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Guidelines for Acute Decompensated Heart Failure Treatment

Article  in  Annals of Pharmacotherapy · May 2004

DOI: 10.1345/aph.1D481 · Source: PubMed

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Cardiology

Guidelines for Acute Decompensated Heart Failure Treatment

Robert J DiDomenico, Hayley Y Park, Mary Ross Southworth, Heather M Eyrich, Richard K Lewis,

Jamie M Finley, and Glen T Schumock

OBJECTIVE: To describe the development of guidelines for the treatment of acute decompensated heart failure (ADHF) in the
emergency department/observation unit (ED-OU) setting for hospitals that are part of a group purchasing organization (GPO).
DATA SOURCES: A MEDLINE search (1966–March 2003) using the following search terms: cardiotonic agents; diuretic; dobutamine;
heart failure, congestive; milrinone; natriuretic peptide, brain; nesiritide; nitroglycerin; vasodilator agents, was conducted.
STUDY SELECTION AND DATA EXTRACTION: Relevant articles in the English language were identified. All randomized studies and
meta-analyses for each category of drugs were included.
DATA SYNTHESIS: A group consensus method was used to develop guidelines. An expert panel reviewed and revised the guidelines.
The final guidelines were approved June 1, 2003, and are described here. They are organized based upon a patient’s
symptomatology at the time the diagnosis of ADHF is made. Patients with evidence of volume overload require intravenous
diuretics and/or intravenous vasodilators to alleviate the symptoms of ADHF. Patients with signs and symptoms of low cardiac
output require inotropic support to manage their ADHF. A timeline for diagnosis, treatment, reassessment, and disposition is
provided and encourages an early, aggressive approach to treating patients with ADHF.
CONCLUSIONS: Hospitalization for ADHF is common and costly. Consensus guidelines for the treatment of ADHF did not previously
exist, resulting in inconsistent and inefficient treatment. Consequently, hospitals struggling with the treatment of ADHF may find
these guidelines and the process by which they were developed useful.
KEY WORDS: emergency department, guidelines, heart failure, observation unit.

Ann Pharmacother 2004;38:649-60.

Published Online, 24 Feb 2004, www.theannals.com, DOI 10.1345/aph.1D481
THIS ARTICLE IS APPROVED FOR CONTINUING EDUCATION CREDIT ACPE UNIVERSAL PROGRAM NUMBER: 407-000-04-015-H01

ongestive heart failure is a common clinical syndrome
C associated with significant morbidity and mortality. In
2003, it was estimated that 4.9 million people in the US
were diagnosed with heart failure, and an additional
550 000 new cases are diagnosed each year.1 For patients
Author information provided at the end of the text.
This project was funded, in part, by a grant from Scios, Inc.; howev-
er, the guidelines described herein were developed independently,
without any influence from the sponsor. Dr. Southworth has re-
ceived research support, and both Drs. DiDomenico and South-
worth have received honoraria for speaking on behalf of Scios, Inc.
Dr. Lewis is Continuing Education Administrator with ProCE, Inc.,
which has had Scios, Inc., as a program sponsor.
with heart failure, the mortality rate is approximately 50%
within 5 years of establishing the diagnosis.1,2
Acute decompensated heart failure (ADHF) is the pri-
mary diagnosis for close to one million hospital admis-
sions in the US and the secondary diagnosis for nearly 2
million hospitalizations.3 In 2003, estimated direct and in-
direct costs for the treatment of heart failure in the US to-
taled $24.3 billion.1 Early hospital readmission for heart
failure is common; approximately 20% of patients are
readmitted within 30 days and 50% within 6 months.2 Giv-
en the prevalence of heart failure in the US and the stag-
gering resources used in caring for patients with this diag-
nosis, methods for improving the management of heart
failure should be a priority of public health.

