Damianus Journal of Medicine; Prompt diagnosis and management of acute heart failure syndrome

Vol.10 No.2 Juni 2011: hal. 91–96

TINJAUAN PUSTAKA

PROMPT DIAGNOSIS AND MANAGEMENT

OF ACUTE HEART FAILURE SYNDROME

Leonardo P. Suciadi*, Bambang B. Siswanto**

ABSTRACT
Gagal jantung akut merupakan kondisi dengan gejala dan tanda gagal jantung *
Emergency & Trauma Center,
yang terjadi dalam onset cepat, dan disebabkan oleh gangguan fungsi jantung Siloam Hospitals Kebun Jeruk).
baik itu disfungsi sistolik atau diastolic, gangguan katup akut, aritmia maupun **
ketidaksesuaian antara preload dengan afterload. Penyebabnya bisa berasal Departemen Kardiologi dan
dari beragam mekanisme, namun kondisi ini merupakan kegawatdaruratan Vaskular Pusat Jantung Nasional
sehingga penting untuk segera dideteksi dan diberikan terapi yang tepat Harapan Kita/Fakultas Kedokteran
untuk menekan angka mortalitas dan morbiditas. Terdapat 7 profil klinis dari Universitas Indonesia)
sindrom gagal jantung akut; acute decompensated heart failure (ADHF),
edema pulmoner akut, syok kardiogenik, gagal jantung akut pada sindrom
koroner akut, gagal jantung kanan terisolir, gagal jantung high-output dan
gagal jantung hipertensif. Pengenalan profil klinis tersebut akan sangat penting
dalam menentukan terapi yang tepat. Diagnosa dibuat berdasarkan
anamnesa yang cermat, pemeriksaan fisik serta disokong dengan berbagai
pemeriksaan penunjang seperti foto rontgen dada, ekokardiografi dan tes
biomarker di laboratorium. Tujuan utama terapi adalah mengatasi gejala
yang ada dan menstabilkan hemodinamik, terutama menjamin oksigenisasi
serta perfusi jaringan.
Kata kunci: gagal jantung akut, profil klinis, diagnosis, terapi

INTRODUCTION gency department, could play an important role to man-

Acute Heart Failure Syndrome (AHFS) is one of the
most common cause of hospital admission in patients
>65 years of age in USA, accounting for more than 1
million hospital admissions annually, with more than 6
millions hospital days, and it has risen 175% from 1979
to 2004.1 Approximately 80% of these patients initially
present to the Emergency Department.2 Between 1992
and 2001, there were 10.5 million Emergency Depart-
ment visits for AHFS in USA, with an admission rate of
70-80%.3 These numbers are projected to increase
along with increasing number of elderly population, in-
creasing success of management of myocardial inf-
arction patients, advanced in long term treatment of
patients with chronic heart failure.2,3
AHFS is an emergency condition that need early diag-
nosis and prompts treatment to cut down the morbid-
ity and mortality. From a large Indonesia ADHERE
(Acute Decompensated Heart Failure Registry) study
2006, the in-hospital mortality in 5 hospitals in Indone-
sia ranges from 6 % to 12% and the 4 years mortality
is 50 %, with re-hospitalization rate is 29%.4 Primary
care physicians, especially they who work at emer-
age these patients at the time of hospital admission.
Many conditions could mimic symptoms and signs of
AHFS in daily practice, and recognizing early signs of
AHFS is challenging. Knowing pathophysiology and
clinical features as well as proper treatment of AHFS
are mandatory at this point because failure to early
diagnosis and prompt treatment will results in mortal-
ity. The aim of this manuscript is to describe how to
diagnose and make early management of this syn-
drome.
Acute heart failure syndrome
Acute heart failure (AHF) is defined as a rapid onset in
the signs and symptoms of HF, secondary to cardiac
dysfunction whether it is related to systolic or diastolic
dysfunction, cardiac arrhythmias, valvular abnormali-
ties or preload-afterload mismatch. These diverse aeti-
ologies often interact resulting to a life threatening con-
dition that requires urgent treatment.5 AHF is not a dis-
ease but rather it is a syndrome caused by different
mechanism, and it may be either new HF or worsening
of pre-existing chronic HF. A number of common causes
and precipitating factors of AHF can be seen at Table

