77 - CJ 66 0068

Circulation Journal
Official Journal of the Japanese Circulation Society

JCS GUIDELINES
http://www. j-circ.or.jp
Guidelines for Treatment of Acute Heart Failure (JCS 2011)

– Digest Version –
JCS Joint Working Group
Table of Contents
Updating the Guidelines∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2157 2. Renal Failure∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2188
1. Preamble∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2157 3. Hepatic Congestion∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2189
2. Updating the Guidelines∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2158 4. Pneumonia∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2189
I General Matters∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2159 5. Pulse Abnormalities∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2189
1. Definition∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2159 6. Chronic Obstructive Pulmonary Disease∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2192
2. Epidemiology∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2163 VI Treatment Strategies for Heart Failure With
3. Signs/Symptoms and Causes∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2164 Preserved EF∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2192
4. Treatment Strategies∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2165 1. Definition of Heart Failure With Preserved EF∙∙∙∙∙∙∙∙∙∙∙∙∙ 2192
5. Initial Management of Acute Heart Failure∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2165 2. Diagnosis in the Acute Phase of Heart Failure With
II Diagnosis∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2166 Preserved EF∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2192
1. Procedures for Diagnosis and Triage for Treatment∙∙∙∙ 2166 3. Treatment in the Acute Phase of Heart Failure With
2. Procedures for Diagnosis in the Emergency Room∙∙∙∙∙ 2166 Preserved EF∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2192
3. Diagnostic Procedures in ICU/CCU∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2170 4. Blood Pressure Control∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2193
5. Rate Control in Atrial Fibrillation∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2193
III Treatment∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2170
6. Medical Therapy in the Chronic Phase of Heart
1. Treatment Strategies∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2170 Failure With Preserved EF∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2193
2. Early Diagnosis and Treatment∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2172
VII Treatment Strategies for Biventricular Failure∙∙∙∙ 2193
3. Determination of Targets of Treatment and
Management∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2173 1. Pathophysiology and Treatment of Biventricular
4. Medical Therapy∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2174 Failure∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2193
5. Nonpharmacologic Treatment∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2178 2. Right Heart Failure∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2194
6. Nursing∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2183 VIII Transition to Chronic Heart Failure and
7. Recommended Requirements for Medical Practice Timing of Discharge∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2194
and Equipment∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2186 IX Palliative Care∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2195
IV Treatment Strategies for Heart Failure by Cause∙∙∙∙ 2186 1. Introduction∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2195
1. Ischemic Heart Disease∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2186 2. Proposals for Palliative Care (Support Model)∙∙∙∙∙∙∙∙∙∙∙∙∙ 2195
2. Hypertensive Urgency∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2187 3. Summary∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2196
3. Idiopathic Cardiomyopathy∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2187 X Flowchart of Treatment∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2196
4. Myocarditis∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2187 XI Summary∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2196
5. Valvular Heart Disease∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2188 References∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2197
V Concomitant Conditions and Their Management∙∙∙∙ 2188
1. Anemia∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙∙ 2188 (Circ J 2013; 77: 2157 – 2201)
Updating the Guidelines

in population proportion of elderly people but also a result
1. Preamble from excellent life-saving activity in cardiovascular territory
such as that in acute myocardial infarction (AMI). From a
The number of patients with acute heart failure who are clini- cohort study, it is estimated that the number of patients with
cally characterized with orthopnea and congestion is steadily heart failure will increase by 0.6% every year over at least the
increasing in developed countries. This tendency reflects a rise next 30 years in Japan.1 Those patients with heart failure who
Released online June 12, 2013

Mailing address: Scientific Committee of the Japanese Circulation Society, 18F Imperial Hotel Tower, 1-1-1 Uchisaiwai-cho, Chiyoda-ku,
Tokyo 100-0011, Japan. E-mail: meeting@j-circ.or.jp
This English language document is a revised digest version of Guidelines for Treatment of Acute Heart Failure reported at the Japanese
Circulation Society Joint Working Groups performed in 2010 (Website: http://www.j-circ.or.jp/guideline/pdf/JCS2011_izumi_d.pdf).
Joint Working Groups: The Japanese Circulation Society, The Japanese Association for Thoracic Surgery, The Japanese Society of Hyper-
tension, The Japanese Society of Pediatric Cardiology and Cardiac Surgery, The Japanese Society for Cardiovascular Surgery, The
Japanese College of Cardiology, The Japanese Association of Cardiac Rehabilitation, The Japanese Society of Electrocardiology, The
Japanese Heart Failure Society, The Japan Society of Ultrasonics in Medicine, The Japanese Heart Rhythm Society
ISSN-1346-9843 doi: 10.1253/circj.CJ-66-0068
All rights are reserved to the Japanese Circulation Society. For permissions, please e-mail: cj@j-circ.or.jp
Circulation Journal Vol.77, August 2013

2158 JCS Joint Working Group
are also suffering from various complications demand an enor- and 19th, 2011, to carefully evaluate where evidence may be
mous economic and labor burden on healthcare systems. Be- lacking and how to improve the current situation. The timing
sides, these burdens will be imposed on the next and subse- and topics chosen for updating were based on consensual deci-
quent generations. Therefore, the coming healthcare systems sion making by the Joint Working Groups. The volition of
should be designed to avoid increase of the burden in any way. members and collaborators for updating the guidelines is out-
This is one of reasons why some strategies to prevent from lined below, and there is a significant consensus on the follow-
worsening and recurrence of heart failure are seriously empha- ing issues. Considering the comprehensive cost benefit, the
sized even in the acute phase. recommendations in the Guidelines for Treatment of Acute
Toward this end, the Japanese Circulation Society (JCS) Heart Failure should reflect not only near-term rescue treat-
developed the Guidelines for Treatment of Acute Severe Heart ment and treatment to overcome cardiac crisis, but also the
Failure in 2000,2 and issued Guidelines for Treatment of Acute ideal state of acute heart failure treatment with the perspective
Heart Failure (JCS2006) in 2006.3 These efforts show the real- of long-term prognosis (e.g., intervention aimed at myocardial
ized intention of JCS to promote the standardization of thera- reverse remodeling), better ways to facilitate patients’ (includ-
py of heart failure to the fullest extent possible. After 5 years ing the elderly’s) abilities to achieve an independent gait at
of follow-up, a partial revision of the guidelines under the discharge, and appropriate treatment of acute heart failure that
Joint Working Groups on the 2011 Guidelines for Treatment truly allows rehabilitation of patients into society (with atten-
of Acute Heart Failure (Chair, Tohru Izumi) has been request- tion to the importance of cardiac rehabilitation). Base on this
ed by the 2010 Science Committee of JCS (Chair, Masatsugu ascertained premise, the Joint Working Groups addressed the
Hori). revision of the following 11 issues: (1) detecting acute heart
failure in an early stage; (2) promptly relieving patients’ symp-
tom; (3) promptly resolving the cardiopulmonary emergency;
2. Updating the Guidelines (4) identifying the cause of the heart failure; (5) choosing a
definitive treatment; (6) achieving stable hemodynamics; (7)
The Joint Working Groups on the 2011 Guidelines for Treat- intervening in the acute phase with the perspective of long-
ment of Acute Heart Failure was set up in April 2010, com- term prognosis (e.g., cardiac reverse remodeling); (8) promot-
prising 11 members recommended by the JCS, the Japanese ing early ambulation and early discharge; (9) preventing wors-
Society of Hypertension, the Japanese Association for Tho- ening and recurrence of disease; (10) providing desirable
racic Surgery, the Japanese Society of Pediatric Cardiology hospice care and terminal care; and (11) achieving resolution
and Cardiac Surgery, the Japanese Society for Cardiovascular of the noted conflicts. This guideline was incorporated by evi-
Surgery, the Japanese College of Cardiology, the Japanese dence obtained in Japan, although the newest editions of the
Association of Cardiac Rehabilitation, the Japanese Society of AHA (American Heart Association) and ESC (European So-
Electrocardiology, the Japanese Heart Failure Society, the Japan ciety of Cardiology) guidelines were consulted. Consistency
Society of Ultrasonics in Medicine, and the Japanese Heart with other guidelines was ensured, and easily understandable
Rhythm Society, and 21 study collaborators. figures and tables were to be provided. All members and col-
In the previous update, the guidelines were organized bear- laborators made efforts to accomplish this task in total coop-
ing in mind the following issues: (1) the management of acute eration.
heart failure should be described extensively with equal atten- However, as is true in all fields of medicine, scientific ratio-
tion to each of the topics; (2) acute-stage management useful nale is not enough to make recommendations for diagnosis
for the long-term prognosis should be identified; (3) treatments and treatment according to evidence-based medicine when
not covered by insurance should also be described if they are there are insufficient supporting clinical studies in Japan. Ac-
highly useful for patients; (4) the level of advanced medical cording to precedent in the development of guidelines, the va-
technology included in the guidelines should remain practical; lidity of recommendations was tested from various aspects by
and (5) thorough discussion among members and collabora- using the results of literature searches and data obtained from
tors, and a consensus of the independent assessment commit- the Japanese people, on the basis of the wisdom and experi-
tee, are necessary for adopting topics for a region lacking in ence of experts in Japan. The results of recent studies were
evidence. These intentions were accepted favorably, and that used as much as possible. When there was no evidence avail-
subsequently the outcomes of acute treatment of heart failure able, discussions were frequently held to achieve consensus
were improved in clinical practice. In Japan, every patient is based on the measures often used by specialists.
covered by health insurance, and has free access to health care. Classification of recommendations and levels of evidence
This situation has exerted a positive influence on the forma- are shown explicitly in this set of guidelines. There are 4 class-
tion of a healthcare environment that allows standardization es of recommendation.
and beneficial advances various aspects, such as the use of risk
profiling by the Nohria-Stevenson classification and artificial Class I: There is evidence and/or general agreement that a
respiratory management with non-invasive positive-pressure given procedure or treatment is useful/effective.
ventilation (NPPV), acute treatment using human atrial natri- Class II: There is conflicting evidence and/or divergence of
uretic polypeptide (hANP), proper use of Swan-Ganz catheter- opinion about the usefulness/efficacy of a procedure
guided procedures, early introduction of angiotensin-convert- or treatment. There are two subclasses:
ing enzyme (ACE) inhibitors or β-blockers, spread of cardiac Class IIa: The weight of evidence/opinion is in favor of use-
rehabilitation, and guidance at the time of discharge based on fulness/efficacy.
brain natriuretic peptide (BNP, N-Terminal pro-BNP [NT-Pro Class IIb: Usefulness/efficacy is less well established by evi-
BNP]) assay and so on. However, it is true that there have dence/opinion.
been still further improvements possible for clinical practice Class III: There is evidence and/or general agreement that a
in Japan since the current guideline was published. procedure/treatment is not useful/effective and in
A thorough identification and discussion of problems was some cases may be harmful.
carried out by members and collaborators on February 18th

JCS Guidelines for Management of Acute Heart Failure 2159
There are 3 levels of evidence: In principle, this set of guidelines provides information on
procedures or treatments currently feasible or covered by
Level A: Data are derived from multiple, randomized, multi- healthcare insurance. Promising methods of diagnosis and treat-
center, interventional clinical trials that each include ment that may be clinically applicable in the near future are
at least 400 patients, or from meta-analyses. also described briefly for the readers’ reference. New recom-
Level B: Data are derived from multiple, randomized, multi- mendations for terminal care and hospice care in the clinical
center, interventional clinical trials each including practice of heart failure are also included. These are important
less than 400 patients, from well-designed compara- issues for a healthcare in Japan, and recommendations on
tive studies, or from large-scale cohort studies. these issues become more refined and acceptable to both pa-
Level C: Recommendations are a consensus opinion of ex- tients and healthcare providers through the review process in
perts, in the absence of data from randomized inter- the near future.
ventional clinical trials.
I General Matters
(2) Hypertensive acute heart failure: Signs and symptoms of
1. Definition heart failure are accompanied by high blood pressure with
a chest X-ray compatible with acute pulmonary conges-
Acute heart failure is defined as the rapid onset or exacerbation and pulmonary edema.
tion of signs and symptoms secondary to increased ventricular (3) Acute cardiogenic pulmonary edema: Pulmonary edema
end-diastolic pressure and decreased perfusion of major or- (verified by chest X-ray) accompanied by severe respira-
gans that are caused by acute loss of compensation of pump- tory distress, with rales over the lung and orthopnea, with
ing function of the heart due to its organic and/or functional O2 saturation usually less than 90% on room air prior to
abnormalities. Acute heart failure may occur as a newly devel- treatment.
oped condition or an acute exacerbation of chronic heart fail- (4) Cardiogenic shock: Significant impairment of microcircu-
ure, and may range in severity from mild to life-threatening. lation of peripheral tissues and major organs induced by
Acute heart failure is classified into the following 6 catego- heart failure after correction of pre-load. There is a con-
ries. Table 1 summarizes hemodynamic profiles of the 6 cat- tinuum from low output syndrome to cardiogenic shock.
egories of acute heart failure.4 (5) High output heart failure: Characterized by high cardiac
output, usually with high heart rate (caused by thyrotoxi-
(1) Acute decompensated heart failure: De novo or as decom- cosis, anemia, shunt disease, beriberi heart, Paget’s dis-
pensation of chronic heart failure with signs and symp- ease, iatrogenic, or by other mechanisms), with warm pe-
toms of acute heart failure, which are mild and do not ripheries, pulmonary congestion, and sometimes with low
fulfill criteria for cardiogenic shock, pulmonary edema, or blood pressure as in septic shock.
hypertensive acute heart failure. (6) Right sided acute heart failure: Characterized by low out-
Table 1. Hemodynamic Profiles of the 6 Categories of Acute Heart Failure

Decreased blood
Mean Killip Forrester Peripheral
Heart rate SBP Cardiac index flow in major
PAWP classifi- classifi- Diuresis hypoperfu-
(bpm) (mmHg) (L/min/m2) organs including
(mmHg) cation cation sion
the brain
1. Acute decompen- Increase/ Decrease, Decrease, Slight II II Present/ Present/ Absent
sated heart failure decrease normal/ normal/ increase decrease# absent
increase increase
2. Hypertensive Increase in Increase Increase/ Increase II to IV II to III Present/ Present/ Present, with CNS
acute heart failure many cases decrease decrease absent symptoms*
3. Acute cardiogenic Increase Decrease, Decrease Increase III II/IV# Present Present/ Absent/present#
pulmonary edema normal/ absent
increase#
4. Cardiogenic shock
(1)
low output Increase Decrease, Decrease Increase III to IV III to IV# Decrease Present Present
syndrome normal
(2) Severe cardio- >90 <90 Decrease Increase IV IV Oliguria Significant Present
genic shock
5. High output heart Increase Increase/ Increase Increase/ II I to II Present Absent Absent
failure decrease no increase
6. Right sided acute Decrease in Decrease Decrease Decrease I# I, III# Present/ Present/ Present/absent
heart failure many cases decrease absent
CNS, central nervous system; PAWP, pulmonary artery wedge pressure; SBP, systolic blood pressure.
An increase in mean PAWP is defined as that by ≥18 mmHg. *Present in patients with hypertensive urgency. #Modified to fit the circumstances
in Japan.
Adapted from Eur Heart J 2005; 26: 384 – 416,4 with permission from Oxford University Press.

Figure 1. Nohria-stevenson classification.
Table 2. Epidemiological Surveys in Japan

HIJC-HF JCARE-CARD ATTEND
Study design Retrospective Prospective Prospective
observational study observational study observational study
Participants Acute heart failure Exacerbation of heart failure Acute heart failure
Basic statistics
No. of participants 3,578 2,675 1,110
Areas of registration 8 prefectures 47 prefectures 20 prefectures
No. of institutions 15 164 32
Mean age (years) 69.8±13.9 71.0±13.4 73±14
Sex
Males (n, %) – 1,598 (59.8) (58.9)
Females (n, %) 1,287 (40.7) – –
BMI (kg/m2) 21.4±3.7 22.3±4.1 –
Patient characteristics
History of hospitalization for heart failure (n, %) 1,090 (33.5) 1,223 (45.7) (37.4)
Past illness
Hypertension 1,711 (54.1) 1,406 (52.8) (70.6)
Diabetes 993 (31.4) 798 (29.9) (34)
Dyslipidemia 814 (25.7) 657 (24.8) –
Atrial fibrillation 1,151 (36.4) 937 (35.0) (40)
COPD – 175 (6.7) (9)
NYHA classification at hospitalization
Class I – 31 (1.2) 8 (0.7)
Class II – 305 (11.4) 134 (12.1)
Class III (30.4) 1,192 (44.6) 434 (39.1)
Class IV (34.6) 1,147 (42.9) 524 (47.2)
Cardiac disease causing heart failure
Coronary artery disease 1,060 (33.5) 856 (32.0) (33.2)
Cardiomyopathy 658 (20.8) 586 (21.9) (Dilated: 12.7)
Valvular heart disease 731 (23.1) 742 (27.8) (17.3)
Hypertensive heart disease 365 (11.5) 658 (24.4) (18.4)
ATTEND, Acute Decompensated Heart Failure Syndromes; BMI, body mass index; COPD, chronic obstructive pulmonary disease; HIJC-HF,
Heart Institute of Japan-Department of Cardiology-Heart Failure; JCARE-CARD, Japanese Cardiac Registry of Heart Failure in Cardiology;
NYHA, New York Heart Association.
Data are expressed as number of patients and percentage (in parenthesis).
The data of the ATTEND study include the results of an interim study in 1,110 patients.

