Turn back

the tide of

cardiogenic
pulmonary
edema
Find out how to recognize
patients at risk for this sudden
and life-threatening disorder
and what to do if it occurs.
BY MARCIA BIXBY, RN, CCRN, CS, MS

WHEN PULMONARY EDEMA arises secondary to

a cardiac disorder, it can develop suddenly and
threaten survival. In this article, Ill describe whos
at risk for pulmonary edema, how to manage it,
and how to help a patient with a cardiac condition
prevent it from recurring. Although pulmonary
edema can have noncardiac origins (see What else
can cause pulmonary edema?), cardiac causes are
more common, so Ill focus on cardiogenic pulmonary edema here.
Whos at risk?

Pulmonary edema develops when fluid accumulates in

the alveoli and airways. Patients at high risk include
those with heart failure, acute myocardial infarction
affecting 25% or more of the left ventricle, damaged or
dysfunctional mitral valves, arrhythmias (including
new-onset atrial fibrillation or ventricular tachycardia),
and fluid overload. In these patients, a reduced ejection
fraction and excessive left ventricular end-diastolic
pressure means that blood backs up into the pulmonary venous system, increasing pressure in the pulmonary vasculature and forcing intravascular fluid
into the alveoli and airways (see Air, water, and trouble).
Impaired gas exchange leads to progressive acidemia,
respiratory distress, and, without treatment, death.
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Nursing2005, Volume 35, Number 5

Heeding ominous signs

Warning signs of impending pulmonary edema

include weak peripheral pulses, capillary refill time
greater than 3 seconds, peripheral cyanosis, tachycardia, tachypnea, and decreased SpO2 with dyspneaall
indications of reduced cardiac output (CO). Vasoconstriction from compensatory mechanisms in patients
with heart failure also can lead to decreased pulse
quality. If you notice these signs in your patient, notify
the primary care provider. If the patient is at risk for
pulmonary edema, assess him frequently to catch
these early signs of trouble:
Hypertension. As forward blood flow decreases, the
body compensates by constricting blood vessels, leading to increased peripheral vascular resistance and
afterload, making the left ventricle work harder to
eject its blood volume and maintain normal CO.
Tachycardia. To compensate for decreased forward
blood flow and activation of the sympathetic nervous
system (a compensatory response to decreased CO),
the patients heart rate increases.
Signs and symptoms of myocardial ischemia. Increased
myocardial workload at a time of decreased myocardial blood flow starts a cycle of ischemia that can lead
to pump failure, hypotension, and pulmonary edema
if not treated.
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CONTACT
HOURS

Alveolus

Air, water, and trouble

Normally, pulmonary capillary hydrostatic
pressure and capillary oncotic pressure
are in balance. But in pulmonary edema,
elevated pulmonary venous pressure
leads to an increase in hydrostatic pressure, pushing fluid from the intravascular
compartment into the lungs interstitial
spaces, then into the alveoli, impairing
gas exchange. Without prompt treatment,
the patient can rapidly go into acute respiratory failure.

Normal alveolus

Capillary
beds

Congested alveolus
Capillary

Alveolus

Normal
blood flow

www.nursing2005.com

Pulmonary edema
Capillary

Alveolus

Interstitial
space

Increased
hydrostatic pressure

Congested
interstitium

Alveolus

Large amount of fluid

forced into the alveolus

Greatly increased
hydrostatic pressure

Nursing2005, May

57

 Premature ventricular contractions

(PVCs) and other arrhythmias.
Myocardial ischemia can trigger
PVCs and other arrhythmias, further impairing CO.
Respiratory distress. Excess interstitial fluid in the alveoli and airways impairs gas exchange. This
leads to respiratory distress and
hypoxemia, which contributes to
myocardial ischemia. Initial signs
and symptoms of respiratory distress, which may be subtle, include
increased respiratory rate, feeling
short of breath, decreased SpO2,
and crackles in the lung bases on
auscultation. As pulmonary edema
worsens, so do symptoms of respiratory distress, and crackles
become increasingly audible

oxygen levels decrease and carbon

dioxide levels increase, the patient
will become restless, agitated, confused, and progressively lethargic.
Turning back the tide

Although treatment for pulmonary

edema may vary depending on the
underlying cause, interventions
aim to increase tissue oxygenation
and perfusion, maintain perfusion
to vital organs, control heart rate
and rhythm, normalize blood pressure (BP), and decrease the work
of breathing.
Your patient will feel panicky as
he struggles to breathe. So as
youre administering treatment,
reassure him that your interventions will ease his distress and help

and mechanical ventilation.

