Download Recommendations for the Evaluation and Management of the

SOCIETY
OF
CHEST PAIN CENTERS RECOMMENDATIONS
Society of Chest Pain Centers Recommendations for the
Evaluation and Management of the Observation Stay Acute
Heart Failure Patient
A Report From the Society of Chest Pain Centers Acute Heart Failure
Committee
WRITING COMMITTEE MEMBERS
Heart Failure Executive Committee
Co-Chairs:
W. Frank Peacock, MD, Cleveland Clinic Foundation, Cleveland, OH
Gregg C. Fonarow, MD, FACC, Ahmanson-UCLA Cardiomyopathy Center, David Geffen School of Medicine at UCLA, Los Angeles, CA
Heart Failure Diagnosis Subcommittee
Chair:
Members:
Douglas S. Ander, MD, Emory University School of Medicine, Atlanta,
GA
Alan Maisel, MD, La Jolla VA Medical Center, San Diego, CA
Judd E. Hollander, MD, From the University of Pennsylvania, Philadelphia, PA
James L. Januzzi Jr, MD, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Clyde W. Yancy, MD, Baylor Heart & Vascular Institute, Dallas, TX
Heart Failure Risk Stratification Subcommittee
Co-chairs:
Members:
Sean P. Collins, MD, MSc, University of Cincinnati, Cincinnati, OH
Mihai Gheorghiade, MD, Northwestern Memorial Hospital, Bluhm Cardiovascular Institute of Northwestern, Chicago, IL
Neal L. Weintraub, MD, University of Cincinnati, Cincinnati, OH
Alan B. Storrow, MD, Vanderbilt University Medical Center, Nashville,
TN
Peter S. Pang, MD, Northwestern University Feinberg School of Medicine,
Chicago, IL
William T. Abraham, MD, FACP, FACC, FAHA, The Ohio State University Medical Center, Columbus, OH
Brian Hiestand, MD, MPH, The Ohio State University Medical Center,
Columbus, OH
Heart Failure Treatment Subcommittee
Co-chairs:
Members:
J. Douglas Kirk, MD, University of California, Davis Medical Center, Sacramento, CA
Gerasimos Filippatos, MD, University of Athens Hospital, Athens, Greece
Mihai Gheorghiade, MD, Northwestern Memorial Hospital, Bluhm Cardiovascular Institute of Northwestern, Chicago, IL
Peter S. Pang, MD, Northwestern University Feinberg School of Medicine,
Chicago, IL
Phillip Levy, MD, MPH, Wayne State University School of Medicine,
Detroit, MI
Ezra A. Amsterdam, MD, FACC, University of California School of
Medicine and Medical Center, Davis and Sacramento, CA
© 2008 Lippincott Williams & Wilkins
83
Society of Chest Pain Centers Acute Heart Failure Committee
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Heart Failure Discharge Criteria Subcommittee
Co-chairs:
Members:
Deborah B. Diercks, MD, FACEP, University of California, Davis Medical Center, Sacramento, CA
Ezra A. Amsterdam, MD, FACC, University of California School of Medicine and Medical Center, Davis and
Sacramento, CA
David F. Gaieski, MD, FACEP, University of Pennsylvania, Philadelphia, PA
Diane Gurney, RN, MS, CEN, Cape Cod Hospital, Hyannis, MA
Heart Failure Patient Education Subcommittee
Co-chairs:
Members:
Robin J. Trupp, PhD(c), MSN, APRN, BC, FAHA, The Ohio State University College of Nursing, Columbus,
OH
Brian Hiestand, MD, MPH, The Ohio State University Medical Center, Columbus, OH
Gail Dodge, RN, MSN, CEN, FreemanWhite, Inc., Charlotte, NC
Christy O. Hayes, MSN, APRN, Wake Forest University Baptist Hospital, Winston-Salem, NC
Chadwick D. Miller, MD, Wake Forest University School of Medicine, Winston-Salem, NC
Elsie Selby, MSN, ARNP, CCNS, CCRN, Ephraim McDowell Regional Medical Center, Danville, KY
Peer Reviewers
Raymond D. Bahr, MD, FACC, St. Agnes Healthcare, Baltimore, MD
Andra L. Blomkalns, MD, University of Cincinnati, Cincinnati, OH
James McCord, MD, FACC, Henry Ford Hospital, Wayne State University, Detroit, MI
Richard M. Nowak, MD, MBA, FACEP, FAAEM, Henry Ford Health System, Detroit, MI
Robert J. Stomel, DO, FACC, Cardiovascular Clinical Associates, Farmington Hills, MI
RELATIONSHIP WITH INDUSTRY: WRITING GROUP AND PEER REVIEWERS
WRITING COMMITTEE MEMBERS
Co-Chairs:
Gregg C. Fonarow, MD
Grant/research support from GlaxoSmithKline, Medtronic, Scios, Pfizer, NHLBI
Consultant to GlaxoSmithKline, Medtronic, Scios, Nitromed, Astra Zeneca, Otsuka, Amgen
Regular speaker for GlaxoSmithKline, Medtronic, Nitromed, Astra Zeneca, Novartis, Pfizer
W. Frank Peacock, MD
Grant/research support from Abbott, Biosite, Brahms, CHF Solutions, Heartscape, Inovise, Inverness, PDL,
Scios, The Medicines Co
Regular speaker for Abbott, Beckman-Coulter, Biosite, Ortho Clinical Diagnostics, PDL, Scios
Stock shareholder of Vital Sensors
Scientific advisory board member at Abbott, Biosite, Inovise, Inverness, Ortho Clinical Diagnostics, Vital
Sensors
William T. Abraham, MD, FACP, FACC, FAHA
No financial interests or commercial affiliations
Ezra A. Amsterdam, MD, FACC
Consultant to Pfizer, Biosite, Advogent, Merck, Sanofi, BMS, Heartscape
Regular speaker for Pfizer, Biosite, Advogent, Merck, Sanofi, BMS, Heartscape, Astra Zeneca, GSK
Douglas S. Ander, MD
No financial interests or commercial affiliations
Sean P. Collins, MD, MSc
Grant/research support from Biosignetics, Inovise Medical Inc, NIH/NHLBI
Consultant to Scios, Abbot Point-of-Care, PDL BioPharma, Astellas and Otsuka Pharmaceuticals
Deborah B. Diercks, MD, FACEP
Grant/research support from Dade-Behring
Consultant to Astellas
Regular speaker for Scios
Gail Dodge, RN, MSN, CEN
No financial interests or commercial affiliations
84
© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008 Kay Holmes, RN, BSN, MSA, The Society of Chest Pain Centers,
Columbus, OH
Gerasimos Filippatos, MD
No financial interests or commercial affiliations
David F. Gaieski, MD, FACEP
No financial interests or commercial affiliations
Mihai Gheorghiade, MD
Grant/research support from National Institutes of Health, Otsuka, Sigma Tau, Merck, Scios
Consultant to Debbio Pharm, Errekappa Terapeutici, GlaxoSmithKline, Protein Design Labs, Medtronic,
Johnson and Johnson, Solvay
Honoraria receved from Abbot, AstraZeneca, GlaxoSmithKline, Medtronic, Otsuka, Protein Design Labs, Scios
Inc., and Sigma Tau for speaking and presenting engagements
Diane Gurney, RN, MS, CEN
No financial interests or commercial affiliations
Christy O. Hayes, MSN, APRN
No financial interests or commercial affiliations
Brian Hiestand, MD, MPH
No financial interests or commercial affiliations
Judd E. Hollander, MD
Grant/research support from Inverness Medical, Biosite, Siemens, Sanofi-Aventis, Abbott
Consultant to Sanofi-Aventis, GSK, PCL, BMS, Genentech, Astra Zeneca, Baxter, The Medicines Company, Otsuka
America
Stock shareholder of mutual funds with various holdings
Honorarium/expenses: Sanofi-Aventis, Biosite, Scios, GSK, PDL, BMS, Ethicon, The Medicines Company, Genentech
Kay Holmes, RN, BSN, MSA
Employed by The Society of Chest Pain Centers
James L. Januzzi Jr, MD
Grant/research support from Roche Diagnostics, Inverness Medical Innovations, Dade Behring
Consultant to Roche Diagnostics, Dade Behring, Inverness Medical, Biosite, Ortho
Regular speaker for Roche Diagnostics
J. Douglas Kirk, MD
Consultant to Biosite JNC, Otsuka, Sanofi-Aventis
Regular speaker for Sanofi-Aventis, Biosite
Phillip Levy, MD, MPH
Grant/research support from The Medicines Company, ProMedDx, LLC
Consultant to Electrosonics Medical, Inc
Alan Maisel, MD
Grant/research support from Bayer, Abbot, Roche
Consultant to Biosite
Regular speaker for Scios
Chadwick D. Miller, MD
Grant/research support from Biosite, Schering-Plough Pharaceuticals, Bristol-Myers Squibb/Sanofi Pharmaceuticals
Partnership, Heartscape Technologies Inc, Inovise Medical, Breathquant Medical LLC, Johnson & Johnson, Scios
Inc.
Consultant to Molecular Insight, The Medicines Company
Peter S. Pang, MD
Grant/research support from PDL BioPharma
Consultant to PDL Biopharma, Otsuka
Honoraria received from Otsuka, Solvay Pharmaceuticals
Elsie Selby, MSN, ARNP, CCNS, CCRN
No financial interests or commercial affiliations
Alan B. Storrow, MD
© 2008 Lippincott Williams & Wilkins
85
Society of Chest Pain Centers Acute Heart Failure Committee
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Grant/research support from Inverness Medical Innovations, Biosignetics, PDL BioPharma, Abbott Diagnostics,
Roche Diagnostics
Consultant to Molecular Insight Pharaceuticals, Abbott Diagnostics, The Medicines Company, Sanofi-Aventis,
Otsuka Pharmaceuticals
Robin J. Trupp, PhD(c), MSN, APRN, BC, FAHA
No financial interests or commercial affiliations
Neal L. Weintraub, MD
Grant/research support from National Institutes of Health, Pfizer Corporation
Clyde W. Yancy, MD
Grant/research support from Scios
Consultant to Otsuka, Scios
Peer Reviewers
Raymond D. Bahr, MD, FACC
No financial interests or commercial affiliations
Andra L. Blomkalns, MD
James McCord, MD, FACC
Grant/research support from Brahms Diagnostics, Molecular Insight
Regular speaker for Biosite Diagnostics
Richard M. Nowak, MD, MBA, FACEP, FAAEM
No financial interests or commercial affiliations
Robert J. Stomel, DO, FACC
No financial interests or commercial affiliations
86
© 2008 Lippincott Williams & Wilkins
SOCIETY
OF
CHEST PAIN CENTERS RECOMMENDATIONS
Table of Contents
Preamble ............................................................................................................................87
Diagnosis............................................................................................................................90
Risk Stratification ..............................................................................................................95
Acute Heart Failure Treatment .......................................................................................102
Discharge Criteria............................................................................................................110
Patient Education.............................................................................................................115
© 2008 Lippincott Williams & Wilkins
87
SOCIETY
OF
CHEST PAIN CENTERS RECOMMENDATIONS
Preamble
Committee Co-Chairs: W. Frank Peacock, MD, and Gregg C. Fonarow, MD, FACC
eart failure is a leading cause of morbidity and mortality in the United States.1
Approximately 5 million patients in the United States have heart failure. In addition,
heart failure patients are responsible for 12 to 15 million physician office visits per year
and 6.5 million hospital days.2 Each year, there are 1.1 million hospitalizations where
heart failure was the primary admission diagnosis and another 2.4 million where heart
failure was a secondary diagnosis. Heart failure accounts for 3.6% of the total national
hospital bill and 5.8% of all Medicare charges. It was the second leading principal
diagnosis for hospital admissions among Medicare patients in 2004.3
The United States is currently in the midst of a heart failure epidemic. With over 1.1
million hospitalizations annually, it is common for heart failure patients to have frequent
emergency department (ED) visits, most culminating in inpatient hospitalization. Many
heart failure patients stabilize within the first few hours of presentation, yet once admitted
for inpatient hospitalization, remain hospitalized for a mean of 6 days while medications
are adjusted. Although permitted to be virtual units, optimal short-stay observation units
are designated areas, commonly located adjacent to EDs, that accommodate patients who
require a brief period of observation or therapy. They have been developed as an extension
of emergency services, providing continued patient management to better define diagnoses, treat certain conditions, and to reduce costs and inappropriate admissions and
discharges. The ultimate goal is to improve the quality of medical care through extended
observation and treatment, while reducing inappropriate admissions and healthcare costs.
Short stay observation units have been demonstrated to provide effective and cost-efficient
care for a variety of conditions, including chest pain and asthma. Initial experience
suggests that certain heart failure patients may be safely and effectively managed on
short-stay observation units, avoiding a more prolonged hospitalization. Thus, observation
stay monitoring and treatment is a highly desirable option for selected heart failure
patients. Methods to develop and support this patient care pathway are needed.
The Society of Chest Pain Centers (SCPC) is a nonprofit patient-centric organization
whose primary mission is to reduce cardiovascular morbidity and mortality through
education and accreditation. To further that mission, it is a natural progression for the
SCPC to engage in the assembly of consensus recommendations for the care of the heart
failure patient using a short-stay treatment and management strategy.
The SCPC is committed to improving medical practice, education, prevention,
management, and evaluation of the short-stay heart failure patient. Expert analysis of the
available data documenting benefits and risks of diagnostic strategies and therapies can
produce helpful consensus recommendations, facilitating the provision of cost-effective,
high-quality care. This may help to result in more optimal patient clinical outcomes. The
committees performed an assessment of the current evidence and best practice standards
to develop written recommendations applicable to clinical practice.
Heart failure experts were charged with completing an extensive literature review
and rigorous analysis to weigh the strength of evidence based on patient clinical outcomes
and the efficacy of current data to assure recommendations provided quality, cost-effective
care for the patient suffering from heart failure. The experts focused on patients that may
be considered candidates for care in the observation unit setting.
These recommendations are intended to assist health care providers in their practice
and to provide guidance in clinical decision making. Compiling best practice standards for
H
Copyright © 2008 by Lippincott Williams & Wilkins
ISSN: 1535-282X/08/0702-0088
DOI: 10.1097/HPC.0b013e318177dc74
88
© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
the diagnosis, risk stratification, treatment, discharge instructions, and patient education provides evidence for the evaluation and management of the observation stay heart failure
patient presenting to the ED. The recommendations are intended to enhance, not replace clinical judgment. Their
healthcare provider, taking into account all of the circumstances presented by that patient, must make the ultimate
judgment regarding care of individual patients.
Definition
For the purposes of this project, recommendations are
written for the Evaluation and Management of the Observation Stay Acute Heart Failure Patient. These recommendations represent all relevant evidence-based best practice supported through peer published research and consider
consensus insight from years of expert clinical experience.
The goal of these recommendations is to provide a basis to
educate physicians and help them form clinical judgments
applicable to their medical practice. Finally, because of the
consensus nature of much of the content of these recommendations, after their completion they were distributed to a
panel of reviewers and to the SCPC Board for approval and
endorsement. They have also been distributed to the relevant
national societies for comments and endorsement.
• There have been various definitions applied for acute heart
failure, also referred to as acute decompensated heart failure or acute heart failure syndromes. Acute heart failure has
been defined as new onset of decompensated heart failure
or decompensation of chronic established heart failure with
symptoms sufficient to warrant presentation to the ED or
hospital.4 The European Society of Cardiology defined
acute heart failure as the rapid onset of symptoms and signs
secondary to abnormal cardiac function that may occur
with or without previous cardiac disease.5 Cardiac dysfunction can be related to systolic or diastolic dysfunction, to
abnormalities in cardiac rhythm, or to preload and afterload mismatch. Other definitions include a gradual or rapid
change in signs and symptoms compatible with heart failure, resulting in a need for new and urgent intravenous
therapy or urgent significant augmentation of existing therapy in patients with established or newly developed left
ventricular dysfunction.6 Acute heart failure represents a
board spectrum of clinical presentations from acute onset of pulmonary edema to gradual worsening of symptoms in a patient with established heart failure. Thus the
term acute heart failure syndromes has also been suggested.6 The clinical classification of patients with acute
heart failure continues to evolve and reflects ongoing
changes in the understanding of the pathophysiology of
this syndrome.7 For these consensus recommendations,
the term acute heart failure is applied, with the main
focus being on those patients presenting to an ED where
monitoring and management in an ED/outpatient observation unit may be appropriate. The final written recommendations will be reviewed every 3 years to include the
results of the most up to date data and research.
© 2008 Lippincott Williams & Wilkins
SCPC Recommendations for Observation Stay AHF
Committee Member Selection
The chairs and each subcommittee chair were selected
by the Recommendation Committee Chairperson with approval of the SCPC Board to develop this recommendation
document. Each subcommittee chairperson submitted the
names of no more than 7 individuals they would like to
participate in creating the recommendations specific to their
area. Nominations were then submitted to the SCPC Board
for final approval. As committees were selected, the need to
maintain a geographical distribution of members was considered to allow for differences in medical practices across the
country. Further, to insure collaboration with other professional organizations, selecting committee members with ties
to other national organizations was also encouraged.
䡲 The Recommendations Committee Chairpersons, of the
SCPC, will appoint subcommittee chairpersons to write the
appropriate section of the recommendations.
䡲 The Subcommittee Chairpersons are responsible for submission of the final recommendations to the Recommendations Committee Chairpersons for feedback and comments.
䡲 Publication of the recommendations will be done in
collaboration with the SCPC.
䡲 Dissemination of the recommendations will occur from
the SCPC with the assistance of the Recommendation
Committee Chairpersons.
The writing group made efforts to avoid any actual,
potential, or perceived conflicts of interest that might arise as
a result of an outside relationship or personal interest of a
member of the writing committee. All members of the writing
committee, as well as peer reviewers of the document, were
asked to provide disclosure statements of all such relationships that might be perceived as real or potential conflicts of
interest. These statements were reviewed by the co-chairs and
reported as part of this document.
Evidence Gathering and Review
• All evidence must be deemed credible for inclusion and
integration into the guidelines. The subcommittee chairpersons must assure all recommendations are based on the
most currently available data. All sources of data, including
peer reviewed publications, published abstracts, and expert
consensus may be considered at the discretion of the
Subcommittee Chair. The recommendations committee
chairpersons will serve to adjudicate controversies that
cannot be resolved within subcommittees.
The recommendations made in this document employed 3 categories of strength to the recommendation. The
recommendations were categorized as “recommended,”
“considered,” and “not recommended.” The phrase “is recommended” should be taken to mean that the therapy or
management process should be followed as often as possible
in individual patients, with exceptions carefully delineated.
The phrase “considered” means that patients should or may
receive the intervention with discretion, allowing for individ-
89
Society of Chest Pain Centers Acute Heart Failure Committee
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
ualization of approach. The phrase “not recommended” is
used when the available evidence is sufficient to determine
that the therapy or management process is not helpful or may
be harmful or that the evidence is considered to be insufficient or too premature to apply.
The level of evidence were cited with each recommendation: the SCPC recommendation development process used
3 grades to characterize the type of evidence available to
support specific recommendations (A, B, or C) (see Table 1).
The recommendations listed in this document are evidence based whenever possible. These consensus recommendations are intended to assist healthcare providers in clinical
decision making by describing a range of generally acceptable approaches for the diagnosis, triage, monitoring, and
management of acute heart failure patients presenting to the
TABLE 1. Relative Weight of Evidence Used to Develop the
SCPC Consensus Recommendations Types of Evidence
Level A
Randomized, controlled, clinical trials
Level B
Cohort and case-control studies
Post hoc, subgroup analysis, and meta-analysis
Prospective observational studies or registries
Level C
Expert opinion
Observational studies–epidemiologic findings
Clinical experience
90
ED. The recommendations attempt to define practices that meet
the needs of most patients under most circumstances. These
recommendations are intended to compliment but not replace
the guidelines of the American College of Cardiology/American
Heart Association and those of the Heart Failure Society of
America. It is hoped these consensus recommendations for the
care of the heart failure patient will be useful to the practicing
clinician using a short-stay treatment and management strategy.
REFERENCES
1. Peacock WF. Short Stay Management of Heart Failure. 1st ed. Philadelphia, Pa: Lippincott, Williams & Wilkins; 2006.
2. Hunt S, Abraham W, Chin M, et al. ACC/AHA 2005 guideline update for
the diagnosis and management of chronic heart failure in the adult: a
report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2005;112:e156.
3. Russo M. The cost of end stage heart failure. Scientific session presented
at American Heart Association Cardiology Conference, Chicago, IL,
November 12–15, 2006.
4. Fonarow GC, Adams KF Jr, Abraham WT, et al, for the ADHERE
Scientific Advisory Committee, Study Group, and Investigators. Risk
stratification for in-hospital mortality in acutely decompensated heart
failure: classification and regression tree analysis. JAMA. 2005;293:572–
580.
5. Nieminen MS, Bohm M, Cowie MR, et al. Executive summary of the
guidelines on the diagnosis and treatment of acute heart failure: the task
force on acute heart failure of the European Society of Cardiology. Eur
Heart J. 2005;26:384 – 416.
6. Gheorghiade M, Zannad F, Sopko G, et al. Acute heart failure syndromes:
current state and framework for future research. Circulation. 2005;112:
3958 –3968.
7. Adams KF, Lindenfeld J, Arnold JMO, et al. For the Heart Failure Society
of America. HFSA 2006 comprehensive heart failure practice guideline.
J Card Fail. 2006;12:e1– e122.
© 2008 Lippincott Williams & Wilkins
SOCIETY
OF
CHEST PAIN CENTERS RECOMMENDATIONS
Diagnosis
Douglas S. Ander, MD, Committee Chair, Alan Maisel, MD, Judd E. Hollander, MD,
James L. Januzzi, Jr, MD, Clyde W. Yancy, MD, Gregg C. Fonarow, MD, FACC,
and W. Frank Peacock, MD; of the Society of Chest Pain Centers Acute Heart Failure Committee
Abstract: Making the definitive diagnosis of heart failure in the acute
care setting can be difficult. In the emergency department this needs to
be done rapidly, frequently, and accurately, without access to a patient’s
health records and while simultaneously initiating the appropriate diagnostic and therapeutic interventions. This section reviews the diagnostic strategies available to the physician confronted with a patient in
whom the differential diagnosis includes acute heart failure.
