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PEDIATRIC CARDIAC EMERGENCIES
375
blood pressure. If the patient remains in shock after
you’ve given the saline boluses, you might start a
peripheral pressor for support while waiting for the
prostaglandins to kick in.
PR: One of my technical nightmares is the thought of
starting an IV on a 3-day-old infant. Would you start
with an intraosseous line (IO) initially? Can prosta-
glandins be given through an intraosseous line?
KB: I wouldn’t spend too much time trying to get an
IV; while we are doing our initial evaluation, I would
expect the nurse to try to get an IV. I wouldn’t hesi-
tate about putting an IO in an infant. Prostaglandins
can be given through the IO as well. The newer IO
access devices, particularly the intraosseous lines
that are more like a hand drill, have markedly
changed our threshold for using intraosseous lines.
They are easier and faster than getting an IV in the
best of hands.
PR: Do you see any need for putting in a femoral line
for central access?
CT: As long as you are able to give the prosta-
glandins, and the baby is responding and able to
maintain some degree of hemodynamic stability, I
would not waste time putting a femoral line in at
this point.
SG: Until when can one cannulate an umbilical vein,
and would that be feasible in this case?
KB: My understanding is that it is feasible until about
day seven of life, particularly if you still have the
umbilical stump present, and you can slice down to
nondesiccated stump material. The biggest problem
with the umbilical vein catheterization is that the vast
majority of emergency physicians haven’t done one,
or may have never even seen one done, so practically
this may not be useful.
PR: I haven’t done one since before the implementa-
tion of the intraosseous route; the problem we had
with umbilical vein catheterization was not the tech-
nical diffi culty, but picking the vessel, since there are
two arteries and one vein and it’s hard to remember
which is which. I think that many of the umbilical cut
downs ended up being intraarterial instead of intrave-
nous. I’m not sure that it makes that much of a differ-
ence, but it probably refl ects the fact that we don’t do
these procedures very often.
KB: Although it is diffi cult to remember all of the
congenital metabolic abnormalities that children
can have, all of them have the potential to result in
hypoglycemia. Without having to remember the indi-
vidual genetic problem, one may be able to fi x all
of these patients simply by keeping the glucose at a
proper level.
PR: What diagnostic tests would you want to utilize
before giving any therapy to this child or while you
are giving the therapy, as in this age group one should
probably intubate and start a prostaglandin infusion as
soon as possible; you can then try to fi gure out which
particular disease is the culprit? Is there an age con-
straint for an echocardiogram (ECHO), or is there any
other initial diagnostic maneuver that might help?
SG: Checking a hemoglobin would be very useful, as
anemia could cause this presentation. With a normal
oxygen saturation, we might worry about peripheral
cyanosis-type diseases, such as methemoglobinemia.
There are no constraints to obtaining an echocardio-
gram. Not only are there no constraints, this test will
likely be diagnostic, and should be done as expedi-
tiously as possible.
CT: After intubating this patient, it will be useful to
look at the infant’s response to oxygenation and intu-
bation. If the baby’s oxygenation improves to 100%,
this is probably sepsis, but if the oxygenation is still
80% post-intubation, then one begins to think that
this is not a new pneumonia or sepsis; some other
disease process is preventing the child from oxygen-
ating the blood.
PR: How do you choose a prostaglandin to infuse?
KB: Prostaglandin-E1 is the only one we routinely use
for infant infusion in the ED. The dose is between
0.05 mcg/kg/min and 0.1 mcg/kg/min. As we men-
tioned, there seems to be a relationship between the
strength of the infusion and the side effects. I would
plan on the patient becoming apneic.
PR: Once you’ve started your prostaglandin infusion,
intubated the child, ordered an ECHO, and spoken
with the pediatric intensive care unit physician and
hopefully a pediatric cardiologist, what else do you
need to do in the ED for this child?
CT: This child will also probably benefi t from a
20 cc/kg bolus of normal saline to help support the
CHAPTER 27
376
this child has a respiratory infection, particularly
RSV, or anything that raises intrathoracic pressure,
even dehydration for any reason, he may present with
low oxygen saturation.
PR: Are they more prone to bacterial infections like
endocarditis?
KB: Surprisingly, endocarditis seems to be quite
rare in these children, despite all of their artifi cial
hardware and the underdeveloped immune system
of an infant. Their biggest problems are the result
of simple viral infections causing them to stop or
limit feeding. As tenuous as they are to begin with,
they very quickly decompensate if they don’t have
enough intravascular volume to keep their blood
pressure in a reasonable range, and often present
in shock.
