Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3970_Библиотеки_им_академика_М_И_Перельмана.pdf
CARDIAC TOXINS AND DRUG-INDUCED HEART DISEASE
255
idiopathic dilated cardiomyopathy. Eur Heart J.
1996;17:251–257.
Gavazzi A, De Maria R, Parolini M, Porcu M. Alcohol 63
abuse and dilated cardiomyopathy in men. Am J
Cardiol. 2000;85:1114–1118.
Salisbury AC, House JA, Conard MW, Krumholz HM, 64
Spertus JA. Low-to-moderate alcohol intake and health
status in heart failure patients. J Card Fail. 2005;11:
323–328.
Abramson JL, Williams SA, Krumholz HM, Vacarrino 65
V. Moderate alcohol consumption and risk of heart
failure among older persons. JAMA. 2001;285:
1971–1977.
Tolstrup J, Gronbaek M. Alcohol and athero-66
sclerosis: recent insights. Curr Atheroscler Rep.
2007;9:116–124.
Femia R, Natali A, L’Abbate A, Ferrannini E. Coronary 67
atherosclerosis and alcohol consumption: angiographic
and mortality data. Arterioscler Thromb Vasc Biol.
2006;26:1607–1612.
Janszky I, Mukamal KJ, Orth-Gomer K, et al. 68
Alcohol consumption and coronary atherosclerosis
progression—the Stockholm Female Coronary Risk
Angiographic Study. Atherosclerosis. 2004;176:311–319.
da Luz PL, Coimbra SR. Wine, alcohol and atheroscle-69
rosis: clinical evidences and mechanisms. Braz J Med
Biol Res. 2004;37:1275–1295.
Penumathsa SV, Maulik N. Resveratrol: a promising 70
agent in promoting cardioprotection against coro-
nary heart disease. Can J Physiol Pharmacol. 2009;87:
275–286.
Wu JM, Wang ZR, Hsieh TC, et al. Mechanism of car-71
dioprotection by resveratrol, a phenolic antioxidant
present in red wine (Review). Int J Mol Med. 2001;
8:3–17.
Wang Z, Zou J, Cao K, et al. Dealcoholized red 72
wine containing known amounts of resveratrol sup-
presses atherosclerosis in hypercholesterolemic rabbits
without affecting plasma lipid levels. Int J Mol Med.
2005;16:533–540.
Maxwell JC, Rutkowski BA. The prevalence of meth-73
amphetamine and amphetamine abuse in North
America: a review of the indicators, 1992–2007. Drug
Alcohol Rev. 2008;27:229–325.
Rasmussen N. America’s fi rst amphetamine epidemic 74
1929–1971: a quantitative and qualitative retrospective
with implications for the present. Am J Public Health.
2008;98:974–985.
Albertson TE, Kenyon NJ, Morrissey B. Amphetamines 75
and derivatives. In: Shannon MW, ed. Haddad and
Winchester’s Clinical Management of Poisoning and
Drug Overdose. 4th ed. Philadelphia: Saunders/Elsevier;
2007:781–790.
Fernandez-Sola J, Fatjo F, Sacanella E, et al. Evidence 50
of apoptosis in alcoholic cardiomyopathy. Hum Pathol.
2006;37:1100–1110.
Aistrup GL, Kelly JE, Piano MR, Wasserstrom JA. 51
Biphasic changes in cardiac excitation-contraction cou-
pling early in chronic alcohol exposure. Am J Physiol
Heart Circ Physiol. 2006;291:H1047–H1057.
Fernandez-Sola J, Nicolas JM, Oriola J, et al. 52
Angiotensin-converting enzyme gene polymor-
phism is associated with vulnerability to alcoholic
cardiomyopathy. Ann Intern Med. 2002;137:321–326.
Wooley JA. Characteristics of thiamin and its relevance 53
to the management of heart failure. Nutr Clin Pract.
2008;23:487–493.
Dancy M, Bland JM, Leech G, Gaitonde MK, 54
Maxwell JD. Preclinical left ventricular abnormali-
ties in alcoholics are independent of nutritional sta-
tus, cirrhosis, and cigarette smoking. Lancet. 1985;1:
1122–1125.
Witte KK, Nikitin NP, Parker AC, et al. The effect of 55
micronutrient supplementation on quality-of-life and
left ventricular function in elderly patients with chronic
heart failure. Eur Heart J. 2005;26:2238–2244.
Ettinger PO, Wu CF, De La Cruz C, et al. Arrhythmias 56
and the “holiday heart”: alcohol-associated cardiac
rhythm disorders. Am Heart J. 1978;95:555–562.
Mukamal KJ, Tolstrup JS, Friberg J, Jensen G, Gronbaek 57
M. Alcohol consumption and risk of atrial fi brillation
in men and women: the Copenhagen City Heart Study.
Circulation. 2005;112:1736–1742.
Steinbigler P, Haberl R, Konig B, Steinbeck G. P-wave 58
signal averaging identifi es patients prone to alcohol-
induced paroxysmal atrial fi brillation. Am J Cardiol.
2003;91:491–494.
Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 59
2006 Guidelines for the management of patients with
atrial fi brillation: A report of the American College of
Cardiology/American Heart Association Task Force
on Practice Guidelines and the European Society
of Cardiology Committee for Practice Guidelines.
Circulation. 2006;114:e257–e354.
Carley S, Ali B, Mackway-Jones K. Towards evi-60
dence based emergency medicine: best BETs from the
Manchester Royal Infi rmary. Acute myocardial infarc-
tion in cocaine induced chest pain presenting as an
emergency. Emerg Med J. 2003;20:174–175.
