Guidelines on the diagnosis and treatment of acute heart failure

36 Pages·2005·0.49 MB·English

EuropeanHeartJournal
doi:10.1093/eurheartj/ehi117
ESC Guidelines
Guidelines on the diagnosis and treatment of
acute heart failure—full text
The Task Force on Acute Heart Failure of the
European Society of Cardiology
Endorsed by the European Society of Intensive Care Medicine (ESICM)
Task Force Members, Markku S. Nieminen, Chairperson* (Finland),
Michael B¨ohm (Germany), Martin R. Cowie (UK), Helmut Drexler (Germany),
Gerasimos S. Filippatos (Greece), Guillaume Jondeau (France),
Yonathan Hasin (Israel), Jose´ Lopez-Sendon (Spain),
Alexandre Mebazaa{ (France), Marco Metra (Italy),
Andrew Rhodes{ (UK), Karl Swedberg (Sweden)
ESC Committee for Practice Guidelines (CPG), Silvia G. Priori(Chairperson) (Italy), MariaAngeles AlonsoGarcia
(Spain), Jean-Jacques Blanc (France), AndrzejBudaj (Poland), MartinR.Cowie (UK), Veronica Dean(France),
JaapDeckers (The Netherlands), Enrique FernandezBurgos (Spain), JohnLekakis(Greece), BertilLindahl
(Sweden), Gianfranco Mazzotta(Italy), Jo˜ao Morais (Portugal), AliOto (Turkey), Otto A.Smiseth (Norway)
Document Reviewers,Maria AngelesAlonso Garcia(Co-CPG Review Coordinator) (Spain), KennethDickstein
(Co-CPGReviewCoordinator)(Norway),AnibalAlbuquerque(Portugal),PedroConthe(Spain),MariaCrespo-Leiro
(Spain),RobertoFerrari(Italy),FerencFollath(Switzerland),AntonelloGavazzi(Italy),UweJanssens(Germany),
MichelKomajda (France), Jo˜aoMorais(Portugal), Rui Moreno(Portugal),Mervyn Singer (UK),Satish Singh(UK),
Michal Tendera(Poland),Kristian Thygesen (Denmark)
Table of Contents 4.1. The viciouscycle in theacute failing
heart . . . . . . . . . . . . . . . . . . . . . 6
Preamble. . . . . . . . . . . . . . . . . . . . . . . . . . 2 4.2. Myocardial stunning . . . . . . . . . . . . 7
1. Introduction . . . . . . . . . . . . . . . . . . . . 2 4.3. Hibernation . . . . . . . . . . . . . . . . . 7
2. Epidemiology,aetiology,and 5. Diagnosis ofAHF . . . . . . . . . . . . . . . . . 7
clinical context . . . . . . . . . . . . . . . . . . 3 5.1. Clinical evaluation . . . . . . . . . . . . . 7
I. Definitions, diagnosticsteps, instrumentation, 5.2. Electrocardiogram . . . . . . . . . . . . . 8
andmonitoring ofthe patient with AHF. . . . . . 4 5.3. Chest X-rayandimaging techniques . . . 8
3. Definition andclinical classification ofAHF . . 4 5.4. Laboratory tests. . . . . . . . . . . . . . . 8
3.1. Definition. . . . . . . . . . . . . . . . . . . 4 5.5. Echocardiography . . . . . . . . . . . . . . 9
3.2. The clinicalsyndrome ofAHF . . . . . . . 5 5.6. Other investigations . . . . . . . . . . . . 9
4. Pathophysiology of AHF . . . . . . . . . . . . . 6 6. Goals of thetreatment ofAHF . . . . . . . . . 9
6.1. Organization ofthe treatment ofAHF . . 10
*Correspondingauthor.Chairperson:MarkkuS.Nieminen,Divisionof 7. Instrumentation andmonitoring ofpatients in
Cardiology, Helsinki University Central Hospital, Haartmaninkatu 4, AHF . . . . . . . . . . . . . . . . . . . . . . . . . 10
00290Helsinki,Finland.Tel:þ358947172200;fax:þ3589471740 7.1. Non-invasive monitoring . . . . . . . . . . 11
15.E-mailaddress:markku.nieminen@hus.fi
7.2. Invasive monitoring. . . . . . . . . . . . . 11
{MembersoftheEuropeanSocietyofIntensiveCareMedicine
&TheEuropeanSocietyofCardiology2005.Allrightsreserved.ForPermissions,pleasee-mail:[email protected]
Page2of36 ESCGuidelines
II. Treatment ofAHF. . . . . . . . . . . . . . . . . . . 12 Consensus Documents published in peer-reviewed jour-
8. General medical issues in the nals between 1985 and 1998 have shown that methodo-
treatment of AHF . . . . . . . . . . . . . . . . . 12 logical standards were not complied with in the vast
9. Oxygen andventilatory assistance . . . . . . . 12 majority of cases. It is therefore of great importance
9.1. Rationale forusingoxygen in AHF . . . . 12 that guidelines and recommendations are presented in
9.2. Ventilatorysupportwithoutendotracheal formats that are easily interpreted. Subsequently, their
intubation (non-invasive ventilation). . . 13 implementation programmes must also be well con-
9.3. Mechanicalventilationwithendotracheal ducted. Attempts have been made to determine
intubation in AHF . . . . . . . . . . . . . . 13 whether guidelines improve the quality of clinical prac-
