Beruflich Dokumente
Kultur Dokumente
Michael C. Scott,
MD
a,b
, Michael E. Winters,
MD
a,
KEYWORDS
Congestive heart failure Acute decompensated heart failure
Noninvasive positive pressure ventilation Nitrates
Angiotensin converting enzyme inhibitors Diuretics Inotropes
KEY POINTS
Many patients with acute decompensated heart failure do not have intravascular volume
overload.
The foundation of emergency department management of acute decompensated heart
failure is the use of noninvasive positive pressure ventilation and nitrate medications.
Diuretics should not be used until optimal preload and afterload reduction has been
achieved.
Morphine, nesiritide, b-blockers, and intraaortic balloon pump should not routinely be
used in the management of patients with acute heart failure in the emergency department.
INTRODUCTION
Congestive heart failure (CHF) remains the most common reason for hospitalization in
the United States for people aged 65 years and older, with more than 1 million patients
admitted for this condition each year.1,2 Despite improvements in diagnosis and treatment, approximately 300,000 deaths each year can be attributed to CHF. Furthermore, the in-hospital mortality rate can be as high as 12% for patients admitted
with an acute exacerbation of CHF.2 Patients with acute decompensated heart failure
(ADHF) frequently present to the emergency department (ED) for evaluation; many of
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them are critically ill, requiring immediate treatment. In 2007, CHF accounted for 6.3%
of ED patients requiring hospital admission.3 It is imperative that the emergency physician be expert in the rapid assessment and treatment of patients with ADHF. The
article focuses on the management of the ED patient with ADHF, with attention to
therapies that improve patient symptoms, morbidity, and mortality.
PATHOPHYSIOLOGY
The European Society of Cardiology has classified acute heart failure into distinct
clinical syndromes (Box 1).6,7 Some patients present with overlapping features, but
their appropriate classification is important, because each requires a specific therapeutic approach.
Box 1
Classification of acute heart failure
Acute decompensated heart failure
Hypertensive acute heart failure
Pulmonary edema
Cardiogenic shock
Right heart failure
Acute coronary syndrome complicated by acute heart failure
Adapted from Dickstein K, Cohen-Solal A, Filippatos G, et al. ESC guidelines for the diagnosis
and treatment of acute heart failure 2008. Eur J Heart Fail 2008;10:968.
CAUSES
Regardless of the underlying pathophysiology, the most common complaint of ED patients with ADHF is dyspnea. Additional symptoms can include orthopnea, paroxysmal nocturnal dyspnea, decreased exercise tolerance, peripheral edema,
weakness, and fatigue. Depending on the classification and cause, patients with
ADHF can present with either hypertension or hypotension. Although most patients
are tachycardic, bradycardia can be seen in the setting of medication toxicity (eg,
b-blocker, digoxin) or high-degree atrioventricular block. Physical examination findings in patients with ADHF include pulmonary edema, peripheral edema, jugular
venous distention, hepatomegaly, hepatojugular reflux, and a third heart sound.
DIAGNOSTIC TESTING
The diagnostic evaluation of the patient with suspected ADHF generally includes electrocardiogram, chest radiography (CXR), bedside echocardiogram, and laboratory
analysis.
Electrocardiogram
A CXR should also be obtained as soon as possible to evaluate for findings consistent
with ADHF. Typical CXR findings of ADHF include pulmonary edema, hilar fullness,
Box 2
Precipitants of acute decompensated heart failure
Medication noncompliancea
Dietary noncompliancea
Acute coronary syndrome
Arrhythmias
Acute valvular dysfunction
Hypertensive crisis
Infection
Anemia
a
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As with other critical illnesses, the use of bedside ultrasonography and echocardiography has become a keystone in the diagnosis and management of ADHF in the
ED. The portability and rapidity of ultrasound as a diagnostic modality lends itself quite
well to this setting. The finding of diffuse b-lines (Fig. 2), although not truly specific to
ADHF, helps the emergency physician to refine the differential diagnosis in the setting
of undifferentiated dyspnea. Furthermore, the ability to evaluate ejection fraction,
exclude other causes of dyspnea such as pleural or pericardial effusion, and evaluate
for diastolic or valvular dysfunction makes bedside echocardiography an enormously
valuable tool in the evaluation of the ED patient with ADHF.
