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radiate to the arms, shoulders or jaw; it can be
associated with diaphoresis, shortness of breath, or
a sense of impending doom. However, several etiologies (esophageal spasm, gastroesophageal reflux
disease, musculoskeletal pain, etc.) may mimic typical angina. Additionally, ACS may present with
atypical symptoms and may be subsequently misdiagnosed. Patients with atypical symptoms tend to
be female, diabetic, and elderly. Regardless of the
types /natures of CP, at a minimum, patientsshould
be adequately risk stratified for ACS. Yet with its
limited sensitivity and specificity for ACS, accurate
risk stratification based solely on clinical examination is not recommended.
Risk Scores
Since clinical evaluation lacks precision at identifying CP patients as high risk (c-stat 0.55), several
risk scoring systems have been developed to stratify patients into low, moderate, or high risk for
ACS. Patients with high risk are likely to benefit
from immediate reperfusion therapy, while those
of intermediate to low risk may benefit from
observation. A number of validated risk scoring
systems exist, and include Thrombolysis in Myocardial Infarction (TIMI), Platelet Glycoprotein
IIb/IIIa in Unstable Angina Using Integrilin
Therapy (PURS UIT), and the Global Registry of
Acute Coronary Events (GRACE) risk scores. It is
open to debate as to which risk score is superior
in deter mining risk. A cohort study of 460 ACS
patients by de Araújo et al. looked at the predictive ability of these three risk scores to predict
death or MI within 1 year. It found that in terms
of predictive accuracy, the GRACE score (c-stat
0.715, CI: 0.672–0.756) outperformed both the
PURSUIT (c-stat 0.630, CI: 0.584–0.674) and the
TIMI scores (c-stat 0.585, CI: 0.539–0.631).
18
However, Lee et al. performed an analysis on
4,743 patients presenting to the ED with potential
ACS and found less variation between the scoring
systems for predicting death, MI, and revascularization within 30 days. The TIMI score had the
best predictive value (0.757 CI: 0.728–0.758),
followed by GRACE (0.728 CI 0.701–0.755) and
PURSUIT scores (0.691 CI 0.662–0.720).
19
Ultimately, regardless of which score is utilized, all have
sufficient predictive value and may be used to
determine patients at risk for ischemic events.
Patients at low to moderate risk are good candidates for OU admission.
Criteria for the Observation Unit
Inclusion Criteria
Patients of low to intermediate risk are candidates
for admission to the OU for further evaluation.
Appropriate OU candidates would include:
1. CP that is potentially related to ischemic heart
disease or CP that is unlikely related to
ischemic heart disease but the patient has a
significant history of coronary artery disease
2. Stable vital signs and hemodynamic
presentation (no hypotension, hypoperfusion,
or mental status change)
3. Comorbidities requiring low intensity of care
4. Negative or indeterminate ECG
5. Negative or indeterminate cardiac biomarkers
Exclusion Criteria
Patients who are at high risk for ACS are not
appropriate candidates and should be admitted
for hospital management. These patients may
have:
1. Ischemic changes on ECG (acute ST-changes,
new left bundle branch block and newly
inverted T-waves believed to be ischemic in
origin)
2. Cardiac marker results consistent with acute
myocardial infarction (e.g., significantly
elevated or rising)
3. Unlikely probability of going home within
24 hours
4. High risk by scoring system
Observation Unit Evaluation
CP has been the number one reason for admission and discharge from the OU between
2001 and 2008.
20
Although the majority of
patients admitted to the CP OU will have a final
diagnosis that is either musculoskeletal, gastroesophageal, or nonspecific in origin, the main
focus is the rule-out of an ACS. Existing rapid
rule-out protocols use a multi-marker or delta
biomarkers approach, which may exclude non
ST-elevated myocardial infarction (NSTEMI) in
as little as 90 minutes. However, these protocols
are for a certain subset of patients at low risk for
ACS and if ruled out, they should not be admitted
to the OU unless they require further evaluation.
Several noncardiac acute etiologies of chest pain
Chest Pain
025
20:47:21
(pneumonia, pneumothorax, pulmonary
embolus, etc.) may also benefit from placement
intheOU(seepneumoniaChapter29,pneumothorax Chapter30, and abdominal pain Chapter 45).
OUs provide an intermediate location for up
to 24 hours of monitoring and evaluation in individuals with low to moderate suspicion for ACS.