(Crit Pathways in Cardiol 2008;7: 91–95)
Making the Diagnosis of Heart Failure When
Patients Present With Symptoms Possibly
Related to Acute Heart Failure
Making the definitive diagnosis of heart failure (HF) in
the acute care setting can be difficult. In the emergency
department (ED) this needs to be done rapidly, frequently
without access to a patient’s health records while simultaneously initiating the appropriate diagnostic and therapeutic
interventions. The physician must determine the etiology of
symptoms in patients with suspected HF based on the initial
history, physical examination, diagnostic studies (laboratory
data, electrocardiogram, and radiography), as well as response to empiric therapy.
PubMed was searched in a systematic manner using a
combination of search terms relevant to each topic specific to
early diagnosis available in the emergency department setting. References from articles and guidelines so identified
were also evaluated for additional pertinent literature.
The Initial History and Physical Examination
The most common symptom of HF is dyspnea.1,2 However, dyspnea is also common in the general population. Even
in well persons, a lack of physical fitness may result in
exertional dyspnea. Multiple other medical conditions also
produce dyspnea, including chronic obstructive pulmonary
disease (COPD), asthma, pneumonia, and myocardial ischemia (Table 1). In several studies and registries of presumed
HF, up to 40% of patients had a history of COPD.1–5
Therefore, in the acute care setting, a chief complaint of
dyspnea is very nonspecific. Other components of a complete
history include assessment of abdominal distention, paroxysmal nocturnal dyspnea, orthopnea, fatigue, weakness, nausea,
and vomiting. The presence of paroxysmal nocturnal dysCopyright © 2008 by Lippincott Williams & Wilkins
ISSN: 1535-282X/08/0702-0091
pnea, orthopnea, or dyspnea on exertion increases the likelihood of HF, whereas their absence decreases its likelihood.6
One of the more reliable indicators that dyspnea is due to an
acute exacerbation of HF is a previous history of HF.1,2,6,7
However, approximately 20% of patients admitted with acute
heart failure have a history of COPD.3 A history is most
beneficial when combined with other information but by itself
will make the accurate diagnosis of HF challenging.
Auscultation for an S3 gallop, assessment for jugular
venous distension (JVD), auscultation for pulmonary rales,
and assessment for leg edema should be part of the initial
evaluation of a patient with suspected HF, and the presence of
these signs increases the likelihood of HF.6 The absence of
rales, edema, or JVD lowers the probability of HF.6 An S3 is
difficult to detect in the emergency department. Electronic
identification of an S3 should improve detection and diagnosis of HF, although studies have yet to show an effect on
patient outcome.8
Chest Radiography
Chest radiographs are considered a standard component
of the initial assessment of a patient with presumed HF. The
presence of pulmonary venous congestion, interstitial edema,
alveolar edema, and cardiomegaly increase the likelihood of
HF.6 Although most patients have cardiomegaly, the absence
of pulmonary venous congestion or edema should not exclude
the diagnosis of HF. In one study, radiographic evidence of
pulmonary congestion was absent in 53% of patients with
moderately elevated pulmonary capillary wedge pressure
(PCWP) and 39% of patients with significantly elevated
PCWP.9 Data from the Acute Decompensated Heart Failure
National Registry revealed that 18.7% of patients with HF,
had no signs of pulmonary congestion on the emergency
department chest radiograph.8 Studies have also shown that
agreement among clinicians in chest x-ray interpretation is
“moderate to almost perfect” for interstitial edema, but only
“moderate” for cardiomegaly and vascular redistribution.7
Chest radiographs should be part of the initial evaluation of a
patient with suspected HF, but absence of findings should not
exclude the diagnosis.
Electrocardiography
Electrocardiography (ECG) should be routinely performed in the evaluation of dyspnea and a suspicion of HF.
Its greatest value lies in its ability to identify potential
etiologies of HF such as acute coronary syndrome and
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
91
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Ander et al
TABLE 1. Differential Diagnosis of Dyspnea
Cardiac
Pulmonary
Other
Acute coronary syndrome/acute myocardial infarction
with or without mechanical complication
Aortic dissection
Arrhythmias
Valvular disease
Chronic obstruction pulmonary disease
Pneumonia
Pneumothorax
Pulmonary embolism
Anemia
Deconditioning
Obesity
tachy- or bradyarrhythmias. The ECG is limited in its
ability to indicate cardiac decompensation, although left
ventricular systolic dysfunction is rare in the presence of a
totally normal ECG.6
In summary, when an emergency physician analyzes all
the information readily available in the ED including history,
physical examination, radiography, and electrocardiogram,
the diagnosis or exclusion of HF can still be challenging.
Care must be taken and a high degree of suspicion applied
when patients present to the ED with dyspnea as a chief
complaint. Despite its limitations, a thorough history and
physical examination can aid the physician in determining the
fluid volume and systemic perfusion status of the patient and
therefore aid in treatment decisions.
Utility of Natriuretic Peptide Levels as a
Diagnostic Tool
Natriuretic peptides (NPs), brain natriuretic peptide
(BNP) and N-terminal prohormone brain natriuretic peptide
(NT-proBNP), are useful blood tests to both rule in and rule
out HF.1,2,5,10,11 In the Breathing Not Properly trial, a multinational trial of 1586 patients presenting to 7 EDs with acute
dyspnea, BNP levels were additive to the accuracy of the
clinicians’ HF diagnosis. BNP levels were associated with
New York Heart Association Functional Class and were the
single most accurate predictor of HF. A BNP cutoff of 100
pg/mL had a sensitivity of 90%, specificity of 76%, and an
accuracy of 83%. BNP was the strongest predictor of a HF
diagnosis compared with the clinical indicators of HF (rales,
cephalization, edema, and JVD).1 An elevated BNP is associated with an odd ratio of 29.6 for HF. The addition of BNP
levels to clinical judgment would have improved the diagnostic accuracy from 74.0% to 81.5% (P ⬍ 0.0001) in
patients with a high pretest probability of HF.4 BNP levels
were confirmatory both when the clinician was certain that
the dyspnea was due to HF and when they were certain that
there was a non-HF cause of dyspnea. When the clinician was
unsure (clinical probability ⬎20% and ⬍80%), a BNP level
ⱖ100 pg/mL correctly identified 74% of the cases.4 Similar
evidence exists that NT-proBNP is a useful tool in the
diagnosis and management of HF. NT-proBNP levels accurately reflect the severity of HF.1,10,11 Like BNP, NT-proBNP
92
has high negative predictive values at appropriate cutpoints.11
The largest studies on the clinical utility of NT-proBNP
in the diagnosis of HF are the N-terminal Pro-BNP Investigation of Dyspnea in the Emergency Department (PRIDE)
and International Collaborative of NT-proBNP (ICON) studies.10,11 The PRIDE study was a prospective investigation of
600 patients with dyspnea which compared NT-proBNP levels to the clinical diagnosis of HF. The median NT-proBNP
among the 209 (35%) patients with HF was 4054 versus 131
pg/mL among the 390 patients (65%) who did not have HF
(P ⬍ 0.001). In PRIDE, an NT-proBNP level of ⬍300 pg/mL
had a negative predictive value excluding HF of 99%,
whereas a cut-point of ⬎900 pg/mL gave similar sensitivity,
specificity, and positive predictive value for HF as the BNP
cut-point of 100 pg/mL as reported in other studies.1 Similar
to reported data for BNP, NT-proBNP plus clinical judgment
was superior to either NT-proBNP or clinical judgment alone.
The ICON study was a pooled analysis of 1273 patients with
dyspnea, of whom 720 had HF. In ICON, NT-proBNP was a
powerful diagnostic and prognostic indicator. Also, the value
of an NT-proBNP ⬍300 pg/mL to exclude HF was reinforced.
Although a single cut-point for NP provide excellent
sensitivity, specificity, and positive predictive value for HF,
the importance of age must be recognized as a cause of
elevated natriuretic peptide levels in the absence of HF. Age
is an independent predictor of elevated BNP levels (ie, ⬎100
pg/mL).12 The ICON investigators showed that age adjusted
NT-proBNP rule in cut-points should be 450, 900, and 1800
pg/mL for the age groups of ⬍50, 50 –75, and ⬎75 years,
respectively, and improved the positive predictive value from
76% to 88%, compared with a single cut-point.11
Besides age, other variables that affect the interpretation of NP levels include gender, renal function, body mass
index (obesity), acute coronary syndrome, and right heart
strain from a variety of causes.13,14 It is critical to recognize
that other cardiovascular conditions can raise NP levels. This
includes cardiac and noncardiac pathology that causes myocardial stress and includes pulmonary hypertension and right
ventricular dysfunction secondary to pulmonary embolism,
acute coronary syndrome, atrial fibrillation, or COPD with
cor pulmonale. Although a 2 cut-point approach (level below
which HF is very unlikely and a second level above which HF
is very likely) provides high diagnostic accuracy, this does
leave a “gray zone” of BNP and NT-proBNP values where
clinical acumen and ancillary testing are often required to
make a correct diagnosis. In patients with prior assessment of
NP when clinically compensated, may allow for comparison
of NP levels and facilitate the diagnosis of decompensation of
heart failure.
Noninvasive Bioimpedance Technology
Noninvasive monitoring systems using bioimpedance
(BI) technology may provide a convenient and useful proxy
to the collection of invasive hemodynamic measurements.
Impedance is proportional to flow, gathering data during the
cardiac cycle, allows the calculation of cardiac output, sys© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
temic vascular resistance, and thoracic fluid volume.15 BI
may add in the diagnosis of HF and management of acute
heart failure.15–17 The precise role that BI should play in the
ED is still undefined and large scale studies are still needed to
assess its ED utility.
Diagnosis
tures can precipitate HF. In addition, pulmonary artery pressures (systolic and diastolic) can be estimated by the Doppler
echocardiogram. Contemporary echocardiogram devices,
which provide excellent cardiac imaging, can be readily
applied in the ED to obtain crucial information on the
presence and severity of cardiac abnormalities.
Recommendations
It is recommended that patients undergo a history and
physical examination when presenting with symptoms suspicious for acute heart failure. A chest radiograph and electrocardiogram should be components of the initial evaluation to
assist in confirming the diagnosis, but more importantly to
eliminate items from the differential diagnosis, determine the
etiology and for patients with chronic heart failure, determine
a precipitant. Level of Evidence: B.
It is recommended that measurement of natriuretic
peptide levels (BNP or NT-proBNP) together with standard
clinical evaluation is useful for improving the diagnostic
accuracy for acute heart failure. Consider an alternative
diagnosis in patients with normal natriuretic peptide levels.
Level of Evidence: A.
Bioimpedance monitoring may be considered as an aid
in the diagnosis and management of acute heart failure. Level
of Evidence: C.
If This is the First Onset of Acute Heart Failure
What are the Investigations Needed to
Determine the Etiology of the Problem?
Patients presenting with symptoms consistent with the
diagnosis of HF but no previous history require an investigation to determine the etiology of the HF. In this subset of
patients with new onset of HF, the clinician should evaluate
the patient for potential precipitants of HF, including myocardial ischemia/injury, arrhythmias, anemia, renal insufficiency, and thyroid disease. An electrocardiogram will provide evidence of structural heart disease and information
regarding acute ischemia, infarction, and arrhythmias. A
chest radiograph will reveal evidence of an increased cardiac
silhouette and increased pulmonary venous pressure. A complete blood count should be obtained, which may reveal
anemia. Electrolytes, in particular sodium, should be ordered
to check for hyponatremia. Renal function should be assessed
because an elevated creatinine may demonstrate pre-existing
or new renal impairment. Measurement of cardiac biomarkers
including serum troponins and NPs may be indicated as part
of the initial evaluation. Troponins are important for both
diagnosis and prognosis in acute ischemic syndromes, and are
prognostic in HF.18,19 Natriuretic peptides (BNP or
NT-proBNP) are useful for diagnosis and severity assessment
of HF, and have strong prognostic utility.5 A thyroid stimulating hormone level is indicated to determine if the patient
has hyper- or hypothyroidism. A urine-drug screen, in particular to assess for cocaine, should be included in the initial
evaluation of patients with new onset of HF. Echocardiography is an invaluable tool in assessing patients presenting with
possible HF, and provides information on cardiac chamber
size, left ventricular function, valve morphology and status,
and pericardial disease. Abnormalities of any of these struc© 2008 Lippincott Williams & Wilkins
Recommendations
It is recommended that the initial evaluation of patients
with new onset of HF should include exacerbating factors, the
following studies are obtained: electrocardiogram, chest radiograph, complete blood count, serum electrolytes, creatinine, thyroid function, troponin (T or I), NP (BNP or NTproBNP), and consideration of a urine-drug screen. Although
rarely necessary in the ED, an echocardiogram is part of the
evaluation of patients with new onset of HF, and should occur
sometime during their hospitalization. Level of Evidence: C.
It is recommended that patients with a diagnosis of
acute heart failure undergo evaluation as outlined in Table 2.
It is recommended that in the initial evaluation of
patients with acute heart failure the following studies are
obtained: complete blood count, serum electrolytes, blood
urea nitrogen (BUN), creatinine, thyroid function, troponin
(T or I), NP (BNP or NT-proBNP), and urine-drug screen,
electrocardiogram and chest radiograph. An echocardiogram
should be part of the evaluation of patients with new onset of
acute heart failure.
The clinician should seek precipitants of HF in patients
with a pre-existing history of HF (Table 3). The identifiable
reversible causes should be addressed in conjunction with the
treatment of the HF. Acute coronary syndrome, arrhythmias,
valvular causes, infection, and noncompliance with therapy
are common precipitating factors for acute heart failure noted
on admission.3 Patient related factors such as noncompliance
with medication and diet should be addressed. The importance of patient and family education cannot be overestimated. Several studies have found that education decreases
hospital readmissions.20 –22
Certain medications should be avoided by patients
with HF. This should be addressed while pursuing a
precipitant for acute heart failure, and should be part of
patient education. It is felt that patients already treated
with angiotensin-converting enzyme (ACE) inhibitors are
at increased risk of an acute decompensation when they are
started on a nonsteroidal anti inflammatory drug (NSAID)
therapy.23,24 The Wafarin/Aspirin Study in Heart Failure
TABLE 2. Initial Evaluation of Patients With a Diagnosis of
Acute Heart Failure
Assess clinical severity of heart failure by history and physical
examination
Determine the etiology of heart failure
Evaluate for acute coronary syndrome or active myocardial ischemia
Evaluate for atrial or ventricular arrhythmias
Identify any exacerbating factors for heart failure
Identify significant comorbidities which influence therapy
Assess cardiac structure and function, if not previously evaluated
93
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Ander et al
Congestion
at rest
TABLE 3. Precipitants of Acute Heart Failure Exacerbations
Noncompliance
Ischemic events
Uncontrolled hypertension
Valvular disease
Cardiac arrhythmias
Noncardiac events
Medications
Diet
Acute myocardial infarction
Cardiac ischemia
Atrial fibrillation with a rapid ventricular
response
Ventricular tachycardia
Bradycardia
Conduction abnormalities
Pulmonary embolus
Anemia
Systemic infection
Thyroid disorders
Stress
Illicit drugs
Alcohol
Adverse effects of medications
and Wafarin Antiplatelet Trial in Chronic Heart Failure
trials found a substantial excess of hospitalizations for
worsening heart failure for patients receiving aspirin.25,26
Normally prostaglandins act as renal arteriole vasodilators.
However, in certain at-risk populations, loss of this vasodilation, related to the interaction between NSAIDs (including aspirin) and ACE inhibitors, can result in a reduction in renal perfusion and an increase in systemic-vascular
resistance. NSAIDs and higher doses of aspirin should be
avoided in patients with HF, in particular those being
treated with ACE inhibitors or those with renal insufficiency. Likewise, calcium channel blockers are currently
not recommended as vasodilator therapy for HF.27 Patients
should be preferentially treated both with ACE inhibitors
and beta blockers in the outpatient settings.
Cardiac ischemia is a leading cause of HF and a cause
of acute exacerbations.28 Although not every exacerbation of
chronic HF will require a workup for an ischemic etiology,
the clinician should be aware of this potential and treat it
accordingly. Cardiac arrhythmias have been associated with a
worse prognosis in HF.29 In the acute care setting, cardiac
arrhythmias, such as atrial fibrillation, ventricular arrhythmias, and conduction abnormalities, can be precipitants of
exacerbations. Treatment should focus on the hemodynamic
effects of the arrhythmia.
No
Yes
No
Warm and Dry
A
Warm and Wet
B
Yes
Cold and Dry
D
Cold and Wet
C
Low
perfusion
at rest
FIGURE 1. Bedside assessment of hemodynamic status and
corresponding therapeutic intervention. A indicates well
compensated. If symptomatic, typically require minor adjustments in medications and follow-up. B, Fluid overloaded and
well perfused. Vasodilators and diuretics are the treatment
modalities. C, Diminished perfusion and fluid overloaded.
For those with elevated systemic vascular resistance, vasodilators and diuretics should improve cardiac output. Inotropic
support may be required. For symptomatic hypotension,
consider addition of a pressor agent. D, Poor perfusion and
dry. Typically require a fluid bolus. Addition of inotropic support and pressors for patients unresponsive to the initial bolus. Adapted from Stevenson.31
hemodynamic category, and then appropriate therapy can be
selected. Fluid overload can be assessed by the presence or
absence of dyspnea, orthopnea, pulmonary rales, elevated
jugular venous pressure, a third heart sound, and hepatomegaly. Perfusion can be estimated by evaluating for the presence
or absence of fatigue, nausea, symptomatic hypotension, and
cool extremities (Table 4).
Assessment using these historical and physical diagnosis clues needs to be made in the aggregate and supplemented
TABLE 4. Clinical Bedside Assessment of Acute Heart
Failure
Evidence of congestion
Recommendation
It is recommended that in patients diagnosed with acute
heart failure, potential precipitants should be investigated and
corrected. Level of Evidence: C.
Assessment of Volume and Perfusion Status in
Acute Heart Failure
Categorizing HF patients using a hemodynamic classification system (Fig. 1) is useful. Based on the initial history
and physical examination, patients can be placed into a
94
Evidence of diminished perfusion
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Jugular venous distention
Hepatojugular reflex
Third heart sound
Edema
Hepatomegaly
Rales
Fatigue
Nausea
Narrow pulse pressure
Cool extremities
Symptomatic hypotension
© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
with diagnostic testing (chest radiograph, NP levels, BI).
Even a combination of clinical findings and imaging has a
poor predictive value for identifying patients with elevated
PCWP.9 In particular, absence of rales cannot exclude congestion.30 A clear chest radiograph may not be indicative of
normal filling pressures.9 Currently clinical assessment provides the best estimate of the patient’s hemodynamic status.
The hemodynamic classification system provides the
physician with a framework for the initial assessment and
treatment of the HF patient. This framework is based on
imprecise measures; therefore the initial treatment must be
guided by sound clinical judgment and must be adjusted
depending on the initial response to the therapeutic interventions. Until better and more accurate diagnostic modalities
are available the physician should use the framework presented in this section to develop their therapeutic plan.
12.
13.
14.
15.
16.
17.
Recommendation
It is recommended that the initial evaluation of a patient
with acute heart failure includes a history, physical examination, and diagnostic workup to determine the degree of fluid
overload and whether systemic hypoperfusion is present or
absent. Level of Evidence: C.
REFERENCES
1. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of
B-type natriuretic peptide in the emergency diagnosis of heart failure.
N Engl J Med. 2002;347:161–167.
2. Dao Q, Krishnaswamy P, Kazanegra R, et al. Utility of B-type natriuretic peptide in the diagnosis of congestive heart failure in an urgentcare setting. J Am Coll Cardiol. 2001;37:379 –385.
3. Nieminen MS, Brutsaert D, Dickstein K, et al. EuroHeart Failure Survey
II (EHFS II): a survey on hospitalized acute heart failure patients:
description of population. Eur Heart J. 2006;27:2725–2736.
4. McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide
and clinical judgment in emergency diagnosis of heart failure: analysis
from Breathing Not Properly (BNP) Multinational Study. Circulation.
2002;106:416 – 422.
5. Harrison A, Morrison LK, Krishnaswamy P, et al. B-type natriuretic
peptide predicts future cardiac events in patients presenting to the
emergency department with dyspnea. Ann Emerg Med. 2002;39:131–
138.
6. Wang CS, FitzGerald JM, Schulzer M, et al. Does this dyspneic patient
in the emergency department have congestive heart failure? JAMA.
2005;294:1944 –1956.
7. Badgett RG, Lucey CR, Mulrow CD. Can the clinical examination
diagnose left-sided heart failure in adults? JAMA. 1997;277:1712–1719.
8. Collins SP, Lindsell CJ, Storrow AB, et al.; and the Adhere Scientific
Advisory Committee IaSG. Prevalence of negative chest radiography
results in the emergency department patient with decompensated heart
failure. Ann Emerg Med. 2006;47:13–18.
9. Chakko S, Woska D, Martinez H, et al. Clinical, radiographic, and
hemodynamic correlations in chronic congestive heart failure: conflicting results may lead to inappropriate care. Am J Med. 1991;90:353–359.
10. Januzzi JL, van Kimmenade R, Lainchbury J, et al. NT-proBNP testing
for diagnosis and short-term prognosis in acute destabilized heart failure:
an international pooled analysis of 1256 patients: the International
Collaborative of NT-proBNP Study. Eur Heart J. 2006;27:330 –337.
11. Januzzi JL Jr, Camargo CA, Anwaruddin S, et al. The N-terminal
© 2008 Lippincott Williams & Wilkins
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
Diagnosis
Pro-BNP investigation of dyspnea in the emergency department
(PRIDE) study. Am J Cardiol. 2005;95:948 –954.
Knudsen CW, Clopton P, Westheim A, et al. Predictors of elevated
B-type natriuretic peptide concentrations in dyspneic patients without
heart failure: an analysis from the Breathing Not Properly Multinational
Study. Ann Emerg Med. 2005;45:573–580.
Redfield MM, Rodeheffer RJ, Jacobsen SJ, et al. Plasma brain natriuretic
peptide concentration: impact of age and gender. J Am Coll Cardiol.
2002;40:976 –982.
McCullough PA, Duc P, Omland T, et al. B-type natriuretic peptide and
renal function in the diagnosis of heart failure: an analysis from the
Breathing Not Properly Multinational Study. Am J Kidney Dis. 2003;
41:571–579.
Summers RL, Shoemaker WC, Peacock WF, et al. Bench to bedside:
electrophysiologic and clinical principles of noninvasive hemodynamic
monitoring using impedance cardiography. Acad Emerg Med. 2003;10:
669 – 680.
