient receiving continuous IV infusions of vasoactive
medications requires ECG monitoring and frequent meas-
urement of vital signs.
For more information, see Chapters 23 and 30 in Smeltzer, S. C.,
Bare, B. G., Hinkle, J. L., & Cheever, K. H. (2010). Brunner
and Suddarth’s textbook of medical-surgical nursing (12th ed.).
Philadelphia: Lippincott Williams & Wilkins.

Pulmonary Embolism
PE refers to the obstruction of the pulmonary artery or one of
P its branches by a thrombus (or thrombi) that originates some-
where in the venous system or in the right side of the heart.
Gas exchange is impaired in the lung mass supplied by the
obstructed vessel. Massive PE is a life-threatening emergency;
death commonly occurs within 1 hour after the onset of symp-
toms. It is a common disorder associated with trauma, surgery
(orthopedic, major abdominal, pelvic, gynecologic), pregnancy,
HF, age more than 50 years, hypercoagulable states, and pro-
longed immobility. It also may occur in apparently healthy peo-
ple. Most thrombi originate in the deep veins of the legs.

Clinical Manifestations
Symptoms depend on the size of the thrombus and the area
of the pulmonary artery occlusion.
• Dyspnea is the most common symptom. Tachypnea is the
most frequent sign.