Obtain a specimen for ABG
analysis. If the patient doesnt have
a patent intravenous (I.V.) device,
establish I.V. access as soon as possible.
If his systolic BP is above 100
mm Hg, administer sublingual
nitroglycerin to decrease afterload
and preload. Give a sublingual
dose of 0.3 or 0.4 mg every 5 minutes for up to three doses while
establishing an I.V. infusion, as Ill
discuss shortly.
As ordered, give a diuretic, typically furosemide, to increase
venous capacitance, decrease left
ventricular filling pressure, and
improve symptoms. The recommended dosage is 0.5 to 1 mg/kg

Your patient will feel panicky as he struggles to breathe. So as youre administering treatment,
toward the apex of the lungs. On
chest X-ray, pulmonary edema
appears as diffuse haziness in the
lung fields.
As his respiratory distress
increases, the patient will want to
sit up; lying down makes breathing
even harder and raises his respiratory rate. Because of peripheral
vasoconstriction, his SpO2 reading
wont be reliable.
Reduced urine output. Decreased
CO decreases the glomerular filtration rate, increasing sodium and
water retention and reducing urine
output. During the acute phase of
pulmonary edema, monitoring
your patients hourly urine output
via an indwelling urinary catheter
can help you assess his response to
treatment and guide further interventions.
Cough and frothy, pink-tinged
sputum. Proteins and red blood
cells in the fluid in the alveoli turn
the patients sputum pink and
frothy, a characteristic of pulmonary edema.
Mental status changes. As blood
58

Nursing2005, Volume 35, Number 5

him breathe easier.

If his BP allows, place him in a
sitting position with his legs
dependent. This increases lung volume and capacity, which eases the
work of breathing, and reduces
venous return to the heart.
Next, administer high-flow supplemental oxygen at 5 to 6 liters/
minute by simple face mask or at
10 to 15 liters/minute by nonrebreather mask with reservoir.
Connect the patient to a cardiac
monitor and pulse oximeter. (Keep
in mind that pulse oximetry readings may be inaccurate because of
decreased peripheral perfusion.
Assess his oxygenation via arterial
blood gas [ABG] analysis.)
Increase oxygen delivery concentrations, trying to keep the
patients SpO2 at 90% or above,
until his respiratory distress
resolves or he needs mechanical
ventilation. If supplemental oxygen isnt sufficient, administer
noninvasive continuous positive
airway pressure ventilation as
ordered or assist with intubation

I.V. Furosemide-induced diuresis

peaks in 30 to 60 minutes.
Next, as long as the patients BP
is adequate, slowly administer
morphine, which has hemodynamic effects as well as analgesic
and sedative ones. Morphine
causes peripheral vasodilation,
reducing venous return to the
central circulation and preload. It
also reduces afterload by causing
mild arterial vasodilation and
reduces the patients anxiety. Give
frequent small doses every 5 to 30
minutes (2 to 4 mg I.V. over 1 to
5 minutes) titrated to patient
response.
Other medications may be
ordered depending on the patients
BP and clinical signs and symptoms. Because these drugs are
vasodilators, administer dosages
precisely and titrate to patient
response. These medications
include:
I.V. nitroglycerin or nitroprusside, to decrease afterload and preload in patients whose systolic BP
is greater than 100 mm Hg
www.nursing2005.com

 catecholamines, for patients in

decompensated heart failure.
These drugs, which include
dopamine and dobutamine, produce vasodilation and increase
myocardial contractility and CO.
However, at higher dosages, these
drugs may increase heart rate, further impair perfusion, and
increase ischemia. They arent
indicated unless first-line therapies are unsuccessful.
Other drug options

Antiarrhythmics such as amiodarone, digitalis, or beta-blockers

may be indicated if the patients
cardiac rhythm is the cause of his
pulmonary edema.
Nesiritide, a synthetic form of

Lab tests: Seeking

the cause

What else can cause pulmonary

edema?

