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ACUTE HEART FAILURE
165
dilatation, as furosemide does, long before it produces
diuresis. Morphine also was thought to be a good way
to lower peripheral resistance, as well as to interfere
with the vicious cycle of hypoxia and adrenalin pro-
duction by the patient. For years this seemed to work
pretty well, so why do we think it’s no longer useful?
AM: There are some studies indicating that when you
give morphine and furosemide, you get peripheral
vasodilatation in the wrist and forearm.
2,3
Based on
those studies, people extrapolated and assumed that if
you had vasodilatation in the wrist and forearm, then
you must also be getting a decrease in right heart fi lling
pressures, but this was only an extrapolation. When
they actually studied this using pulmonary artery (PA)
catheters, they found that when you give morphine
and furosemide peripherally, you often obtain a slight
increase in wedge pressures, so patients actually get
a little bit worse.
4,5
There are studies indicating that
furosemide activates the renin-angiotensin-aldosterone
system, which is an endogenous pressor system. This
may transiently cause an increase in afterload. It’s not
until the diuretic effect actually kicks in, which can be
an hour or two later, that central preload will drop.
6–8
To summarize, when giving diuretics, rather than
a central improvement there is mild worsening; then,
about an hour later, when diuresis begins, there is a
drop in the wedge pressure. Similarly, morphine has
been found to be a myocardial depressant; the few
PA catheter studies show that giving morphine to
patients with cardiogenic pulmonary edema worsens
the cardiac index.
4,9
EU: I fi nd afterload reduction with ACE inhibitors
particularly useful for the hemodialysis patient who
presents in pulmonary edema, as it may buy time until
the hemodialysis team comes in for defi nitive care.
that we tend to forget about, and that is the patient
with cor pulmonale or “blue bloater” rather than the
“pink puffer.” This is the patient who has chronic
obstructive pulmonary disease (COPD), and who
presents with an enormous volume overload per-
haps triggered by an acute fl are-up of bronchitis with
worsening hypoxia. This causes the patient not only
to have the presentation of someone with acute con-
gestive failure, but the appearance of someone who
has acute respiratory failure. How we can distinguish
these patients, or does it matter? Can we just lump
A patient who is somnolent or unconscious is not
going to be able to tolerate bilevel positive airway
pressure (BiPAP) or continuous positive airway pres-
sure (CPAP); these patients will certainly need intuba-
tion. If a patient comes in markedly hypotensive or in
shock, it is necessary to actively manage the airway.
As in all of emergency medicine, fi rst take care of the
airway, and then care for breathing and circulation.
PR: I think that’s a useful fi rst distinction. In the
patient who presents with pump failure, one of the
critical fi rst steps in management is to perform intuba-
tion to reduce the work of respiration. These patients
will not respond to CPAP and to volume manipula-
tion; they’re going to need pump assistance.
WB: I would focus on three things: fi rst, make sure
the patient is not in extremis. Then, supply some form
of high fl ow oxygen, at least initially a non-rebreather
facemask. Lastly, start high dose nitrates, either sub-
lingual, topical, intravenous, or some combination
thereof.
SG: I would avoid topical nitrates in this patient as
their effect on blood pressure is inconsistent, and their
absorption is erratic due to both patient diaphoresis
and the nature of a transdermal absorption.
WB: After nitrates, I use noninvasive positive pres-
sure ventilation aggressively. Lastly, I’ve added ACE
inhibitors to my armamentarium, either enalaprilat or
sublingual captopril. I have begun to stay away from
furosemide, and I try not to use morphine if at all
possible. I’ve recently developed several prehospital
protocols for EMS agencies that removed furosemide
as a fi rst line drug, and made its use dependent upon
a base station medical command. For EMS, we have
also signifi cantly deemphasized morphine, and added
sublingual captopril.
AM: Maryland has developed similar EMS proto-
cols. Formerly, the paramedics would automatically
give morphine and furosemide, but now morphine
has been completely excluded from the protocol, and
furosemide can only be given upon medical com-
mand. Similarly, the state protocols have also incor-
porated sublingual captopril into prehospital CHF
protocols.
1
PR: Could you explain why this is the case? Most of
us grew up in the period where we were told you had
to unload the heart, and you had to produce venous
CHAPTER 12
166
compromise, I would arrange admission, even with a
rapid positive response to intervention. Patients with
similar presentations to this case can be treated aggres-
sively, observed over a number of hours, and then reeval-
uated as to their response to work of breathing and
the effectiveness of their perfusion. Diagnostic testing
on the front end of the evaluation of congestive heart
failure is largely limited to taking an adequate focused
history and performing an appropriate physical exam-
ination. I do think it’s appropriate to consider that,
when a patient is in congestive heart failure, why did
that patient decompensate? One should always con-
sider acute cardiac ischemia, realizing that shortness
of breath can be an anginal equivalent that is present
in many patients with acute myocardial infarction. It’s
very appropriate to perform an EKG. I would check
at least two sets of cardiac markers using troponins
spaced at least 3 hours apart. I would also consider in
the history whether the etiology is related to dietary
indiscretion. Was the patient celebrating with a large
holiday feast where people ate a lot of salty food that
caused the decompensation? Did the patient stop using
his routine outpatient therapy? I would also consider
respiratory infections, as they can also cause someone
with tenuous cardiac function to tip the balance and
decompensate.