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Downloaded from aop.sagepub.com by guest on October 11, 2013
RJ DiDomenico et al.
While national guidelines exist for treatment of many
acute cardiovascular conditions such as acute coronary syn-
dromes, ischemic stroke, and life-threatening arrhythmias,4-
7
there have been no consensus guidelines for the manage-
ment of ADHF. Guidelines that do exist for heart failure fo-
cus on chronic rather than acute treatment of this disease.8
For conditions such as ADHF where there is a lack of ran-
domized controlled trials, using a systematic approach to
gather expert opinion is one method to create knowledge-
based measures.9 Consensus statements that incorporate the
available literature with expert opinion can be used as a
guideline until higher levels of evidence are published.
A significant barrier to the development of consensus
guidelines is the high cost associated with their prepara-
tion, implementation, and evaluation. Therefore, consensus
guidelines are generally reserved for conditions where the
cost of therapy is high and/or there is confusion about pa-
tient selection, drug choice, and drug regimen. Therapies
for ADHF are not well studied, leading to inconsistent and
inefficient treatment of patients afflicted with this disease.
As a result, the costs of treating ADHF continue to soar.
Consequently, there is a mandate for consensus guidelines
for the treatment of ADHF.
The purpose of this article is to describe the develop-
ment of treatment guidelines for the diagnosis and treat-
ment of ADHF in the emergency department/observation
unit (ED -OU) setting for hospitals that are part of a na-
tional group purchasing organization (GPO). These guide-
lines focus on the management of drug therapy (drug se-
lection and monitoring, management of adverse events)
during the initial 24 hours of care for ADHF patients.
Data Sources
Mercy Resource Management Inc. (MRMI) is a GPO
that represents over 250 hospital and non-hospital healthcare
facilities located across the US. At the time that these guide-
lines were developed, MRMI membership was comprised
of 4 large-owner systems (Catholic Healthcare East, based
in Newton Square, PA, with facilities throughout the eastern
US and Florida; CHRISTUS Health, based in Dallas, with
facilities in Texas, Utah, Arkansas, Louisiana, and Mexico;
Mercy Chicago, based in Chicago; and Trinity Healthcare,
based in Michigan, with hospitals across the US but concen-
trated in the Midwest), as well as a group of independent
healthcare facilities throughout the US. In addition to the tra-
ditional contracting and purchasing services associated with
a GPO, MRMI provides members with a variety of value-
added programs including multi-hospital drug use evalua-
tion and quality improvement projects, pharmacy service
certification programs, drug prescribing guidelines, continu-
ing education, staff development, and other programs.
In early 2003, MRMI began a project to develop, imple-
ment, and evaluate the use of guidelines for the treatment
of ADHF in the ED -OU. Previous studies have shown
that a major limitation to the development of practice
guidelines is the lack of adequate personnel resources at
individual institutions to police this process.10 To minimize
650 ■ The Annals of Pharmacotherapy ■ 2004 April, Volume 38
this obstacle, MRMI sought to develop such guidelines
centrally for use by all of its member hospitals.
Guidelines for treatment and management of ADHF
were developed by MRMI between January and June
2003. A project team comprised of MRMI staff (JMF and
RKL) and 4 university-based consultants (RJD, HME,
MRS, and GTS) coordinated the effort. A group consensus
method was used to develop the guidelines following a
modified Delphi/RAND method.11,12 The process occurred
in 3 main steps: a systematic review of the literature, draft
guidelines by the project team, and review of proposed
guidelines by an expert panel.
A systematic literature search using MEDLINE was
conducted by the project team to identify evidence sup-
porting the use of diuretics, vasodilators, inotropes, and
neurohormonal agents for the management of ADHF. Rel-
evant articles in the English language were identified. All
randomized studies and meta-analyses for each category of
drugs were included. Once reviewed, evidence from these
articles was used to determine drug selection and drug reg-
imens for each indication. These data were then formatted
as draft guidelines.
Key articles and draft guidelines were mailed to members
of the Expert Panel. Members were asked to review and rate
the items in the guidelines. A standing committee within
MRMI was used as the Expert Panel. This committee con-
sisted of representatives from each of the owner systems that
comprised MRMI. Members of the committee were selected
for their expertise and experience in pharmacotherapeutics.
A majority of panel members were clinical pharmacists, and
all were involved in Pharmacy and Therapeutics Committee
activities in their hospitals and health systems. In addition,
the Expert Panel included non-MRMI clinical practitioners
and academicians with national reputations as thought lead-
ers in ADHF (cardiologist; emergency medicine physician;
clinical pharmacists specializing in inpatient cardiology/criti-
cal care, outpatient heart failure/heart transplant, and emer-
gency medicine; experts in health economics).
Feedback from panel members was aggregated by the
project team in preparation for a face-to-face meeting of
the group. The Expert Panel meeting occurred on April 3,
2003. An open discussion occurred and consensus was
reached as to the content included in the guidelines. The
project team amended the guidelines based on consensus
reached during this meeting. The final document was ap-
proved at a second meeting on June 1, 2003.
Description of Guidelines
The timeline for key elements of the guidelines is de-
picted in Figure 1 and the guidelines developed are shown
in Figure 2. A physician order set for ADHF management
in the ED -OU was developed and is presented in Figure 3.
TIMELINE FOR ASSESSMENT AND TREATMENT
Figure 1 depicts the timeline for the diagnosis of ADHF,
initiation of treatment, assessment of response, and patient
www.theannals.com

