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PERICARDITIS
235
Table 16-2. Differentiating acute pericarditis and Acute
Coronary Syndromes (ACS)
Acute
Pericarditis ACS
Chest pain history
• Quality
• Duration
• Positional
• Radiation
Sharp, stabbing,
intermittent
Hours to days
Yes, worse with
supine position
Patient often sitting
up, leaning for-
ward; trapezius
ridge specifi cally,
also neck, jaw,
shoulder/arms
Dull, pressure-
like, squeezing
Minutes to hours
No
Neck, jaw,
shoulder/arms
Examination
• Friction rub
Present—no respi-
ratory variation
Usually not
present
Electrocardiogram
• ST elevation
• PR depression
• T-wave
inversion
• Q waves
Diffuse, concave
upward
Diffuse (elevated
in aVR)
After ST elevations
resolve
Absent
Regional, convex
Absent
Present with ST
elevations
May be present
Table 16-3. Indications for hospitalization for patients
with acute pericarditis
Cardiac Tamponade
Large Pericardial Effusion
Anticoagulation Therapy
Immunocompromised State
HIV
Extensive Myocardial Involvement
Elevated Troponin
Traumatic Etiology
Fever
Subacute Onset
Conventional Treatment Failure
Cardiac tamponade is the most worrisome •
complication, as evidenced by hypotension, elevated
jugular venous pressure, and pulsus paradoxus, and
must be treated emergently with pericardiocentesis
and drainage.
Most cases of acute pericarditis are self-limited and •
can be managed with supportive care, including
NSAIDs, aspirin, and colchicine.
Several factors are associated with potential •
risk for complications and poor outcome and
are indications for inpatient hospitalization
(Table 16-3).
References
Troughton RW, Asher CR, Klein AL. Pericarditis. 1 Lancet.
2004;363:717–727.
Chan TC, Brady WJ, Pollack M. Electrocardiographic 2
manifestations: acute myopericarditis. J Emerg Med.
1999;17:865–872.
Imazio M, Trinchero R. Myopericarditis: etiology, manage-3
ment, and prognosis. Internat J Cardiol. 2008;127:17–26.
Launbjerg J, Fruergaard P, Hesse B, et al. Long-term 4
risk of death, cardiac events and recurrent chest pain
in patients with acute chest pain of different origin.
Cardiology. 1996;87:60–66.
Spodick DH. Acute pericarditis—current concepts and 5
practice. JAMA. 2003;289:1150–1153.
Imazio M, Cecchi E, Demichelis B, et al. Myopericarditis 6
versus viral or idiopathic acute pericarditis. Heart.
2008;94:498–501.
Lange RA, Hillis LD. Acute pericarditis. 7 N Engl J Med.
2004;351:2195–2202.
Tingle LE, Monia D, Calvert CW. Acute pericarditis. 8 Am
Fam Physician. 2007;76:1509–1514.
Patients with signifi cant complications, such as large
pericardial effusions with or without tamponade physio-
logy, may require emergent drainage and hospitalization.
Similarly, patients may present with cardiac decom-
pensation as a result of constrictive pericarditis, and
require inpatient care. Other poor prognostic signs and
indications for admission include fever above 38ºC
(100.4ºF), subacute onset (over several weeks), antico-
agulant therapy, immunocompromised state, evidence
of myocardial involvement (myopericarditis), elevated
troponin levels, conventional treatment failure, and a
traumatic etiology for the acute pericarditis.
Section IV: Decision making
The patient’s presentation must be differentiated •
from other causes of chest pain, such as acute
coronary syndromes.
Careful history and examination and a 12-lead •
EKG can be of great utility in making the diagnosis
(Table 16-2).
CHAPTER 16
236
Imazio M, Demichelis B, Cecchi E, et al. Cardiac tro-15
ponin I in acute pericarditis. J Am Coll Cardiol.
2003;42:2144–2148.
Cheitlin MD, Armstrong WF, Aurigemma GP, et al. ACC/16
AHA/ASE 2003 guideline update for the clinical appli-
cation of echocardiography: summary article: a report
of the ACC/AHA Task Force on Practice Guidelines.
Circulation. 2003;108:1146–1162.
Schifferdecker B, Spodick DH. Nonsteroidal anti–infl am-17
matory drugs in the treatment of pericarditis. Cardiol
Rev. 2003;11:211–217.
Imazio M, Bobbio M, Cecchi E, et al. Colchicine in 18
addition to conventional therapy for acute pericardi-
tis—results of the colchicine for acute pericarditis trial.