Singer DE, Albers GW, Dalen JE, et al. Antithrombotic 61
therapy in atrial fi brillation: American College of Chest
Physicians Evidence-Based Clinical Practice Guidelines
(8th Edition). Chest. 2008;133:546S–592S.
Prazak P, Pfi sterer M, Osswald S, Buser P, Burkart 62
F. Differences of disease progression in conges-
tive heart failure due to alcoholic as compared to
CHAPTER 17
256
Lauwers LF, Roelants A, Rosseel PM, Heyndrickx B, 93
Baute L. Oral antimony intoxications in man. Crit Care
Med. 1990;18:324–326.
Peters HA, Croft WA, Woolson EA, Darcey BA, 94
Olson MA. Seasonal arsenic exposure from burn-
ing chromium-copper-arsenate-treated wood. JAMA.
1984;251:2393–2396.
Pigott DC, Liebelt EL. Arsenic and arsine. In: 95
Shannon MW, ed. Haddad and Winchester’s Clinical
Management of Poisoning and Drug Overdose. 4th ed.
Philadelphia: Saunders/Elsevier; 2007:781.
Beckman KJ, Bauman JL, Pimental PA, Garrard C, 96
Hariman RJ. Arsenic-induced torsade de pointes. Crit
Care Med. 1991;19:290–292.
Aposhian HV. Mobilization of mercury and arsenic 97
in humans by sodium 2,3-dimercapto-1-propane sul-
fonate (DMPS). Environ Health Perspect. 1998;106
Suppl 4:1017–1025.
Insley BM, Grufferman S, Ayliffe HE. Thallium 98
poisoning in cocaine abusers. Am J Emerg
Med.1986;4:545–548.
Lorenc JD. Inhalant abuse in the pediatric population: 99
a persistent challenge. Curr Opin Pediatr. 2003;15:
204–209.
Williams DR, Cole SJ. Ventricular fi brillation following 100
butane gas inhalation. Resuscitation. 1998;37:43–45.
Murphy NG, Benowitz NL, Goldschlager N. 101
Cardiovascular toxicology. In: Shannon MW, ed.
Haddad and Winchester’s Clinical Management of
Poisoning and Drug Overdose. 4th ed. Philadelphia:
Saunders/Elsevier; 2007:133–156.
Webb DJ, Muirhead GJ, Wulff M, et al. Sildenafi l cit-102
rate potentiates the hypotensive effects of nitric oxide
donor drugs in male patients with stable angina. J Am
Coll Cardiol. 2000;36:25–31.
Anderson JL, Adams CD, Antman EM, et al. ACC/103
AHA 2007 guidelines for the management of patients
with unstable angina/non-ST-elevation myocar-
dial infarction: a report of the American College
of Cardiology/American Heart Association Task
Force on Practice Guidelines. J Am Coll Cardiol.
2007;50:e1–e157.
Parker JD, Bart BA, Webb DJ, et al. Safety of intra-104
venous nitroglycerin after administration of sildenafi l
citrate to men with coronary artery disease: a double-
blind, placebo-controlled, randomized, crossover trial.
Crit Care Med. 2007;35:1863–1868.
Gupta A, Lawrence AT, Krishnan K, Kavinsky CJ, 105
Trohman RG. Current concepts in the mechanisms and
management of drug-induced QT prolongation and
torsade de pointes. Am Heart J. 2007;153:891–899.
Indik JH, Pearson EC, Fried K, Woosley RL. Bazett 106
and Fridericia QT correction formulas interfere with
Derlet RW, Albertson TE. Emergency department pre-76
sentation of cocaine intoxication. Ann Emerg Med.
1989;18:182–186.
Bashour TT. Acute myocardial infarction resulting from 77
amphetamine abuse: a spasm-thrombus interplay? Am
Heart J. 1994;128:1237–1239.
Westover AN, Nakonezny PA, Haley RW. Acute myo-78
cardial infarction in young adults who abuse amphet-
amines. Drug Alcohol Depend. 2008;96:49–56.
Ayres PR. Amphetamine cardiomyopathy. 79 Ann Intern
Med. 1983;98:110.
Rasmussen S, Corya BC, Glassman RD. Valvular heart 80
disease associated with fenfl uramine-phentermine. N
Engl J Med. 1997;337:1773.
Kaku DA, Lowenstein DH. Emergence of recreational 81
drug abuse as a major risk factor for stroke in young
adults. Ann Intern Med. 1990;113:821–827.
Chin KM, Channick RN, Rubin LJ. Is methamphet-82
amine use associated with idiopathic pulmonary arte-
rial hypertension? Chest. 2006;130:1657–63.
Welling TH, Williams DM, Stanley JC. Excessive oral 83
amphetamine use as a possible cause of renal and
splanchnic arterial aneurysms: a report of two cases.
J Vasc Surg. 1998;28:727–731.
Dihmis WC, Ridley P, Dhasmana JP, Wisheart JD. 84
Acute dissection of the aorta with amphetamine mis-
use. BMJ.1997;314:1665.
Brennan K, Shurmur S, Elhendy A. Coronary artery 85
rupture associated with amphetamine abuse. Cardiol
Rev. 2004;12:282–283.
Alexander CS. Cobalt-beer cardiomyopathy. A clinical 86
and pathologic study of twenty-eight cases. Am J Med.
1972;53:395–417.
Morin Y, Daniel P. Quebec beer-drinkers’ cardiomyo-87
pathy: etiological considerations. Can Med Assoc J.
1967;97:926–928.
Shannon MW. Lead. In: Shannon MW, ed. 88 Haddad
and Winchester’s Clinical Management of Poisoning
and Drug Overdose. 4th ed. Philadelphia: Saunders/
Elsevier; 2007:781–790.