10. Medical treatment. . . . . . . . . . . . . . . . 13 tice andthe utilization ofhealth resources.
10.1. Morphineandits analogues in AHF . . 13 TheESCCommitteeforPracticeGuidelines(CPG)super-
10.2. Anticoagulation. . . . . . . . . . . . . . 14 vises and coordinates the preparation of new Guidelines
10.3. Vasodilators inthe treatment ofAHF . 14 and Expert Consensus Documents produced by Task
10.4. ACE inhibitorsin AHF . . . . . . . . . . 15 Forces, expert groups, or consensus panels. The chosen
10.5. Diuretics. . . . . . . . . . . . . . . . . . 15 expertsinthesewritingpanelsareaskedtoprovidedisclos-
10.6. b-Blocking agents . . . . . . . . . . . . 17 ure statements of all relationships they may have which
10.7. Inotropic agents . . . . . . . . . . . . . 18 mightbeperceivedasrealorpotentialconflictsofinterest.
11. Underlying diseases andco-morbidities These disclosure forms are kept on file at the European
in AHF. . . . . . . . . . . . . . . . . . . . . . . 21 Heart House,headquartersofthe ESC.The Committeeis
11.1. Coronary arterydisease . . . . . . . . . 21 also responsible for the endorsement of these Guidelines
11.2. Valvular disease . . . . . . . . . . . . . 23 andExpertConsensusDocumentsorstatements.
11.3. Management ofAHFdue toprosthetic TheTaskForcehasclassifiedandrankedtheusefulness
valvethrombosis . . . . . . . . . . . . . 23 orefficacyoftherecommendedprocedureand/ortreat-
11.4. Aorticdissection . . . . . . . . . . . . . 24 ments and the Level of Evidence as indicated in the
11.5. AHFandhypertension . . . . . . . . . . 24 tables that follow.
11.6. Renal failure . . . . . . . . . . . . . . . 24
11.7. Pulmonary diseases and
ClassesofRecommendations
bronchoconstriction . . . . . . . . . . . 25
11.8. ArrhythmiasandAHF . . . . . . . . . . 25 ClassI Evidenceand/orgeneralagreementthatagiven
11.9. Peri-operative AHF. . . . . . . . . . . . 27 diagnosticprocedure/treatmentisbeneficial,
12. Surgicaltreatment of AHF . . . . . . . . . . . 27 useful,andeffective
ClassII Conflictingevidenceand/oradivergenceof
12.1. AHFrelated tocomplications ofAMI . 27
opinionabouttheusefulness/efficacyofthe
13. Mechanical assist devices andheart
treatment
transplantation . . . . . . . . . . . . . . . . . 28
ClassIIa Weightofevidence/opinionisinfavourofuse-
13.1. Indication . . . . . . . . . . . . . . . . . 28
fulness/efficacy
13.2. Hearttransplantation . . . . . . . . . . 30 ClassIIb Usefulness/efficacyislesswellestablishedby
14. Summary comments. . . . . . . . . . . . . . . 30 evidence/opinion
References. . . . . . . . . . . . . . . . . . . . . . . . . 31 ClassIII(cid:1) Evidenceorgeneralagreementthatthetreat-
mentisnotuseful/effectiveandinsomecases
maybeharmful
(cid:1)UseofClassIIIisdiscouragedbytheESC.
Preamble
Guidelines and Expert Consensus Documents aim to
presentalltherelevantevidenceonaparticularissuein Levelsofevidence
order to help physicians to weigh the benefits and risks
LevelofevidenceA Dataderivedfrommultiplerandom-
ofaparticulardiagnosticortherapeuticprocedure.They izedclinicaltrialsormeta-analyses
shouldbehelpfulineverydayclinicaldecision-making. LevelofevidenceB Dataderivedfromasinglerandom-
A great number of Guidelines and Expert Consensus izedclinicaltrialsorlargenon-
Documents have been issued in recent years by the randomizedstudies
European Society of Cardiology (ESC) and by different LevelofevidenceC Consensusofopinionoftheexperts
organizations and other related societies. This profusion and/orsmallstudies,retrospective
studiesandregistries
canputatstaketheauthorityandvalidityofguidelines,
which can only be guaranteed if they have been devel-
oped by an unquestionable decision-making process.
This is one of the reasons why the ESC and others have 1. Introduction
issued recommendations for formulating and issuing
Guidelines andExpertConsensus Documents. The aim of these guidelines is to describe the rationale
In spite of the fact that standards for issuing good behind the diagnosis and treatment of acute heart
quality Guidelines and Expert Consensus Documents are failure (AHF) in the adult population. These guidelines
well defined, recent surveys of Guidelines and Expert arewrittenforallspecialistscaringforpatientswithAHF.
ESCGuidelines Page3of36
The Committee for Practice Guidelines (CPG) of the
Table1 CausesandprecipitatingfactorsinAHF
European Society of Cardiology(ESC) nominated the Task
Force for the AHF guidelines. The Task Force included
(1) Decompensationofpre-existingchronicheartfailure
representatives from the Heart Failure Associationof the
(e.g.cardiomyopathy)
ESC and members of the European Society of Intensive
(2) Acutecoronarysyndromes
Care Medicine (ESICM). The Task Force recommendations
(a) myocardialinfarction/unstableanginawithlarge
were circulated among a review board and approved by extentofischaemiaandischaemicdysfunction
theCPG,andbytheESICM. TogetherwiththeGuidelines (b) mechanical complication of acute myocardial
for the diagnosis and treatment of chronic heart failure1 infarction
these Guidelines form the recommendations on diagnosis (c) rightventricularinfarction
andtreatmentofheartfailure. (3) Hypertensivecrisis
The recommendations are also published as a shorter (4) Acutearrhythmia(ventriculartachycardia,ventricular
document,2 andas apocket guideline. Updatedversions fibrillation,atrialfibrillationorflutter,othersupraven-
triculartachycardia)
willbe prepared in duecourse.