Circulation. 2005;112:2012–2016.
Imazio M, Demichelis B, Parrini I, et al. Management, 19
risk factors, and outcomes in recurrent pericarditis. Am
J Cardiol. 2005;96:736–739.
Barbaro G, Klatt EC. HIV infection and the cardiovascu-9
lar system. AIDS Rev. 2002;4:93–103.
Cassimatis DC, Atwood JE, Engler RM, et al. Smallpox 10
vaccination and myopericarditis: a clinical review. J Am
Coll Cardiol. 2004;43:1503–1510.
Vasquez A, Butman SM. Pathophysiologic mechanisms 11
in pericardial disease. Curr Cardiol Rep. 2002;4:26–32.
Maisch B, Seferovic PM, Ristic AD, et al. Guidelines on 12
the diagnosis and management of pericardial disease—
executive summary of the task force on the diagnosis
and management of pericardial disease of the European
Society of Cardiology. Eur Heart J. 2004;25:587–610.
Ginzton LE, Laks MM. The differential diagnosis of acute 13
myopericarditis from the normal variant: new electrocar-
diographic criteria. Circulation. 1982;65:1004–1009.
Bonnefoy E, Godon P, Kirkorian G, et al. Serum cardiac 14
troponin I and ST segment elevation in patients with
acute pericarditis. Eur Heart J. 2000;21:832–836.
237
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.
Cardiac toxins and drug-induced
heart disease
Jeffrey Green
1
& Richard Harrigan
2
1
Associate Professor of Emergency Medicine, U.C. Davis School of Medicine,
Sacramento, CA, USA
2
Professor of Emergency Medicine, Temple University School of Medicine,
Philadelphia, PA, USA
17
Section I: Case presentation
A 66-year-old woman presented to the emergency
department (ED) with worsening dyspnea and
orthopnea over several days. She denied chest pain,
abdominal pain, nausea, or emesis. She also had a
mild intermittent global headache. She reported a dry,
non-productive cough, but denied fever and chills.
She was compliant with her medications.
The past medical history included congestive heart
failure (CHF), with an ejection fraction of 10–20%,
hypertension, diabetes mellitus type II, chronic
obstructive pulmonary disease (COPD), and a chole-
cystectomy. Medications included aspirin, nitro-
glycerin tablets, furosemide, digoxin, metoprolol,
pantoprazole, citalopram, albuterol/ipratropium, and
fl uticasone/salmeterol. She was allergic to clarithro-
mycin and azithromycin. She smoked cigarettes, and
did not use alcohol or illicit drugs.
On physical examination, the vital signs were: tem-
perature 36.1˚C (96.9˚F), pulse 60 beats/min, respira-
tions 24 breaths/min, blood pressure 154/82 mmHg,
and O
2
saturation 98%. The skin was nondiapho-
retic. The eyes had no conjunctival pallor. The neck
had jugular venous distention. The lungs had bilat-
eral rales and expiratory wheezes. Cardiovascular
examination showed a regular rate and rhythm with
a III/VI holosystolic murmur radiating to the axilla.
The abdomen was soft, nontender, without masses or
bruits. The extremities had equal pulses with symmet-
ric peripheral edema.
Laboratory studies were: BUN 63 mg/dL, creatinine
2.4 mg/dL, a hematocrit at her baseline of 30.1%,
BNP 2370 pg/mL, and troponin I <0.05 ng/mL. A
chest X-ray study showed mild-to-moderate pulmo-
nary edema. The EKG is shown in Figure 17-1.
While awaiting admission to an inpatient bed, a
bradycardic rhythm was noted on the telemetry moni-
tor, and a rhythm tracing was obtained (Figure 17-2).
The patient’s clinical status remained stable, with no
change in blood pressure.
Section II: Case discussion
Dr Peter Rosen: This patient appears to have a vari-
ety of causes for her congestive heart failure, includ-
ing hypertension and probably some degree of mitral
regurgitation. It seems her heart is not doing very
well at baseline with an ejection fraction of 20%,
and it also sounds like she is beginning to fail in
terms of being unable to cope with her daily living
requirements. I’m a little puzzled as to why a BNP
was ordered on this patient; I don’t know what a
BNP would tell you that you don’t already know.
Was this part of an ED protocol or the universal
poor practice of ordering laboratory tests because
they are available?