A 12-lead electrocardiogram can help

Noncardiac causes of pulmonary edema include:
identify the underly pulmonary embolus
ing cause of cardio cardiopulmonary bypass
genic pulmonary
rapid removal of pneumothorax
acute respiratory distress syndrome
edema, such as
transfusion-related acute lung injury
myocardial ischemia
infectious pneumonia
or infarction and
opioid overdose
tachyarrhythmias or
high altitude
bradyarrhythmias,
cerebral hemorrhage
guiding treatment
eclampsia.
choices.
Chest X-rays on
admission or at
symptom onset can rule out other
causes for the patients respiratory
distress, such as pneumothorax. In
a patient with heart failure, you

reassure him that your interventions will ease his distress.

brain-type natriuretic peptide
(BNP), is used to treat patients in
acutely decompensated heart failure. This drug promotes diuresis
and causes vasodilation, decreasing
venous return, preload, and afterload. Monitor the patient for
hypotension caused by the drugs
hemodynamic effects.
Phosphodiesterase inhibitors such
as milrinone increase myocardial
contractility and cause vasodilation, improving CO and reducing
afterload and preload.
Angiotensin-converting enzyme
inhibitors such as captopril or
enalapril may be used for their
afterload-reducing effects,
which increase CO and renal
perfusion.
Depending on the underlying
cause of pulmonary edema, other
diagnostic and therapeutic interventions may include coronary
angiography, intra-aortic balloon
pump therapy, surgical interventions such as coronary artery revascularization or valve repair, or ventricular assist device therapy.
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may see cardiomegaly, alveolar

edema, or pleural effusion on
X-ray.
Arterial blood gas analysis early
in pulmonary edema and respiratory distress may reveal hypoxemia
and respiratory alkalosis with a
decreased PaCO2. (Tachypnea
blows off carbon dioxide as the
body tries to cope with the acidbase imbalance.) As respiratory
distress worsens, the patients
PaCO2 will rise and acidosis occurs.
A plasma BNP level helps to
determine if the patients dyspnea
is from heart failure or a noncardiac cause. In a patient with
heart failure, BNP is released from
myocardial muscle cells in times of
volume or pressure overload on
the left ventricle. A BNP level
greater than 100 picograms/ml
generally indicates heart failure.
Checking the patients serum
cardiac markers, such as myoglobin, creatine kinase MB isoforms,
and cardiac troponins, can help
determine if myocardial damage
has occurred and if a myocardial

infarction triggered the pulmonary edema.

A two-dimensional
transthoracic echocardiogram can be
obtained at the bedside. This noninvasive
test evaluates the cardiac chamber
and valves, as well as the hearts
pumping function and ejection
fraction. The test can help identify
the underlying cause of cardiogenic pulmonary edema, such as
mitral regurgitation, which increases intravascular hydrostatic pressure.
A transesophageal echocardiogram (TEE) provides clearer
images of cardiac structures via a
specialized scope containing an
ultrasound probe, which is inserted
into the esophagus. Some structures, such as the atria, are better
imaged by TEE than a transthoracic echocardiogram, but the
patient may need to be sedated for
TEE, which is more invasive.
Nursing2005, May

59

Preventing future problems

Before your patient is discharged,

teach him about his underlying disease, medications, and dietary and
lifestyle restrictions. Make sure he
understands the early signs and
symptoms of worsening heart failure and pulmonary edema and
when to call his health care
provider or seek immediate medical
treatment. Early intervention can
prevent further myocardial damage
and cardiovascular collapse.
Give your patient a card to
record his medications, dosages,
and BP. This information will help
his health care provider evaluate
how hes responding to his medications or changes in dosages.
Advise him to lose weight if hes
overweight. He should follow a
low-sodium diet (less than 2
grams/day of sodium) to help prevent heart failure from worsening.
A nutritionist can help him and his
family review meal choices and
options.

He should weigh himself at the

same time each day, naked and
after he urinates, and mark his
weight on a calendar or chart, so
he can see trends. Teach him to call
his health care provider if he gains
3 pounds (1.4 kg) in 2 to 3 days;
this is a warning sign of worsening
heart failure and increasing risk of
pulmonary edema.
Encourage him to enroll in a
cardiac rehabilitation program for
regular exercise tailored to his
condition. If he smokes, encourage him to stop. Explain how
nicotine constricts arteries, reducing blood supply to the heart and
worsening respiratory problems.
Refer him to a smoking cessation
program.
Finally, supplement your teaching with written information he
can take home and review later.

you can help your patient stem

the tide of pulmonary edema and
prevent another crisis in the
future.
SELECTED REFERENCES
American Heart Association. Handbook of Emergency Cardiovascular Care. Dallas, Tex., American Heart Association, 2004.
Cotter G, et al. Pulmonary edema: New insight
on pathogenesis and treatment. Current Opinion
in Cardiology. 16(3):159-163, May 2001.
Hunt SA, et al. American College of Cardiology/
American Heart Association (ACC/AHA) Task
Force on Practice Guidelines (Committee to
Revise the 1995 Guidelines for the Evaluation
and Management of Heart Failure). ACC/AHA
guidelines for the evaluation and management
of chronic heart failure in the adult: Executive
summary. Circulation. 104(24):2996-3007, December 11, 2001.
Macklin MM. Managing heart failure: A case
study approach. Critical Care Nurse. 21(2):3651, April 2001.
Marcia Bixby is a clinical nurse specialist in surgical
critical care at Beth Israel Deaconess Medical Center
in Boston, Mass., and a nursing education consultant.
The author has disclosed that she has no significant
relationship with or financial interest in any commercial companies that pertain to this educational activity.