If the person were not in extremis or exhibiting sig-
nifi cant respiratory compromise, and had a positive
response to therapy and excellent medical follow-up,
then I would consider discharging the patient from the
ED. Follow-up is critically important, because many
of us forget that congestive heart failure has a very
high mortality rate with a large number of people
dying in the fi rst year after the diagnosis. For this rea-
son, even if we do turn them around quickly in the
ED and they are appropriate discharge candidates, we
must assure adequate medical follow-up in the short-
term and long-term.
PR: The statistics that I’ve read are absolutely fright-
ening. I recall data from a couple of years ago that,
after the acute onset of congestive failure, well over
80% will be dead within 2 years.
Yet, years ago our cardiac beds were fi lled with
CHF patients who would lie around for 2 or 3 weeks
while we diuresed 20 or 30 pounds from them. We
didn’t have very good diuretics. It seemed as though
there were many more patients who were chronically
overloaded, and who, to a large degree, fared much
them together and use a similar therapeutic approach,
and only worry about primary lung disease if we hear
physical signs of bronchoconstriction?
SG: This is a classic emergency medicine question: the
patient presents short of breath, and you don’t know
if the cause is COPD or CHF. This was part of the con-
troversy when BNP as a marker for CHF was devel-
oped. Do you really need to know the whether this is
CHF or COPD? Traditionally, the shotgun approach
was to treat the patient for both diseases, and then
an hour or two later see what was the true etiology
of their respiratory diffi culty. The issues are several-
fold. First, we’re using medications that don’t clearly
have benefi t but, at the same time, don’t clearly have
detriment, such as a beta-agonist in a patient with
acute CHF. Although there is some rather old data
that suggest that some beta-agonists may have utility
in patients with CHF, most studies have not shown
benefi t, but also have yet to show an adverse affect.
At the same time, if you start treating a patient with
steroids whom you think is having a COPD exacerba-
tion but who actually has CHF and cardiac ischemia,
you may be impairing the cardiac remodeling taking
place during the infarction evolution. This is the argu-
ment against a shotgun approach and to suggest that
there should be some sort of rapid approach to sort
out whether the patient really has CHF. Unfortunately,
this has led to rampant overutilization of BNP as a
marker for CHF.
PR: Often the patient’s history can help sort the diag-
nosis out. I’ve seen a fair number of patients who
were mistreated as COPD patients because they were
wheezing, yet there was no prior history of asthma
or chronic bronchitis, and they clearly were in acute
congestive failure. While I have no problem in using
diagnostic tests that help sort things out, I fi nd it the
very antithesis of emergency medicine to wait 2 hours
for a BNP level while your patient is choking to death
and needing emergent therapy. A critical issue in the
management of a patient like this who doesn’t sound
as critically ill as many patients can be, is can we turn
him around in the ED? Does he need admission? What
should be the follow up once we get his pulmonary
overload turned around?
WB: In most cases, you can identify admission can-
didates when you walk into the room. If someone
presents in extremis or having signifi cant respiratory
ACUTE HEART FAILURE
167
to know, “Why are you admitting this patient?”, not
realizing that an hour ago, the patient was on the
verge of intubation. The second scenario includes the
patients who are much more aggressively managed
with loop diuretics than they were even 15 or 20 years
ago. Although the loop diuretic is an effective agent
in terms of removing fl uid, this is often one of the
wrong approaches. High-dose furosemide over a very
short period of time may make the patient relatively
hypovolemic, resulting in acute renal failure. In these
patients we have to be quite cautious, but it’s very
hard to convince many inpatient physicians to admit
these patients because they don’t see someone who
is in extremis; today you have to be quite ill to even
qualify for a non-ICU bed.
PR: One of the curses of our crowded hospitals and our
crowded EDs is that we often reach for therapies that
are suboptimal, because even if we’re willing to be the
patient’s advocate, there just aren’t any beds. We can’t
achieve the same benefi t that an inpatient admission
would. I think this problem is going to increase over
time. We are seeing more and more patients who are
having their acute ischemia managed well, but their
chronic heart disease is advancing inexorably, and we
don’t do a very good job managing this. The fi nal issue
that I’d like to address is rate disturbance as the trigger
of this congestive failure. We have many patients who
are in chronic atrial fi brillation. Is there something we
can use to slow their rate? Or should we try to convert
them to a sinus rhythm? Is there something we should
use beyond the treatment for heart failure?