Table 3. Characteristics of Patients With Acute Heart Failure: Comparison Between Epidemiological Studies in Japan and Western
Countries
ATTEND ADHERE OPTIMIZE-HF EHFS II
n=1,110 n=187,565 n=48,612 n=3,580
Demographics
Age (years; mean ± SD) 73±14 72±14 73±14 70±13
Males (%) 59 49 48 61
Comorbidities (%)
Hypertension 71 74 71 63
Diabetes 34 44 42 33
Atrial fibrillation/flutter 40 31 31 39
Etiology
Ischemic (%) 33 57 46 30
Hypertensive (%) 18 N/A 23 11
Clinical status on hospitalization
De novo acute heart failure (%) 63 24 13 37
Orthopnea (%) 69 34 27 N/A
Peripheral edema (%) 68 65 65 N/A
Serum creatinine level (mg/dL; mean ± SD) 1.4±1.5 1.8±1.6 1.8±1.8 N/A
Brain natriuretic peptide 1,063±1,158 Median 843 1,273±1,330 N/A
Heart rate (bpm; mean ± SD, median) 99±30 N/A 87±22 Median 95
SBP (mmHg; mean ± SD) 147±38　　 144±33　　 143±33　　 N/A
(median, mmHg) 141　　 N/A N/A 135　　
LVEF <40% 57 47 48.8 46
Outcomes
Length of stay (days, median) 21 4.3 N/A 9
(days, mean) 31 N/A 6.4 N/A
In-hospital mortality (%) 7.7 3.8 3.8 6.7
ADHERE, Acute Decompensated Heart Failure Patients National Registry; EHFS II, EuroHeart Failure Survey II; LVEF, left ventricular ejection
fraction; N/A, not applicable; OPTIMIZE-HF, Organized Program To Initiate lifesaving treatMent In hospitaliZEd patients with Heart Failure;
SD, standard deviation. Laboratory findings at admission are expressed with percentage, mean ± SD or median. Adapted from Am Heart J
2010; 159: 949 – 955,11 with permission from Elsevier Inc.
Table 4. Treatment During the Early Phase of Hospitalization

Items n (%) Items n (%)
No. of patients 1,100 Nonpharmacologic treatment
Intravenous drugs Continuous positive airway pressure 241 (21.7)
Diuretics 894 (80.4) Bilevel positive airway pressure 160 (14.4)
Carperitide 770 (69.4) Endotracheal intubation 123 (11.1)
Isosorbide dinitrate 102 (9.2)　　 Swan-Ganz catheterization 223 (20.1)
Nitroglycerine 289 (26.0) Pacing 52 (4.7)
Nicorandil 118 (10.6) Cardiac resynchronization therapy 27 (2.4)
Inotropes, any 230 (20.7) Implantable cardioverter defibrillators 29 (2.6)
Dobutamine 141 (12.7) Hemodialysis 39 (3.5)
Dopamine 122 (11.0) Continuous hemodiafiltration 41 (3.7)
Norepinephrine 69 (6.2) Percutaneous coronary intervention 107 (9.6)　　
Milrinone 31 (2.8) Coronary artery bypass grafting 15 (1.4)
Olprinone 8 (0.7) Valve replacement 19 (1.7)
Digoxin 72 (6.5) Intraaortic balloon pumping 40 (3.6)
Calcium channel blockers 91 (8.2) Percutaneous cardiopulmonary support 7 (0.6)
Left ventricular assist system 1 (0.1)
Adapted from Am Heart J 2010; 159: 949 – 955,11 with permission from Elsevier Inc.
put syndrome with increased jugular venous pressure, in- commonly with the New York Heart Association (NYHA) clas-
creased liver size and hypotension. sification,5 and the Killip’s classification that is based on signs
and symptoms of AMI,6 and the Forrester classification based
The nature and severity of heart failure are classified most on hemodynamic conditions.7 In both classifications, mortal-

Figure 2. Prescriptions at discharge:

comparison between Japan and
Western countries. ACE, angiotensin-
converting enzyme; ARB, angioten-
sin II receptor blocker. Adapted from
Am Heart J 2010; 159: 949 – 955,11
with permission from Elsevier Inc.
Table 5. Criteria for Diagnosis of Congestive Heart Failure: Framingham Criteria

Diagnosis of heart failure requires the simultaneous presence of at least 2 major criteria or 1 major criterion in conjunction with 2 minor criteria.
[Major criteria]
- Paroxysmal nocturnal dyspnea or orthopnea
- Neck-vein distention
- Rales
- Cardiomegaly
- Acute pulmonary edema
- Protodiastolic gallop (S3 gallop)
- Increased venous pressure (≥16 cm H2O at right atrium)
- Increased circulation time (≥25 sec)
- Hepatojugular reflux
[Minor criteria]
- Ankle edema
- Nocturnal cough
- Dyspnea on ordinary exertion
- Hepatomegaly
- Pleural effusion
- Decrease in vital capacity by one third from maximum recorded
- Tachycardia (heart rate ≥120 bpm)
[Major or minor criteria]
Weight loss of 4.5 kg or more in 5 days in response to treatment. When the weight loss is attributable to the treatment of heart failure, it is
considered 1 major criterion. Otherwise it is considered a minor criterion.
ity rates are higher among patients classified into more severe patients were classified into profiles A, B, C, and L (Figure 1),
categories. short-term mortality rates (including cases of heart transplan-
The Nohria-Stevenson classification is useful for risk profil- tation) were higher in patients with profiles B and C.8
ing of patients with heart failure based on peripheral circula-
tion and pulmonary auscultation findings. In a study where

Table 6. Signs and Symptoms of Acute Heart Failure

Congestive signs and symptoms
Left heart failure
Symptoms: Dyspnea, shortness of breath, tachypnea, orthopnea
Signs: Bubbling rales, wheezing, pink foamy sputum, third or fourth heart sound
Right heart failure
Symptoms: Right hypochondrium pain, anorexia, abdominal fullness, epigastric discomfort, fatigability
Signs: Hepatomegaly, increased hepatobiliary enzymes, neck-vein distention
Signs of pulmonary congestion are not apparent in patients with severe right heart failure
Signs and symptoms of low output syndrome
Symptoms: Disturbance of consciousness, restlessness, memory disorder
Signs: Cold sweat, cold limbs, cyanosis, hypotension, oliguria, agitated or confused
Table 7. Causes and Precipitating Factors of Acute Heart Table 8. Pathophysiological Mechanisms and Related
Failure Factors in Heart Failure
1.
Acute decompensated heart failure: e.g., cardiomyopathy, I. Cardiac abnormalities
specific cardiomyopathy and old myocardial infarction 1. Structural abnormalities
2. Acute coronary syndromes a) Myocardium or myocyte: Abnormal excitation-contraction
a) Myocardial infarction/unstable angina with large extent of coupling, β-adrenergic desensitization, hypertrophy, necro-
ischemia and ischemic dysfunction sis, fibrosis, and apoptosis
b)
Complication of acute myocardial infarction (e.g., mitral b) Left ventricular chamber: Remodeling (dilatation, increased
valve insufficiency, ventricular septal perforation) sphericity, aneurysmal dilatation, or wall thinning)
c) Right ventricular infarction c) Coronary arteries: Obstruction, inflammation
3. Hypertension 2. Functional abnormalities
4. Acute arrhythmia: Ventricular tachycardia, ventricular fibrilla- a) Mitral valve regurgitation
tion, atrial fibrillation or flutter, other supraventricular tachy- b) Intermittent ischemia, myocardial stunning, or hibernating
cardia myocardium
5. Valvular regurgitation (endocarditis, rupture of chordae tendin- c) Supraventricular and ventricular arrhythmias
eae, exacerbation of pre-existing valvular regurgitation, aortic
dissection) d) Altered ventricular interaction
6. Severe aortic valve stenosis II. Biologically active tissue and circulating substances
7. Acute severe myocarditis (fulminant myocarditis) 1.
Humoral factors of the rennin-angiotensin-aldosterone
system
8. Takotsubo cardiomyopathy
2. Sympathetic nervous system: Norepinephrine
9. Cardiac tamponade, constrictive pericarditis
3. Vasodilators: Bradykinin, nitric oxide, and prostaglandins
10. Congenital heart disease: e.g., atrial septal defect, ventricu-
lar septal defect 4. Natriuretic peptides
11. Aortic dissection 5. Cytokines: Endothelin, tumor necrosis factor, and interleu-
kins
12. Pulmonary (thrombosis) embolism
6. Vasopressin
13. Pulmonary hypertension
7. Matrix metalloproteinases
14. Postpartum cardiomyopathy
III. Other factors
15. Non-cardiovascular precipitating factors
1. Genetic background, including effects of sex
a) Lack of compliance with medical therapy
2. Age
b) Excessive water/salt consumption
3. Environmental factors, including use of alcohol, tobacco, and
c) Infections, particularly pneumonia or septicemia toxic drugs
d) Severe brain insult 4. Coexisting conditions: diabetes, hypertension, renal disease,
e) After major surgery coronary artery disease, anemia, obesity, sleep apnea, and
f ) Reduction in renal function depression
g) Asthma, chronic obstructive pulmonary disease Adapted from N Engl J Med 2003; 348: 2007 – 2018.14 Copyright
© 2003 Massachusetts Medical Society. All rights reserved.
h) Drug abuse, treatment with drugs that may reduce cardiac
function
i ) Alcohol abuse
j ) Phaeochromocytoma
k) Overwork, insomnia, emotional or physical stress 2. Epidemiology
16. High output syndromes
a) Septicemia
Because no formal epidemiological survey of acute heart fail-
b) Thyrotoxicosis
ure has been conducted in Japan, the actual status and trend of
c) Anemia
this disease have not yet been clarified. In 2008, the Ministry
d) Shunt disease of Health, Labour and Welfare estimated that there were
e) Beriberi heart 47,500 patients with heart failure and 27,900 patients hospital-
f ) Paget’s disease ized for this disease per day.9 Considering current trends of

Figure 3. Initial management of acute heart failure. ACLS, advanced cardiac life support; BLS, basic life support; NPPV, non-
invasive positive-pressure ventilation; PEEP, positive end-expiratory pressure.
disorders causing this condition, acute heart failure is highly

likely to become more common in the future. A detailed epi-
3. Signs/Symptoms and Causes
demiological survey of acute heart failure must be conducted
promptly and practical measures should be taken according to 1. Signs and Symptoms
survey results in the light of the medical expenses in Japan. Physicians should evaluate patients for signs and symptoms
by obtaining a complete medical history taking and conduct-
1. Characteristics of Patients With Acute Heart Failure ing a physical examination according to the criteria for con-
Data on characteristics of patients are essential to establish gestive heart failure used in the Framingham study (Table 5).13
standard treatment for acute heart failure. Such data have been
reported in three epidemiological surveys, i.e., the HIJC-HF (1) Symptoms
(Heart Institute of Japan-Department of Cardiology-Heart See Table 6. Physicians should note that patients with heart
Failure) Registry,10 the ATTEND (Acute Decompensated failure may not always have the listed symptoms, and some
Heart Failure Syndromes) Registry,11 and the JCARE-CARD patients may have “hidden heart failure”, where patients do
(Japanese Cardiac Registry of Heart Failure in Cardiology not notice the presence of heart failure (see Chapter II).
study) evaluating the patients hospitalized with exacerbating
heart failure.12 Table 2 outlines the characteristics of the pa- (2) Signs
tients evaluated in these surveys.10–12 See Table 6 also.
2. Comparison With Epidemiological Data in Western 2. Disorders Causing Acute Heart Failure
Countries Table 7 lists disorders causing acute heart failure and the fac-
Epidemiological data obtained in the ATTEND Registry are tors that worsen it.2 Table 8 summarizes the pathophysiology
compared with those in Western counries.11 Table 3 shows con- and mechanisms of the onset of acute heart failure.14
dition at hospitalization and its outcome. Table 4 is content of
treatment during the early phase of hospitalization, and Figure 2
is comparative data in prescriptions at discharge among them.

Table 9. Algorithm for the Early In-Hospital Management of Patients With Acute Heart Failure: Clinical Scenario
Management at admission
- Non-invasive monitoring (SaO2, BP, temperature) - Laboratory tests
- O2 - BNP or NT-pro BNP when diagnosis is uncertain
- NPPV as indicated - ECG
- Physical examination - Chest X-Ray
CS 1 CS 2 CS 3 CS 4 CS 5
SBP
SBP > 140 mmHg SBP < 100 mmHg ACS Right ventricular failure
100 to 140 mmHg
- Symptoms develop - Symptoms develop - Rapid or gradual onset - Symptoms and signs - Rapid or gradual onset
abruptly gradually, together of symptoms of acute heart failure - No pulmonary edema
- Predominantly diffuse with a gradual increase - Predominantly signs of - Evidence of ACS - Right ventricular
pulmonary edema in body weight hypoperfusion - Isolated elevation of dysfunction
- Minimal systemic - Predominantly - Minimal systemic and cardiac troponin is - Signs of systemic
edema (patient may systemic edema pulmonary edema inadequate for CS 4 venous congestion
be euvolemic or hypo- - Minimal pulmonary - Elevation of filling pres- classification
volemic) edema sure
- Acute elevation of - Chronic elevation of Two subsets:
filling pressure often filling pressure, includ- (1) Clear hypoperfusion
with preserved LVEF ing increased venous or cardiogenic shock
- Vascular pathophysi- pressure and elevated (2) No hypoperfusion or
ology pulmonary arterial cardiogenic shock
pressure
- Manifestations of
organ failure (renal
impairment, liver
dysfunction, anemia,
hypoalbuminemia)
Treatments
- NPPV and nitrates - NPPV and nitrates - Volume loading with - NPPV - Avoid volume loading
- Diuretics are rarely - Diuretics if systemic initial fluid challenge if - Nitrates - Diuretics if SBP
indicated unless chronic fluid retention no overt fluid retention; - Cardiac catheterization >90 mmHg and
volume overload - Inotrope lab systemic chronic fluid
- PAC if no improvement - Follow guideline retention
- If BP fails to improve recommended - Inotropes if SBP
above 100 mmHg and management for ACS <90 mmHg
hypoperfusion persists, (aspirin, heparin, reper- - If SBP fails to improve
then consider vasocon- fusion therapy) above 100 mmHg, then
strictors - IABP begin vasoconstrictors
Treatment objectives
- Decrease dyspnea - Decrease heart rate - Maintain/improve SBP
- Improve well being - Urine output >0.5 mL/kg/min - Restore adequate perfusion
ACS, acute coronary syndrome; BNP, brain natriuretic peptide; BP, blood pressure; CS, clinical scenario; IABP, intraaortic balloon pumping;
NT-pro BNP, N-terminal pro-brain natriuretic peptide; PAC, pulmonary artery catheter; SaO2, arterial oxygen saturation.
Adapted from Crit Care Med 2008; 36(Suppl): S129 – S139,19 with permission from Wolters Kluwer Health.
Specifically, measures should be taken to treat dyspnea, as

4. Treatment Strategies well as congestion and hypoperfusion of organs to save the
life.15–17 Patients for whom active interventions were initiated
1. Basic Principle in the emergency room show lower mortality rates, shorter
Patients with acute heart failure are treated to (1) rescue and durations of hospitalization, shorter stays in intensive care units/
stabilize vital signs; (2) improve symptoms such as dyspnea; cardiac care units (ICU/CCU), and lower rates of ICU admis-
and (3) reduce organ congestion. Treatment must be initiated sion as compared with patients for whom treatment was initi-
as soon as possible to stabilize and maintain the condition by ated in the ward.18
using cost-effective and low-risk methods.
2. Preparations for Accepting Patients and Evaluation of
2. Points to Be Checked Vital Signs
Figure 3 shows a chart of approach to diagnosis, points to be Before accepting the patient, medical staff members should
checked, and emergent treatment methods for acute heart prepare instruments, such as an automatic blood pressure moni-
failure. tor, a pulse oximeter and an ECG monitor, devices to establish
intravenous lines, drugs for cardiopulmonary resuscitation, a
defibrillator, and devices for endotracheal intubation, to be ready
5. Initial Management of Acute Heart Failure for immediate use, considering the worst scenario such as respi-
ratory arrest and cardiopulmonary arrest. When the patient ar-
1. Purpose and Significance rives, treatment should be started immediately under continuous
Saving the life and alleviating distress should be prioritized. monitoring of blood pressure, pulse rate, and oxygen saturation.

3. Treatment formed quickly even by general clinicians (see Figure 3 and

Procedures of early intervention should be able to be per- Table 9).19
II Diagnosis
1. Procedures for Diagnosis and 2. Signs and Symptoms for Acute Phase Diagnosis
(1) Symptoms
Triage for Treatment Signs/symptoms of acute heart failure are classified into those
due to congestion and those due to peripheral hypoperfusion
Figure 4 shows a flowchart of how to diagnose acute heart resulting from decreased cardiac output (Table 6).
failure. The severity of congestion can be evaluated on the basis of
Physicians should evaluate patients to differentiate the pres- non-invasive estimation of central venous pressure (Figure 5).
ence/absence of common disorders that cause heart failure
(Tables 7 and 8) and to distinguish the most treatable ones (2) Cardiac Auscultation
that may be effectively remedied with emergent surgery and In patients with low output heart failure, the first heart sound
emergent cardiac catheterization. is often diminished, while the third and fourth heart sounds are
often audible. A ventricular or atrial gallop may be heard. Car-
diac auscultation is useful in the diagnosis of acute mitral re-
2. Procedures for Diagnosis gurgitation due to ventricular septal perforation or papillary
in the Emergency Room muscle rupture, which requires emergent surgery. Prompt di-
agnosis and determination of the appropriate timing of surgery
1. Assessment of General Condition become feasible by using auscultation and echocardiography.
At the time of arrival, the patient should be inspected for gen-
eral condition by an evaluation of vital signs and the typical (3) Measurement of Systemic Blood Pressure
signs and symptoms of acute heart failure. In patients presenting with both hypertension and acute heart
failure, acute heart failure may result from untreated hyperten-
sion (see Section 2 of Chapter IV), or hypertension may be
Figure 4. Procedures for diagnosis of acute heart failure.