Balestra DJ. Adult chronic lead intoxication. A clinical 89
review. Arch Intern Med. 1991;151:1718–1720.
Baum CR. Mercury, Heavy metals and inorganic 90
agents. In: Shannon MW, ed. Haddad and Winchester’s
Clinical Management of Poisoning and Drug Over-
dose. 4th ed. Philadelphia: Saunders/Elsevier; 2007:
1111–1116.
Guallar E, Sanz-Gallardo MI, van’t Veer P, et al. 91
Mercury, fi sh oils, and the risk of myocardial infarc-
tion. N Engl J Med. 2002;347:1747–1754.
Yoshizawa K, Rimm EB, Morris JS, et al. Mercury and 92
the risk of coronary heart disease in men. N Engl J
Med. 2002;347:1755–1760.
CARDIAC TOXINS AND DRUG-INDUCED HEART DISEASE
257
Love JN. Acebutalol overdose resulting in fatalities.120
J Emerg Med.2000;18:341–344.
Love JN, Enlow B, Howell JM, Klein-Schwartz W, 121
Litovitz TL. Electrocardiographic changes associ-
ated with beta-blocker toxicity. Ann Emerg Med.
2003;42:156–157.
Baud FJ, Megarbane B, Deye N, Leprince P. Clinical 122
review: Aggressive management and extracorporeal
support for drug-induced cardiotoxicity. Crit Care.
2007;11:207–215.
Salhanick SD. Calcium channel antagonists. In: 123
Shannon MW, Borron SW, Burns MJ, eds. Haddad
and Winchester’s Clinical Management of Poisoning
and Drug Overdose. 4th ed. Philadelphia: Saunders/
Elsevier; 2007: Available at: “UrlBlockedError.aspx”
www.mdconsult..com/das/book/body. Accessed Sept-
ember 18, 2009.
Proano L, Chiang WK, Wang RY. Calcium channel 124
blocker overdose. Am J Emerg Med.1995;13:444–450.
Brass BJ, Winchester-Penny S, Lipper BL. Massive vera-125
pamil overdose complicated by noncardiogenic pulmo-
nary edema. Am J Emerg Med.1996;14:459–461.
Holstege CP, Baer AB. Other sodium channel block-126
ing agents. In: Chan TC, Brady WJ, Harrigan RA,
et al., eds. ECG in Emergency Medicine and Acute
Care. Philadelphia: Elsevier Mosby; 2006:274–278.
Nieman JT, Bessen HA, Rothstein RJ, Laks MM. 127
Electrocardiographic criteria for tricyclic antidepressant
cardiotoxicity. Am J Cardiol. 1986;57:1154–1159.
Liebelt EL, Francis PD, Woolf AD. ECG lead aVR 128
versus QRS interval in predicting seizures and arrhyth-
mias in acute tricyclic antidepressant toxicity. Ann
Emerg Med. 1995;26:195–201.
Nanagas KA, Furbee RB. Class IA antiarrhythmics: 129
Quinidine, procainamide, and disopyramide. In:
Shannon MW, Borron SW, Burns MJ, eds. Haddad and
Winchester’s Clinical Management of Poisoning and
Drug Overdose. 4th ed. Philadelphia: Saunders/Elsevier;
2007: Available at: “UrlBlockedError.aspx” www.
mdconsult..com/das/book/body. Accessed September 18,
2009
Floyd J, Morgan JP, Perry MC. Cardiotoxicity of 130
anthracycline-like chemotherapy. 2009 Available at;
www.utdol.com. Accessed June 8, 2010.
Floyd J, Morgan JP, Perry MC. Cardiotoxicity of nonan-131
thracycline cancer chemotherapeutic agents. 2009.
Available at; www.utdol.com. Accessed June 8, 2010.
measurement of drug-induced changes in QT interval.
Heart Rhythm. 2006;3:1003–1007.
Al-Khatib SM, LaPointe NM, Kramer JM, Califf RM. 107
What clinicians should know about the QT interval.
JAMA. 2003;289:2120–2127.
De Bruin ML, Pettersson M, Meyboom RH, Hoes AW, 108
Leufkens HG. Anti-HERG activity and the risk of drug-
induced arrhythmias and sudden death. Eur Heart J.
2005;26:590–597.
Roden DM, Lazzara R, Rosen M, et al. Multiple mech-109
anisms in the long-QT syndrome. Current knowledge,
gaps, and future directions. The SADS Foundation Task
Force on LQTS. Circulation. 1996;94:1996–2012.
Zeltser D, Justo D, Halkin A, et al. Torsade de pointes 110
due to noncardiac drugs: most patients have eas-
ily identifi able risk factors. Medicine (Baltimore).
2003;82:282–290.
Roden DM. Taking the “idio” out of “idiosyn-111
cratic”: predicting torsades de pointes. Pacing Clin
Electrophysiol. 1998;21:1029–1034.
Newman LS, Feinberg MW, LeWine HE. A bitter tale. 112
N Engl J Med. 2004;351:594–599.
Lapostolle F, Borron SW. Digitalis. In: Shannon MW, 113
Borron SW, Burns MJ, eds. Haddad and Winchester’s
Clinical Management of Poisoning and Drug Overdose.
4th ed. Philadelphia: Saunders/Elsevier; 2007: 1001.
Holstege CP, Kirk MA. Digitalis. In: Chan TC, Brady 114
WJ, Harrigan RA, et al, eds. ECG in Emergency
Medicine and Acute Care. Philadelphia: Elsevier
Mosby; 2006:255–260.
Williamson KM, Thrasher KA, Fulton KB, et al. 115
Digoxin toxicity: An evaluation in current clinical prac-
tice. Arch Intern Med. 1998;158:2444–2449.
