Pulmonary edema is a condition associated with increased loss of fuid from the

pulmonary capillaries into the pulmonary interstitium and alveoli. Pulmonary edema
of cardiac origin most commonly results from an increase in pulmonary capillary
pressure caused by an elevation of left atrial pressure (pulmonary capillary wedge
pressure) associated with left ventricular failure or valve disease (e.g., mitral or
aortic regurgitation, mitral or aortic stenosis). Pulmonary hypertension can also
lead to elevated capillary pressures and pulmonary edema. The physical factors and
dynamics of edema formation are discussed elsewhere.
Pulmonary edema, a medical emergency, is an accumulation of fluid in the lungs. Most often
a consequence of congestive heart failure, pulmonary edema typically occurs when the heart is
unable to pump blood out through the arteries as quickly as it is returned to the heart through the
veins.
Failure of the left side of the heart (left ventricle) causes blood to accumulate in the veins of the
lungs (pulmonary veins), producing a dangerous rise in blood pressure within these veins.
Sustained high pressure in the pulmonary veins eventually forces some fluid from the blood into
the surrounding microscopic air sacs (alveoli), which transfer oygen to the bloodstream. !s the
alveoli fill with fluid, they can no longer provide adequate amounts of oygen to the body.
Symptoms, especially severe breathing difficulty, develop over the course of a few hours and
may be life"threatening. !lthough the outlook for pulmonary edema is favorable if the
underlying disorder is treated in a timely fashion, the overall outcome for the patient depends
upon the nature of the underlying disorder. !dults at high risk for heart failure are most
commonly affected.
! less common form of the disease, high-altitude pulmonary edema (which may occur while
mountain"climbing, for instance), is also life"threatening if not treated quickly. Strenuous activity
upon arrival at high altitudes may cause a dangerous rise in the pressure in the pulmonary veins,
forcing fluid out of the veins into the alveoli. !fter people become acclimated to the altitude,
strenuous activity does not pose such a risk.
#igh"altitude pulmonary edema most often affects young adults under age $% who are
unacclimati&ed to the altitude but otherwise in good health. Symptoms appear within $' to ($
hours and necessitate immediate descent to a lower altitude for treatment. (!ir travelers are
generally not at risk for this disorder because commercial airplane cabins are pressuri&ed.)
What Causes Pulmonary Edema?
)ongestive heart failure due to high blood pressure, aortic or mitral valve disease, or
cardiomyopathy is a common cause of pulmonary edema.
! heart attack may cause pulmonary edema.
! variety of other conditions, such as lung infections, etensive burns, liver or kidney
disease, #odgkin*s disease, pneumothora or nutritional deficiencies, may lead to
pulmonary edema in some cases.
+verdoses of heroin, morphine and other narcotics may lead to pulmonary edema.
,apid ascent to high altitudes followed immediately by heavy eertion may cause high"
altitude pulmonary edema.
Pulmonary edema is acute, severe left ventricular failure with pulmonary venous
hypertension and alveolar flooding. Findings are severe dyspnea, diaphoresis, whee&ing, and
sometimes blood"tinged frothy sputum. -iagnosis is clinical and by chest "ray. .reatment
is with +$, /0 nitrates, diuretics, and sometimes morphine and short"term /0 positive
inotropes, endotracheal intubation, and mechanical ventilation.
/f left ventricular (10) filling pressure increases suddenly, plasma fluid moves rapidly from
pulmonary capillaries into interstitial spaces and alveoli, causing pulmonary edema.
!lthough precipitating causes vary by age and country, about one half of cases result from
acute coronary ischemia2 some from decompensation of significant underlying heart failure
(#F), including diastolic dysfunction #F due to hypertension2 and the rest from
arrhythmia, an acute valvular disorder, or acute volume overload often due to /0 fluids.
-rug or dietary nonadherence is often involved.
Symptoms and Signs
3atients present with etreme dyspnea, restlessness, and aniety with a sense of suffocation.
)ough producing blood"tinged sputum, pallor, cyanosis, and marked diaphoresis are
common2 some patients froth at the mouth. Frank hemoptysis is uncommon. .he pulse is
rapid and low volume, and 43 is variable. Marked hypertension indicates significant cardiac
reserve2 hypotension with systolic 43 5 677 mg #g is ominous. /nspiratory fine crackles are
widely dispersed anteriorly and posteriorly over both lung fields. Marked whee&ing (cardiac
asthma) may occur. 8oisy respiratory efforts often make cardiac auscultation difficult2 a
summation gallop9merger of :rd (S:) and 'th (S') heart sounds9may be present. Signs of
right ventricular (,0) failure (eg, neck vein distention, peripheral edema) may be present.