Figure 5. Non-invasive estimation of central venous pressure.
Table 10. Indications for Swan-Ganz Catheterization in Patients With Heart Failure

Class I, Level of Evidence: C
- Cardiogenic shock not responding promptly to appropriate fluid administration.
- Pulmonary edema associated with hypotension or shock/near shock that does not respond to appropriate treatment measures.
- A diagnostic measure to confirm whether the cause of pulmonary edema is cardiogenic or noncardiogenic.
Class II, Level of Evidence: C
- Assessment of intravascular volume status, ventricular end-diastolic pressure, and cardiac function in patients with heart failure not
responding to conventional treatment.
- Assessment of cardiac hemodynamics in patients with non-metabolic chronic lung disease or examination to rule out left heart failure.
- A diagnostic measure to investigate the cause and clinical/hemodynamic significance of systolic murmur newly developed in patients with
acute heart failure.
Class III, Level of Evidence: C
- A routine approach in the assessment, diagnosis, and treatment of heart failure.
Table 11. Assessment at Hospital Admission of Patients With Acute Heart Failure

Class I
- 12-lead ECG, arterial blood gas analysis, hematology and blood chemistry, plasma BNP (NT-pro BNP) (Level of Evidence: C)
- Chest X ray, echocardiography, Doppler echocardiography (Level of Evidence: C)
caused by acute heart failure. Physicians should consider the tients with AMI, physicians should perform Swan-Ganz cath-
possibility of heart failure with preserved ejection fraction (EF) eterization to predict the prognosis and determine treatment
in the treatment of patients’ acute heart failure resulting from strategies by using the Forrester classification.7 Although the
untreated or poorly controlled hypertension (see Chapter VI). Forrester classification is widely used for patients with acute
In 2008, Mebazaa, and Gheorghiade et al. proposed a heart failure, the threshold values for pulmonary artery wedge
clinical scenario to roughly classify the types of acute heart pressure (PAWP) and cardiac index may not always be helpful
failure according to the initial systolic blood pressure upon for patients with acute decompensated heart failure. Alterna-
arrival at the hospital or immediately after hospital admission, tively, the Nohria-Stevenson classification categorizes patients
and design a treatment strategy for each individual patient with heart failure into 4 hemodynamic profiles based on the
(Table 9).19 Clear evidence has not been established for the clinical findings of congestion and hypoperfusion (Figure 1).21
efficacy of the scenario, and validation studies are awaited. This classification is useful in the assessment of the severity
of acute heart failure.
3. Classification of Severity
Swan-Ganz catheterization is not always necessary for all 4. 12-Lead ECG and ECG Monitoring
patients with acute heart failure, and should be indicated based In patients with acute heart failure, the 12-lead ECG should be
upon the characteristics of the patients (Table 10).20 In pa- repeated at periodic intervals (Table 11). ECG monitoring is

Figure 6. Chest X-ray findings of heart failure: schema.
Table 12. Echocardiographic Parameters Used in the Diagnosis and Treatment of Acute Heart Failure
1. Abnormal left ventricular function
- Left ventricular ejection fraction (LVEF)
2. Increased left ventricular filling pressure
- Left ventricular inflow velocity pattern: The ratio of early diastolic filling velocity to atrial filling velocity (E/A), the deceleration time (DT) of
the E wave
- Tissue Doppler imaging: Early diastolic movement of the mitral annulus (E’ wave) (See Figure 7)
- Systolic pressure gradient between right ventricle and right atrium calculated on the basis of the tricuspid regurgitation jet velocity
- Respiratory variation in inferior vena cava diameter (See Figure 8)
- Estimated pulmonary artery systolic pressure (using the above two parameters)
3. Low output syndrome
- Left ventricular outflow tract velocity-time index (velocity-time index, VTI)
4. Abnormal right ventricular function
- The size of the right ventricle and right atrium
- Abnormal findings in at least one of the parameters of the right ventricular systolic function (fractional area change [FAC]; tricuspid annular
plane systolic excursion [TAPSE]; and right ventricular index of myocardial performance [RIMP])
- Estimated pulmonary artery systolic pressure
necessary. er in the follow-up of patients with acute heart failure. In pa-

tients with acute heart failure in whom cardiac contractility is
5. Arterial Blood Gas Analysis, Hematology, and Blood maintained, NT-proBNP levels plays a key role in the diagno-
Chemistry sis of heart failure with preserved EF.21 Aspartate aminotrans-
Arterial blood gas analysis should be performed to diagnose ferase (AST) (glutamate oxaloacetate transaminase [GOT]),
respiratory failure and acidosis. Oxygen administration should alanine aminotransferase (ALT) (glutamic-pyruvic transami-
be initiated promptly, after a blood sample is obtained when- nase [GPT]) and total bilirubin levels increase in patients with
ever possible (Table 11). right heart failure.
An increase in levels of creatine kinase (CK), especially
CK-MB, and an increase in troponin T levels strongly suggest 6. Chest X-Ray (Including Portable Chest X-Ray Machines)
the presence of AMI. An increase in levels of troponin T or I Chest X-ray should be examined to determine the nature and
is observed in 30 to 50% of patients with acute heart failure location of pulmonary congestion in patients to make the di-
without AMI. Renal/hepatic function tests, and the presence agnosis and efficacy evaluation of acute heart failure. See
or absence of anemia, electrolyte abnormality, and infections Figure 6.
and/or inflammation are also important in the assessment of
the causes of heart failure. Because plasma BNP levels in- 7. Echocardiography and Doppler Echocardiography
creases to 100 pg/mL or more in most patients with acute heart (Table 12)
failure with substantial pulmonary congestion, it can be used The roles of echocardiography and Doppler echocardiography
in the diagnosis of the condition. NT-proBNP is a useful mark- in the diagnosis and treatment of acute heart failure are (1) to

Figure 7. E/E’ before and after treatment of heart failure. E/E’, early diastolic filling velocity/peak early diastolic velocity of the
mitral annulus.
Figure 8. Enlargement of the inferior vena cava and respiratory variation in inferior vena cava diameter.
detect the presence of hemodynamic abnormalities, abnormal 8. Other Examinations

pump function resulting in increased ventricular filling pres- Cardiac magnetic resonance (CMR) imaging and radionuclide
sure, and decreased cardiac output; and (2) to obtain findings (radioisotope) imaging are useful in patients in whom it is dif-
of underlying disease. See Figures 7 and 8. ficult to determine whether ischemia is involved in acute heart
failure. Contrast computed tomography (CT) is necessary in

Table 13. Monitoring of Patients With Acute Heart Failure

Class I (Level of Evidence: C)
- ECG monitoring
- Blood pressure
- Pulse oximeter (SaO2)
- Estimation of hemodynamics using echocardiography or Doppler echocardiography
- Determination of hemodynamics by Swan-Ganz catheterization (for Class I indications listed Table 10)
Class IIa (Level of Evidence: C)
- Arterial line
- Central venous line
- Determination of hemodynamics by Swan-Ganz catheterization (for Class II indications listed in Table 10)
Class III (Level of Evidence: B)
- Routine determination of hemodynamics by Swan-Ganz catheterization in the treatment
patients suspected to have aortic dissection. 2. Evaluation for Causative Conditions
When conditions causing acute heart failure can be specified,
appropriate treatment strategies can be planned. Patients with
3. Diagnostic Procedures in ICU/CCU acute heart failure should be evaluated for the presence/ab-
sence of ischemic heart disease (coronary artery disease) and
Patients who do not require emergent surgery or catheteriza- non-ischemic heart diseases (myocardial disease, valvular heart
tion are transferred to the ICU/CCU where initial treatment disease, and others). See Tables 7 and 8.
is continued. Comprehensive evaluation through (1) cardiac
hemodynamic monitoring, (2) investigation to identify the 3. Search for Precipitating Factors of Acute Heart Failure
cause of acute heart failure, (3) identification of precipitating Identifying precipitating factors of acute heart failure is impor-
factors of acute heart failure, and (4) evaluation of complica- tant to ensure the most effective treatment of the condition.
tions is necessary to ensure appropriate treatment of acute heart Recurrence or exacerbation of heart failure cannot be pre-
failure. vented without addressing or eliminating the causes and pre-
cipitating factors of the acute heart failure. Precipitating fac-
1. Cardiac Hemodynamic Monitoring (Table 13) tors of acute heart failure include extreme fatigue, infections,
The pathologic condition of patients with acute heart failure anemia, mental stress, and discontinuation of oral drugs. See
changes moment to moment. Patients should also be moni- Tables 7 and 8.
tored for efficacy of treatment over time. Patients with acute
heart failure should be observed for physical signs/symptoms, 4. Diagnosis of Complications
blood pressure, heart rate, timed urine volume, arterial partial Patients with severe heart failure or diabetes, and elderly pa-
pressure of oxygen (PaO2), and estimated pulmonary arterial tients, should be carefully observed for infections. Renal func-
pressure by Doppler echocardiography, among other param- tion may often be decreased in association with acute heart
eters. failure. The mortality risk of patients with acute heart failure
increases when complications are present.
III Treatment
heart failure by using the Killip classification, the Nohria-
1. Treatment Strategies Stevenson classification (Figure 1),8 echocardiography, and
arterial blood gas analysis, as well as whenever necessary
1. Treatment Goals Swan-Ganz catheterization for hemodynamic assessment. Pa-
Treatment goals for acute heart failure are (1) making a prompt tients with findings suggestive of congestion should be evalu-
diagnosis, evaluating its severity and starting appropriate treat- ated for pulmonary and/or systemic congestion. Patients with
ment in the acute phase; (2) initiating appropriate medical ther- pulmonary congestion should be treated with vasodilators and
apy considering the patient’s long-term prognosis to ensure those with systemic congestion should be treated mainly with
myocardial protection after the patient’s condition is stabi- diuretics.22 Intravenous catecholamines are required for pa-
lized, and promoting early ambulation as possible; and (3) tients with peripheral circulatory failure or hypotension (less
providing comprehensive patient/family education in terms of than 90 mmHg). Patients with intractable acute heart failure
life style, medications, and diet before discharge to prevent not responding to medical therapy should be treated with re-
rehospitalization due to exacerbation of heart failure. spiratory support with endotracheal intubation, extracorporeal
ultrafiltration method (ECUM), continuous hemodiafiltration
2. Basic Policy of Treatment (CHDF), intraaortic balloon pumping (IABP), percutaneous
Patients should be initially treated in the emergency room ac- cardiopulmonary support (PCPS), and/or ventricular assist sys-
cording to Figure 3. Treatment methods should be based on tem (VAS), among other methods. After discharge from the
the results (Figure 9) of an evaluation of the severity of acute emergency room or ICU/CCU, patients are treated in the car-

Figure 9. Flow chart for the management of acute heart failure. CHDF, continuous hemodiafiltration; CRT-D, cardiac resynchro-
nization therapy defibrillator; ECUM, extracorporeal ultrafiltration method; ICU, intensive care unit; PCPS, percutaneous cardiopul-
monary support; QOL, quality of life; SAS, specific activity scale; VAS, ventricular assist system.
Table 14. Use of β-Blockers in Patients With Acute Decompensated Heart Failure

Class IIa
- Continuing β-blocker therapy at the same or reduced doses during acute exacerbation of heart failure in patients receiving β-blocker
therapy. (Level of Evidence: B)
- Initiating PDE inhibitors during acute exacerbation of heart failure in patients receiving β-blocker therapy. (Level of Evidence: C)
PDE, phosphodiesterase.
diovascular or general ward. Patients who can walk and are promptly. Patients receiving β-blockers should be treated ac-
considered to be able to perform light activities of daily living cording to methods shown in Table 14.
are discharged home from hospital and are managed in the
ambulatory setting. Treatment goals for patients in the ambu- (2) Hypertensive Acute Heart Failure
latory setting are improving long-term prognosis; preventing Hypertensive acute heart failure is caused by hypertension.
rehospitalization; improving quality of life (QOL), and pre- Blood pressure management is the basis of treatment (see
venting the exacerbation of heart failure. Physicians should Tables 15 and 32).
refer to the guidelines for the diagnosis and treatment of chron-
ic heart failure for its management in the ambulatory setting. (3) Acute Cardiogenic Pulmonary Edema
Table 15 lists recommendations for the treatment of acute
(1) Acute Decompensated Heart Failure cardiogenic pulmonary edema.
Acute decompensated heart failure is classified into (1) newly
developed acute heart failure, and (2) acute exacerbation of (4) Cardiogenic Shock
chronic heart failure. In both cases, treatment should follow Table 16 lists recommendations for the initial treatment of
the basic treatment strategies (Figure 9). For patients with acute cardiogenic shock. Patients should be treated according to the
decompensated heart failure, it is effective to identify the pre- basic treatment strategies shown in Figures 3 and 17.
cipitating factors of heart failure (Table 7) and to treat them

Table 15. Treatment of Acute Cardiogenic Pulmonary Edema

Class I
- Oxygen administration (maintain SaO2 >95% and PaO2 >80 mmHg) (Level of Evidence: C)
- NPPV for patients not responding to oxygen administration (Level of Evidence: A)
- Sublingual, spray, or intravenous nitrates (Level of Evidence: B)
- Intravenous furosemide (Level of Evidence: B)
- Intravenous catecholamines for patients with hypotension (Level of Evidence: C)
- Intravenous nitroprusside for patients with acute heart failure due to hypertensive urgency, aortic valve insufficiency, or mitral valve regur-
gitation (Level of Evidence: C)
- Calcium channel blockers (e.g., nicardipine) for patients with acute pulmonary edema associated with significant hypertension (Level of
Evidence: C)
- Nitrates for patients with acute pulmonary edema associated with significant hypertension (Level of Evidence: C)
- Loop diuretics for patients with acute pulmonary edema associated with significant hypertension (Level of Evidence: C)
- Carperitide for patients with acute pulmonary edema associated with significant hypertension (Level of Evidence: C)
- Artificial respiration with endotracheal intubation for patients who do not respond well to NPPV, or have disturbance of consciousness or
difficulty of expectoration (Level of Evidence: C)
Class IIa
- Intravenous carperitide (Level of Evidence: B)
- Intravenous PDE inhibitors (for patients without ischemia) (Level of Evidence: A)
- Torasemide during transition to chronic phase (Level of Evidence: C)
- Adenylate cyclase activators (for patients without ischemia) (Level of Evidence: C)
Class IIb
- Intravenous PDE inhibitors (for patients with ischemia) (Level of Evidence: A)
- Intravenous carperitide for patients with renal dysfunction (Level of Evidence: B)
- Intravenous morphine (Level of Evidence: B)
- Adenylate cyclase activators (for patients with ischemia) (Level of Evidence: C)
Class III
- Antialdosterones for patients with renal dysfunction and hyperkalemia (Level of Evidence: C)
- Sublingual nifedipine for patients with hypertensive urgency (Level of Evidence: C)
PaO2, arterial partial pressure of oxygen.
Table 16. Treatment of Cardiogenic Shock

Class I
- Volume loading for patients with decreased circulating blood volume (Level of Evidence: C)
- Use of catecholamines (Level of Evidence: C)
- Concomitant use of inotropes (with catecholamines and PDE inhibitors) (Level of Evidence: C)
- Mechanical circulatory support (IABP and PCPS) for patients not responding to medical therapy (Level of Evidence: C)
- Intravenous epinephrine during cardiopulmonary arrest (Level of Evidence: B)
- Endotracheal epinephrine during cardiopulmonary arrest (at a dose 2 to 2.5 times higher than the intravenous dose) (Level of Evidence: C)
Class IIa
- NPPV (Level of Evidence: A)
- VAS for patients with intractable heart failure that is not responding to medical therapy or may be recoverable or is indicated for heart
transplantation (Level of Evidence: B)
Class III
- Intracardiac injections during cardiac arrest (Level of Evidence: C)
(5) Acute Right Heart Failure

See Section 2 of Chapter VII.
2. Early Diagnosis and Treatment
(6) High Output Heart Failure 1. Treatment in the Emergency Room
The treatment of the underlying disease/condition that induced At the arrival in the emergency room, patients should be
the high output heart failure should be prioritized. When no checked for vital signs and consciousness, and their conditions,
improvement is observed after treatment of the cause, physi- and should be treated according to basic life support (BLS)
cians should investigate other types of underlying heart dis- and advanced cardiac life support (ACLS) guidelines.23 The
ease. patients should then receive treatment to alleviate major symp-

Table 17. Respiratory Management in Patients With Acute Heart Failure

Class I
- NPPV for patients not responding to oxygen administration (Level of Evidence: A)
- Artificial respiration with endotracheal intubation in patients who cannot receive NPPV (Level of Evidence: C)
Table 18. Initial Management of Acute Heart Failure in the Emergency Room

Respiratory management
- Airway management: Class I, Level of Evidence: C
- Oxygen administration: Class I, Level of Evidence: C
- NPPV such as CPAP and bilevel PAP for patients in whom oxygenation is inadequate despite oxygen administration (see Tables 16 and
17): Class I, Level of Evidence: A
- Endotracheal intubation for patients in whom oxygenation is inadequate despite oxygen administration (See Tables 16 and 17): Class I,
Level of Evidence: C
Treatment of underlying disease (whenever possible)
- Thrombolysis/percutaneous transluminal coronary angioplasty for acute myocardial infarction: Class I, Level of Evidence: A
- Considering indications of surgery for patients with acute aortic dissection: Class I, Level of Evidence: C
- Temporary pacing for patients with bradyarrhythmia: Class I, Level of Evidence: C
- Pericardiocentesis and drainage for the treatment of cardiac tamponade: Class I, Level of Evidence: C
- Thrombolysis for patients with unstable hemodynamics such as prolonged shock or hypotension in the early stage of acute pulmonary throm-
boembolism: Class I, Level of Evidence: C
Medical therapy for each aspect of acute heart failure
- Sublingual, spray, or intravenous nitrates: Class I, Level of Evidence: B
- Intravenous epinephrine during cardiopulmonary arrest: Class I, Level of Evidence: B
- Intravenous diuretics for acute pulmonary edema: Class I, Level of Evidence: C
- Nitroglycerin and calcium channel blockers (e.g., nicardipine) for patients with acute pulmonary edema associated with significant hyper-
tension: Class I, Level of Evidence: C
- Catecholamines for cardiogenic shock: Class I, Level of Evidence: C
- Mechanical circulatory support for patients in whom no improvement in hemodynamics has been achieved after medical therapy: Class I,
Level of Evidence: C
- Prompt transfer to CCU for the treatment of acute coronary syndrome after initial management in emergency room: Class I, Level of
Evidence: C
- Intravenous morphine: Class IIb, Level of Evidence: B
- Sublingual nifedipine during hypertensive urgency: Class III, Level of Evidence: C
- Intracardiac injections during cardiac arrest: Class III, Level of Evidence: C
CCU, cardiac care unit; CPAP, continuous positive airway pressure; PAP, positive airway pressure.
toms, and correct pathological conditions (Tables 17 and 18, 4. Measurements of Urine Volume and Body Weight
and Figure 3).
5. Blood Pressure
2. Intervention to Correct the Causative Condition and
Precipitating Factors 6. Heart Rate
When the causative condition and precipitating factors are iden-
tified and require prompt intervention, treatment should be pri- 7. Arterial Oxygen Saturation
oritized. Table 19 lists the goals of the listed treatment and manage-
ment.
3. Determination of Targets of 8. Cardiac Rehabilitation
Treatment and Management (1) Significance of Cardiac Rehabilitation in Patients
With Acute Heart Failure
1. Bed Rest Level The goals of cardiac rehabilitation in patients with acute heart
failure are (1) facilitating early ambulation to prevent conse-
2. Placement of Urinary Catheter and Establishment of quences of prolonged bed rest (e.g., physical/mental decon-
Venous Lines ditioning, bedsores, and pulmonary embolism); (2) establish-
ing/sharing a plan for a prompt and safe discharge from hospital
3. Hydration and Meals and social rehabilitation; (3) improving QOL by increasing
exercise capacity; and (4) preventing severe heart failure and

Table 19. Targets of Treatment and Management

Bed rest level
- Resting in the Fowler’s position: Class IIa, Level of Evidence: C
- Allowing more physical activity promptly after obtaining stable hemodynamics: Class I, Level of Evidence: C
- Use of elastic stockings to prevent venous thrombosis for patients requiring long-term bed rest: Class I, Level of Evidence: A
Establish venous lines
- Establishing more than one venous lines using large cannulae: Class I, Level of Evidence: C
- Introduction of a Swan-Ganz catheter to monitor hemodynamics and assess treatment efficacy: Class IIb, Level of Evidence: C
Meals and nutrition
- Prohibition of oral nutrition/food intake until circulation and diuresis are stabilized: Class I, Level of Evidence: C
- Limit salt intake
Urine output
- Achieving a urine output of ≥40 mL/hr: Class I, Level of Evidence: C
- Fluid removal to reduce body weight by ≤1 to 1.5 kg/day in patients with congestion: Class I, Level of Evidence: C
Blood pressure
- Drip infusion of nitroglycerin and calcium channel blockers (e.g., nicardipine) for the treatment of significant hypertension: Class IIa, Level
of Evidence: C
Heart rate
- Rate control (using digitalis or other drugs) for the treatment of atrial fibrillation: Class I, Level of Evidence: C
- Aggressive rate control therapy for the treatment of sinus tachycardia (excluding severe cases): Class IIb, Level of Evidence: C
Arterial oxygen saturation
- Oxygen administration to ensure an oxygen saturation level of 95 to 98%: Consider CPAP, NPPV and endotracheal intubation for patients
with lower oxygen saturation after oxygen therapy: Class I, Level of Evidence: C
Table 20. Mental Support for Patients in the Early Stage of Acute Myocardial Infarction
(1) Allow the patient time to meet his/her family members from an early stage of treatment.
(2) Listen to the patient carefully.
(3) Explain the purposes and methods of examinations and procedures to alleviate the patient’s concern.
(4) Address the patient in a familiar way to encourage the patient to talk about his/her concern and questions.
(5) Ensure a sufficient amount of sleep.
(6) Allow the patient to get a change of pace to prevent excessive stress from bed rest or restriction of visits.
(7) Explain the examinations, treatment, and rehabilitation plans to help the patient to imagine his/her life in the future.
(8) Suspect the possibility of restlessness and CCU syndrome when uneasiness and insomnia continue, and take preventive measures.
rehospitalization through comprehensive patient education and after by a multidisciplinary team.24 Ambulatory cardiac reha-
disease management. bilitation that is performed as a part of the disease manage-
ment program after discharge is also effective in improving
(2) Physical/Exercise Therapy exercise capacity and QOL, and preventing rehospitalization.25
Patients with dyspnea at rest due to pulmonary congestion and
fever and patients in whom the IABP is inserted through the
groin need complete bed rest, and are not recommended to 4. Medical Therapy
participate in physical or exercise therapy. Patients without
symptoms at rest should undergo low-intensity physical/exer- Table 21 lists the recommended dosage regimens of intrave-
cise therapy. nous drugs used for the treatment of acute heart failure in Japan.
(3) Mental Support and Counseling 1. Sedation

Mental support during the early stage of acute heart failure is (1) Morphine Hydrochloride
important in alleviating emotional distress and improving QOL Blood pressure may decrease in patients with hypotension,
of patients during hospitalization. Table 20 summarizes the bradycardia, and/or advanced atrioventricular (AV) block.
procedures of mental support. Morphine hydrochloride should not be administered to patients
with intracerebral hemorrhage, decreased consciousness, bron-
(4) Patient Education and Disease Management chial asthma, or chronic obstructive pulmonary disease (COPD),
Comprehensive patient education on how to manage heart fail- in principle. Morphine hydrochloride may worsen the progno-
ure and prevent rehospitalization should be initiated early dur- sis in patients complicated with unstable angina. Because mor-
ing the hospital visit. phine hydrochloride may cause respiratory arrest, a bag valve
It is effective for patients with acute heart failure at high mask or other equipment suitable for non-breathing patients
risk of rehospitalization to receive a “disease management should be ready for use (Class IIb, Level of Evidence: B)
program” that is initiated before discharge and continued there- (Table 18).