EU: If you have someone who is in CHF with rapid
atrial fi brillation, I would be very leery of using a
beta-blocker for the theoretical pump disturbance
that will go along with it. Instead I fi nd much of the
time, just by noninvasive pulmonary management
and aggressive nitroglycerin therapy, you’re able to
improve breathing. Then the atrial fi brillation, or at
least the rapid ventricular response, tends to respond
appropriately, and you’re at a level of heart rate that’s
not so tenuous. I would tend to avoid chemical or
electrical cardioversion as more often than not, these
patients have chronic atrial fi brillation, which won’t
convert anyway, and if they do convert, they would be
at high risk for stroke.
PR: What about the patient with valvular heart dis-
ease from endocarditis and CHF? When should you
better in the hospital, I suppose because they had bed
rest, oxygen, and a careful diet. Since that no longer
seems to be a possible utilization of a hospital bed, are
we just overlooking people like this, or has the quality
of congestive failure changed over the years so that
we’re seeing a different kind of patient?
EU: I think it’s a bit of both. There hasn’t been a lot of
great innovation. In fact, most of the therapies, aside
from positive pressure ventilation, are just old school
therapies.
SG: I believe we have gotten better at keeping these
patients out of the ED. Often dobutamine courses will
be done as a day therapy or in observation units. This
is more a refl ection of improved outpatient clinic care
and diffi culty sustaining long-term inpatient care then
a refl ection of therapeutic advances.
PR: Do you think our international diets are becom-
ing more salt-laden?
SG: Congestive heart failure has very high mortality
and morbidity, and patients don’t seem to realize how
sick they really are. Patients want to go out and live
the way they enjoy living, and life is so much easier
than it was even 10 years ago. Certainly around the
world, but especially in the United States, accessibility
to any sort of food at any sort of time, in any sort of
place, is incredible, and that factors into dietary indis-
cretion. This is a lifestyle that is very diffi cult to alter,
especially when there is no perception that CHF is as
deadly or perhaps more deadly than diseases such as
cancer or other major killers.
PR: Do you have diffi culty getting your CHF patients
admitted?
WB: Most large teaching hospitals today are func-
tioning at or above capacity, so I think my experience
is similar to most. Not only housestaff, but admit-
ting physicians in general, look at this patient and
say, “Well, they just need a little more furosemide,
and I’ll see them in a couple of days, or a couple of
weeks.” There are two scenarios to talk about: One
is the patient who does present with signifi cant respi-
ratory compromise. This patient might be under-
perfused. The emergency physician approaches the
problem aggressively, improves the situation, and
by the time the admitting physician sees the patient,
the situation looks completely different: the patient
looks well. Therefore, the admitting physician wants
CHAPTER 12
168
failure, usually with acute pulmonary edema. They
would start with a mild fl u syndrome, but within
48 hours, were in bubbling pulmonary edema.
AM: We’ve also seen a few cases of myocarditis
presenting as CHF in relatively young people. When
you have a young person who is in CHF, you have to
consider viral myocarditis.
PR: What about the congestive heart failure of preg-
nancy? Many of us don’t see much of this, as the
pregnant patients go to the labor and delivery (L&D)
fl oors. There are many hospitals in this country where
there are no L&D fl oors. Yet, we see many patients
who come in short of breath during late pregnancy.
Most of us think more of pulmonary embolus than
congestive failure, and yet heart failure must be con-
sidered in these patients. Do you have any experience
with this entity?
SG: What’s interesting about the cardiomyopathy of
pregnancy is that it can be prepartum (within a month
of delivery) or post-partum (within 4–5 months of
delivery), and more often than not, left ventricu-
lar function will return to normal over the ensuing
course of months. It is often missed initially as women
who are short of breath prepartum or postpartum are
thought to more likely to have pulmonary emboli.
Although the etiology of the cardiomyopathy remains
unclear, advanced maternal age, multiparity, African
descent, pregnancy with multiple fetuses, eclampsia,
cocaine abuse, and long term oral tocolytic therapy
may help predict which patients will develop this
cardiomyopathy. The trick is to recognize that this
is in fact congestive heart failure, and once you’ve
recognized it as CHF, then begin much of the same
the treatment. The only medications to avoid are
ACE inhibitors and ARBs (Angiotensin II Receptor
Blockers), as they may be teratogenic.
Case resolution
The patient was felt to be suffering from an acute heart
failure syndrome, likely due to acute vascular dys-
function, based on the acute progression of his symp-
toms, physical examination, and CXR study fi ndings
of cardiogenic pulmonary edema. As the patient was
alert and well perfused, CPAP at 10 mmHg on 100%
oxygen was initiated. Rapid administration and
titration of IV nitroglycerin was begun. In addition,
start thinking of endocarditis in a patient presenting
with symptoms of congestive heart failure?