Laboratory Testing
In the patient with suspected ADHF, a complete blood count should be obtained to
exclude anemia, along with a basic metabolic panel to evaluate for renal dysfunction.
Cardiac biomarkers (eg, troponin I) are commonly obtained and increased in many patients with ADHF.8 Although increases in troponin might simply reflect the severity of
heart failure and not myocardial necrosis, elevated values are associated with
increased short-term mortality.8
Fig. 2. Lung ultrasound showing finding of a b-line (arrows). Note the extension fully to the
end of the field. Multiple, diffuse b-lines suggests the presence of fluid in the lung fields, as
in pulmonary edema.
A common laboratory test obtained in the patient with ADHF is the measurement of
B-type natriuretic peptide (BNP) or the N-terminal proBNP (NT-proBNP).9 BNP is
released from cardiac myocytes in response to volume overload and has been used
in the evaluation of ED patients with undifferentiated dyspnea. In general, BNP values
of less than 100 pg/mL indicate that ADHF is an unlikely cause of dyspnea, whereas
values of greater than 400 pg/mL strongly suggest the presence of ADHF.9 Although
NT-proBNP has a different half-life and different cutoff values for ADHF than BNP,
both are degradation products of a common precursor and are clinically interchangeable. Importantly, ADHF is not the only cause of increases in BNP or NT-proBNP. Any
condition that increases the stretch of the left or right ventricle (eg, pulmonary embolism) can result in elevated BNP and NT-proBNP levels. In addition, elevated BNP and
NT-proBNP levels can also be seen in older patients and those with renal dysfunction.
In contrast, obese patients often have lower values of BNP and NT-proBNP. Optimal
cutoff values for both BNP and NT-proBNP in these patient populations remain
controversial; therefore, values must be interpreted within the clinical context of the
patients history, the clinical presentation, and prior BNP or NT-proBNP values.
Regardless of the cause, increases in BNP and NT-proBNP are associated with
increased in-hospital mortality and therefore have prognostic importance.10
EMERGENCY DEPARTMENT TREATMENT
Patients with ADHF often present to the ED in extremis and require rapid treatment.
Similar to other critical conditions, patients with suspected ADHF should be placed
on a cardiac monitor and continuous pulse oximetry and should be given
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nitroprusside might increase the mortality rate among patients with acute myocardial
infarction.19
ACE inhibitors are effective at reducing afterload and have been used in the ED
treatment of patients with ADHF. Several small studies on ACE inhibitors in patients
with ADHF demonstrated improvement in hemodynamic markers.20,21 In addition, a
single-center study demonstrated reduced rates of intubation and intensive care
unit admission for patients who received sublingual captopril as a component of their
ED treatment.22 Importantly, current guidelines from the American College of Emergency Physicians include ACE inhibitors in the treatment options for ED patients
with ADHF.23 The most commonly used ACE inhibitors in studies of patients with
ADHF are enalaprilat and captopril. Enalaprilat can be given intravenously at a dose
of 1.25 mg over 5 minutes, whereas captopril can be administered via intravenous
or sublingual routes.
Traditionally, diuretic medications have been considered the mainstay of pharmacologic therapy for patients with ADHF. Because the majority of acutely ill ED patients
with ADHF are not volume overloaded, indiscriminate administration of diuretics could
be harmful.5 Adequate renal perfusion is necessary for these medications to be effective. As a result, the role of diuretics in the ED management of patients with ADHF is
limited.19 The administration of a diuretic should not supersede known effective therapies, namely NPPV and nitrates. When a diuretic is deemed appropriate, furosemide
is used most commonly. For patients not routinely taking furosemide as an outpatient,
an initial dose of 20 to 40 mg can be given. For patients already prescribed furosemide, an initial intravenous dose equivalent to their oral outpatient dose can be given.
Studies comparing high- and low-dose diuretic therapy, as well as those comparing
intermittent bolus dosing with continuous infusions, have not demonstrated superior
outcomes with any dose or method.
