June
2007, Volume 11, Number 3
CJON book excerpt series
Pulmonary
Edema
Susan A. Ezzone,
MS, RN, CNP
This
excerpt, chapter 32 from the book Clinical Manual for the Oncology Advanced
Practice Nurse (2nd ed.), edited by Dawn Camp-Sorrell, MSN, FNP, AOCNฎ,
and Rebecca A. Hawkins, MSN, ANP, AOCNฎ, is a part of a series of
clinically relevant reprints that appear regularly in the Clinical Journal
of Oncology Nursing.
IVII. Definition:
Clinical syndrome resulting in leakage of fluid from the pulmonary capillaries
and veins into the interstitium and alveoli of the
lungs (Dada & Sznajder, 2003)
VIII. Physiology/Pathophysiology (Cotter, Kaluski,
& Vered, 2005)
A.
1. According to
Starlings Law, the flow of fluid from the pulmonary capillaries to the lungs
equals the removal of fluid by pulmonary lymphatics.
2. To prevent
pulmonary edema, an active process of sodium (Na+) transport by an osmotic
process removes fluid from the alveoli as a protective mechanism.
B. Pathophysiology
1. Pulmonary edema
occurs when fluid accumulates in the alveolar spaces.
2. Cardiogenic pulmonary edema may occur because of an
increase in the hydrostatic pressure gradient associated with an altered hemodynamic status, such as in CHF. An elevated PCWP occurs
because of left ventricular dysfunction (Cotter et al., 2005).
3. Noncardiogenic pulmonary edema is caused by leakage of
fluid from pulmonary capillaries with a decrease in plasma oncotic
pressure and elevation of capillary pressure, producing interstitial and
intra-alveolar edema.
a) This type of
pulmonary edema may be caused by several clinical conditions that result in
fluid and protein accumulation in the alveoli.
b) May be caused by
many clinical conditions that cause injury to the lungs, such as acute
respiratory distress syndrome and inflammatory damage to the alveolar capillary
membrane (Cotter et al., 2005)
4. Neurogenic pulmonary edema may occur because of head
trauma, intracranial or subarachnoid hemorrhage, and
some neurologic disorders (Cotter et al., 2005).
5. Decreased lung and
small airway compliance may result in altered ventilation, hypoxia, and
respiratory failure.
6. Hypoxia reduces
the ability to actively transport Na+, leading to alveolar edema (Dada & Sznajder, 2003).
VIII. Clinical
features (Cotter et al., 2005)
A. Etiology: See Table
32-1.
B. Types of pulmonary
edema (see Table 32-1)
C. History
1. History of cancer
and cancer treatment
2. Current
medications: Prescribed and over-the-counter
3. History of
presenting symptom(s): Precipitating factors, onset, location, and duration
4. Changes in ADLs
D. Signs and symptoms
1. Dyspnea, orthopnea
2. Anxiety or feeling
of impending doom
3. Frothy-pink or
salmon-colored sputum
4. Cough
5. Cyanosis, pallor
6. Diaphoresis
7. Unable to lie flat
8. Poor prognostic
symptoms (Cotter et al., 2005)
a) Hypoxia
b) High or low blood
pressure
c) High heart rate
d) High respiratory
rate
e) Increased PCWP
E. Physical exam
1. Vital signs
a) Tachypnea
b) Tachycardia
c) Hypotension
2. Integument exam:
Skin pallor and livedo reticularis
(skin discoloration with mottled appearance)
3. Pulmonary exam
a) Abnormal breath
sounds with occasional
wheezing
b) Abnormal breathing
pattern with use of accessory muscles
4. Cardiac exam
a) Pulsus alternans, alternating weak
and strong pulse, may be a sign of left ventricular failure in CHF
b) Heart sounds with
presence of S3, S4, and harsh murmur
c) JVD
d) Peripheral edema
of extremities
IIIV. Diagnostic
tests (see Table 32-1)
A. Laboratory
1. ABGs
a) Hypoxia (oxygen
saturation < 90% and PaO2 < 60 mm Hg)
b) Hypercapnia (CO2 > 4555 mm Hg)
c) Acidosis (pH <
7.35 nEq/liter). Early findings of pulmonary edema
may be respiratory alkalosis because of hyperventilation.
2. Serum albumin: May
be low (normal = 3.65 g/dl)
3. Blood urea
nitrogen and creatinine to evaluate kidney function
to ensure that renal perfusion is occurring
4. Liver function
tests to evaluate hepatic function (elevation in alanine
aminotransferase, aspartate
aminotransferase and bilirubin
are seen with right ventricular failure and hepatic congestion)
5. Plasma brain natriuretic peptide levels may be increased in
cardiovascular pulmonary edema (Cotter et al., 2005).
