Acute Pulmonary Edema

Maryl R. Johnson, MD
Address
Heart Failure/Cardiac Transplant Program, Northwestern Memorial
Hospital/Northwestern University Medical School, 250 East Superior
Street, Suite 512, Chicago, IL 60611, USA.
Current Treatment Options in Cardiovascular Medicine 1999, 1:269–276
Current Science Inc. ISSN 1092-8464
Copyright © 1999 by Current Science Inc.

Opinion statement
Patients with acute cardiogenic pulmonary edema require rapid assessment and
therapy to prevent progression to respiratory failure and cardiovascular collapse. The
goal of therapy is to decrease the pulmonary capillary wedge pressure by decreasing
intravascular volume and shifting the blood volume into peripheral vascular beds.
Mainstays of therapy include morphine sulfate (a venodilator and an anxiolytic),
furosemide (a venodilator and diuretic), nitroglycerin preparations (venodilators),
and, in some cases, aminophylline, nitroprusside, and beta-adrenergic agents or
milrinone. Patients who do not respond to more conservative measures may require
interventional procedures, including Swan-Ganz catheterization or arterial pressure
monitoring, continuous positive airway pressure or mechanical ventilation, intra-
aortic balloon counterpulsation, and mechanical removal of fluid. Because the prog-
nosis for patients with acute cardiogenic pulmonary edema depends on identification
and correction of the underlying disease process, it is essential to define the cause of
the edema during and after stabilization of the patient. Evaluation should include
Doppler echocardiography, cardiac catheterization, and coronary angiography.

Introduction
Pulmonary edema is an abnormal accumulation of present with both acute pulmonary edema and cardio-
extravascular lung water caused by leakage of fluid from genic shock.
the pulmonary capillaries and venules into the pul- Acute pulmonary edema has one of the most classic
monary interstitium and alveoli. Although pulmonary and most dramatic clinical presentations of any medical
edema can be related to increased permeability of the disorder. The affected patient has shortness of breath and
vascular membranes, decreased plasma oncotic pressure, extreme air hunger resulting from altered gas exchange
or increased tissue oncotic pressure, the focus of this arti- and pulmonary compliance. Because of significant sym-
cle is on cardiogenic pulmonary edema, in which an ele- pathetic stimulation, the patient may be diaphoretic and
vated pulmonary capillary wedge pressure drives the may seem apprehensive, anxious, or even agitated. If cere-
transudation of fluid. The increase in extravascular lung bral perfusion is compromised or hypoxia is far
water decreases lung volumes and lung compliance, advanced, the patient may be confused, somnolent, or
increases airway resistance and ventilation-perfusion almost comatose. A patient with pulmonary edema will
mismatching, and decreases gas exchange. This results in be tachypneic and tachycardic, but the blood pressure
an increase in the work of breathing, hypoxemia, and, may be high, normal, or low, depending on the under-
because of the sympathetic stimulation that occurs, an lying clinical condition. A decrease in peripheral per-
increase in peripheral vascular resistance. Acute pulmo- fusion may cause cyanosis, and the patient may cough up
nary edema is not a primary disease process but a mani- frothy pink sputum. Lung examination will show moist
festation of many cardiac disease processes that produce rales and perhaps rhonchi and wheezing if the extra-
an increased pulmonary capillary wedge pressure. vascular lung water produces reactive airways.
Pulmonary edema may be the initial presentation of The focus of this article is patient management, not
a patient with no previous cardiac history or may repre- patient evaluation or differential diagnosis, but in the
sent an acute exacerbation of a chronic condition. Man- case of acute pulmonary edema, it is difficult to separate
agement of it may require modification in patients who these topics. Any patient with acute cardiogenic pulmo-
270 Myocardial Disease