disposition. Although the collection and synthesis of pa-
tient-specific clinical information takes time, we believe
the diagnosis of ADHF should be established within 2
hours after presentation to the ED -OU. Intravenous thera-
py should be initiated within 2 hours of establishing the di-
agnosis (≤4 h from the initial ED -OU contact). Within 2
hours of initiating intravenous therapy for ADHF, the pa-
tient’s response should be assessed and additional therapy
added as necessary. Over the following 6 –8 hours, re-
assessment of the patient’s response should continue. Ulti-
mately, within 12 hours of the initial ED -OU contact, the
patient’s disposition should be determined (eg, hospital ad-
mission or discharge home). Transfer out of ED -OU to the
patient’s final destination should then proceed, within 24
hours of the initial ED -OU contact.
ADHF TREATMENT ALGORITHM
Treatment of ADHF is generally based on the presence
or absence of pulmonary congestion (ie, volume overload)
and an assessment of the patient’s cardiac output.13-15 On
the left side of Figure 2, treatment recommendations are
given for patients with ADHF experiencing signs and
symptoms of volume overload. The right side of the algo-
rithm provides treatment recommendations for patients
with low cardiac output. Although this algorithm focuses
on parenteral therapy during the initial 24 hours, continua-
tion of patients’ chronic heart failure medications, includ-
ing chronic β-blocker therapy, is advised.8
Figure 1. Timeline for the management of acute decompensated heart failure (ADHF) in the emergency department/observation unit. CO = cardiac output; ED =
emergency department; ICU = intensive care unit; mod-sev = moderate to severe.
www.theannals.com
Guidelines for Acute Decompensated Heart Failure Treatment
Volume Overload
Patients with ADHF may present with varying degrees
of volume overload. To aid clinicians in determining the
severity of volume overload, common signs and symptoms
are provided in box A of Figure 2. Patients with mild vol-
ume overload (C) should be treated with intravenous di-
uretic therapy, typically loop diuretics (D). For the purpos-
es of this algorithm, diuretic dosages expressed are for in-
travenous furosemide, although equivalent doses of other
loop diuretics may be used. In patients taking oral diuretic
therapy at home, the total daily dose should be given as an
intravenous bolus, with a maximum initial dose equivalent
to furosemide 180 mg.16 Patients not taking oral diuretics
at home should be given an intravenous bolus of furose-
mide 40 mg,16 although patients with renal insufficiency
may require an even larger dose to produce the desired ef-
fect.17,18
Monitoring of diuretic use is driven by urine output
goals. For patients with normal renal function, the goal
urine output is ≥500 mL in the first 2 hours, whereas an ac-
ceptable urine output for patients with serum creatinine
>2.5 mg/dL is ≥250 mL (Table 1).16 If the patient fails to
attain adequate diuresis after the initial bolus, the previous
dose may be doubled (Figure 2, box F) and should be ad-
ministered within 2– 4 hours of the first dose to induce
more rapid diuresis (Figure 1).16 Electrolyte deficiencies,
particularly hypokalemia and hypomagnesemia, are the
most common adverse effects experienced with intra-
venous diuretic therapy, although hypotension, azotemia,
The Annals of Pharmacotherapy ■ 2004 April, Volume 38 ■ 651
RJ DiDomenico et al.

and renal dysfunction are also possible. A management 3).16 Patients with an inadequate response to furosemide
strategy for electrolyte disturbances in this setting has been should also be assessed for the presence of signs and
proposed and is included in the standing orders (Figure symptoms of moderate to severe volume overload (Figure

Figure 2. Acute decompensated heart failure (ADHF) treatment algorithm. AJR = abdominal jugular reflex; BiPAP = bilevel positive airway pressure; BNP = b-na-
triuretic peptide; CI = cardiac index; CPAP = continuous positive airway pressure; DOE = dyspnea on exertion; HJR = hepatojugular reflex; JVD = jugular venous
distention; PCWP = pulmonary capillary wedge pressure; PND = paroxysmal nocturnal dyspnea; SBP = systolic blood pressure; SCr = serum creatinine; SOB =
shortness of breath; SVR = systemic vascular resistance.

652 ■ The Annals of Pharmacotherapy ■ 2004 April, Volume 38 www.theannals.com

 Guidelines for Acute Decompensated Heart Failure Treatment

2, box E). If volume overload is present, these patients
may require additional therapy.
Because patients with more severe volume overload are
more likely to have an inadequate response to intravenous
diuretic therapy alone, the initial pharmacologic regimen
should be more aggressive. The initial drug regimen for
patients with moderate to severe volume overload and sys-
tolic blood pressure >90 mm Hg (Figure 2, box E) should
include both an intravenous diuretic and a parenteral va-
sodilator (F). Intravenous diuretics should be given as de-
scribed above for mild volume overload. However, either
intravenous nitroglycerin or nesiritide should be added to
intravenous diuretics to produce a more rapid response and
more effectively relieve the signs and symptoms of con-
gestion in these patients.
Intravenous nitroglycerin should be initiated as a contin-
uous infusion and may be increased every 5 minutes as
necessary (Table 1). If nesiritide is used, it should be ad-
ministered as an intravenous bolus of 2 µg/kg followed by
a continuous infusion of 0.01 µg/kg/min. If a satisfactory
response to nesiritide is not seen after 3 hours, considera-
tion may be given to increasing the dose as shown in Table
1. Hypotension is the most common adverse effect from
both intravenous nitroglycerin and nesiritide. Figure 4 pro-
vides guidance for the management of hypotension associ-
ated with vasodilators. Patients who fail to respond to in-
travenous diuretics, intravenous vasodilators, or both may
also be suffering from low cardiac output and may require
additional therapy to relieve symptoms.
Low Cardiac Output