CHAPTER 17
238
Dr Richard Harrigan: The BNP was likely ordered
for both reasons. The early working diagnoses
were COPD and CHF; if the X-ray study were
nondiagnostic, or if there were a delay in obtain-
ing the X-ray study, the BNP could help. Invariably,
it does seem that the X-ray is fi nished in a timely
fashion, you also have the clinical diagnosis, and the
BNP results arrive later and aren’t useful in many
cases.
PR: They also fell into a common trap thinking that
because a patient has asthma, COPD must be present.
While there is some overlap between the two diseases,
Figure 17.1 Cardiotoxic drugs (1).
Figure 17.2 Cardiotoxic drugs (2).
CARDIAC TOXINS AND DRUG-INDUCED HEART DISEASE
239
RH: The principal symptoms of digoxin toxicity are
gastrointestinal, including nausea, vomiting, abdomi-
nal cramping, and diarrhea. Neurologic symptoms
can include headache, confusion, hallucinations, or
delirium at higher levels. The classic visual complaints
are less common.
PR: When you see an EKG like this, should you
start with dig toxicity? As I recall, the most common
abnormality with dig toxicity is premature ventricular
contraction. Is there any other explanation for this
kind of block?
RH: There is a clue on this EKG that suggests
digoxin. There is a mixture of excitability and atrio-
ventricular (AV) nodal suppression with an acceler-
ated atrial beat at about 150 beats per minute—an
atrial tachycardia—with a delayed ventricular rate
at the same time. There is also evidence of digoxin
effect: scooping- or coving-type ST-segment depres-
sion that is best seen in leads V5 and V6 on this EKG,
and on the V5 rhythm strip on the bottom. I would
assume this was digoxin toxicity if I knew the patient
was taking digoxin.
SG: If digoxin were not on the patient’s medication
list, either the patient managed to fi nd a digoxin source
and take it without a prescription or the dysrhythmia
must have another etiology. Electrolyte abnormali-
ties cause many abnormal rhythms. Hyperkalemia,
in particular, is notorious for causing a variety of
abnormal rhythms, and although this is not a classic
hyperkalemic dysrhythmia, this could have resulted
from intrinsic conduction disease as well. Part of dis-
covering the etiology in this case may require a better
knowledge of the medical history.
RH: Nevertheless, seeing dig effect should make
you think that the patient is taking this medication
even when the patient isn’t forthcoming with a com-
plete medication list. This doesn’t predict toxicity,
however.
PR: Dig effect does not mean dig toxicity, but par-
oxysmal atrial tachycardia (PAT) with block almost
always does. With good evidence that she is on dig,
and that she is digitoxic, what are your indications for
using Digibind fragments to reverse the toxicity?
RH: There are a number of different views about
when to administer Digibind. It is easy to administer
it’s unlikely that this patient’s heart failure is related to
cor pulmonale. Were the examining physicians aware
of an abnormal heart beat, or was this only noted on
cardiac monitoring?
RH: They thought she was in a regular rhythm, which
she did have initially on the EKG. They did notice a
slow heart rate. This was thought to be related to the
metoprolol and digoxin, and to her age as well. At 65
years old, perhaps her conduction system had begun
to degenerate.
PR: I noticed she is taking a powerful diuretic, furo-
semide, without taking a potassium supplement. I’m
somewhat surprised that her potassium was normal,
but it may be an alternate explanation for her ulti-
mate illness. There was a time when all patients with
hypertension were treated with diuretics without
potassium. Many of them also had heart failure, and
were being treated with a form of digitalis. The most
common reason for dig toxicity in those days was
hypokalemia. Digoxin was a relatively late-comer
to digitalis therapy. For years we used digitalis leaf,
and then we used digitoxin, which was thought to
be preferable because it was longer acting. This
meant that when you became dig-toxic, you could
expect to be dig-toxic for a month. Today we use less
“dig,” and when we do, we use the shorter-acting
digoxin so we are not as sensitized to the potential
for dig toxicity. I’m not sure the long-acting agents
are even available, yet it’s still unwise to use digoxin
and a diuretic without accompanying potassium
replacement.
Dr Shamai Grossman: I suspect that the patient had
some known renal failure. In the setting of someone
who has chronic renal insuffi ciency, giving potassium
may not be ideal.
PR: Taking furosemide isn’t ideal in renal failure either.