SG: What do you need to worry about when this
patient becomes an adult? What kinds of things
would you need to keep in mind when a patient pres-
ents to the ED with a history of having had congeni-
tal heart disease?
KB: The greatest challenge I experience with these
patients is fi nding them a physician. Adults with
a history of congenital heart disease tend to have
extraordinarily complex anatomical alterations,
and will often fall through the cracks, unless they
are well set up with a pediatric cardiologist. They
are similar to 40-year-old patients with cystic fi bro-
sis. They often don’t have a medical home or a phy-
sician following them, and this is why enlisting a
pediatric cardiologist is very important. Moreover,
the adult cardiologists don’t usually take care of
these problems.
PR: These cases can be very scary to the emergency
physician, particularly one who doesn’t see critical
infants very often. To summarize, check the blood
sugar, check the oxygen, and see if the child responds
to oxygenation. Don’t be afraid to put an intraosseous
line in quickly, be sure to look at the age of the child,
and administer your prostaglandins promptly to keep
the shunt open.
Case resolution
The physician intubated the patient, and adminis-
tered prostaglandin at a rate of 0.05 mcg/kg/min.
PR: If the baby’s pulse rate did not slow down with
a fl uid and prostaglandin infusion, what would be
your next step? Would you have any concern that
you are dealing with a dysrhythmia that needs
cardioversion?
SG: Unless there was electrocardiographic evidence of
a dysrhythmia, I would not worry about one. If the
heart rate doesn’t slow down, then I would try and
obtain an ECHO sooner rather than later, because
perhaps you are dealing with something that you are
not going to be able to fi x in an ED and need an oper-
ative intervention.
PR: Can you summarize the most common ductal-
dependent congenital lesions?
CT: More important than the specifi c diagnoses is
to remember the two-way communication between
your left-sided circulation and your right-sided
circulation. I think of ductal-dependent lesions as
either blood fl ow being obstructed and not fl owing
to the lungs, or not fl owing to the systemic circula-
tion. If you can keep the communication open, then
you can distribute the blood where it needs to go.
For example, in left-sided obstructive lesions, if you
have a coarctation of the aorta or a hypoplastic left
ventricle, then by maintaining patency of the ductus
arteriosus, you can move the blood that is congest-
ing the pulmonary system into the circulation. With
gray or cyanotic babies who are in shock or with
congenital heart abnormalities like tricuspid atre-
sia, tetralogy of Fallot, or transposition obstructing
blood fl ow to the lungs, you want to open the ductus
so the systemic circulation can infuse the lungs and
oxygenate the blood.
PR: After the fi rst life-saving surgery, what compli-
cations will bring the child back to the ED: sepsis,
failure of the shunt, or congestive heart failure?
CT: With a hypoplastic left heart, congestive failure is
possible in that ventricle, as the right ventricle needs
to supply the systemic circulation. The lungs are sup-
plied by fi rst a synthetic shunt, and second from an
anastamosis of the superior vena cava and inferior
vena cava to the pulmonary arteries, and they can
have heart failure if the ventricle fails. These patients
are very preload dependent as the blood supplied to
the lungs is a passive system, and they need an ade-
quate intravascular volume. More commonly, when
PEDIATRIC CARDIAC EMERGENCIES
377
Initial workup, history and physical
As these infants are typically critically ill, initial
resuscitation efforts should begin immediately. The
infant should be placed on supplemental oxygen if
in respiratory distress. Intravenous access should be
established rapidly; if unable to place a peripheral
line quickly, an umbilical line or intraosseous access
should be performed. An umbilical line can be placed
until the stump has desiccated, between 7–14 days
after birth. The physician should obtain a brief pedi-
atric history, focusing on events surrounding birth
for both the neonate and mother, and a description
of the onset of the current symptoms. If the patient is
febrile, this may point toward an infectious etiology
and a septic infant. Questioning about diaphoresis,
tachypnea, or fatigue, or diffi culties during feeding
is often helpful.
9
Feeding is often the most stressful
activity for an infant.