OUs have been proven to improve outcomes,
decrease LOS, reduce costs, and improve overall
patient satisfaction. Evaluations revolve predominantly around serial cardiac markers, serial
ECGs, and stress testing. Although telemetry is
commonly available for use in the OU, a study
of 248 patients in a CP OU demonstrated that
telemetry did not improve detection rates of cardiac events or admissions for arrhythmias compared to patients without telemetry.
21
Serial Electrocardiogram (ECG)
The ECG is an important part of the investigation
of potential ACS. The ECG evolution of an AMI
typically begins with hyperacute T waves, progresses to ST-elevation, which is then followed
by Q and inverted T waves. Although the specificities for ECGs are adequate, they ultimately lack
sufficient sensitivity for discharge decision
making. Further, ECG changes are not specific
to ACS and other diagnoses should be considered
(Table 22.1). The initial ECG has a poor sensitivity (55.4%) for detecting an MI while serial ECGs
modestly improve the sensitivity to 68.1%.
22
One
study found nondiagnostic ECGs (secondary ST
and T segment changes, < 2 mm ST elevation,
previous ischemic changes, etc.) were associated
with missed MI and unstable angina (UA).
23
Delayed clinical presentations may increase the
difficulty to interpret ECGs and may contribute
to a decreased sensitivity. In fact, after 12 hours
ECGs may start to normalize and interpretations
may become more difficult. To prevent misinterpretation of normalizing ECG, serial assessment
may reveal evolving changes. It is recommended
that a baseline ECG be obtained within 10 minutes
of arrival to the ED and repeated thereafter if
clinical suspicion remains. Compared to a single
ECG, serial ECGs could adjudicate 16.2% more
AMIs and improve diagnostic utility.
24
Cardiac Markers
In the absence of a diagnostic ECG , cardiac
markers (e.g., CK-MB, troponin) serve as a
primary tool for ruling out ACS. In the setting
of an anginal equivalent, elevation of cardiac
markers above the 99th percentile of the upper
reference limit is highly associated with cardiac
necrosis from ACS. However, depe nding on the
assay platform utilized, cardiac marker studies
may take 8–12 hours from the initial ischemic
event before becoming diagnostic for ACS. In
Table 22.1: ECG Differentials for STEMI
Increased T-wave Amplitude
– Acute Myocardial Infarction
– Benign Early Repolarization
– Hyperkalemia
– Left Ventricular Hypertrophy
ST-Elevation
– Acute Myocardial Infarction
– Benign Early Repolarization
– Left Ventricular Hypertrophy
– Left or Right Bundle Branch Block
– Left Ventricular Aneurysm
– NonSpecific Intraventricular Conduction Defect
– Pericarditis
– Pulmonary Embolism
– Takotsubo Cardiomyopathy
– J wave of Osborne
Q-waves
– False Lead Poling
– Hypertrophic Obstructive Cardiomyopathy
– Left Bundle Branch Block
– Left Ventricular Hypertrophy
– Preexcitation in Wolf Parkinson White
T-wave Inversion
– Acute Myocarditis
– Long QTc
– Pacemaker
– Pericarditis
– Persistent Juvenile T-Wave Pattern
– Pulmonary Embolism
– Stroke
– Takotsubo Cardiomyopathy
Tertius T. Tuy and W. Frank Peacock
025
20:47:21
fact, even when using newer higher sensitivity
troponins, approximately 30% of patients with
confirmed NSTEMI had initially negative cardiac markers.
25
Newer troponin platforms demonstrate little improvement in diagnostic
accuracy when performed i n serial fashion at
least 3 hours after symptom onset. Therefore
the 2011 European Society of Cardiology
(ESC) recommendations are that a second set
of cardiac markers should be repeated in as little
as 6 hours from the onset of symptoms. Other
professional societies (ACCF/AHA, ACEP, etc.),
which have not updated their guidance, still
have recommendations suggesting that serial
troponin measures are required for 8–12 hours
after symptom onset
4,26
, or 90 min after an
initially negative baseline troponin value for
patients presenting within 8 hours of symptoms.
26
Because ED patients may spend hours
waiting for their serial c ardiac markers to
return, the OU provides an alternate location
for patients to be evaluated while minimizing
the costs associated with ED or in-hospital
room.