This patient may be between a rock and a hard place;
perhaps worsening renal failure, rather than potas-
sium changes with furosemide, led to digoxin toxic-
ity. In any event, I can see why the clinicians were not
particularly alert to digoxin toxicity. I was also sur-
prised that she didn’t manifest some other symptoms
of dig toxicity, such as nausea and vomiting or optical
complaints such as color changes. Often patients feel
dizzy and become more aware of irregularities in their
heart beat.
CHAPTER 17
240
PR: Since we are moving away from using digoxin for
heart failure, do you think that is a reason to stop this
patient’s digitalis?
SG: Digoxin doesn’t work acutely, and in the short-
term there are other medicines that are effective
and should be used for rate control in atrial fi bril-
lation. Therefore, I have no problem with suppress-
ing digoxin, particularly when it’s causing conduction
problems. Long term, digoxin remains unique as
an effective cardiac inotrope, and could always be
restarted later.
PR: Before we had easy access to digoxin levels, we
used clinical parameters to decide whether a patient
was suffi ciently digitalized. If a patient’s rate were
slow, we felt we were where we needed to be. One
of the clinical tests for adequate digitalization was to
give a dose of atropine, and if the heart speeded up,
we thought we needed more digoxin. Given the fact
that this patient’s heart rate is already slow, would
you expect to see a very high level even before the
laboratory value comes back?
EU: A high digoxin level wouldn’t surprise me in this
case, more so because of the EKG fi ndings of atrial
tachycardia with AV block. The vague neurologic
complaints would have also clued me in.
PR: Is there a role for hemodialysis in digoxin toxic-
ity, particularly in a patient with concomitant renal
failure?
RH: Dialysis doesn’t play a role in removing
digoxin or the digoxin bound with Fab fragments.
Hemodialysis does not enhance elimination due to the
large volume of distribution of digoxin. Nevertheless,
most patients recover well after receiving Digibind. If
days later they do deteriorate, there may be a role for
plasma exchange to rid the body of the digoxin-Fab
fragments, particularly if there is a concern that the
complex may come apart and cause a high rebound
digoxin level.
PR: I thought the problem with giving Fab fragments
was that it removes all of digoxin’s effectiveness, and
may worsen the patient’s heart failure. This patient’s
CHF already seems to be worsening, and I wonder if
that’s why they chose not to use the Fab fragments.
RH: I agree. Although this patient was oxygenating,
her reserve with an ejection fraction of 10–20% is
the Fab fragments when the patient is at or near car-
diac arrest from a ventricular dysrhythmia; otherwise,
the indications seem to be less agreed upon, and some-
what subjective. This patient didn’t receive Digibind,
although I believe she should have. Digibind may be
appropriate for ventricular dysrhythmias, AV nodal
conduction disease such as a Mobitz II second-degree
AV block, or a third-degree AV block, especially with a
very slow escape rhythm. Hyperkalemia (K⫹ ⬎5) in
a patient who has taken an acute digoxin overdose,
with the high potassium signaling poisoning of the
sodium-potassium-ATPase pump, is another possible
indication for Digibind. Lastly, a digoxin level of 10
or above, regardless of the clinical status, or if the
amount of digoxin ingested is ⬎10 mg for adults or
⬎4 mg in a child, are all indications for the adminis-
tration of Digibind.
SG: There is a well-established view that if you have a
patient who can be safely and effectively paced without
giving them Fab fragments, you should. The thinking
behind this is that the random use of Fab fragments
is too expensive a cost for our healthcare system to
sustain. This view always bothered me because I think
that subjecting someone to the discomfort of pacing
or the danger of transvenous pacing when we have a
drug that can reduce its effect raises some diffi cult ethi-
cal issues.
PR: Given this patient has chronic renal failure, and we
don’t know whether it is acutely worsening, would that
change your thinking about reversing the digoxin with
Fab fragments?
Dr Edward Ullman: Renal failure doesn’t equate to a
need for Fab fragments.
PR: Given that this also could be beta-blocker toxic-
ity, would you entertain giving this patient some glu-
cagon, despite the fact that the patient’s glucose was
not bad at 176 mg/dL?
SG: If I decided to treat the patient for digoxin tox-
icity because I thought that’s probably what it was,
I wouldn’t start glucagon. If Fab fragments didn’t
work, and it wasn’t clear that this was dig toxicity,
and the patient had a subsequent digoxin level that
was zero or near zero, then I’d seriously consider
glucagon, but I wouldn’t use it empirically in this
case.
CARDIAC TOXINS AND DRUG-INDUCED HEART DISEASE
241
can increase the dig level. We don’t use all of these
agents very frequently in the ED, but we do frequently
use nonsteroidal antiinfl ammatory drugs (NSAIDS).