The history can guide the physical examination. If
congenital heart disease is suspected, blood pressure
readings and oxygen saturations in both the arms
and the legs should be obtained. A general guide-
line is any number less than 70 plus the age in years
for the systolic blood pressure indicates a pediatric
patient is hypotensive. The general appearance of
the neonate should be noted, looking for signs of
dehydration or signs of fl uid overload, which may
suggest heart failure. If the infant is crying, deter-
mine if this improves or worsens the cyanosis, as
improvement in color with crying suggests a pul-
monary etiology. On cardiac auscultation, a third
heart sound can be physiologic, but the presence of
a fourth heart sound is almost always pathologic.
The chest should be auscultated and percussed for
evidence of fl uid. Central and peripheral cyanosis
can be distinguished by evaluating the mucus mem-
branes, lips, and nail beds. The extremities should
be evaluated for capillary refi ll, clubbing, tempera-
ture and moisture of skin, as well as the quality of
pulses.
3,10
A crucial aspect of the evaluation centers on dis-
criminating between noncardiac etiologies and cardiac
etiologies. In this case, a hyperoxia test is very helpful.
In a standard hyperoxia test, the infant is placed on
100% oxygen for 10 minutes. If the arterial oxygen-
ation is greater than 150 mmHg as measured on an
arterial blood gas, a respiratory cause is more likely.
If the oxygenation is less than 100 mmHg, congenital
The child was subsequently transferred to a tertiary
referral center where he was admitted to the ICU.
The patient had an echocardiogram demonstrating
a hypoplastic left-heart syndrome, and he under-
went surgery the next day. After a weeklong stay
in the ICU, he was transferred to the fl oor for an
additional 5 weeks prior to discharge home with his
parents. The patient will require close cardiology
follow up for examination and echocardiography as
an outpatient.
Section III: Concepts
Background/epidemiology
Congenital heart disease occurs in 4–12 per 1000
live births.
1–3
Increasingly, congenital heart disease
can be detected in utero.
4
Despite this progress in
early detection, some studies indicate up to 25% of
patients with congenital heart disease are discharged
home after birth undiagnosed.
5
Many infants are
asymptomatic at birth, but deteriorate rapidly as the
amount of blood fl ow through the pulmonary circu-
lation increases and the foramen ovale and ductus
arteriosus close over the fi rst days to weeks of life. In
cyanotic congenital heart disease, the patient has a
right to left shunt, allowing the deoxygenated blood
to bypass the lungs and pass directly through the cir-
culation. These infants are dependent on the presence
of a patent ductus arteriosus to allow deoxygen-
ated blood to fl ow back into the pulmonary arteries
from the aorta.
6
To obtain an oxygen saturation of
85%, at least 3–5 g/dL of deoxygenated hemoglobin
is needed in the neonatal circulation.
7
Infants with
lesions such as hypoplastic left-heart syndrome and
aortic coarctation, which obstruct blood fl ow from
the heart to the rest of the body, require a patent
ductus to maintain their systemic circulation, and
will present in profound shock when the ductus
closes. Furthermore, neonates do not have the same
ability to increase their stroke volume, and thus rely
on tachycardia to increase their cardiac output in
response to stressors. Therefore, changes in volume
status, such as dehydration or a relative bradycardia,
can have disastrous effects on the cardiac output.
This helps to explain why neonates will compen-
sate by increasing the systemic vascular resistance
to maintain blood pressure, and will clinically have
cool, pale extremities.
8
CHAPTER 27
378
arterial blood gas on room air. A second sample should
be taken after administration of 100% oxygen for 10
minutes (hyperoxia test). A chest radiograph is helpful
to determine if there is a pulmonary cause of the cyano-
sis; this also allows one to assess if the pulmonary blood
fl ow is increased or decreased, as well as note the pres-
ence of a pneumothorax or a pleural effusion and the
appearance of the cardiac silhouette. In many instances,
the chest radiograph will be unremarkable. An EKG
can evaluate dysrhythmias, axis deviation, hypertrophy,
strain, and metabolic abnormalities, but may appear
normal despite life-threatening pathology.
14
Management
It is common to witness oxygen saturations of less than
70% in patients with ductal-dependent lesions. To
maintain patency of the ductus arteriosus, administer
prostaglandin-E1 as a continuous infusion; the initial
dose is 0.05–0.1 mcg/kg/min.
6,15,16
This dosage may
also be given via the IO route. Patients with ductal-
dependent lesions should not be left on a 100% non-
rebreather mask, as the high level of oxygen actually
triggers closure of the ductus arteriosus. Depending
on the stability of the patient, the child may need to
be intubated for airway protection and as protection
against apnea, one of the more serious side effects of
prostaglandin administration. There often is time to
utilize rapid sequence intubation, preparing a spec-
trum of styletted endotracheal tubes ranging from
2.5–4.0, depending on the age of the infant. Recent
evidence, however, suggests that in the stable patient,
intubation prior to transfer may actually produce more
complications in the infant, and therefore should be
deferred until the tertiary care destination is reached.