WB: Endocarditis is a diffi cult diagnosis to make,
very insidious even in the acute forms, such as with a
Staphylococcus aureus type presentation. The patients
will likely present in pulmonary edema, and in a busy
and noisy ED in a patient who has signifi cant work of
breathing and related respiratory noises, it’s often dif-
fi cult to detect the murmurs that would lead you down
that pathway. In someone with a history of IV drug
abuse, the diagnosis may be a little easier. Frequently,
patients don’t admit to drug abuse. I always try to
look at the forearms and other prominent vein areas.
The IV drug abuser who is relatively young, who
presents with signs and symptoms of heart failure,
should prompt a consideration of endocarditis. This
doesn’t mean that you need to pursue the diagnosis
with blood cultures, but you should at least consider
endocarditis. Transthoracic echocardiography isn’t
very helpful; if you don’t see vegetations, you haven’t
ruled anything out. While transesophageal echo is a
much more helpful study, it’s also much more diffi cult
to obtain in the ED.
AM: If you have a patient with endocarditis who now
presents with CHF, would you say that almost always
the CHF is due to signifi cant valvular dysfunction that
perhaps even a transthoracic echocardiogram might
be sensitive enough to pick up?
WB: If a patient presents with signifi cant heart failure
due to endocarditis, and you can demonstrate valvu-
lar dysfunction on a trans-thoracic echocardiogram,
you would at least have part of your answer. In terms
of making the diagnosis of endocarditis, like many
syndromes that are diffi cult to diagnose, they tend
to evolve in front of your eyes over the following 24,
48, 72 hours. In the ED, we do not have the luxury
of that kind of serial observation. The emergency
physician who is thinking clearly is always asking
why; in a young person who may have some drug use
history, he needs to ask the question, “Why is this
person demonstrating signifi cant mitral dysfunction,
or why does this person have signifi cant aortic insuf-
fi ciency?” If there’s really no other explanation for it,
consider endocarditis.
PR: One of the things that I was beginning to see more
frequently at the start of this century were young
people with viral syndromes presenting in congestive
ACUTE HEART FAILURE
169
now often required to deliver both acute and ongoing
heart failure care.
14
Defi nitions and pathophysiology
of acute heart failure
The term “acute heart failure syndromes” emerged
from meetings of an international workgroup that
was convened primarily to establish uniform terminol-
ogy and defi nitions in heart failure. The workgroup
defi ned acute heart failure syndromes as the “gradual
or rapid deterioration in heart failure signs and symp-
toms resulting in a need for urgent therapy.”11 The
American College of Emergency Physicians (ACEP)
Clinical Policies Committee uses the term “acute heart
failure syndromes” in their updated guidelines.
11
Two separate categories of AHF syndromes, fi rst
suggested by Cotter, et al. in 2002
16
have been adopted
by the European Society of Cardiology in their guide-
lines on diagnosis and treatment of AHF.
17
The fi rst
is termed acute decompensated cardiac failure. These
patients suffer from a progressive, relatively slow
(days to weeks) deterioration of chronic heart failure.
This is typically attributed to noncompliance with
medications, dietary indiscretions, or myocardial dys-
function (Figure 12-1). These patients are typically
fl uid-overloaded and benefi t from diuretic therapy,
fl uid restriction, dietary compliance, improved phar-
macotherapy, or other interventions (such as revascu-
larization or resynchronization).
12
The second is termed acute vascular failure or
dysfunction. This is a rapidly progressive condition
associated with high blood pressure and severe acute
dyspnea, a common ED presentation in patients with
acute heart failure syndromes. The acute presentation
in these patients is most likely caused by a combina-
tion of increased vascular resistance and decreased
cardiac contractility (Figure 12-1). This can occur
even if the ejection fraction is relatively good. This
suggests a largely vascular problem, and not a fl uid
overload problem. Recent data from registries such as
ADHERE suggest that this second category is actually
the most common type of AHF in unselected popula-
tions.
13
Acute decompensated cardiac failure tends to
be overrepresented in studies of patients in academic
tertiary care centers, which may be the reason that a
majority of the academic teaching has been focused
on therapy of fl uid overload (diuretics) rather than on
therapy of vascular dysfunction (vasoactive agents).
1.25 mg IV enalapril was administered, followed by
furosemide 40 mg IV, with an ensuing diuresis of
1.0 liter of urine within 90 minutes of presentation.
The patient’s respiratory rate, physical appearance,
and subjective dyspnea began to improve within the
fi rst 15 minutes. Initial laboratory data returned with
a normal chemistry profi le, a BNP level of 1360 pg/dL,
and a normal digoxin level. The patient was admitted
to the ICU for close monitoring.
An inpatient echocardiogram showed a worsening
EF of 35%, compared with a previous EF of 50%.
A nuclear stress test was negative for acute ischemia.
The cardiology team optimized the patient’s medica-
tions, and the patient was discharged home 4 days
later in stable condition.
Section III Concepts
Background
Heart failure is a worldwide problem of epidemic
proportions, and represents a tremendous cost bur-
den to health care.