There is literature suggesting a rising dig level with
indomethacin, as well as other NSAIDS. You may be
in a dangerous situation where a patient’s renal perfu-
sion may be compromised, and you impair it further
with an NSAID, ultimately causing a dig toxic rhythm
in the face of worsening renal failure.
PR: Is the use of Fab fragments a contraindication
for surgery, assuming she has some degree of mitral
regurgitation that someone may want to fi x?
RH: I agree that when the heart is irritated, as it is
here with digoxin, that that situation has to be quelled
before any surgical stress on the heart can be superim-
posed on the clinical situation.
PR: I think she has a failing heart in the sense that
the medications that we are giving her aren’t going
to improve her cardiac output that much. I wouldn’t
have had the nerve to hold off on the Fab; I haven’t
all that much faith in dig levels. I would have thought
hers would be higher given the toxicity, and I’m not
sure that the dig level is a refl ection of dig activity
anyway. This is a tough case and I think that it is a
very interesting one, but I’m not sure what we have to
offer this patient in long-term therapy.
SG: Digoxin is only one of the many medications
we give that has potential for adverse outcomes, and
needs careful monitoring of many different metabolic
parameters. As we use less digoxin, we encounter
more issues with other cardiac medications, such as
calcium channel blocker and beta-blocker toxicity. I
think that although we may not have to fi ght at the
digitalis front as much as we used to, there are many
new battles to be fought.
Case resolution
The patient was observed on telemetry; digoxin and
metoprolol were held. Digoxin levels were monitored
serially, and fell from an initial level of 2.1 ng/ml to
0.8 ng/mL by the second hospital day. She had no
worsening of her dysrhythmias, and her heart fail-
ure improved with treatment. The EKG improved to
atrial tachycardia with 2:1 block, and then reverted to
atrial fi brillation; rate control was achieved with oral
limited. She is already in CHF, with impaired kidney
function.
PR: This is a tough patient: she doesn’t fi t criteria for
dialysis, but it’s an ominous picture. I don’t know if
she fi ts criteria for replacing her mitral valve, as we
don’t have any detailed information about her valve,
but we have a patient who is in pulmonary edema
with mitral regurgitation, with diabetes and renal fail-
ure, who has digoxin toxicity. What can you do for
her heart failure short of dialysis?
SG: You can try high-dose diuretics. High-dose
diuretics are more likely to work in patients who still
make urine, and may be useful. Preload reduction
with intravenous nitroglycerin or afterload reduction
with an ACE inhibitor may also be useful. There are a
number of case reports of using an ACE inhibitor as a
bridge to dialysis, and this might be that scenario.
PR: Would it worry you that she already has a dry
nonproductive cough, which is supposedly associated
with ACE inhibitors?
SG: No, simply because you have a cough from what
is likely an intrinsic respiratory illness or perhaps as a
manifestation of her heart failure, I wouldn’t assume
that the patient is at risk for a worsened cough from
an ACE inhibitor. The cough from an ACE inhibitor
is a unique side effect from the drug and associated
with a delayed sensitization.
PR: Would you consider changing the diuretics?
EU: If you are going to continue her on the digoxin,
then you have to be very careful about further wors-
ening the renal function with more or higher doses of
diuretics. ACE inhibitors might help to optimize the
renal function in house, but it’s not clear that another
diuretic will lessen the risk of renal failure.
RH: Although we are not prescribing a lot of digoxin,
we do cross paths with it, and we have to be care-
ful what drugs we add that may precipitate toxicity
down the road. While digoxin is not in the same tier
of complications as is warfarin, where you have to
look up almost any drug that you add for concerns
regarding effect on the international normalized
ratio (INR), there are a lot of drug interactions with
digoxin, including quinidine, verapamil, tetracy-
cline, erythromycin, and cyclosporine. All of these
CHAPTER 17
242
life than cocaine itself, can cause coronary artery
vasospasm and a delayed AICS.
9
Additionally, there
is some evidence that cocaine withdrawal is related
to the development of myocardial ischemia.
12
The
toxic effect cocaine has on the cardiovascular system
appears to be disproportionately increased by con-
comitant use of both tobacco and alcohol. Alcohol
ingestion with cocaine leads to the development of
cocaethylene, a unique metabolite that causes direct
myocardial depression and increased coronary ath-
erosclerosis, independent of the coronary artery
spasm caused by cocaine.