17
Regardless, the FiO
2
of the oxygen should remain as
close to 40% as possible. If dehydration is also a con-
cern, small fl uid boluses should be administered at
10–20 mL/kg. Attempts should also be made to get
the patient to a tertiary referral center as soon as pos-
sible to obtain a pediatric ECHO, and for evaluation
by pediatric cardiologists. In recent years, telemedicine
has come to the aid of smaller hospitals to facilitate
and expedite care.
18
Disposition
Most of these patients presenting with newly
diagnosed CHD, should be admitted to the pediatric
heart disease is more likely.
3,10,11
Since an arterial blood
gas may not be feasible in all situations, it is more
straightforward to place the infant on 100% oxygen
and note the response. If the saturation fails to improve,
cardiac disease is the more likely explanation.
Etiologies/differential diagnosis
The differential diagnosis of a critically-ill infant is
broad, but a basic evaluation can generally guide the
initial resuscitation. Sepsis is one of the most com-
mon causes of critical illness in newborns. The infec-
tious etiologies include pneumonia, bronchiolitis, and
meningitis.
12
Central nervous system abnormalities
include shallow breathing from a perinatal asphyxia
and encephalopathy.
13
Less common congenital mal-
formations include diaphragmatic hernias or tracheoe-
sophageal fi stulas. One would expect an improvement
of the cyanosis with oxygen administration with a
diaphragmatic hernia, and a tracheoesophageal fi stula
may be distinguished by exacerbations during peri-
ods of feeding. Other pulmonary etiologies include a
pneumothorax or pleural effusions; these can be iden-
tifi ed on physical examination and further testing.
Infantile botulism or muscular dystrophy should also
be considered with a fl oppy infant.
Lastly, the differential diagnosis of cyanotic congeni-
tal heart diseases (CHD) includes the causes of right to
left shunts: tetralogy of Fallot, transposition of the great
arteries, tricuspid atresia, total anomalous pulmonary
venous return, truncus arteriosis, pulmonary atresia,
Ebstein’s anomaly, and single ventricle states such as
the hypoplastic left-heart syndrome. Fortunately, the
initial resuscitation is similar for each of these lesions,
so it is not necessary to determine the likely etiology to
begin effectively stabilizing the infant.
Testing
Patients who present with altered consciousness should
have a blood glucose obtained as soon as possible.
Thereafter, all patients should have a baseline chemistry
panel to evaluate for a metabolic acidosis. A complete
blood count should also be obtained, looking at the
white blood cell count as a marker for possible infec-
tion, as well as for erythrocytosis, a marker of chronic
cyanosis. The I/T ratio, or immature to total ratio, for
white blood cells is also frequently requested. An umbil-
ical artery line should be placed to obtain a baseline
PEDIATRIC CARDIAC EMERGENCIES
379
Section IV: Decision making
A targeted history and physical examination can •
help distinguish between cardiac and noncardiac
etiologies in the cyanotic infant.
Initial resuscitation involves rapid intravenous or •
intraosseous access, oxygen administration, and pro-
staglandin administration as indicated (Figure 27-1).
See Table 27-1 for specifi c characteristics of •
cyanotic congenital heart disease.
intensive care unit. It is often prudent to administer
broad spectrum antibiotics, as sepsis is typically still
on the differential diagnosis list.
If the child deteriorates into pulseless electrical
activity or cardiac dysrhythmia while still in the
ED, standard pediatric advance life support path-
ways should be followed.
19
Inotropic agents, such
as dopamine at 5–20 mcg/kg/min or dobutamine
at 5–20 mcg/kg/min, can be added for pressure
support.
Figure 27.1 Cyanotic congenital heart disease
(6,20)
.