B. Radiography (see
Table 32-1): Chest x-ray
1. Noncardiogenic: Bilateral consolidative
pattern, interstitial edema
2. Cardiogenic: Diffuse bilateral infiltrates, cardiomegaly
C. Other: Hemodynamic monitoring
1. Pulmonary arterial
pressure measurements with elevated PCWP (normal = 612 mm Hg)
2. Systemic vascular
resistance may be elevated (normal = 8001,200 dynes/sec/m2)
3. Electrocardiogram
(EKG): Abnormal in cardiogenic induced
IIIV. Differential
diagnosis: Table 32-1 lists common causes of pulmonary edema.
A. CHF (see Chapter
40)
B. Obstruction of
pulmonary lymphatics by tumor compression
C. CLS (see Chapter
27)
D. Acute respiratory
distress syndrome
E. Early phase of
septic shock (see Chapters 121 and 140)
IIVI. Treatment:
Goal is to decrease pulmonary venous and capillary pressure, improve cardiac
output, and correct underlying pathology. Patient is hospitalized for
management (Cotter et al., 2005).
A. Drug therapy
1. Use of loop
diuretics (e.g., furosemide, bumetanide,
torsemide) causes vasodilation
and decreases pulmonary congestion. Doses of 0.51 mg/kg may be used.
2. Administer metolazone (thiazide diuretic)
520 mg po once a day for treatment of CHF.
3. Vasodilators cause
vasodilation, therefore decreasing pulmonary vascular
pressure.
a) Nitroprusside is started at an IV infusion of 0.5 mcg/kg/minute and titrated to achieve the desired effect;
average dose is 0.50.8 mcg/kg/minute.
b) Nitroglycerin is
started at an IV infusion of 1020 mcg/minute, and the dose is increased by
510 mcg/minute every 510 minutes until the desired effect occurs.
4. Morphine sulfate
may be given to cause venous dilation at doses of 13 mg IV push. The dose is
repeated every two to three hours as needed up to a total of 1015 mg.
5. Aminophylline may be given at 5 mg/kg IV infusion for
symptoms of wheezing.
6. In patients with
ventilator-induced lung injury, dopamine and beta-adrenergic agonists (terbutaline and isoproterenol)
improved clearance of pulmonary edema (Dada & Sznajder,
2003).
7. Dysrhythmia control
B. Oxygen therapy
1. Oxygen therapy
often is used, and dose is titrated to patient response. Intubation and
mechanical ventilation may be necessary.
2. Continuous
positive airway pressure (PAP) and bilevel-PAP have
been found to be superior to oxygen therapy in decreasing the need for
mechanical ventilation (Park et al., 2004).
C. Swan Ganz catheter may be placed to evaluate the cause of
pulmonary edema.
D. Position patient in
semi-Fowler position.
E. Obtain daily weight
to monitor fluid status.
F. Obtain frequent
intake and output measurements.
IVII. Follow-up
A. Daily physical
assessment and evaluation of response to treatment is necessary.
B. Diagnostic studies,
such as chest x-ray and ABGs, may be done to evaluate
patient condition.
VIII. Referrals
A. Pulmonary consult:
To evaluate lung status and assist with medical management as needed
B. Respiratory therapy:
May be needed for oxygen therapy, ventilatory
management, percussion, or respiratory treatments
References
Cotter, G., Kaluski,
E., & Vered, Z. (2005). Pulmonary edema.
In M.P. Fink, E. Abraham, J.L. Vincent, & P.M. Kochanek
(Eds.), Textbook of critical care (5th ed., pp. 719734).
Dada,
Park, M., Sangean,
M., Volpe, M.S., Feltrim, M., Nozawa,
E., Leite, P., et al. (2004). Randomized,
prospective trial of oxygen, continuous positive airway pressure, and bilevel positive airway pressure by face mask in acute cardiogenic pulmonary edema. Critical Care
Medicine, 32, 24072415.
From Clinical
Manual for the Oncology Advanced Practice Nurse (2nd ed., pp. 213217),
edited by Dawn Camp-Sorrell, MSN, FNP, AOCNฎ, and Rebecca A.
Hawkins, MSN, ANP, AOCNฎ, Pittsburgh, PA: Oncology Nursing Society. Reprinted with permission.
Digital
Object Identifier: 10.1188/07.CJON.457-459