Springfield CL, Sebat F, Johnson D, et al. Utility of impedance cardiography to determine cardiac vs. noncardiac cause of dyspnea in the
emergency department. Congest Heart Fail. 2004;10(suppl 2):14 –16.
Neath SX, Lazio L, Guss DA. Utility of impedance cardiography to
improve physician estimation of hemodynamic parameters in the emergency department. Congest Heart Fail. 2005;11:17–20.
Sato Y, Yamada T, Taniguchi R, et al. Persistently increased serum
concentrations of cardiac troponin T in patients with idiopathic dilated
cardiomyopathy are predictive of adverse outcomes. Circulation. 2001;
103:369 –374.
Latini R, Masson S, Anand IS, et al. Prognostic value of very low plasma
concentrations of troponin T in patients with stable chronic heart failure.
Circulation. 2007;116:1242–1249.
West JA, Miller NH, Parker KM, et al. A comprehensive management
system for heart failure improves clinical outcomes and reduces medical
resource utilization. Am J Cardiol. 1997;79:58 – 63.
Rich MW, Beckham V, Wittenberg C, et al. A multidisciplinary intervention to prevent the readmission of elderly patients with congestive
heart failure. N Engl J Med. 1995;333:1190 –1195.
Philbin EF. Comprehensive multidisciplinary programs for the management of patients with congestive heart failure. J Gen Intern Med.
1999;14:130 –135.
Hall D, Zeitler H, Rudolph W. Counteraction of the vasodilator effects
of enalapril by aspirin in severe heart failure. J Am Coll Cardiol.
1992;20:1549 –1555.
Garcia Rodriguez LA, Hernandez-Diaz S. Nonsteroidal anti-inflammatory drugs as a trigger of clinical heart failure. Epidemiology. 2003;14:
240 –246.
Massie BM, Krol WF, Ammon SE, et al. The Warfarin and Antiplatelet
Therapy in Heart Failure trial (WATCH): rationale, design, and baseline
patient characteristics. J Card Fail. 2004;10:101–112.
Cleland JGF, Findlay I, Jafri S, et al. The Warfarin/Aspirin Study in
Heart failure (WASH): a randomized trial comparing antithrombotic
strategies for patients with heart failure. Am Heart J. 2004;148:157–164.
Betkowski AS, Graff R, Chen JJ, et al. Panel-reactive antibody screening
practices prior to heart transplantation. J Heart Lung Transplant. 2002;
21:644 – 650.
Goldberger JJ, Peled HB, Stroh JA, et al. Prognostic factors in acute
pulmonary edema. Arch Intern Med. 1986;146:489 – 493.
Dries DL, Exner DV, Gersh BJ, et al. Atrial fibrillation is associated with
an increased risk for mortality and heart failure progression in patients
with asymptomatic and symptomatic left ventricular systolic dysfunction: a retrospective analysis of the SOLVD trials. Studies of Left
Ventricular Dysfunction. J Am Coll Cardiol. 1998;32:695–703.
Stevenson LW, Perloff JK. The limited reliability of physical signs for
estimating hemodynamics in chronic heart failure. JAMA. 1989;261:
884 – 888.
Stevenson LW. Tailored therapy to hemodynamic goals for advanced
heart failure. Eur J Heart Fail. 1999;1:251–257.
95
SOCIETY
OF
CHEST PAIN CENTERS RECOMMENDATIONS
Risk Stratification
Sean P. Collins, MD, MSc, Mihai Gheorghiade, MD, Committee Co-Chairs; Neal L. Weintraub, MD,
Alan B. Storrow, MD, Peter S. Pang, MD, William T. Abraham, MD, FACP, FACC, FAHA,
Brian Hiestand, MD, MPH, Gregg C. Fonarow, MD, FACC, and W. Frank Peacock, MD; of the
Society of Chest Pain Centers Acute Heart Failure Committee
Abstract: The goal of the Society for Chest Pain Centers Heart
Failure Risk Stratification Recommendations Committee was to
review the available literature and currently published guidelines to
provide recommendations for acute heart failure providers to assist
with risk stratification. To accomplish this, we focused on 2 areas:
(1) risk stratification upon emergency department presentation, and
(2) risk stratification after initial therapy.
(Crit Pathways in Cardiol 2008;7: 96 –102)
H
eart failure is a disease of epidemic proportions, whose
incidence and prevalence continue to increase. In 2005,
over 1 million hospital discharges with a primary diagnosis of
heart failure consumed 3% of the total national healthcare
budget.1–3 Over 80% of the admissions originated in an
emergency department (ED) and accounted for a majority of
expenditures, yet it has been suggested up to 50% could be
discharged home after initial therapy.4 – 6 However, patients
with acute heart failure (AHF) have an in-hospital mortality
of 4% to 7%, and a 60-day mortality and recidivism rate of
10% and 25%, respectively.7–10 Further, current AHF guidelines for ED and hospital disposition are based on little or no
empirical evidence. This results in overestimation of risk and
risk aversion causing unnecessary admissions and prolonged
hospital lengths-of-stay.5,11–16
Over the last 3 decades, several observational trials
have been performed attempting to identify high-risk AHF
features. A few others have attempted to identify low-risk
features of patients with AHF. It is clear that a lack of
high-risk features does not necessarily mean the patient is at
low-risk of subsequent adverse events. Further, level of
acuity upon initial presentation does not always correlate with
subsequent near term event risk. Consider 2 patients as
examples of different risk profiles. The first patient appears
gravely ill upon ED presentation (hypoxia, significant hypertension, and tachypnea) and requires intense therapy for the
first 2 hours that includes an intravenous vasodilator and
noninvasive ventilation. However, once their acute symptoms
are brought under control, they may actually be at low-risk of
near term events (5 days). This is in stark contrast to the
Copyright © 2008 by Lippincott Williams & Wilkins
ISSN: 1535-282X/08/0702-0096
96
mildly ill patient who presents with a low normal blood
pressure, renal dysfunction, and low serum sodium. Although
their initial therapy is much less intense, their risk of near
term events is significantly higher.7,8,17
In the last decade, several major societies have published their recommendations for the management of heart
failure. The Society for Chest Pain Centers Heart Failure Risk
Stratification Recommendation Committee reviewed the major observational studies and society recommendations, focusing on results that were relevant to ED patients with AHF.
Further, we focused on 2 time points for risk determination:
(1) data that would be available within the first 2 hours of ED
presentation and (2) available data after initial therapy at the
time of ED disposition.
PubMed was searched in a systematic manner using a
combination of search terms specific to risk stratification of
patients with AHF presenting to an ED. Preferences were
given to studies that enrolled patients in the ED, studied AHF,
and looked at near and intermediate term events (within 30
days of ED presentation). References from the articles identified by the search criteria were also examined for other
pertinent articles. Specific inclusion and exclusion criteria
were delineated under each question of interest. Predictive
instruments are almost always generated from observational
cohort studies. Although this is appropriate, it limits the
strength of evidence to Level B in the majority of situations.
Only when the predictive instrument is studied as a decision
rule (against standard physician judgment) would the trial be
in the form of a prospective randomized trial. Further, although we have focused on trials that have evaluated ED
patients with AHF, there is inherent difficulty in inferring
individual patient-based risks from population-level data. As
such, our recommendations are meant to be used in conjunction with, and not in lieu of, physician discretion.
Heart Failure Risk Stratification Upon ED
Presentation
Clinical Variables Useful for Initial Risk Stratification
Our search strategy examined risk stratification, prognosis, or mortality in manuscripts addressing heart failure in
the ED and resulted in 23 studies. The majority of these
focused on predicting inpatient mortality and many used data
not routinely available to the emergency physician. Further,
only a minority of the investigations attempted to identify
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Risk Stratification
patients at low-risk of subsequent events; lack of high-risk
cannot be interpreted as low-risk.
vated BUN, (3) elevated creatinine, (4) low SBP, (5) ischemic changes on ECG, and (6) positive troponin.
High-Risk Features Upon ED Presentation
Selker et al18 developed a model to predict acute
hospital mortality from data available to the ED physician
within the first 10 minutes of presentation (patients’ age,
systolic blood pressure 关SBP兴 and findings and electrocardiography 关ECG兴 abnormalities). The model was prospectively
validated for mortality, but its validity for morbidity and
other acute sequelae is unknown. Additionally, the ability of
the model to differentiate a low-risk patient who can be safely
discharged home has not been assessed; the model was
developed to identify the high-risk patient. Chin and Goldman19 developed a risk model using a larger number of
variables (vital signs, comorbidities, ECG findings, and laboratory data). The model is successful in predicting morbidity
and mortality, but it cannot delineate the low-risk patient.
Katz et al20 developed a model that could predict 81% of
complications. This model was based on ED information but
included a 4-hour diuresis measure, making it unsuitable for
use as a decision-making tool early in the emergency setting;
delaying decision making in the ED can result in a potentially
life-threatening delay in admission and treatment. Additionally, the model missed 19% of cardiopulmonary complications, making it unsuitable for safe implementation.
In one of the largest studies to date, classification and
regression tree methodology was used on 45 variables in 65,275
patients with heart failure to predict in-hospital mortality.21 The
model is capable of predicting a risk for mortality as low as 2.1%
and demonstrates that ED data can be used to identify low-,
moderate-, and high-risk patient groups. Although this model is
perhaps the most elegant available to date, it remains highly
limited because only 39 of more than 100 variables available to
the ED physician were considered, and the model was designed
only to predict inpatient mortality. An additional issue yet to be
addressed in risk models using ED data is the relationship
between the events modeled and the acute presentation for heart
failure. It is not possible to show that the adverse outcomes were
related to the acute event without intensive, prospective, evaluation of outcomes.
Further, several recent studies have retrospectively
evaluated cohorts of AHF patients enrolled in registries and
clinical trials of novel therapeutic agents to identify markers
of risk.22–25 Patients on admission with SBP ⬍120 mm Hg
had an almost 3-fold increased risk of in-hospital mortality
compared with patients with SBP ⬎140 mm Hg (7.2% vs
2.5% P ⬍ 0.001).22 Further low serum sodium upon hospital
admission (⬍135 mmol/L) has been associated with increased in-hospital and postdischarge mortality and increased
rates of readmission.23 Finally, renal dysfunction (elevated
blood urea nitrogen 关BUN兴 or creatinine) upon hospital admission has also been associated with increased rates of
in-hospital and postdischarge mortality.24,25
These limitations notwithstanding, the previous studies
serve as a good foundation for identifying variables consistently associated with patients at high-risk of adverse events.
Recurrent features include (1) low serum sodium, (2) ele-
Low-Risk Features Upon ED Presentation
Two studies have attempted to identify low-risk features
of ED patients with AHF. Diercks et al26 studied a prospective
convenience sample of patients with AHF to identify a low-risk
cohort of patients with AHF suitable for observation unit (OU)
management. Patients with an SBP over 160 mm Hg at ED
presentation and a normal initial cardiac Troponin I were significantly more likely to be discharged from the OU and not
experience any 30-day adverse events (death, readmission, myocardial infarction, arrhythmias). Auble et al27 retrospectively
examined a statewide database to identify variables predictive of
a low-risk of inpatient death or serious complications. Recursive
partitioning was used to classify 17.2% of patients as low-risk
(0.3% mortality, 1.0% inpatient complications). The resultant
model was somewhat cumbersome, but also identified serum
sodium, SBP and creatinine as differentiators between low-risk
and high-risk.
© 2008 Lippincott Williams & Wilkins
Natriuretic Peptides for Initial ED Risk Stratification
A search strategy examining natriuretic peptides, heart
failure, ED, and mortality or risk stratification identified 7
original studies that have investigated the diagnostic utility and
clinical impact of measuring natriuretic peptides in patients with
dyspnea.28 –34 A study of 325 ED patients demonstrated the
ability of brain natriuretic peptide (BNP) to predict future cardiac events.29 Patients presenting to the ED with dyspnea had
BNP levels drawn and were followed for 6 months for the
combined end point of death (both cardiac and noncardiac),
hospital admission with a cardiac diagnosis, and repeat ED visits
for heart failure. The area under the receiver operating characteristic curve was 0.87 (95% confidence interval 关CI兴 ⫽ 0.83–
0.92) for the ability of BNP to predict a combined end point. The
cumulative probability of a heart failure event within 6 months
was 51% in the 67 patients with a BNP level ⬎ 480 pg/mL,
compared with 2.5% in the 205 patients with BNP values ⬍230
pg/mL. BNP has also been shown to predict adverse events
better than a physician’s ability to decide disposition strategy
based on the level of severity.34 Finally, in a retrospective
analysis of 77,467 patients from the Acute Decompensated
Heart Failure National Registry, there was a near linear relationship between BNP quartiles and in-hospital mortality.31 Similar
findings have been reported for N-terminal prohormone brain
natriuretic peptide (NT-proBNP).32,35–37 In a pooled analysis of
1256 patients, NT-proBNP was a significant predictor of subsequent adverse events.32 A NT-proBNP concentration ⬎5180
pg/mL was strongly predictive of death by 76 days (odds ratio ⫽
5.2, 95% CI ⫽ 2.2– 8.1, P ⬍ 0.001).
Previous Guideline Recommendations
In general, heart failure guidelines have addressed
chronic heart failure to a much greater extent than AHF.
Further, recommendations for risk stratification and disposition are even less robust. The 1994 guidelines published by
the Agency for Health Care Policy and Research provided
recommendations for hospital admission criteria based on the
lowest level of evidence, Level C (expert opinion).16 The
97
Collins et al
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
1995 American College of Cardiology (ACC)/American
Heart Association (AHA) guidelines limit their disposition
recommendations (Class I and II) to hospital admission for
new onset heart failure, chronic heart failure with mild to
moderate decompensation, or chronic heart failure complicated by acutely threatening events or clinical situations.
However, criteria for these conditions are not specifically
defined. The 2005 American College of Cardiology/American Heart Association guidelines update addressed the evaluation and management of chronic heart failure and provide
no insight into acute heart failure disposition decisions.12 In
2006, the Heart Failure Society of America published detailed guidelines on heart failure management.38 It did provide conceptual discharge criteria (ie, follow-up scheduled
before discharge, optimal volume status achieved, etc) for all
patients with AHF and patients with advanced heart failure
and recurrent admissions. However, it did not address specific
ED disposition criteria in an objective manner. In 2007, the
American College of Emergency Physicians published AHF
recommendations.39 Although the document addressed 4 specific areas of diagnosis and treatment, there were no recommendations regarding ED disposition.
Recommendations
It is recommended that a positive cardiac troponin
levels be evaluated and treated in an inpatient bed for the
patients with renal dysfunction (BUN ⬎40 mg/dL or creatinine ⬎3 mg/dL), low serum sodium (⬍135 mEq/L), low SBP
(⬍100 mm Hg), new ischemic changes on ECG. Level of
Evidence: B.
Consider patients with substantial elevation in presentation natriuretic peptides levels (BNP ⬎1000 pg/mL or
NT-BNP ⬎5000 pg/mL), or borderline low-normal blood
pressure (SBP 100 –120 mm Hg) be evaluated and treated in
an inpatient bed.
Other Considerations for Acute Heart Failure
Observation Unit Management
Previous OU experiences also suggest there are other
features available upon presentation which would preclude an
OU stay.40 – 42 Those patients with the following features are
considered poor candidates for OU management: (1) poor
social support/follow-up, (2) new-onset AHF where a rapid
outpatient etiologic workup is not available, (3) those on
intravenous infusions being actively titrated, (4) significant
comorbidities requiring acute intervention, (5) significantly
elevated respiratory rate (⬎32 breaths/min) or requiring noninvasive ventilation at the time of OU entry, and (6) signs of
poor perfusion at the time of OU entry.
Although initial risk stratification is based on variables
available upon ED presentation, a patient’s hemodynamic profiles may change based on initial therapy allowing reassessment
and consideration for OU management. For example, consider
the patient who presents to the ED with significant hypertension
and hypoxia requiring aggressive titration of an intravenous
vasodilator and noninvasive ventilation. After initial therapy, the
patient is weaned from noninvasive ventilation and is on a stable
dose of a vasodilator. Although their initial symptoms suggested
98
they would be excluded from the OU, reassessment suggests
they may benefit from OU management. Continual reassessment
before and during OU management is key to determining patients whose symptoms are moving toward decreased congestion
and clinical stability.
Recommendations
It is recommended that patients with a positive cardiac
troponin, renal dysfunction (BUN ⬎40 mg/dL or creatinine
⬎3 mg/dL), low serum sodium (⬍135 mEq/L), low SBP
(⬍100 mmHg), or new ischemic ECG changes be evaluated
in an inpatient bed. Level of Evidence: B (Table 3).
Inpatient management is recommended for patients
with the following features: (1) new onset of AHF where a
rapid outpatient etiologic workup is not available, (2) those
on intravenous infusions being actively titrated, (3) significant comorbidities requiring acute intervention, (4) significantly elevated respiratory rate (⬎32 breaths/min) or requiring noninvasive ventilation at the time of OU entry, and (5)
signs of poor perfusion at the time of OU entry. Level of
Evidence: C.
Consider inpatient management for patients with the following features: (1) poor social support or (2) poor follow-up.
Risk Stratification After Initial Therapy
Response to Therapy and its Relationship to Prognosis
Therapy for AHF is often begun shortly after ED
presentation. A patient’s initial response to therapy may
influence subsequent treatment and disposition decisions.
There is a paucity of data available that has attempted to
determine an objective relationship between response to therapy and subsequent adverse events (Table 2).
Small randomized, controlled trials had suggested that
pulmonary artery catheters provided some benefit in the treatment of AHF.43 However, recent findings have suggested they
do not improve subsequent mortality or hospitalization in highrisk patients (Evaluation Study of Congestive Heart Failure and
Pulmonary Artery Catheterization Effectiveness Trial 关ESCAPE兴),
and their utilization in ED patients with AHF is neither cost
nor time efficient.44 Katz et al20 found 4-hour urinary output
less than 1 L to be indicative of lack of response to initial
therapy, and a marker of high-risk. Similarly, Brophy et al45,46
found that the amount of diuretic administered and minimal
diuresis were markers of high-risk for adverse outcomes. Esdaile
et al46a also found that poor response to therapy in the first 24
hours may suggest a patient at high-risk of in-hospital mortality.
Conversely, prospectively studied, readily available safe endpoints after AHF therapy have yet to be identified.
Natriuretic Peptide Levels After Initial Therapy
and Before Hospital Discharge
Small studies have yielded conflicting results as to
whether changes in BNP levels correlate with changes in
pulmonary capillary wedge pressure.47,48 A recent study
suggests that although some inpatient trials have achieved a
statistically significant decline in natriuretic peptide levels,
© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
many outpatient trials have produced a change that does not
exceed the biologic variance of the assays.49 Depending on
the assay, the day-to-day percentage decrease in natriuretic
peptide level suggesting clinical improvement is 27% to 39%.
The within-day decrease suggesting clinical improvement is
10% to 20%. Because of the preliminary finding, suggesting
BNP changes as a result of the therapy, several investigators
have evaluated the association of changes in natriuretic peptide levels after therapy with subsequent adverse events.
Data that examine the change in natriuretic peptide
levels after ED or OU therapy are virtually nonexistent.
Although extrapolating inpatient data to OU patients is problematic, a few preliminary studies are worth discussing.
Natriuretic peptide levels drawn just before hospital discharge have been associated with subsequent adverse events.
Elderly patients with AHF and elevated predischarge BNP
Risk Stratification
levels (⬎500 pg/mL) have been shown to have increased
hazard ratios for death or readmission at 6 months when
compared with those patients with low BNP levels (⬍200
pg/mL).50 Similar findings were reported in patients of all
ages hospitalized with AHF.51,52 Patients with predischarge
BNP values greater than the 75th percentile (696 pg/mL) had
a greater risk of 30-day readmission when compared with the
remainder of the cohort (56% vs 4%, P ⬍ 0.001).51
Inpatients that have minimal changes in NT-proBNP
during admission have an increased risk of events compared
with those subjects with larger changes in serial values.28
Further, one outpatient investigation targeted a reduction in
natriuretic peptide levels with therapy and found a slight
decrease in subsequent adverse events at 10-month followup.53 These results have yet to be validated externally or
duplicated in the acute setting.
TABLE 1. Past Modeling Studies With Reported Outcomes and Variables Found to Be Significant Risk Indicators
Author, Year
N
Subject Type
Outcome
Significant Variables
Filippatos,24 2007
Gheorghiade,23 2007
Formiga,25 2007
Diercks,26 2006*
Rohde,57 2006
302
48,612
414
499
779
I
I
I
E
I
R
R
R
P
R
60-d death/readmission
In-hospital and 30-d mortality
In-hospital mortality
LOS ⬍24 h, 30-d events
In-hospital mortality
Gheorghiade,22 2006
Barsheshet,58 2006
48,612
1,122
I
I
R
R
In-hospital and 30-d mortality
In-hospital mortality
Burkhardt,59 2005
Auble,27 2005*
385
33,533
I
I
R
R
Fonarow,21 2005
Klein,60 2005
Felker,61 2004
65,275
949
949
I
I
I
R
R
R
Observation Unit discharge
Inpatient complications and
mortality
Inpatient mortality
Days hospitalized over 2 mo
60-d mortality/readmission
Lee,62 2003
Harjai,63 2001
4,031
434
I
I
R
R
30 d and 1 yr mortality
30-d readmission
Butler,64 1998
120
I
R
Inpatient complications†
Villacorta,65 1998
Chin,66 1997
57
257
I
I
R
R, S
Inpatient and 6-mo death
60-d readmission and death
Chin,19 1996
Selker,18 1994
Brophy,45 1993
435
401
153
I
I
E
R
PA, R
P
Inpatient complications†
Inpatient mortality
LOS and 6-mo mortality
Esdaile,46a 1992
191
I
PA, R
Inpatient mortality
Katz,20 1988
216
E
R
2-d complications†
55
I
PA, R
Inpatient and 1-yr mortality
BUN ⬎40 mg/dL
Na2⫹ ⬍ 135 mmol/L
Barthel index, creatinine, edema
SBP, troponin I
SBP ⬍124 mm Hg, Cr ⬎1.4 mg/dL,
BUN ⬎37 mg/dL, Na ⬍136
SBP ⬍120
Age, glucose, female sex, creatinine,
low SBP, New York Heart
Association Functional Class III/IV
BUN
Na2⫹, SBP, white blood cell count,
pH, creatinine
BUN, creatinine, SBP
Na2⫹
Age, SBP, BUN, Na2⫹, hemoglobin,
No. past admits, class IV symptoms
Age, SBP, respiratory rates, BUN, Na2⫹
Sex, chronic obstructive pulmonary
disease, prior admits
O2 saturation, creatinine, pulmonary
edema
Na2⫹, sex
Marital status, comorbidity index,
admit SBP, No ST-T wave changes
on ECG
Initial SBP, RR, Na2⫹, ST-T changes
Age, SBP, T-wave flattening, heart rate
Left atrial size, cardiac ischemia,
minimal diuresis
Age, chest pain, cardiac ischemia,
valvular disease, arrhythmia,
new onset, poor clinical response
4-h diuresis, history of pulmonary
edema, T-wave abnormalities,
jugular venous distention
Admit SBP, dyspnea, peak
creatine phosphate kinase
Plotnick,67 1982
Study Type
I indicates inpatients; R, retrospective chart review; E, emergency; PA, patient assessment; S, Survey.