Telemetry, Pulse oximetry, Temperature
Supplemental oxygen
IV/IO access
Obtain blood pressure in upper/lower extremities
Blood glucose
Perform physical exam
CBC, Chemistry panel, Blood cultures
Urinalysis
EKG
Chest X ray
Perform Hyperoxia Challenge test
Oxygen saturation fails to improve:
Continue to suspect cyanotic congenital
heart disease
Oxygen saturation improves:
Evaluate for other causes of cyanosis,
e.g., sepsis
Consider Intubation
Fluid bolus 10–20 ml/kg NS
Administer Prostaglandin drip at
0.05 microgram/kg/min
STAT ECHO
Pediatric cardiology consult
Transfer to tertiary care/admit to PICU
Hypoxic Infant
Initial Management
Labs and
Diagnostic testing
Special tests
CHAPTER 27
380
Table 27-1. Rate control medications for atrial fi brillation with rapid ventricular response.
Etiology Percentage
of CHD*
Anatomy Chest X-ray Findings EKG Findings
Tetrology of Fallot 10%
Right ventricle outfl ow •
obstruction
RVH•
VSD•
Overriding aorta•
Decreased pulmonary
fl ow
Boot-shaped heart
RVH
Right axis deviation
Transposition of the
great arteries
5%
Aorta arises from right •
ventricle
Requires either PDA •
or VSD
Egg-shaped heart RVH, LVH
Right axis deviation
Tricuspid atresia 1–2%
RV and RA not connected•
Boot-shaped heart RVH, Right axis
deviation
LVH in severe cases
Total anomalous
pulmonary
venous return
1%
Pulmonary venous blood •
drains to right atrium or
systemic circulation
Pulmonary venous
congestion
RVH, Right axis
deviation
Truncus arteriosus
⬍1%
Single artery supplies •
pulmonary, coronary, and
systemic blood
Right aortic arch
⫹/⫺ evidence of CHF
RVH, LVH
Pulmonary atresia
⬍1%
RVH•
Blood fl ows through PFO•
Right atrial enlargement RVH, Right axis
deviation
Ebsteins’s anomaly
⬍1%
Tricuspid valve develops •
in RV
Smaller functioning RV•
Cardiomegaly (sometimes
described as box or
funnel shaped)
Hypoplastic left-
heart syndrome
⬍1%
Underdeveloped mitral/aortic •
valve and left ventricle
Hypoplasia of ascending aorta•
Blood supply via PDA•
Frequently associated with •
coarctation of aorta
Increased pulmonary
fl ow
Cardiomegaly
RVH, Right axis
deviation
*
The majority of congenital heart disease can be attributed to acyanotic heart disease presentations.
Abbreviations: RVH–Right Ventricle Hypertrophy, VSD–Ventricular Septal Defect, PFO–Patent Foramen Ovale, PDA–Patent
Ductus Arteriosus, RV–Right Ventricle, RA–Right Atrium, and LVH–Left Ventricular Hypertrophy.
Adapted from: Yee L. Cardiac emergencies in the fi rst year of life. Emerg Med Clin North Am. 2007;25(4):981–1008,
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outcome of heart disease in live-born children: A prospective analysis of 91,823 live-born children. Pediatr Cardiol.
1989;10(4):205–211.
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383
Cardiovascular Problems in Emergency Medicine: A discussion-based review, First Edition.
Edited by Shamai A. Grossman and Peter Rosen.
© 2011 John Wiley & Sons, Ltd. Published 2011 by John Wiley & Sons, Ltd.
Index
abciximab, benefi ts of, 29
abdominal aortic aneurysm (AAA), 288
case discussion, 283–7
case presentation, 283
case resolution, 287–8
decision making, 293
defi nition of, 288
diagnosis, 290–2
ultrasound, 291
unenhanced CT scan, 291, 292
epidemiologic risk factors, 288
management, 289
pathogenesis, 288
perioperative risk, 289–90
predictor of, 289
presentation, 290
risk of rupture, 289
surveillance, 289
treatment, 292–3
AC controller/charger unit, 370
acidemia, 154
ACI TIPI score, 352
actue valvular regurgitation, 203
fl owchart for, 206
acute aortic regurgitation, 203
acute cerebrovascular accident (CVA), 52
acute coronary syndrome (ACS), 6, 7, 19, 27, 41, 58,
111, 313, 334, 338, 350
case discussion, 309–12
case presentation, 309
decision making, 323–4
defi nition of, 313
diagnosis of, 64
EKG evolution in STEMI, 317
dynamic change of ST-segment, 318–20
hyperacute T waves, 317–18
Q waves, 319–20
electrocardiogram (EKG), 314
notable challenges to interpretation, 321–3
and risk stratifi cation, 314
role of, 320–1