Inotropic medications should be considered in patients with ADHF who manifest
signs of cardiogenic shock. Bedside echocardiography performed by the emergency
physician can be immensely helpful in identifying patients who might benefit from
inotropic support. Current guidelines generally recommend initiating inotropic medications after optimizing administration of nitrates and diuretics.24,25 Dobutamine and milrinone are the most common inotropic medications used in these patients. A
dobutamine infusion can be initiated at 2.5 mg/kg per minutes and titrated by 2.5 mg/
kg per minute every 10 minutes to a maximum dose of 20 mg/kg per minute. These 2
agents have important differences in mechanism and duration of action. Although
dobutamine stimulates adrenergic receptors, resulting in increased contractility and
reduced afterload milrinone inhibits phosphodiesterase, the resultant increase in
cyclic adenosine monophosphate causes increased contractility and diastolic relaxation, as well as vasodilation and, therefore, decreased afterload. Because it does not
rely on sympathetic receptors, it may be preferred in patients on chronic b-blocker
therapy. Furthermore, milrinone has more potent vasodilatory effects, making it
more attractive than dobutamine in patients with severe pulmonary hypertension.
Finally, it is important to note that milrinones half-life is 2 to 4 hours, whereas dobutamine has a half-life of just 2 minutes.26 If the patients blood pressure remains inadequate despite inotropic therapy, a vasopressor medication (ie, norepinephrine,
epinephrine) can be initiated. It is important to recall that inotropic medications can
have the significant adverse effects of hypotension and tachydysrhythmias. As a result,
they should not be used routinely for all patients with ADHF. In fact, several studies
suggested an increase in mortality rate when these agents were used liberally.27,28
The use of morphine in the treatment of ADHF has long been considered standard
care, even though no well-designed, randomized trials have established its efficacy for
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these purposes. Over the past 10 to 15 years, evidence has been mounting to suggest
that morphine is actually not helpful in the treatment of ADHF and very likely could
carry significant harm. Sacchetti and colleagues22 reported an increased rate of
mechanical ventilation and admission to the intensive care unit for ADHF patients
treated with morphine and Peacock and associates29 found an increased likelihood
of mortality. These studies are based on retrospective reviews and are, therefore,
subject to the flaws inherent in such research, but they are far from unique in suggesting that morphine might very well worsen the effects of ADHF.30 Given these unsettling findings, we recommend against the use of morphine in the management of
ED patients with ADHF.
Nesiritide, a recombinant form of BNP with vasodilatory and diuretic properties,
received initial positive reviews as well as approval for use by the US Food and
Drug Administration, but controversy arose when 2 metaanalyses indicated a significant increase in kidney injury and a trend toward increased mortality among ADHF patients receiving this drug.31,32 The ASCEND-HF trial failed to demonstrate a reduction
in the 30-day mortality rate and the rate of rehospitalization for patients with ADHF
receiving nesiritide.33 The same trial also demonstrated significantly higher rates of
hypotension in patients randomized to the nesiritide group compared with patients
in the control group. As a result, nesiritide should not be used commonly in the treatment of ED patients with ADHF.
b-Blocker medications are an integral component of the outpatient management of
patients with chronic heart failure. In general, these medications are not used in
patients with ADHF, because of their negative inotropic effects. For patients who
take these medications routinely, it is common to withhold them during an acute exacerbation of chronic heart failure. However, recent guidelines indicate that withholding
b-blocker therapy from patients with chronic heart failure is not beneficial and recommend continuing the medication at its previously prescribed doses during an episode
of ADHF.25 The decision to continue b-blocker therapy for ED patients with ADHF is
best left to the inpatient team in consultation with the patients cardiologist.
Mechanical Assistance
Patients with ADHF who come to the ED are usually critically ill and require immediate
treatment. In contrast with traditional teaching, many of them are not volume overloaded. The foundation of ED management of patients with ADHF is rapid initiation
of NPPV along with aggressive titration of nitrates. For patients who do not respond
to escalating doses of nitrates, afterload reduction with an ACE inhibitor can be
considered. A diuretic should not be administered before these critical interventions
have been completed, but can be given after optimal preload and afterload reduction
has been achieved. Short-term inotropic therapy can be considered in select patients
with cardiogenic shock and ADHF who fail to respond to standard therapy. Morphine,
nesiritide, b-blockers, and placement of an IABP are not recommended for routine use
in the ED management of patients with ADHF.
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