Dam J Med Volume 10, Nomor 2, 2011 91

 DAMIANUS Journal of Medicine
1. Generally, AHF could be induced by one or a combi-
nation of hemodynamic mechanisms including in-
creased afterload due to systemic or pulmonary hy-
pertension or high output states (septicemia, anemia,
thyrotoxicosis); increased preload due to volume over-
load; decreased cardiac contractility due to significant
infarct or other myopathies; or diastolic dysfunction.5,6
Identifying the underlying factor is very crucial in strat-
egy to manage patients with AHF.
Table 1. Several precipitating factors of AHF
Ischaemic heart disease
† Acute coronary syndromes
† Mechanical complications of acute MI
† Right ventricular infarction
Circulation failure
† Septicaemia
† Thyrotoxicosis
† Anaemia
† Shunts
† Cardiac tamponade
† Pulmonary embolism
Valvular
† Valve stenosis or regurgitation
† Endocarditis
† Aortic dissection
Look into its pathophysiology, there are three phases
of AHF; Initiation, amplification and final vicious cycle.6
The disturbance in hemodynamic processes leads to
the genesis of the initial phase of AHF which com-
prises both backward failure (increased LV filling pres-
sure lading to pulmonary congestion) and forward fail-
ure (peripheral hypoperfusion). This phase is marked
as acute diastolic dysfunction on echocardiography.
Once initiated, AHF is amplified through several mecha-
nisms; myocardial necrosis as measured by troponin
release (PRESERVD-HF study), respiratory failure and
leakage of the alveolar-capillary membrane, RV fail-
ure, renal failure, and arrhythmias especially atrial
tachyarrhythmias which is a strong predictor of recur-
rent events and death.7 Finally the patients fall into
92 Dam J Med Volume 10, Nomor 2, 2011
genic shock.5 Data from ESC-HF Pilot Survey8 showed
that acute decompensated HF was most frequent pre-
sentation of AHF (75% of the cases) in clinical setting.
The patients presenting with cardiogenic shock have
the worst short-term prognosis with the highest in-hos-
pital mortality rate so that patients presenting with this
clinical profile should be aggressively treated. Whereas,
the lowest mortality rate is in those with hypertensive
HF. Furthermore, there are three major independent
determinants of death in AHF, those are low systolic
blood pressure, older age, and reduced renal function.8
Drugs induced: NSAID, COX inhibitors,
thizolidinediones
Decompensation of pre-existing chronic HF
† Lack of adherence
† Volume overload
† Infections, especially pneumonia
† Cerebrovascular insult – severe brain injury
† Major surgery
† Renal dysfunction
† Asthma, COPD
† Drug abuse
† Alcohol abuse
Hypertensive crisis
Acute arrhythmia
Myopathies
† Postpartum cardiomyopathy
† Acute myocarditis
vicious cycle leading into severe cardiovascular failure
with low cardiac output, hypoxemia, activated neuro-
hormonal and inflammatory modulators, vasoconstric-
tion, decreased peripheral perfusion, respiratory fail-
ure, and if untreated, multi-organ failure and death.
The clinical presentation of AHF reflects a spectrum of
conditions. Some classifications have been applied in
order to giving guide how to manage every distinct pre-
sentation of AHF and also to predict prognosis of the
patients. The patients with AHF will usually present in
one of 7 clinical categories; worsening or acute dec-
ompensated chronic HF, pulmonary oedema, hyper-
tensive heart failure, high output failure, AHF in acute
coronary syndrome, isolated RV failure, and cardio-
 Prompt diagnosis and management of acute heart failure syndrome
Acute Coronary Syndromes is the commonest cause
of acute new-onset HF.
Other useful clinical classification of AHF after acute
MI is the Killip-Kimball Class. Specifically, Killip class
I patients had no evidence of heart failure; Killip class II
patients had mild heart failure with rales involving one
third or less of the posterior lung fields and systolic
blood pressure of 90 mmHg or higher; Killip class III