Table 21. Intravenous Drugs Used for the Treatment of Acute Heart Failure in Japan
Drugs Dosage regimens
Morphine An ampule of 5 to 10 mg is diluted, and 2 to 5 mg is administered intravenously over 3 minutes.
Furosemide The dose of an intravenous infusion is 20 to 120 mg, and the dose of continuous infusion is around 2 to 5 mg/hr.
Digoxin A dose of 0.125 to 0.25 mg is administered slowly. The effective blood concentration is 0.5 to 1.0 ng/mL. The patient
should be carefully observed for toxicity.
Dopamine The dose ranges between 0.5 and 20 μg/kg/min. It increases renal blood flow at ≤5 μg/kg/min, exerts positive inotropic
action at 2 to 5 μg/kg/min, and constricts blood vessels and increases blood pressure at ≥5 μg/kg/min.
Dobutamine The dose ranges between 0.5 and 20 μg/kg/min. It dilates peripheral blood vessels and decreases pulmonary capil-
lary pressure at ≤5 μg/kg/min.
Norepinephrine The dose ranges between 0.03 to 0.3 μg/kg/min.
Milrinone It is given as a bolus injection at 50 μg/kg followed by continuous infusion at 0.1 to 0.75 μg/kg/min. Treatment is
started with continuous infusion in many cases.
Olprinone It is given as a bolus injection at 10 μg/kg followed by continuous infusion at 0.1 to 0.3 μg/kg/min. Treatment is started
with continuous infusion in many cases.
Colforsin daropate Treatment is started at 0.1 to 0.25 μg/kg/min, which is adjusted according to hemodynamics and heart rate. Care
should be taken because it may increase heart rate.
Nitroglycerin It is infused continuously at 0.5 to 10 μg/kg/min. Care should be taken because it may cause vascular resistance.
Isosorbide dinitrate It is given at 1 to 8 mg/hr, 0.5 to 3.3 μg/kg/min. Care should be taken because it may cause vascular resistance.
Nicorandil It is infused continuously at 0.05 to 0.2 mg/kg/hr.
Nitroprusside Continuous infusion is started at 0.5 μg/kg/min, and adjusted according to the hemodynamics (0.5 to 3 μg/kg/min).
Carperitide Continuous infusion is started at 0.025 μg/kg/min (in some cases at 0.0125 μg/kg/min), and adjusted according to the
hemodynamics (up to 0.2 μg/kg/min). The most commonly used dose is between 0.05 and 0.1 μg/kg/min.
Table 22. Diuretic Treatment in Patients With Acute Heart Failure

Class I
- Furosemide (intravenous injection or oral administration) for patients with pulmonary congestion or edema associated with acute heart
failure (Level of Evidence: B)
- Spironolactone (oral administration) for patients with severe chronic heart failure (NYHA functional Class III or IV) (Level of Evidence: B)
Class IIa
- Intravenous carperitide (Level of Evidence: B)
- Torasemide during transition from acute heart failure to chronic phase management (Level of Evidence: B)
- Continuous infusion of furosemide in patients not responding to repeated bolus intravenous furosemide (Level of Evidence: B)
Class IIb
- Multiple diuretics for patients in whom the effect of furosemide is reduced (concomitant use of loop diuretics and thiazides, or spironolac-
tone) (Level of Evidence: C)
- Intravenous carperitide for patients with renal dysfunction (Level of Evidence: B)
Class III
- Antialdosterones for patients with renal dysfunction or hyperkalemia (Level of Evidence: C)
2. Diuretics treatment of acute heart failure associated with ischemic heart

Table 22 lists recommendations on diuretic treatment for pa- disease.
tients with acute heart failure.
(3) Carperitide
3. Vasodilators In prospective surveillance in the clinical setting in Japan,
(1) Nitrates carperitide is often given at a dose of 0.05 to 0.1 μg/kg/min
The previous JCS guidelines3 and the current American Col- (maximum recommended dose: 0.2 μg/kg/min),28 and is a
lege of Cardiology (ACC)/AHA guidelines26 have described known, highly effective in the treatment for patients with de-
that sublingual tablets, nasal sprays, and intravenous injections compensated heart failure caused by cardiomyopathy, hyper-
of nitroglycerin and isosorbide dinitrate (ISDN) are effective tensive heart disease, or valvular heart disease (Class IIa,
in the treatment of pulmonary congestion in patients with acute Level of Evidence: B) (Table 15). Ultra-low doses of carper-
heart failure or acute decompensated heart failure (Class I, itide (0.0125 to 0.025 μg/kg/min) do not always impair renal
Level of Evidence: B) (Tables 15 and 18). function.
(2) Nicorandil (4) Phosphodiesterase Inhibitors

It has been reported that repeated bolus intravenous adminis- Phosphodiesterase (PDE) inhibitors selectively inhibit PDEs
tration of nicorandil prior to reperfusion therapy for AMI may involved in the decomposition of cyclic adenosine monophos-
improve coronary microcirculation and attenuate reperfusion phate (cAMP), to increase the level of cAMP in the myocar-
injury.27 Nicorandil is thus expected to be effective in the dium and vascular smooth muscle cells without affecting β

Table 23. ACE inhibitors, ARBs, Antialdosterones, and Carperitide as Myocardial Protective Agents
ACE inhibitors and ARBs
- In patients with stabilized acute heart failure, start ACE inhibitors and ARBs from a small dose, and increase the dose gradually (Class I,
Level of Evidence: A)
- In the acute phase, use ACE inhibitors and ARBs appropriately according to the type and severity of heart failure (Class IIa, Level of
Evidence: B)
- In patients with severely unstable hemodynamics, avoid ACE inhibitors and ARBs (Class IIb, Level of Evidence: C)
Antialdosterones (Class I, Level of Evidence: A)
Carperitide (Class IIa, Level of Evidence: B)
receptors, and thereby increase the myocardial contractility (2) Digitalis

and exert a vasodilating effect (see Section 4.4 of Chapter III). In patients with acute heart failure, digitalis is indicated for the
treatment of heart failure induced by tachycardias such as atrial
(5) ACE Inhibitors and Angiotensin II Receptor Blockers fibrillation (Tables 19 and 39). Treatment with digitalis is not
In the treatment of chronic heart failure, ACE inhibitors have recommended for patients with acute heart failure due to AMI
been established as a first-line therapy for patients ranging or myocarditis. Digitalis is contraindicated for patients with
from asymptomatic heart failure to symptomatic, severe heart bradycardia, second or third degree AV block, sick sinus syn-
failure. Because patients with acute heart failure may often drome, Wolff-Parkinson-White (WPW) syndrome, hypertro-
have an increase in circulating blood volume, but not all pa- phic obstructive cardiomyopathy, hypokalemia, or hypercal-
tients have excessive fluid retention as is often observed in cemia.
patients with chronic heart failure, physicians should carefully
observe for hypotension due to adverse drug reactions to these (3) PDE Inhibitors
drugs when they are given to patients with acute heart failure PDE inhibitors are effective even in patients not responding to
(Class IIa, Level of Evidence: C) (Table 23).29 catecholamines because they exert their effects without affect-
ing β receptors; possess both vasodilator and positive inotro-
4. Inotropes pic effects and are associated with a smaller increase in myo-
Inotropes are effective in improving hemodynamics and clin- cardial oxygen consumption as compared with catecholamines;
ical findings for a short period of time, but may negatively and are less prone to induce resistance to nitrates. PDE in-
affect long-term prognosis by causing arrhythmias, myocar- hibitors exert their actions promptly after the initiation of in-
dial ischemia, or myocardial injury. Physicians should care- travenous administration and improve hemodynamics in a
fully select inotropes and use them at an appropriate dose and nearly dose related manner (for non-ischemic heart failure,
duration. Class IIa, Level of Evidence: A; for ischemic heart failure,
Class IIb, Level of Evidence: A)30 (Tables 15 and 40).
(1) Catecholamine Inotropes In patients who are receiving β-blockers for the treatment
1) Dobutamine of the acute decompensated heart failure, dopamine and dobu-
Dobutamine at a dose of 10 μg/kg/min or lower does not in- tamine do not exert inotropic effects because β receptors are
crease heart rate or myocardial oxygen consumption substan- blocked, while PDE inhibitors and adenylate cyclase activa-
tially, and may be readily used for patients with ischemic heart tors such as colforsin daropate (for non-ischemic heart failure,
disease. However, dobutamine should be given with dopamine Class IIa, Level of Evidence: C; for ischemic heart failure,
or norepinephrine to patients in whom dobutamine mono- Class IIb, Level of Evidence: C) favorably increase cardiac
therapy cannot maintain blood pressure or ensure adequate output and decrease pulmonary capillary pressure31 (Tables 15
diuresis. and 40).
2) Dopamine (4) Adenylate Cyclase Activators (Colforsin Daropate)

Dopamine at a dose of 2 μg/kg/min or lower induces diuresis Adenylate cyclase activators are inotropes available only in
by dilating renal arteries to increase the glomerular filtration Japan. These drugs act as inodilators as PDE inhibitors do.
rate and directly affects renal tubules. At a dose of 2 to 10 μg/ However, adenylate cyclase activators have slower onset of
kg/min, it exerts positive inotropic action, increases heart rate action and induce a larger increase in heart rate as compared
and constricts blood vessels. At a dose of 10 to 20 μg/kg/min, with PDE inhibitors. Physicians should carefully observe for
it increases vascular resistance. proarrhythmic adverse reactions during treatment. It has been
suggested that the co-administration of PDE inhibitors and
3) Norepinephrine low-dose adenylate cyclase activators is effective in the treat-
Norepinephrine is administered to patients with cardiogenic ment of acute heart failure. (for non-ischemic heart failure,
shock that do not respond to other inotropes or restoration of Class IIa, Level of Evidence: C; for ischemic heart failure,
circulating blood volume. Because it increases mean arterial Class IIb, Level of Evidence: C) (Tables 15 and 40)
blood pressure by increasing peripheral vascular resistance, it
increases myocardial oxygen consumption but decreases blood (5) Calcium Sensitizers (Pimobendan, Levosimendan
flow in the kidney, brain, and other organs. Monotherapy with [Not Approved in Japan])
norepinephrine as an inotropes should be avoided. However, In the LIDO (Levosimendan Infusion versus Dobutamine) trial
norepinephrine is required for patients complicated with septic where patients with low output heart failure received levosi-
shock. mendan or dobutamine, levosimendan improved hemodynam-
ics better than dobutamine with less mortality rate.32 In the

Table 24. The Effects of Antiarrhythmic Drugs on Cardiac Function: Classification of Drugs Proposed by the Members of Sicilian
Gambit
Ion channels Receptors Pumps Clinical efficacy ECG findings
Drug Na Na-K LV Sinus Extra-
Ca K If α β M2 A1 PR QRS JT
Fast Med Slow ATPase function rhythm cardiac
Lidocaine ○ → → ● ↓
Mexiletine ○ → → ● ↓
Procainamide A ● ↓ → ● ↑ ↑ ↑
Disopyramide A ● ○ ↓ → ● ↑↓ ↑ ↑
Quinidine A ● ○ ○ → ↑ ● ↑↓ ↑ ↑
Propafenone A ● ↓ ↓ ○ ↑ ↑
Aprindine I ○ ○ ○ → → ● ↑ ↑ →
Cibenzoline A ○ ● ○ ↓ → ○ ↑ ↑ →
Pirmenol A ● ○ ↓ ↑ ○ ↑ ↑ ↑→
Flecainide A ○ ↓ → ○ ↑ ↑
Pilsicainide A ↓ → ○ ↑ ↑
Bepridil ○ ● ● ? → ○ ↑
Verapamil ○ ● ● ↓ ↓ ○ ↑
Diltiazem ● ↓ ↓ ○ ↑
Sotalol ● ● ↓ ↓ ○ ↑ ↑
Amiodarone ○ ○ ● ● ● → ↓ ● ↑ ↑
Nifekalant ● → → ○ ↑
Nadolol ● ↓ ↓ ○ ↑
Propranolol ○ ● ↓ ↓ ○ ↑
Atropine ● → ↑ ● ↓
ATP ■ ? ↓ ○ ↑
Digoxin ■ ● ↑ ↓ ● ↑ ↓
Relative intensity of blockage: ○ = low; ● = moderate; and ● = strong.
A = activated channel blocker, I = inactivated channel blocker, ■ = agonist.
ATP, adenosine triphosphate.
Modified from Members of the Sicilian Gambit, Antiarrhythmic therapy: a pathophysiologic approach. New York: Futura Publishing Company,
Inc; 1994.
RUSSLAN (Randomized Study on Safety and Effectiveness (2) In patients with pulmonary congestion and a systolic blood
of Levosimendan in Patients with Left Ventricular Failure due pressure of less than 90 mmHg, treatment should be start-
to an Acute Myocardial Infarct) trial in patients with left ven- ed with dopamine 2 to 5 μg/kg/min. Although in most
tricular failure complicating AMI, patients receiving levosi- patients blood pressure often increases after the dose of
mendan experienced a lower risk of both death and exacerba- dopamine is increased up to 10 μg/kg/min, patients with
tion of heart failure than did patients receiving placebo.33 no increase in blood pressure after dopamine infusion at
However, in the SURVIVE (Survival of Patients with Acute 15 μg/kg/min should be treated with norepinephrine con-
Heart Failure in Need of Intravenous Inotropic Support) trial tinuous drip infusion at 0.03 to 0.3 μg/kg/min. In patients
in patients with acute decompensated heart failure, levosimen- with cardiogenic shock norepinephrine increases afterload
dan did not improve long-term prognosis as compared with on the heart with decreased contractility, and therefore
dobutamine.34 Further studies should be carried out. treatment with low-dose norepinephrine must be as short
as possible. Patients requiring a large dose of norepineph-
5. Vasopressors rine should start promptly mechanical circulatory support
(1) In patients with pulmonary congestion and a systolic blood such as IABP and PCPS to decrease the use of norepi-
pressure of 90 mmHg or more, inotropic vasodilators such nephrine.
as PDE inhibitors and adenylate cyclase activators should (3) In patients with pulmonary congestion and a systolic blood
be considered. When blood pressure decreases, the drugs pressure of less than 70 mmHg, a co-administration of do-
should be replaced by or used with dobutamine. Dobuta- pamine and norepinephrine should be considered. Recent
mine drip infusion should be initiated at a dose of 2 to reports have suggested a co-administration of dobutamine
5 μg/kg/min, and should be increased whenever necessary and norepinephrine is effective in the treatment of multi-
up to 10 μg/kg/min. Even when the restoration of blood ple organ failure. Mechanical circulatory support devices
pressure is insufficient, the drugs should be replaced by or such as IABP and PCPS should be used whenever neces-
used with dopamine. After blood pressure is stabilized, sary.
venous dilators such as nitroglycerin should be adminis-
tered concomitantly to patients with severe pulmonary con- 6. Myocardial Protective Agents
gestion. Patients with a timed urine volume of 1 mL/kg/hr Survival should be prioritized in the treatment of acute heart
or less should be additionally treated with diuretics. failure. When survival is ensured, treatment should be given

Figure 10. BLS algorithm in the 2010

AHA Guidelines for CPR and ECC.
AHA, American Heart Association;
CPR, cardiopulmonary resuscitation;
ECC, emergency cardiovascular care.
Cited from Circulation 2010; 122
(Suppl 3): S685 – S705,41 with permis-
sion from Wolters Kluwer Health.
to improve long-term prognosis and QOL. Considering the unless they have bradycardia, advanced AV block, broncho-
fact that the acute decompensated heart failure accounts for a spasm, cardiogenic shock, or other intractable conditions. In
considerable number of acute heart failures, physicians should the latter group of patients, physicians should consider dose
try to protect the myocardium during the acute phase to im- reduction or discontinuation of β-blockers (Class IIa, Level
prove long-term prognosis. of Evidence: B) (See Table 14). The long-term prognosis of
See Table 23 for the use of (1) ACE inhibitors and angio- patients with heart failure who discontinued β-blockers due to
tensin II receptor blockers (ARBs); (2) antialdosterones; and acute exacerbation is poor.37
(3) carperitide.
7. Antiarrhythmic Drugs
(4) β-Blockers Various types of arrhythmias may develop in patients with
Although treatment with β-blockers has long been initiated heart failure. Antiarrhythmic drugs should be carefully used
during the stable phase of chronic heart failure, physicians because many antiarrhythmic drugs possess negative inotropic
should try to start the treatment in an early stage of acute heart and proarrhythmic effects. Antiarrhythmic treatment in patients
failure.35 Patients with signs/symptoms of heart failure or left with heart failure should be limited to the minimum necessary.
ventricular dysfunction due to AMI should especially start Table 24 summarizes the effects of antiarrhythmic drugs on
treatment with β-blockers in an early stage at least prior to cardiac function.38,39 When antiarrhythmic drugs are used in
discharge. In patients hospitalized with acute heart failure who patients with heart failure, physicians should consider the neg-
were using ACE inhibitors or ARBs, β-blockers should be ative inotropic effects when selecting appropriate medication.
initiated prior to discharge, unless contraindicated (the ESC
Guidelines for the diagnosis and treatment of acute and chron-
ic heart failure 2008) (Class I, Level of Evidence: A)36 (See 5. Nonpharmacologic Treatment
Table 41).
In patients hospitalized with acute decompensated heart 1. Emergent Treatment and ACLS
failure who were receiving β-blockers, β-blockers should not (1) Patients With Cardiopulmonary Arrest
be discontinued and should be continued whenever possible, Patients with cardiopulmonary arrest should receive cardio-