S E L EC T E D W E B S I T E

Staying vigilant

By staying vigilant during patient

assessment and intervening early,

Cardiogenic pulmonary edema

http://www.emedicine.com/med/topic1955.htm
Last accessed on April 4, 2005.

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Turn back the tide of cardiogenic pulmonary edema

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Turn back the tide of cardiogenic pulmonary edema

GENERAL PURPOSE To help nurses recognize patients at risk for cardiogenic pulmonary edema and what to do if it occurs.
LEARNING OBJECTIVES After reading the preceding article and taking this test, you should be able to: 1. Identify the pathophysiology
and warning signs of pulmonary edema. 2. Discuss the diagnostic studies and treatment strategies for pulmonary edema. 3. Describe
patient education related to cardiogenic pulmonary edema.
6. If his BP allows, place the patient in
a sitting position with his legs dependent to
a. decrease lung volume.
b. increase lung capacity.
c. increase venous return to the heart.
d. decrease venous capacitance.

1. Factors that place a patient at high risk

for cardiogenic pulmonary edema include
a. heart failure.
b. high altitude.
c. cerebral hemorrhage.
d. opioid overdose.
2. In patients at high risk for pulmonary
edema, a reduced ejection fraction can
a. decrease left ventricular end-diastolic
pressure.
b. decrease pressure in the pulmonary vasculature.
c. increase pressure in the pulmonary vasculature.
d. increase pressure in the aorta.

7. Sublingual nitroglycerin may be given

to your patient in pulmonary edema to
a. decrease afterload and increase preload.
b. decrease afterload and decrease preload.
c. increase afterload and increase preload.
d. increase afterload and decrease preload.
8. Which medication can be given to
increase myocardial contractility and CO?
a. morphine
b. dopamine
c. furosemide
d. nitroglycerin

3. Which isnt a warning sign of impending pulmonary edema?

a. hypertension
b. tachycardia
c. tachypnea
d. increased SpO2

9. Pharmacologic actions of morphine

include
a. peripheral vasodilation.
b. increased venous return to the heart.
c. increased preload.
d. arterial vasoconstriction.

4. Which is a compensatory mechanism

for decreasing CO?
a. tachycardia
b. hypotension
c. PVCs
d. increased urine output

10. Milrinone is classified as

a. a synthetic BNP.
b. an antiarrhythmic.
c. a phosphodiesterase inhibitor.
d. an angiotensin-converting enzyme
inhibitor.

5. Respiratory distress in pulmonary

edema is caused by
a. bronchial hyperresponsiveness.
b. air leaking into the pleural space.
c. sudden occlusion of the pulmonary
arterial tree by a blood clot.
d. excess interstitial fluid in the alveoli.

11. Arterial blood gas analysis in a

patient with tachypnea and early pul-

monary edema generally reveals

a. respiratory alkalosis.
b. metabolic alkalosis.
c. respiratory acidosis.
d. metabolic acidosis.
12. A plasma BNP level of 950
picograms/ml indicates that a patients
dyspnea is most likely due to
a. cardiac ischemia.
b. myocardial infarction.
c. pneumothorax.
d. heart failure.
13. Teach your patient with pulmonary
edema to
a. recognize the early signs and symptoms
of worsening heart failure.
b. eat a low-potassium diet if hes taking a
diuretic.
c. monitor his weight weekly.
d. limit sodium intake to 4 grams/day.
14. The recommended initial I.V. dosage
of furosemide for a nonhypotensive
154-pound (70-kg) patient in cardiogenic
pulmonary edema is
a. 15 to 30 mg.
b. 35 to 70 mg.
c. 75 to 100 mg.
d. 110 to 125 mg.
15. Tell your patient to notify his primary health care provider if he gains
a. 1 pound over 2 to 3 days.
b. 1 pound over 2 weeks.
c. 3 pounds over 2 weeks.
d. 3 pounds over 2 to 3 days.

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