10
Recent data from the American
Heart Association (AHA) estimates that nearly fi ve
million individuals are living in the United States with
heart failure (2.3% of the general population), and
an additional 550,000 new cases are diagnosed each
year.
11
Acute heart failure (AHF) is the most common
cause for hospital admission in patients 65 years of
age.
12
The ED plays a critical role in the management
of acute heart failure syndromes, since approximately
80% of patients hospitalized for the condition are
admitted through the ED. There are approximately
one million admissions to US hospitals for AHF each
year, accounting for more than six million hospital
days and $12 billion in charges. Moreover, the prog-
nosis of patients admitted with AHF is dismal, with
greater than 20% of patients being readmitted with
heart failure (HF) and more than 20% dying during
the fi rst year after admission.
13
Further contributing to the burden of heart failure in
the United States is the impact of an aging population,
along with hospital and ED crowding.
14
The Institute
of Medicine’s Report on Emergency Medicine fi nds
that from 1993 to 2003, the number of EDs decreased
by 425, and the number of hospital beds decreased
by 198,000.
13,15
As many patients are “boarded” in
the ED, sometimes for up to 48 hours before an inpa-
tient bed becomes available, emergency physicians are
CHAPTER 12
170
symptoms reported include dyspnea on exertion
progressing to dyspnea at rest, orthopnea, periph-
eral edema, and paroxysmal nocturnal dyspnea. The
progression of symptoms before ED presentation
may take hours to days; however, an episode of acute
Vascular dysfunction is very important because it
may be the most commonly encountered reason for
patients presenting in AHF. Steep increases in after-
load, combined with poor systolic function, result
in an acute increase in left ventricular end-diastolic
pressure and a decrease in cardiac output. This model
may explain the presence of pulmonary congestion
despite (only) modest fl uid accumulation.
Standard teaching has been that acute heart failure is
mainly due to fl uid overload. However, in many cases,
an acute increase in afterload is often the precipitant
of AHF in many patients, leading to the rapid devel-
opment of pulmonary congestion even in the absence
of fl uid overload. More than 50% of patients present-
ing with cardiogenic pulmonary edema are euvolemic
or hypovolemic.
12
Therefore, the key to treatment of
AHF in many cases is to focus on afterload reduction
and fl uid redistribution, rather than aggressive diuresis.
(Figures 12-2, 12-3, 12-4, Table 12-1).
Initial CHF workup: history and physical
examination
A signifi cant number of patients presenting with AHF
syndrome have a prior history of CHF. Common
Cardiac Pathway Vascular Pathway
Mild to Moderately
Impaired Cardiac
Contractility Reserve (Cpo)
Inflammatory/
Neurohormonal Activation
Arterial Resistance/
Stiffness
Central Fluid
Redistribution
Low Cardiac
Contractility
Reserve (Cpo)
Non-adherence
Over Diuresis
Renal
Impairment
Forward Failure
(Effective Blood
Volume )
“Low CVS
perfusion”
Acute Decrease in
Contractility
Reserve (Cpo)
Fluid
Accumulation
Troponin “Leak”
Pulmonary
Congestion
Diastolic Dysfunction
Wedge
Figure 12.1 Initiation phase
of AHF. Reprinted from Am
Heart J, 155(1), Cotter G,
Felker GM, Adams KF, The
pathophysiology of acute
heart failure–is it all about
fl uid accumulation?,
pages 9–18, Copyright
2008, with permission from
Elsevier.
Figure 12.2 Normal physiology. Reprinted from Am
Heart J, 155(1), Cotter G, Felker GM, Adams KF, The
pathophysiology of acute heart failure–is it all about
fl uid accumulation?, pages 9–18, Copyright 2008, with
permission from Elsevier.
ACUTE HEART FAILURE
171
Figure 12.3 Pulmonary edema from 3 mechanisms.
Reprinted from Am Heart J, 155(1), Cotter G, Felker GM,
Adams KF, The pathophysiology of acute heart failure–is it
all about fl uid accumulation?, pages 9–18, Copyright 2008,
with permission from Elsevier.
Figure 12.4 Goals of therapy for acute heart failure.
Reprinted from Am Heart J, 155(1), Cotter G, Felker GM,
Adams KF, The pathophysiology of acute heart failure–is it
all about fl uid accumulation?, pages 9–18, Copyright 2008,
with permission from Elsevier.
ischemia or acute valvular dysfunction may cause
symptoms to progress much faster. Physical exami-
nation fi ndings typically include tachycardia and
hypertension (increased catecholamine production),
tachypnea, hypoxia, and diaphoresis. Auscultation
of the lungs reveals rales or wheezes, and cardiac
auscultation may be notable for an S3 heart sound.
The remainder of the examination may fi nd jugular
venous distension (JVD), hepatojugular refl ux, and
peripheral edema.
