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Acute Heart Failure

Syndromes
KELOMPOK C

DEFINITION
AHFS

can be defined as new onset or gradual or rapidly worsening HF signs and


symptoms requiring urgent therapy. Irrespective of the underlying cause (e.g.,
ischemic event) or precipitant (e.g., severe hypertension), pulmonary and
systemic congestion due to elevated ventricular filling pressures with or without a
decrease in cardiac output is a nearly universal finding in AHFS (5).

Coronary

artery disease(CAD), hypertension, valvular heart disease, and/or atrial


fibrillation, as well as noncardiac conditions such as renal dysfunction, diabetes,
anemia, and medications (i.e., nonsteroidal anti-inflammatory drugs, glitazones),
may also contribute to these abnormalities (5,911). The majority of AHFS
patients have worsening chronic HF; after initial management resulting in
stabilization, they should no longer be consideredacute but chronic HF.

EPIDEMIOLOGY
Incidence and prevalence:

One hundred to 400 new cases of heart failure are diagnosed per 100,000 persons per year

One thousand or more new cases are diagnosed per 100,000 persons over age 65 per year

There are approximately 1,000 to 2,000 cases of heart failure per 100,000 persons

Five thousand or more cases are diagnosed per 100,000 persons over age 65; heart failure is the most common inpatient
diagnosis in the U.S. in patients over age 65

Heart failure occurs at some stage in patients with most forms of severe heart disease, regardless of the underlying cause

Heart failure leads to a total of 12 to 15 million office visits per year

Demographics:

Incidence increases with age

Heart failure is more common in men than in women between 40 and 75 years of age, but among persons over age 70, both
sexes are affected equally

The prevalence of heart failure is estimated to be 25% greater in black persons than in white persons

Dilated and hypertrophic forms of cardiomyopathy may run in families, and specific genetic defects are known. Susceptibility
to myocardial infarction, which is a frequent cause of heart failure, may have a genetic component. Hypertension is frequently
familial. Hemochromatosis can lead to both cardiomyopathy and accelerated coronary artery disease

RISK FACTORS

Obesity

Obstructive sleep apnea

Cigarette smoking

Pregnancy

Infection, especially pulmonary infection

Diabetes

Physical inactivity

Renal insufficiency

CLINICAL CLASIFICATION

PATHOPHYSIOLOGY
AHFS are characterized by severe hemodynamic and neurohormonal abnormalities
that may cause myocardial injury and/or renal dysfunction or may be a result of it
These abnormalities may be caused or precipitated by ischemia, hypertension, atrial
fibrillation, other noncardiac conditions (e.g., renal insufficiency), or untoward drug
effects

Congestion

Myocardial injury

Renal impairment

Untoward drug effects

Congestion

High LV diastolic pressure resulting in pulmonary and systemic congestion with or without
low cardiac output is the main reason for presentation in the majority of patients . Systemic
congestion manifests clinically by jugular venous distention with or without peripheral
edema and gradual increases in BW are often seen ..

High LV diastolic pressure, by itself, may contribute to the progression of HF by further


causing activation of neurohormones, subendocardial ischemia, and/or changes in LV size
and shape (remodeling) that often results in mitral insufficiency.

Body weight is often used as a marker of congestion in both inpatient and outpatient
settings. However, recent data suggest a more complex relationship among BW, congestion,
and outcomes. Although an increase in BW predicts hospitalization, a reduction in BW in
response to different therapies may not necessarily result in decreased hospitalization or
mortality.

Myocardial injury

Troponin release often occurs in AHFS, particularly in patients


with CAD. This likely reflects myocardial injury, which may
be related to hemodynamic and/or neurohormonal
abnormalities or the result of an ischemic event (MI).

Injury may also be the consequence of a high LV diastolic


pressure, further activation of neurohormones, and/or inotropic
stimulation, resulting in a supply and demand mismatch
(increased myocardial oxygen demand and decreased coronary
perfusion. These conditions may precipitate injury, particularly
in patients with CAD, who often have hibernating and/or
ischemic myocardium. This is supported by experimental data
in dogs where stimulation of hibernating myocardium with
low-dose dobutamine resulted in myocardial necrosis

Renal impairment

In AHFS, renal abnormalities promote sodium and water retention.

Renal dysfunction resulting from neurohormonal or hemodynamic


abnormalities (vasomotor nephropathy) may be preventable or
reversible and it is often referred as the cardio-renal syndrome.

In a given patient, distinguishing between vasomotor nephropathy


from abnormalities related to intrinsic kidney disease is often difficult
and remains an important area for research.

Both intrinsic/pre-existing structural kidney disease and potential


contributors to renal injury from acute heart failure (HF) syndromes
characterize the cardio-renal syndrome. Figure illustration by Rob
Flewell.

Untoward drug effects

Nonpotassium-sparing intravenous (IV) loop diuretics are


first-line agents to alleviate congestive symptoms. High-dose
administration of IV loop diuretics has been associated with
worse outcomes in HF patients.