Figure 11. ACLS cardiac arrest circular algorithm. ET, endotracheal; IO, intraosseous; IV, intravenous; P ETCO2, end-tidal carbon
dioxide tension; VF, ventricular fibrillation; VT, ventricular tachycardia. Cited from Circulation 2010; 122 (Suppl 3): S729 – S767,40
with permission from Wolters Kluwer Health.
pulmonary resuscitation (CPR) on the basis of ACLS accord- In patients who do not respond to NPPV and treatment of
ing to “the 2010 AHA Guidelines for Cardiopulmonary Re- pulmonary congestion (see Section 1 and 2 of Chapter III), and
suscitation and Emergency Cardiovascular Care”.40 The major show no improvement in respiratory condition and arterial
change in the 2010 AHA Guidelines is a change in the CPR blood gas, or patients who have a consciousness disorder, loss
sequence of steps from “A-B-C” (Airway-Breathing-Chest of cough reflex, or difficulty in expectoration, artificial respira-
compressions) to “C-A-B” (Chest compressions-Airway- tion under endotracheal intubation is indicated (Class I, Level
Breathing) (Figure 10).41 As Figure 11 shows, high-quality of Evidence: C) (Table 17). Table 25 summarizes the criteria
CPR should be continued to facilitate complete recovery and for weaning from PEEP and artificial respiration, and those for
ambulatory discharge.40 extubation.
2. Artificial Respiration 3. Types and Indications of Mechanical Circulatory

In patients with acute heart failure, oxygen administration Support Devices (IABP, PCPS, and VAS)
should be started with a nasal cannula or face mask at 2 to (1) Purpose and Strategies for Acute Decompensated
6 L/min (Table 16). In patients with a PaO2 of less than Heart Failure Treatment by the Use of Mechanical
80 mmHg (arterial oxygen saturation [SpO2] of less than 95%) Circulatory Support Devices
or an arterial partial pressure of carbon dioxide (PaCO2) of Mechanical circulatory support devices are indicated for pa-
50 mmHg or more, or patients in whom symptoms such as tients with heart failure who are refractory to medical thera-
tachypnea, forced respiration, and orthopnea are not improved py.42 Mechanical circulatory support devices include the IABP,
or are worsening, NPPV should be initiated promptly (see cardiopulmonary support devices (PCPS such as veno-arterial
Section 1 and 2 of Chapter III). [V-A] bypass and extracorporeal membrane oxygenation

Table 25. Indications of PEEP and Criteria for Discontinuation and Extubation

[Indications]
1. A PaO2 ≤60 mmHg during artificial respiration under endotracheal intubation with 50% oxygen.
2. NPPV with or without endotracheal intubation in patients with acute pulmonary edema.
3. Patients with high PCWP and respiratory failure despite treatment with drugs such as diuretics, vasodilators, and inotropes for acute
heart failure.
4. Prevention of pulmonary edema in patients requiring volume expansion for the treatment of low output syndrome.
[Criteria for discontinuation of PEEP]
1. A PaO2 ≥80 mmHg with PEEP 0 (ZEEP) and 50% oxygen.
2. Patients with decreased PCWP (<18 mmHg as a guide), and improved physical findings (e.g., rales and abnormal third heart sound
[gallop]) and chest X-ray.
[Criteria for extubation]
1. A tidal volume of ≥200 ml.
2. A PaO2 of ≥80 mmHg with ZEEP and 40% oxygen.
3. Patients who can receive NPPV such as CPAP after extubation.
PCWP, pulmonary capillary wedge pressure; ZEEP, zero end-expiratory pressure.
Table 26. Types and Characteristics of Mechanical Circulatory Support Devices

PCPS, V-A bypass,
IABP Extracorporeal VAS Implantable VAS
ECMO
Placement Percutaneous Percutaneous, surgical Surgical Surgical
Flow volume Increase CO by ≤40% 2.0 to 3.0 L/min 3 to 5 L/min Up to 10 L/min (depend on
type of device used)
Assisted ventricle Left heart Left heart/right heart Left heart/right heart Left heart
Pulmonary support No support Possible No support No support
Duration Days to weeks Days to weeks Months (years when the device Months to years
is replaced appropriately)
Place of use Only in hospital Only in hospital Only in hospital May be used after
discharge to home
ECMO, extracorporeal membrane oxygenation; V-A, veno-arterial.
[ECMO]), and VAS. Table 26 summarizes the characteristics and 12).

of these procedures. Short- and mid-term circulatory supports Enhanced external counterpulsation (EECP), a noninvasive
are indicated for patients who cannot be weaned off cardiopul- circulatory support device that is expected to function simi-
monary bypass; those with extensive myocardial infarction; larly to the IABP, has been developed and is being investi-
those with fulminant myocarditis with hemodynamic compro- gated in patients with heart failure.44
mise; and those with severe allograft rejection after heart trans-
plantation. Mechanical circulatory support is used as a bridge (ii) Contraindications
to recovery or to long-term device. Long-term mechanical IABP is contraindicated for patients with moderate or severe
circulatory support devices are used to bridge to transplanta- aortic valve insufficiency, those with thoracic or abdominal
tion in patients with intractable heart failure that meet the cri- aortic dissection, and those with aortic aneurysm. Careful con-
teria for heart transplantation (e.g., patients with dilated car- sideration is required to determine whether the IABP should
diomyopathy, dilated phase hypertrophic cardiomyopathy be used in patients with severe aortic atherosclerosis and those
[D-HCM], or ischemic cardiomyopathy). with arteriosclerosis obliterans of the lower extremities.
(2) Indications for Mechanical Circulatory Support (iii) Major Complications

Devices Major complications of the IABP include leg ischemia, hem-
1) IABP orrhage, balloon rupture, arterial injuries (including arterial
(i) Indications43 dissection), cholesterol embolization, spinal cord injury (spi-
The IABP is a simple circulatory support device that is used nal artery ischemia), and abdominal organ ischemia (intestinal
in patients with acute heart failure not responding well to ischemia).
medical therapy or those with cardiogenic shock (Class I,
Level of Evidence: B) (Table 16). The IABP is also useful in 2) PCPS (V-A Bypass, ECMO)
preventing infarct expansion in patients with acute coronary PCPS is a method of cardiopulmonary support using a closed-
syndrome, alleviating anginal pain, preventing impending in- circuit cardiopulmonary bypass system that contains a cen-
farction, and treating severe arrhythmias due to ischemia or trifugal pump and an extracorporeal membrane oxygenator
low output syndrome (Class IIa, Level of Evidence: B) (ECMO). Using the centrifugal pump, blood is taken via a
(Figures 9 and 12). It has been reported that prophylactic use cannula inserted into the right atrium through the femoral vein,
of IABP is beneficial in high-risk patients undergoing coronary oxygenized with ECMO, and returned into the femoral artery.
revascularization (Class IIa, Level of Evidence: B) (Figures 9 Children and patients whose femoral artery and vein are not

Figure 12. Indications of mechanical circulatory support devices and treatment strategies in patients with acute heart failure.
percutaneously accessible should undergo open chest surgery while on the waiting list; and (3) the risks of surgery.45–47 For
to cannulate the right atrium and ascending aorta directly (V-A patients who have been repeatedly hospitalized and are resis-
bypass). V-A bypass is commonly maintained for about 1 week, tant to medical therapy, physicians should be attuned to the
but can be used continuously for several weeks. V-A bypass appropriateness and optimal timing of VAS support. The
may also be performed as a respiratory support (ECMO). 6-month survival rate of patients who are inotrope-dependent
is less than 50%. Such patients should be referred to institu-
(i) Indications tions where VAS surgery can be performed in order to ensure
PCPS is indicated for patients requiring cardiopulmonary re- timely and successful intervention.48,49 Social workers and
suscitation for cardiopulmonary arrest or cardiogenic shock psychiatrists should also be consulted to discuss the social and
(Class I, Level of Evidence: B) (Tables 16 and 18); those psychological issues for patients indicated for VAS.
with intractable heart failure requiring respiratory and circula-
tory support (Class IIa, Level of Evidence: C) (Tables 17 [Extracorporeal Ventricular Assist System]
and 26), low output syndrome after open heart surgery (Class Extracorporeal VAS uses diaphragm-type pulsatile pneumatic
IIa, Level of Evidence: C) (Figure 9), drug-resistant intrac- pumps and can provide biventricular support. Extracorporeal
table arrhythmias and severe respiratory failure. VAS can be used in patients of small body size. The inflow
cannula may be placed in either the left atrium or left ventri-
(ii) Contraindications cle, and blood is returned to the ascending aorta through the
Patients with severe arteriosclerosis obliterans, moderate or outflow cannula.
severe aortic regurgitation, bleeding diathesis, recent cerebro-
vascular accident or head injury and drug-resistant sepsis are (i) Indications
considered to be relative contraindications for PCPS. Extracorporeal VAS placement is indicated for patients who
are expected to have enough recovery of their own ventricular
(iii) Complications function to be eligible for weaning from mechanical support
Complications of PCPS include hemorrhage from the access within several months, and for patients who require biven-
sites for outflow and inflow cannulae, vascular damage, lower tricular support. Extracorporeal ventricular support is also in-
limb thrombosis or ischemia, retroperitoneal hematoma, neu- dicated for patients whose body size is too small for intratho-
rological complications, infections, and pulmonary disorders. racic VAD placement and for whom the surgery will be
performed for the purpose of bridging to transplantation.
3) Ventricular Assist System
VAS is indicated for patients with low output syndrome that (ii) Contraindications
is refractory to maximal medical therapy and short-term me- Extracorporeal VAS placement is contraindicated for (1) pa-
chanical circulatory supports such as IABP and PCPS, in whom tients with multiple organ failure who are not expected to re-
the major organs and peripheral tissues are not sufficiently cover despite maximal medical therapy; (2) patients with can-
oxygenated (Class IIa, Level of Evidence: B) (Tables 16 and cer or other malignant diseases with poor prognoses; (3)
18).42 In patients indicated for heart transplantation, VAS patients with central nervous system disorders with poor prog-
should be introduced at the appropriate timing considering (1) noses (including those with cerebral infarction or cerebral
the expected waiting time for transplant; (2) the mortality risk hemorrhage); and (4) patients with intractable serious infec-

Table 27. Management With Pacing (Cardiac Resynchronization Therapy and Other Types of Pacing)
Class I
- Temporary emergent pacing should be performed promptly in patients with bradycardia causing compromised hemodynamics or transient
cerebral ischemia who do not respond to atropine. (Level of Evidence: C)
Class IIb
- There are no established indications of cardiac resynchronization therapy during the very acute phase of heart failure. (Level of Evidence: C)
(ii) Contraindications
Table 28. Indications of Hemofiltration Methods for Patients
With Acute Heart Failure Contraindications for implantable VAS are similar to those for
Class IIa
extracorporeal VAS. In addition, patients who will not be able
to manage their devices at home and who are not expected to
1) Hemofiltration
be socially rehabilitated are also contraindicated for implant-
a) Extracorporeal ultrafiltration method, Level of Evidence: B
able VAS surgery.
b) Continuous veno-venous hemofiltration, Level of Evidence:
B
(iii) Complications
Only for patients with volume overload and stable hemo-
dynamics.
In addition to complications commonly observed with the use
of extracorporeal VAS, the implantable VAS may be more
Class IIb
frequently associated with anorexia and gastrointestinal per-
2) Hemodialysis
foration due to gastrointestinal compression by the implanted
a) Hemodialysis, Level of Evidence: B device. Other complications include gastrointestinal hemor-
b) Peritoneal dialysis, Level of Evidence: B rhage due to degradation of von Willebrand factor, and aortic
3) Hemodiafiltration valve insufficiency.
a) Continuous hemodiafiltration, Level of Evidence: C
4. Management With Pacing (Cardiac Resynchronization
Therapy and Other Types of Pacing)
See Table 27.
tions, severe respiratory failure, or a bleeding diathesis. Extra-
corporeal VAS is not recommended for patients with moder- 5. Acute Hemofiltration
ate or severe aortic valve insufficiency, or patients with severe For those patients with acute heart failure and acute decom-
calcification of the ascending aorta. pensated heart failure, hepatic congestion and edema may de-
velop in association with pulmonary congestion and excessive
(iii) Complications fluid retention. During the acute phase treatment, excessive
Physicians should carefully observe patients for complications water should be quickly removed from the body. Patients with
of extracorporeal VAS including hemorrhage; infections (e.g., renal dysfunction in whom diuresis cannot be achieved require
at cannula insertion areas or pump pocket, and/or sepsis); cra- acute hemofiltration (Table 28).
nial nerve disorder (e.g., cerebral infarction or hemorrhage);
arrhythmias; pericardial effusion (including tamponade); de- 6. Indications and Methods of Surgical Treatment in
vice malfunction; right heart failure; hemolysis; hepatic, renal, Patients With Acute Heart Failure (Cardiac
pulmonary, and multiple organ failure; and device-related em- Tamponade and Acute Valvular Disease)
bolisms including myocardial infarction. Patient may also ex- (1) Cardiac Tamponade
perience mood change such as adjustment disorder or depres- Cardiac tamponade is a condition caused by the accumulation
sion. of fluid in the pericardial space, resulting in decreased venous
return during the diastolic phase that reduces ventricular fill-
[Implantable Ventricular Assist System] ing. It causes a decrease in cardiac output and venous conges-
Currently available implantable VAS are continuous flow tion, and patients often show a rapid deterioration and develop
pumps (centrifugal or axial pumps), and are used for assisting cardiogenic shock within minutes from the onset of acute
only the left ventricle. In both types of continuous flow pumps, cardiac tamponade.
the inflow cannula is placed at the apex of the left ventricle, When cardiac tamponade with overt hemodynamic com-
and the outflow cannula is placed at the ascending aorta. promise requires urgent removal of pericardial fluid, echocar-
diography-guided pericardiocentesis is conducted. In patients
(i) Indications with unsuccessful pericardiocentesis or recurrence of hemor-
Implantable VAS is used as a bridge to transplant for patients rhagic cardiac tamponade, surgical drainage by pericardioto-
with intractable heart failure who have low output syndrome my through a subxiphoid approach or open chest surgery should
that is refractory to maximal medical therapy or short-term be performed. Cardiac tamponade occurring immediately after
mechanical circulatory support such as an IABP and in whom cardiac surgery, caused by aortic dissection, post-infarction
short-term devices are not adequate enough to support periph- heart rupture, or trauma requires emergent surgical correction.
eral circulation. Patients must be able to self-manage the de-
vice at home for a long period of time and are expected to be (2) Acute Valvular Heart Disease
socially rehabilitated. Patients are also required to understand Acute valvular heart disease may occur in any of the four valves
the limitations and complications associated with VAS place- of the heart, but left heart valvular disease is the most common
ment and must have adequate family and social support. and requires urgent surgical treatment. Figure 13 shows a
treatment algorithm for acute valvular heart disease.50–53

Figure 13. Treatment strategies for acute valvular heart disease. TEE, transesophageal echocardiography. Adapted from Circu-
lation 2009; 199: 3232 – 3241,53 with permission from Wolters Kluwer Health.
7. Treatment of Mechanical Complications Associated of the medical team to obtain vital signs, physical findings,
With Acute Myocardial Infarction (Left Ventricular and laboratory data that are necessary to establish treatment
Free Wall Rupture, Ventricular Septal Perforation, strategies and goals of treatment according to the clinical
and Papillary Muscle Dysfunction) scenario (Table 9) and the Nohria-Stevenson classification
Mechanical complications associated with AMI are caused by (Figure 1). These findings should guide selection of the ap-
destruction of the fragile myocardium during the early stage propriate treatment for each individual patient.20,57,58 Nurses
of AMI, resulting in left ventricular free wall rupture, ven- should also try to alleviate symptoms, keep the patient in the
tricular septal perforation, or mitral regurgitation due to papil- Fowler position to reduce the cardiac load, and observe the
lary muscle dysfunction, depending on the lesion and size of patient continuously for cardiac hemodynamics and signs/
the infarction. These conditions may lead to cardiogenic shock, symptoms during the treatment (Table 13).
and require emergent surgery (Class I, Level of Evidence: C)
(Figure 14).54,55 2. Nursing of Patients Under Respiratory Management
and/or Mechanical Circulatory Support
Respiratory management in patients with acute heart failure
6. Nursing includes oxygen administration using a nasal cannula or an
oxygen mask with reservoir bag, NPPV, and artificial respira-
1. Nursing in the Initial Assessment of Acute Heart Failure tion with endotracheal intubation. While the patient is receiv-
In the initial assessment of acute heart failure, physicians must ing oxygen administration, nurses should observe the patient’s
establish an appropriate treatment strategy and goals of treat- general conditions including respiration, and should monitor
ment without delay. A prolonged duration from the onset of the SpO2 (oxygenation index) continuously to confirm wheth-
acute heart failure to the initiation of vasoactive drugs will er SpO2 is being maintained at 95% or more. Prompt introduc-
worsen the prognosis.56 Nurses should cooperate as members tion of NPPV is recommended for patients with severe venti-