Bismuth C, Gaultier M, Conso F, Efthymiou ML. 116
Hyperkalemia in acute digitalis poisoning: Prognostic
signifi cance and therapeutic implications. Clin Toxicol.
1973;6:153–162.
Lapostolle F, Borron SW, Verdier C, et al. Digoxin-117
specifi c Fab fragments as single fi rst-line therapy in dig-
italis poisoning. Crit Care Med. 2008;36:3014–3018.
Love JN, Howell, JM, Litovitz TL, Klein–Schwartz W. 118
Acute beta blocker overdose: factors associated with
the development of cardiovascular mortality. J Toxicol
Clin Toxicol. 2000;38:275–281.
Taboulet P, Cariou A, Berdeaux A, Bismuth C. 119
Pathophysiology and management of self-poisoning
with beta-blockers. J Toxicol Clin Toxicol. 1993;31:
531–551.
258
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.
Cardiomyopathy
Alden Landry
1
& Shamai Grossman
2
1
Instructor in Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center,
Fellow, Commonwealth Fund/Harvard University, Minority Health Policy Fellowship,
Boston, Massachusetts, USA
2
Director, Cardiac Emergency Center and Clinical Decision Unit, Beth Israel Deaconess
Medical Center, Assistant Professor of Medicine, Harvard Medical School, Boston,
Massachusetts, USA
18
Section I: Case presentation
A 35-year-old woman was brought to the emergency
department (ED) with complaints of shortness of
breath for the past 2 weeks, which worsened over
the prior day. She had experienced the symptoms
even with simple tasks such as washing dishes or
walking up stairs. She denied chest pain with the
shortness of breath, but did think that her legs were
more swollen than before. She stated that she did not
feel her heart beat fast intermittently. Her husband
noted that his wife had been breathing more heav-
ily at night, and had also complained of decreased
energy.
The past medical history was unremarkable except for
a prior appendectomy and tonsillectomy as a child.
The patient was 5 weeks postpartum after an uncom-
plicated fi rst pregnancy that was carried to term. She
did not associate her symptoms with the recent preg-
nancy nor with new motherhood.
The initial vital signs were: blood pressure 112/76
mmHg, heart rate 72 beats/min, respiratory rate
22 breaths/min, and temperature 36.8ºC (98.2ºF).
The patient was mildly obese, and was sitting upright
in mild respiratory distress. The physician noted a
mild 2/6 systolic ejection murmur with no rubs or gal-
lops. There was moderate jugular venous distention
in the external jugular veins. There were crackles at
the base of both lungs. There was trace-pitting edema
in the ankles to the mid-calves. The remainder of the
examination was unremarkable.
The physician ordered a battery of laboratory tests.
A complete blood count and serum electrolytes
were all normal. The patient was noted to have an
elevated beta-naturetic pepide (BNP) level. An EKG
was done, and was notable for a left axis deviation,
but was otherwise normal. A chest X-ray study was
performed that showed an enlarged cardiac silhou-
ette and mild vascular congestion, most prominent in
the lung bases. The cardiology and obstetric services
were consulted.
Section II: Case discussion
Dr Peter Rosen: In looking at the presenting com-
plaints of this patient, I would not immediately think
that this patient had a cardiac problem. We have a
patient who is 5 weeks postpartum; it’s not unusual
for patients to have weakness and fatigue and leg
swelling postpartum, even this far out, and swell-
ing may have been present all along the pregnancy.
One of the things I would be concerned about here
is pulmonary embolus (PE), which has a higher inci-
dence not just toward the end of pregnancy, but also
in the fi rst 2 months thereafter(1A). I think that part
of the initial workup should include a workup for PE.
Nevertheless, there are a number of heart diseases that
CARDIOMYOPATHY
259
and you can have eclampsia even after delivery, even
though one of the therapies for severe eclampsia is
delivery, to terminate the pregnancy. This diagnosis
may be missed because you don’t think of it; after
all, the patient is no longer pregnant. Similarly, rheu-
matic heart disease can be subtle when you can’t hear
the murmur, and since we don’t see much rheumatic
fever, we may stop thinking about it as a complica-
tion of pregnancy. Congenital valve disease can also
be well-tolerated until pregnancy, but here I would
suspect that the murmurs would be louder, and the
patient would probably be aware of that murmur for
years, and may have had a cardiac workup prior to
the pregnancy. Are there any symptoms or signs that
quickly point you towards a cardiomyopathy, or is it
a diagnosis of exclusion?
SG: First, I would think about the stage of the preg-
nancy; if the patient is third trimester or postpartum,
cardiomyopathy is within the differential, especially
in late third trimester. If we’re earlier in pregnancy,
the likelihood of cardiomyopathy is minimal. Next I
would consider the past medical history, including a
history of similar symptoms. If a patient has no his-
tory of a murmur, and suddenly has one, that would
make me think that it was brought on specifi cally by
the pregnancy. If the patient has a history of a coagu-
lopathy, then I might consider a thrombotic disease
rather than a cardiomyopathy. If on physical exami-
nation there are fi ndings of volume overload, I don’t
think I could differentiate between a cardiomyopa-
thy and another cardiac or even noncardiac etiology.
Ultimately, this is going to depend on some diagnostic
testing to better decide whether this is cardiomyopathy
or something else.
PR: My understanding is that, by defi nition, it can’t be
cardiomyopathy if it occurs earlier than the last 5 weeks
of pregnancy, but it can occur as long as 5 months after
delivery. I think that whenever I see an artifi cial defi -
nition of time-constraint, I always wonder why it’s so
important to have that time-constraint, and since the
etiology isn’t well-known, but has been suggested to
be postviral myocarditis, it would seem that it could
develop at any point in pregnancy, and not just in the
last trimester. Perhaps it takes the volume overload and
the work of carrying the heavy fetus to decompensate.