18
JVD and a third heart sound (S3)
have been reported to have low sensitivities (30%
and 24%, respectively) for diagnosing AHF.
19
When
AHF is associated with cardiogenic shock, evidence
of poor tissue perfusion, including skin mottling or
pallor, may be evident. Unfortunately, vital signs and
physical examination fi ndings have relatively low
sensitivity (70%) for AHF.
20
As many as one-third
of patients presenting with dyspnea and similar vital
signs have COPD, and many also have risk factors
for pulmonary embolism and acute MI.
20,21
This pres-
ents a quandary for the clinician, as these alternative
diseases can mimic AHF syndrome, thereby com-
plicating one’s ability to make an accurate clinical
diagnosis.
In some patients, signifi cant mechanical lesions that
evolve or deteriorate rapidly can lead to decreased
myocardial contractility, leading to subsequent AHF.
The most common such mechanical lesion is acute
mitral regurgitation. In acute mitral regurgitation, an
audible systolic thrill is often present, and the mur-
mur often is harsh.
22
It may be auscultated over the
back of the neck, vertebra, or sacrum, and may radi-
ate to the axilla, back, and left sternal border.
22
Other
causes of mechanical lesions that may cause an AHF
event are ischemic or nonischemic papillary muscle
rupture, mechanical valve malfunction due to throm-
bosis or pannus, infective endocarditis, ventricular
septal rupture, and aortic dissection causing severe
ischemia or aortic regurgitation. Overall, the preva-
lence of such mechanical lesions as the primary cause
of AHF appears to be low.
12
Table 12-1. Major etiologies of cardiogenic pulmonary
edema.
• Exacerbation of chronic left ventricular failure
• Acute myocardial ischemia/infarction
• Severe systemic hypertension
• Left-sided valvular disorders
• Acute tachydysrhythmias and bradydysrhythmias
Reprinted with permission from Elsevier from: Mattu
A, Martinez JP, Kelly BS, Modern management of
cardiogenic pulmonary edema. Emerg Med Clin N Am.
2005;23(4):1105–1125.
CHAPTER 12
172
The presence of cardiomegaly, often considered
one of the most reliable radiographic abnormali-
ties associated with systolic dysfunction, may be
absent in patients who have rapidly-developing
CPE.
33
Radiographs can be diffi cult to interpret in
patients who develop chronic lung abnormalities
or may have scarring that impairs image quality or
mimics vascular redistribution.
18
Image quality may
also be impaired in obese patients and patients with
COPD.
34
Previous research suggest that a combination of
medical history, physical examination, and chest
radiograph fi ndings can suggest a diagnosis of acute
heart failure syndrome.
35–37
Although signs, symp-
toms, and scoring systems can be highly suggestive
of acute heart failure syndromes, they lack suffi cient
accuracy to serve as a defi nitive diagnostic strategy.
11
(Table 12-3). Furthermore, these scoring systems have
not been extensively validated in the acute setting,
Initial testing
Electrocardiogram (EKG)
An electrocardiogram should be performed in all
patients presenting with possible AHF syndrome.
The EKG should be assessed for acute dysrhyth-
mias, signs of acute coronary syndrome includ-
ing ST-segment elevation myocardial infarction,
and signs of electrolyte abnormalities (i.e., hyper-
kalemia in renal failure). If the EKG shows evidence
of acute myocardial ischemia (acute MI) appropri-
ate anti-ischemia and reperfusion therapies should
be pursued. Severe bradyarrhythmias along with
normal or elevated right-heart fi lling can induce
elevations in pulmonary capillary hydrostatic pres-
sures, leading to cardiogenic pulmonary edema
(CPE). Tachydysrhythmias may lead to CPE caused
by poor diastolic fi lling, which also leads to eleva-
tions in pulmonary capillary hydrostatic pressures.
Along with initial stabilization measures, treatment
of CPE in either case is simply based on correc-
tion of the underlying dysrhythmia using standard
Advanced Cardiac Life Support protocols.
18
Most
registries have reported that atrial fi brillation occurs
in 30–42% of patients admitted with AHF.
12
While
one study shows that the occurrence of new dys-
rhythmias, mainly atrial fi brillation, is a strong
predictor of recurrent events and death in patients
admitted for AHF, the precise role of dysrhythmia in
the pathogenesis of AHF remains unknown.
12
A widened QRS of 120ms has been suggested as a
clinical marker of poor prognosis in heart failure and
reduced left ventricular ejection fraction (LVEF). It
has also been reported to be associated with increased
mortality and sudden death in heart failure, as well as
an independent predictor of cardiac death in a gen-
eral medical population.
23–27
However, as these obser-
vations were not made in the acutely decompensated
patient presenting with an unknown diagnosis, the
application of this into routine ED clinical practice
is unclear.
28
Chest radiograph
The classic radiographic fi ndings of CPE are listed in
Table 12-2.
29,30
However, these “classic” radiographic
fi ndings may not be seen at the time of initial presen-
tation.