(5) Valvularregurgitation/endocarditis/ruptureofchordae
tendinae,worseningofpre-existingvalvular
regurgitation
2. Epidemiology, aetiology, and
(6) Severeaorticvalvestenosis
clinical context (7) Acuteseveremyocarditis
(8) Cardiactamponade
The combination of the aging of the population in many (9) Aorticdissection
countries and improved survival after acute myocardial (10) Post-partumcardiomyopathy
infarction (AMI) has created a rapid growth in the (11) Non-cardiovascularprecipitatingfactors
(a) lackofcompliancewithmedicaltreatment
number of patients currently living with chronic heart
(b) volumeoverload
failure (CHF), with a concomitant increase in the
(c) infections,particularlypneumoniaorsepticaemia
number of hospitalizations for decompensated heart
(d) severebraininsult
failure. Heart failure is the leading cause of hospital
(e) aftermajorsurgery
admissions in the Medicare population in the United (f) reductioninrenalfunction
States.3 In Europe, Scottish data show that both the (g) asthma
number of’ ‘first ever’ diagnosis, and principal and sec- (h) drugabuse
ondary diagnosis of heart failure, hospitalizations have (i) alcoholabuse
increased.Inahospitalregistrysurvey4.7%ofhospitaliz- (j) phaeochromocytoma
ations in women, and 5.1% in men, were due to heart (12) Highoutputsyndromes
(a) septicaemia
failure (in any diagnostic position), and was highly age-
(b) thyrotoxicosiscrisis
related.4 While some hospitalizations are due to new
(c) anaemia
onsetofAHF,mosthospitalizationsarecausedbydecom-
(d) shuntsyndromes
pensationofCHF.Thecrudeincidenceofheartfailureof
allgradesofseverityvariesfrom2.3to3.7perthousand
per annum.1,5,6
Coronary heart disease is the aetiology of AHF in paroxysmal atrial arrhythmias. Hospitalization due to
60–70% of patients,7,8 particularly in the elderly popu- life threatening arrhythmia was reported in 8%. The
lation. In younger subjects, AHF is frequently caused by heartfailuresyndromewasaccompaniedwithhyperten-
dilated cadiomyopathy, arrhythmia, congenital or valvu- sionorleftventricularhypertrophy(LVH)in53%,diabetes
larheartdisease,ormyocarditis.Thecausesandcompli- in 27%, with renal problems in 17%, and respiratory
cations ofAHF aredescribed inTable 1. diseasein32%.Theprevalenceofmyocardialdysfunction
The large number and long duration of hospitalization inacutemyocardialinfarctpatientsisupto30–35%12and
associatedwithAHFordecompensatedCHFcreateasub- in unstableangina patients 9%.13
stantialeconomicburdenonthehealthcaresystem.The Patients with AHF have a very poor prognosis. In the
management of heart failure in the United States con- largest randomized trial to date in patients hospitalized
sumes nearly $20 billion annually, 10% of all health care with decompensated heart failure, the 60-day mortality
dollars spent on cardiovascular disease.9 Around 75% of rate was 9.6% and the combined rate for mortality or
expenditure on heart failure relates to in-patient care. rehospitalization within 60 days was 35.2%.8,12 Mortality
Advanced heart failure and related acute decompensa- is high particularly in patients with AMI accompanied by
tion have become the single most costly medical severe heart failure, with a 30% 12 month mortality.14
syndromein cardiology.10,11 Likewise, in acute pulmonary oedema a 12% in-hospital
AHForCHFisoftenacombinationofcardiacandother and40%1-yearmortalityhavebeenreported.15Thepre-
end-organdisease,particularlymetabolicdisease.Inthe dictors of mortality are high pulmonary capillary wedge
Euroheart Failure survey8 of patients hospitalized with pressure (PCWP(cid:2)16mmHg), low serum sodium,
heart failure, mitral regurgitation was found in the increased left ventricular dimension, and low peak
echo substudy in 29% of patients, aortic regurgitation oxygen consumption.16,17
in 7%, aortic stenosis in 7%, and mitral stenosis in 3%. About 45% of patients hospitalized with AHF will be
Furthermore, 44% of the patients gave a history of rehospitalized at least once (and 15% at least twice)
Page4of36 ESCGuidelines
withintwelvemonths.18,19Estimatesoftheriskofdeath
n
or rehospitalizations within60 daysof admission forthis sio NSms
dstiusedaiesed.v7a,8r,y20f–r2o3m30to60%,dependingonthepopulation Endorganhypoperfu 2 þ,withCsympto 2 þ þ 2þ2/
I. Definitions, diagnostic steps, on et
io3n.fstthrDueemfipneainttiitoeanntitaonwnd,itcahlninAdiHcmaFlocnlaitsosirfiincagtion of AHF Hypoperfusi þ2/ þ2/ þ2/ þ þþ 2þ2,/acuteons
3.1. Definition
Acuteheartfailureisdefinedastherapidonsetofsymp- esis 2 low 2
tmoamysoacncdursiwgnitshseocrownditahroyuttoparbenvoiorumsaclacradridaicacdifsuenacsteio.nT.hIet Diur þ þ/ þ Low Very þþ/
cardiacdysfunctioncanberelatedtosystolicordiastolic
dysfunction, to abnormalities in cardiac rhythm, or to
/
p
acdpinacir(gseiurTAt)dltHhiaoneiAdoenaFacfeccdhdtpcuceAdaaracotaHeytnelnmriisqFdtnef,ppuduinfarceiewantreafnceichtswllosetesuiacimcirnrotutohlethinpornog)aeaiidnAntednroisHentseraomiaFtlofmaftpintmcesarCiasmudletasHdti(aayeeTFhatatna)cempcdntbuarhewdeletrw.ecnetsidoItiettt2homfd.nhai)etospn:islueioowungtntfronitestpvsfeahorunt(ealiodfi(volnnneiilndfoeeecunworsosotfiylfhtvyomCerosneHrkepsianFoveat.tooertefwmroanoanssr-fl PCWPCongestionKillimmHgForrester MildKIIFII/elevation–IVFII–III.18KII/ ElevatedKIIIFII/ .16KIII–IVFI–III/ .18KIVFIV/ þ2KIIFI–II//LowFI ayoverlaptheseclassifications.¼centralnervoussystem.