The treatment recommendations for ADHF

Table 1. Monitoring Parameters for Medications Used to Treat
Acute Decompensated Heart Failure
Drug Monitoring Parameters
Diuretics symptom relief
vital signs
BUN, creatinine, electrolytes
urine output, goal:
normal renal function:
>500 mL within 2 h of iv
furosemide
renal insufficiency: >250 mL
within 2 h of iv furosemide
Nitroglycerin symptom relief
vital signs every 15 min until
on stable dose, then every
30 min for 1 h, then every
4h
urine output
may require ICU stay to
titrate infusion
if pulmonary artery catheter
in place, PCWP, SVR, CI
Inotropes telemetry
symptom relief
vital signs every 15 min until
on stable dose, then every
30 min for 1 h, then every
4h
urine output
may require ICU stay to
titrate infusion
if pulmonary artery catheter
in place, PCWP, SVR, CI
Nesiritide symptom relief
vital signs every 15 min for
1 h, then every 30 min for
1 h, then every 4 h
urine output
BUN, creatinine, electrolytes
BUN = blood urea nitrogen; CI = cardiac index; ICU = intensive care unit; PCWP =
pulmonary capillary wedge pressure; SBP = systolic blood pressure; SVR = sys-
temic vascular resistance.
Titration Parameters
starting dose: 5–10 µg/min
dose can be increased by
increments of 10–20 µg/min
every 5 min if necessary until
desired response achieved
dobutamine
dose can be increased by
increments of up to 2.5 µg/kg/min
every 5–15 min if necessary
until desired response achieved
milrinone
may take several hours to reach
steady-state concentrations
consider 50 µg/kg iv bolus over
10 min if immediate response
desired and BP will tolerate
(SBP >100 mm Hg)
dose titration should occur slowly
poor symptom relief and/or sub-
optimal diuretic response ≥3 h
after nesiritide initiation and
SBP >90 mm Hg
consider titrating nesiritide
nesiritide 1 µg/kg iv push, ↑ infu-
sion by 0.005 µg/kg/min
maximum: 0.03 µg/kg/min
after 1st dosage adjustment, may
up-titrate every hour thereafter
patients displaying signs and symptoms of low
cardiac output are depicted in box B of Figure
2. Patients with evidence of low cardiac output
should be considered for inotropic support.
Drug selection is based on 2 variables: con-
comitant therapy with an oral β-blocker and
baseline blood pressure (G). ADHF patients
with low cardiac output and systolic blood
pressure <90 mm Hg should be treated with
dobutamine initially (I). Additionally, these pa-
tients may require vasopressor support if symp-
tomatic hypotension develops. Patients with
low cardiac output and adequate blood pressure
(systolic blood pressure >90 mm Hg) who are
also taking β-blockers chronically may be giv-
en milrinone preferentially (H).8 Patients with
low cardiac output and adequate blood pressure
without concomitant β-blocker therapy may re-
ceive either milrinone or dobutamine.
Dobutamine should be initiated as a contin-
uous infusion and may be increased to achieve
the desired response (Table 1). Milrinone is
administered as a continuous infusion starting
at a dose of 0.375 µg/kg/min, although the ini-
tial dose must be lowered in patients with renal
insufficiency. To avoid hypotension, adminis-
tration of an intravenous bolus of milrinone is
discouraged. Milrinone has a half-life of ap-
proximately 2–3 hours; therefore, dose titra-
tion must occur slowly (Table 1). Patients with
low cardiac output who fail to respond to in-
otropic therapy should be evaluated for the
presence of very low cardiac output and may
require additional therapy.
Patients showing signs of very low cardiac
output (J) require more aggressive management.
Typically, these patients require admission to an
intensive care unit for close monitoring and may
require the placement of a pulmonary artery
catheter to more accurately assess their hemo-

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RJ DiDomenico et al.

Congestive Heart Failure Order Set

For Acute Decompensated Congestive Heart Failure Patients
Emergency Department Order Sheet

Date Time Primary Diagnosis: Acute Decompensated Congestive Heart Failure

Secondary Diagnosis: ________________________________________
Vital signs q4h and as directed by medications (see individual medications)

❏ Labs: Basic metabolic panel, calcium, magnesium, phosphorus, CBC, PT/INR, PTT, BNP, CK, CK-
MB, Troponin, O2 saturation
❏ Digoxin level (if outpatient medication)
❏ Patient Weight: ______________________
❏ Ins and Outs
❏ 12 Lead ECG
❏ AP and lateral
❏ Foley catheter prn heavy diuresis
❏ Diet: <2.4g Na, low fat
❏ Fluid restriction: 1800 mL/24h; if Na <131 mg/dL, restrict fluid to 1500 mL/24h

Intravenous Furosemide
❏ If furosemide naïve, furosemide 40 mg IVP x 1 dose
❏ If on furosemide as outpatient
Total daily dose as IV _____________ mg: maximum 180 mg
• Goal: >500 mL urine output within 2 hours for normal renal function
>250 mL urine output within 2 hours if renal insufficiency
• If goal urine output not met within 2 hours, double the furosemide dose to a maximum of 360 mg
IV
• Monitor symptom relief, vital signs, BUN, SCr, electrolytes

Nesiritide
❏ 2 µg IV push followed by 0.01 µg/kg/min IV infusion
❏ If symptomatic hypotention during infusion, discontinue nesiritide
• Monitor symptom relief, vital signs q15m × 1 hour, then q30min × 1 hour, then q4h, urine
output, electrolytes, BUN, SCr, magnesium, calcium, phosphorus
❏ If poor symptom relief or diuretic response ≥3 hours after nesiritide therapy initiation AND SBP
≥90 mm Hg, may consider titration of nesiritide
• Nesiritide 1 µg/kg IVP and increase infusion by 0.005 µg/kg/min
• May increase infusion rate q1h after first dosage, increase to a maximum dose of
0.03 µg/kg/min

Nitroglycerin 50 mg/250 mL
❏ 5 µg/min IV infusion; titrate dose q5min by 10–20 µg/min to achieve symptom relief
• Monitor symptom relief, vital signs q15min until stable dose, then q30min × 1 hour, then q4h,
ECG, urine output