nary edema should be managed with the general stabi- controversies in the treatment of acute pulmonary
lizing measures delineated herein, but it is essential to edema are also briefly presented. Further information
define the underlying pathophysiology because it may about pulmonary edema and its therapy is summarized
affect acute management and will certainly modify elsewhere [1•–3•,4,5].
long-term therapy. Cardiovascular processes that com-
monly result in pulmonary edema include myocardial PROGNOSIS
ischemia or infarction, valvular heart disease (including The prognosis for patients with acute cardiogenic pul-
mitral stenosis, aortic stenosis, mitral regurgitation, and monary edema depends greatly on the ability to define
aortic regurgitation), hypertension, arrhythmias, heart and correct the underlying disease process. Early in the
block, acute papillary muscle rupture with consequent evaluation and management of patients with pul-
severe mitral regurgitation, and development of a ven- monary edema, transthoracic Doppler and two-dimen-
tricular septal defect. Progressive decompensation of a sional echocardiography should be performed to define
patient with underlying left ventricular dysfunction may cardiac function, determine intracardiac pressures, and
also produce acute pulmonary edema. In this setting, detect evidence of valvular heart disease. Patients in
precipitating factors to consider include excess fluid or whom transthoracic Doppler echocardiography is inad-
salt intake and noncompliance with prescribed medical equate should undergo transesophageal echocardiog-
regimens. Massive volume overload can produce acute raphy. Patients with any suggestion of ischemic cardiac
pulmonary edema, but this is rare unless the patient has disease should undergo cardiac catheterization and cor-
concomitant cardiac or renal dysfunction. onary angiography, either early in the course (if acute
The response of pulmonary edema to therapy is as intervention for myocardial ischemia or infarction is
dramatic as its presentation. In this article, treatment of anticipated) or later, to define the cause of pulmonary
acute pulmonary edema is discussed in terms of gen- edema. Follow-up management should include appro-
eral treatment measures, specific pharmacologic ther- priate dietary and pharmaceutical management to pre-
apy, and procedures that may be necessary. Some vent recurrence of acute pulmonary edema.

Treatment
• The goal of therapy for acute pulmonary edema is to decrease pulmonary
capillary and venous pressure, either by removing fluid from the body or
by shifting fluid to other vascular territories. It is important to maintain
adequate cardiac output; to do this, one must maintain myocardial per-
fusion. Although patients with acute pulmonary edema generally have
high systemic vascular resistance, the presenting blood pressure may be
low, normal, or high. Patient management is modified to reflect these
various presentations.
• Initial diagnostic evaluation should occur in concert with initial therapeu-
tic management and should include the following components: focused
history and physical examination; 12-lead electrocardiography; laboratory
studies, including complete blood count and measurement of electrolytes,
blood urea nitrogen, creatinine, and cardiac enzymes; digital pulse oxime-
try; arterial blood gas analysis; and chest radiography.
• General therapeutic management should include the following elements:
placement of the patient in a seated position, with legs dangling if possi-
ble (this position increases lung volume and capacity and decreases respi-
ratory work, venous return, and pulmonary capillary wedge pressure);
administration of oxygen (this may be optimized with continuous positive
airway pressure or mechanical ventilation); establishment of intravenous
access; continuous electrocardiographic monitoring; and continuous digi-
tal pulse oximetry.
• Although rotating tourniquets (to decrease venous return) and phlebot-
omy (to decrease intravascular volume) have been used in the treatment of
pulmonary edema, they are considered outdated and are rarely needed,
given the availability of the pharmacologic and mechanical measures
described here.
 Acute Pulmonary Edema Johnson 271

Pharmacologic treatment
• In acute pulmonary edema, the goals of pharmacologic treatment and the
goals of general treatment measures are the same, but pharmacologic treat-
ment should also be targeted at improving myocardial efficiency by
decreasing oxygen consumption and maximizing forward cardiac output.
• In general, both diuretics and nitrate preparations are indicated in the ther-
apy of pulmonary edema, but several recent studies suggest that intrave-
nous nitrates may actually provide more benefit than diuretics. In a series
of 24 cases of cardiogenic pulmonary edema, 50-mg boluses of intravenous
nitroglycerin were given every 1 to 2 minutes, and 20 of 24 cases showed
significant improvement after 30 minutes [6]. In a randomized trial that
compared 3 mg of intravenous isosorbide dinitrate given every 5 minutes
with 80 mg of intravenous Lasix (Hoechst Marion Roussel, Kansas City,
MO) given every 15 minutes plus intravenous isosorbide dinitrate given at
a rate of 1 mg/h (increased every 10 minutes by 1 mg/h), the group receiv-
ing only intravenous isosorbide dinitrate had a decreased need for mechan-
ical ventilation and a striking decrease (53%) in the incidence of
myocardial infarction [7].
• Although these studies speak to the benefits of intravenous nitroglycerin
preparations in patients with acute cardiogenic pulmonary edema, it seems
that the vasodilatory effect of nitroglycerin would be most beneficial in sit-
uations where acute pulmonary edema occurs in the absence of significant
total body volume overload [8] or in the presence of acute myocardial
ischemia. Indeed, in my opinion, both diuretics and nitrate preparations
are essential in the treatment of acute pulmonary edema. Their relative
importance depends on the underlying clinical situation.