*Identified markers of low-risk.
†
Complications include mortality.
© 2008 Lippincott Williams & Wilkins
99
Collins et al
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Summary: Risk Stratification After Initial Therapy
Although clinical improvement may be apparent (diuresis, decreased tachypnea, blood pressure, and heart rate)
the impact of response to initial therapy on subsequent risk
has not been thoroughly evaluated. Future research must
objectively quantify the impact of response to therapy on
initial risk in those patients receiving treatment for AHF.
Determination of objective endpoints of therapy that describe
a patient at low-risk of subsequent adverse events are necessary to facilitate safe discharge at the earliest point after
initial therapy. The lack of objective endpoints contributes to
the high ED admission rate in patients with AHF.
Recommendations
Inpatient management is recommended for patients
with a poor response to initial therapy, indicated by a lack of
urinary output or lack of improvement in vital signs. Level of
Evidence: B.
Serial natriuretic peptide levels may prove useful for
assessing response to therapy if there are significant changes
in levels with therapy. However, at this point routine serial
natriuretic peptide testing in the OU is not recommended.
Level of Evidence: C.
Health Behavior and its Impact on Subsequent
Adverse Events
Several studies have identified markers of poor health
behavior that predict late adverse events in patients with AHF.
Vinson et al54 identified nonadherence (medication and diet) and
previous AHF admissions to be associated with 90-day readmission. Krumholz et al55 found poor social support was associated
with increased AHF-related readmissions during one-year follow-up. Rich et al56 found implementation of a nurse-directed
disease intervention program aimed at education, dietary and
medication assessment, discharge planning, and close outpatient
follow-up reduced 90-day AHF hospital readmissions. These
inpatient studies have identified health behavior as a risk factor
for late events. The impact of this risk on decision making and
short- and intermediate-term risk, as quantified prospectively,
has yet to be determined.
The OU presents a unique window of opportunity
where concurrent treatment, risk stratification, and bedside
teaching can occur. This is an ideal environment for those
patients with adherence issues, where resuming outpatient
medications concurrent with 12 to 24 hours of acute therapy
provides symptom resolution. Simultaneous bedside education and arrangement of close outpatient follow-up facilitates
safe, early OU discharge.
Preliminary data suggests that OU utilization for AHF
is safe, resource conservative, and may be a reasonable
alternative in patients with poor health behavior.40 – 42 A
sequential group design study analyzed the impact of OU
management as an alternative to hospital admission in a
nonhigh-risk cohort of ED patients with AHF.42 Total
charges were significantly lower for OU patients (median
$4203, range $2518 –$17,485) than for admitted patients
(median $8398, range $4283 – $34,604) (P ⫽ 0.001). Inpatient charges and pharmacy charges were also significantly
100
TABLE 2. Potential Modifiable Risk Markers in AHF
Source
Past medical history
Physical examination
Laboratory findings
Ancillary studies
Marker
Coronary artery disease
Systolic blood pressure, respiratory rate, oxygen
saturation
BUN, creatinine, sodium, natriuretic peptide levels
Ischemic ECG changes suggesting coronary
artery disease
less for OU patients (P ⬍ 0.001 and P ⫽ 0.042, respectively).
Further, there were 6 events among admitted patients (18.8%)
and 4 events among OU patients (14.8%) (P ⫽ 0.482). All
events included a readmission for AHF. All but one event
included an AHF-related ED visit.
Summary
Previous studies have identified several markers of highrisk in ED patients with AHF (Table 1). Impaired renal function,
low blood pressure, hyponatremia, ischemic ECG changes, elevated troponins, and elevated natriuretic peptides all have been
shown to be predictors of adverse events. Still lacking is a large,
prospective ED-based study that determines all levels of risk, not
just those at high-risk. Lack of high-risk cannot be equated with
low-risk. Further, objective markers of safe endpoints of therapy
are not well delineated. Not only do objective risk factors need
to be identified, but those amenable to intervention should also
be studied (Table 2). Modifiable objective endpoints would be
expected to drive early, aggressive therapy and disposition
decisions. Clinical trials have traditionally focused on improvement in symptoms and overall mortality. However, perhaps a
reasonable alternative would be to target prospectively objective
markers (creatinine, systolic blood pressure, natriuretic peptide
levels) with treatment pathways and novel therapies. Changes in
TABLE 3. Criteria to Identify AHF Patients for Observation
Stay
Recommended
Stable hemodynamic and respiratory status
SBP ⱖ100 mm Hg on presentation
BUN ⬍40 mg/dL
Creatinine ⬍3.0 mg/dL
Absence of ischemic ECG changes and/or elevated cardiac troponin
levels
Pre-existing heart failure
No intravenous vasoactive infusions being actively titrated
No significant comorbities requiring acute interventions
Respiratory rate (⬍32 breaths/min) and not requiring noninvasive
ventilation at the time of OU entry
No signs of poor perfusion
At least partial response to initial therapy with increased urine output
and/or improvement in vital signs
Consider
SBP ⬎120 mm Hg
Adequate social support
Adequate follow-up
BNP ⬍1000 pg/mL or NT-BNP ⬍5000 pg/mL
© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
these intermediate markers would be expected to lead to improvements in traditional endpoints such as hospital length-ofstay, recidivism, and mortality. There has yet to be a randomized
trial that has evaluated the efficacy of a prediction rule dictating
therapy (goal-directed therapy) compared with standard physician decision making.
This paradigm shift is necessary if we expect to be able to
alter disposition decisions from prolonged inpatient admissions
to either ED discharge or brief OU management. Until we are
able to determine a cohort of ED patients at low-risk of subsequent adverse events, the OU represents a reasonable alternative
to inpatient admission for further treatment and risk stratification
in patients who do not have high-risk ED features (Table 3).
16.
17.
18.
19.
REFERENCES
20.
1. O’Connell JB, Bristow M. Economic impact of heart failure in the
United States: a time for a different approach. J Heart Lung Transplant.
1994;13:S107–S112.
2. Stevenson LW, Braunwald E. Recognition and management of patients
with heart failure. In: Goldman L, Braunwald E, eds. Primary Cardiology. Philadelphia: WB Saunders; 1998:310 –329.
3. American Heart Association. Heart Disease and Stroke Statistics–2004
Update. Available at: http://www.americanheart.org/downloadable/
heart/ 1079736729696HDSStats2004UpdateREV3-19-04.pdf. Accessed
December 24, 2007.
4. Graff L, Orledge J, Radford MJ, et al. Correlation of the agency for
health care policy and research congestive heart failure admission
guideline with mortality: peer review organization voluntary hospital
association initiative to decrease events (PROVIDE) for congestive heart
failure. Ann Emerg Med. 1999;34:429 – 437.
5. Smith WR, Poses RM, McClish DK, et al. Prognostic judgments and
triage decisions for patients with acute congestive heart failure. Chest.
2002;121:1610 –1617.
6. Polanczyk CA, Rohde LE, Philbin EA, et al. A new casemix adjustment
index for hospital mortality among patients with congestive heart failure.
Med Care. 1998;36:1489 –1499.
7. Adams KF Jr, Fonarow GC, Emerman CL, et al. Characteristics and
outcomes of patients hospitalized for heart failure in the United States:
rationale, design, and preliminary observations from the first 100,000
cases in the Acute Decompensated Heart Failure National Registry
(ADHERE). Am Heart J. 2005;149:209 –216.
8. Cleland JG, Swedberg K, Follath F, et al. The EuroHeart Failure survey
programme—a survey on the quality of care among patients with heart
failure in Europe. Part 1: patient characteristics and diagnosis. Eur
Heart J. 2003;24:442– 463.
9. Cuffe MS, Califf RM, Adams KF Jr, et al. Short-term intravenous
milrinone for acute exacerbation of chronic heart failure: a randomized
controlled trial. JAMA. 2002;287:1541–1547.
10. Publication Committee for the VMAC Investigators. Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart
failure: a randomized controlled trial. JAMA. 2002;287:1531–1540.
11. Rame JE, Sheffield MA, Dries DL, et al. Outcomes after emergency
department discharge with a primary diagnosis of heart failure. Am
Heart J. 2001;142:714 –719.
12. Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 guideline
update for the diagnosis and management of chronic heart failure in the
adult-summary article a report of the American College of Cardiology/
American Heart Association Task Force on Practice Guidelines (writing
committee to update the 2001 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol. 2005;46:1116 –1143.
13. Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the
evaluation and management of chronic heart failure in the adult: executive summary. J Heart Lung Transplant. 2002;21:189 –203.
14. Heart Failure Society of America. HFSA guidelines for the management
of patients with heart failure due to left ventricular systolic dysfunction–
pharmacological approaches. Congest Heart Fail. 2000;6:11–39.
15. Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Evaluation and
21.
© 2008 Lippincott Williams & Wilkins
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
Risk Stratification
Management of Heart Failure). Guidelines for the evaluation and management of heart failure. J Am Coll Cardiol. 1995;26:1376 –1398.
Konstam M, Dracup K, Baker D. Clinical Practice Guidelines No 11:
heart failure: evaluation and care of patients with left-ventricular systolic
dysfunction. Provid Stud Res Note Agency Health Care Policy Res.
1994;94.
Fonarow G, Abraham WT, Albert NM, et al. Characteristics, treatment
and outcomes of patients hospitalized for heart failure with preserved
systolic function: a report from OPTIMIZE-HF. J Am Coll Cardiol.
2006;47(suppl A):47.
Selker HP, Griffith JL, D’Agostino RB. A time-insensitive predictive
instrument for acute hospital mortality due to congestive heart failure:
development, testing, and use for comparing hospitals: a multicenter
study. Med Care. 1994;32:1040 –1052.
Chin MH, Goldman L. Correlates of major complications or death in
patients admitted to the hospital with congestive heart failure. Arch
Intern Med. 1996;156:1814 –1820.
Katz MH, Nicholson BW, Singer DE, et al. The triage decision in
pulmonary edema. J Gen Intern Med. 1988;3:533–539.
Fonarow GC, Adams KF Jr, Abraham WT, et al.; for the ADHERE
Scientific Advisory Committee, Study Group, and Investigators. Risk
stratification for in-hospital mortality in acutely decompensated heart
failure: classification and regression tree analysis. JAMA. 2005;293:572–
580.
Gheorghiade M, Abraham WT, Albert NM, et al.; for the OPTIMIZEHF 关Organized Program to Initiate Lifesaving Treatment in Hospitalized
Patients with Heart Failure兴 Investigators and Coordinators. Systolic
blood pressure at admission, clinical characteristics, and outcomes in
patients hospitalized with acute heart failure. JAMA. 2006;296:2217–
2226.
Gheorghiade M, Abraham WT, Albert NM, et al. Relationship between
admission serum sodium concentration and clinical outcomes in patients
hospitalized for heart failure: an analysis from the OPTIMIZE-HF
registry. Eur Heart J. 2007;28:980 –988.
Filippatos G, Rossi J, Lloyd-Jones DM, et al. Prognostic value of blood
urea nitrogen in patients hospitalized with worsening heart failure:
insights from the Acute and Chronic Therapeutic Impact of a Vasopressin Antagonist in Chronic Heart Failure (ACTIV in CHF) study. J Card
Fail. 2007;13:360 –364.
Formiga F, Chivite D, Manito N, et al. Predictors of in-hospital mortality
present at admission among patients hospitalised because of decompensated heart failure. Cardiology. 2007;108:73–78.
Diercks DB, Peacock WF, Kirk JD, et al. ED patients with heart failure:
identification of an observational unit-appropriate cohort. Am J Emerg
Med. 2006;24:319 –324.
Auble TE, Hsieh M, Gardner W, et al. A prediction rule to identify low-risk
patients with heart failure. Acad Emerg Med. 2005;12:514 –521.
Bayés-Genı́s A, Lopez L, Zapico E, et al. NT-ProBNP reduction percentage during admission for acutely decompensated heart failure predicts long-term cardiovascular mortality. J Card Fail. 2005;11(suppl
5):S3–S8.
Harrison A, Morrison LK, Krishnaswamy P, et al. B-type natriuretic
peptide predicts future cardiac events in patients presenting to the
emergency department with dyspnea. Ann Emerg Med. 2002;39:131–
138.
Cheng V, Kazanagra R, Garcia A, et al. A rapid bedside test for B-type
peptide predicts treatment outcomes in patients admitted for decompensated heart failure: a pilot study. J Am Coll Cardiol. 2001;37:386 –391.
Fonarow GC, Peacock WF, Phillips CO, et al. Admission B-type
natriuretic peptide levels and in-hospital mortality in acute decompensated heart failure. J Am Coll Cardiol. 2007;49:1943–1950.
Januzzi JL, van Kimmenade R, Lainchbury J, et al. NT-proBNP testing
for diagnosis and short-term prognosis in acute destabilized heart failure:
an international pooled analysis of 1256 patients: the International
Collaborative of NT-proBNP study. Eur Heart J. 2006;27:330 –337.
Yu CM, Sanderson JE. Plasma brain natriuretic peptide–an independent
predictor of cardiovascular mortality in acute heart failure. Eur J Heart
Fail. 1999;1:59 – 65.
Maisel A, Hollander JE, Guss D, et al. Primary results of the Rapid
Emergency Department Heart Failure Outpatient Trial (REDHOT). A
multicenter study of B-type natriuretic peptide levels, emergency de-
101
Collins et al
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
partment decision making, and outcomes in patients presenting with
shortness of breath. J Am Coll Cardiol. 2004;44:1328 –1333.
35. Kirk V, Bay M, Parner J, et al. N-terminal proBNP and mortality in
hospitalised patients with heart failure and preserved vs. reduced systolic
function: data from the prospective Copenhagen Hospital Heart Failure
Study (CHHF). Eur J Heart Fail. 2004;6:335–341.
36. Januzzi JL Jr, Sakhuja R, O’Donoghue M, et al. Utility of aminoterminal pro-brain natriuretic peptide testing for prediction of 1-year
mortality in patients with dyspnea treated in the emergency department.
Arch Intern Med. 2006;166:315–320.
37. Chen AA, Wood MJ, Krauser DG, et al. NT-proBNP levels, echocardiographic findings, and outcomes in breathless patients: results
from the ProBNP Investigation of Dyspnea in the Emergency Department (PRIDE) echocardiographic substudy. Eur Heart J. 2006;
27:839 – 845.
38. Heart Failure Society of America. HFSA 2006 comprehensive heart
failure practice guideline. J Card Fail. 2006;12:e1– e2.
39. Silvers SM, Howell JM, Kosowsky JM, et al. Clinical policy: critical
issues in the evaluation and management of adult patients presenting to
the emergency department with acute heart failure syndromes. Ann
Emerg Med. 2007;49:627– 669.
40. Peacock WF, Albert NM. Observation unit management of heart failure.
Emerg Med Clin North Am. 2001;19:209 –232.
41. Peacock WF, Young J, Collins S, et al. Heart failure observation units:
optimizing care. Ann Emerg Med. 2006;47:22–33.
42. Storrow AB, Collins SP, Lyons MS, et al. Emergency department
observation of heart failure: preliminary analysis of safety and cost.
Congest Heart Fail. 2005;11:68 –72.
43. Ivanov RI, Allen J, Sandham JD, et al. Pulmonary artery catheterization:
a narrative and systematic critique of randomized controlled trials and
recommendations for the future. New Horiz. 1997;5:268 –276.
44. Binanay C, Califf RM, Hasselblad V, et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the
ESCAPE trial. JAMA. 2005;294:1625–1633.
45. Brophy JM, Deslauriers G, Boucher B, et al. The hospital course and
short term prognosis of patients presenting to the emergency room with
decompensated congestive heart failure. Can J Cardiol. 1993;9:219 –
224.
46. Brophy JM, Deslauriers G, Rouleau JL. Long-term prognosis of patients
presenting to the emergency room with decompensated congestive heart
failure. Can J Cardiol. 1994;10:543–547.
46a. Esdaile JM, Horwitz RI, Levinton C, et al. Response to initial therapy
and new onset as predictors of prognosis in patients hospitalized with
congestive heart failure. Clin Invest Med. 1992;15:122–131.
47. O’Neill JO, Bott-Silverman CE, McRae AT III, et al. B-type natriuretic
peptide levels are not a surrogate marker for invasive hemodynamics
during management of patients with severe heart failure. Am Heart J.
2005;149:363–369.
48. Kazanegra R, Cheng V, Gaccia A, et al. A rapid test for B-type
natriuretic peptide (BNP) correlates with falling wedge pressures in
patients treated for decompensated heart failure: a pilot study. J Card
Fail. 2001;7:21–29.
49. Wu AH. Serial testing of B-type natriuretic peptide and NTpro-BNP for
monitoring therapy of heart failure: the role of biologic variation in the
interpretation of results. Am Heart J. 2006;152:828 – 834.
50. Valle R, Prevaldi C, D’Eri A, et al. B-type natriuretic peptide predicts
102
51.
52.
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
postdischarge prognosis in elderly patients admitted due to cardiogenic
pulmonary edema. Am J Geriatr Cardiol. 2006;15:202–207.
Verdiani V, Nozzoli C, Bacci F, et al. Pre-discharge B-type natriuretic
peptide predicts early recurrence of decompensated heart failure in
patients admitted to a general medical unit. Eur J Heart Fail. 2005;7:
566 –571.
Logeart D, Thabut G, Jourdain P, et al. Predischarge B-type natriuretic
peptide assay for identifying patients at high risk of re-admission after
decompensated heart failure. J Am Coll Cardiol. 2004;43:635– 641.
Troughton RW, Frampton CM, Yandle TG, et al. Treatment of heart
failure guided by plasma aminoterminal brain natriuretic peptide
(N-BNP) concentrations. Lancet. 2000;355:1126 –1130.
Vinson JM, Rich MW, Sperry JC, et al. Early readmission of elderly
patients with congestive heart failure. J Am Geriatr Soc. 1990;38:1290 –
1295.
Krumholz HM, Amatruda J, Smith GL, et al. Randomized trial of an
education and support intervention to prevent readmission of patients
with heart failure. J Am Coll Cardiol. 2002;39:83– 89.
Rich MW, Beckham V, Wittenberg C, et al. A multidisciplinary intervention to prevent the readmission of elderly patients with congestive
heart failure. N Engl J Med. 1995;333:1190 –1195.
Rohde LE, Goldraich L, Polanczyk CA, et al. A simple clinically based
predictive rule for heart failure in-hospital mortality. J Card Fail.
2006;12:587–593.
Barsheshet A, Garty M, Grossman E, et al. Admission blood glucose
level and mortality among hospitalized nondiabetic patients with heart
failure. Arch Intern Med. 2006;166:1613–1619.
Burkhardt J, Peacock WF, Emerman CL. Predictors of emergency
department observation unit outcomes. Acad Emerg Med. 2005;12:869 –
874.
Klein L, O’Connor CM, Leimberger JD, et al. Lower serum sodium is
associated with increased short-term mortality in hospitalized patients
with worsening heart failure: results from the Outcomes of a Prospective
Trial of Intravenous Milrinone for Exacerbations of Chronic Heart
Failure (OPTIME-CHF) study. Circulation. 2005;111:2454 –2460.
Felker GM, Leimberger JD, Califf RM, et al. Risk stratification after
hospitalization for decompensated heart failure. J Card Fail. 2004;10:
460 – 466.
Lee DS, Austin PC, Rouleau JL, et al. Predicting mortality among
patients hospitalized for heart failure: derivation and validation of a
clinical model. JAMA. 2003;290:2581–2587.
Harjai KJ, Nunez E, Turgut T, et al. The independent effects of left
ventricular ejection fraction on short-term outcomes and resource utilization following hospitalization for heart failure. Clinical Cardiol.
1999;22:184 –190.
Butler J, Hanumanthu S, Chomsky D, Wilson JR. Frequency of low-risk
hospital admissions for heart failure. Am J Cardiol. 1998;81:41– 44.
Villacorta H, Rocha N, Cardoso R, et al. Hospital outcome and shortterm follow-up of elderly patients presenting to the emergency unit with
congestive heart failure. Arq Bras Cardiol. 1998;70:167–171.
Chin MH, Goldman L. Correlates of major complications or death in
patients admitted to the hospital with congestive heart failure. Arch
Intern Med. 1996;156:1814 –1820.
Plotnick GD, Kelemen MH, Garrett RB, et al. Acute cardiogenic
pulmonary edema in the elderly: factors predicting in-hospital and
one-year mortality. South Med J. 1982;75:565–569.
© 2008 Lippincott Williams & Wilkins
SOCIETY
OF
CHEST PAIN CENTERS RECOMMENDATIONS
Acute Heart Failure Treatment
J. Douglas Kirk, MD, Gerasimos Filippatos, MD, Committee Co-Chairs; Mihai Gheorghiade, MD,
Peter S. Pang, MD, Phillip Levy, MD, MPH, Ezra A. Amsterdam, MD, W. Frank Peacock, MD,
and Gregg C. Fonarow, MD, FACC; of the Society of Chest Pain Centers Acute Heart
Failure Committee
Abstract: Emerging concepts in the short term management of
acute heart failure have fostered changes in therapeutic targets and
the expectations of emergency department and in-hospital treatment
options. Investigators and clinicians are now reconsidering how
intravenous diuretics, vasodilators, and inotropes commonly used to
alleviate congestion and restore hemodynamic stability should be
administered; which acute heart failure patients should receive them;
and the long-term morbidity and mortality implications of these
decisions. This section evaluates these various therapeutic options
for patients appropriate for short stay unit management.