____________________________________________________ _________________________
Physician Signature Date

Figure 3. Physician order set for the initial management of acute decompensated heart failure in the emergency department/observation unit. AP = anterior/posterior;
BNP = b-natriuretic peptide; BUN = blood urea nitrogen; CBC = complete blood cell count; CK = creatine kinase; CK-MB = creatine kinase MB isoenzyme; ECG = elec-
trocardiogram; INR = international normalized ratio; IVP = intravenous push; PT = prothrombin time; PTT = partial thromboplastin time; SBP = systolic blood pressure;
SCr = serum creatinine.
(continued on page 655)

654 ■ The Annals of Pharmacotherapy ■ 2004 April, Volume 38 www.theannals.com

 Guidelines for Acute Decompensated Heart Failure Treatment

Congestive Heart Failure Order Set

For Acute Decompensated Congestive Heart Failure Patients
Emergency Department Order Sheet

Dobutamine 500 mg/250 mL

❏ 2.5 µg/kg/min IV infusion and titrate dose every 5 minutes to desired response to a maximum dose
of 20 µg/kg/min
• Monitor symptom relief, vital signs q15min until stable dose, then q30min × 1 hour, then
q4h; ECG; urine output

Milrinone 20 mg/100 mL
❏ 0.375 µg/kg/min
• Monitor symptom relief, vital signs q15min until stable dose, then q30min × 1 hour, then
q4h; ECG; urine output

❏ Digoxin ________________________________________________
Dose Route Frequency

❏ Lisinopril PO ________________________________________________
Dose Frequency

❏ Losartan PO ________________________________________________
Dose Frequency

❏ Metoprolol PO ________________________________________________
Dose Frequency

❏ Spironolactone PO ______________________________________________
Dose Frequency

Electrolyte Replacement
❏ Potassium
level (mEq/L) IV dose (over 1 h) PO dose When to recheck potassium
3.7–3.9 20 mEq 40 mEq 12 hours or next morning
3.4–3.6 20 mEq × 2 doses 40 mEq × 2 doses 6 hours or next morning
3.0–3.3 20 mEq × 4 doses 40 mEq × 3 doses 4 hours after last dose
<3.0 20 mEq × 6 doses Give IV only 1 hour after last dose
• If Clcr <30 mL/min, reduce dose by 50%

❏ Magnesium
level (mEq/L) IV dose PO dose (Mg oxide) When to recheck magnesium
1.9 Give PO only 140 mg Next morning
1.3–1.8 1 g MgSO4 for every Give IV only Next morning
0.1 below 1.9
(max 6 g)
<1.3 8 g MgSO4 Give IV only 6 hours after last dose
or next morning

• MgSO4 1–2 g, infuse over 1 hour

• MgSO4 3–6 g, infuse ≤2 g/hour

____________________________________________________ _________________________
Physician Signature Date

Figure 3 (continued). Clcr = creatinine clearance; ECG = electrocardiogram.

www.theannals.com The Annals of Pharmacotherapy ■ 2004 April, Volume 38 ■ 655

RJ DiDomenico et al.
dynamics. Patients with very low cardiac output who also
have sufficient blood pressure (systolic blood pressure >90
mm Hg) may benefit from the addition of intravenous di-
uretic therapy and intravenous vasodilators (F).
Explanation of Drug Therapy Recommendations
DIAGNOSIS OF ADHF
The diagnosis of ADHF incorporates various pieces of
clinical information including, but not limited to, history
and physical, chest X-ray, laboratory values, and diagnos-
tic imaging studies. Recently, elevated b-natriuretic peptide
(BNP) serum levels have been shown to correlate with
ADHF diagnosis, New York Heart Association functional
class, and mortality.19-21 In one analysis, elevated BNP lev-
els >100 pcg/mL were associated with an 83% accuracy of
differentiating ADHF from other causes and an odds ratio
of 29.60 (17.75– 49.37) of predicting ADHF.19 However,
elevations in BNP levels alone are not accurate in diagnos-
ing ADHF. In the same analysis, patients with ADHF had
significantly higher BNP levels (mean ± SD; 675 ± 450
pcg/mL) than patients with underlying left-ventricular
function without evidence of ADHF (mean ± SD; 346 ±
390 pcg/mL), p < 0.001, and patients with normal left-ven-
tricular function without ADHF symptoms (110 ± 225
pcg/mL), p < 0.001. This would imply that a BNP level
>100 pcg/mL without other evidence of ADHF is insuffi-
Figure 4. Algorithm for the management of hypotension associated with parenteral vasodilator therapy in acute decompensated heart failure. ACE = angiotensin-
converting enzyme; ED = emergency department.
656 ■ The Annals of Pharmacotherapy ■ 2004 April, Volume 38
cient to make the diagnosis. The ADHF guidelines devel-
oped here recommend an assessment of BNP levels (Fig-
ure 3) to aid in the diagnosis. However, elevated BNP lev-
els (>100 pcg/mL) in the absence of other signs and symp-
toms of ADHF may not be useful.
EARLY INITIATION OF THERAPY
The guidelines described here promote an early aggres-
sive approach to initiating drug therapy for patients with
ADHF. Emerging data suggest that early initiation of intra-
venous vasoactive therapy reduces hospital length of stay.
A preliminary analysis of 1414 patients from ADHERE
(Acute Decompensated Heart Failure National Registry)
indicates that length of stay in patients receiving vasoac-
tive therapy (intravenous vasodilators, nesiritide, or in-
otropes) in the ED -OU decreased by 3.1 days compared
with patients in whom vasoactive therapy was initiated in
the hospital (6.3 ± 6.6 vs 9.4 ± 10.9 days; p < 0.004).22
DIURETICS
Diuretics are effective in providing symptomatic relief
and should be the first-line treatment for patients experi-
encing pulmonary congestion or peripheral edema from
fluid overload. However, there is little evidence that diuretics
are effective in improving outcomes associated with ADHF.
Diuretics have been shown to cause neurohormonal activa-
www.theannals.com