Figure 14. Guidelines for treatment of acute heart failure due to acute coronary syndrome. PCI, percutaneous coronary interven-
tion; LVAS, left ventricular assist system.
lation disorder. Patient cooperation is essential for successful PCPS are bedridden and are thus prone to pulmonary throm-
implementation of NPPV. Patients and families should be suf- boembolism, bedsores, and pulmonary disorders, preventive
ficiently informed about NPPV, and appropriate care such as measures for these complications are necessary.62 Patients using
eliminating discomfort with the mask should be given. While VAS require postoperative management after implantation, as
the patient is receiving NPPV, the respiratory condition, fitting well as observation for the functioning of the device and pres-
of the mask, and presence/absence of air leakage should be ence/absence of hemorrhage and thromboembolism, and in-
checked. While the patient is receiving artificial respiration, fection control. Because patients using VAS are prone to de-
tidal volume, respiratory minute volume, airway pressure, re- pression, anxiety, feelings of irritation, and fear of death, a
spiratory rate, respiratory sounds, SpO2 percentage, end-tidal team of cardiologists, nurses, psychiatrists, clinical psycho-
carbon dioxide concentration (ETCO2), and the presence/ab- therapists, and psychiatric liaison nurses should offer mental
sence of patient-ventilator dyssynchrony should be checked. support.63 Family members of patients using VAS need practi-
It is also important to prevent the development of atelectasis cal support to reduce the burden of patient care as well as
and ventilation-associated pneumonia (VAP). Frequent pos- mental support.
tural changes, oral care, regular changing of ventilator circuits, Patients who require sedation to stabilize their condition
subglottic aspiration, and observation of the VAP bundle are should be evaluated regularly using appropriate criteria such
effective in the prevention of these complications.59–61 as the Richmond Agitation Sedation Scale (RASS), and ob-
In patients with mechanical circulatory support, nurses should served for neurological findings such as convulsion and pupil
cooperate with physicians and clinical engineers to maintain signs.64
stable hemodynamics, ensure safe use of the devices, and
continuously check the blood pressure, water balance, level of 3. Patient Education During the Early Stage of Acute Heart
consciousness, presence/absence of ventricular arrhythmias, Failure
and peripheral circulation state. In patients undergoing IABP, Prevention of the exacerbation of heart failure is essential to
nurses should check the position of the balloon catheter and improve the prognosis and QOL, and reduce excessive medi-
the functioning of the IABP, and also check for hemorrhage at cal costs.65 The most common precipitating factors of heart
the insertion site and the presence/absence of hematoma. Pa- failure include insufficient control of the salt and water bal-
tients with PCPS should be observed for limb ischemia, pe- ance, poor adherence to medical therapy, and insufficient re-
ripheral nerve disorder, and thromboembolism, receive ap- striction of activity, all of which are preventable.66
propriate infection control, and be maintained with appropriate Comprehensive patient education is important to prevent
sedation and analgesia. Because patients receiving an IABP or rehospitalization. Appropriate pre-discharge patient education

Table 29. Education and Counseling for Patients With Heart Table 30. Risk Factors for Developing Delirium
Failure and Their Family Members and Caregivers
1. Precipitating factors
1. General topics CNS disorders
Explanation of pathophysiology of heart failure e.g., cerebrovascular disorders, brain tumor, brain injuries,
and encephalomeningitis
Physical changes (signs and symptoms)
Non-CNS disorders
Psychological responses
Hemodynamic disorders (hypotension, low output syndrome,
Prognosis and heart failure)
2. Monitoring and management of symptoms Respiratory disorders (e.g., hypopnea, apnea, and pulmo-
Symptoms of exacerbation of heart failure nary infarction)
Daily self-monitoring of body weight Infections
Measures to be taken when symptoms are getting worse Metabolic disorders (e.g., hyperglycemia/hypoglycemia, dehy-
Measures to treat psychological symptoms dration, renal/hepatic failure, and electrolyte abnormality)
3. Diet therapy Endocrine disorders (e.g., thyroid disorders, parathyroid disor-
ders, and adrenal disorders)
Restriction of salt and water
Collagen disease
Restriction of alcohol
Surgical invasion
Adherence strategies
Addictive and abused substances
4. Medical therapy
e.g., alcohol, cocaine, psychostimulants, and benzodiaze-
Nature of each drug, dosing, and side effects pines
Concomitant drugs Drugs
How to manage complex medical therapy Steroids, anticholinergics, antihistamines, anesthetics, H2
Cost issues blockers, digitalis, lidocaine, β-blockers, antiparkinson drugs,
Adherence strategies lithium, and morphine
5. Activities and exercise 2. Predisposing factors
Work and leisure activities Advanced age
Exercise therapy Male sex
Sexual activities Cerebrovascular disorders (chronic phase)
Adherence strategies Alzheimer’s disease, and other factors
6. Risk factor modification 3. Facilitating factors
Smoking cessation Change of environment due to hospitalization
Body weight control for obese patients Excessive stimuli experienced in ICU/CCU
Management of dyslipidemia, diabetes, and hypertension Sleep disturbing factors
Noises and inappropriate lightning
Source: Moser DK, Riegel B. Management of heart failure in the
outpatients setting. In: Mann DL, editor. Heart failure: A compari- Mental stress
son to Braunwald’s heart disease. Philadelphia: Saunders, 2004: Physical stress
772.
e.g., pain, itching, pollakiuria
Sensory deprivation
e.g., absence of eyeglass or hearing aid, and eye surgery
by nurses improves the prognosis of heart failure.67
Nurses Restrained condition
should provide patient education repeatedly from the early Adapted from Japanese Journal of Nursing Techniques 2011;
phase of hospitalization to immediately before discharge to 57(Suppl): 9 – 16.79
facilitate early discharge and prevent recurrence68–70 (Table 29).
Patient support using disease management programs by a mul-
tidisciplinary team consisting of physicians, nurses, pharma-
cists, physiotherapists, dietitians, and clinical psychotherapists prognosis as well as significant mental stress due to having a
is effective.24 Especially in elderly patients with heart failure, life-threatening illness and receiving advanced mechanical
a patient’s ability to perform self-care behavior should be as- support. Nurses should closely communicate with patients and
sessed71 to build appropriate self-care methods that fit the liv- their family members to alleviate their anxiety.
ing environment of individual patients from the early phase of Delirium develops in about 30% of elderly patients hospi-
hospitalization, and patients and family members should be talized for an acute exacerbation of heart failure.76,77 Delirium
educated repeatedly until the time of discharge. makes the treatment difficult, prolongs hospitalization, and in-
creases mortality rate.78 Prevention of delirium is important to
4. Mental and Psychological Support ensure the smooth progress of treatment of acute heart failure.
Depression is common among patients hospitalized for acute Factors involved in the development of delirium include pre-
heart failure or an acute decompensated heart failure.72,73 De- cipitating factors, predisposing factors, and facilitating factors
pression and anxiety worsen the QOL and the long-term prog- (Table 30).79 Effective measures to prevent delirium include
nosis of heart failure.74,75 Patients should undergo screening close communication between the patient, family members,
and mental disorders should be appropriately treated and man- and medical staff members; support to ensure the patient has
aged by a team of psychiatrists, psychosomatic physicians, sufficient sleep at night; early ambulation; avoidance of un-
clinical psychotherapists, and psychiatric liaison nurses. Pa- necessary physical restriction; treatment of dehydration; ap-
tients receiving intensive care and those using VAS and their propriate vision and hearing support in elderly patients; ap-
family members may have anxiety about their disease and its propriate sensory stimulation using music; early introduction

Table 31. Recommended Requirements for Medical Service and Equipment

Medical service
Class I
- 24-hour emergency service by cardiologists (Level of Evidence: C)
Class II
- Availability of intensive treatment of patients with severe cardiovascular disorders (e.g., CCU, HCU, and ICU) (Level of Evidence: C)
- 24-hour emergency service by cardiac surgeons (emergent surgery) and nephrologists (dialysis and ultrafiltration) (Level of Evidence: C)
- Education of nurses specialized in the treatment of cardiovascular disorders (Level of Evidence: C)
In-hospital examinations
Class I
[Items that should be available 24 hours a day]
- Blood chemistry, arterial blood gas analysis, and chest X-ray (Level of Evidence: C)
- ECG, echocardiography, and angiography (Level of Evidence: C)
Class II
[Special examination items additionally required to determine treatment strategies of sub-acute phase of hospitalization]
- Holter ECG, cardiac electrophysiological study, cardiac radionuclide imaging, X-ray, CT, and CMR (Level of Evidence: C)
Special devices
Class I
- ECG, blood pressure and arterial oxygen saturation monitors (Level of Evidence: C)
- Swan-Ganz catheterization to determine and monitor cardiac output (Level of Evidence: C)
- Artificial respiration devices (Level of Evidence: C)
- External pacemakers (Level of Evidence: C)
- Dialysis and ultrafiltration devices (Level of Evidence: C)
- Intraaortic balloon pumping (Level of Evidence: C)
- Percutaneous cardiopulmonary bypass assist devices (Level of Evidence: C)
- Ventricular assist system (Level of Evidence: C)
CMR, cardiac magnetic resonance; CT, computed tomography; HCU, high care unit.
of self-care activities; and maintaining temporal orientation the patient from the acute to chronic phase of heart failure,
using clocks and calenders.80,81 Patients with delirium should multidisciplinary team of healthcare professionals should pro-
be assessed objectively,82–85 and receive appropriate medical vide a discharge plan and patient education to facilitate early
therapy under the direction of a physician. discharge and prevent recurrence.70,81
5. Multidisciplinary Approaches to the Management of

Acute Heart Failure
7. Recommended Requirements for
In the initial assessment of acute heart failure, physicians, nurs- Medical Practice and Equipment
es, and emergency response personnel should cooperate to
collect and evaluate the data necessary for the prompt and Medical institutions treating patients with acute decompen-
appropriate assessment of the patient’s clinical condition. Dur- sated heart failure should assess their conformity to the recom-
ing intensive care, a multidisciplinary approach involving phy- mended requirements listed in Table 31. Although these re-
sicians, nurses, specialized nurses, certified nurses, clinical en- quirements are established as the goals for medical institutions
gineers, clinical laboratory technicians, pharmacists, clinical treating acute decompensated heart failure, these have not
psychotherapists, certified artificial heart technicians, and cer- been validated using statistical procedures. There are regional
tified respiratory therapists should be taken to stabilize hemo- and institutional differences in the conformity to these require-
dynamics and respiration to ensure patient survival and im- ments. Each medical institution should provide appropriate
prove the general medical condition by maintaining medical care according to the level of available medical treatment, and
devices safely and appropriately, supporting the activities of build relationships with local clinics to facilitate a smooth
daily living, and providing mental support. In the transition of transition from before to after discharge.
IV Treatment Strategies for Heart Failure by Cause

2. Ischemic Cardiomyopathy
1. Ischemic Heart Disease Patients with acute exacerbation of ischemic cardiomyopathy
should be treated similarly to those who have acute decompen-
1. Acute Myocardial Infarction sated heart failure. However, the progression of coronary le-
Figure 14 summarizes guidelines for the treatment of acute sions may be involved in the acute decompensated heart fail-
heart failure due to AMI.86 ure due to previous myocardial infarction. In such patients,
physicians should consider revascularization as in the case of

Table 32. Drugs for the Treatment of Hypertensive Urgency

Class I
- The use of nitroglycerine, calcium channel blockers (e.g., nicardipine), carperitide, ACE inhibitors, and ARBs for the treatment of hyperten-
sive urgency associated with pulmonary edema (Level of Evidence: C)
Class III
- Sublingual nifedipine for the treatment of hypertensive urgency (Level of Evidence: C)
Table 33. Treatment of Acute Heart Failure Due to Fulminant Myocarditis

Class I
- IABP, PCPS, external pacemaker, and LVAS (Level of Evidence: C)
Class IIa
- Catecholamines, and PDE III inhibitors (Level of Evidence: C)
- Steroids for the treatment of giant cell myocarditis or eosinophilic myocarditis (Level of Evidence: C)
Class IIb
- High-dose immunoglobulin therapy, and steroid therapy for patients other than those with special types of myocarditis (Level of Evidence: C)
- Carperitide (Level of Evidence: C)
patients with multivessel disease and hibernating myocardium. In some patients HCM progresses to D-HCM. Patients with
D-HCM should be treated similarly to those with dilated car-
diomyopathy. Because the prognosis of D-HCM is often poor,
2. Hypertensive Urgency heart transplantation should be considered for these patients.
Patients who need urgent antihypertensive treatment should be 2. Dilated Cardiomyopathy
given intravenous drugs such as nitroglycerin and calcium Patients with acute heart failure due to dilated cardiomyopathy
channel blockers. The addition of carperitide is effective in should receive treatment to decrease left ventricular filling
patients with severe pulmonary congestion (Table 32). ACE pressure and improve low output syndrome, as in the case of
inhibitors, ARBs, and calcium channel blockers are used in heart failure due to other causes. After improvement of con-
the long-term treatment. gestion, ACE inhibitors should be administered at an optimal
In general, patients with hypertensive urgency receive treat- dose, and β-blockers should be initiated starting with a low
ment to decrease mean atrial pressure by about 25% in the first dose with careful monitoring of heart rate and blood pressure.
1 to 2 hours, and then to decrease gradually to around 160/ Physicians should use diuretics to treat excessive fluid reten-
100 mmHg over 2 to 6 hours. An excessive decrease in blood tion, digitalis to control pulse rate during atrial fibrillation,
pressure that may cause ischemia of major organs should be warfarin to prevent thrombosis, and amiodarone to manage
avoided. Although immediate-release nifedipine capsules have severe ventricular arrhythmias.
been administered sublingually to some patients with hyper- Patients with heart failure not responding well to medical
tensive urgency, sublingual nifedipine should not be given to therapy should be considered for cardiac resynchronization
these patients because sublingual treatment does not allow for therapy (CRT) or valvuloplasty for the treatment of functional
control the speed and degree of the blood pressure reduction.87 mitral valve insufficiency. Patients with intractable disease who
do not responded to these procedures are indicated for VAS as
a bridge to heart transplantation. Hospice care is an option for
3. Idiopathic Cardiomyopathy patients who are not indicated for heart transplantation.
1. Hypertrophic Cardiomyopathy 3. Specific Cardiomyopathy Requiring Careful Attention

Patients with acute heart failure due to left ventricular outflow Special attention should be paid to reversible or treatable acute
tract stenosis have a decrease in left ventricular output. Pa- heart failure. These types of heart failures (e.g., tachycardia-
tients with HCM are treated to reduce preload using fluid ad- induced cardiomyopathy, some types of acute myocarditis,
ministration, β-blockers and class I antiarrhythmic drugs, con- takotsubo cardiomyopathy, or drug-induced cardiomyopathy)
trol cardiac contractility and tachycardia.88 Patients with may improve with catheter ablation, or other interventions to
ventricular tachycardias or tachycardiac paroxysmal atrial fi- treat tachycardias, treatment with immunosuppressants includ-
brillation should be actively treated with defibrillation, and ing steroids, careful observation of the natural course, and/or
should be considered for amiodarone treatment without delay. discontinuation of culprit drugs whenever possible. Differen-
Because the incidence of atrial fibrillation is high among pa- tial diagnoses should be actively performed even in patients in
tients with HCM, it is important to administer anticoagulants the acute phase to determine appropriate treatment strategies
to prevent cardiogenic embolism. Treatment with inotropes without delay.
for low output syndrome and nitrates for chest pain may wors-
en symptoms of HCM.
The pathophysiology of HCM not associated with left ven- 4. Myocarditis
tricular outflow tract stenosis is characterized by diastolic dys-
function. These patients should be treated similarly to those 1. Intervention According to the Cause
with heart failure with preserved EF. No antiviral drugs are available for the treatment of viral myo-

carditis. Allergy or autoimmune processes may play roles in substances by suppressing immune function,90,91 but the effi-
special types of myocarditis such as giant cell myocarditis and cacy of steroid pulse therapy in this patient population has not
eosinophilic myocarditis, and steroids and immunosuppres- been confirmed. High-dose immunoglobulin therapy92,93 and
sants are considered effective for these diseases.89 Steroids and plasmapheresis are under investigation.
immunosuppressants should not be used aggressively unless Patients with myocarditis should be treated by considering
the specific cause of myocarditis is confirmed with myocar- the above-described circumstances (Table 33). Especially pa-
dial biopsy. tients in the acute phase of fulminant myocarditis should be
transferred to large hospitals that can provide specialized treat-
2. Maintaining Hemodynamics to the Time of Spontaneous ment by experienced staff members, and should receive sys-
Improvement temic treatment including mechanical circulatory support, when
Patients in the acute phase of myocarditis often experience necessary.
cardiogenic shock, AV block, ventricular tachycardia, ven-
tricular fibrillation, and asystole. When arrhythmias such as
AV block and ventricular fibrillation develop, external pacing 5. Valvular Heart Disease
or direct current defibrillation should be used. IABP or PCPS
should be introduced when cardiogenic shock or low output Because patients with acute heart failure associated with val-
syndrome develops (see Section 5.3 of Chapter III). vular heart disease did not recover despite maximal medical
therapy, patients who require operative intervention should
3. Treatment of Myocardial Dysfunction Due to undergo surgery in a timely manner.94,95 Readers should refer
Inflammatory Substances to the “Guidelines for Surgical and Interventional Treatment
Short-term, high-dose steroid therapy (steroid pulse therapy) of Valvular Heart Disease (JCS 2007)” for detailed indications
is used to treat myocardial dysfunction due to inflammatory for surgical treatment.94
V Concomitant Conditions and Their Management
1. Anemia (Table 34) 2. Renal Failure (Table 35)
Both in patients with acute heart failure and in those with Acute heart failure is often complicated with renal dysfunc-
chronic heart failure, anemia is an independent prognostic fac- tion, which is an independent factor associated with poor prog-
tor. Transfusion is the main procedure to treat anemia in pa- nosis, as in the case of chronic heart failure. Excessive use of
tients with acute heart failure because of its quick effect. How- diuretics may worsen renal function. To protect the kidneys,
ever, the efficacy of transfusion in patients with acute heart diuretics should be used at a dose appropriate to alleviate renal
failure has not been investigated in detail, and remains uncer- congestion without delay.19
tain. Transfusion is indicated for patients in whom significant Carperitide, a vasodilator, exerts renal protective effects, and
anemia is a cause of exacerbation of heart failure, who require has been demonstrated to protect the kidneys during open heart
prompt improvement of their condition, and in whom only surgery and to prevent contrast-induced nephropathy.96,97 It
transfusion is expected to improve their condition. has not been determined whether carperitide consistently ex-
erts renal protective effects in patients with acute heart failure
when they receive the drug after the onset of heart failure.98
Table 34. Treatment of Anemia in Patients With Acute Heart Failure

Class IIb
- Treatment of anemia with iron supplementaion, erythropoietin, and/or darbepoetin during the chronic phase of heart failure. (Level of
Evidence: B)
- Transfusion is indicated for patients in whom significant anemia is a cause of exacerbation of heart failure, who require prompt improve-
ment of the condition, and in whom only transfusion is expected to improve the condition. (Level of Evidence: C)
Table 35. Treatment of Renal Failure in Patients With Acute Heart Failure

Class IIa
- There is no single procedure to protect the kidneys in patients with acute heart failure. Physicians should try the most effective methods to
stabilize hemodynamics according to systolic blood pressure and the severity of congestion. (Level of Evidence: B)
Table 36. Treatment of Hepatic Congestion in Patients With Acute Heart Failure

Class IIa
- There is no single procedure to protect the liver in patients with acute heart failure. Physicians should try the most effective methods to
stabilize hemodynamics according to systolic blood pressure and the severity of congestion. (Level of Evidence: C)