13,14
Tobacco appears to
increase the degree of coronary artery spasm caused
by cocaine, and it independently decreases microvas-
cular blood fl ow.
3
Patients with a cocaine-related AICS tend to
develop complications earlier than patients with a
non-cocaine-related AICS. In one study, more than
90% of complications for cocaine-related acute MI
(including CHF, dysrhythmias, and cardiogenic shock)
occurred within 24 hours of presentation.
15
On the
other hand, short-term mortality appears to be lower,
and the likelihood of surviving a sudden cardiac arrest
is higher, in patients with cocaine-related AICS.
16
The
better prognosis for patients with a cocaine-associ-
ated AICS is believed to be related to their overall
younger age and therefore lower level of underlying
coronary atherosclerosis. Patients who have had chest
pain and then abstain from further cocaine use have
signifi cantly better long-term outcomes than patients
who continue to abuse cocaine.
17
The presentation of a cocaine-related AICS is vari-
able. Cocaine has been implicated as a cause in up to
25% of acute MI in patients aged 18–45 years, but
it has also been known to cause an AICS in patients
more than 60 years of age.
18,19
A detailed social his-
tory, including drug habits, frequency of use, and
most recent use, should be elicited from all patients
with symptoms consistent with a possible AICS. Urine
screening for cocaine metabolites should be consid-
ered in any young person with chest pain, as underre-
porting is common, and confi rmed cocaine use could
affect short-term management strategies. About 45%
of patients with a cocaine-associated AICS present
with chest pain; the pain is most commonly described
as substernal (71%) and pressure-like (47%). Other
common presenting symptoms of acute MI among
cocaine abusers are dyspnea (60%), diaphoresis
(44%), and less commonly palpitations, dizziness,
metoprolol. She was discharged home on metoprolol
but without digoxin.
Section III: Concepts
Recreational toxins
Cocaine
Cocaine is the second most commonly used illicit
drug, after marijuana, in the United States. More
than 20% of Americans have tried cocaine, and 5.5%
of Americans abused cocaine at least once in 2002.
Men are twice as likely as women to abuse cocaine.
1
Cocaine-related complaints accounted for approxi-
mately 450,000 ED visits in 2005, more than any
other illicit drug, and 40% of cocaine-related ED vis-
its were for chest pain.
2
Cocaine is an alkaloid extracted from the leaves of
the Erythroxylon coca bush, which is found mostly
in South America. It is ingested in one of two forms:
as a hydrochloride salt or as freebase. The hydro-
chloride salt is water-soluble and is usually taken
intranasally (snorting) or intravenously (mainlin-
ing). Cocaine ingestion causes catecholamine release
and increased sympathetic tone, which leads to a
faster heart rate, increased myocardial muscle con-
tractility, and oxygen consumption. Cocaine reduces
myocardial oxygen supply by causing coronary
artery vasoconstriction via increased alpha-adrener-
gic smooth muscle contraction and decreased nitric
oxide production.
3–5
It induces a prothrombotic state
by increasing platelet production and aggregation,
and it causes systemic hypertension by increasing
both the cardiac index and arterial smooth muscle
vasoconstriction.
6–8
Cocaine ingestion is known to cause several cardio-
vascular complications, including angina, myocardial
ischemia and infarction, hypertensive emergency,
cardiomyopathy, dysrhythmias, and endocarditis.
9
The incidence of acute myocardial infarction (MI)
among ED patients with cocaine-associated chest
pain is approximately 1–6%, and another 15% of
patients have an acute ischemic coronary syndrome
(AICS).
10
The adjusted risk of MI is 24 times greater
in the fi rst hour after cocaine use; however, cocaine
has been implicated as a causative factor in an AICS
as much as a week after use.
11
It is thought that the
metabolites of cocaine (benzoylecgonine and ecgo-
nine methyl ester), which have a much longer half
CARDIAC TOXINS AND DRUG-INDUCED HEART DISEASE
243
bleeding and other complications than nonabusers;
fi brinolytics should be given only to those patients
suffering an acute ST elevation myocardial infarction
when early percutaneous intervention is not possible.
28
Drug-eluting coronary stents should be considered for
only the patients with a high probability of complying
with long-term antiplatelet therapy.
2
Patients with a possible cocaine-associated AICS
should be treated with benzodiazepines early in their
management. Benzodiazepines relieve chest pain,
decrease heart rate, systolic blood pressure, and car-
diac index in patients with cocaine-associated chest
pain.