Morphine sulfate
Morphine is a narcotic analgesic. By acting on opiate receptors in the brain, it pro-
duces central nervous system depression, providing both analgesia and sedation. It
is also a venodilator and thus increases venous capacitance and decreases venous
return. The decrease in systemic vascular resistance and anxiety produced by mor-
phine decreases myocardial oxygen demand.
Standard dosage Morphine is given intravenously in increments of 1 to 4 mg every few minutes until
respiratory status improves or the patient develops hypotension, respiratory
depression, or altered mental status.
Contraindications Relative contraindications include intravascular volume depletion and hypotension
because morphine given in these settings can further decrease blood pressure.
Morphine should be used with caution in patients with respiratory insufficiency
and respiratory or metabolic acidosis. The narcotic antagonist naloxone should be
available whenever morphine is given.
Main drug interactions Other medications known to have depressive effects on the central nervous system
should be used with caution when administered in conjunction with morphine. The
effects of morphine may be exaggerated and prolonged by phenothiazines,
monoamine oxidase inhibitors, and imipramine-like drugs.
Main side effects Nausea, vomiting, abdominal cramps, constipation, visual changes, constricted
pupils, mental status changes, dizziness, sweating, headaches, circulatory
depression, and respiratory depression.
Cost/cost effectiveness The cost of morphine varies considerably depending on the formulation and
packaging, ranging from $0.06 to $3.16/mg.

Furosemide
Furosemide is a loop diuretic. It inhibits sodium and chloride reabsorption in the
kidneys and also produces venous dilatation, an effect that is especially helpful in
the treatment of pulmonary edema.
272 Myocardial Disease

Standard dosage In a patient not already receiving furosemide, an initial intravenous dose of 20 to
40 mg should be given. In patients already receiving furosemide, the usual oral
dose should be doubled and given intravenously (if information on the usual oral
dose is available). If diuresis does not occur within 1 to 2 hours, the previously
given dose can be doubled and the regimen repeated until an adequate diuretic
response is achieved or the clinician decides that additional methods of fluid
removal must be tried.
Contraindications During pregnancy, furosemide should be used only in life-threatening situations
because it has been known to cause fetal abnormalities.
Main drug interactions The diuresis induced by furosemide can lead to potassium depletion, which can
exacerbate digitalis toxicity. Similarly, if hyponatremia develops, lithium toxicity
may result. Furosemide also increases the ototoxicity of the aminoglycosides and
ethacrynic acid.
Main side effects Hypotension, electrocardiographic changes (related to electrolyte depletion),
chest pain, dry mouth, hypochloremia, hypokalemia, hyponatremia, hyper-
glycemia, hypomagnesemia, pancreatitis, jaundice, tinnitus, hearing loss,
and hyperuricemia.
Special points Furosemide is a venous dilator, but Francis et al. [9] found that when intravenous
furosemide was given to patients with chronic heart failure, increases in mean
arterial pressure, pulse rate, and systemic vascular resistance and a decrease in
the stroke work index occurred during the first 1 to 2 hours. These effects were
thought to be due to direct stimulation of the renin-angiotensin-aldosterone sys-
tem and the sympathetic nervous system. Patients in this study were not receiv-
ing vasodilators or beta-blockers, so it is unclear whether these effects occur in
patients already receiving optimized medical therapy for congestive heart failure.
Although physicians using furosemide to treat acute pulmonary edema should be
aware of these potential acute and short-lived “adverse” effects of intravenous
furosemide, furosemide remains a mainstay of therapy for pulmonary edema.
Cost/cost effectiveness Although other intravenous loop diuretics are effective in the treatment of acute
pulmonary edema [10], the long-term availability of generic furosemide makes it a
very cost-effective choice. Reported costs for intravenous furosemide range from
$0.004 to $0.21/mg. Other loop diuretics, including bumetanide, ethacrynic acid,
and torsemide, can be used in patients who do not respond to furosemide. For
comparative purposes, intravenous bumetanide costs $1.78 to $3.75/mg, and
intravenous torsemide costs $0.11 to $0.20/mg.