SG: The etiologies of peripartum cardiomyopathy
even today are still unclear. Therefore, because we
seem to present during pregnancy. While we don’t see
as many of them as often as we once did, it is not
uncommon for valvular heart disease to worsen dur-
ing pregnancy, and sometimes have pregnancy as the
fi rst manifestation of it. Do you have any experience
along those lines? How do these patients present?
Dr Shamai Grossman: In patients who are pregnant,
like with any patient who presents to the ED, you
always need to consider the worst possible diagno-
sis, which may be rare, as well as the more common
ones; only once you’ve decided there is no catastro-
phe, and you’ve ruled out any of the more ominous
causes of their problem, can you begin to attribute
their current presentation to some of the more benign
etiologies. For instance, if a pregnant patient comes
in with leg swelling and nonspecifi c symptoms such
as feeling more weak or overwhelmed, or just unable
to function with the daily activities of living, you can
only assume that those symptoms are related to the
pregnancy itself and not some other etiology only
after you’ve thoroughly evaluated the patient. Given
that our postpartum patient presents acutely dyspneic
with leg swelling, you must consider that this patient
has some other disease than pregnancy or the post-
partum physiology. The diseases that I would be
concerned about would be unmasked valvular heart
disease, pulmonary embolus, and perhaps a cardio-
myopathy. All of these can present with acute short-
ness of breath, and all of these diseases can present
with edema. However, if you are considering pulmo-
nary embolus, then you would think the etiology was
from a deep venous thrombosis, and expect unilat-
eral, rather than bilateral, lower extremity edema. If
you were thinking about cardiomyopathy or valvular
heart disease, you would expect the patient to present
volume-overloaded, and with valvular heart disease
you would expect a very noticeable murmur as well.
These diseases may be the most ominous that occur
in pregnancy, but a pregnant woman can also present
just like any other patient, and the disease may be
simply coincidental to the pregnancy.
PR: I remember a number of women with mitral valve
disease whose murmurs were not very loud, prob-
ably because they were diastolic. The systolic fl ow
murmur of pregnancy can last for at least a month
postpartum, since some women diurese the expanded
volume of pregnancy more slowly than others.
Edema of pregnancy can also represent eclampsia,
CHAPTER 18
260
congestive heart failure, you may see cardiomegaly,
which, in a 35-year-old woman, would be unusual.
Even if this patient were still pregnant, in the third tri-
mester, I would have no concern about doing a chest
X-ray study, given that this study has very minimal
amounts of radiation exposure to the patient, and
could give you some very useful information. These
are the two tests that I would start with in the ED,
coupled with a standard metabolic work up including
a complete blood count, serum electrolytes, and renal
function.
PR: One can obtain a decent chest X-ray study and
even shield the fetus, so the presence of a third-trimester
pregnancy certainly wouldn’t stop me from ordering
that test.
SG: My understanding as well is that the radiation
from a chest X-ray study is the equivalent of what one
gets when one goes on an airplane. Although third-
trimester women are concerned about going on an
airplane because of the possibility of going into labor
on the airplane, the radiation does not preclude them
from fl ying.
PR: What about an echocardiogram? Is that at all use-
ful in this entity?
SG: An echocardiogram would be the test of choice.
Although an echocardiogram is not always easily
available in the ED, it does need to be included in
this patient’s work up. Regardless of whether the
EKG or chest X-ray study suggest a possible cardio-
myopathy, I would want an echocardiogram to better
evaluate this patient. However, there is nothing in this
patient’s medical history to suggest that I must do the
echocardiogram in the ED. If this patient is admitted,
I would get the echocardiogram while this patient is
in the hospital, to better understand the etiology of
her symptoms.
PR: What would make you admit this patient? Is it
the new onset cardiac disease, or is it the possibility of
cardiomyopathy? Is it that these patients may do very
well, but can also do very poorly, and it’s hard to pre-
dict which patient is going to fall into which group?
SG: I believe it is a mixture of all of those things.
First, as with any patient, when we evaluate them in
the ED, we have to decide whether they are sick or
not sick. Does this patient look to be in decompen-
sated heart failure, or does the patient have ongoing
don’t really know the etiology, in terms of classify-
ing this as a disease entity, all we are left with is its
timing.
PR: There have been a number of different suggested
etiologies, none of which have been proven, in part
because this is still a pretty rare disease, and in part
because some of the suggestions were too farfetched.
For example, it is hard to understand physiologically
the use of tocolytics during labor as a cause of cardio-
myopathy. Infectious etiologies are also hard to prove,
as most of these patients don’t have an infection his-
tory, and this infection doesn’t appear to affect the
fetus the way that other third-trimester infections
often do. It’s hard to imagine a viral infection that
can affect the mother’s heart but not affect the fetus.
I think that we have to accept that we don’t know
the cause of this disease, but when you see pregnant
patients with symptoms of heart failure, weakness
and swelling, then, at this point, this becomes a dis-
ease entity that needs to cross your mind. One of the
things that strikes me as I read this presentation is that
there are a number of other disease entities that are
rare in late pregnancy and early puerperium that one
also is reluctant to think about, but may have similar
symptomatology as well. One of these is postpartum
depression. Not every patient who has this appears
depressed. They can complain of poor appetite and
some of the vegetative symptoms of depression more
than the psychiatric symptoms; it’s something that I
would think about in a patient who may be losing
weight, can’t eat, has fatigue, and complains of inabil-
ity to do simple tasks, such as housework or caring
for a new baby. Another is metabolic failure. We’ve
all seen patients who appear to be stable, but gradu-
ally develop symptoms that don’t fi t any single disease
complex. Whenever I hear symptoms from a patient
that I can’t add together, one of the entities that enters
my mind is metabolic disease, such as adrenal failure,
such as diabetes or thyroid failure, and I think that
these also can be triggered by pregnancy. Having said
that, let’s move down the path of cardiomyopathy.