(Crit Pathways in Cardiol 2008;7: 103–110)
A
cute heart failure (AHF) has historically been viewed as
a transient event, characterized by systolic dysfunction,
low cardiac output, and fluid overload. This pathophysiologic
model was thought to be relatively consistent across patient
groups, only varying in its severity.1–3 Consequently, shortterm treatment strategies such as intravenous diuretics, targeted at rapidly alleviating fluid congestion, were adopted
without clinical trials evaluating long-term safety and efficacy issues. Diuretics, along with the subsequent use of
vasodilator therapy, eventually became standard care. Emerging data from several heart failure registries have largely
challenged this model by revealing a more complex and
distinct pathophysiologic entity.4,5 Before this, the unique
AHF pathophysiology and diverse patient types were largely
underappreciated or unobserved. Registry data have shown
that the AHF population is not a homogeneous group of
chronic heart failure patients, but rather multiple types of
heart failure patients with various forms of acute decompensation, combinations of comorbidities, and varying degrees of
severity.4,5
Therapeutic Options
A PubMed search of congestive heart failure, emergency department (ED) therapy, and outcomes or guidelines
found that multiple pharmacologic agents are used to manage
AHF.6,7 Most were not designed specifically for the management of AHF, but their use is common and largely empiric.8
Copyright © 2008 by Lippincott Williams & Wilkins
ISSN: 1535-282X/08/0702-0103
Collectively, these agents effectively restore hemodynamic
function, reduce dyspnea, and alleviate congestion.9 –13 However, treatment success is limited as no agent has been shown
to reduce post-discharge mortality or readmission rates, and
patients frequently remain symptomatic after treatment.2 A
common thread in these failed trials is the timing of therapeutic intervention; specifically a delay between the onset of
symptoms or hospital presentation and randomization to therapy, which can be as much as 48 hours. During this interval,
prerandomization treatment can alter patient’s symptoms and
change their hemodynamic status, affecting the clinical targets or even worse, altering important safety measures such
as mortality. The following is a brief overview of the pharmacologic agents whose use in an observation unit would be
appropriate. In addition, the use of noninvasive ventilation for
the treatment of respiratory embarrassment because of acute
pulmonary edema is also described.
Diuretics
Nonpotassium sparing diuretics (ie, loop diuretics) are
often the first-line approach to rapidly reduce fluid overload
and relieve symptoms. Because of this, they are a central
component to AHF management and their use is endorsed by
guidelines from both the United States6 and Europe.7 Despite
the obvious clinical utility of diuretics, it is important for
clinicians to understand the potential adverse effects of diuretics and their possible limitations in patients with AHF.
Clinicians should critically reconsider the degree to which
current standard of care relies on diuretics for AHF treatment
because of both the wealth of data indicating the deleterious
side effects of these agents in the short term and the emerging
data suggesting that chronic diuretic use may increase the
morbidity and mortality of patients with chronic heart failure.14 –16 However, these limitations must be balanced with
the fact that there are few alternatives and the long history of
their effective use.
A number of studies have reported adverse effects
including hypotension, electrolyte abnormalities, renal dysfunction, and maladaptive neurohormonal activation, especially when used at high doses.14 –17 Despite their use for
decades, clinical targets of diuretic therapy in AHF are not
well defined. Large-scale randomized controlled trials to
define the best strategy for their use (dose and duration) and
their effects on clinical outcomes have not been conducted.
Clear dosing guidelines are lacking, and dosing choices and
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
103
Kirk et al
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
administration methods tend to be empiric.11 However, several small studies in patients with advanced chronic heart
failure suggest that continuous infusion of furosemide preceded by a loading dose may be superior to the common
practice of using single or intermittent bolus injection of an
equal dosage.18,19
Cotter et al20 described the deleterious effects of moderate-high dose furosemide in 20 patients with refractory
heart failure, demonstrating a decrease in mean arterial blood
pressure, deterioration in renal function, and more hypokalemia compared with treatment with low dose furosemide
despite similar improvement in symptoms and urine output.
The author also reported results in 104 patients presenting
with severe pulmonary edema, and hypoxemia randomized to
either high-dose nitrate plus low dose furosemide versus
high-dose furosemide plus low dose nitrates. Adverse events,
including in-hospital death, need for mechanical ventilation,
and myocardial infarction occurred more frequently in the
high-dose furosemide group than in the high-dose nitrate
group.21
Until there are further therapeutic advances, diuretics
will remain a mainstay of treatment in congested patients
because of the ability of these agents to rapidly reduce fluid
overload, an important and central component to AHF management. More importantly, using these agents judiciously
with close monitoring of fluid balance and electrolytes seem
to be a sound approach given the contradictory safety and
efficacy data. Clinical trials evaluating doses, routes of administration, duration of treatment, and clinical outcomes are
sorely needed.
Vasodilators
Vasodilator therapy includes a diverse group of agents
(eg, nitrates, nesiritide, nitroprusside) that produce multiple,
similar hemodynamic changes in the failing circulatory system. They are frequently used in the treatment of AHF
patients with congestion and normal or elevated blood pressure. In the Acute Decompensated Heart Failure National
Registry (ADHERE), nesiritide and nitroglycerin were the
most commonly used intravenous vasoactive agents, given to
13% and 9% of patients, respectively.4 Intravenous nitroglycerin relaxes vascular smooth muscle by stimulating guanylate
cyclase, leading to venodilation at low doses (30 – 40 ␮g/min)
and arteriolar dilation at higher doses (250 ␮g/min).12 It
reduces left ventricular (LV) filling pressures and pulmonary
congestion without compromising stroke volume or increasing myocardial oxygen demand.
Nitroglycerin is generally considered safe by most
physicians who are quite familiar with it and are comfortable
using it. In addition to the intravenous form, it is also
available in sublingual and topical preparations. The latter are
frequently used in the ED but no clinical trial data exist
describing its utility. Transient increases in serum creatinine
have been observed,22 but treatment does not seem to worsen
overall renal function.23 Nitroglycerin may stimulate neurohormonal activity (eg, increase aldosterone and epinephrine
levels), and patients often develop tolerance, especially when
doses are increased to produce short term hemodynamic
104
benefit.13 Because of this, nitroglycerin administration often
requires careful titration and monitoring. In some institutions,
titration of intravenous nitroglycerin requires admission to
the intensive care unit (ICU), which in those cases would
preclude its use in the observation unit setting.
However, the evidence base for its specific use in AHF is
sparse. Several small-scale studies established the ability of
nitroglycerin to improve hemodynamic function in a dosedependent manner,13,24,25 whereas others have shown the use of
high dose intravenous nitroglycerin or isosorbide dinitrate to
treat pulmonary edema because of hypertensive crisis to be more
effective than standard dosing or repeat furosemide administration.26 –31 These substantial doses have been given with a low
incidence of hypotension (⬍4%) and no report of adverse
neurologic or cardiac events. This approach to treatment however, requires diligent hemodynamic monitoring.
Moreover, it has been evaluated in AHF in only one
randomized, double-blind, placebo-controlled study, the vasodilation in the acute management of congestive heart failure (VMAC) trial.32 In this trial, nitroglycerin produced a
nonsignificant pulmonary capillary wedge pressure (PCWP)
reduction versus placebo. Other improvements in hemodynamic function and global assessment were evident with
nitroglycerin, as were reductions in dyspnea, although most
improvements did not reach statistical significance versus
control or the comparator nesiritide. Adverse events such as
headache and abdominal pain were more common in nitroglycerin than with nesiritide but there were no differences in
clinical outcomes.
Nesiritide, a recombinant form of human brain natriuretic peptide, is also indicated for the treatment of AHF. It
prevents excess salt and water retention, promotes vascular
relaxation, and suppresses sympathetic outflow. Nesiritide
exerts vasodilatory effects on arterial, venous, and coronary
vessels, leading to increased cardiac output.33 Studies of
nesiritide in the treatment of AHF have documented beneficial effects on hemodynamics (reductions in PCWP and
systemic vascular resistance and increases in cardiac output)
and symptoms, compared with placebo.34,35 In VMAC, nesiritide had a faster onset of action and produced a greater and
more sustained reduction in PCWP than did nitroglycerin or
placebo.32 It significantly improved dyspnea compared with
placebo but not compared with nitroglycerin.
The safety of nesiritide has been called into question by
2 meta-analysis.36,37 The first, a 5-trial meta-analysis (n ⫽
797) reported that nesiritide induced increases in serum
creatinine levels of more than 0.5 mg/dL in 21% of treated
patients versus 15% of patients who received control therapy
(P ⫽ 0.003).36 The second meta-analysis of 3 randomized
double-blind studies (n ⫽ 862) that included AHF patients
treated with nesiritide or control therapy reported a trend
toward an increased risk of 30-day mortality with nesiritide,
although the difference failed to achieve statistical significance.37 However, caution is warranted in interpreting the
meta-analysis results. The studies were not powered or designed to assess mortality or renal dysfunction as a primary or
secondary end point, and meta-analyses are inherently limited
© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
by an inability to control for baseline characteristics and
various concomitant or control treatments.38,39
Angiotensin-converting enzyme (ACE) inhibitors have
also been used in the setting of AHF. As a class, they are
effective antihypertensives and provide antagonism of the
renin-angiotensin-aldosterone system, making them ideal
agents for heart failure treatment. There is an abundance of
data which show substantial benefit of their use in chronic
heart failure (ie, disease regression, symptom improvement,
and decreased mortality),40 – 42 but few studies have been
conducted in the acute setting. However, the results from
these limited trials are encouraging with demonstration of
rapid symptom improvement and a reduced need for mechanical ventilation after a single dose of sublingual captopril (25
mg) or the intravenous (IV) administration of enalaprilat
(1.25 mg).43,44 Because of the absence of large, placebo
controlled trials and the potential for adverse events such as
hypotension and renal dysfunction, ACE inhibitors are not
currently considered standard of care in the management of
AHF. However, these limited data and anecdotal reports of
successful use in the observation unit setting are encouraging
and warrant further investigation to determine this class of
drug’s utility in these patients.
Another common medication used as a “vasodilator” in
the treatment of AHF that deserves comment is morphine
sulfate. Morphine is thought to produce mild veno-dilatation
with an associated reduction in preload. In addition, morphine
may induce respiratory relaxation and exert a calming effect
on those with agitation due to dyspnea. The evidence in favor
of morphine use for AHF is limited at best, with most of its
support anecdotal. There are retrospective data, however,
which demonstrate an association between morphine and
adverse outcomes such as endotracheal intubation, need for
intensive care unit admission and prolonged hospital length
of stay.45,46 In a recent report from the ADHERE registry,
morphine use was associated with increased in-hospital mortality.47 Despite morphine’s longstanding use in AHF, the
possibility exists that the risks outweigh any benefits. Because of these safety concerns, morphine’s routine use cannot
be recommended. Additional studies are needed before definitive recommendations either for or against can be provided.
Oxygen Therapy and Ventilatory Support
The majority of patients who present with AHF will
require some form of oxygen supplementation. Nasal cannula
delivery for mild dyspnea and a nonrebreather facemask for
moderate dyspnea will generally be sufficient. Those with
severe dyspnea, particularly those with acute pulmonary
edema, often require ventilatory support. The need for endotracheal intubation and mechanical ventilation should be a
clinical decision based on careful assessment of the patient.
Noninvasive ventilation using continuous positive airway
pressure (CPAP) or bilevel positive airway pressure (BiPAP)
has been shown to be quite effective in reducing the need for
intubation and a trend toward a mortality benefit.48 Its use
should be considered in all patients with intact mental status
who show early signs of respiratory embarrassment or fatigue. However, caution must be exercised, as it is not an
© 2008 Lippincott Williams & Wilkins
Treatment
alternative to mechanical ventilation in patients who clearly
have respiratory failure, and it should not be used as “bridging therapy” in anticipation of endtracheal intubation.
Although both methods of noninvasive ventilation
(CPAP and BiPAP) seem to offer benefit, controversy exists
regarding relative superiority. Both diminish preload and
cardiac filling pressures to a similar degree, but hemodynamic manifestations vary, with BiPAP producing a more
rapid decrease in blood pressure and CPAP resulting in a
greater initial reduction in mean PCWP.49,50 BiPAP may
have a slight advantage with regard to measures of respiratory
status, as prior studies have demonstrated more rapid dyspnea
resolution and more profound improvement in the PO2 and
PCO2.49,50 With respect to clinical outcomes, the situation is
not entirely clear. A single, prospective comparison trial did
suggest a higher rate of myocardial infarction with use of
BiPAP, but this has not been found in subsequent investigations.49,51,52 A recent meta-analysis found a significant mortality reduction for patients treated with CPAP but not BiPAP, with no overall difference in effect on intubation rate.53
However, the recent 3CPO trial demonstrated no significant
outcome differences between BiPAP versus CPAP and no
mortality benefit of noninvasive ventilation in general.54
Based on the available evidence, it is difficult to distinguish
one method as superior, and there is likely to be general
equivalence in clinical practice.
Approximately 5% of all AHF patients and up to 40%
of those with acute pulmonary edema will require mechanical
ventilation.45,55,56 For most of these individuals, signs of
impending respiratory failure such as severe dyspnea, tachypnea, diaphoresis, fatigue, and confusion will be readily
apparent. In others, however, findings may be more subtle.
Objective parameters which indicate potential need for mechanical ventilation include persistent hypoxia (SaO2 ⬍90)
despite supplemental oxygen, hypercarbia (PaCO2 ⬎55 mm
Hg) and acidosis (pH ⬍7.25).57
AHF Classification
AHF patient types have not been well elucidated or
matched with specific treatment strategies in prospective
randomized studies, and selection of existing treatments is
largely empiric because of the paucity of randomized clinical
trial data.58 In addition, some of the few AHF specific
treatments may cause myocardial injury,1 impair renal function,36 and increase mortality risk,37 further complicating
decision-making. Although AHF is associated with a poor
prognosis, only recently have guidelines from the United
States and Europe6,7 begun to address management of these
patients. The European Society of Cardiology guidelines
were the first to classify patients with AHF into distinct
clinical conditions.7 However, this classification is complex
and is based on pathophysiology, clinical phenotype and
disease severity on presentation. Moreover, most of these
conditions are not practically well defined. Despite the publication of these guidelines, there are no inclusive, evidenceand consensus-based treatment algorithms that address the
individual treatment needs of each type of patient with AHF.
Useful recommendations should focus on therapeutic management, with particular emphasis on identifying AHF pa-
105
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Kirk et al
tient types and matching them to specific treatment strategies.
Management algorithms are likewise helpful, and should
supplement any recommendations.
A novel method of categorizing AHF patient types has
recently been described by heart failure experts.1–3,59 – 61 This
classification is based upon hemodynamic characteristics at
presentation in addition to a clinical symptom profile that
suggest AHF (dyspnea because of pulmonary congestion,
peripheral edema, weight gain, fatigue, history of heart failure). Although most EDs don’t have the luxury of obtaining
hemodynamic parameters such as PCWP or cardiac output
via invasive means, they do have a reliable and easily obtainable parameter — the blood pressure. AHF patients can
be classified into those with normal (120 –160 mm Hg),
elevated (⬎160 mm Hg) or low (⬍120 mm Hg) systolic blood
pressure at presentation. The exact pathophysiology, clinical
characteristics, and appropriate treatment options of each of
these patient types has yet to be fully clarified, but recommendations based largely on observational data and expert consensus
can be suggested. Because virtually all patients with hypotension
are unstable by definition, recommendations for the group with
low blood pressure at presentation will not be discussed or
provided as these patients would not be candidates for care in an
observation unit. Clinical characteristics of the remaining 2
groups are described in Table 1.1,4,7
AHF Patients With Normal Systolic Blood
Pressure at Presentation
These patients are common and may represent nearly
half of the AHF population.4 Blood pressure is normal (systolic blood pressure range of 120 –160 mm Hg) and there is
usually a history of progressive worsening of chronic heart
failure. In this group, symptoms and signs develop gradually,
over days-weeks, and not only pulmonary but also systemic
congestion (jugular venous distension and peripheral edema)
is present. The ejection fraction is usually reduced. Management is often difficult as many patients are refractory to
therapy and continue to have signs of congestion despite the
initial improvement in symptoms. Moreover, in a number of
patients the clinical and/or radiographic signs of pulmonary
congestion are not evident, despite elevated left ventricular
filling pressures.1,4,6,7 These patients benefit from more intense diuresis, with a therapeutic goal of relieving congestion
TABLE 1. Clinical Characteristics of AHF Patient Types
Normal SBP at Presentation
(Vascular Failure)
Elevated SBP at Presentation
(Cardiac Failure)
SBP 120–160 mm Hg
Dyspnea
Pulmonary edema (⫾)
Rales (⫾)
Peripheral edema
Gradual symptom onset (d/wk)
Weight gain
Mild to moderate PCWP elevation
Decreased systolic function
SBP ⬎160 mm Hg
Dyspnea
Pulmonary edema
Rales
Peripheral edema (⫾)
Rapid symptom onset
Minimal weight gain
Moderate to severe PCWP elevation
Preserved systolic function
106
and reducing total body fluid and peripheral edema. The
addition of nitrates may be helpful to control symptoms in
patients with relatively elevated blood pressure.
Treatment of this group is depicted in Figure 1 and is
initiated with an intravenous loop diuretic. The lowest effective dose should be used, with an estimated starting dose
equivalent to the patient’s daily outpatient oral dose given
intravenously, or 20 mg of furosemide in the diuretic naive
patient. The patient’s renal function and response to diuretics
should be measured and the blood pressure reassessed. Patients who respond appropriately with ample diuresis and
clinical improvement may be admitted to an observation unit
and continuously reassessed for symptomatic improvement.
Those with a partial response and those with a relatively
elevated blood pressure may benefit from the addition of an
intravenous vasodilator.
However, the patient who fails to improve, is resistant
to diuretic therapy, has poor renal function, or develops
hypotension should be admitted to the hospital for further
management. In a select number of these patients, the addition of an IV vasodilator may be warranted. Unfortunately,
those patients with an initial systolic blood pressure (SBP) in
the low normal range (90 to 120 mm Hg) may “run out” of
blood pressure after initial diuresis, and caution must be
exercised to maintain adequate perfusion. Because some
vasodilators require careful titration, admission to the ICU
may be appropriate, particularly in patients with renal insufficiency or those with inadequate urine output. If at any point
the patient becomes hypotensive, the dose of the vasodilator
should be reduced or discontinued if persistent. Evidence of
hypoperfusion may warrant initiation of an IV inotrope, with
guidance based upon hemodynamic measurements. As such,
these latter patients would clearly not be candidates for
observation unit management any further.
AHF Patients with Elevated Systolic Blood
Pressure at Presentation
Data from the ADHERE registry demonstrate that 50%
of AHF patients had an elevated SBP on presentation.4
Occasionally referred to as vascular failure,1 these patients
typically have a SBP ⬎160 mm Hg and are more often
women, older, and more likely to have diastolic dysfunction
with relatively preserved left ventricular function.1,5 Symptom onset is generally abrupt and severe dyspnea is the
predominant complaint although signs of end-organ hypoperfusion may be present. Acute pulmonary edema is the hallmark of this syndrome and is usually evident on examination
(rales) and chest radiography (pulmonary edema). However,
response to therapy is typically just as rapid in patients who
are aggressively treated. Accordingly, the clinical target is
blood pressure control with early, aggressive vasodilation,
more so than diuresis. This is particularly true when pulmonary congestion is related to fluid mal-distribution, rather
than an increase in total fluid volume.1,2,7
Upon first patient contact, either in the prehospital
setting or in the ED, treatment ensues with the immediate use
of sublingual nitroglycerin, which is easily and rapidly administered (Fig. 2). This typically produces dramatic im© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
AHF patient with
SBP 120-160 mmHg
IV loop diuretic
Reassess for
clinical improvement
•
•
Partial response
Elevated SBP
•
•
•
•
•
Good response
Good urine output
Good renal function
Normal SBP
Troponin negative
Treatment
Consider
additional
therapy
Add IV vasodilator
(nitroglycerin, nesiritide)
Worsens
Good
Response
Admit to ED
observation unit
•
•
•
•
•
•
Poor response
Poor urine output
Poor renal function
Diuretic resistant
Low SBP(<90 mm Hg)
Troponin negative
No
improvement
Admit to
Hospital
Continued
improvement
Consider
discharge
Admit to hospital
FIGURE 1. Treatment algorithm for the AHF patient with normal systolic blood pressure at presentation.
provement within minutes.62 An IV vasodilator (nitroglycerin
or nesiritide) should then be added and renal function, blood
pressure, and the response to therapy should be assessed.
Topical nitrates could be considered as an alternative to an IV
vasodilator in those patients who are less ill or in those in who
use of an IV vasodilator is not feasible. If the patient fails to
respond accordingly or has other evidence of high risk,63
admission to the ICU is recommended. Persistent signs of
pulmonary congestion despite adequate blood pressure control or signs of systemic volume overload may warrant the
addition of an intravenous loop diuretic. Diuretics should be
prescribed at the lowest possible effective dose to achieve
symptomatic improvement, to avoid adverse effects such as
prerenal azotemia or diuretic resistance. If the patient responds adequately to initial therapy, admission to an observation unit is appropriate, unless ongoing titration of the
vasodilator necessitates ICU admission.
•
AHF patient with
SBP>160 mmHg
•
•
Good
response
Good urine
output
SBP normalized
Summary of Recommendations
Management of AHF Based on Systolic Blood
Pressure at Presentation
It is recommended that AHF be classified based on
hemodynamic characteristics (SBP) at presentation in addition to a clinical symptom profile that suggest AHF (dyspnea
because of pulmonary congestion, peripheral edema, weight
gain, fatigue, history of heart failure). Level of Evidence: C.
• AHF patients can be classified into those with normal
(120 –160 mm Hg), elevated (⬎160 mm Hg) or low (⬍120
mm Hg) SBP at presentation.
• Recommendations focus on matching these AHF patient
types to specific treatment strategies.
• Management algorithms are provided and should supplement these recommendations.
Admit to ED
observation unit
Immediate
sublingual nitroglycerin
Continued
improvement
Consider discharge
No
improvement
Consider additional
therapy
Worsens
Topical/IV vasodilator
(nitroglycerin, nesiritide)
Add IV loop diuretic
if volume overloaded
Reassess for
clinical improvement
•
•
•
•
•
Admit to
hospital
Poor response
Poor urine output
SBP <90 or >210 mmHg
Troponin elevated
Respiratory embarrassment
FIGURE 2. Treatment algorithm for the AHF patient with elevated systolic blood pressure at presentation.