patients had pulmonary oedema with rales involving
more than one third of the posterior lung fields and
systolic blood pressure of 90 mm Hg or more; and
Killip class IV patients had cardiogenic shock with any
rales and systolic blood pressure of less than 90 mm
Hg. In a multivariate analysis of patients after acute
MI, higher Killip class was associated with higher mor-
tality at 30 days (2.8% in Killip class I vs 8.8% in class
II vs 14.4% in class III/IV; P<.001) and 6 months (5.0%
vs 14.7% vs 23.0%, respectively;(P<.001). 9 The
Forrester Classification or Wet/Dry-Warm/Cold Profile
is also based on clinical signs and hemodynamic char-
acteristics after acute MI, identifying sufficiency of pe-
ripheral perfusion or existence of pulmonary conges-
tion in AHF setting. The patients with wet-cold profile
have the highest mortality rate in hospital stay.5,6
Diagnosis
The diagnosis of AHF is made by careful assessment
of the clinical presentation focused on history taking
and physical examination. Confirmation of the diagno-
sis is provided by appropriate investigations such as
chest X-ray, echocardiography and laboratory test in-
cluding specific biomarkers and arterial blood gas
analysis. Although ECG is non-diagnostic in HF, it
should be performed to figure out some underlying
pathologic processes such as acute coronary syn-
dromes and arrhythmias.5,6 Figure 1 depicts initial evalu-
ation of patients with suspected AHF.
The presenting symptoms of AHF could be classified
generally into backward symptoms and afterward symp-
toms. Backward symptoms can be related to pulmo-
nary congestion as result of increase LV filling pres-
sure, or to systemic venous congestion as result of
RV filling pressure (Table 2). Some studies reported
no differences in the symptoms of HF in the proportion
of the patients with either reduced (LVEF < 40%) or
preserved (LVEF > 40%) LV function, but the severity
is greater in patients with reduced LV function.6 Other
diverse symptoms can be found relating to different
underlying causes of AHF.
Dam J Med Volume 10, Nomor 2, 2011
Figure 1. Initial evaluation of patients suspected Heart
Failure
Assess symptoms and signs
Known heart
disease of chronic
HF? X-ray conges-
tion? Abnormal
blood gasses? N
Natriuretic peptide? o
Abnormal ECG?
Yes Consider non-
cardiac origin
Evaluate by
echocardiography
HF confirmed
Plan treatment
strategy
Assess clinical
profile, severity, l
r ma
and aetology using No
further investigation
Adapted from ESC Guidelines for the treatment of
acute and chronic heart failure 2008.
Dyspnea is the most common presenting symptoms
of AHF, occurring in approximately 90% cases.10 Dif-
ferentiating dyspnea from cardiac origin with non-car-
diac (pulmonary diseases, musculoskeletal, anemia,
gastrointestinal problems, obesity and anxiety) origin
is crucial, although many times it is challenging, as
this symptom is not a monopoly of cardiac problem.
As a subjective symptom, dyspnea presents in many
ways. Dyspnea on exertion, especially following a light
exertion (such as with dressing) is often the first type
of dyspnea felt by the patients so that it is important to
be noted in early stage of HF.6 As HF develops, ortho-
pnea, PND and dyspnea at rest might present. PND
may occur in patients with severe HF, usually mani-
fest by abrupt awakening due to acute dyspnea about
1-2 hours after lying on the bed which is gradually re-
lieved by sitting. This is considered to be related to
increased venous return from the periphery in recum-
bency position.6,11
Physical examination of patients with AHF is impor-
tant not only to diagnose AHF, but also to make clini-
cal profiles of patients guiding physician to determine
proper therapy next. Bibasilar late inspiratory rales or
crackles can be found by careful chest auscultation.
Although this is a classical finding in AHF, in the case
of decompensated chronic HF, rales is often not heard
because of enlarged lymphatics in this condition.6 Third
93
 DAMIANUS Journal of Medicine

