Diagnosis and Management

of
Acut Heart Failure
Gusti Rifansyah, dr, SpJP, FIHA

1
 Overview
Introduction

Definition and Classification

Epidemiology

Pathophysiology

Clinical Manifestations

Diagnostic Evaluation

Management

Clinical Outcomes and Prognosis 2

 Introduction
The past two decades → dramatic advances in the
treatment of chronic heart failure (CHF) →
significantly improved the survival

Acute heart failure (AHF) had initially been ignored but

during the last decade, there has been growing interest
in this field.
New data → new insights into AHF & a growing
literature has evolved 3
Definition and Classification

A rapid onset or change in the sign

and symptoms of HF, resulting in
the need for urgent therapy

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 Classification
Pulmonary
Clinical Classifications
oedema
(Developed by Stevenson & colleagues)
High Output Acutely
Failure Decompensated
Dry and warm Wet and warm
Chronic HF
De (I) Acute(II) on
Novo Chronic
Dry and cold Wet and cold
Cardiogenic
(III) (IV)
Shock Hypertensive
AHF
Right HF
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 Pathophysioogy

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 Causes and Precipitating Factors of
Acut Heart Failure
Ischemic heart disease Circulatory failure
- Acut Coronary Syndromes -Septicaemia
- Mechanical complications of AMI -Thyrotoxicosis
- RV infarction - Anemia
- Shunts
- Tamponade
- Pulmonary embolism

Valvular Decompensation of pre-existing chronic

- Valve stenosis HF
- Valvular regurgitation - Lack of adherence
- Endocarditis - Volume overload
- Aortic dissection - Infections

Myopathies -Cerebrovascular insult

- Postpartum cardiomyopathy - Surgery
- Acute myocarditis - renal disfunction

Hypertension/Arrhytmia - Asthma, COPD

-Drug Abuse
-Alcohol abuse

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 SYMPTOMS & SIGNS

Predominantly related to volume overload

Predominantly related to hypoperfusion

Other signs and symptoms of acute heart failure

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 LABORATORY TEST
Serum electrolytes:(Na,K)
25-30% with Na < 135 mEq/L
3% with K<3,6meq/L,8%>5.5mEq/L
Renal Function :
BUN, Creatinin ↑
Liver Function :
61% liver disfunction→dose
adjusments
Hematological studies:
50% anemia (Hb<12g/dl)
Natriuretic Peptides
(BNP, nt-pro-BNP, ANP)
DIAGNOSTIC TEST
Biomarkers of
Myocardial injury
Troponin or CK-MB
Other :
CRP (C-reactive protein)
D-dimers
ABG (arterial Blood gases
Chest Radiography
ADHERE: >80% congestion
Electrocardiogram
EFICA : 13%Normal, 29%ischemic
changes, 25% AF
Echocardiogram
→evaluating the etiology of AHF.
EHFS II: systolic disfunction (66%),
diastolic disfunction (56%), MR
(43%), TR(30%
Pulmonary Artery Catheter
Provides important &clinically
relevant hemodynamic data9
 Phonocardiography

Other Potensial External impedance

cardiography (ICG)
Diagnostic

Internal thoracic impedance

Implantable hemodynamic
monitors
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 Management
Intermediate
Immediate (in hospital) Long-term &
(ED/ICU/ICCU) Pre-discharge
• Stabilize & optimize
• Improve treatment • Optimize chronic oral
symptoms • Life saving therapy
• Restore pharmacological • Minimize the side
oxigenation therapy effects of treatments
• Device therapy in • Plan follow up
• Improve organ
appropriate patients
perfusion & strategy
• Lab. Monitoring
hemodynamics • Educate & life style
• Diagnostic
• Limit evaluations
adjusment
cardiac/renal • Education about HF • Prevent early
damage • Minimize hospital readmission
• Minimize ICU length of stay • Improve quality of
length of stay life and survival

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 •Advanced
ExacerbatingHF :factors
addressed
• Oral medication regimen
• Atbeleast near
stable foroptimal
24 hours volume
status achieved
HFSA • No intravenous
• Transition from
vasodilators or intravenous
inotropic
guidelines toagent
oral7diuretic completed
to2410hours
for days
Discharge ••Education
Ambulation completed
prior to
• Atdischarge
least neartooptimal
assess
Criteria pharmacological
functional capacity therapy
•achieved
Plans for post-discharge
• Follow-up
management clinic visit
scheduled

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13
Treatment strategies
Worsening Systolic Blood Pressure
Volume Renal
>100 mm Hg 90-100 mm Hg <90 mm Hg
Overload[*] Function
Yes Yes Vasodilator Vasodilator (cautiously)[§] Inotrope and/or d
Diuretics (consider infusion and/or inotrope Consider norepinephrine or
or combination therapy)[†] Diuretics (consider infusion other vasopressor
Consider ultrafiltration[‡] or combination therapy)[†] Diuretics (consider infusion or
combination therapy)[†]
Yes No Vasodilator Vasodilator (cautiously)[§]
-Recheck volume status
Diuretics and/or inotrope -Inotrope and/or dopamine
Consider ultrafiltration[‡] -Consider norepinephrine or
other vasopressor
-Diuretics (consider continuous
infusion or combination
therapy)
No Yes Vasodilator for hypertensive Vasodilator (cautiously)[‡] -Recheck volume status
HF and/or inotrope -? Volume repletion
-Inotrope and/or dopamine
-Consider norepinephrine or
other vasopressor
No No Vasodilator Consider “normotensive -Recheck volume status
cardiogenic shock” (then -? Volume repletion
treat as if SBP <90 mm Hg) -Inotrope and/or dopamine
-Consider norepinephrine or
other vasopressor 14
 Pharmacological
Therapies......