cardiogenicshock,pulmonaryoedema,orhyperten- mNS
nC
(((iiiivii))) HPsfawmacuCefcwogbaairlencurvulayviheooaiiactindtlrpellidanomchtuucodcieireckadorrmcihororaoeelnrmretnenypgicespdlecssaeeahaeunaarioehxrsnntooessrfepfiyer.iuoitivceisvedclensvesafekaetpeediurlritlsaolotmnrryiyhiicteoerasssbAcohatc,nddsoypHec.eout(ieurrdko9Fhsmermeslsy:g0f:eeuuesopisr%ahcnneCatvaraStydogrleaopniilspvilogryrnhiftia(ehoedenncfuvndraepidscdecoodereorBihoroegmeelramiPobfaeemnffissnruryofncpp,etdatpsd(eaiaihdciTcrryhisot9oaavtersniin0epstebbylgpiahoorbnnnlmlhmrmiieeaoryotnziypodcrmeipedwb2ickrt.adrcuHoldi)ect,ouct,miiogThvsholpsewbaahetbsdtadydrrioalesrurteeetecrrahtobpnsfreaufimfuyserccatOtn,enedXmeaeei2hhscu-srtdwdseeerptdesacurainaaaiuirenoontraoyrrtstldpdehnostt.,---) monclinicalandhaemodynamiccharacteristics HeartrateSBPCI2mmHgLminm// þ2LownormalLownormal///HighHighþUsuallyHigh2/increased þLownormalLow þLownormalLow,,2.2 .90,90,1.8 þþþ2/UsuallylowLowLow eneralrules.diacoutputsyndromeissubjectiveandtheclinicalpresentatio¼¼cardiacindex;PCWPpulmonarycapillarywedgepressure;
(v) .tsHoadwtuoiyirufriiomasn6rgitnnerhm0dhpem.eayrusbestooTtehppawum,oh,mnmetuieeptrutiirhiauaawpspetrtstuuohlitr,oiatteefoshcwlarrglaaiiyi(oeleartB,urndchlsPrw,ioiy0wecopnrap.igitro5tsituoehesithlmrnsionmoncsuxihlbuuhcou/iistrycagnkmeseorhegahpaos/vrotf.ictyhisirhchtdc,o)3ekecee,m0s.aorrnhirnzmcwatomlgeeoncimedetwrkaoshacH.etbfhtcigmyoeoaaa)nrinrhag,da(iip,sacginamauanhdnclusd/sccP)seooo,easarunordgwtrdgmelpaeioitbattuesw’ehycts-- Table2Terminologyandcom Clinicalstatus IAcutedecompensatedcongestiveheartfailureIIAcuteheartfailurewithhypertensionhyperten-/sivecrisisIIIAcuteheartfailurewithpulmonaryoedema(cid:1)IVaCardiogenicshock/lowoutputsyndromeIVbSeverecardiogenicshockVHighoutputfailureVIRight-sidedacuteheartfailure TheabovevaluesinTable2areg(cid:1)Thedifferentiationfromlowcar¼SBPsystolicbloodpressure;CI
ESCGuidelines Page5of36
(vi) Right heart failure is characterized by low output pulmonary congestion (rales, abnormal chest X-ray),
syndrome with increased jugular venous pressure, and haemodynamically on the basis of a depressed
increased liversize andhypotension. cardiac index ((cid:3)2.2L/min/m2) and elevated pulmonary
capillary pressure (.18mmHg). The original paper
VariousotherclassificationsoftheAHFsyndromeareuti-
defined the treatment strategy according to the clinical
lizedincoronarycareandintensivecareunits.TheKillip
and haemodynamic status. Mortality was 2.2% in group
classification is based on clinical signs and chest X-ray
I, 10.1% in group II, 22.4% in group III, and 55.5% in
findings,andtheForresterclassificationisbasedonclini-
group IV.
calsignsandhaemodynamiccharacteristics.Theseclassi-
fications have been validated in AHF after AMI and thus
arebestappliedtodenovoAHF.Thethird‘clinicalsever- 3.1.3. ‘Clinical severity’ classification. The clinical
ity’classificationhasbeenvalidatedinacardiomyopathy severity classification is based on observation of the
service24 and is based on clinical findings.25 It is most peripheral circulation (perfusion) and on auscultation of
applicable tochronic decompensated heart failure.24 the lungs (congestion). The patients can be classified as
Class I (Group A) (warm and dry), Class II (Group B)
3.1.1. Killip classification. The Killip classification was (warm and wet), Class III (Group L) (cold and dry), and
designed to provide a clinical estimate of the severity
Class IV (Group C) (cold and wet). This classification
ofmyocardial derangement in thetreatment of AMI:26
has been validated prognostically in a cardiomyopathy
service28 and is therefore applicable to patients with
. Stage I—No heart failure. No clinical signs of cardiac
decompensation; CHF, whetherhospitalized oroutpatients.