tion and systemic vasoconstriction.17,18,23,24 Consequently, he-
modynamic improvements with diuretics are somewhat at-
tenuated and relief of symptoms may be incomplete (diuretic
resistance), increasing the risk of rehospitalization.15 Al-
though diuretic resistance can be overcome by administer-
ing the agent as a continuous infusion or combining a loop
and thiazide diuretic, patients with ADHF may derive more
benefit from the addition of intravenous vasoactive therapy
(vasodilator or inotrope).17,18,25-27
VASODILATORS
Vasodilators promote a rapid reversal of the decompen-
sated state by improving resting hemodynamics. Vasodila-
tors have been shown to significantly reduce ventricular
filling pressures (pulmonary capillary wedge pressure
[PCWP], or preload) within 24– 48 hours and reduce my-
ocardial oxygen consumption.15,28 Vasodilators can also de-
crease systemic vascular resistance (SVR, or afterload),
decrease ventricular workload, increase stroke volume, and
improve cardiac output.15
Nitroglycerin is a vasodilator commonly used to relieve
pulmonary congestion in patients with ADHF. While an
effective vasodilator, frequent dose titration of intravenous
nitroglycerin is often necessary to produce the desired
hemodynamic effects and symptomatic relief. In fact, dos-
es ≥140–160 µg/min may be necessary to sufficiently de-
crease PCWP and alleviate symptoms of ADHF.29-32 Un-
fortunately, early tachyphylaxis can occur in patients re-
ceiving intravenous nitroglycerin, necessitating additional
titration and higher doses.33 Because intravenous nitroglyc-
erin requires frequent dose titration and may cause dose-
dependent hypotension, patients are often monitored in an
intensive care unit and may require invasive hemodynamic
monitoring while being treated with this drug.
Nesiritide is the newest addition to the treatment arsenal
for ADHF. It is a recombinant form of human BNP, an en-
dogenous neurohormone produced in the ventricles in re-
sponse to the increased wall stress that occurs from volume
overload in patients with ADHF. Nesiritide has been shown
to improve hemodynamics and alleviate the symptoms of
ADHF (dyspnea, global clinical status).34-36 Because the ef-
fects of nesiritide are predictable and sustained at the rec-
ommended dosage, titration of the infusion rate is not com-
monly required nor is invasive hemodynamic monitoring.
Therefore, patients treated with nesiritide may not require
as close monitoring as may be necessary with other va-
sodilators (ie, nitroglycerin or nitroprusside), perhaps
negating the need for intensive care unit stays.
When compared with intravenous nitroglycerin in the
VMAC (Vasodilation in the Management of Acute Con-
gestive Heart Failure) study, nesiritide produced greater re-
ductions in the PCWP within 15 minutes, and these effects
were sustained through 24 hours (PCWP –8.2 mm Hg in
the nesiritide group vs – 6.3 mm Hg in the nitroglycerin
group at 24 h; p = 0.04).36 Through 48 hours, the PCWP
remained lower in nesiritide-treated patients compared
with those receiving nitroglycerin, although the differences
www.theannals.com The Annals of Pharmacotherapy
Guidelines for Acute Decompensated Heart Failure Treatment
were no longer statistically significant. Symptomatic im-
provement was similar in both groups at both 3 and 24
hours. Patients treated with nesiritide experienced fewer
adverse effects compared with those given nitroglycerin,
although the incidence of hypotension was similar.
In addition to the beneficial hemodynamic benefits and
symptomatic relief seen with nesiritide, studies suggest
that nesiritide may reduce hospital readmissions for
ADHF. Hospital readmission for ADHF within 30 days
was less common in patients treated with nesiritide com-
pared with nitroglycerin in the VMAC study (7% vs 13%,
respectively; p values not reported).36 One study demon-
strated similar trends when nesiritide was compared with
dobutamine (4% readmission for heart failure with nesiri-
tide vs 13% with dobutamine; p = 0.081).37 In the PROAC-
TION (Prospective Randomized Outcomes Study of Acutely
Decompensated Congestive Heart Failure Treated Initially in
Outpatients with Natrecor) study, nesiritide was associated
with a 57% reduction in hospital readmissions within 30 days
compared with standard therapy (p = 0.058).38 While each of
these findings was not statistically significant, they are en-
couraging and deserve more investigation.
Because intravenous vasodilators rapidly improve
hemodynamics, resulting in more rapid symptomatic im-
provement, we believe they should be initiated early in the
treatment course for ADHF. Patients who fail to respond
adequately to intravenous diuretics or who present with
moderate to severe signs of congestion are candidates for in-
travenous vasodilator therapy provided they have adequate
systolic blood pressure (>90 mm Hg).
INOTROPES
Historically, inotropes have been the mainstay for adju-
vant therapy for ADHF because of their beneficial effects
on hemodynamic parameters, namely improved cardiac