Table 2. Common presenting symptoms of Acute Hearf Failure

Pulmonary congestion Systemic venous congestion Others

 Dyspnea; dyspnea on exertion,
orthopnea,paroxysmal nocturnal
dyspnea (PND), dyspnea at rest.
 Non productive cough.
 Wheezing or cardiac asthma.
 bilateral pedal-pretibial oedema.  Palpitation.
 Abdominal discomfort, bloating, or  Angina.
pain at right upper quadrant.
 Fatigue.
 Nausea, anorexia.
 Depression
 weight gain
 Sleep disturbance
 Increasing abdominal girth

heart sound is another classical finding by cardiac
auscultation of AHF patients, related to low ventricular
compliance or increase ventricular filling pressure.
Because this extra sound is low pitch, using the bell of
stethoscope with patient slight left lateral decubitus
will ease to find this.11 Elevated jugular venous pres-
sure (JVP) is perhaps the most useful clinical finding
for detecting AHF especially in decompensated chronic
HF setting, associated with elevated pulmonary capil-
lary wedge pressure (PCWP).6 Abdomino-jugular re-
flux as result of applying midabdominal pressure for 10
seconds or more also suggests an elevated PCWP.11
It is important to be noted that although both third heart
sound and increased JVP are very specific for detect-
ing AHF (> 90%), these signs are not sensitive in many
cases (< 40%).12 Hepatomegaly, ascites and bilateral
pretibial-pedal pitting oedema are easily found, accom-
panying elevated JVP in decompensated chronic HF
patients. Cool clammy periphery along with low sys-
tolic blood pressure and rapid-weak pulse suggest low
perfusion. Arrhythmias detected by cardiac ausculta-
tion or pulse palpation are not uncommon.6
Some confirmatory investigations are needed in mak-
ing diagnosis of AHF. Chest X-ray should be performed
as soon as possible at admission for all patients with
AHF to assess the degree of pulmonary congestion
and to differentiate from other pulmonary or cardiac
pathologies. Arterial blood gas analysis usually shows
hypoxemia with metabolic acidosis. Pulse oximetry
can be used for practical reason, but it does not pro-
vide information about pCO2 or acid-base status.5
Natriuretic peptides (BNP and NT-proBNP) are very
useful in determining diagnosis and prognosis of pa-
tients with AHF. Increased natriuretic peptides value
has a negative predictive value for ruling out HF. Gen-
erally, BNP cutoff 100 pg/mL can be used to rule out
HF and cutoff 400 pg/mL to rule in HF. The higher BNP
value, the worse prognosis of patients, so that more
aggressive therapy should be made for these patients.13
Echocardiography with Doppler is an essential tool for
the evaluation of the functional and structural changes
underlying or associated with AHF. All patients with
AHF should be evaluated as soon as possible.5
MANAGING PATIENTS WITH ACUTE HEART
FAILURE SYNDROME
The immediate goals of treatment in AHF are to im-
prove symptoms and to stabilize haemodynamic con-
dition especially oxygenation and tissue perfusion.5
Planning follow up strategy is needed in hospitalized
patients and also long-term management if the acute
episode leads to chronic HF. Initial treatment in AHF
can be seen at Figure 2. Oxygen therapy and relieving
patients' distress are the initial treatment at admis-
sion. Non-invasive ventilation with positive pressure
(NIPPV) is recommended as soon as possible in ev-
ery patients with respiratory distress caused by acute
pulmonary oedema, but this respiratory assist should
be used with caution in cardiogenic shock as
haemodynamic compromises would worsen. Intuba-
tion and mechanical ventilation should be restricted to
patients who is failed with NIPPV or with increased
respiratory failure or exhaustion as assessed by hy-
percapnia.5
A specific treatment strategy should be based on dis-
tinguishing the clinical conditions. In acute decompen-
sated HF condition, vasodilators along with loop di-
uretics are recommended. Higher dose of diuretics is
usually needed. Morphine is usually indicated in pa-
tients with pulmonary oedema, along with loop diuret-
ics and vasodilators. Lowering blood pressure with ti-
trated vasodilators simply improve symptoms of pa-
tients with hypertensive HF. Fluid resuscitation is sug-
gested along with inotropic agents to support patients
with right HF. Patients with cardiogenic shock need
more aggressive therapy including fluid challenge in
small amount (250 mL) followed by an inotrope. An
Intra-Aortic Balloon Pump (IABP) and intubation should
be considered.5,6 Selecting agents according to sys-
tolic blood pressure can be seen at Figure 3.