Figure 15. Severity classification of pneumonia. CRP, C-reactive protein; FiO2, fraction of inspired oxygen; MRSA, methicillin-re-
sistant Staphylococcus aureus.
Drip infusion of inotropes including dopamine, which has been pain), infiltrates in chest X-ray, inflammation (C-reactive pro-
indicated to increase renal blood flow, has not been confirmed tein [CRP] levels and white blood cell count [WBC]), and the
to exert renal protective effects in the clinical setting. No drugs results of bacteriological examination.
have been demonstrated to protect the kidneys in this patient
population. 1. Selection of Antimicrobial Drugs for Empirical Therapy
Hemofiltration should be considered for patients who can- The severity of pneumonia is classified, and appropriate anti-
not achieve sufficient diuresis and improvement of hemody- microbial drugs are selected, according to Figure 15.
namics and symptoms with medical therapy. Physicians should refer to the Guidelines for the Manage-
ment of Hospital-Acquired Pneumonia in Adults proposed by
the Japanese Respiratory Society in 2008 for selection of drugs
3. Hepatic Congestion (Table 36) (Table 37).100
In patients with acute heart failure, liver disease develops as a

result of hepatic congestion and low output syndrome. Im- 5. Pulse Abnormalities
provement of hemodynamics is essential to treat the hepatic
congestion.99 1. Arrhythmias in Patients With Acute Heart Failure
Arrhythmias requiring management during the early stage of
acute heart failure include (1) severe bradycardia, (2) paroxys-
4. Pneumonia mal supraventricular tachycardia, (3) atrial fibrillation/flutter,
and (4) ventricular tachycardias (see Section 4.7 of Chapter III).
Most cases of pneumonia developing after hospitalization for
acute heart failure are hospital-acquired pneumonia. Hospital- (1) Severe Bradycardia
acquired pneumonia is defined as pneumonia developing more Temporary pacing is indicated for patients with advanced or
than 48 hours after hospitalization. Pneumonia is diagnosed third degree AV block who have disturbance of consciousness
on the basis of symptoms (fever, cough, sputum, and chest or heart failure. Temporary pacing is also indicated for pa-

Table 37. Selection of Antimicrobial Drugs

1. Selection of antimicrobial drugs for mild pneumonia (Group A)
- Ceftriaxone (CTRX, Rocephin®), 1 to 2 g per dose, 1 or 2 doses per day, div (the maximal dose is 4 g/day).
- Sulbactam/ampicillin (SBT/ABPC, Unasyn®-S), 3 g per dose, 2 to 4 doses per day, div.
-
Panipenem/betamipron (PAPM/BP, Carbenin®), 0.5 to 1 g per dose, 2 to 4 doses per day (the maximal dose is 2 g/day).
[Alternative drugs]
Ceftriaxone →
Cefotaxime (CTX, Claforan®), 1 to 2 g per dose, 2 to 4 doses per day, div (the maximal dose is 4 g/day).
2. Selection of antimicrobial drugs for moderate pneumonia (Group B)
(1) Group 1, monotherapy
- Tazobactam/piperacillin (TAZ/PIPC, Zosyn®), 4.5 g per dose, 3 or 4 doses per day, div.
- Imipenem/cilastatin (IPM/CS, Tienam®), 0.5 to 1 g per dose, 2 to 4 doses per day (the maximal dose is 2 g/day).
- Meropenem (MEPM, Meropen®), 0.5 to 1 g per dose, 2 to 4 doses per day, div (the maximal dose is 2 g).
[Alternative drugs]
Imipenem, meropenem →
Doripenem (DRPM, Finibax®), 0.25 to 0.5 g per dose, 2 or 3 doses per day, div (the maximal dose is 1.5 g).
Biapenem (BIPM, Omegacin®), 0.3 g per dose, 2 or 3 doses per day, div (the maximal dose is 1.2 g).
(2) Group 2, concomitant use should be performed in particular conditions*
- Cefepime (CFPM, Maxipime®), 1 to 2 g per dose, 2 to 4 doses per day, div (the maximal dose is 4 g).
±
- Clindamycin (CLDM, Dalacin®S), 600 mg per dose, 2 to 4 doses per day (the maximal dose is 2,400 mg).
[Alternative drugs]
Cefepime →
Cefpirome (CPR, Keiten® or Broact®), 1 to 2 g per dose, 2 to 4 doses per day, div (the maximal dose is 4 g/day).
Cefozopran (CZOP, Firstcin®), 1 to 2 g per dose, 2 to 4 doses per day, div (the maximal dose is 4 g/day).
* When aspiration or anaerobic infection is suspected.
(3) Group 3, concomitant use should be performed in principle
- Ceftazidime (CAZ, Modacin®), 1 to 2 g per dose, 2 to 4 doses per day, div (the maximal dose is 4 g).
+
- Clindamycin (CLDM, Dalacin S®), 600 mg per dose, 2 to 4 doses per day (the maximal dose is 2,400 mg).
[Alternative drugs]
Ceftazidime →
Aztreonam (AZT, Azactam®), 1 to 2 g per dose, 2 to 4 doses per day, div (the maximal dose is 4 g).
Sulbactam/cefoperazone (SBT/CPZ, Sulperazon®),* 1 to 2 g per dose, 2 to 4 doses per day, div (the maximal dose is 4 g).
*As in the case of clindamycin, sulbactam and cefoperazone are metabolized in the liver and are useful for patients with renal
dysfunction.
- Ciprofloxacin (CPFX, Ciproxan®), 300 mg per dose, 2 doses per day, div.
+
- Sulbactam/ampicillin (SBT/ABPC, Unasyn®-S), 3 g per dose, 2 to 4 doses per day, div.
[Alternative drugs]
Ciprofloxacin →
Pazufloxacin (PZFX, Pasil® or Pazucross®), 500 mg per dose, 2 doses per day, div.
Sulbactam/ampicillin →
Clindamycin (CLDM, Dalacin®S), 600 mg per dose, 2 to 4 doses per day (the maximal dose is 2,400 mg).
3. Selection of antimicrobial drugs for severe pneumonia (Group C)
The following drugs are used in addition to those listed for Group B.
- Amikacin (AMK, Amikacin® or Biklin®), 200 to 400 mg/day divided into 2 doses.
or
- Ciprofloxacin (CPFX, Ciproxan®),*1 300 mg per dose, 2 doses per day, div.
[Alternative drugs]
Ciprofloxacin →
Pazufloxacin (PZFX, Pasil® or Pazucross®), 500 mg per dose, 2 doses per day, div.
Amikacin →
Gentamicin (GM, GENTACIN®), 80 to 120 mg/day, divided into 2 or 3 doses.
Tobramycin (TOB, Tobracin®), 180 mg/day, divided into 2 to 3 doses.
Isepamicin (ISP, Isepacin® or Exacin®), 400 mg/day, divided into 1 or 2 doses.
Arbekacin (ABK, Habekacin®)*2, 150 to 200 mg/day, once daily.
*1 Use CPFX only when quinolones are not selected from Group B.
*2 Arbekacin is anti-MRSA drug but is also effective against Pseudomonas (P.) aeruginosa.
(Table 37 continued the next page.)

4. Selection of antimicrobial drugs for drug-resistant bacteria

(1) Patients with suspected MRSA infection
- Vancomycin (VCM, Vancomycin Hydrochloride for Injection [0.5 g]), 0.5 to 1 g per dose, 2 to 4 doses per day, div over ≥60 minutes (the
daily dose is 2 g).
TDM should be performed to achieve the peak drug concentration at 20 to 40 μg/mL and the trough drug concentration at 5 to 10 μg/mL.
The trough drug concentration should be adjusted to 10 to 15 μg/mL in patients with severe pneumonia and those infected with strains
with high MIC.
- Teicoplanin (TEIC, TARGOCID® [200 mg for Injection]), treatment should be started at 400 mg, followed by additional 400 mg 12 hours
after the first dose. From the third dose on, the drug should be administered every 24 hours, div.
When TDM is used, the trough drug concentration should be adjusted in 10 to 20 μg/mL. It takes 2 or 3 days to achieve a steady state.
- Linezolid (LZD, ZYVOX® Tablets and Injection 600 mg), 600 mg per dose, 2 doses per day, div or po.
- Dose adjustment is not necessary even in patients with renal disorder. Linezolid is absorbed well after po administration, and achieves
similar tissue concentrations after both po administration and div. Patients should be carefully observed for thrombocytopenia and other
adverse drug reactions and the development of drug-resistant bacteria. The duration of treatment is commonly ≤14 days, and should
not exceed 28 days.
- Arbekacin (ABK, HABEKACIN® INJECTION 75, 100, 200 mg), 150 to 200 mg per dose, once daily, div.
When TDM is used, the trough and peak drug concentration should be targeted at ≤2 μg/mL and 9 to 20 μg/mL, respectively. Once daily
administration is effective.
(2) When ESBL-producing organisms are detected
Physicians should select appropriate antimicrobial drugs according to the results of drug-susceptibility testing, in principle. However, it has
been reported that penicillins and cephalosporins are not effective against them regardless of their susceptibility to these drugs.
Carbapenems should be the first line treatment because ESBL-producing organisms are often susceptible to them. Quinolones have also
been reported to be effective. Because Acinetobacter species are susceptible to sulbactam (SBT) and tazobactam (TAZ), which are
β-lactamase inhibitors having antimicrobial activity, sulbactam/cefoperazone (SBT/CPZ, Sulperazon®) and tazobactam/piperacillin (TAZ/
PIPC, Zosyn®) may be selected.
(3) When MDRP is detected
MDRP is defined as P. aeruginosa that is resistant to all of the small number of antimicrobial drugs (e.g., carbapenems and other β-lactam
antimicrobials, quinolones, and aminoglycosides) effective against it. MDRP is one of the most important causes of hospital-acquired
infections. MDRP infection, when once developed, is the most intractable bacterial infection in Japan because no effective antimicrobial
drugs are available (Colistin® is used in some countries, but is not approved in Japan). The most important measure to prevent MDRP
infection is infection control in the hospital because hospital-acquired transmission is the main route of infection. Multiple antimicrobial
treatment is recommended for patients with MDRP infection. Because the effects of concomitant use differ among strains, in vitro evalua-
tion of the concomitant use should be performed.
div, intravenous drip infusion; ESBL, extended-spectrum beta-lactamase; MDRP, multi-drug resistant Pseudomonas aeruginosa; MIC,
minimum inhibitory concentration; po, per os; TDM, therapeutic drug monitoring.
Source: The JRS (Japanese Respiratory Society) Guidelines for the Management of Hospital-Acquired Pneumonia in Adults, 2008.100
tients with bradycardia and atrial fibrillation who experience (3) Atrial Fibrillation and Atrial Flutter
symptomatic asystole for 3 to 5 seconds or longer and asymp- Patients with unstable hemodynamics due to atrial fibrillation/
tomatic patients with a mean heart rate of less than 40 bpm. flutter should be treated with direct current defibrillation or
Advanced AV block often develops in patients with myocar- atrial pacing to restore sinus rhythm without delay. In patients
dial infarction involving the right coronary artery. Because with stable hemodynamics, prevention of embolism and rate
AV block may progress as myocardial ischemia progresses in control should be prioritized. Physicians should be aware of
such patients, they should undergo temporary pacing to main- the risk of embolism in patients receiving immediate defibril-
tain regular heart rate and reperfusion of the culprit lesion lation. Patients within 48 hours after the onset of atrial fibril-
without delay (Class I). lation/flutter and patients in whom the presence of left atrial
thrombus can be ruled out with transesophageal echocardiog-
(2) Paroxysmal Supraventricular Tachycardia raphy should be treated with heparin. Patients more than 48
Patients in whom prolonged sinus tachycardia affects the treat- hours after the onset of atrial fibrillation/flutter, patients with
ment of heart failure should be given slow infusion of intrave- unknown onset time, and patients in whom the presence of left
nous β-blockers such as propranolol under hemodynamic mon- atrial thrombus is suspected on transesophageal echocardiog-
itoring. Patients with undiagnosed tachycardia with a normal raphy should receive anticoagulant therapy with warfarin.
R-R interval should be treated with vagal stimulation such as Rate control is best achieved with digitalis (start with digoxin
the Valsalva maneuver. Direct current defibrillation should be 0.25 mg intravenously, administer 0.25 mg every 2 hours to
considered whenever hemodynamics deteriorates. Patients in the maximum total dose of 1.00 mg). Adequate rate control is
whom tachycardia persists but hemodynamics are stable should more difficult to achieve in patients with atrial flutter than in
be treated with adenosine 10 mg (administer intravenously those with atrial fibrillation, and sinus rhythm control with
over 1 to 2 seconds; note that the use for this purpose is not drugs is also more difficult in the former. Catheter ablation
covered by the National Health Insurance [NHI] of Japan) or may be considered for patients with persistent treatment-resis-
calcium channel blockers (verapamil 5 mg or diltiazem 10 mg; tant atrial flutter. In patients with organic heart disease, espe-
administer intravenously over about 5 minutes). Special care cially those with cardiomyopathy as the underlying disease,
should be taken concerning the use of verapamil, because it amiodarone is effective both in rate control and maintenance
may often decrease blood pressure. Patients in whom tachy- of sinus rhythm. Oral administration of amiodarone is not suit-
cardia persists or patients with atrial tachycardias should be able for acute phase treatment because the onset of effect is
considered for the treatment with sodium channel blockers such slow. However, oral amiodarone is selected as a rhythm con-
as cibenzoline and pilsicainide. trol drug for long-term treatment with low risk of exacerbation

Table 38. Treatment of Patients With Heart Failure Associated With COPD

Class IIa
- ACE inhibitors, ARBs, β-blockers, and diuretics are recommended for the treatment of heart failure associated with COPD. Treatment of
COPD should be continued during treatment of heart failure. (Level of Evidence: B)
of heart failure (Class IIb, Level of Evidence: C). fibrillation, it is important to ensure rate control by inhibiting
AV conduction.104 When catheter ablation can restore normal
(4) Ventricular Tachycardia and Frequent Premature sinus rhythm, patients are expected to have recovery to normal
Ventricular Contractions cardiac function and improvement in exercise capacity and
Patients with premature ventricular contractions (PVCs) or QOL105 (Class IIa, Level of Evidence: C).
ventricular tachycardia should be assessed for myocardial isch-
emia and electrolyte abnormality to make differential diagno-
sis. Patients in whom ventricular tachycardia affects hemody-
6. Chronic Obstructive Pulmonary
namics should be considered for direct current defibrillation. Disease (Table 38)
Patients in whom the origin of tachycardia is localized are
indicated for catheter ablation. Although COPD is present among 20 to 30% of patients with
heart failure,106 and is an independent risk factor for cardiovas-
2. Heart Failure Due to Tachycardias cular death,107 the awareness of COPD is still low. It is diffi-
(Tachycardia-Induced Cardiomyopathy) cult to differentiate heart failure from respiratory failure due
Tachycardia-induced cardiomyopathy is a reversible condition to an exacerbation of COPD, but BNP or NT-proBNP levels
where heart failure develops in the presence of persistent or are useful in the diagnosis of heart failure.106,108 In patients
recurrent tachycardia with no other underlying heart disease, with heart failure complicated with COPD, ACE inhibitors,
and discontinues in the absence of tachycardias resulting in β-blockers, and ARBs are recommended.108 β-blockers can be
recovery to normal cardiac function.101 used safely in most patients with heart failure complicated
Because rhythm or rate control therapy may restore left ven- with COPD. It is preferable to introduce β-blockers at a low
tricular function, it is important to differentiate this condition dose and increase the dose slowly.109 Careful attention should
from other irreversible myocardial disorders.102,103 The most be given to patients with uncontrolled asthma. Treatment of
common cause of tachycardia-induced cardiomyopathy is atri- COPD should be continued in parallel to treatment of the heart
al fibrillation, but it is also caused by ectopic atrial tachycardia failure.110,111
or accelerated idioventricular rhythm. In patients with atrial
VI Treatment Strategies for Heart Failure With Preserved EF
1. Definition of Heart Failure With mitral valve stenosis, and other conditions meet the definition
of “heart failure with preserved EF”, but these conditions are
Preserved EF not included in the clinical setting.
Heart failure with reduced EF accounts for about 60% of pa-

tients with heart failure, and heart failure with preserved EF
2. Diagnosis in the Acute Phase of
accounts for about 40%.112,113 The main feature of heart failure Heart Failure With Preserved EF
with preserved EF is diastolic dysfunction not associated with
left ventricular enlargement.114 Because of the absence of pre- During the acute phase, heart failure with preserved EF is di-
load reserve, left ventricular diastolic pressure readily increas- agnosed on the basis of the following signs: (1) the presence
es in association with an increase in blood pressure or physical of heart failure is confirmed or strongly suspected; (2) left
activity, which increases the left atrial pressure and pulmonary ventricular ejection fraction (LVEF) is normal and left ven-
venous pressure and causes difficulty in breathing. In these pa- tricular enlargement is absent; and (3) the presence of other
tients, pulmonary edema develops in the absence of systolic heart diseases such as valvular heart disease or constrictive
dysfunction,115 and their prognosis, including rehospitalization pericarditis is ruled out.
due to heart failure, is poor as in the case of heart failure with Plasma BNP (NT-proBNP) levels increases in patients with
reduced EF.112,113 Heart failure with preserved EF is relatively heart failure with both reduced and preserved EF.119 Echocar-
common among elderly women, and patients often present with diography should be performed to determine LVEF and assess
complications of hypertension, diabetes, chronic kidney dis- the presence/absence of valvular heart disease.
ease, or atrial fibrillation. The pathophysiology of heart failure
with preserved EF is still unclear. It has been pointed out that
functional arterial stiffing and functional mitral regurgitation
3. Treatment in the Acute Phase of Heart
as well as diastolic dysfunction play roles in the development Failure With Preserved EF (Table 39)
of this condition.116–118 In Western countries, the term “dia-
stolic heart failure” is no longer used, and the term “heart fail- Most patients in the acute phase of heart failure with preserved
ure with preserved EF” is used instead. In the broadest sense EF show clinical findings of acute pulmonary edema. Refer to
of the word, constrictive pericarditis, aortic valve stenosis, Table 15 for the treatment of acute pulmonary edema.