Diagnosis
)linical evaluation showing severe dyspnea and pulmonary crackles
)hest "ray
Sometimes serum brain natriuretic peptide (483) or 8"terminal"pro 483 (8."pro"
483)
;)<, cardiac markers, and other tests for etiology as needed
! )+3- eacerbation can mimic pulmonary edema due to 10 failure or even that due to
biventricular failure if cor pulmonale (see )or 3ulmonale) is present. 3ulmonary edema
may be the presenting symptom in patients without a history of cardiac disorders, but )+3-
patients with such severe symptoms usually have a history of )+3-, although they may be
too dyspneic to relate it.
! chest "ray, done immediately, is usually diagnostic, showing marked interstitial edema.
4edside measurement of serum 483=8."pro483 levels (elevated in pulmonary edema2
normal in )+3- eacerbation) is helpful if the diagnosis is in doubt. ;)<, pulse oimetry,
and blood tests (cardiac markers, electrolytes, 4>8, creatinine and, for severely ill patients,
!4<s) are done. ;chocardiography may be helpful to determine the cause of the pulmonary
edema (eg, M/, valvular dysfunction, hypertensive heart disease, dilated cardiomyopathy)
and may influence the choice of therapies. Hypoemia can be severe. )+$ retention is a
late, ominous sign of secondary hypoventilation.
!reatment
!reatment of cause
+$
/0 diuretic
8itrates
/0 inotropes
Morphine
0entilatory assistance
/nitial treatment includes identifying the cause2 677? +$ by nonrebreather mask2 upright
position2 furosemide
7.% to 6.7 mg=kg /0 or by continuous infusion % to 67 mg=h2 nitroglycerin
7.' mg sublingually q % min, followed by an /0 drip at 67 to $7 mcg=min, titrated upward at
67 mcg=min q % min as needed to a maimum :77 mcg=min if systolic 43 is @ 677 mm #g.
Morphine
, 6 to % mg /0 once or twice, has long been used to reduce severe aniety and the work of
breathing but is decreasingly used, as noninvasive ventilatory assistance with bilevel
positive airway pressure (4i3!3) is helpful if hypoia is significant. /f )+$ retention is
present or the patient is obtunded, tracheal intubation and assisted ventilation are required
(see .racheal /ntubation).
Specific additional treatment depends on etiologyA
For acute M/ or another acute coronary syndrome, thrombolysis or direct
percutaneous coronary angioplasty with or without stent placement
For severe hypertension, an /0 vasodilator
For supraventricular or ventricular tachycardia, direct"current cardioversion
For rapid atrial fibrillation, cardioversion is preferred. .o slow the ventricular rate,
an /0 B"blocker, /0 digoin
, or cautious use of an /0 )a channel blocker
/n patients with acute M/, fluid status before onset of pulmonary edema is usually normal,
so diuretics are less useful than in patients with acute decompensation of chronic #F and
may precipitate hypotension. /f systolic 43 falls 5 677 mm #g or shock develops, /0
dobutamine
and an intra"aortic balloon pump (counterpulsation) may be required.
Some newer drugs, such as /0 483 (nesiritide
) and )a"sensiti&ing inotropic drugs (levosimendan, pimobendan), vesnarinone, and
ibopamine, may have initial beneficial effects but do not appear to improve outcomes
compared to standard therapy, and mortality may be increased.
+nce patients are stabili&ed, long"term #F treatment is begun (see see .reatment).
"ey Points
#cute pulmonary edema can result from acute coronary ischemia, decompensation
of underlying #F, arrhythmia, an acute valvular disorder, or acute volume overload.
3atients have severe dyspnea, diaphoresis, whee&ing, and sometimes blood"tinged
frothy sputum.
)linical eamination and chest "ray are usually sufficient for diagnosis2 ;)<,
cardiac markers, and sometimes echocardiography are done to identify cause.
.reat the cause and give +$ and /0 furosemide
and=or nitrates as needed2 try noninvasive ventilatory assistance initially but use
tracheal intubation and assisted ventilation if necessary.