© 2008 Lippincott Williams & Wilkins
107
Kirk et al
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Early Treatment of AHF
• It is recommended that all AHF patients should have therapy
started as early as possible, in the prehospital setting and in the
emergency department. Level of Evidence: B.
Non-Invasive Ventilation
• Noninvasive ventilation could be considered in AHF patients with respiratory embarrassment to prevent the need
for intubation and its subsequent complications. Level of
Evidence: B.
• Noninvasive ventilation is not recommended when there is
a need for emergent intubation.
• A superior method (CPAP versus BiPAP) has not been
established and there is likely to be general equivalence in
clinical practice.
Diuretics
• In general, loop diuretics are only recommended when there is
evidence of systemic volume overload. Level of Evidence: B.
• Loop diuretics may be considered helpful in addition to
vasodilators in AHF patients with elevated SBP, but they
are less effective as monotherapy. Level of Evidence: B.
• Loop diuretics are recommended as first line therapy in
AHF patients with normal SBP and gradual onset of dyspnea
and increase of body weight because of the likelihood of high
filling pressures and systemic edema. Level of Evidence: B.
• It is recommended that the lowest effective dose of a loop
diuretic should be used initially, with an estimated starting dose equivalent to the patient’s daily outpatient oral
dose given IV, or 20 mg of furosemide in the diuretic
naive patient. The dose can be up-titrated according to
renal function, blood pressure, and history of chronic
diuretic use. Level of Evidence: B.
• The initial use of high doses of loop diuretics are not recommended because they may be detrimental to renal function and
decrease patient tolerability of potential life saving therapies
(eg, ACE inhibitors). Level of Evidence: B.
• Continuous infusion of a loop diuretic could be considered
after the initial IV bolus. Level of Evidence: C.
• It is recommended that patients receiving loop diuretics
should be re-evaluated in 30 – 60 minutes. Therapeutic
targets include symptomatic improvement, improvement in
physical findings, hemodynamic improvement, oxygen saturation, and diuresis. Level of Evidence: B.
• It is recommended that electrolytes should be monitored
closely based upon patient response (eg, urine output).
Level of Evidence: B.
Vasodilators
• Vasodilator therapy (nitroglycerin or nesiritide) is recommended as first line therapy in AHF patients with elevated
SBP. Level of Evidence: B.
108
• The blood pressure below which vasodilators should not be
used varies among patients and clinical settings. Level of
Evidence: B.
• In those patients with elevated SBP, it is recommended to
administer nitroglycerin spray or tablets sublingually early
(prehospital or in the ED), prior to starting an IV vasodilator. Level of Evidence: B.
• With IV vasodilator therapy, frequent blood pressure measurement is recommended to avoid large drops in blood
pressure. Level of Evidence: B.
• Topical nitrates could be considered as an alternative to an IV
vasodilator in those patients who are less ill or in those in who
use of an IV vasodilator is not feasible. Level of Evidence: C.
Other Medications
• The routine use of morphine is not recommended. If used,
caution should be exercised due to concerns regarding
safety. Level of Evidence: B.
• Beta blockers, ACE inhibitors, angiotensin receptor blockers, and/or aldosterone antagonists should be continued
(per home medication regimen) unless the patient has
symptomatic hypotension, bradycardia, is in cardiogenic
shock, or has significant hyperkalemia. In patients not
previously treated with these life-saving therapies, those
without contraindications should have them initiated at the
lowest starting dose during this visit.
REFERENCES
1. Gheorghiade M, De Luca L, Fonarow GC, et al. Pathophysiologic
targets in the early phase of acute heart failure syndromes. Am J Cardiol.
2005;96(suppl 6A):11G–17G.
2. Gheorghiade M, Zannad F, Sopko G, et al. Acute heart failure syndromes: current state and framework for future research. Circulation.
2005;112:3958 –3968.
3. Cotter G, Moshkovitz Y, Milovanov O, et al. Acute heart failure: a novel
approach to its pathogenesis and treatment. Eur J Heart Fail. 2002;4:
227–234.
4. Adams KF Jr, Fonarow GC, Emerman CL, et al. Characteristics and
outcomes of patients hospitalized for heart failure in the United States:
rationale, design, and preliminary observations from the first 100,000
cases in the Acute Decompensated Heart Failure National Registry
(ADHERE). Am Heart J. 2005;149:209 –216.
5. Cleland JG, Swedberg K, Follath F, et al. The EuroHeart Failure survey
programme—a survey on the quality of care among patients with heart
failure in Europe. Part 1: patient characteristics and diagnosis. Eur
Heart J. 2003;24:442– 463.
6. Adams KF, Lindenfeld J, Arnold JMO, et al. For the Heart Failure
Society of America. HFSA 2006 comprehensive heart failure practice
guideline. J Card Fail. 2006;12:e121– e122.
7. Nieminen MS, Bohm M, Cowie MR, et al. Executive summary of the
guidelines on the diagnosis and treatment of acute heart failure: the task
force on acute heart failure of the European Society of Cardiology. Eur
Heart J. 2005;26:384 – 416.
8. Gheorghiade M, Mebazaa A. Introduction to acute heart failure syndromes. Am J Cardiol. 2005;96(suppl 6A):1G– 4G.
9. Bayram M, De Luca L, Massie MB, et al. Reassessment of dobutamine,
dopamine, and milrinone in the management of acute heart failure
syndromes. Am J Cardiol. 2005;96(suppl):47G–58G.
10. Brater DC. Diuretic therapy. N Engl J Med. 1998;339:387–395.
11. Stough WG, O’Connor CM, Gheorghiade M. Overview of current
noninodilator therapies for acute heart failure syndromes. Am J Cardiol.
2005;96(suppl):41G– 46G.
12. Moazemi K, Chana JS, Willard AM, et al. Intravenous vasodilator
therapy in congestive heart failure. Drugs Aging. 2003;20:485–508.
© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
13. Elkayam U, Bitar F, Akhter MW, et al. Intravenous nitroglycerin in the
treatment of decompensated heart failure: potential benefits and limitations. J Cardiovasc Pharmacol Ther. 2004;9:227–241.
14. Gottlieb SS, Brater DC, Thomas I, et al. BG9719 (CVT-124), an A1
adenosine receptor antagonist, protects against the decline in renal
function observed with diuretic therapy. Circulation. 2002;105:1348 –
1353.
15. Jhund PS, McMurray J, Davie AP. The acute vascular effects of
furosemide in heart failure. Br J Clin Pharmacol. 2000;50:9 –13.
16. Weinfeld MS, Chertow GM, Stevenson LW. Aggravated renal dysfunction during intensive therapy for advanced chronic heart failure. Am
Heart J. 1999;138:285–290.
17. Cooper HA, Dries DL, Davis CE, et al. Diuretics and risk of arrhythmic
death in patients with left ventricular dysfunction. Circulation. 1999;
100:1311–1315.
18. Lahav M, Regev A, Ra’anani P. Intermittent administration of furosemide vs continuous infusion preceded by a loading dose for congestive
heart failure. Chest. 1992;102:725–731.
19. Dormans TP, van Meyel JJ, Gerlag PG, et al. Diuretic efficacy of high
dose furosemide in severe heart failure: bolus injection versus continuous infusion. J Am Coll Cardiol. 1996;28:376 –382.
20. Cotter G, Weissgarten J, Metzkor E, et al. Increased toxicity of highdose furosemide versus low-dose dopamine in the treatment of refractory congestive heart failure. Clin Pharmacol Ther. 1997;62:187–193.
21. Cotter G, Metzkor E, Kaluski E, et al. Randomised trial of high-dose
isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema.
Lancet. 1998;351:389 –393.
22. Heywood JT. Temporal characteristics of serum creatinine elevations in
patients receiving nesiritide and nitroglycerin. Presented at: Heart Failure Society of America 9th Annual Scientific Sessions; September 20,
2005; Boca Raton, FL. Abstract 255.
23. Burger AJ. Clinical predictors of worsening renal function in patients
hospitalized for heart failure. Presented at: Heart Failure Society of
America 9th Annual Scientific Sessions; September 19, 2005; Boca
Raton, FL. Abstract 345.
24. Elkayam U, Roth A, Kumar A, et al. Hemodynamic and volumetric
effects of venodilation with nitroglycerin in chronic mitral regurgitation.
Am J Cardiol. 1987;60:1106 –1111.
25. Loh E, Elkayam U, Cody R, et al. A randomized multicenter study
comparing the efficacy and safety of intravenous milrinone and intravenous nitroglycerin in patients with advanced heart failure. J Card Fail.
2001;7:114 –121.
26. Nashed AH, Allegra JR. Intravenous nitroglycerin boluses in treating
patients with cardiogenic pulmonary edema. Am J Emerg Med. 1995;
13:612– 613.
27. Nashed AH, Allegra JR, Eskin B, et al. Prospective trial of the treatment
of acute cardiogenic pulmonary edema with IV nitroglycerin boluses.
Ann Emerg Med. 1997;30:382.
28. Cotter G, Faibel H, Barash P, et al. High-dose nitrates in the immediate
management of unstable angina: optimal dosage, route of administration,
and therapeutic goals. Am J Emerg Med. 1998;16:219 –224.
29. Levy P, Hexdall A, Gordon P, et al. A randomized trial of bolus
nitroglycerin for the treatment of acute congestive heart failure. Acad
Emerg Med. 2003;10:544 – b-5-b.
30. Levy P, Compton S, Welch R, et al. Treatment of severe decompensated
heart failure with high-dose intravenous nitroglycerin: a feasibility and
outcome analysis. Ann Emerg Med. 2007;50:144 –152.
31. Levy P, Compton S, Dunne R, et al. Need for mechanical ventilation is
reduced by the use of high-dose nitroglycerin for patients with acute
cardiogenic pulmonary edema: results of an open-label trial. Acad
Emerg Med. 2006;13:s107.
32. Publication Committee for the VMAC Investigators. Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart
failure: a randomized controlled trial. JAMA. 2002;287:1531–1540.
33. Levin ER, Gardner DG, Samson WK. Natriuretic peptides. N Engl
J Med. 1998;339:321–328.
34. Mills RM, LeJemtel TH, Horton DP, et al. For the Natrecor Study Group.
Sustained hemodynamic effects of an infusion of nesiritide (human b-type
natriuretic peptide) in heart failure: a randomized, double-blind, placebocontrolled clinical trial. J Am Coll Cardiol. 1999;34:155–162.
© 2008 Lippincott Williams & Wilkins
Treatment
35. Colucci WS, Elkayam U, Horton DP, et al. For the Nesiritide Study Group.
Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated congestive heart failure. N Engl J Med. 2000;343:246 –253.
36. Sackner-Bernstein JD, Skopicki HA, Aaronson KD. Risk of worsening
renal function with nesiritide in patients with acutely decompensated
heart failure. Circulation. 2005;111:1487–1491.
37. Sackner-Bernstein JD, Kowalski M, Fox M, et al. Short-term risk of
death after treatment with nesiritide for decompensated heart failure: a
pooled analysis of randomized controlled trials. JAMA. 2005;293:1900 –
1905.
38. Abraham WT. Nesiritide and mortality risk: individual and pooled
analyses of randomized controlled trials. Rev Cardiovasc Med. 2005;6:2.
39. Teerlink J, Massie BM. Nesiritide and worsening of renal function: the
emperor’s new clothes? Circulation. 2005;111:1459 –1461.
40. The Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). The CONSENSUS Trial Study Group. Effects of enalapril on
mortality in severe congestive heart failure. N Engl J Med. 1987;316:
1429 –1435.
41. The SOLVD Investigators. Effect of enalapril on survival in patients
with reduced left ventricular ejection fractions and congestive heart
failure. N Engl J Med. 1991;325:293–302.
42. The SOLVD Investigators. Effect of enalapril on mortality and the
development of heart failure in asymptomatic patients with reduced left
ventricular ejection fractions. N Engl J Med. 1992;327:685– 691.
43. Hamilton RJ, Carter WA, Gallagher EJ. Rapid improvement of acute
pulmonary edema with sublingual captopril. Acad Emerg Med. 1996;3:
205–212.
44. Annane D, Bellissant E, Pussard E, et al. Placebo-controlled, randomized, double-blind study of intravenous enalaprilat efficacy and safety in
acute cardiogenic pulmonary edema. Circulation. 1996;94:1316 –1324.
45. Sacchetti A, Ramoska E, Moakes ME, et al. Effect of ED management on
ICU use in acute pulmonary edema. Am J Emerg Med. 1999;17:571–574.
46. Hoffman JR, Reynolds S. Comparison of nitroglycerin, morphine and
furosemide in treatment of presumed pre-hospital pulmonary edema.
Chest. 1987;92:586 –593.
47. Peacock WF, Hollander J, Diercks D, et al. Morphine for acute decompensated heart failure: valuable adjunct or a historical remnant? Acad
Emerg Med. 2005;12:97b–98b.
48. Collins SP, Mielniczuk LM, Whittingham HA, et al. The use of noninvasive ventilation in emergency department patients with acute cardiogenic pulmonary edema: a systematic review. Ann Emerg Med. 2006;
48:260 –269, 9 e1-4.
49. Mehta S, Jay GD, Woolard RH, et al. Randomized, prospective trial of
bilevel versus continuous positive airway pressure in acute pulmonary
edema. Crit Care Med. 1997;25:620 – 628.
50. Philip-Joet FF, Paganelli FF, Dutau HL, et al. Hemodynamic effects of
bilevel nasal positive airway pressure ventilation in patients with heart
failure. Respiration. 1999;66:136 –143.
51. Levitt MA. A prospective, randomized trial of BiPAP in severe acute
congestive heart failure. J Emerg Med. 2001;21:363–369.
52. Nava S, Carbone G, DiBattista N, et al. Noninvasive ventilation in
cardiogenic pulmonary edema: a multicenter randomized trial. Am J
Respir Crit Care Med. 2003;168:1432–1437.
53. Masip J, Roque M, Sánchez B, et al. Noninvasive ventilation in acute
cardiogenic pulmonary edema: systematic review and meta-analysis.
JAMA. 2005;294:3124 –3130.
54. Cleland JG, Abdellah AT, Khaleva O, et al. Clinical trials update from
the European Society of Cardiology Congress 2007:3CPO, ALOFT,
PROSPECT and statins for heart failure. Eur J Heart Fail. 2007;9:1070 –
1073.
55. Pang D, Keenan SP, Cook DJ, et al. The effect of positive pressure
airway support on mortality and the need for intubation in cardiogenic
pulmonary edema: a systematic review. Chest. 1998;114:1185–1192.
56. Yan AT, Bradley TD, Liu PP. The role of continuous positive airway
pressure in the treatment of congestive heart failure. Chest. 2001;120:
1675–1685.
57. Masip J, Paez J, Merino M, et al. Risk factors for intubation as a guide
for noninvasive ventilation in patients with severe acute cardiogenic
pulmonary edema. Intensive Care Med. 2003;29:1921–1928.
58. Gheorghiade M, Mebazaa A. The challenge of acute heart failure
syndromes. Am J Cardiol. 2005;96(suppl 6A):86G– 89G.
109
Kirk et al
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
59. Kirk JD, Costanza MR. Managing patients with acute decompensated
heart failure. Clin Courier. 2006;23:1–14.
60. Gheorghiade M, Abraham WT, Albert NM, et al. For the OPTIMIZE- HF
关Organized Program to Initiate Lifesaving Treatment in Hospitalized
Patients with Heart Failure兴 Investigators and Coordinators. Systolic
blood pressure at admission, clinical characteristics, and outcomes in
patients hospitalized with acute heart failure. JAMA. 2006;296:2217–
2226.
61. Filippatos G, Zannad F. An introduction to acute heart failure
110
syndromes: definition and classification. Heart Fail Rev. 2007;12:
87–90.
62. Bussmann W, Schupp D. Effect of sublingual nitroglycerin in emergency treatment of severe pulmonary edema. Am J Cardiol. 1978;41:
931–936.
63. Fonarow GC, Adams KF Jr, Abraham WT, et al. For the ADHERE
Scientific Advisory Committee, Study Group, and Investigators. Risk stratification for in-hospital mortality in acutely decompensated heart failure:
classification and regression tree analysis. JAMA. 2005;293:572–580.
© 2008 Lippincott Williams & Wilkins
SOCIETY
OF
CHEST PAIN CENTERS RECOMMENDATIONS
Discharge Criteria
Deborah B. Diercks, MD, FACEP, Committee Chair; Ezra A. Amsterdam, MD, FACC,
David F. Gaieski, MD, FACEP, Diane Gurney, RN, MS, CEN, W. Frank Peacock, MD,
and Gregg C. Fonarow, MD, FACC; of the Society of Chest Pain Centers Acute Heart
Failure Committee
Abstract: The goal of the Society of Chest Pain Centers Heart
Failure Discharge Recommendations Committee was to review the
available literature and currently published guidelines to provide
recommendations for acute heart failure providers regarding observation unit discharge criteria. Explicit and validated criteria for
discharging patients from the emergency department or observation
unit are lacking. We propose the utilization of criteria that reflect
improvement in fluid overload, which is the most common feature of
patients admitted with heart failure.
(Crit Pathways in Cardiol 2008;7: 111–115)
T
he decision to discharge a patient from an observation
unit or emergency department (ED) is based upon the
overall assessment that the patient has clinically improved
and can be managed further as an outpatient. This is usually
based on a combination of the patient’s subjective report and
the physician’s judgment. It has been noted, however, in
hospitalized patients with heart failure that almost 50% are
discharged with persistent symptoms.1 Explicit and validated
criteria for discharging patients from the ED or observation
unit are lacking. Care must be taken to avoid premature
discharge of patients with acute heart failure (AHF). The
discharge criteria recommended in this presentation seek to
balance the need for adequate symptom relief and acceptable
readmission rates with the requirements for a cost-effective
management strategy.
The goal of the Society of Chest Pain Centers Heart
Failure Discharge Recommendations Committee was to review the available literature and currently published guidelines to provide recommendations for AHF providers regarding observation unit discharge criteria. We propose the
utilization of criteria that reflect improvement in fluid overload, which is the most common feature of patients admitted
with heart failure. PubMed was searched in a systematic
manner using a combination of search terms specific to the
discharge criteria of patients with AHF presenting to an
ED for care. Priority was given to studies that enrolled
patients in the ED, investigated AHF, and looked at near
and intermediate-term events (within 30 days of ED pre-
Copyright © 2008 by Lippincott Williams & Wilkins
ISSN: 1535-282X/08/0702-0111
sentation). References from the articles identified by the
initial search criteria were reviewed to identify other
pertinent studies. Specific inclusion and exclusion criteria
were delineated under each question of interest. In this
section, we focus on the question regarding what criteria
can be used to identify patients suitable for discharge from
the ED.
In most of patients who present with AHF, fluid overload (congestion) results in the symptoms and physical findings that prompt the ED visit.2–5 Signs of fluid overload
include jugular venous distension, edema, and weight gain.3,6,7
Dyspnea, orthopnea, dizziness, and decreased exercise tolerance
are the key symptoms of pulmonary congestion and reduced
cardiac output. It has been demonstrated that the presence of
these signs and symptoms is associated with an increased
rate of recidivism and adverse events postdischarge.3
Therefore, evaluation for and alleviation of these findings
are crucial steps when considering whether a patient is
stable for discharge. It is important to appreciate, however,
that there can be marked improvement in signs and symptoms of AHF in patients who have an ongoing elevation in
cardiac filling pressures. Improvement in symptoms related to congestion coupled with hemodynamic evidence
of decreased volume overload is a reasonable combined
goal for the acute management of patients with heart
failure in the observation unit setting.
Improvement in Clinical Congestion
Unlike patients in the inpatient setting, the evaluation
of clinical congestion in the observation unit or ED must
focus on parameters that are sensitive to rapid change. Objective measures of improvement in congestion including a
reduction in jugular venous pressure (JVP), resolution of
rales, edema and orthopnea, and change in the patient’s
weight from presentation to discharge represent potential
criteria to use in the observation unit setting.
It is recommended that at the time of discharge improvement in symptoms of congestion, as measured by a
decrease in dyspnea, is documented. Level of Evidence: C.
Dyspnea and orthopnea are key symptoms that prompt
patients to seek emergency care for AHF, and improvement in
these symptoms is an essential component in the treatment
of volume overload. Currently, there is no validated measure of dyspnea,8 although 5 or 7 point Likert scales have
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
111
Diercks et al
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
been used to assess dyspnea in clinical trials.8 Orthopnea
has been shown to correlate with clinical and hemodynamic congestion.9 In patients who report worsening in
this symptom upon admission, improvement should be
noted at the time of discharge.
It is recommended that at the time of discharge, the
patient be able to ambulate without symptoms of significant
dyspnea above baseline and without orthostatic symptoms.
Level of Evidence: B.
Dyspnea on exertion is a common symptom present at
the time of discharge.7 In addition, it has been shown to be
a reliable marker of hemodynamic congestion.10,11 Orthostatic hypotension, manifesting as the symptom of lightheadedness, is a marker for over-diuresis. In the observation unit setting, a patient’s ability to ambulate without
symptoms allows the evaluating physician to assess for
persistent fluid overload and evaluate for potential overdiuresis. Before discharge, patients should walk around the
ED. Ideally, they should be able to ambulate for 3 to 6
minutes with minimal dyspnea (over baseline) and without
lightheadedness; if they are unable to do this and discharge will
still occur, a clear rationale for the discharge needs to be
documented in the chart.
At the time of discharge, improvement in other signs
and symptoms such as reduced body weight and decreased
edema, rales, and JVP should be considered as indicators of
decreased congestion. Level of Evidence: B.
Other parameters can be used to identify the presence
of clinical congestion. However, in patients who clinically are
improved based on symptoms, it is not suggested that these
factors be used as sole discharge criteria.
Body Weight
Increasing body weight in patients with heart failure is
a result of sodium and water retention in the setting of acute
decompensation. Reduction of body weight during observation unit management is primarily a function of diuresis.
Urine output is a reasonable surrogate for weight loss while in
the observation unit but body weight should be recorded at
regular intervals because change in body weight plays a more
important role in the outpatient management of patients with
heart failure.
Edema
Diuretic therapy usually results in improvement in
lower extremity edema and anasarca. Elevation of the lower
extremities during bed rest can also increase fluid return to
the right side of the heart and decrease lower extremity
edema. In addition, the supine position enhances renal blood
flow and may promote diuresis.
