Management of

Acute Heart Failure

Anna Fuji Rahimah
M. Saifur Rohman

Department of Cardiology and Vascular Medicine

Brawijaya University Dr. Saiful Anwar General Hospital Malang
 Introduction
Current management of acute
coronary syndrome has
resulted in an improved
survival after acute
myocardial infarction.
A rapid growth in the number
of patients currently living
with chronic heart failure.
Decompensation of
preexisting chronic heart
failure may cause acute heart
failure (AHF).
Eur Heart J 2005;26:384-416
Introduction
Precipitants and
causes
In patients with pre-existing HF
there is often a clear
precipitant or trigger
an arrhythmia or discontinuation
of diuretic therapy in a patient
with HF-REF
volume overload or severe
hypertension in patients with
HF-PEF
It is essential that these factors
be identified and incorporated
into the treatment strategy

European Heart Journal (2012) 33, 17871847

European Heart Journal (2008) 29, 23882442
Clinical classification
Treatment of acute heart failure
The key drugs are oxygen, diuretics, and vasodilators
Opiates and inotropes are used more selectively
Non-invasive ventilation (commonly)
Invasive ventilation (in only a minority of patients)
SBP, heart rhythm and rate, SpO2 using a pulse oximeter, and urine
output should be monitored until the patient is stabilized

Diuretics Vasodilators Inotropes Natriuretic

peptides
Reduce Decrease Augment Vasodilate;
fluid preload contractility reduce fluid
volume and volume;
afterload counteract
RAAS/SNS

RAAS = renin-angiotensin-aldosterone system European Heart Journal (2012) 33, 17871847

SNS = sympathetic nervous system Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7S12
 Assessment of Haemodynamic Profile
Sign of congestion:
Congestion at rest Orthopnea,
elevated JVP,

No Yes edema,
pulsatile hepatomegaly,
Low perfusion at rest

ascites,
rales,

No A B louder S3,
P2 radiation left ward,
abdomino-jugular reflex
Warm & dry Warm & wet

Cold & dry Cold & Wet

Yes L C
Sign of low perfusion:
Narrow pulse pressure, cool extremities,
low urine output, altered mental status,
hypotension, inadequate response to IV
diuretics, prerenal azotemia
European Heart Journal of Heart Failure, 2005; 7:323-331
 Patient Treatment Selection
Dry WET Diuretic
Vasodilator

War A B
m

Inotropic drugs :
Dobutamine
Cold Milrinone
Levosimendan

L C
Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7S12.
Goals of
treatment
Pharmacological therapy:
Acute management
Oxygen
To treat hypoxaemia (SpO2 <90%)
Oxygen should not be used routinely in non-hypoxaemic
patients as it causes vasoconstriction and a reduction in
cardiac output

European Heart Journal (2012) 33, 17871847

Pharmacological therapy:
Acute management
Diuretics
Most patients with dyspnoea caused by pulmonary oedema
obtain rapid symptomatic relief from administration of an
i.v. diuretic, as a result of both an immediate venodilator
action and subsequent removal of fluid
The optimum dose and route of administration (bolus or
continuous infusion) are uncertain
The high-dose strategy was associated with greater
improvement in a number of secondary outcomes (including
dyspnoea)

European Heart Journal (2012) 33, 17871847

Pharmacological therapy:
Acute management
Opiates
Opiates such as morphine may be useful in some patients
with acute pulmonary oedema
anxiety and relieve distress associated with dyspnoea.
venodilators,
reducing preload,
sympathetic drive.
induce nausea (necessitating the concomitant
administration of an antiemetic)
depress respiratory drive (potentially increasing the need
for invasive ventilation)
European Heart Journal (2012) 33, 17871847
Pharmacological therapy:
Acute management
Vasodilators
Although preload and afterload and stroke volume,
there is no robust evidence that they relieve dyspnoea or
improve other clinical outcomes.
Probably most useful in patients with hypertension
Should be avoided in patients with a systolic blood pressure
<110 mmHg.
Excessive falls in blood pressure should also be avoided
because hypotension is associated with higher mortality
Vasodilators should be used with caution in patients with
significant mitral or aortic stenosis
European Heart Journal (2012) 33, 17871847
 Pharmacological therapy:
Acute management
Inotropes
E.g. dobutamine
for patients with such severe reduction in cardiac output that vital
organ perfusion is compromised
hypotensive (shocked)
Cause sinus tachycardia may induce myocardial ischaemia and
arrhythmias

! prevalence of iv. inotropes infusion that cannot be weaned

without symptomatic hypotension, recurrent renal dysfunction
Dependence on iv. inotrope can be avoided by weaning infusion
within 1-2 weeks and reducing or stopping other medication that
decrease blood pressure and renal function (Nitrate, CCB, NSAID)

European Heart Journal (2012) 33, 17871847

Pharmacological therapy:
Acute management
Vasopressors
E.g. norepinephrine
sometimes given to severely ill patients with marked
hypotension
blood pressure and redistribute cardiac output from the
extremities to the vital organs
in LV afterload
have adverse effects similar to those of inotropes
restricted to patients with persistent hypoperfusion despite
adequate cardiac filling pressures
European Heart Journal (2012) 33, 17871847
Pharmacological therapy:
Acute management
Dopamine
In large doses (>5 mg/kg/min) dopamine has inotropic and
vasoconstrictor activity
At lower doses (<3 mg/kg/min) dopamine may have a
selective renal arterial vasodilator activity and promote
natriuresis
may cause hypoxaemia
Arterial oxygen saturation should be monitored, and
supplemental oxygen administrated as required.

European Heart Journal (2012) 33, 17871847

Pharmacological therapy:
After stabilization
Angiotensin-converting enzyme inhibitor/angiotensin
receptor blocker
Beta-blocker
Mineralocorticoid (aldosterone) receptor antagonist
Digoxin
Non-pharmacological/non-device therapy [restrict sodium
intake to <2 g/day and fluid intake to <1.52.0 L/day]

European Heart Journal (2012) 33, 17871847

Monitoring after stabilization
HR, rhythm, BP, and oxygen saturation should be monitored
continuously for at least the first 24 h of admission, and
frequently thereafter.
Symptoms relevant to HF (e.g. dyspnoea) and related to the
adverse effects of treatments used (e.g. dizziness) should be
assessed at least daily.
Fluid intake and output, weight, and the jugular venous
pressure and extent of pulmonary and peripheral oedema
(and ascites if present) should be measured daily to
evaluate the correction of volume overload.
BUN, creatinine, potassium, and sodium should be
monitored daily during i.v. therapy and when RAAS
antagonists are being initiated or if the dose of any of these
drugs is changed.

European Heart Journal (2012) 33, 17871847

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