29
Hypertension associated with cocaine abuse
should be treated initially with benzodiazepines, but
if sympathomimetic symptoms are controlled with IV
benzodiazepines and the patient remains hypertensive,
treatment with phentolamine (a direct alpha-adrener-
gic blocker), sodium nitroprusside, or nitroglycerin
can be utilized.
30
Beta-adrenergic blockers increase the rate of
coronary vasospasm in animal models exposed
to cocaine, likely due to the effects of unopposed
alpha-sympathetic stimulation on coronary smooth
muscle cells.
31
Labetalol (a combined alpha- and
beta-adrenergic antagonist, which has theoreti-
cal advantages over pure beta-adrenergic block-
ing agents) has been shown to increase the rate of
seizure and death in cocaine animal models, and
should be avoided in the acute setting. The cur-
rent ACC/AHA guidelines recommend withholding
all beta-adrenergic blockers from patients with a
cocaine-associated AICS due to the increased risk of
coronary vasoconstriction.
32
Nitroglycerin reduces cocaine-associated chest pain,
reverses coronary vasoconstriction and effectively
treats hypertension.
29
Phentolamine reverses cocaine-
associated hypertension and coronary vasoconstric-
tion and, as mentioned previously, it can be used in
patients not responding to benzodiazepine and nitro-
glycerin therapy.
30
Calcium channel blockers have no
proven effi cacy in patients with a cocaine-associated
AICS, and are harmful in patients with heart failure.
Antiplatelet and antithrombotic agents are indicated
for a cocaine-associated AICS due to the direct pro-
thombotic effects of cocaine.
2
Patients with a high probability for a cocaine-induced
AICS should be admitted to a monitored bed; low-to-
moderate risk patients without other coronary risk fac-
tors can be safely evaluated in an observation unit. In
nausea, and anxiety.
10
Patients may present with
symptoms of anxiety and restlessness related to the
sympathomimetic stimulation of cocaine, but these
symptoms are variable. In fact, “speedballing” (con-
comitant use of heroin and cocaine) may cause an ini-
tially depressed sensorium.
20
The initial electrocardiogram (EKG) is abnormal in
55–80% of patients with a cocaine-associated AICS,
but the fi ndings are nonspecifi c. Benign early repolar-
ization is a common fi nding that is not caused by the
cocaine, and very few patients with J-point elevation
and cocaine use have an acute MI.
21
Other common
fi ndings are left ventricular hypertrophy, nonspecifi c
T-wave abnormality, and ST-segment elevation or
depression. In one study, the EKG is 36% sensitive
and 89% specifi c for an AICS in cocaine users.
10
A
chest X-ray study should be performed on all patients
with cardiopulmonary symptoms following cocaine
abuse. Crack cocaine use can lead to the development
of a pneumothorax and “crack lung,” which is a syn-
drome of hypoxia, hemoptysis, and eventual respi-
ratory failure associated with bilateral pulmonary
infi ltrates on the chest X-ray study. It occurs after the
ingestion of freebase cocaine.
22
Patients who abuse cocaine are at increased risk of
developing rhabdomyolysis, which makes interpre-
tation of serum myoglobin and total creatine kinase
levels unreliable for risk stratifi cation of a possible
AICS; as such, serum troponin T and I levels are the
most accurate markers for an AICS in patients abus-
ing cocaine.
23,24
Patients with cocaine-associated chest
pain who are considered a low risk for an AICS based
on clinical presentation and EKG fi ndings have a low
rate (⬍3%) of fi xed or reversible defects on myocar-
dial perfusion imaging.
25
Cocaine use is associated
with concentric left ventricular hypertrophy, which
can mask localized wall-motion abnormalities, mak-
ing echocardiography an insensitive test for detec-
tion of a cocaine AICS.
26
The majority of cocaine
users (55–80%) with proven acute MI have evidence
of underlying coronary artery disease on cardiac
catheterization.
27
Patients with a possible cocaine-associated AICS
should be treated similarly to those with a non-co-
caine-associated AICS, with a few notable exceptions.
Patients with EKG evidence of an acute MI should be
treated with emergent cardiac catheterization. There is
evidence that patients who abuse cocaine who receive
IV fi brinolytics are more likely to have intracranial
CHAPTER 17
244
patients with a history of excessive drinking for more
than 10 years, though subclinical decreased left ven-
tricular function can occur with as little as 5 years of
heavy drinking. Most cases occur during the fourth to
sixth decades of life.