Rales
Documentation of rales on physical examination in
patients with heart failure is common. Improvement in this
finding normally occurs as fluid congestion resolves. However, it is unclear how responsive this clinical finding is to
volume reduction over a short interval.
112
Jugular Venous Pressure
Assessment of JVP is routinely performed at the time
of ED presentation and observation unit admission. An
elevated JVP has been associated with increased risk of
recidivism and, therefore, it is potentially useful as a discharge criterion.12,13 Although clinical studies suggest that a
JVP ⬍8 cm is optimal and reflects euvolemia, a reduction in
JVP from the value present on initial ED evaluation should
represent an improvement in pulmonary vascular congestion
and may serve as an indicator of safe discharge.
It is recommended that at the time of discharge, no
significant alterations in serum creatinine or serum electrolytes are present. Level of Evidence: B.
Significant alterations in serum electrolytes and renal
function can identify patients who are not suitable for discharge from the observation unit. Studies evaluating patients
hospitalized with heart failure have shown that an increase in
serum creatinine between 0.3 to 0.5 mg/dL above baseline is
associated with prolonged hospitalization and increased mortality.14,15 Extrapolation from these studies suggests that an
increase in serum creatinine identifies a high risk group of
patients. Similarly, a serum sodium level of ⬍136 mEq/L has
been demonstrated to correlate with increased 30 day and 1
year mortality. In patients with a normal serum sodium level
at baseline, a decrease in their serum sodium to ⬍136 mEq/L
should be an indicator of the need of admission.16 –18 Prospective studies performed in the observation unit are needed
to assess the utility of these markers in this setting.
There are numerous other markers associated with poor
prognosis and adverse events that may not be suitable as
discharge criteria for an observation unit. An elevated B-type
natriuretic peptide (BNP) level has been associated with poor
prognosis.19,20 By contrast, studies have shown that a decrease in BNP during hospitalization is associated with improved outcome.21 In one study Cheng et al21 evaluated 72
subjects with heart failure and reported that decreasing BNP
was associated with a lower event rate at 30 days. The optimal
threshold appeared to be ⬍430 pg/mL, which was similar to the
level above which patients are identified as at high risk for AHF.
In a large study of ED patients, discharge with a BNP ⬎480
pg/mL was associated with a 6-month congestive heart failure
related adverse event of 43%. If the discharge BNP was ⬍230
pg/mL, the 6-month event rate was 2.5%.22 Maisel et al,23 in
another ED-based study, demonstrated the limits of clinical
examination in the assessment of AHF; they reported that if
BNP was assessed in a blinded fashion, there was no difference
between the BNP levels of patients admitted to the hospital
versus those of patients discharged to home. However, there was
a significant increase in the rate of death at 30 and 90 days in
subjects based on the degree of elevation in BNP levels. Despite
these studies, serial measures of BNP over a short period of time,
such as the duration of observation unit management, may not
have value because of lack of rapid responsiveness of BNP to
changes in left ventricular distention. This may be related to a
delay in decrease in production and release of BNP relative to
more rapid hemodynamic improvement. Therefore, BNP testing
cannot be used as the sole measure to identify patients suitable
for discharge.
© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
It is recommended that before discharge, several goals
must be met including: the reasons for acute decompensation
have been identified and (partially) reversed; transition from
intravenous to oral diuretic has been completed; patient and
family education has been addressed; the initial outpatient
pharmacologic regimen has been established; compliance
with Joint Commission core measures for heart failure has
occurred; and a follow-up clinic visit is arranged for between
7 and 10 days after discharge. Level of Evidence: C.
Appropriate discharge from the ED or observation unit
must be combined with adequate follow-up. Explicit instructions, including diet recommendations and an outpatient medication schedule, are mandatory and must comply with the
Joint Commission core measures for the management of
AHF. In patients with known chest failure who are already on
outpatient therapy, patient reeducation about the current treatment plan should occur, explicitly delineating changes in the
treatment regimen and what medications have been added to
or eliminated from the previous regimen. In those patients
with a new diagnosis of heart failure and no prior outpatient
treatment regimen, the prescribed treatment regimen should
follow established treatment guidelines (Table 1). Use of a
checklist to assist in this process is practical way to assure
compliance (Appendix Table).
Discharge Criteria
The risk of hospital readmission is highest shortly after
observation unit or hospital discharge. Appropriate discharge
planning and a systematic transition of care to the outpatient
physicians, coupled with careful monitoring of patients soon
after discharge, may decrease the likelihood of readmission.
A subset of patients may become rapidly congested after
discharge. Timely follow-up can be performed by telephone
or during a clinic visit and should include assessment of the
patient’s volume status, adherence to and understanding of
the new medical regimen, and adherence to a salt-restricted
diet. An example of an observation unit checklist is shown in
the Appendix Table.
The mandate that the Joint Commission Accreditation Health Care Organizations core measures be addressed before discharge requires that several complex tasks
be accomplished. These include the following15:
1. Heart failure (HF) patients will be discharged home with
a copy of written instructions and, ideally, educational
materials addressing activity level, diet, discharge medications, follow-up appointment, home weight monitoring,
and warnings about what to do if symptoms worsen.
2. HF patients need documentation in the hospital record that
left ventricular function was assessed before ED arrival,
TABLE 1. Discharge Recommendations
It is recommended at the time of discharge that change in symptoms of congestion, as measured by improvement in dyspnea, is documented.
Level of Evidence: B
It is recommended at the time of discharge that the patient be able to ambulate without an exacerbation or recurrence of symptoms including significant
dyspnea above baseline and orthostasis.
Level of Evidence: B
At the time of discharge improvement in other signs such as decreased rales, edema, and jugular venous pressure, and a decrease in body weight should
be considered as parameters of decreased congestion.
Level of Evidence: B
It is recommended at the time of discharge that no significant alterations in serum electrolytes, with an emphasis on serum sodium and creatinine, are present.
Level of Evidence: A
It is recommended that prior to discharge several goals must be met including: the reasons for acute decompensation have been identified and (partially)
reversed; transition from intravenous to oral diuretic has been completed; patient and family education has been addressed; the initial outpatient
pharmacologic regimen has been established; compliance with Joint Commission core measures for heart failure has occurred; and a follow-up clinic
visit is arranged for between 7 and 10 d after discharge.
Level of Evidence: C
TABLE 2. Recommendation for Pharmacologic Therapy Based on the Heart Failure Society of America Recommendations24
Patients with impaired systolic function (ejection fraction 关EF兴 ⬍40%)
1. ACE inhibitor therapy is recommended for heart failure patients with reduced left ventricular ejection fraction (LVEF) (⬍40%).
2. ARBs are recommended for patients with reduced LVEF who have a contraindication to ACE inhibitor because of chronic cough or a prior episode
of angioedema.
3. It is recommended that evidence-based, low dose beta blocker therapy be administered prior to discharge in stable heart failure patients with reduced
LVEF.
4. It is recommended that beta blocker therapy be continued in most patients experiencing a symptomatic exacerbation of heart failure during chronic
maintenance treatment. A temporary reduction of dose in this setting may be considered. Abrupt discontinuation in patients with symptomatic
exacerbation should be avoided. If discontinued or reduced, beta blockers should be reinstated or the dose should be gradually increased before the
patient is discharged.
Patients with preserved systolic function
1. ARBs or ACE inhibitors should be considered in patients with HF and preserved LVEF.
2. Beta blocker treatment is recommended in patients with HF and preserved LVEF who have hypertension or have had prior myocardial infarction.
© 2008 Lippincott Williams & Wilkins
113
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Diercks et al
during hospitalization, or is planned in a timely fashion
after discharge.
3. Patients with left ventricular systolic dysfunction who
have no contraindications to treatment with an angiotensin
converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) should be prescribed either an ACE
inhibitor or ARB at hospital discharge.
4. HF patients with a history of smoking cigarettes (currently
or within the past year) must be given smoking cessation
advice or counseling during the observation unit stay.
14.
15.
16.
17.
18.
CONCLUSIONS
The criteria proposed have not been extensively studied
in the observation unit setting. However, they represent
variables that can easily be assessed and applied in this
setting (Table 2). Although these criteria are based on observation unit treatment, it is important that effective integration
of an outpatient management plan occurs. Discharge criteria
should reflect an improvement in the parameters that are the
goals of the treatments rendered.
19.
20.
21.
22.
REFERENCES
1. Gheorghiade M, Filippatos G, De Luca L, et al. Congestion in acute
heart failure syndromes: an essential target of evaluation and treatment.
Am J Med. 2006;119:S3–S10.
2. Adams KF Jr, Fonarow GC, Emerman CL, et al. Characteristics and
outcomes of patients hospitalized for heart failure in the United States:
rationale, design, and preliminary observations from the first 100,000
cases in the Acute Decompensated Heart Failure National Registry
(ADHERE). Am Heart J. 2005;149:209 –216.
3. Gheorghiade M, Abraham WT, Albert NM, et al. Systolic blood pressure
at admission, clinical characteristics, and outcomes in patients hospitalized with acute heart failure. JAMA. 2006;296:2217–2226.
4. Cleland JG, Swedberg K, Follath F, et al. The EuroHeart Failure survey
programme—a survey on the quality of care among patients with heart
failure in Europe. Part 1: patient characteristics and diagnosis. Eur
Heart J. 2003;24:442– 463.
5. O’Connor CM, Stough WG, Gallup DS, et al. Clinical characteristics, and
outcomes of patients hospitalized for decompensated heart failure: observations from the IMPACT-HF Registry. J Card Fail. 2005;11:200 –205.
6. Gattis WA, O’Connor CM, Gallup DS, et al. Predischarge initiation of
carvedilol in patients hospitalized for decompensated heart failure.
Results of the initiation management predischarge: process for assessment of carvedilol therapy in heart failure (IMPACT-HF) trial. J Am
Coll Cardiol. 2004;43:1534 –1541.
7. Yu CM, Wang L, Chau E, et al. Intrathoracic impedance monitoring in
patients with heart failure: correlation with fluid status and feasibility of
early warning preceding hospitalization. Circulation. 2005;112:841– 848.
8. Teerlink JR. Dyspnea as an end point in clinical trials therapies for acute
decompensated heart failure. Am Heart J. 2003;145:S26 –S33.
9. Beck da Silva L, Mielniczuk L, Laberge M, et al. Persistent orthopnea
and the prognosis of patients in the heart failure clinic. Congest Heart
Fail. 2004;10:177–180.
10. Shah MR, Hasselblad V, Gheorghiade M, et al. Prognostic usefulness of
the six-minute walk in patients with advanced congestive heart failure
secondary to ischemic or nonischemic cardiomyopathy. Am J Cardiol.
2001;88:987–993.
11. Rostagno C, Olivo G, Comeglio M, et al. Prognostic value of 6-minute
walk corridor test in patients with mild to moderate heart failure:
comparison with other methods of functional evaluation. Eur J Heart
Fail. 2003;5:247–252.
12. Butman SM, Ewy GA, Standen JR, et al. Bedside cardiovascular examination in patients with severe chronic heart failure: importance of rest or
inducible jugular venous distention. J Am Coll Cardiol. 1993;22:968 –974.
13. Drazner MH, Rame JE, Phil M, et al. Prognostic importance of elevated
114
23.
24.
jugular venous pressure and a third heart sound in patients with heart
failure. N Engl J Med. 2001;345:574 –581.
Lee DS, Austin PC, Rouleau JL, et al. Predicting mortality among
patients hospitalized for heart failure. JAMA. 2003;290:2581–2587.
The Joint Commission. A comprehensive review of development
for core measures. Available at: http://www.jointcommission.
org/NR/rdonlyres/48DFC95A-9C05-4A44-AB05⫽769D5253014/0/
AComprehensiveReviewofDevelopmentforCoreMeasures.pdf. Accessed November 17, 2007.
Sica DA. Hyponatremia and heart failure–pathophysiology and implications. Congest Heart Fail. 2005;11:274 –277.
Oren RM. Hyponatremia in congestive heart failure. Am J Cardiol.
2005;95:2B–7B.
Forman DE, Butler J, Wang Y, et al. Incidence, predictors at admission
and impact of worsening renal function among patients hospitalized with
heart failure. J Am Coll Cardiol. 2004;43:61– 67.
Logeart D, Thabut G, Jourdain P, et al. Predischarge B-type natriuretic
peptide assay for identifying patients at risk of re-admission after
decompensated heart failure. J Am Coll Cardiol. 2004;43:635– 641.
Kazanegra R, Cheng V, Garcia A, et al. A rapid test for B-type
natriuretic peptide (BNP) correlates with falling wedge pressures in
patients treated for decompensated heart failure: a pilot study. J Card
Fail. 2001;7:21–29.
Cheng V, Kazanagra R, Garcia A, et al. A rapid bedside test for B-type
peptide predicts treatment outcomes in patients admitted for decompensated heart failure: a pilot study. J Am Coll Cardiol. 2001;37:386 –391.
Harrison A, Morrison L, Krishnaswamy P, et al. B-type natriuretic peptide
predicts future cardiac events in patients presenting to the emergency
department with dyspnea. Ann Emerg Med. 2002;39:131–138.
Maisel A, Hollander JE, Guss D, et al. Primary results of the Rapid
Emergency Department Heart Failure Outpatient Trial (REDHOT). A
multicenter study of B-type natriuretic peptide levels, emergency department decision making, and outcomes in patients presenting with
shortness of breath. J Am Coll Cardiol. 2004;44:1328 –1333.
Heart Failure Society of American. HFSA 2006 comprehensive heart
failure practice guideline. J Card Fail. 2006;12:e1– e2.
APPENDIX
ACE Inhibitors
ACE inhibitors are recommended in all patients with HF and
LVEF ⱕ40%, unless a contraindication or intolerance to
ACE inhibitors is documented in the medical record. Those
with renal insufficiency should be started on lower doses of
ACE inhibitors and should have frequent monitoring of
electrolytes and creatinine.
Contraindications to ACE inhibitors: allergy or intolerance, angioedema, hyperkalemia (K ⬎5.5 mmol/L), pregnancy, symptomatic hypotension, systolic blood pressure
(SBP) ⬍80 mm Hg, and bilateral renal artery stenosis. Consider hold parameter of SBP ⬍80 mm Hg.
ARBs should be used as an alternative treatment in
patients with ACE inhibitor intolerance.
Beta Blocker
Beta blockers are recommended in all patients with HF
and LVEF ⱕ40%, unless a contraindication or intolerance to
beta blockers is documented in the medical record. Use only
evidence-based beta blockers (carvedilol, metoprolol succinate, or bisoprolol). Patients should be compensated and not
on intravenous inotropes.
Contraindications: symptomatic bradycardia, significant reactive airway disease, shock, 2nd or 3rd degree heart
block without a pacemaker.
© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Start at low HF dosing. Consider hold parameter of
SBP ⬍80 mm Hg and heart rate ⬍40.
Discharge Criteria
Start at very low HF dosing. It is essential to very
closely monitor serum potassium and renal function.
LVEF
Aldosterone Antagonist
Aldosterone antagonists are recommended in patients
with HF and LVEF ⱕ40% and moderate to severe symptoms,
unless a contraindication to aldosterone antagonists is documented in the medical record.
Evaluation of LVEF with echocardiography should
occur in all patients with newly diagnosed HF during admission. In patients with established HF, evidence must be
present in the medical record that LVEF was evaluated before
admission, ideally within the past 1 to 2 years.
APPENDIX
HEART FAILURE OBSERVATION UNIT DISCHARGE CHECKLIST
Please complete all boxes for each HF indicator:
Admit Date: _________ Time: ___________ Discharge Date: _________ Time: ___________
Attending Physician: _________________________ HF Etiology: ____________________________________
Ejection Fraction: _______ Date Assessed: _______ Method:
Echocardiogram
YES
Complete All Boxes for Each HF Indicator
Angiotensin-converting enzyme inhibitor (if LVSD)
Angiotensin receptor blocker (if LVSD and ACE inhibitor not tolerated)
Beta blocker (if LVSD, use only evidence-based)
Aldosterone antagonist (if LVSD and moderate-severe HF symptoms)
Most recent left ventricular ejection fraction (_____%)
Date of most recent LVEF (____________)
Anticoagulation for atrial fibrillation or flutter (permanent or paroxysmal) or
other indications
Assessment of smoking status
Smoking cessation counseling for current or recent smokers
(have quit within the last year)
Cardiac catheterization
NO
MUGA scan
Reason Not Done/
Contraindications
□ NA
□ NA
□ NA
□ NA
□ CI
□ CI
□ CI
□ CI
□ NA
□ CI
□ NA
□ NA
Education
2-gram sodium diet
Fluid restriction if indicated
Monitoring of daily weights
What to do if HF symptoms worsen
Physical activity level counseling
Follow-up appointments
Review of medications
HF patient education handout
HF patient discharge contract
NA indicates not applicable or not indicated; CI, contraindication documented either by physician or by registered nurse per
verbal discussion with physician.
© 2008 Lippincott Williams & Wilkins
115
SOCIETY
OF
CHEST PAIN CENTERS RECOMMENDATIONS
Patient Education
Robin J. Trupp, PhD(c), MSN, APRN, BC, FAHA, Brian Hiestand, MD, MPH, Committee Co-Chairs;
Gail Dodge, RN, MSN, CEN, Christy O. Hayes, MSN, APRN, Chadwick D. Miller, MD,
Elsie Selby, MSN, ARNP, CCNS, CCRN, W. Frank Peacock, MD, and Gregg C. Fonarow, MD, FACC;
of the Society of Chest Pain Centers Acute Heart Failure Committee
Abstract: Managing heart failure is complex because of the requisite
polypharmacy resulting from evidence based care, dietary limitations,
lifestyle modifications, and the need for frequent contact and follow-up.
Therefore, it is not surprising that adherence to the prescribed medical
regimen is frequently suboptimal, serving as the major cause for heart
failure exacerbations that lead to hospitalizations. In fact, over 70% of
hospitalizations in the United States have been directly attributed to one
or more of the following: failure to follow medication regimens, failure
to follow dietary limitations, or failure to seek care with worsening
symptoms (Michalsen A et al, Heart. 1998;437– 441, Vinson JM. J Am
Geriatr Soc. 1990;38:1290 –1295). This translates to the largest portion of healthcare expenditures being consumed by acute heart
failure, usually beginning in the emergency department followed by
observation or inpatient treatment. After discharge, these patients
are at an increased risk for readmission, with rates between 36% and
75%, and for increased mortality rates (Whellan D et al, Am J Manag
Care. 1999;5:499 –507). Age, gender, coronary artery disease, diabetes,
and nonadherence to the medical regimen are risk factors for readmission (Rich MW et al, J Gen Intern Med. 1993;8:585–590).
The goal of the Society for Chest Pain Centers Patient Education
Recommendations Committee was to evaluate relevant literature
and published guidelines to produce recommendations relevant to
patient education in the setting of acute heart failure. We focused on
patient adherence to medications, dietary restrictions, lifestyle modification, and symptom recognition.
(Crit Pathways in Cardiol 2008;7: 116 –121)
M
anaging heart failure is complex because of the requisite polypharmacy resulting from evidence-based care,
dietary limitations, lifestyle modifications, and the need for
frequent contact and follow-up. Therefore, it is not surprising
that adherence to the prescribed medical regimen is frequently suboptimal, serving as the major cause for heart
failure exacerbations that lead to hospitalizations. In fact,
over 70% of hospitalizations in the United States have been
directly attributed to one or more of the following: failure to
follow medication regimens, failure to follow dietary limitations, or failure to seek care with worsening symptoms.1,2
This translates to the largest portion of healthcare expendiCopyright © 2008 by Lippincott Williams & Wilkins
ISSN: 1535-282X/08/0702-0116
116
tures being consumed by acute care of worsening heart
failure, usually beginning in the ED followed by inpatient
treatment. Postdischarge, these patients are at increased risk
for readmission, with rates between 36% and 75%, and for
increased mortality, rates.3 Age, gender, coronary artery disease, diabetes, and nonadherence to the medical regimen are
risk factors for readmission.4
Most patients with chronic disease, including heart
failure, are not well educated on managing their disease
processes. Office visits with healthcare providers are frequently attenuated and provide inadequate time for addressing chronic conditions or establishing clearly defined plans of
care. Patient education necessary to understand the underlying pathology or treatment regimens is suboptimal. The end
result is a passive, ill-informed patient who receives episodic,
reactive care, driven primarily by exacerbations, rather than a
proactive, comprehensive approach to managing chronic illnesses. Thus, educational strategies to improve adherence, to
increase awareness for signs and symptoms of worsening
heart failure, and to facilitate the adoption of lifestyle modifications are essential to reducing the morbidity, mortality,
and financial outcomes of heart failure.
Adherence to prescribed medical regimens, including
both pharmacologic and nonpharmacologic interventions, has
a significant impact on both the short- and long-term management of heart failure. Such therapeutic strategies have
been well proven to slow disease progression, reduce hospital
admissions, and improve overall symptom control.5 However, despite the importance of these interventions, numerous
barriers to adherence exist. Barriers may include lack of
understanding of perceived benefit, lifestyle modifications,
absence of social support, powerlessness, financial concerns,
and time constraints. These barriers complicate the ability
and willingness of the patients to adhere to the prescribed
medical regimen. In addition, in the haste to shorten length of
stay and reduce healthcare expenditures, clinicians may simply treat the symptoms and fail to identify nonmedical causes
for the decompensation. By taking the time to do a thorough
assessment to identify barriers and then target problem areas,
clinicians can better use the time spent with each patient,
leading to a more individualized treatment plan and enhanced
adherence. This can particularly benefit high-risk patients
such as those who live alone, the elderly, those with multiple
comorbidities, or those with a new diagnosis of heart failure.
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
PubMed was searched in a systematic manner using a
combination of search terms relevant to each topic as well as
specific to patient education. References from articles and
guidelines so identified were also evaluated for additional
pertinent literature.
Patient Education in the Emergency
Department or Observation Setting
Both the American College of Cardiology or American
Heart Association (ACC/AHA) guidelines for the management of chronic heart failure and the Heart Failure Society of
America (HFSA) guidelines focus on outpatient care in adults
and recommend that patients receive education regarding
their disease process.6,7 The goals of patient education are
manifold; in addition to learning how to recognize early signs
of decompensation, appropriate education can decrease the
likelihood of nonadherence to medication plans and dietary
requirements. However, patients with heart failure are often
faced with an extensive list of medications for both heart
failure and any comorbidities, making compliance challenging. As discussed previously, medication nonadherence is one
of the leading causes of admission and emergency department
(ED) visits for acute heart failure.1,8 –10 Therefore, attention
has centered on whether patient education regarding medication use can improve outcomes. Unfortunately, there are no
trials of ED or observation unit-based education programs for
patients with heart failure.9 However, teaching and education
is a cornerstone of previous successful observation unit heart
failure programs.11–13 Although this represents an opportunity for later research, in the interim, ED and observation
medicine clinicians must extrapolate results from studies
based in other healthcare settings.