Troponin, CK-MB, and Myoglobin
When cardiac necrosis occurs, creatinine kinase
MB isoform, myoglobin, and cardiac troponin are
released into the blood stream. Although sensitivities and specificities vary with time (Table 22.2),
cardiac troponins tend to have the greatest specificity and sensitivity among the three. Thus the
ACC/AHA and the ESC suggests that cardiac
troponins should the marker of choice for cardiac
necrosis when available. Interpretation and application of cardiac biomarkers requires knowledge
on their natural history following cardiac insult.
27
Cardiac troponin becomes detectable within 3–6
hours of myocardial necrosis, peaks at 12 hours
and may remaining elevated for approximately 14
days. High sensitivity troponin tests are capable of
detecting cardiac necrosis earlier and can identify
reinfarction (using delta values). Of the other
markers, myoglobin and CK-MB peak at about
4 and 12 hours, and remain elevated for 12 and
24–48 hours respectively. Therefore, CK-MB and
myoglobin can also be used when there is suspicion for infarction or reinfarction.
Table 22.2: Standard Cardiac Biomarkers
Onset Peak Disappearance Advantages Disadvantages Sensitivity
(Initial/
Serial)*
Specificity
(Initial/
Serial)*
Myoglobin 2
hours4hours
8–12 hours – Short half-
life allows
detection
of reinfarction
– Rapid ruleout of AMI
– Nonspecific to
cardiac muscle
49%/89% 91%/87%
CKMB 4
hours
12–24
hours
2–3 days – Short half-life
allows detection
of reinfarction
– Slightly
nonspecific to
cardiac muscle
(large amount of
skeletal muscle
damage:
rhabdomyolysis,
muscular
degeneration,
trauma)
42%/79% 97%/96%
Troponin
I/T
3–6
hours12hours
7–14 days – Able to
detect recent
infarct
– Specific
to myocytes
– Difficult to detect
reinfarction
39%/
90–100%
93%/
83–96%
* Sensitivity and specificity in detection of acute myocardial infarction
Chest Pain
025
20:47:21
Provocative Stress Test and/or
Imaging
In selected ACS patients with negative serial biomarkers and ECGs, provocative stress tests may
be indicated.
28–33
However, there is some contention whether a stress test while in the OU confers
a mortality benefit compared to an early outpatient stress test.
34
Depending on the institution, a variety of
stress tests may be implemented during the OU
stay. Exercise stress tests (assessed by ECG or
echocardiogram) are cost-efficient, easily performed, and provide insight into presence of
inducible ischemia from physiologic stress.
A study compared ED-initiated cardiac treadmill
exercise stress testing with admitted patients.
35
The average patient charge was $467 with a LOS
of 5.5 hours for the ED stress test patients, while
the inpatient average patient charge was $2,340
with a 2-day LOS.
35
For individuals who cannot
meet the target heart rate for a variety of reasons
(inability to exercise, structural deficits, extreme
pain), a pharmacological stress test may be used
instead.
Although exercise stress tests are commonly
implemented, there are other modalities of cardiac imaging that can be used to evaluate the
likelihood of ACS. Another technique of imaging,
myocardial perfusion imagin g (MPI) uses
technetium-99m and coronary artery vasodilators
to provide information about relative blood flow
to the myocardium. In detecting coronary artery
disease MPI has a good sensitivity of 92% and a
decent specificity of 63–71%.
33
This should be
considered for women as exercise treadmill test
in women has poor negative predictive value
(68%) for coronary artery disease and may misrepresent the presence or absence of coronary
artery disease in 36%.
36
Computer tomography angiogram (CTA) can
also provide insight into whether there is significant coronary plaque or stenosis. In fact CTA had
a sensitivity of 100% and specificity of 54% for
detection of a coronary plaque.
37
In the Rule-out
Myocardial Infarction using Computer Assisted
Tomography (ROMICAT) study, CTA was used
for rapid rule-ou t of low risk ACS patients in the
ED. ROMICAT demonstrated that low-risk CP
patients with a negative CTA had 100% negative
predictive value for coronary artery disease and
could be discharged home immediately.
37
Cardiac magnetic resonance (CMR) imaging
can provide information about cardiac function,
ischemia, viability, and coronary anatomy. In
individuals with negative ECGs and cardiac
markers, dobutamine stress CMR was more sensitive (86.2 vs. 74.3%) and specific (85.7 and
69.8%) for detecting 50% stenosis than a stress
echo.
38
When using adenosine, perfusion CMR
had a sensitivity and specificity for detecting coronary artery disease of 90% and 81%
respectively.