output.39,40 However, large-scale clinical trials evaluating
dobutamine and milrinone for ADHF are lacking. The use
of dobutamine is supported by several small studies docu-
menting improved hemodynamics in ADHF patients.41-43
However, evidence from larger morbidity and mortality tri-
als demonstrates a lack of efficacy in many ADHF patients
and has revealed some safety concerns in those given in-
otropic support.44-47 Inotropes increase heart rate, increase
myocardial oxygen demand, aggravate ischemia, precipitate
arrhythmias, and cause hypotension.44,48-50 The PRECE-
DENT (Prospective Randomized Evaluation of Cardiac Ec-
topy with Dobutamine or Nesiritide Therapy) trial demon-
strated that dobutamine increases the incidence of ventricu-
lar ectopy and ventricular tachycardia compared with
nesiritide, whereas symptomatic hypotension was less
common.50 The only large-scale, placebo-controlled study
evaluating the use of milrinone (OPTIME-CHF; Out-
comes of a Prospective Trial of Intravenous Milrinone for
Exacerbations of Chronic Heart Failure) in patients with
ADHF failed to demonstrate significant improvements in
total days hospitalized, symptomatic relief, or mortality
compared with placebo.44 Milrinone was, however, associ-
■ 2004 April, Volume 38 ■ 657
RJ DiDomenico et al.
ated with an increased incidence of adverse effects com-
pared with placebo, particularly sustained hypotension and
tachyarrthmias. The American Heart Association and
American College of Cardiology discourage intermittent
outpatient inotropic support for patients with severe heart
failure due to the increased mortality and other adverse
outcomes associated with this approach (Class III recom-
mendation).8
Given the lack of compelling evidence supporting their
use and the increased incidence of adverse effects, inotrop-
ic support for patients with ADHF should be reserved for
patients showing signs of low or very low cardiac output
(Figure 1). Because milrinone is prone to causing hypoten-
sion, patients with systolic blood pressure <90 mm Hg
should receive dobutamine preferentially. For ADHF pa-
tients with adequate blood pressure, selection of inotropic
support should be dependent on the presence or absence of
concomitant β-blocker therapy. Because dobutamine ex-
erts its effects by stimulating β-adrenergic receptors, much
higher doses are required to overcome the effects of chron-
ic β-blocker therapy in order to significantly increase car-
diac output. In contrast, concomitant β-blocker therapy in
ADHF does not attenuate the response to milrinone.51 For
ADHF patients on chronic β-blocker therapy, milrinone is
preferred.8 In patients not receiving concomitant β-block-
ers, either inotrope may be used.
Limitations
Several limitations were identified in the development
and implementation phases of the proposed ADHF guide-
lines including awareness, physician support, coordination
of efforts among various groups of clinicians, formulary
restrictions, and time constraints. To increase awareness
and elicit feedback from various clinicians, we performed
several educational inservices, developed an ADHF order
set (Figure 3), and tailored the guidelines to satisfy any in-
stitution-specific policies or restrictions. To date, multiple
institutions have implemented the ADHF guidelines, and
their clinical impact is being studied at 3 of those hospitals.
Summary
Evidence-based therapies for the treatment of ADHF are
severely lacking. The current standards of care to treat
ADHF (intravenous diuretics, nitroglycerin, inotropic sup-
port) are based largely on small studies documenting im-
provements in hemodynamic endpoints with little emphasis
on cardiovascular outcomes. Because of the paucity of data,
ADHF is unlike most acute cardiac conditions in that it has
previously been without consensus guidelines for appropriate
management. In describing our efforts here, we hope to en-
courage others to target ADHF as a public health priority and
adopt therapeutic approaches that maximize patient health
without exhausting healthcare and economic resources.
Robert J DiDomenico PharmD, Clinical Assistant Professor, De-
partment of Pharmacy Practice; Affiliate Faculty, Center for Pharma-
coeconomic Research, University of Illinois at Chicago, Chicago, IL
658 ■ The Annals of Pharmacotherapy ■ 2004 April, Volume 38
Hayley Y Park PharmD, Research Fellow, Center for Pharma-
coeconomic Research
Mary Ross Southworth PharmD, Clinical Assistant Professor,
Department of Pharmacy Practice and Section of Cardiology, Uni-
versity of Illinois at Chicago
Heather M Eyrich PharmD, Clinical Assistant Professor, Depart-
ment of Pharmacy Practice, University of Illinois at Chicago
Richard K Lewis PharmD MBA, Vice President, Pharmacy Ser-
vices, Mercy Resource Management, Inc., Naperville, IL; Clinical
Assistant Professor, Department of Pharmacy Practice, University
of Illinois at Chicago
Jamie M Finley PharmD, Coordinator of Clinical Pharmacy Pro-
grams, Mercy Resource Management, Inc., Naperville, IL; Clinical
Assistant Professor, Department of Pharmacy Practice, University