. Stage II—Heart failure. Diagnostic criteria include
rales, S3 gallop and pulmonary venous hypertension. 3.2. Theclinical syndromeofAHF
Pulmonary congestion with wet rales in the lower half AHFisaclinicalsyndrome,withreducedcardiacoutput,
of thelung fields; tissuehypoperfusion,increaseinthepulmonarycapillary
. Stage III—Severe heart failure. Frank pulmonary wedge pressure, and tissue congestion. The underlying
oedema with ralesthroughoutthe lungfields; mechanism may be cardiac or extra-cardiac, and may
. StageIV—Cardiogenicshock.Signsincludehypotension be transient and reversible with resolution of the acute
(SBP(cid:3)90mmHg),andevidenceofperipheralvasocon- syndrome or may induce permanent damage leading to
striction such asoliguria, cyanosis, anddiaphoresis. chronic heart failure. The cardiac dysfunction can be
related to systolic or diastolic myocardial dysfunction
3.1.2. Forrester classification. The Forrester AHF (mainlyinducedbyischaemiaorinfection),acutevalvu-
classification was also developed in AMI patients, and lardysfunction,pericardialtamponade,abnormalitiesof
describes four groups according to clinical and haemo- cardiacrhythm,orpreload/afterloadmismatch.Multiple
dynamic status (Figure 1).27 Patients are classified extra-cardiac pathologies may result in AHF by changing
clinically on the basis of peripheral hypoperfusion (filli- the cardiac loading conditions for example (i) increased
form pulse, cold clammy skin, peripheral cyanosis, afterload due to systemic or pulmonary hypertension or
hypotension, tachycardia, confusion, oliguria) and massive pulmonary emboli, (ii) increased preloaddue to
Figure1 Clinicalclassificationofthemodeofheartfailure(Forresterclassification).HI–IVreferstohaemodynamicseverity,withreferencefiguresfor
cardiacindexandpulmonarycapillarypressuresshownontheverticalandhorizontalaxes,respectively.CI–IVreferstoclinicalseverity.
Page6of36 ESCGuidelines
increased volume intake or reduced excretion due to left heart. Extra-cardiac pathologies may include severe
renal failure or endocrinopathy, or (iii) high output hypertension, high output states (anaemia, thyrotoxi-
state due to infection, thyrotoxicosis, anaemia, and cosis),andneurogenicstates(braintumoursortrauma).
Paget’s disease. Heart failure can be complicated by Physical examination of the cardiovascular system,
co-existing end-organ disease. Severe heart failure can including the apex beat, the quality of the heart sounds,
also induce multi-organ failure, whichmay be lethal. the presence of murmurs, and auscultation of the lungs
Appropriatelong-termmedicaltherapyand,ifpossible, for fine rales and expiratorywheezing (‘cardiac asthma’)
anatomical correction of the underlying pathology may maybeindicativeofthemaindiagnosis.
prevent further AHF syndrome ‘attacks’ and improve the In left heart backward failure patients should be
poorlong-termprognosisassociatedwiththissyndrome. treated mainly with vasodilation and the addition of
Theclinical AHF syndromemay be classifiedas predo- diuretics, bronchodilators, and narcotics, as required.
minantly left or right forward failure, left or right back- Respiratory support may be necessary. This can either
ward failure, ora combinationof these. be with continuous positive airway pressure (CPAP) or
non-invasive positive pressure ventilation, or in some
3.2.1. Forward (left and right) AHF. Forward acute circumstances invasive ventilation may be required
heart failure may be mild-to-moderate with only effort following endotracheal intubation.
fatigue, up to severe with manifestations of reduced
tissueperfusionatrestwithweakness,confusion,drowsi- 3.2.3. Right-heart backward failure. The syndrome of
ness, paleness with peripheral cyanosis, cold clammy acute right heart failure is related to pulmonary and
skin,lowbloodpressure,filliformpulse,andoliguria,cul- rightheartdysfunction,includingexacerbationsofchro-
minating in the full blown presentation of cardiogenic nic lung disease with pulmonary hypertension, or acute
shock. massive lung disease (e.g. massive pneumonia or pul-
This syndrome may be induced by a large variety of monaryembolism),acuterightventricularinfarction,tri-
pathologies. An adequate history may indicate the main cuspid valve malfunction (traumatic or infectious), and
diagnosis for example (i) acute coronary syndrome with acute or subacute pericardial disease. Advanced left
the relevant risk factors, past history, and suggestive heart disease progressing to right sided failure should
symptoms; (ii) acute myocarditis with a recent history alsobeconsidered,andsimilarlylongstandingcongenital
suggestive of acute viral infection; (iii) acute valvular heart disease with evolving right ventricular failure
dysfunction with a history of chronic valve disease or should be taken into account. Non-cardiopulmonary
valve surgery, infection with the possibility of bacterial pathologies include nephritic/nephrotic syndrome and
endocarditis, or chest trauma; (iv) pulmonary embolism end-stage liver disease. Various vasoactive peptide-
with a relevant history and suggestive symptoms; or (v) secreting tumours should also be considered.
pericardial tamponade. The typical presentation is with fatigue, pitting ankle
Physicalexaminationofthecardiovascularsystemmay oedema, tenderness in the upper abdomen (due to liver
be indicative of the main diagnosis, for example by dis- congestion), shortness of breath (with pleural effusion),
tended neck veins and paradoxical pulse (pericardial and distension of the abdomen (with ascites). The full-
tamponade),muffledheartsoundsrelatedtomyocardial blownsyndromeincludesanasarcawithliverdysfunction
systolic dysfunction, or the disappearance of artificial andoliguria.