9
Men make up more than 85%
of cases, but this difference can largely be attributed
to the prevalence of alcoholism by gender, although
they constitute a minority of cases, women appear
to develop cardiac dysfunction at a lower cumulative
alcohol dose than men.
40,41
Patients may present with
symptoms as mild as a limited exercise tolerance, or
as severe as decompensated heart failure. Symptoms
include fatigue, dyspnea, orthopnea, and paroxysmal
nocturnal dyspnea.
All patients presenting with symptoms of heart fail-
ure should be queried for acute and chronic alcohol
consumption habits, with appropriate referral for
counseling whenever possible. Counseling and group
therapy are the only effective methods for decreasing
drinking habits, which is the most successful treatment
for alcoholic cardiomyopathy.
42
Patients with alcoholic
cardiomyopathy may suffer from other stigmata of
alcohol-related syndromes, including hepatic cirrhosis,
malnourishment, alcoholic ketoacidosis, electrolyte
abnormalities, and delirium tremens. Alcoholics with
hepatic cirrhosis frequently have asymptomatic ven-
tricular dysfunction, which should be considered in
their acute management.
43,44
Physical examination fi ndings of alcoholic car-
diomyopathy closely resemble those of idiopathic
dilatated cardiomyopathy. Patients may have a nar-
row pulse pressure because systemic vasoconstriction
causes an elevated diastolic pressure. Other fi ndings
include a presystolic gallop, displaced apical impulse,
and a murmur of mitral regurgitation, auscultated
best at the apex. Peripheral edema and an elevated
jugular venous pressure may occur due to fl uid reten-
tion.
9
There appears to be a relationship between the
malnourishment common among alcoholics and the
development of alcoholic cardiomyopathy.
44–46
The
physical examination should include an assessment
for malnourishment, which commonly presents in
alcoholics as atrophy and skeletal myopathy of the
shoulders and pelvic girdle.
47,48
An irregular pulse or
tachycardia may be present, which would be consis-
tent with an alcohol-induced dysrhythmia.
The etiology of alcoholic cardiomyopathy is not
fully understood, but it appears that several mecha-
nisms are involved. Alcohol has a direct toxic effect
one study, patients with cocaine-associated chest pain
stratifi ed as low-to-moderate risk for AICS were moni-
tored with serial cardiac enzymes for 9 hours from ini-
tial presentation and then discharged. Fewer than 1%
of patients discharged have had a postobservation MI
at one-year follow-up.
33
Other studies of 9–12 hour
observation periods for low-risk patients have similar
results.
34
Cocaine use can cause signifi cant myocardial dys-
function, caused by direct myocardial toxicity and
coronary artery vascoconstriction. Adulterants and
virulent organisms administered with the cocaine can
also cause myocarditis or endocarditis. Treatment for
myocardial dysfunction includes abstinence from the
drug in addition to standard therapy.
35
Cocaine can cause atrial dysrhythmias, most com-
monly supraventricular tachycardia and atrial fi bril-
lation, with intravenous fl uids and benzodiazepines
generally being effective for reversal. Beta-adrenergic
blockers should be avoided in this population.
Ventricular dysrhythmias can occur due to increased
sympathetic tone and direct sodium channel block-
ade, with intravenous sodium bicarbonate, 1 to 2
mEq/kg, being the treatment of choice.
36
There has
been some concern that lidocaine might increase dys-
rhythmic complications, but the clinical experience
fi nds it to be effi cacious; it should be considered sec-
ond-line therapy for any wide complex dysrhythmia
not responsive to sodium bicarbonate.
37
Intravenous cocaine use can cause endocarditis, usu-
ally of left-sided valves, in contradistinction to other
intravenous drug-associated endocarditis, which pref-
erentially affects the right-sided valves. Cocaine use
has also been associated with aortic dissection and
rupture. One study of 38 patients with aortic dissec-
tion fi nds that 37% of the cases are related to cocaine
use, most within 12 hours of ingestion.
38
Cocaine use
is associated with an increased risk of ruptured intra-
cerebral aneurysms, likely due to increased systemic
blood pressure.
Alcohol
There are approximately 18 million alcohol-
ics in the United States, and 8% of ED visits are
related to alcoholism or inappropriate drinking.
39
Cardiovascular complications of heavy drinking and
alcoholism include alcoholic cardiomyopathy, the
“holiday heart” syndrome, and atrial fi brillation/fl ut-
ter. Alcoholic cardiomyopathy typically presents in