Dobutamine, milrinone, and levosimendan improve


hemodynamics; however, these effects may be associated with
increased myocardial oxygen consumption (tachycardia and
increased contractility) and hypotension due to their
vasodilatory effects.

Decreasing coronary perfusion due to hypotension in the


presence of increased myocardial oxygen demand may result
in myocardial injury, particularly in patients with CAD who
often have ischemic or hibernating myocardium.

Hypotension associated with the use of vasodilators may also


result in myocardial and renal hypoperfusion and possibly
injury.

MANAGEMENT OF ACUTE
HEART FAILURE SYNDROME

Pharmalogical Treatment

Acute Management
Oxygen
Oxygen

may be given to treat


hypoxaemia (SpO2 ,90%), which is
associated with an increased risk of
short-term mortality.

Oxygen

should not be used routinely in


non-hypoxaemic patients as it causes
vasoconstriction and a reduction in
cardiac output.

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. A
recent, small, prospective RCT compared 12hourly bolus injection with continuous infusion
and low-dose (equal to pre-existing oral dose)
with highdose (2.5 times previous oral dose)
using a 2 2 factorial design.

Opiates

Opiates such as morphine may be useful in


some patients with acute pulmonary oedema as
they reduce anxiety and relieve distress
associated with dyspnoea. Opiates are also
thought to be venodilators, reducing preload,
and may also reduce sympathetic drive.
Conversely,
opiates
induce
nausea
(necessitating the concomitant administration
of an antiemetic, one of which, cyclizine, has
vasoconstrictor
activity)
and
depress
respiratory drive, potentially increasing the
need for invasive ventilation.

Vasodilators

Although vasodilators such as nitroglycerine


(Table 20) reduce preload and afterload and
increase stroke volume, there is no robust
evidence that they relieve dyspnoea or improve
other clinical outcomes. Vasodilators are
probably most useful in patients with
hypertension and 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 in patients with AHF.
Vasodilators should be used with caution in
patients with significant mitral or aortic
stenosis.

Nesiritide

Nesiritidea human BNP that acts mainly as a


vasodilatorwas recently shown to reduce
dyspnoea by a small but statistically significant
amount when added to conventional treatment
(mainly diuretic)

Inotropes

Use of an inotrope such as dobutamine should


usually be reserved for patients with such
severe reduction in cardiac output that vital
organ perfusion is compromised. Such patients
are almost always hypotensive (shocked).
Inotropes cause sinus tachycardia and may
induce myocardial ischaemia and arrhythmias.

Vasopressors

Drugs with prominent peripheral arterial


vasoconstrictor action such as norepinephrine
are sometimes given to severely ill patients
with marked hypotension. These agents are
given to raise blood pressure and redistribute
cardiac output from the extremities to the vital
organs.

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, although this is uncertain.
Dopamine may cause hypoxaemia.

After stabilization

Angiotensin-converting
enzyme
/angiotensin receptor blocker

inhibitor

In patients with reduced EF not already


receiving an ACE inhibitor (or ARB), this
treatment should be started as soon as possible,
blood pressure and renal function permitting.

Beta-blocker

In patients with reduced EF not already


receiving a beta-blocker, this treatment should
be started as soon as possible after
stabilization, blood pressure and heart rate
permitting

Mineralocorticoid
antagonist

(aldosterone)

receptor

In patients with reduced EF not already


receiving an MRA, this treatment should be
started as soon as possible, renal function and
potassium permitting

Digoxin

In patients with reduced EF, digoxin may be


used to control the ventricular rate in AF,
especially if it has not been possible to uptitrate the dose of beta-blocker. Digoxin may
also provide symptom benefit and reduce the
risk of HF hospitalization in patients with
severe systolic HF

Non-pharmacological/non-device

therapy
Ventilation Non-invasive ventilation
Continuous

positive airway pressure


(CPAP) and non-invasive positive
pressure ventilation (NIPPV) relieve
dyspnoea
and
improve
certain
physiological measures (e.g. oxygen
saturation) in patients with acute
pulmonary oedema.

Endotracheal intubation and invasive ventilation

The primary indication for endotracheal intubation and


invasive ventilation is respiratory failure leading to
hypoxaemia, hypercapnia, and acidosis. Physical
exhaustion, diminished consciousness, and inability to
maintain or protect the airway are other reasons to
consider intubation and ventilation.

Mechanical circulatory support Intra-aortic balloon


pump

The conventional indications for an intra-aortic balloon


pump (IABP) are to support the circulation before
surgical correction of specific acute mechanical
problems (e.g. interventricular septal rupture and acute
mitral regurgitation), during severe acute myocarditis
and in selected patients with acute myocardial ischaemia
or infarction before, during, and after percutaneous or
surgical revascularization.

Ventricular

assist devices

Ventricular

assist devices and other


forms of mechanical circulatory support
(MCS) may be used as a bridge to
decision orvlonger term in selected
patients

Ultrafiltration
Venovenous

isolated ultrafiltration is
sometimes used to remove fluid in
patients with HF, although is usually
reserved for those unresponsive or
resistant to diuretics.

REFERENCES