Diuretics Cardiac myosin

activators

Vasodilator Natriuretic peptides

Potensial Future
Therapies
Adenosin antagonis

Vasopressin
antagonis
Endothelin antagonis
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 Therapy Indications/ Contraindications/ Adverse effect
Description caution
Vasodilators
Adrenergic
Adrenergic
-Nitrat
Loop diuretic :
agonists -- Pulmonary congestion/oedema
AHF with congestion and -Hypotension, severe
-Hypotension --Hypovolaemia
hypotension,
agonists -Potent - Preload
-Dobutamin
overload
-Hypoperfusion, SBP < 90 mmHg hiponatraemia, - dependent or aortic
acidosis
HR > 100 bpm → headache,
- -Tachycardia
Hyponatremiaabdominal
- PDEIs (Milrinone venodilators→↓pulmonary
-Inotropy, chronotropy
-Positive inotrope & chronotropy stenosisto
& lusitropy unlikely respond
- Renal disfunction→dose - --pain
Hypokalaemia
tachycardia
hypotension (-)
& Enoximone) venous & ventricle
→vasorelaxation
(through infilling
increases pressure,
vascular - NSAID→↓efficacy
smooth cAMP
in intracellular muscle adjustment of diuretic - -Arrhytmia
Hypomagnesemia
- Peripheral
↓oksigen & pulmonary vasodilatation,
& Ca) → demand
improve CO & ↓ afterload - -Hyperuricaemia
? mortality
↓after&preload
-Arterial vasodilators→↓afterload, - Neurohormonal
-Improve renal perfusion
CO↑→useful
--Ca
low dose →for Myocardial
vasodilatation activation
- Ca sensitizer ischemia sensitization of the contractile - hypotension
( Levosimendan) protein→inotropic effect - Ototoxicity
- smooth muscle K-channels opening→
- Nitroprusside -Hipertensive
-precursor toAHF
the(↑afterload),
synthesis of - active myocardial ischemia
-Advanced HF ! - Hypotension, Cyanide
- Dopamin peripheral vasodilatation
moderate to severe
norephinephrin, MR →” side effect (nausea,
- 80 hs half-life agonist of both - high dose→ limb &
- aadrenergic
pro drug →&Nitric oxide + reseptors,
dopaminergic Coronary steal
end phenomenon”
organ ischemia dysphoria),
cyanida
and an inhibitor of NE uptake thiocyanate toxicity,
- induces a balanced reduction
- low dose→improve in flow
renal blood light sensitive
afterload & preload
- intermediate dose→inotropy &
- avasoconstriction
very short half-life→monitor!
-Tapering doses→avoid rebound
hypertension

- Nesiritide -Acutely decompensated

- Cardiogenic shock (when CHFthe - Should- not
Highbesistemic
administered
vascular - Hypotension,
- Epinephrin & -recombinant human BNP for replacing diuretics headache (less than
Norepinephrin combination of an inotropic fails) resistence !
- potent vasodilatation → ↓
- balanced vasodilator & vasoconstrictor organic nitrates)
venous
effect & ventricle filling - ? ↓ renal function,
pressures, CO↑
- increasing inotropy independent of ↑mortality
myocardial catecholamine stores
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 Various targets for therapies used in the
management of acute decompensated heart failure
Potensial Future Therapies
-Inotropic agent
Cardiac Myosin Activators
-Directly improving the work of the cardiac motor unit→accelerate the
(CK-1827452)
strong binding of the activated myosin-actin
- ↑ EF

- dual mechanism of action inhibition of the Na+/K+ -

ATPase→↑intracellular Ca & inotropy, stimulasi SERCA2a→rapid Ca
Istaroxime uptake into sarcoplasma reticulum→ improve myocardial relaxation
-Improve both systolic & diastolic function without ↑ O2 demand

Natriuretic peptides -potent vasodilators( > nesiritide)

-Carperitide - ↓PCWP, sistemic vasc.resistance,↑ nt-pro-BNP, ↑CO
- Ularitide
Adenosin antagonis - effective in patient with diuretic resistance
(BG9719, KW-3902) - ↑urine output&GFR, synergistically with furosemid

Vasopressin antagonis -↓PCWP, RA pressure, ↑urine output without change cardiac index /
(Conivaptan, Tolvaptan, hemodynamic
Lixivaptan) -Tolvaptan : ↓ Body weight & improved serum sodium conc.
- ↓ LV filling pressure, ↓afterload, ↑CO
Endotelin Antagonis
- trial was terminated 18
(Tezosentan)
 Clinical Outcome & Prognosis
Mortality
Study Patients (n) Rehospitalization Mortality In- Post-Discharge
Hospital
Jong (Ontario; 1994-7) 38,702 N/A N/A 11.6% 30 d

33.1% 1 yr
Lee (Ontario, 1997- 4,031 N/A 8.7% 10.6% 30 d
2001)
31% 1 yr
OPTIME-HF (US) 949 35.2% 60 d[*] 3.0% 9.6% 60 d
IMPACT-HF Registry 567 25.7% 60 d 2.6% 8.5% 60 d
(US)
ADHERE (US) 187,565 N/A 3.8% N/A
OPTIMIZE-HF (US) 41,267 29.5% 60-90 d 3.8% 8.0% 60-90 d
EHFS I (EU) 11,327 24% 12 wk 6.9% 13.5% 12 wk
Rudiger (Zürich- 312 N/A 8% 11% 30 d
Helsinki)
18% 12 wk

29% 1 yr
Tavazzi (Italy) 2,807 38.1% 6 mo 7.3% 12.8% 6 mo
Zannad (France) 581 N/A N/A 27.4% 4 wk[†]
46.5% 1 yr[†]
EHFS II (EU) 3,580 N/A 6.7% N/A 19
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