What kind of workup is going to help us to confi rm
or reject that diagnosis?
SG: There are a number of things that we do routinely
on many patients in the ED that may be reasonable
in this case, such as an EKG looking for ventricular
hypertrophy and conduction disease, and a chest
X-ray study. Although you may not see overt signs of
CARDIOMYOPATHY
261
complaints to be found on their presentation in the
ED. So if this 35-year-old woman presents with short-
ness of breath, lower extremity swelling, and increased
fl uid on examination or chest X-ray study, it would be
appropriate to give this patient a diuretic to try to
achieve a diuresis. Diuretics would be an appropri-
ate therapy in both the pre-partum and postpartum
patient.
PR: We don’t need to be concerned about the fetus in
this patient, because she has delivered. Is there a role
for beta-blockade?
SG: In the acute setting, I would not use beta-blockers
in this patient. Beta-blockers should not be used in a
patient who is currently in congestive heart failure,
even if that patient presents in rapid atrial fi brillation.
Instead, if the patient remains with a rapid ventricu-
lar response, despite diuresis, I would use a calcium
channel blocker for rate control. In the long term she
may benefi t from beta-blockade therapy for conges-
tive heart failure, but not in the acute setting.
PR: What about afterload reduction? What would
you use for that?
SG: I would stay away from angiotensin-converting
enzyme inhibitors (ACE) inhibitors and angiotensin
II receptor blockers in the prepartum patient as they
are contraindicated any time in pregnancy due to the
high risk of adverse fetal effects. Nitrates, however,
reduce both preload and afterload, and are consid-
ered safe. Given that this patient has already deliv-
ered, you might want to use an ACE inhibitor as well.
I don’t think that this case mentioned whether this
patient was breastfeeding, but ACE inhibitors, or at
least captopril, are not recommended by the manufac-
turer while nursing because it crosses into the moth-
er’s milk; the data is less clear with lisinopril. Given
that, I would also stay away from ACE inhibitors if
the mother were nursing.
PR: Given her current congestive failure, she’s likely
going to have to come up with a substitute feeding
pattern for her child anyway, so maybe that’s a deci-
sion that can be predicated on how she appears clini-
cally, and whether or not she needs to be admitted.
I’m not sure that we would want to put her child into
the hospital as well if we could avoid it. The long-term
prognosis for postpartum cardiomyopathy seems to
be biphasic, with a rather high initial mortality rate,
symptoms that look unchanged over the course of the
week or longer? Were it to be the latter, I would be
less concerned that the patient needs an emergent hos-
pitalization. That would not preclude a need for an
evaluation in an expeditious fashion, but the patient
may not need it in the hospital. However, I think that
your concerns are well-founded in that some of these
patients, despite looking well and having had rela-
tively slow onset symptoms, can develop acute wors-
ening fairly rapidly, and, more often than we’d like,
end up with a poor outcome.
PR: It’s always hard to take a new mother away from
her infant, and I think that some of our admission
decisions are distorted by the reality that we want to
preserve the mother’s ability to care for her baby. Yet
this is one instance in which you need to unhesitat-
ingly call for admission once you think that you are
dealing with a cardiomyopathy.
Could you quickly review for us the cardiomyo-
pathies, and how we decide which one is which, and
what are the concerns we need to focus upon for the
individual entities?
SG: There are a number of classifi cations of cardio-
myopathies; one of the more common classifi cations
divides the cardiomyopathies into “dilatated” and
“restrictive” cardiomyopathies. The dilatated cardio-
myopathies include ischemic cardiomyopathy, valvu-
lar cardiomyopathy, viral cardiomyopathy, which you
alluded to as a possible etiology within our postpartum
and peripartum patients, and then there are genetic
cardiomyopathies. The restrictive cardiomyopathies
include infi ltrative diseases like amyloid and sarcoido-
sis, and noninfi ltrative such as idiopathic hypertrophic
subaortic stenosis or hypertrophic cardiomyopathy,
and the more obscure storage diseases like hemochro-
matosis and Fabry’s disease.
PR: What are some of the early therapeutic concerns
that we should be thinking about and undertaking in
the ED?
SG: You may differentiate somewhat between the
pregnant patient with peripartum cardiomyopathy
and the postpartum patient, as once you’ve delivered
the baby, you may not need to worry about the fetal
effects of your medication. In all patients, we should
be able administer some of the standard medications
used for any other patient presenting with congestive
heart failure, which would be the most likely set of
CHAPTER 18
262
onboard to achieve any effect, and on average, it will
take much longer. In addition, digoxin isn’t particu-
larly effective in patients who have increased sympa-
thetic tone, which is true of most patients we see in
the ED. With this in mind, I would say there is no
need to start digoxin in the ED; rather, I would start
it after the patient is admitted to a hospital bed, and
had a chance to quiet down. You may then see some
benefi t in the long term.
PR: I take it from your comments that this kind of
patient would not be a good candidate for an emergency
observation unit or chest pain center holding unit.
SG: I would agree with that. Generally, the role of
observation units should be limited to patients who
you think will be able to have a very rapid turn-
around, with a likelihood of 85% or better that they
will be adequately improved enough to be discharged
within 24 hours. I don’t think it that likely that 85%
of the time a patient like this will be ready for dis-
charge within 24 hours.