Nitroprusside
Nitroprusside is a venous and arterial dilator that is beneficial in the treatment of
patients with pulmonary edema who do not respond to more conservative therapies,
especially patients with mitral regurgitation, aortic regurgitation, or hypertension.
Its venodilatory characteristics decrease preload, and its arteriolar-dilating char-
acteristics decrease afterload, optimizing cardiac performance.
Standard dosage Nitroprusside is started at a dosage of 0.1 mg/kg/min; this dosage is increased as
necessary and as tolerated by blood pressure.
Contraindications Significant hypotension or intravascular volume depletion.
Main drug interactions Nitroprusside interacts with other vasodilators to enhance their blood pressure–
lowering and vasodilatory side effects.
Main side effects Hypotension, headache, and thiocyanate toxicity (particularly in patients with
renal insufficiency).
Special points Because of its potent vasodilatory effects, nitroprusside should be given only in an
intensive care setting with continuous arterial pressure monitoring. In patients
with acute pulmonary edema, Swan-Ganz catheter monitoring is also frequently
used when nitroprusside is given.
Cost/cost effectiveness A 24-hr infusion of nitroprusside at 1 mg/kg/min in a 70-kg male would cost
$12.60. (The average wholesale price is used for cost calculations; however,
because of contracts and bulk orders, this amount is rarely paid.)
 Acute Pulmonary Edema Johnson 273

Nitroglycerin preparations
Nitroglycerin is a smooth muscle relaxant. At lower doses, it dilates veins,
producing a decrease in preload. At higher doses, it dilates arteries, producing a
decrease in afterload. It also dilates the coronary circulation and improves
coronary perfusion.
Standard dosage In patients with pulmonary edema, nitrate preparations should be given sub-
lingually or intravenously to allow adequate drug absorption. Because of the
peripheral and mesenteric vasoconstriction that accompanies pulmonary edema,
topical and oral routes of administration are unreliable. Nitroglycerin, 0.4 mg,
should be given sublingually every 5 to 10 minutes as required and tolerated by
blood pressure. In the monitored, in-hospital (emergency department or intensive
care) setting, nitroglycerin may be given intravenously, with a starting dosage of
0.3 to 0.5 mg/kg/min, which is increased as needed and tolerated.
Contraindications Nitroglycerin should be used with caution in patients with borderline hypotension
and should be used in hypotensive patients only if inotropic and pressor agents
are available. It should not be given to patients who may have increased intra-
cranial pressure.
Main drug interactions The vasodilating effects of nitrate preparations may be additive with those of other
vasodilators, particularly alcohol. Intravenous nitroglycerin may interfere with the
anticoagulant effects of heparin.
Main side effects Headache, dizziness, weakness, lightheadedness, syncope, tachycardia, hypo-
tension, orthostasis, skin rash, dry mouth, nausea, and vomiting.
Special points In countries where intravenous preparations of isosorbide dinitrate are available,
these preparations may be used in the treatment of acute pulmonary edema, as
previously discussed.
Cost/cost effectiveness An infusion of intravenous nitroglycerin, 0.5 mg/kg/min for 24 hr in a 70-kg
patient, would cost $14.11 to $68.54.

Beta-adrenergic agents
Dopamine benefits patients with acute pulmonary edema because of its renal
vasodilating effects (which enhance renal perfusion and improve urinary output)
and its cardiac effects (which improve cardiac output). In hypotensive patients,
the vasoconstrictive effects of higher doses of dopamine will maintain blood pres-
sure and perfusion of vital organs. Dobutamine is a positive inotropic agent that
will improve forward cardiac output; it is particularly useful in patients with
underlying left ventricular dysfunction. Dobutamine is indicated only for the
short-term treatment of hospitalized patients with cardiac decompensation due to
decreased contractility.
Standard dosage For renal or mesenteric vasodilatory effects, dopamine, 2 to 3 mg/kg/min, is
recommended. To achieve positive inotropic effects, dosages of 5 to 10 mg/kg/min
are used. Dopamine at more than 10 mg/kg/min is a vasopressor. (It may improve
blood pressure, but it also increases systemic vascular resistance and may further
impede cardiac performance.) Dobutamine is given at a dosage of 5 to 10
mg/kg/min. In the setting of acute pulmonary edema, continuous electrocardio-
graphic monitoring should be employed during drug administration.
Contraindications Beta-adrenergic agents are contraindicated in patients with idiopathic hyper-
trophic subaortic stenosis.
Main drug interactions In patients undergoing aggressive diuresis, electrolyte balance (particularly mag-
nesium and potassium levels) must be maintained. If it is not, the arrhythmogenic
effects of dopamine and dobutamine may be enhanced.
Main side effects Tachycardia, hypertension, arrhythmias, hypotension, nausea, headache, chest
pain, palpitations, shortness of breath, and thrombocytopenia.
Cost/cost effectiveness An infusion of renal dose dopamine (2 mg/kg/min) for 24 hr in a 70-kg patient
would cost $0.40 to $56.25. Dobutamine infused at 5 mg/kg/min for 24 hr in a
70-kg patient would cost $6.05 to $302.40.
274 Myocardial Disease