valvesoundsoranappropriatemurmurindicatingavalv- History and physical examination should confirm the
ular problem. syndrome of acute right heart failure, indicate the
InforwardAHFimmediatemanagementshouldinclude suspected diagnosis and guide further investigation,
supportive treatment to improve cardiac output and which is likely to include ECG, blood gases, D-dimer,
tissue oxygenation. This canbe achieved with vasodilat- chest X-ray, cardiac Doppler-echocardiography, pulmon-
ing agents, fluid replacement to achieve an optimal ary angiography,or chest CTscan.
preload, short-term inotropic support and (sometimes) In right heart backward failure fluid overload is
intra aortic ballooncounterpulsation. managed with diuretics, including spironolactone and
sometimes with a short course of low dose (‘diuretic
3.2.2. Left-heart backward failure. Left-heart back- dose’) of dopamine. Concomitant treatment may
wardfailuremayberelatedtoleftventriculardysfunction includeantibioticsforpulmonaryinfectionandbacterial
with varying degrees of severity from mild-to-moderate endocarditis; Caþþ channel blockers, nitric oxide, or
with only exertional dyspnoea, to pulmonary oedema prostaglandins for primary pulmonary hypertension; and
presentingwithshortnessofbreath(drycough,sometimes anticoagulants, thrombolytics, or thrombectomy for
withfrothysputum),pallororevencyanosis,coldclammy acute pulmonary embolism.
skin,andnormalorelevatedbloodpressure.Fineralesare
usuallyaudibleoverthelungfields.ChestX-rayshowspul- 4. Pathophysiology of AHF
monarycongestion/oedema.
Pathologyoftheleftheartmayberesponsibleforthis 4.1. Theviciouscycle intheacute failing heart
syndrome, including: myocardial dysfunction related to The final common denominator in the syndrome of AHF
chronicexistingconditions;acuteinsult suchasmyocar- is a critical inability of the myocardium to maintain a
dial ischaemiaorinfarction;aorticandmitralvalvedys- cardiac output sufficient to meet the demands of the
function;cardiacrhythmdisturbances;ortumoursofthe peripheral circulation. Irrespective of the underlying
ESCGuidelines Page7of36
cause of AHF a vicious cycle is activated that, if not consumptiontopreventischaemiaandnecrosisfollowing
appropriately treated, leads to chronic heart failure reduced bloodflow tothemyocardium.41
and death. This is shown in Figure 2, and is described Hibernating myocardium and stunning can co-exist.
in detail elsewhere.29–34 Hibernation improves in time with reinstitution of blood
InorderforpatientswithAHFtorespondtotreatment flow and oxygenation, whilst stunned myocardium
the myocardial dysfunction must be reversible. This is retains inotropic reserve and can respond to inotropic
particularlyimportantinAHFduetoischaemia,stunning stimulation.36 Since these mechanisms depend on the
or hibernation, where a dysfunctional myocardium can duration of myocardial damage, a rapid restoration of
return tonormal when appropriately treated. oxygenation and blood flow is mandatory to reverse
these pathophysiological alterations.
4.2. Myocardial stunning
Myocardial stunning is the myocardial dysfunction that 5. Diagnosis of AHF
occurs following prolonged ischaemia, which may persist
in the short-term even when normal blood flow is ThediagnosisofAHFisbasedonthesymptomsandclini-
restored. This phenomenon has been described exper- calfindings,supportedbyappropriateinvestigationssuch
imentally35aswellasclinically.36Mechanismsofdysfunc- as ECG, chest X-ray, biomarkers, and Doppler-echo-
tion are excessive oxidative stress,37 changes in Caþþ cardiography(Figure3).Thepatientshouldbeclassified
homeostasis,andCaþþ desensitizationofcontractilepro- according to previously described criteria for systolic
teins,38 as well as myocardial depressant factors.39 The and/or diastolic dysfunction (Figure 4), and by the
intensity and duration of stunning is dependent on the characteristics of forward or backward left or right
severityanddurationoftheprecedingischaemicinsult.36 heart failure.
4.3. Hibernation 5.1. Clinical evaluation
Hibernation is defined as an impairment of myocardial Systematic clinical assessment of the peripheral circula-
function due to severely reduced coronary blood flow tion, venous filling, and peripheral temperature are
although myocardial cells are still intact. By improving important.
blood flow and oxygenation, hibernating myocardium Right ventricular filling in decompensated heart
can restore its normal function.40 Hibernation can be failure may usually be evaluated from the central jugular
regarded as an adaptive mechanism to reduce oxygen venous pressure. When the internal jugular veins are
Figure2 PathophysiologyofthesyndromeofAHF.Followingacutecriticalevents,LVdeteriorationoccursrapidlyandrequiresurgentmedicaltreat-
ment.Thepathophysiologyofthesyndromeofheartfailureissummarized.Mechanical,haemodynamic,andneurohormonalchangesaresimilarbut
notidenticaltothoseobservedinCHF.Thetimecourseofdevelopmentorreversalofthesechangesvariesconsiderablyandstronglydependsonthe
underlyingcauseofleftventriculardeteriorationaswellaspreexistingcardiovasculardisease.However,changesdeveloprapidlyandthereforeAHF
isconsiderablydifferenttothesyndromeofCHF.
Page8of36 ESCGuidelines
determine the aetiology of AHF and assess the loading
conditions of the heart. It is essential in the assessment
ofacutecoronarysyndromes.42–44TheECGmayalsoindi-
cate acute right or left ventricular or atrial strain, peri-
myocarditis and pre-existing conditions such as left and
rightventricularhypertrophyordilatedcardiomyopathy.
Cardiacarrhythmiashouldbeassessedinthe12-leadECG
as well asin continuous ECGmonitoring.