PR: Are there any dysrhythmias that this condition
induces that we need to be alert for, or are there any
drugs that we could commence that would lower their
likelihood of onset?
SG: I believe these patients are like any patients with
cardiomyopathy. They are at a higher risk for having
both atrial and ventricular dysrhythmias. However, I
don’t know of any data that has shown that prophy-
lactic medications for dysrhythmias are useful. The
data from the CASS study in the 1970s, where they
tried suppressing ventricular dysrhythmias during
myocardial infarctions, found that rather than help
people, it increased mortality. With this study, the use
of prophylactic dysrhythmics fell by the wayside.
PR: How about intubation? Are these patients likely
to require it, and if so, is it prudent to undertake that
in the ED, where we are used to emergency airway
management, rather than letting the patient get up to
a unit where they have to call for help from the anes-
thesiology service?
SG: I think that again depends on the individual patient,
and the clinical appearance in the ED. A patient who
is in respiratory distress should be intubated in the
ED, because we are the experts in emergency intuba-
tion. However, a patient who presents, such as the
one in this case, with a satisfactory respiratory status
but with the majority recovering almost completely.
I don’t know that we can determine which direction
this patient will take in the ED, but clearly it’s a sig-
nifi cant disease that we need to take very seriously. As
emergency physicians, we may be inclined to do less
since we don’t see this frequently, and thus may not
realize how rapidly these patients can deteriorate. This
patient doesn’t sound like she’s particularly sick given
this presentation. Would you admit this patient?
SG: I probably would admit her for a number of rea-
sons. First, although the mother doesn’t want to be
taken away from her child, sometimes the only way
to really treat the mother is by arranging for some-
one else to care for the child. This may be the only
way to get a patient to be compliant, and to obtain
the appropriate workup. In addition, this patient also
has a number of symptoms that have been worsening
over the course of the prior day, although she has had
several weeks of symptoms. Lastly, she’s not able to
function with the daily tasks of living, such as taking
care of her newborn, which amplifi es her daily tasks
enormously. Hopefully by admitting her we would
enable the workup to take place in a more expeditious
fashion, and get her on the road to recovery quickly.
PR: If the patient were still pregnant, presenting dur-
ing the third trimester of her pregnancy, then clearly
she would need to be admitted to the obstetrics ser-
vice. Is there any value to the early delivery of these
patients?
SG: Many of the patients seem to go to caesarean
section for other reasons, but I don’t believe there is
clear data to suggest emergent delivery as therapeutic
for this maternal disease. Perhaps this lack of data is
because this cardiomyopathy is found more often in
the postpartum patient.
PR: Other than trying to unload the heart, is there a role
for early digitalization of these patients in the ED?
SG: I believe digoxin, in general, doesn’t really have a
role in the ED. Basically this goes back to the defi nition
of what we term an emergency department. Starting
any medication in which you can’t see the effect in the
ED is hard to justify. That said, we give antibiotics for
a wide variety of infections, and we don’t see the ben-
efi t. The problem is that digoxin takes many hours in
order to produce a benefi t. At a minimum, it will take
2–3 hours to have an adequate amount of medication
CARDIOMYOPATHY
263
as she does not have concomitant sepsis or renal fail-
ure, and so I don’t see what should preclude one from
ordering it.
PR: How do you feel about doing a CT scan on this
patient as opposed to just a simple chest X-ray study?
SG: It depends on what you are looking for. If you
are looking for a cardiomyopathy, then the study of
choice is an echocardiogram. If you are looking for
a pulmonary embolus, then a CT scan would be a
better choice. I think that this is where you might go
back to our earlier question and say, well, what test
does this patient actually need in the ED? We talked
about whether the patient actually needed an emer-
gent echocardiogram; if that echocardiogram is going
to preclude the patient from going for a CT scan, and
she is still pregnant, then it might be very useful to get
that echocardiogram emergently. I may not need to
know whether this is a cardiomyopathy defi nitively in
the ED just to treat the patient, but it would be use-
ful to know if this is truly a cardiomyopathy to avoid
doing a potentially dangerous test on this patient and
exposing a fetus to CT scan radiation. In our patient,
as she is postpartum, if you had a reasonable concern
that this is a pulmonary embolus and not a cardio-
myopathy, then a CT scan would be a reasonable test
to do. Given her presentation, pulmonary embolus is
lower down on my differential diagnosis tree, and I
probably wouldn’t pursue a CT scan on this patient.
PR: I’m not sure that I would have diagnosed her
immediately with a cardiomyopathy, and I suspect
that I would have initially obtained a CT scan look-
ing for a pulmonary embolus.
Case resolution
The patient was admitted to the obstetrics service for
monitoring and workup. The patient also underwent
a CT angiogram of the chest to evaluate for pulmo-
nary embolism, which was negative for clot, but did
show pulmonary edema and vascular congestion.
An echocardiogram was obtained, and showed nor-
mal valve structure and function. Nevertheless, mild
diastolic dysfunction was noted as well as slight left
ventricular enlargement. The ejection fraction was
measured at 55%. The patient was started on furo-
semide for a short course of diuresis, and on an ACE
inhibitor that was continued as an outpatient. The
probably shouldn’t require intubation, hopefully at
all, during the hospitalization. Although, unfortu-
nately, there is no good way to predict which patient
is going to end up deteriorating unless she has already
begun to deteriorate while in the ED.
PR: What kind of bed would you want to request for
this patient? Can they go to a step-down unit or can
they go to a regular fl oor bed?