39
Immediate Management of Newly
Confirmed ACS in the OU
During the OU stay, if patients are identified as
high risk for an ACS event (positive serial biomarkers or ECGs, a clinical presentation consistent with ACS, or developing new or worsening
heart failure symptoms) they should receive
guideline-consistent ACS care. This includes antiplatelet and antithrombotic therapy. Oxygen,
nitrates, and morphine have no demonstrated
mortality benefits
40–42
and their use could be
given for symptomatic treatment. Beta-blockade
may be considered (except when there is evidence
of heart block, hypotension, and/or acute heart
failure). The physician should decide whether the
patient is a candidate for either reperfusion therapy or medical management, and hospital admission to the appropriate intensive care unit should
be arranged. Subsequent management of ACS
should be done on an inpatient basis.
Disposition
Low-risk patients who have had an acute ACS
excluded may be candidates for early discharge
without a myocardial perfusion evaluation. The
ASPECT study reported outcomes in patients
with TIMI risk scores of zero at zero and 2-hour
serial biomarker testing results and found early
discharge, rather than OU stress testing, an
effective strategy.
43
The decision on whether
higher-risk patients require immediate evocative
myocardial perfusion evaluation, or may be discharged for outpatient stress testing, is less clear.
Patients discharged with elevated risk (elevated
cardiac markers, ST-depressions, advanced age,
or history of HF) can have up to 14-fold increase
in mortality and they may benefit from earlier
stress testing.
4
Tertius T. Tuy and W. Frank Peacock
025
20:47:21
Chest Pain Center Quality
Improvement
While a number of professional societies (AHA,
ACC, ESC) provide extensive recommendations
on the management of patients with confirmed
ACS, few detail specific “best practices” for the
patient with suspected but unconfirmed ACS. The
Society of Chest Pain Centers and Providers
(SCPCP) currently accredits CP OUs on their
process for evaluating patients with suspected
ACS. While little objective data exists establishing
improved outcomes after any quality certification
process (e.g., Joint Commission Certification),
using the Centers for Medicare and Medicaid
Studies database, SCPCP accreditation is associated with markedly greater rates of guideline
compliance than nonaccredited CP centers.
44
Summary
In the management of CP, the observation unit
serves as a location to safely determine if an ACS
exists. Patients who have low to intermediate suspicion for ACS may be effectively managed
during the < 24-hour placement. Observed care,
serial cardiac markers and ECGs, as well as provocative stress test and imaging are the foundation for OU care. Therefore, in this selected
patient population, the OU strategy can be used
without incurring added risk and reduces the
unnecessary cost associated with prolonged inpatient admission stay. Once ACS and other serious
pathology have been ruled out, patients may be
safely discharged and managed in an outpatient
setting.
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Subpart IVA
Chapter
23
Clinical – Cardiac
Heart Failure
Jieun Kim, MD
W. Frank Peacock, MD, FACEP
Introduction
Heart failure (HF) has been a consistently
increasing burden in both clinical management
and health care spending. Annual expenditures
on HF management are massive. Beyond costs,
HF is becoming one of the major causes of mortality in the United States.
1
More than 4 million
Medicare beneficiaries have HF and approximately half will die within 5 years.
1
In 2008, the
overall prevalence of HF reached 5.7 million
people, with estimated direct and indirect cost
of HF alone to exceed 37.2 billion dollars.
2
The
majority of the HF cost is due to inpatient hospitalization. Because the incidence of HF is
expected to increase dramatically due to the
aging population and improved survival from
acute coronary syndrome (ACS), new strategies
to decrease the clinical burden and economic
costs are needed.
Based on American College of Cardiology/
American Heart Association (ACC/AHA) and
Agency for Healthcare Research and Quality
(AHRQ) guidelines, it has been suggested that
up to 50% of admitted HF patients are low-risk
and may be candidates for outpatient therapy.
3
In
this context, the HF observation unit (OU) can be
an innovative alternative means of managing
selected HF patients in an acute setting. Clinical
management in the OU can provide specialized
care for HF patients and is reported to shorten
hospital length of stay (LOS), reduce the number
of intensive care unit (ICU) admissions, and
decrease the rate of 30-day hospital readmissions,
thus reducing health care cost without difference
in outcome.
4
In a prospective observational study, emergency departm ent (ED) HF patients of equivalent
severity who were admitted as inpatients were
compared to those treated in the ED OU. The
study found no significant difference in outcome,
but major benefits from ED OU management in a
decrease in time from ED triage to disposition,
reduced mean bed hours of inpatient 58.5 hours
to 25.7 hour in ED OU, and significant cost
savings from $7824 as an inpatient to $4203 from
ED OU.
