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 (5,9–11). 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: Demographics:
 One hundred to 400 new cases of heart failure Incidence increases with age
are diagnosed per 100,000 persons per year
 Heart failure is more common in men than in
 One thousand or more new cases are diagnosed women between 40 and 75 years of age, but
per 100,000 persons over age 65 per year among persons over age 70, both sexes are
affected equally
 There are approximately 1,000 to 2,000 cases of
heart failure per 100,000 persons  The prevalence of heart failure is estimated to be
25% greater in black persons than in white
 Five thousand or more cases are diagnosed per persons
100,000 persons over age 65; heart failure is the
most common inpatient diagnosis in the U.S. in Dilated and hypertrophic forms of
patients over age 65 cardiomyopathy may run in families, and
specific genetic defects are known.
 Heart failure occurs at some stage in patients Susceptibility to myocardial infarction, which is
with most forms of severe heart disease, a frequent cause of heart failure, may have a
regardless of the underlying cause genetic component. Hypertension is frequently
 Heart failure leads to a total of 12 to 15 million familial. Hemochromatosis can lead to both
office visits per year 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
 Non–potassium-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 12-
hourly 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
 Nesiritide—a human BNP that acts mainly as a
vasodilator—was 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 inhibitor
/angiotensin receptor blocker
 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 (aldosterone) receptor
antagonist
 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 up-
titrate 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