18
Up to a 12 hour delay can occur between
the abrupt onset of CPE symptoms and the develop-
ment of signifi cant radiographic abnormalities.
31,32
Table 12-2. Classic radiographic fi ndings of cardiogenic
pulmonary edema.
Cardiomegaly (underlying CHF)
Pulmonary vascular redistribution
Thickening of interlobular septa (Kerley B lines)
Alveolar edema
Pleural effusions
Bilateral infi ltrates in a “bat wing” pattern
Table 12-3. Test characteristics of heart failure
diagnostic scoring systems.
Scoring System Sensitivity Specifi city
Framingham
63%4% 94%1%
Boston*
35%4% 99%0%
NHANES**
62%4% 94%1%
Gheorghiade
55%4% 95%1%
*Test characteristics for a Boston Score greater than 8.
**NHANES, National Health and Nutrition Examination
Survey.
Reprinted with permission of Elsevier from: Collins S,
Storrow AB, Kirk JD, et al. Beyond pulmonary edema:
Diagnostic, risk stratifi cation, and treatment challenges
of acute heart failure management in the emergency
department. Ann Emerg Med. 2008;51(1);45–47.
ACUTE HEART FAILURE
173
(ROC) curve for this test is calculated as 0.91.
11,38
In data derived from the same sample population,
McCullough, et al.
43
report on 1538 subjects for
whom the clinical likelihood of acute heart failure
syndromes was recorded by an emergency physician
who was blinded to the BNP level.
11
In this study, the
area under the curve (AUC) for “estimated congestive
heart failure probability” based on clinical evaluation
alone is 0.86, as compared to 0.90 for a single BNP
measurement and 0.93 for the combination of clinical
evaluation and BNP.
11
Measurement of BNP levels in patients presenting
to the ED with acute dyspnea can assist clinicians in
distinguishing acute heart failure and CPE from other
acute or chronic lung diseases.
44,45
Based on available
data, the ACEP guidelines on AHF recommend that
the addition of a single BNP or NT-proBNP measure-
ment can improve the diagnostic accuracy, compared
to standard clinical judgment alone, in the diagno-
sis of acute heart failure syndrome among patients
presenting to the ED with acute dyspnea (Level B
recommendation).
11
The following are included as cutoffs for ProBNP
and NT-proBNP.
BNP 1 100 pg/dL or NT-proBNP 300 pg/dL: acute
heart failure syndrome unlikely* (Approximate
LR 0.1)
BNP 2 500 pg/dL or NT-proBNP 1,000 pg/dL:
acute heart failure syndrome likely (Approximate
LR 6)
BNP and NT-proBNP measurement have been
compared head to head in a number of prospective
trials with essentially parallel ROC curves and sta-
tistically similar AUCs with respect to the diagnosis
of acute heart failure syndrome. Age, sex, body mass
index, and renal function may infl uence BNP and
NT-proBNP measurements. Several post hoc analyses
show that BNP measurements may retain discrimi-
natory power in various subpopulations, including
individuals with systolic and diastolic heart failure,
underlying pulmonary disease, advanced renal dis-
ease, advanced age, and obesity.
11
An intermediate “grey zone” BNP level in the range
of 100 to 500 pg/mL represents a signifi cant quan-
dary for the ED physician. While an elevated BNP can
be caused by acute heart failure, it can also be caused
making their implementation in the ED somewhat
limited.
11
Additional testing in acute heart failure syndromes
As discussed previously, the clinical diagnosis of
acute heart failure is estimated to be incorrect in
more than 50% of cases, leading to frequent over-
diagnosis and underdiagnosis.
21
Because of the limi-
tations of clinical assessment and chest radiography
in distinguishing acute heart failure from other
causes of acute dyspnea, B-type natriuretic peptide
(BNP) testing has emerged as a diagnostic tool in ED
practice.
18
BNP and NT-proBNP
BNP is an endogenous cardiac neurohormone pro-
duced by cardiac myocytes in response to increased
end-diastolic pressure and volume (increased wall
tension), as occurs in the setting of heart failure. Pre-
proBNP is synthesized within myocytes and cleaved
to proBNP. The latter is released into the circulation
and then cleaved to the active BNP and an inactive
N-terminal fragment, called NT-proBNP. BNP’s main
effect is to counteract the renin-angiotensin-aldoster-
one system by promoting natriuresis, diuresis, and
vasodilatation.
18
Plasma BNP levels increase in the
setting of acute heart failure and CPE.
18
During the
past decade, both BNP and NT-proBNP have been
studied as markers for aiding in the diagnosis of acute
heart failure syndrome in patients presenting with
dyspnea in the acute setting.
11
Elevated levels of BNP
have been demonstrated to correlate with the severity
of left ventricle fi lling pressures, clinical status, short-
term and long-term mortality, and response to inhos-
pital therapy.