5
Furthermore, another study shows that
during the same time period, annualized hospital
costs declined by nearly $100,000, predominately
the result of the 30-day readmission avoidance
advantage in ED OU.
6
Presentation of HF in the
Emergency Setting
The common presentations of acute decompensated heart failure (ADHF) in the ED are shortness of breath, fatigue, and swelling of the legs.
The presentation could be either an acute pump
dysfunction reflecting worsening of cardiac
function, or an insidious presentation as a consequence of pathologic neurohormonal and
hemodynamic cascade from myocardial stress.
Without a worsening of underlying circulatory
function, failure to adhere to prescribed medications or dietary regimes may also lead to ADHF
presentation in the ED.
4, 7
Effective ADHF management in the ED
encompasses two objectives: first, to correctly
diagnose ADHF and second, to initiate an appropriate treatment in a timely manner. Both aspects
of care should be equally emphasized since inability to accomplish either could have deleterious
effects in ADHF patients.
Diagnosis of ADHF
The first challenge of HF management begins in
the ED, where rapid and accurate identification of
ADHF is necessary.
6
HF is a clinical syndrome
and its diagnosis is based on signs and symptoms
from the patient’s initial history and physical
examination, supported by radiographic findings,
and laboratory results, such as biomarkers.
8
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History and Physical Examination
The most common presenting symptom of HF is
dyspnea. Unfortunately, a chief complaint of dyspnea is nonspecific since it can be produced by
multiple other medical conditions such as COPD,
asthma, pneumonia, and myocardial ischemia.
6
Moreover, other typical physical examination
findings of ADHF (e.g., rales, peripheral edema)
are nondiagnostic since they are also a common
presentation of other comorbidities
8
and may be
missing at hospital presentation.
9
For instance, in
one study, rales, edema, and elevated mean jugular
venous pressure were absent in 18 of 43 patients
with a documented pulmonary capillary wedge
pressure (PCWP) > 22 mmHg.
10
Unfortunately,
diagnostic accuracy can further decrease with
other confounding factors, such as gender. Female
patients can present with atypical signs and symptoms of card iovascular disease, which can contribute to diagnostic complexity in ADHF.
11
Radiographic Findings and Biomarkers
Similarly, radiographic features of ADHF are not
always reliable. Pulmonary congestion can be
minimal or absent in patients with significantly
elevated pulmonary artery wedge pressure
12
and
ECG and x-ray findings are either non-specific or
insensitive. In one study, approximately one of
every five patients admitted from the ED with
ADHF had no signs of congestion on chest radiography.
13
In a large registry study (ADHERE),
26% of patients did not have evidence of pulmonary congestion on their initial chest radiograph.
14
Consequently, biomarkers such as serum Btype natriuretic peptide (BNP) and its N-terminal
prohormone (NT-proBNP) have been integrated
into diagnostic decision making in suspected HF
to improve accuracy and help assess the severity of
potential ADHF. BNP levels are associated with
New York Heart Association (NYHA) functional
class, and were reported as the single most accurate
predictor of the presence of HF.
6
In one study, a
BNP cutoff of 100 pg/ml had a sensitivity of 90%,
specificity of 76%, and an accuracy of 83% for the
diagnosis of ADHF. From the PRIDE study,
NTproBNP was shown to have a rule-in cutpoint
of 900 pg/mL with a sensitivity of 90%, specificity
of 85%, and an accuracy of 87%. NT-proBNP’s
rule-out cutpoint of 300 pg/mL has a sensitivity
of 99%, specificity of 68%, and negative predictive
value of 99%.
15
Despite its high sensitivity, BNP
has several confounders that include renal failure
and body mass index (BMI).
16
Therefore, BNP’s
role in diagnosing ADHF should be coupled with
clinical impression.
Noninvasive Bioimpedance Technology
Providing a noninvasive and convenient diagnostic investigation has been evaluated using bioimpedance (BI) technology. BI measures the
reactance and resistance of the body and can
provide plots of a patient’s volume status,
17
thus,
providing real-time hydration status of the
patient. Nevertheless, the precise role of BI in
the ED is still undefined and large-scale studies
are still needed to assess its ED utility.