5.3. ChestX-rayand imagingtechniques
ChestX-rayandotherimagingshouldbeperformedearly
forallpatientswithAHFtoevaluatepre-existingchestor
cardiacconditions(cardiacsizeandshape)andtoassess
pulmonarycongestion.Itisusedbothforconfirmationof
thediagnosis,andforfollow-upofimprovementorunsa-
Figure3 DiagnosisofAHF. tisfactory response to therapy. Chest X-ray allows the
differentialdiagnosisofleftheartfailurefrominflamma-
tory or infectious lung diseases. Chest CTscan with or
without contrast angiography and scintigraphy may be
used to clarify the pulmonary pathology and diagnose
major pulmonary embolism. CT scan, transesophageal
echocardiography,orMRIshouldbeusedincasesofsuspi-
cion ofaorticdissection.
5.4. Laboratorytests
AnumberoflaboratorytestsshouldbeperformedinAHF
patients (Table 3). Arterial blood gas analysis (Astrup)
enables assessment of oxygenation (pO ), respiratory
2
adequacy (pCO ), acid–base balance (pH), and base
2
deficit, and should be assessed in all patients with
Figure4 AssessmentofLVfunctioninAHF.
severe heart failure. Non-invasive measurement with
impractical for evaluation (e.g. dueto venous valves) the pulse oximetry and end-tidal CO can often replace
2
external jugular veins can be used. Caution is necessary Astrup (Level of evidence C) but not in very low
in the interpretation of high measured central venous output, vasocontricted shock states. Measurement of
pressure (CVP) in AHF, as this may be a reflection of venous O saturation (i.e. in the jugular vein) may be
2
decreasedvenouscompliancetogetherwithdecreasedRV
complianceeveninthepresenceofinadequateRVfilling. Table3 LaboratorytestsinpatientshospitalizedwithAHF
Leftsidedfillingpressureisassessedbychestausculta-
tion, with the presence of wet rales in the lung fields Bloodcount Always
Plateletcount Always
usually indicating raised pressure. The confirmation,
INR Ifpatientanticoagulated
classification of severity, and clinical follow up of pul-
orinsevereheartfailure
monary congestion and pleural effusions should be done
CRP Tobeconsidered
using thechest X-ray.
D-dimer Tobeconsidered(maybe
ClassI recommendation, level ofevidenceC falselypositiveifCRP
elevatedorpatienthas
Again,inacuteconditionstheclinicalevaluationofleft beenhospitalizedfor
sided filling pressure may be misleading due to the prolongedperiod)
rapidly evolving clinical situation. Cardiac palpation and UreaandElectrolytes Always
auscultation for ventricular and atrial gallop rhythms (Naþ,Kþ,urea,
(S3, S4) should be performed. The quality of the heart creatinine)
BloodGlucose Always
sounds, and presence of atrial and ventricular gallops
CKMB,cardiacTnI/TnT Always
and valvular murmurs are important for diagnosis and
Arterialbloodgases Insevereheartfailureor
clinicalassessment.Assessmentoftheextentofarterio-
indiabeticpatients
sclerosisbydetectingmissingpulsesandthepresenceof
Transaminases Tobeconsidered
carotidandabdominalbruitsisoftenimportant,particu- Urinanalysis Tobeconsidered
larly in elderly subjects. PlasmaBNPorNTproBNP Tobeconsidered
Otherspecificlaboratorytestsshouldbetakenfordifferentialdiag-
5.2. Electrocardiogram nosticpurposesorinordertoidentifyend-organdysfunction.
A normal electrocardiogram (ECG) is uncommon in AHF. INR¼Internationalnormalizedratioofthromboplastintime;Tnl¼
troponinI;TnT¼troponinT.
The ECG is able to identify the rhythm, and may help
ESCGuidelines Page9of36
useful for an estimation of the total body oxygen An improvement in the haemodynamic parameters
supply–demand balance. (primarily an increase in cardiac output and stroke
Plasma B-type natriuretic peptide (BNP) is released volume and a reduction in the pulmonary capillary
from the cardiac ventricles in response to increased wedgepressureandrightatrialpressure)havetradition-
wall stretch and volume overload and has been used allybeenregardedasbeneficialeffectsofthetreatment
to exclude and/or identify congestive heart failure in of AHF.52–57 An improvement in haemodynamic para-
patientsadmittedfordyspnoeatotheemergencydepart- meters only may be misleading, and a concomitant
ment.1,45Decisioncutpointsof300pg/mLforNT-proBNP improvement in symptoms (dyspnoea and/or fatigue) is
and 100pg/mL for BNP have been proposed, but the generally required.58 These short-term benefits must
older population has been poorly studied. During’ also be accompanied by favourable effects on longer-
‘flash’ pulmonary oedema, BNP levels may remain term outcomes. This is likely to be achieved by avoid-
normal at the time of admission. Otherwise, BNP has ance,or limitation, of myocardial damage.
a good negative predictive value to exclude heart Dyspnoea is the dominant symptom in AHF but is sub-
failure.46 The data are not consistent on reference jective. Objective assessment can be made by standar-
values and on the effect of treatment. Various clinical dized tools, such as the Borg Rating of perceived
conditions may affect the BNP concentration, including exertion,59indexesofdyspnoea,60andvariousvisualana-
renalfailureandsepticaemia.Ifelevatedconcentrations logue scales.61 Changes from the initial assessment may
arepresent,furtherdiagnostictestsarerequired.IfAHF be used asmeasures of improvementor deterioration.