of Illinois at Chicago
Glen T Schumock PharmD MBA FCCP, Director, Center for Phar-
macoeconomic Research, University of Illinois at Chicago; Associ-
ate Professor, Department of Pharmacy Practice, University of Illi-
nois at Chicago
Reprints: Glen T Schumock PharmD MBA FCCP, Center for Phar-
macoeconomic Research, University of Illinois at Chicago, 833 S.
Wood St. (M/C 886), Chicago, IL 60612-7230, fax 312/996-0379,
schumock@uic.edu
We acknowledge the members of the MRMI Pharmacy Clinical Resource Commit-
tee in addition to Drs. Finley and Lewis for assistance in developing the guidelines
described here: Michael Ahrens BSPharm, Heather Brockmiller PharmD, Carlos
Lacy PharmD, Andrea Roberson PharmD, Randy Sasaki PharmD, Patricia Siola
PhD MBA BSPharm, and Leslie Stewart PharmD. Additionally, we would like to rec-
ognize the efforts of the non-MRMI participants of the Expert Panel in addition to
Drs. DiDomenico, Southworth, Eyrich, and Schumock. These individuals are con-
sidered thought leaders in the areas of heart failure and outcomes research and in-
clude Mitchell Saltzberg MD and Charles Emerman MD. Their clinical expertise and
insight was extremely helpful in the development of these guidelines.
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EXTRACTO
OBJETIVO: Describir el desarrollo de unas guías para el manejo de fallo
cardíaco agudo descompensado en el Departamento de
Emergencia/Unidad de Observación en un escenario de hospitales que
son parte de una organización grupal de compra.
EXTRACCIÓN DE DATOS: Un repaso sistemático de la literatura fue
conducido para identificar evidencia de eficacia y seguridad de varios
medicamentos usados en el manejo de fallo cardíaco agudo
descompensado.
SELECCIÓN DE ESTUDIO Y EXTRACCIÓN DE DATOS: Un método consenso
general fue usado para desarrollar unas guías y éstas fueron revisadas
por un panel de expertos. Las guías finales fueron aprobadas el 1 de
junio de 2003.
SÍNTESIS DE DATOS: Las guías finales son descritas e incluídas. Estas
fueron organizadas basadas en la sintomatología del paciente en el
momento del diagnóstico de fallo cardíaco agudo descompensado es
efectuado. Los pacientes con evidencia de sobrecarga de volumen
requieren diurético IV + vasodilatador IV para aliviar los síntomas.
Mientras que los pacientes con síntomas y signos de rendimiento
cardíaco bajo requieren ayuda con agentes inotrópicos. Una guía con el
■ 2004 April, Volume 38 ■ 659
 RJ DiDomenico et al.
período de tiempo asignado para el diagnóstico, tratamiento, re-
evaluación y disposición se provee, y se exhorta una intervención
temprana y agresiva en el tratamiento de los pacientes con fallo cardíaco
agudo descompensado.
CONCLUSIONES: La hospitalización de pacientes con fallo cardíaco agudo
descompensado es común y costosa. Actualmente, unas guías de
consenso general para el tratamiento de fallo cardíaco agudo
descompensado no existen, resultando en un manejo inconsistente e
ineficiente. La creación de éstas guías podrían brindar una solución al
esfuerzo de los hospitales para el manejo de fallo cardíaco agudo
descompensado y el proceso por las cuales estas guías fueron
desarrolladas es de utilidad.
Wilma M Guzmán-Santos
RÉSUMÉ
OBJECTIF: Décrire le processus d’élaboration de lignes directrices pour le
traitement de la décompensation aiguë de l’insuffisance cardiaque
(DAIC) à l’urgence/unité d’observation pour des hôpitaux qui font partie
d’une organisation d’achats de groupe.
REVUE DE LITTÉRATURE: Une revue de la documentation scientifique a été
réalisée afin d’identifier les données probantes d’efficacité et d’innocuité
660 ■ The Annals of Pharmacotherapy ■ 2004 April, Volume 38
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des différents médicaments utilisés dans le traitement de la DAIC. La
méthodologie par consensus de groupe a ensuite été utilisée pour
élaborer les lignes directrices. Un groupe d’experts a ensuite revu et
révisé les lignes directrices proposées. Le document final a été approuvé
le 1er juin 2003.
RÉSUMÉ: L’organisation de ces lignes directrices est basée sur la
symptomatologie présente au moment où le diagnostic de DAIC est
posé. Les patients avec surcharge volémique recevront des diurétiques
IV + des vasodilatateurs IV alors que ceux présentant des signes et
symptômes de bas débit cardiaque recevront une médication inotrope
pour traiter leur épisode de DAIC. Un schéma décrivant les étapes à
réaliser en fonction du temps (diagnostic, traitement, réévaluation, et
hospitalisation/autorisation du congé) est présenté et favorise une
approche de traitement précoce et agressive.
CONCLUSIONS: Les hospitalisations pour une DAIC sont fréquentes et
coûteuses. Actuellement, des lignes directrices pour le traitement de la
DAIC n’existent pas, ce qui peut résulter en un traitement inadéquat. Par
conséquent, les hôpitaux ayant des difficultés avec le traitement de la
DAIC pourraient trouver utiles ces lignes directrices et le processus à
l’aide duquel elles ont été élaborées.
Alain Marcotte
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