6
The Initial Treatment Goal in ED
The goal of initial treatment of ADHF is to stabilize hemodynamics, support oxygenation and ventilation, and to relieve symptoms. The primary
objectives in hemodynamic stabilization are to
lower the pulmonary capillary wedge pressure,
reduce systemic vascular resistance, and provide
a modest improvement in cardiac index.
18
In the
hypertensive patient, these objectives can be
achieved through a reduction in blood pressure
(BP) by vasodilation and diuresis, which will also
increase oxygenation of patients. P atients will
benefit from maintaining a low BP, which will
decrease peripheral vascular resistance and lead
to an immediate clinical improvement.
17
Simultaneously, all suspected ADHF patients
should be monitored for coronary artery disease
(CAD) as well as electrolyte imbalance. CAD is
one of the most common causes of HF, thus,
cardiac markers should be checked to detect any
underlying acute myocardial infarction (AMI).
Concurrently, abnormalities in potassium,
sodium, magnesium, creatinine and BUN should
be monitored since the patient will underg o diuresis. Significant derangement of electrolytes will
need correction and will guide individualized care
with supplemented electrolytes.
The Observation Unit
in the Emergency Setting
The OU can be an alternative option for appropriate patients by providing optimized care to
ADHF patients, thereby, reducing hospital admissions and healthcare costs. Studies have shown
Heart Failure
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that safe and effective HF management strategies
in the ED OU can decrease the number of ED
visits, hospitalizations, and ICU admissions; thus
decreasing costs and improving quality of life and
mortality when compared to non-OU management programs.
11
Outcomes before and after
institution of an ED OU HF protocol found ED
HF revisit rates declined by 56% and the 90-day
HF rehospitalization rate decreased by 64%. Furthermore, the 90-day rates of OU HF readmission
decreased from 18% to 11% and the 90-day death
rate decreased from 4% to 1 %.
27
ED OU management has been shown to reduce hospital LOS
more than 20 hours per patient and provides a
cost saving of approximately $3600 per patient.
5
Studies have suggested that up to 50% of patients
could be discharged home after initial therapy.
3
These patients can be expected to greatly benefit
from OU management as their clinical symptoms
improve sufficiently within a few hours of ED
admission.
The implementation of OU management not
only decreases the overall healthcare costs, but
more importantly can directly benefit patient s as
well. In the OU, patients can receive appropriate
and intensive HF therapy without requiring several days of hospitalization. This enables patients
to receive the full benefit of hospitalization in a
short period of time, thus, preventing an extended
inpatient admission and/or multiple outpatient
visits. For instance, ejection fraction (EF)
measurement can be assessed in the OU and
significant delays as may occur in the outpatient
setting are prevented. Optimization of medication
can be accomplished in a more controlled environment. One recommended ADHF patient management flow chart is presented in Figure 23.1.
OU Entry Criteria
In order to provide optimal care, patients should
be carefully selected and transferred to the HF OU
from the ED. First, patients should have a recent
clinical history consistent with an acute decompensation episode such as shortness of breath,
orthopnea, dyspnea upon exertion, paroxysmal
nocturnal dyspnea, swollen legs or abdomen, or
weight gain associated with fluid retention.
11
Physical examination should be consistent with
findings of ADHF like jugular venous distention,
an audible S3 or S4 heart sound (galloping
rhythms), positive abdominal jugular reflex, rales,
and peripheral edema. Chest radiograph findings
associated with HF include cardiomegaly, pulmonary vascular congestion, Kerley B lines, pulmonary edema, and pleural effusion.
11
Previous
history of HF should be also taken as it has been
shown as one of the most reliable predictors of a
HF diagnosis is a history of ADHF.
19
BNP levels are helpful for the exclusion of HF.
Therefore, patient, eligibility to the HF OU
includes a BNP level of > 100 pg/mL (normal
Double dose of
furosemide+ and
re-administer IV bolus
No addional
diurec needed,
connue to monitor
Volume overload and systolic BP > 100 mmHg
On PO furosemide* as outpaent?
NOYES
Give 40 mg
IV furosemide
Give usual oral dose of
furosemide as IV bolus
Is 2 hour urine output?
> 500 cc if creanine < 2.5 mg/dL
> 250 cc if creanine > 2.5 mg/dL
NO
YES
*Or furosemide equivalent
+
Bolus doses > 160 mg suggest
paent is not likely to succeed
OU management. Inpaent
hospitalizaon should be
considered.
Figure 23.1 Acute
Decompensated Heart Failure
Patient Management Flow Chart
Jieun Kim and W. Frank Peacock
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