Table 39. Treatment of Heart Failure With Preserved Ejection Fraction

Treatment of pulmonary edema (See Table 15)
Class I
- Treatment of congestion with diuretics, nitrates, and carperitide (Level of Evidence: C)
- Intravenous drip infusion of calcium channel blockers (nicardipine or diltiazem) to control severe hypertension (Level of Evidence: C)
Class IIa
- Treatment with digitalis, calcium channel blockers, and β-blockers to control heart rate in patients with atrial fibrillation (Level of
Evidence: C)
Class IIb
- Treatment with inotropes in patients with heart failure with preserved ejection fraction (Level of Evidence: C)
tion 5 of Chapter V.
4. Blood Pressure Control
Patients in the acute phase of heart failure with preserved EF

6. Medical Therapy in the Chronic Phase of
often have a significant increase in blood pressure. Blood pressure Heart Failure With Preserved EF
control should be prioritized, because adequate diuresis may be
achieved and pulmonary congestion may be alleviated by control- Although treatment of the acute and chronic phase of heart
ling blood pressure. Refer to Section 4 of Chapter III for details. failure with preserved EF should aim at an improvement of the
prognosis, no treatment strategies specific to this condition have
been proven effective in large-scale clinical studies. The re-
5. Rate Control in Atrial Fibrillation sults of large-scale clinical studies have suggested the efficacy
of ARBs,120 ACE inhibitors,121 and β-blockers,122 but none of
In patients with heart failure with preserved EF, left ventricu- these drugs have been established as treatment options for this
lar filling highly depends on atrial contraction. Accordingly, condition. Treatment should thus be directed at the cause of
atrial fibrillation significantly affects left ventricular filling and heart failure. Antihypertensive treatment should be given to
deteriorates hemodynamics due to the absence of effective patients with poorly controlled hypertensive heart disease.
atrial contraction and the decreased diastolic time associated Treatment of myocardial ischemia is expected to improve he-
with tachycardia. Rate control therapy is especially important modynamics and symptoms in patients with ischemic heart
in these patients. Refer to Section 4.7 of Chapter III and Sec- disease.
VII Treatment Strategies for Biventricular Failure
1. Pathophysiology and Treatment of doses, PDE III inhibitors mainly exert a positive inotropic ac-
tion, which is further potentiated by concomitant use of dobu-
Biventricular Failure tamine.125 When PDE III inhibitors are used with dobutamine,
both drugs should first be administered at low doses.
1. Biventricular Failure Mainly Due to Increased Patients not responding well to medical therapy should be
Circulating Blood Volume considered for heart transplantation at the initial phase of the
Diuretic drugs are the primary treatment for patients with bi- disease, and physicians should establish detailed treatment strat-
ventricular failure accompanied by increased circulating blood
volume. Inotropes may also be required in patients with se-
verely impaired cardiac function and those with poor re-
sponse to diuretics alone (Table 40). Repeated bolus intrave- Table 40. Treatment of Biventricular Failure
nous injections of diuretics can be given; however, continuous Biventricular failure with increased circulating blood volume
infusions may be effective for patients not responding well to Class I
repeated boluses (Class IIa, Level of Evidence: B) (See - Loop diuretics (Level of Evidence: C)
Table 21). Treatment with natriuretic peptide analogs such as Class IIa
carperitide which protects renal function is considered valu-
- Carperitide (Level of Evidence: B)
able in the treatment of patients who increased circulatory blood
- Ultrafiltration (Level of Evidence: B)
volume due to the cardio-renal relationship. Co-administration
of heparin should be considered to prevent thrombosis. In pa- - Inotropes (dobutamine, PDE inhibitors) (Level of Evidence: C)
tients with diuretic-resistant or severe renal dysfunction, ad- Class IIb
justment of circulating blood volume by extracorporeal ultra- - Thiazides (Level of Evidence: C)
filtration or hemofiltration is effective.123,124 - Tolvaptan (Level of Evidence: B)
Biventricular failure with a significant decrease in cardiac
2. Biventricular Failure Mainly Due to Significant output
Decrease in Cardiac Output Class IIb
The relative contributions of the positive inotropic and vaso- - Inotropes (concomitant use of dobutamine and PDE inhibi-
dilator actions of PDE III inhibitors differ by dose.125 At low tors) (Level of Evidence: C)

egies for such patients including the use of mechanical circula- cases secondary to left heart failure, include a decrease in right
tory support during an acute exacerbation of the condition. ventricular contractility due to right ventricular infarction or
arrhythmogenic right ventricular dysplasia, right ventricular
volume overload due to acute tricuspid valve regurgitation or
2. Right Heart Failure failure of the Fontan circulation, an increase in right ventricu-
lar afterload due to pulmonary embolism or primary pulmo-
1. Right Heart Failure Associated With Left Heart Failure nary hypertension, and right ventricular diastolic dysfunction
In many cases, right heart failure develops secondary to left heart due to cardiac tamponade or constrictive pericarditis.
failure.126 Right heart failure can also cause bowing of the inter- In the treatment of acute right heart failure, physicians should
ventricular septum toward the left due to the increased volume treat the underlying cause, and reduce the right ventricular
load of the right ventricle, thereby impeding left ventricular dia- afterload, enhance the contractility of the right ventricle, and
stolic function and further reducing cardiac output. The coexis- control the right ventricular preload appropriately. PDE III in-
tence of left ventricular systolic dysfunction and right ventricular hibitors as monotherapy or concomitant use of dobutamine are
systolic dysfunction is the largest independent risk factor of poor useful in reducing pulmonary vascular resistance and enhanc-
prognosis.126,127 As right heart failure progresses, functional tri- ing the contractility of the right ventricle. In patients with se-
cuspid valve regurgitation contributes to hepatic congestion and vere pulmonary hypertension who need a significant decrease
portal hypertension resulting in resistance to oral medications in the right ventricular afterload, concomitant use of calcium
due to intestinal edema, hepatorenal syndrome. Because veno- channel blockers, prostaglandins, endothelin antagonists, in-
venous shunts due to portal hypertension increase mixed venous haled nitric oxide (NO), PDE V inhibitors, and/or Rho kinase
oxygen saturation, the cardiac output calculated using the Fick inhibitors are effective.128 Because PCPS may decrease the
method may overestimate the actual cardiac output. right ventricular load and maintain PaO2 at an appropriate level,
PCPS is quite effective in the treatment of patients with acute
2. Acute Right Heart Failure right heart failure and poor pulmonary oxygenation.
The typical causes of acute right heart failure, other than the
VIII Transition to Chronic Heart Failure and Timing of Discharge

When signs/symptoms of heart failure are managed well and has not been established. Patients with heart failure due to
euvolemia can be obtained, according to the evidence, treat- systolic dysfunction should start treatment with β-blockers
ment of chronic heart failure should be initiated and drug doses (Table 41). It is preferable to introduce β-blockers when con-
should be increased to the target doses. During this stage, phy- gestion is absent and the heart failure is stabilized. Physicians
sicians should assess the severity of the myocardial damage should start β-blockers in the in-hospital setting to achieve the
and renal dysfunction that developed after the onset of acute sufficient dose during hospitalization.129 Long-term prognosis
heart failure, and treat these conditions accordingly. is better in patients who start β-blockers during hospitalization
Treatment with ACE inhibitors should be initiated as soon rather than after discharge.130 Some patients who cannot toler-
as possible (Table 41). ARBs should be used for patients who ate β-blockers due to exacerbation of heart failure may begin
cannot receive ACE inhibitors. The efficacy of ACE inhibitors β-blocker treatment safely when the drug is combined with
and ARBs in the treatment of heart failure with preserved EF pimobendan 1.25 or 2.5 mg/day.129
Table 41. Transition to Chronic Heart Failure

Class I
- During the early stage of acute heart failure, treatment with ACE inhibitors (or ARBs when ACE inhibitors cannot be used) should be started
at a low dose and the dose should be increased gradually thereafter. (Level of Evidence: C)
- In patients with heart failure due to systolic dysfunction, treatment with β-blockers should be initiated during hospitalization. (Level of
Evidence: A)
Table 42. Criteria for Discharge of Patients With Acute Heart Failure

1. Reaching the target body weight.
2. Achieving target blood pressure.
3. Absence of shortness of breath or dizziness during daily activities.
4. Stable condition for 24 hours or more after addition or change in dose of oral drugs.
5. Stable condition for 48 hours or more after discontinuation of intravenous treatment.
6. Maintaining the optimal circulating blood volume with oral diuretics.
7. Absence of substantial dehydration.
8. Stable or improving renal function.
9. Adequate control of the triggers or precipitating factors of acute heart failure.
10. Implementation or development of treatment strategies according to the guidelines for the treatment of heart failure.
11. Education of the patient and his/her family about heart failure.

Figure 16. Assessment and targeted implementation of evidence-based therapy in acute heart failure. *Select patients. #Modified
to fit the circumstances in Japan. CAD, coronary artery disease; CRT, cardiac resynchronization therapy; Dor procedure, ven-
tricular reconstructive surgery to restore aneurysmal left ventricle to its normal; ICD, implantable cardioverter defibrillator; LV, left
ventricular. Adapted from J Am Coll Cardiol 2009; 53: 557 – 573,131 with permission from Elsevier Inc.
Treatment of acute heart failure should aim at not only an should be given for each aspect of heart failure (Figure 16).131
improvement in congestion and in other symptoms of heart Because acute heart failure may be caused by a wide variety
failure but also prevention of rehospitalization and an improve- of conditions and diseases, no criteria for discharge have been
ment of prognosis through comprehensive assessment of the established. Table 42 summarizes conditions suitable for dis-
condition and its complications. Evidence-based treatment charge in typical cases.
IX Palliative Care

failure.
1. Introduction Physicians should also refer to the section of “Cardiovascu-
lar Intensive Care” in the “Statement for End-Stage Cardio-
The treatment of heart failure has advanced greatly as the di- vascular Care (JCS 2010)”.133
agnostic and therapeutic technologies have evolved. Today,
the needs for palliative care for patients with end-stage heart
failure who are not expected to recover are increasing.132 Pal- 2. Proposals for Palliative Care (Support Model)
liative care was first advocated mainly for patients with end-
stage cancer, and was developed to alleviate pain in patients 1. Catch the Pain
with treatment-resistant disease and to provide mental support. Patients suffer from not only physical symptoms such as short-
However, palliative care now includes relief of symptoms and ness of breath and palpitations but the “gap between ambitions
phychological care from an acute phase of the disease. When and reality” such as that the patient can no longer move as he/
palliative care is defined as a method to support the life and she wants, and the patient wants to live longer but his/her time
well-being of patients with physical and psychological distress, is now limited. Healthcare professionals should be aware of
healthcare professionals should make every effort not only to the potential for patients’ physical and emotional pain. The
alleviate pain and provide terminal care, but also support every first step is listening to the patient carefully to know his/her
aspect of patients living with heart failure. There is little evi- pain (to establish the gap between ambitions and reality), in
dence regarding effective palliative care for patients with heart addition to paying attention to visible figures such as vital
failure. The present guidelines provide recommendations for signs, blood test results, and imaging findings.
approaches to support patients with treatment-resistant heart

2. Catch the Keys ness when others understand his/her suffering, and should
Healthcare professional should know the patient’s keys to being carefully listen to the patient. Healthcare professionals should
him/herself. Such keys differ among individuals, but the most interact with the patient to listen to him/her carefully using
common keys among patients in the clinical setting are dreams attentive hearing techniques such as repetition, pausing, and
for the future (temporal existence), relationships with others asking. Even if the patient is faced with death, he/she can stay
(relational existence), and the freedom of making one’s own calm when the patient understands he/she is fully supported.
decisions (autonomous existence).134 These keys help the pa- Even though the keys for support differ among individuals,
tient feel peace even when he/she is suffering from pain.135 healthcare professionals can support the well-being of patients
Healthcare professionals should concentrate not only on alle- when they understand their roles in palliative care.
viating the patient’s pain but also knowing their keys in the
clinical setting. 4. Support for Healthcare Professionals
Dreams for the future encourage the patient to reflect on It is not difficult for healthcare professionals to build a good
their experience in the past and live for the future. Even though relationship with the patient if they can help him/her. However,
the time is limited, the patient may be motivated to live to do if they cannot help the patient with treatment-resistant disease,
something he/she wants to do if he/she has dreams for the it is difficult to interact with him/her continuously. Even when
future. The patient may also be motivated if he/she can imag- the best available treatment is provided, the patient’s condition
ine that the tie with family members will last forever even deteriorates gradually. When healthcare professionals are over-
after his/her death. Relationships with others who fully under- whelmed by a feeling of helplessness, they may want to dis-
stand the patient are important. The patient is encouraged by tance themselves from the patient. To keep interacting with
the existence of the patient’s family members, friends, and patients with treatment-resistant heart failure, healthcare pro-
medical staff members who will continue to support him/her fessionals should also be supported emotionally. The true value
throughout the treatment-resistance heart failure. The patient of healthcare professionals is not the power to solve all prob-
may also be encouraged by connecting with pets and nature. lems but the continuity of effort to treat the patient even when
The freedom of making one’s own decisions is a basic human it is not helpful. This is difficult to achieve, and healthcare
right. It is important to value the patient’s decisions on the professionals need support and encouragement.
treatment strategy, place of care, and other matters related to
heart failure treatment.
3. Summary
3. Knowing Healthcare Professionals’ Roles to Support the
Patient Healthcare professionals involved in the treatment of heart
Patients with end-stage treatment-resistant heart failure cannot failure should provide a good standard of care, and should also
be reassured by just giving words of encouragement and un- continue to interact with the patient until the end of his/her
wanted life-sustaining treatment. In palliative care, it is quite life. There is little evidence regarding recommendations for
important to keep good communication with the patient even palliative care for patients with heart failure. Japan is a coun-
when the patient receives unfortunate news. The patient is not try with an aging population and how to care for and interact
encouraged by frank and open discussion only. Healthcare with end-stage patients with heart failure is a major issue.
professionals should understand that the patient feels happi-
X Flowchart of Treatment
Figure 17 summarizes the outline of treatment for acute heart failure.
XI Summary
The present revision of the guidelines reflects the rapid ad- present guideline document also describes the clinical scenar-
vancement of understanding of the pathophysiology of heart ios and the Nohria-Stevenson classification that are common-
failure and treatment methods. Early diagnosis and prompt ly used in the assessment of the pathophysiology of acute phase
treatment are essential for patients with acute heart failure, and heart failure.
a misjudgment may lead to life-threatening conditions. It is Treatment has advanced as well. In addition to conventional
essential to appropriately understand patients’ pathological medical therapy, new methods of respiratory management have
condition without delay. Assessment of clinical symptoms and become available. In this document, carperitide and inotropes
physical findings is especially important as emphasized in the are positioned more clearly, and new drugs are introduced. It
present guideline document. It is also important to use the new- is expected that further studies will facilitate appropriate selec-
est and most appropriate treatment methods for the varied path- tion of treatment options for individual patients according to
ological conditions encountered in each patient, and to evalu- their pathophysiological conditions.
ate the effects and modify the treatment as needed. The prevention of acute heart failure is the most important
Because the understanding of the pathophysiology of heart goal, and this depends on the proper management of chronic
failure and treatment techniques has been greatly advanced, heart failure, as well as treatment of arrhythmias, ischemia,
the present guideline document covers many aspects of this cardiomyopathy, and valvular heart disease. Physicians should
condition. The pathophysiology of acute heart failure second- manage cardiac function, but should also take a multidisci-
ary to diastolic dysfunction has been clarified in detail. The plinary approach to the patient as a whole.

Figure 17. Outline of treatment for acute heart failure. ACLS, advanced cardiac life support; ACS, acute coronary syndrome; BLS,
basic life support; CVVH, continuous veno-venous hemofiltration; ECLS, extracorporeal life support; ECUM, extracorporeal ultra-
filtration method; ET, endotracheal; IABP, intraaortic balloon pumping; LV, left ventricular; LVEF, left ventricular ejection fraction;
NPPV, non-invasive positive pressure ventilation; PDE, phosphodiesterase; PEEP, positive-end-expiratory pressure; SaO 2, arterial
oxygen saturation; SBP, systolic blood pressure; VAS, ventricular assist system.
Finally, the present guideline document provides standard cians will utilize this guideline document in the clinical setting
information regarding the diagnosis and treatment of acute heart by adapting the standard treatment strategies appropriately to
failure, and it is the physicians’ responsibility to determine their patients according to each pathophysiological condition.
treatment strategies for their patients. We expect that physi-
great vessels, 9th ed. Boston: Little, Brown and Company, 1994;
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• Tsutomu Imaizumi, Division of Cardiovascular Medicine, Department
of Internal Medicine, Kurume University School of Medicine
Appendix • Takeshi Nakatani, Department of Transplantation, National Cerebral
Chair: and Cardiovascular Center
• Tohru Izumi, Kitasato University • Keijiro Saku, Department of Cardiology, Fukuoka University School
of Medicine
Members: • Michihiro Yoshimura, Division of Cardiology, Department of Internal
• Atsushi Hirayama, Division of Cardiovascular Medicine, Department Medicine, The Jikei University School of Medicine
of Medicine, Nihon University School of Medicine (The affiliations of the members are as of July 2012)

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Circulation Journal

Official Journal of the Japanese Circulation Society

Guidelines for Treatment of Acute Heart Failure (JCS 2011)

Updating the Guidelines

Released online June 12, 2013

Circulation Journal Vol.77, August 2013

Circulation Journal Vol.77, August 2013

Table 1. Hemodynamic Profiles of the 6 Categories of Acute Heart Failure

Circulation Journal Vol.77, August 2013

Table 2. Epidemiological Surveys in Japan

Circulation Journal Vol.77, August 2013

Table 4. Treatment During the Early Phase of Hospitalization

Circulation Journal Vol.77, August 2013

Figure 2. Prescriptions at discharge:

Table 5. Criteria for Diagnosis of Congestive Heart Failure: Framingham Criteria

Circulation Journal Vol.77, August 2013

Table 6. Signs and Symptoms of Acute Heart Failure

Circulation Journal Vol.77, August 2013

disorders causing this condition, acute heart failure is highly

Circulation Journal Vol.77, August 2013

Specifically, measures should be taken to treat dyspnea, as

Circulation Journal Vol.77, August 2013

3. Treatment formed quickly even by general clinicians (see Figure 3 and

Figure 4. Procedures for diagnosis of acute heart failure.

Circulation Journal Vol.77, August 2013

Figure 5. Non-invasive estimation of central venous pressure.

Table 10. Indications for Swan-Ganz Catheterization in Patients With Heart Failure

Table 11. Assessment at Hospital Admission of Patients With Acute Heart Failure

Circulation Journal Vol.77, August 2013

Figure 6. Chest X-ray findings of heart failure: schema.

necessary. er in the follow-up of patients with acute heart failure. In pa-

Circulation Journal Vol.77, August 2013

detect the presence of hemodynamic abnormalities, abnormal 8. Other Examinations

Circulation Journal Vol.77, August 2013

Table 13. Monitoring of Patients With Acute Heart Failure

Circulation Journal Vol.77, August 2013

Table 14. Use of β-Blockers in Patients With Acute Decompensated Heart Failure

Circulation Journal Vol.77, August 2013

Table 15. Treatment of Acute Cardiogenic Pulmonary Edema

Table 16. Treatment of Cardiogenic Shock

(5) Acute Right Heart Failure

Circulation Journal Vol.77, August 2013

Table 17. Respiratory Management in Patients With Acute Heart Failure

Table 18. Initial Management of Acute Heart Failure in the Emergency Room

Circulation Journal Vol.77, August 2013

Table 19. Targets of Treatment and Management

(3) Mental Support and Counseling 1. Sedation

Circulation Journal Vol.77, August 2013

Table 22. Diuretic Treatment in Patients With Acute Heart Failure

2. Diuretics treatment of acute heart failure associated with ischemic heart

(2) Nicorandil (4) Phosphodiesterase Inhibitors

Circulation Journal Vol.77, August 2013

receptors, and thereby increase the myocardial contractility (2) Digitalis

2) Dopamine (4) Adenylate Cyclase Activators (Colforsin Daropate)

Circulation Journal Vol.77, August 2013

Circulation Journal Vol.77, August 2013

Figure 10. BLS algorithm in the 2010

Circulation Journal Vol.77, August 2013

2. Artificial Respiration 3. Types and Indications of Mechanical Circulatory

Circulation Journal Vol.77, August 2013

Table 25. Indications of PEEP and Criteria for Discontinuation and Extubation

Table 26. Types and Characteristics of Mechanical Circulatory Support Devices

[ECMO]), and VAS. Table 26 summarizes the characteristics and 12).

2. Artificial Respiration 3. Types and Indications of Mechanical Circulatory

(2) Indications for Mechanical Circulatory Support (iii) Major Complications

5. Multidisciplinary Approaches to the Management of