32,38–42
The largest trial to date is a Class II, industry-
sponsored, prospective, multicenter, observational
study
38
that enrolled 1586 subjects with a primary
complaint of “shortness of breath” and compared
a single BNP measurement (Triage; Biosite Inc, San
Diego, CA) against a criterion-standard, fi nal diag-
nosis as determined retrospectively by two cardiolo-
gists blinded to BNP levels.
11
The authors suggest a
cut point of 100 pg/mL yielding a sensitivity of 90%
and specifi city of 76%. Higher cut points result in
improved specifi city, up to 90% at a cut point of 1000
pg/mL but with markedly lower sensitivity.
11
The over-
all area under the receiver operating characteristic
*BNP conversion: 100 pg/mL 22 pmol/L; NT-proBNP
conversion: 300 pg/mL 35 pmol/L
CHAPTER 12
174
and adverse outcomes appears to be linear, several
studies have used a threshold of a 0.3-mg/dL rise
in serum creatinine over baseline to defi ne this risk
level. Changes of this magnitude generally occur in
about one-third of patients admitted for AHF and
are associated with a prolonged and complicated
hospital course, as well as high rates of morbidity
and mortality. Worsening renal function may play
an important role in the progression and propaga-
tion of an AHF episode by leading to greater fl uid
and sodium retention and neurohormonal activa-
tion.
12
Therefore, any signifi cant changes in serum
creatinine from baseline or chronic renal insuffi -
ciency warrant further evaluation in the inpatient or
observation setting.
Management of acute heart failure and cardiogenic
pulmonary edema
Rapid triage and initial stabilization
The goals of management of AHF should focus on
the suspected etiology of the patient’s presentation.
Determine if the patient’s history and physical exam-
ination are consistent with acute decompensated
cardiac failure or acute vascular dysfunction. As
many patients present to the ED with acute vascu-
lar dysfunction, in a majority of cases treatment will
need to focus upon decreasing preload and decreas-
ing afterload to improve LV function and to increase
cardiac output. Implementation of ionotropic sup-
port may be required to improve LV function.
Initial management of patients who experience
severe AHF and CPE should focus on the “ABCs”
of resuscitation.
18
Large bore IV lines should be
inserted to draw needed laboratory tests, and for
needed medication administration. Patients should
be placed in an upright sitting position, connected
to a cardiac monitor and pulse oximeter, and high-
fl ow supplemental oxygen should be provided by
way of a facemask with a fraction of inspired oxy-
gen of 1.0.
18
Patients with AHF should be rapidly triaged to
decide on appropriate treatment and diagnostic test-
ing. Immediate stabilization is necessary in patients
presenting in extremis, including patients with sig-
nifi cant tachypnea, hypoxia, and mental status
changes, to prevent further deterioration. Aggressive
intervention with noninvasive ventilation or pos-
sible endotracheal intubation is recommended to
by other conditions that induce elevated ventricular
wall tension, including cor pulmonale and acute pul-
monary embolism.
21
Falsely low BNP levels can occur
during the fi rst 1–2 hours after symptom-onset in
cases of fl ash pulmonary edema.
46
Cardiac troponins
Electrocardiographic changes and troponin release
may occur in patients with HF without coronary dis-
ease (and may be the result rather than the cause of
the AHF syndrome).
12
Available data suggest that the
incidence for troponin above the threshold for acute
coronary syndrome (ACS) is approximately 20% in
patients with AHF. However, the exact incidence of
frank myocardial ischemia in AHF remains unknown
due to the diffi culty of diagnosing ischemia in patients
admitted with AHF.
12
Although observational data
cited suggest ischemic complications in 20% of AHF
admissions, this number may be lower (troponin leak
can occur even when ischemic heart disease is not
present) or higher (ischemia may occur without sig-
nifi cant troponin leakage).
11
One large study on the incidence and outcome of
clinical HF (N 20,000) in patients with non–ST
elevation ACS has concerning fi ndings.
47
Acute HF
was observed in 11% of the patients, leading to a 9%
1-month mortality and 16% 6-month mortality—
more than triple the mortality observed in patients
without HF. Acute HF is correlated with 30% of
the overall mortality in the study, being the stron-
gest independent negative prognostic factor in the
cohort.
12
Based on this and other studies, patients
presenting with the combination of ACS and AHF
have a poor prognosis, and should be admitted to the
ICU for further management.
12
Patients “ruling in”
for cardiac ischemia or non-ST-segment elevation MI
(NSTEMI) should have urgent cardiology consulta-
tion to help guide further inpatient care, including
possible interventional or cardiac revascularization
procedures.
18
Blood chemistries
In patients with chronic HF, the presence of con-
comitant chronic renal insuffi ciency (CRI) is a strong
risk factor for mortality. Although renal dysfunc-
tion predicts all-cause mortality, it is most predic-
tive of death from progressive HF, suggesting that
renal dysfunction may be a marker of HF severity.
Although the relationship between renal dysfunction