94 Dam J Med Volume 10, Nomor 2, 2011

 Prompt diagnosis and management of acute heart failure syndrome

Figure 2. Initial treatment algorithm in AHF

Immediate symptomatic treatment


Patient distressed or in pain
 > YES > Analgesia, sedation (morphine)

Pulmonary congestion > YES > Medical therapy; diuretic,

vasodilator


SaO2 < 95% > YES > Increase Fi02; consider NIPPV;
mechanical ventilation


Normal heart rate and rhythm > No > Antiarrhythmics, pacing,

cardioversion

NIPPV = Non-Invasive Positive Pressure Ventilator (adapted from ESC Guidelines for the diag-
nosis and treatment of acute and chronic heart failure.

Figure 3. AHP treatment strategy according to systolic blood pressure.

Initial assessment; ABC supports



SBP > 100 mmHg SBP - 100 mmHg SBP < 100 mmHg


Vasodilator (NTG, Vasodilator and/or Fluid resuscitation;

Nitroprusside, inotrope unotrope (dopam-
Nesititide (dobutamine), PDEI ine)

Good response: Poor response:

Stabilize and initiate Inotrope, vasopres-
diuretics, ACEI/ARB, sor, mechanical
beta-blockers support

ABD = Aorway-Breathing Circulation; SBP = Systolic blood pressure; NTC =

Nytroglilcerin; PDEI = Phosphodiesterase Inhibitor (adapted from ESC Guidelines
for diagnosis and treatment of acute and chronic heart failure 2002)

Table 3. Common used agents in AHF therapy

Agent Indication Dose and administering

Diuretics: Symptoms secondary to conges- Initial bolus 20-40 mg i.v continued
tion and fluid overload with infusion of 5-40 mg/h. Higher
furosemide dose is consider in severe overload as
long as the total dose <100 mg in the
1st 6 h and 240 mg during the 1st 24 h
Vasodilators: Hypertensive HF; Drip; start with 10-20 mcg/min,
increase up to 200 mcg/min.
Nitroglycerine
Drip; start 1 mg/h, increase up to 10
Isosorbide dinitrate Pulmonary congestion with SBP mg/h.
>90 mmHg
Nitroprusside Drip 0.3-5 mcg/kg/min.
Nesiritide Bolus 2 mcg/kg + drip 0.015-0.03
mcg/kg/min.

Dam J Med Volume 10, Nomor 2, 2011 95

 DAMIANUS Journal of Medicine

Inotropes: SBP 90-100 mmHg without shock Drip; 2-20 mcg/kg/min

syndrome.
Dobutamine Drip; 2-20 mcg/kg/min
SBP < 90 mmHg with shock
Dopamine Drip; 0.2-1.0 mcg/kg/min
syndrome.
Norepinephrine SBP < 70 mmHg with shock
syndrome; sepsis complicating
AHF.

CONCLUSION 6. O'Connor CM, editors. Managing Acute Decompen-

AHF is an emergency situation in cardiovascular re-
quiring prompt clinical evaluation, early diagnosis and
immediate intervention to cut down the morbidity and
mortality rates. Because this is a common case found
at primary care, recognizing its symptoms and signs
along with proper treatment is important. Diagnosis can
be made by careful history taking and physical exami-
nation, confirmed by Chest-x ray, echocardiography,
laboratory test, and ECG. Furthermore, clinical profile
of patients with AHF should be performed in order to
make suitable strategy to manage the patients. The
goals of initial therapy are to improve symptoms and
stabilize haemodynamic by maintaining oxygenation
and tissue perfusion as early as possible. Proper oxy-
gen therapy, pharmacological agents and devices
should be used to reach these goals.
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