Milrinone
Milrinone is a phosphodiesterase inhibitor with inotropic and vasodilatory effects.
It may be particularly useful in the treatment of pulmonary edema in patients with
left ventricular dysfunction who do not respond to more conservative measures.
Milrinone is indicated only for the short-term intravenous therapy of congestive
heart failure.
Standard dosage Milrinone is given as a loading dose of 50 mg/kg over 10 minutes with a sub-
sequent maintenance infusion of 0.375 to 0.75 mg/kg/min. The infusion rate
should be reduced in patients with renal impairment. In patients who are
relatively hypotensive (particularly patients with known severe left ventricular
dysfunction), the loading dose should be omitted because it may produce
significant hypotension.
Contraindications Milrinone should not be used in patients with idiopathic hypertrophic
subaortic stenosis.
Main drug interactions As with beta-adrenergic agents, it is essential to maintain magnesium and potas-
sium levels to minimize the risk of arrhythmias.
Main side effects Atrial and ventricular arrhythmias, hypotension, chest pain, headaches, tremor,
hypokalemia, and thrombocytopenia.
Special points Infusion of milrinone is safest under continuous arterial pressure monitoring.
Cost/cost effectiveness In a 70-kg patient, a milrinone bolus of 50 mg/kg followed by an infusion of
0.5 mg/kg/min for 24 hr would cost $338.49 to $427.97.

Aminophylline
Aminophylline is a xanthine bronchodilator that relaxes bronchial smooth muscle
and does not depend on activation of the adrenergic receptors for its action. It
stimulates the respiratory center and produces mild diuresis, and it has mild
inotropic and chronotropic effects. Except in settings of marked bronchospasm, it
should not be used in patients with pulmonary edema because of its tachycardic
and arrhythmogenic effects.
Standard dosage 250 mg of aminophylline can be infused intravenously over 5 minutes with contin-
uous electrocardiographic monitoring.
Contraindications Aminophylline preparations should be used with extreme caution in patients with
ischemic heart disease, cardiac arrhythmias, hypertension, or a history of seizures.
Main drug interactions Aminophylline interacts with cimetidine, erythromycin, tacrine, carbamazepine,
rifampin, and beta-blockers.
Main side effects Tachycardia, cardiac arrhythmias, palpitations, chest pain, nervousness,
tremors, headaches, seizures, nausea, vomiting, diarrhea, abdominal pain,
and insomnia.
Special points Given the availability of other management techniques for cardiogenic pulmonary
edema, aminophylline is rarely indicated.
Cost/cost effectiveness Aminophylline for intravenous use costs $0.02 to $0.07/mg; therefore, a 250-mg
bolus of intravenous aminophylline would cost $5.00 to $17.50.

Interventional procedures
• In patients who do not respond readily to initial therapy or who are
hemodynamically unstable, insertion of a Swan-Ganz catheter for direct
monitoring of cardiac filling pressures and cardiac output may be of
benefit in the specific tailoring of therapy. In patients who are relatively
hypotensive, placement of an arterial line should also be considered.
Other procedures that may be needed or beneficial in patients with
pulmonary edema include administration of continuous positive airway
pressure (CPAP), mechanical ventilation, intra-aortic balloon counter-
pulsation, and fluid removal.
 Acute Pulmonary Edema Johnson 275