Although educational needs for the patient with heart
failure are vast and include such topics as the pathophysiology and etiology of heart failure and necessary lifestyle
modifications, given the short-term nature of the patientprovider interaction, education provided in the ED and observation setting must be direct and succinct. During times of
stress, as would be expected in patients presenting with
acute heart failure, retention of any information given is
limited.14 However, previous research has demonstrated
that the ED may serve as a suitable environment to initiate
lifestyle changes because the impact of the “teachable
moment” may be substantial.15,16 If the patient is ultimately hospitalized, the urgency is somewhat lessened, as
the inpatient environment offers additional opportunity for
and the reinforcement of education. This section will
concentrate on the topics of medication and dietary adherence, lifestyle modifications, and recognition of worsening
symptoms as essential elements of patient education within
the observation setting.
Medication and Dietary Adherence
Medication and dietary adherence have profound implications for the management of heart failure. Lack of
adherence as a significant cause of decompensation and
hospitalization has been well documented and has significant
economic repercussions.17 For example, if insufficient med© 2008 Lippincott Williams & Wilkins
Patient Education
ication is taken for the treatment to be fully effective, as
occurs when patients “ration” diuretics to extend the life of a
prescription, subsequent healthcare costs are likely to be
incurred as a result of the need for hospital-based treatment.
It is estimated that only about 10% of patients actually take
their medications as directed.18 Not unexpectedly, better
outcomes are seen with improved adherence to treatment
plans.5 The role of education on medication and dietary
adherence cannot be overemphasized.
Unfortunately, the literature on patient education and
adherence issues specific to the acute care setting remains
sparse. In the majority of studies, patient education is one of
a number of interventions targeting adherence and/or reduced
healthcare expenditures. Therefore, the individual impact of
any educational effort is difficult to identify. However, the
current body of literature does suggest that patient education,
usually in the setting of multidisciplinary heart failure management programs, can enhance medication compliance,
which in turn is associated with decreased hospital utilization
and improved quality of life. Most studies are underpowered
to assess mortality impact, however. The ACC/AHA and
HFSA guidelines support the referral of patients at high risk
for hospital admission or clinical deterioration.6 High risk
patients are defined as those with renal insufficiency, chronic
obstructive pulmonary disease, New York Heart Association
Functional Class II–IV symptoms, frequent hospitalizations,
multiple comorbidities, or history of depression, cognitive
impairment, or nonadherence.7
Medication Adherence
A number of studies have examined the impact of a
variety of interventions for medication adherence. Most successful outcomes related to adherence and medication optimization are seen in multidisciplinary heart failure programs.
Reported improvements include: reduced hospital readmissions,19 –21 shorter lengths of stay during hospitalizations,20
improved quality of life,19,20,22 and improved mortality.22 In
the majority of these studies, nurses served as the primary
educators and leaders of the interventions, and the role of
nurses in educating on heart failure is emphasized in the
guidelines.7 Rich et al21 performed a randomized, controlled
inpatient trial, evaluating the effect of intensified inpatient
education on medication compliance at 30 days after discharge. Patients were randomized to either standard care or to
daily education on the importance of dietary and medication
adherence, as well as attempts to reduce the complexity of the
patient’s regimen. The intervention group had significantly
greater medication compliance at 30 days.4 Studies in which
a pharmacist was directly involved with education and/or
streamlining medication regimens also reported enhanced
adherence to prescription medications.23–25
Because the prevalence of heart failure is associated
with age, it is important to consider the educational needs of
the elderly. Written materials specifically designed to address
these needs, including larger font size, simple sentence structuring, and consistent formats that focus on the purpose,
directions for use and possible side effects for medications,
117
Trupp et al
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
improved the accuracy and rapidity of comprehension for
given information.26
A variety of aides to enhance adherence are available
and may be helpful to those who have difficulty in remembering to take medications. These include devices such as
pill boxes, medication trackers, or timers. For those with
financial constraints, most major pharmaceutical companies offer assistance programs for individuals unable to
afford medications. Social workers could serve as the
liaison for networking needy patients with the appropriate
services and programs.
Recommendations
It is recommended that individualized education regarding the purpose of medications, a complete list of
discharge medications with dosing schedules, and importance of taking as directed be provided. Discussion should
include what should be done if a dose is missed. Level of
Evidence: B.
Identification of individuals at high risk for nonadherence to the therapeutic regimen is recommended. Level of
Evidence: C.
Inpatient, and by extension observation unit-based education programs may increase retention of medication
knowledge and improve medication adherence and should be
considered. Level of Evidence: B.
Graphic-oriented, large text, simpler, and keyed to
specific recall items as opposed to standard medication instruction and educational materials for elderly patients should
be considered. Level of Evidence: B.
The use of pill boxes, timers, or other prompts to
remind patients of medications should be considered. Level
of Evidence: C.
Referral to programs that provide assistance for obtaining medications for those patients with financial barriers to
compliance should be considered. Level of Evidence: C.
Referral to a comprehensive heart failure disease management program may improve the delivery of both educational and clinical care to patients with heart failure should be
considered. Level of Evidence: B.
Dietary Adherence
Despite widespread acceptance, evidence supporting
positive effects of sodium restriction in heart failure is missing. In fact, it is only in the latest renditions of heart failure
guidelines that sodium restriction of 2000 –3000 mg/d have
been included and, even then, are based on expert opinion as
opposed to clinical trial data.6,7 Significant reductions in the
development of cardiovascular disease and in related mortality have been recently reported in individuals who limited
their sodium intake for 10 –15 years.27 These results make the
adoption of salt restricted diets more compelling and of
greater importance to the overall health and well-being of
American society.
Because the average American diet consists of approximately 6000 mg/d, this degree of sodium restriction is a
118
challenge to the patient. Salt substitutes and spices may be
used to improve the palatability of food. However, some salt
substitutes replace sodium chloride with potassium chloride
and should be used with caution, given the potential risk of
hyperkalemia.
Although patients not suffering from advanced heart
failure may be able to tolerate more sodium, limiting intake to
2000 –3000 mg sodium daily is advised, since consumption
will likely exceed the recommendations. In particular, patients, along with family members, in whom an acute visit for
decompensation can be directly attributed to sodium indiscretion, should receive counseling on the components of
sodium restriction. Patients should understand that dietary
indiscretion produces fluid retention and an escalation of symptoms. Efforts should concentrate on helping patients make the
association between their behavior and ensuing symptoms. Instructing patients to simply take an extra diuretic to relieve
symptoms is no longer encouraged, because diuretics contribute
to increased neurohormonal stimulation and a decline in renal
function.5 In addition, nutritional supplements as treatment for
heart failure are not indicated, given the lack of any clinical trials
demonstrating patient benefit.6
Patients presenting to the ED are likely to have advanced heart failure and, as such, may warrant further dietary
sodium restriction to attenuate the expansion of extracellular
fluid volume and the development of edema. Although sodium restriction may palliate the development of edema, it
cannot totally prevent it, as the kidneys are capable of
reducing urinary sodium excretion to less than 10 mmol per
day. Hyponatremia, defined as serum sodium ⬍136 mEq/
dL, may be present and is usually dilutional in nature,
because of total body sodium and water excess. However,
hyponatremia is not a benign finding and is associated with
longer hospital stays as well as higher in-hospital and early
postdischarge mortality.4,27 Treatment consists of fluid
restriction and aggressive use of other strategies to restore
optivolemic states, such as intravenous vasodilators and
ultrafiltration.
Recommendations
About 2000 –3000 mg sodium diet is recommended for
all patients with heart failure. Level of Evidence: B.
Identification of those patients at increased risk for
nonadherence is recommended. Level of Evidence: B.
It is recommended that a low sodium diet and hidden
sources of sodium be reviewed with the patient. Review of
recent dietary intake to uncover possible link to current
decompensation should also occur. Level of Evidence: B.
Patient and family education on dietary restrictions
related to sodium intake should be considered. Level of
Evidence: B.
Fluid restriction of 2000 mL per day in patients with
hyponatremia (serum sodium ⬍136 mEq/dL) should be considered. Level of Evidence: B.
Use of salt substitutes without prior approval, due to
risks of hyperkalemia is not recommended. Level of Evidence: B.
© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Use of nutritional supplements except as required to
treat specific and identified deficiencies is not recommended.
Level of Evidence: C.
Lifestyle Modifications
As with the previous topics, there is currently little
evidence regarding the efficacy of lifestyle modification education for patients in the ED/observation unit. However,
lifestyle modifications have been well documented as effective measures for the chronic management heart failure.
Lifestyle changes, such as weight control, exercise, smoking
cessation, and alcohol abstinence, are all common components of contemporary patient management and of heart
failure management programs.6,7 However, lifestyle issues
receive little attention in the ED or observation unit, because
of the brevity of the interaction and the intensity of care
required.
Exercise
Exercise can lessen symptoms, increase functional capacity, and improve the quality of life of patients with chronic
heart failure. Improvements seen in clinical trials were comparable to that achieved with angiotensin-converting enzyme
inhibitors and beta blockers and were additive to the benefits
of these medications.6 Because restriction of activity promotes physical de-conditioning, adversely affecting clinical
status and contributing to exercise intolerance, most patients
with heart failure are encouraged to engage in regular physical activity.6 However, during periods of acute heart failure
exacerbation, inactivity, and rest are encouraged to prevent
additional stress on the heart.
Smoking Cessation
Tobacco is known to play a central role in the development of coronary artery disease but can also increase
symptoms of heart failure secondary to the hemodynamic
effects associated with its use. Within the ED, education on
the effects of tobacco and nicotine and information on smoking cessation programs and products to assist with withdrawal
should be readily available for staff and patient use.
Alcohol
Current guidelines recommend alcohol intake be limited to 2 or less drinks per day for men and 1 or less drink per
day for women.6,7 Additionally, those with cardiomyopathy
secondary to alcohol use should be advised to avoid any
alcohol consumption, as should individuals with a history of
alcohol abuse.
Recommendations
Smoking cessation information and reinforcement for
all current smokers is recommended. Level of Evidence: C.
Patient referral to a smoking cessation program is
recommended. Level of Evidence: C.
Use of prescriptions for oral or topical medications to
assist with nicotine cravings is recommended. Level of Evidence: C.
© 2008 Lippincott Williams & Wilkins
Patient Education
It is recommended that patients limit alcohol consumption with referral to an abstinence program as indicated.
Level of Evidence: C.
It should be considered to advise patients to avoid
conditions known to provoke shortness of breath, such as
inclement weather, heat, humidity, or poor air quality, etc.
Level of Evidence: C.
Increased physical activity during exacerbation of heart
failure is not recommended. Level of Evidence: C.
Symptom Monitoring
Evidence suggests that high rates of hospitalization are
because, in large part, of a failure to recognize impending
episodes of heart failure decompensation until the opportunity for outpatient intervention has been lost. Unfortunately,
even daily weight monitoring via telemetry fails to decrease
heart failure hospitalization.28 In addition, the signs and
symptoms attributed to worsening heart failure, such as
dyspnea, edema, fatigue, and exercise intolerance, have poor
sensitivity and specificity for an exacerbation, and their
absence does not exclude the presence of elevated filling
pressures.29
Essential elements of patient education promote selfcare and the acquisition of knowledge, skills, strategies, and
motivation necessary for adherence to the treatment plan.7
Even though patients diagnosed with heart failure for years
were more likely to use appropriate self-care strategies than
newly diagnosed patients, these same patients were uncomfortable in evaluating the effectiveness of their own actions.30
Thus, there is dissociation between patient knowledge of
worsening heart failure signs and symptoms and the link to
management strategies to avoid decompensation. This dissociation can be avoided by employing strategies that promote
behavior change, including motivational approaches. Minimally, patients should have knowledge about medications
prescribed and their purpose, sodium restriction and sodium
content of frequently eaten foods, symptoms of worsening
heart failure, and when to call their healthcare provider with
changes.
Currently a number of implanted cardiac devices, such
as cardiac resynchronization therapy, defibrillators, or the
combination of the two, provide longitudinal data on parameters important to heart failure status, such as heart rate
variability, activity, atrial or ventricular arrhythmias, and/or
intrathoracic volume.31–35 Past practice has provided this type
of information retrospectively during a device interrogation
during an office visit; hence its clinical relevance during acute
heart failure has been limited. Now, this current data can be
retrieved via the internet, offering clinicians the ability to
remotely monitor patients from their home environments,
rather than through office visits. These technological advances allow for a proactive approach to managing heart
failure–in many cases prior to symptom development. However, within the ED, when heart failure is exacerbated, reactive care is appropriate and necessary. At this point, the
device diagnostics information is still valuable and can be
downloaded via programmers specific for each manufacturer.
Because the indications for and use of implanted cardiac
devices continue to expand, it is imperative that ED staff gain
119
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
Trupp et al
knowledge and understanding of these devices and the information available to assist with the clinical diagnosis and
management.
9.
Recommendations
It is recommended that the patient receives education
on the common symptoms of worsening heart failure including fatigue, dyspnea, weight gain, bloating, and worsening
edema. A plan for care, including notification of their primary
physician, should be established. Level of Evidence: B.
It is recommended that education on self-care activities
should be reinforced. Level of Evidence: B.
It should be considered that clinicians caring for heart
failure patients become familiar with the heart failure diagnostic data that can be downloaded from implanted cardiac
devices. Level of Evidence: B.
Heart failure patient education materials can be obtained
from the American Heart Association at www.americanheart.
org, the American College of Cardiology at www.cardiosource.
com, the Heart Failure Society of America at www.abouthf.org,
and the American Association of Heart Failure Nurses at www.
aahfn.org.
10.
11.
12.
13.
14.
15.
16.
17.
18.
Summary
For many patients, episodes of acute heart failure may
be largely avoidable through self-monitoring of symptoms
and enhanced adherence to treatment regimens. Unfortunately, during incidents of worsening heart failure, it may be
difficult to provide education to patients on better management of their disease, depending on the severity of the illness
of the patient. A better plan in the early management of acute
heart failure is to begin by treating the decompensation and
alleviating the symptoms. Once stabilized, education and
lifestyle modification should be discussed. Retrieving information from implanted devices may provide additional insight into precipitants for changes in heart failure status.
Education plays an essential role for patients with heart
failure, across the whole spectrum of the disease–from compensated to decompensated states.
19.
20.
21.
22.
23.
24.
25.
REFERENCES
1. Michalsen A, Konig G, Thimme W. Preventable causative factors
leading to hospital admission with decompensated heart failure. Heart.
1998;437– 441.
2. Vinson JM. Early readmission of elderly patients with congestive heart
failure. J Am Geriatr Soc. 1990;38:1290 –1295.
3. Whellan D, Gattis W, Gaulden L, et al. Disease management of congestive heart failure. Am J Manag Care. 1999;5:499 –507.
4. Rich MW, Vinson JM, Sperry JC, et al. Prevention of readmissions in
elderly patient with CHF. Results of a prospective, randomized pilot
study. J Gen Intern Med. 1993;8:585–590.
5. Compliance or concordance: is there a difference? Drugs Ther Perspect.
1999;13:11–12.
6. Hunt S, Abraham W, Chin M, et al. ACC/AHA 2005 guideline update
for the diagnosis and management of chronic heart failure in the adult:
a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2005;112:e154 –
e235.
7. Adams KF, Lindenfeld J, Arnold JMO, et al. Executive summary: HFSA
2006: comprehensive heart failure practice guideline. J Card Fail.
2006;12:10 –38.
8. Cole J, Weatherby L, Walker A. Drug copayment and adherence in
120
26.
27.
28.
29.
30.
31.
chronic heart failure: effect on cost and outcomes. Pharmacotherapy.
2006;26:1157–1164.
Granger B, Swedberg K, Elkman I, et al. Adherence to candesartan and
placebo and outcomes in chronic heart failure in the CHARM programme: double-blind, randomised, controlled clinical trial. Lancet.
2005;366:2005–2011.
Hope C, Wu J, Too W, et al. Association of medication adherence,
knowledge, and skills with emergency department visits by adults 50
years or older with congestive heart failure. Am J Health Sits Pham.
2004;61:2043–2049.
Peacock WF, Young J, Collins S, et al. Heart failure observation units:
optimizing care. Ann Emerg Med. 2006;47:22–33.
Sorrow AB, Collins SP, Lyons MS, et al. Emergency department
observation of heart failure: preliminary analysis of safety and cost.
Congest Heart Fail. 2005;11:68 –72.
Peacock WF, Albert NM. Observation unit management of heart failure.
Emerg Med Clin North Am. 2001;19:209 –232.
Esker JL, Bock BC. Psychological treatments for noncardiac chest pain:
recommendations for a new approach. J Psychoses Res. 2004;56:263–269.
Williams S, Brown A, Patton R, et al. The half-life of the “teachable
moment” for alcohol misusing patients in the emergency department.
Drug Alcohol Depend. 2005;77:205–208.
Dominique J, Quatrain DD, Rosendale B, et al. Acute cortisol administration impairs retrieval of long term declarative memory in humans.
Nat Neurosis. 2000;3:313–314.
Dunbar S, Clark P, Deaton C, et al. Family education and support
interventions in heart failure. Knurs Res. 2005;54:1158 –1166.
Levant Hal M. Negotiating compliance in heart failure: remaining issues
and questions. Eur J Cardiovascular Knurs. 2005;4:298 –307.
Doughty R, Wright S, Pearl A, et al. Randomized, controlled trial of
integrated heart failure management: the Auckland heart failure management study. Eur Heart J. 2002;23:139 –146.
Discharge A, Doyen O, White M. Impact of care at a multidisciplinary
congestive heart failure clinic: a randomized trial. Can Med Assoc J.
2005;173:40 – 45.
Rich M, Gray D, Beckham V. Effect of a multidisciplinary intervention
on medication compliance in elderly patients with congestive heart
failure. Am J Med. 1996;101:270 –276.
Smith B, Forcer E, Sallow B, et al. Disease management produces
limited quality-of-life improvements in patients with congestive heart
failure: evidence from a randomized trial in community-dwelling patients. Am J Manag Care. 2005;11:701–713.
Buoy M, Herding E, Urquhart J. Effect of a pharmacist-led intervention
on diuretic compliance in heart failure patients: a randomized controlled
study. J Card Fail. 2003;9:404 – 411.
Murray M, Young J, Hoke S, et al. Pharmacist intervention to improve
medication adherence in heart failure: A randomized trial. Ann Intern
Med. 2007;146:714 –725.
Varma S, McElnay J, Hughes C, et al. Pharmaceutical care of patients
with congestive heart failure: interventions and outcomes. Pharmacotherapy. 1999;19:860 – 869.
Morrow D, Weiner M, Young J, et al. Improving medication knowledge
among older adults with heart failure: a patient-centered approach to
instruction design. Gerontologist. 2005;45:545–552.
Cook NR, Cutler JA, Obarzenak E, et al. Long term effects of dietary
sodium reduction on cardiovascular disease outcomes: observational
follow-up of the trials of hypertension prevention (TOPH). BMJ 关serial
online兴. 2007; doi:10.1136/bmj.39147.604896.55.
Gheorghiade M, Abraham WT, Albert NM, et al. Relationship between
admission serum sodium concentration and clinical outcomes in patients
hospitalized for heart failure: an analysis from the OPTIMIZE-HF
registry. Eur Heart J. 2007; doi:10.1093/eurheartj/ehl542.
Goldberg L, Piette J, Walsh M, et al. Randomized trial of a daily
electronic home monitoring system in patients with advanced heart
failure: the Weight Monitoring in Heart Failure (WHARF) trial. Am
Heart J. 2003;146:705–712.
Chakko S, Woska D, Martinez H, et al. Clinical, radiographic, and
hemodynamic correlations in chronic congestive heart failure: conflicting results may lead to inappropriate care. Am J Med. 1991;90:353–359.
Carlon B, Riegel B. Self-care abilities of patients with heart failure.
Heart Lung. 2001;30:351–359.
© 2008 Lippincott Williams & Wilkins
Critical Pathways in Cardiology • Volume 7, Number 2, June 2008
32. Adamson P, Magalski A, Braunschweig F. Ongoing right ventricular
hemodynamics in heart failure: clinical value of measurements derived
from an implantable monitoring system. J Am Coll Cardiol. 2003;41:
565–571.
33. Abraham W. Intrathoracic impedance monitoring for early detection of
impending heart failure decompensation. Congest Heart Fail. 2007;13:
113–115.
Patient Education
34. Yu CM, Wang L, Chau E, et al. Intrathoracic impedance monitoring in
patients with heart failure: correlation with fluid status and feasibility of
early warning preceding hospitalization. Circulation. 2005;112:841–
848.
35. Adamson P, Smith A, Abraham W, et al. Continuous autonomic assessment in patient with symptomatic heart failure. Circulation. 2004:2389 –
2394.
APPENDIX
TABLE 1. Recommended Educational Objectives for Patients With Signs and Symptoms of Heart Failure
Medication adherence
Instruction regarding importance of taking medication as prescribed including its purpose, recommend schedule, and what to do if a dose is missed.
Identify those patients at high risk for nonadherence who may benefit from referral to a comprehensive disease management program.
Dietary adherence
A dietary intake of 2000–3000 mg of sodium per day is strongly recommended.
Identify those patients at high risk for nonadherence.
Review sources of high sodium, including hidden sources. Include family members in instruction since they can unknowingly become contributors to a
patient’s decompensation.
Review recent dietary intake to identify possible sodium indiscretion contributing to current decompensation.
Smoking cessation
All current smokers should receive information and reinforcement on smoking cessation.
Refer to smoking cessation program.
Consider prescribing oral or topical agents for nicotine cravings.
Alcohol consumption
Limit alcohol consumption (ⱕ2 drinks/d for men, ⱕ1 drink/d for women).
Refer to abstinence program as needed.
Symptom monitoring
Daily weights should be encouraged, using the same scale, wearing similar clothing, at same time per day.
Notification of clinician with change in weight and/or symptoms; ie weight gain of 3 or more pounds overnight or 5 pounds over 3 d, increased
dyspnea, increase fatigue, dizziness, etc.
© 2008 Lippincott Williams & Wilkins
121