is confirmed, increased levels of plasma BNPand NT-pro Anotherobjectiveoftreatmentisthereductioninthe
BNP carry important prognostic information. The exact clinical signs of heart failure, although these may often
roleof BNPremainstobe fully clarified.47 be difficult to quantify. A reduction in body weight and/
or an increase in diuresis are beneficial effects
5.5. Echocardiography of therapy in congestive and oliguric patients with
Echocardiography is an essential tool for the evaluation AHF.56,62 Similarly, an improvement in oxygen saturation
of the functional and structural changes underlying or andinlaboratorytestssuchasrenaland/orhepaticfunc-
associated with AHF, as well as in the assessment of tion and/or serum electrolytes are meaningful goals of
acutecoronary syndromes treatment.PlasmaBNPconcentrationcanreflecthaemo-
Class Irecommendation, levelof evidenceC dynamic improvement and decreased levels are ben-
eficial. However, short-term haemodynamic benefits
EchocardiographywithDopplerimagingshouldbeused maybedissociatedfromafavourableeffectonprognosis.
toevaluateandmonitorregionalandgloballeftandright Thus,abeneficial(oratleastaneutral)effectonpatient
ventricular function, valvular structure and function, outcome is required in addition to an improvement in
possiblepericardialpathology,mechanicalcomplications symptoms and/orclinical signs.54,58
of acute myocardial infarction, and, on rare occasions, Beneficial effects of therapy on outcome include a
spaceoccupyinglesions.Cardiacoutputcanbeestimated reduction in the duration of intravenous vasoactive
byappropriateDoppleraorticorpulmonarytimevelocity
contour measurements. An appropriate echo-Doppler
Table4 GoalsoftreatmentofthepatientwithAHF
study can also estimate pulmonary artery pressures
(from the tricuspid regurgitation jet) and has been also Clinical
used for the monitoring of left ventricular preload.48–50 #symptoms(dyspnoeaand/orfatigue)
Echocardiography has not been validated with right #clinicalsigns
heart catheterisation inpatients with AHF.51 #bodyweight
"diuresis
"oxygenation
5.6. Other investigations
Laboratory
Incasesofcoronaryarteryrelatedcomplicationssuchas
Serumelectrolytenormalisation
unstable angina or myocardial infarction, angiography #BUNand/orcreatinine
is important and angiography-based revascularization #S-bilirubin
therapy hasbeen shownto improveprognosis.39,42,43 #plasmaBNP
ClassI recommendation, levelofevidence B Bloodglucosenormalisation
Haemodynamic
Coronary arteriography is also often indicated in pro- #pulmonarycapillarywedgepressureto,18mmHg
longed AHF, unexplained by other investigations, as rec- "cardiacoutputand/orstrokevolume
ommended inthe guidelines for diagnosis ofCHF.1 Outcome
#lengthofstayintheintensivecareunit
Insertion of a pulmonary artery catheter (PAC) may
#durationofhospitalisation
assist the diagnosis of and follow up AHF. See Section
"timetohospitalre-admission
7.2.3 forfurther details.
#mortality
Tolerability
6. Goals of the treatment of AHF Lowrateofwithdrawalfromtherapeuticmeasures
Lowincidenceofadverseeffects
The immediate goals are to improve symptoms and to
BUN¼bloodureanitrogen.
stabilizethehaemodynamiccondition(Table4,Figure5).
Page10of36 ESCGuidelines
Figure5 Immediategoalsintreatmentofthepatientswithacuteheartfailure.Incoronarypatientsmeanbloodpressure(mBP)shouldbehigherto
ensurecoronaryperfusion,mBP.70,orsystolic.90mmHg.
therapy,63 the length of stay (both in the intensive care failuremanagement.ThetreatmentofAHFshouldbefol-
unit and in the hospital),54,58,63,64 and a reduction in lowedbyasubsequentHFclinicprogrammewhenappli-
the readmission rate with an increase in the time to cable andas recommendedbyESC guidelines.1
readmission.58,63,64 A reduction in both in-hospital The care and information needs of the acutely ill
and long-term mortality is the major goal of treat- patient and his/her family will usually be addressed by
ment54,58,63,64 although the effect of short-term treat- expert nurses.
ment may bedissociated fromthe long-termeffects. Heart failure staff nurses and cardiologist/heart
Lastly, a favourable safety and tolerability profile is failure/intensive care specialists should be given the
also necessary for any treatment used in patients with opportunity forcontinuing professional education.
AHF. Any agent used in this condition should be associ- Recommendations on the standard structure, nursing
ated with a low withdrawal rate with a relatively low staffandequipmentrequirementsinintensivecardiology
incidence ofuntoward side effects. care units and relevant step-down care units based on
the expert opinion of the Working Group of Acute
Cardiac Careare under preparation.
6.1. Organization ofthetreatmentof AHF
BestresultsareachievedifpatientswithAHFaretreated
promptly by expert staff in areas reserved for heart
failurepatients,beitanemergencyarea,acutecoronary 7. Instrumentation and monitoring of
care, or surgical or medical intensive care. An experi- patients in AHF
enced cardiologist and/or other suitably trained staff
should treat AHF patients. The diagnostic services MonitoringofthepatientwithAHFshouldbeinitiatedas
should provide early access to diagnostic procedures soon as possible after his/her arrival at the emergency
such as echocardiography and coronary angiography, as unit, concurrently with ongoing diagnostic measures
needed. addressed at determining the primary aetiology. The
Treatment of patients with AHF requires a treatment typesandlevelofmonitoringrequiredforanyindividual
planin the hospital system.16,21 patient vary widely depending on the severity of the
Class Irecommendation, levelof evidenceB cardiac decompensation and the response to initial
therapy. Local logistic issues may also be relevant.
Comparative studies have shown shorter hospitali- There are no prospective randomized controlled
zation time in patients treated by staff trained in heart outcome-basedstudiesontheuseofdifferentmonitoring