Continuous positive airway pressure

• Whether administered nasally or by face mask, CPAP increases end-
expiratory volume and recruits alveoli, leading to an increase in oxygenation
due to a decrease in intrapulmonary shunting. It also increases intra-alveolar
pressure and thereby decreases transudation of fluid into the lung spaces,
venous return, and afterload. It also decreases the work of breathing. It does
not directly decrease the amount of lung water, however, and it should there-
fore be used in conjunction with other treatments. Possible side effects include
nasal skin necrosis, gastric distention, aspiration, barotrauma, asphyxia, sub-
gingival emphysema, subcutaneous emphysema, and pneumomediastinum.
• In a study published in 1991 by Bersten et al. [11], 39 patients who were in
respiratory failure due to severe cardiogenic pulmonary edema were ran-
domly assigned to receive oxygen alone or oxygen plus CPAP delivered by
face mask. After 30 minutes, the group receiving CPAP had a greater
decrease in respiratory rate, a greater decrease in Pco2, and a greater increase
in arterial pH and the ratio of arterial oxygen to FiO2. These variables did
not differ between the two groups after 24 hours, but none of the patients
who received CPAP plus oxygen (compared with 35% of patients who
received oxygen alone) required intubation and mechanical ventilation.
The patients who received CPAP also had a shorter stay in the intensive care
unit. No significant complications of CPAP were recorded.
• A subsequent study included 100 patients admitted to the coronary care
unit for the treatment of acute cardiogenic pulmonary edema [12]. As in
the earlier study, patients were randomly assigned to receive oxygen or
oxygen plus CPAP. Patients in the group receiving CPAP had a greater
increase in PaO2 and greater decreases in the intrapulmonary shunt and the
alveolar-arterial oxygen tension gradient associated with a lower rate-
pressure product and higher stroke-volume index. The therapeutic failure
rate (therapeutic failure was defined as the need for tracheal intubation and
ventilator therapy) at 6 hours was 24% in the group receiving CPAP and
50% in the group receiving oxygen.
• A recent retrospective review of 75 patients who had acute severe pulmo-
nary edema treated with adjuvant CPAP reported no adverse events and an
89% rate of tolerance of the CPAP mask [13]. Of note, a study that ran-
domly assigned 30 patients to receive oxygen plus nasal CPAP or oxygen
alone showed not only the previously defined improvement in the ratio of
PaO2 to FiO2 with CPAP but also a decrease in the plasma endothelin-1
concentration. This provides a possible mechanistic explanation for the
benefits of CPAP beyond its purported respiratory and hemodynamic
effects [14]. Thus, when practical, it seems that CPAP should be incor-
porated into the treatment of severe acute pulmonary edema.

Mechanical ventilation
• Mechanical ventilation may be needed to improve oxygenation, decrease
the work of breathing, or treat impending respiratory failure.

Intra-aortic balloon counterpulsation

• The intra-aortic balloon pump improves coronary perfusion and decreases
afterload. Thus, it may be particularly beneficial in the treatment of pul-
monary edema produced by acute myocardial ischemia or infarction or
mitral regurgitation.
• It is contraindicated in patients with significant aortic regurgitation.
276 Myocardial Disease

Fluid removal
• Patients who do not achieve adequate diuresis with diuretics, vasodilators,
and inotropic agents may require mechanical removal of fluid. Removal
can be done with ultrafiltration, arteriovenous filtration, hemodialysis, or
peritoneal dialysis. In one study of 20 patients, continuous venovenous
ultrafiltration for 2.5 hours resulted in an average ultrafiltration volume of
3000 mL and produced a 58% decrease in the intrapulmonary shunt [15].

References and Recommended Reading

Papers of particular interest, published recently, have been highlighted as:
• Of special interest
•• Of outstanding interest
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ican College of Cardiology/American Heart Associa- semide versus high-dose furosemide plus low-dose
tion Task Force on Practice Guidelines (Committee on isosorbide dinitrate in severe pulmonary oedema.
Evaluation and Management of Heart Failure). Lancet 1998, 351:389–393.
J Am Coll Cardiol 1995, 26:1376–1398. 8. Northridge D: Frusemide or nitrates for acute heart
These general guidelines for the treatment of heart failure failure? Lancet 1996, 347:667–668.
include guidelines for the evaluation and management of 9. Francis GS, Siegel RM, Goldsmith SR, et al.: Acute vaso-
acute pulmonary edema and cardiogenic shock. constrictor response to intravenous furosemide in
2.• Emergency Cardiac Care Committee and Subcommit- patients with chronic congestive heart failure. Activa-
tees, American Heart Association: Guidelines for car- tion of the neurohumoral axis. Ann Intern Med 1985,
diopulmonary resuscitation and emergency cardiac 103:1–6.
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