ST-segment depression, 316
T-wave inversion, 314–16
U waves, 316
historical background, electrocardiogram, 313
initially normal or minimally abnormal EKG,
313–14
spectrum of, 43
ST-segment trend monitoring, 316–17, 319, 320
symptoms of, 24
acute decompensated heart failure national registry
(ADHERE), 179
acute heart failure (AHF), 163
ACE inhibitors, utility of, 177
background, 169
blood chemistries, 174
B-type natriuretic peptide (BNP) testing, 173
cardiac troponins testing, 174
case discussion, 163–8
case presentation, 163
case resolution, 168–9
chest radiograph, 172–3
CPAP and BiPAP devices, 175
decision making, 179–80
defi nitions, 169–70
disposition of patients with, 178–9
electrocardiogram (EKG), 172
emergency department observation unit, 179
furosemide, administration, 176
history and physical examination, 170–1
inotropic support, 177–8
catecholamines, 177–8
phosphodiesterase inhibitors, 177–8
morphine sulfate (MS), administration, 176
nebulizers, utility of, 178
nitroglycerin (NTG), use of, 175–6
NT-proBNP testing, 173
pathophysiology, 169–70
pharmacologic therapies, 175, 177–8
potential safety considerations regarding diuretic,
176–7
predictors of inhospital mortality in patients, 179
INDEX
384
Debakey and Stanford classifi cation schemes, 275
decision making, 281
differential diagnosis, 275
EKG, 276
emergency department diagnosis, 279–80
emergency treatment, 280
epidemiology, 274–6
history, 276
imaging studies, 277–9
chest CT image, 279
multidetector CT (MDCT) coronary angiography,
279
transesophageal echocardiogram, 278
laboratory studies, 276
pathophysiology, 274–6
physical examination, 276
prognosis for patients, 281
promising marker for, 277
surgical treatment, 280–1
aortic stenosis (AS), 186, 192, 202
apical ballooning syndrome, 58, 63
aspirin, 40, 234, 367
affects of, 6
atherosclerotic coronary artery disease (ASCAD), 60, 62
associated ischemia, 63
risk factors for, 60
atrial fi brillation, 86–94, 380
acute management, 92–4
background, 89–90
case discussion, 86–9
case presentation, 86
case resolution, 89
decision making, 94
disposition, 94
initial atrial fi brillation workup, 90
rate control medications for, 93
testing, 91–2
atrial natriuretic factor, 102
atrioventricular (AV)
block degrees, 88
conduction, 155
junctional rhythm, 79, 80
nodal, 49
nodal reentry (AVRT), 98
antidromic, 105
orthodromic, 105
orthodromic, reentry mechanism for, 104
nodal reentry tachycardia, 100
node, 73, 101, 154
pacing, 147
synchrony, 155
acute heart failure (AHF) (continued )
rapid triage and initial stabilization, 174–5
syndrome, 179
acute infl ammation of the pericardium, 233
acute mitral regurgitation (MR), 203
acute myocardial infarction (AMI)
complications of, 51
criteria for, 332
defi ned by WHO, 331
EKG changes, 331–2
acute pericarditis/infl ammation of pericardium, 230
acute tamponade, 232
adrenoreceptor activity, 178
advanced cardiac life support (ACLS) strategies, 131
guidelines, 76
advanced life support treatment (ALS) protocols, 130
AFFIRM trial, 93
akinesis, 64
alcoholic cardiomyopathy, 245
alcohol-induced dysrhythmia, 244
alpha-2-agonists, 79
American College of Cardiology (ACC)/American Heart
Association (AHA) guidelines, 7, 48, 350
2004 guidelines, 367
American College of Cardiology and European Society
of Cardiology, 12
American College of Emergency Physicians, 11
American-European Atrial Fibrillation guidelines, 90
American Heart Association (AHA), 63, 124, 130, 133,
139, 140
2005 guidelines, 132
amiodarone, 364
amphetamine abuse and cardiovascular diseases, 246–7
angiotensin-converting enzyme inhibitors (ACE)
inhibitors, 261, 298
antibiotic regimen, for patient with endocarditis, 206–7
anticoagulant drugs, 49
anticoagulant therapy, 48
anticoagulation, 90
antidysrhythmics, 131–2
agents, 154
cause of prolonged QT-related dysrhythmias, 249
drugs, 125, 367
anti-platelet therapy, 29, 111
antithrombotic therapy, 29
anxiety, 192
aortic dissection, 269
case discussion, 269–74
case presentation, 269
case resolution, 274
clinical factors, 275