SG: I think that is a very good question, because part
of that depends on whose service this patient should
go to. Obstetricians have much expertise in dealing
with obstetrical patients and many of the complica-
tions of postpartum, but on the other hand, obste-
tricians are not cardiologists and don’t deal regularly
with cardiomyopathies, and therefore depending on
the institution that you’re in, the patient might go to
either service. The fi rst thing that you need to weigh
is the comfort of the physician taking care of the
patient. In my mind, I think that a cardiology service
might be the most appropriate service to take care of
this patient regardless of whether she is pregnant or
not, with obstetrics consulting particularly for the
peripartum issues or the postpartum issues. I know
that in many institutions, obstetrics cannot admit to
a step-down or intensive care unit whatsoever, so that
may easily take them out of the loop in that scenario.
My preference in this patient would be to admit her
to a cardiology fl oor, probably one such as a step-
down unit or at least dedicated to cardiology patients,
where they can get the expertise of both nursing and
physicians, in dealing with the most pressing issue for
this patient.
PR: I would guess that if the patient was still preg-
nant, she would be admitted to an obstetric service
during the third trimester with a cardiac consult, but
postpartum, I would not see a need for admission to
the obstetric service. As it turns out, this patient was
admitted without much of a workup.
Is this a place where BNP can play a useful role?
SG: That’s a good question. I am unaware of any
studies looking at BNP in postpartum cardiomyopa-
thy patients. In general, if a patient has a markedly
elevated BNP, not 500, but in the thousands, it is very
likely that that patient is volume overloaded. This
should help solidify a diagnosis of cardiomyopathy. I
can’t think of a good reason why BNP would not be
useful in this particular patient population, as long
CHAPTER 18
264
recent viral illness, use of certain medications, preg-
nancy, exposures either environmental or self-infl icted
(alcohol or cocaine), or chronic medical problems
can help with identifying the underlying cause of the
patient’s symptoms. Syncope can be the only present-
ing symptom of a cardiomyopathy, which can be omi-
nous and requires further workup.
The physical examination should focus on the
cardiovascular and pulmonary systems; however,
vigilance for extracardiac abnormalities may help to
discover the underlying cause. Key cardiovascular
fi ndings include distant heart sounds, jugular venous
distention, S3 gallop, enlargement of the liver, or pres-
ence of a hepatojugular refl ux. Peripheral edema is
likely to be present as well. No change in blood pres-
sure as in pulsus paradoxus occurs with the restrictive
forms of the disease. Other symptoms that may be
identifi ed include a goiter or proptosis and exopthal-
mos indicating thyrotoxicosis. Skin changes, such as
increased pigmentation, can help to identify underly-
ing illnesses such as hemochromatosis.
Etiologies of cardiomyopathy
There are numerous causes of cardiomyopathy, rang-
ing from genetic and exposure to infectious and auto-
immune.
3,4
(Table 18-1)
Testing in cardiomyopathy
Initial testing for all patients in which cardiomyopathy
is part of the differential diagnosis list should include a
chest X-ray study and an EKG. Atrial fi brillation or left
ventricular hypertrophy may be the only fi ndings on
the initial EKG. A chest X-ray study is helpful in two
ways. First, it can help to identify cardiomegaly or an
enlarged cardiac silhouette. Second, it can help to reveal
fl uid overload and venous congestion. Radiologic fi nd-
ings of fl uid overload include pleural effusions, Kerley B
lines, interstitial edema, and cephalization of vessels.
5
Laboratory data can be helpful in the workup of car-
diomyopathy as well. Cardiac markers are helpful in
differentiating between ischemic disease and cardiomy-
opathy. However, a grossly elevated troponin may be
evidence for a more severe case and increased mortality.
2
Other helpful laboratory data include a beta-naturetic
peptide that may indicate fl uid overload.
6
Thyroid func-
tion tests, drug screens, and pregnancy testing may help
to indentify more rare causes of the disease as well.
patient remained in the hospital for 3 days and left
after an uneventful course.
Section III: Concepts
Background
Cardiomyopathy is a disease of heart muscle, impor-
tant because it can lead to heart failure, dysrhythmia,
or even death. It is unusual for a cardiomyopathy to
present initially to the ED; it is more likely to be iden-
tifi ed on a routine health check up. However, recogni-
tion of certain characteristics of the illness assists in
making the correct diagnosis, regardless of the locale
of presentation.
Cardiomyopathy is an umbrella term that covers a
number of cardiac diseases. There are three traditional
categories of cardiomyopathy: dilatated, hypertrophic
and restrictive, with dilatated and hypertrophic cardio-
myopathies occurring more frequently than the restric-
tive forms.
1
Determining the underlying cause of the
cardiomyopathy is heavily dependent on the history of
the patient, including the progression of the symptoms,
past medical history, and physical examination fi ndings.
Asking key questions can direct the physician to the eti-
ology of the disease. Appropriate laboratory data and
imaging studies further aid in the ultimate diagnosis.
Initial cardiomyopathy workup: history and physical
The initial workup, as with all ED patients, begins
with obtaining vital signs, identifying patients in
extremis, and initiating immediate resuscitation of the
unstable patient. Patients may present with tachycar-
dia or hypotension, and the administration of intra-
venous fl uids may be enough to stabilize the patient
while more information is collected.
The history of a patient presenting with cardiomyo-
pathy often overlaps with other illnesses, but atten-
tion to detail allows the physician to make the right
diagnosis. Symptoms of the disease include fatigue,
dyspnea (made worse with exertion), orthopnea,
increased edema, ascites, and weight gain. Angina is
an uncommon symptom, but should angina be a part
of the chief complaint, an EKG should be done imme-
diately to rule out other life-threatening diseases such
as a myocardial infarction.
2
The past medical history can be helpful in the
workup of cardiomyopathy. Obtaining a history of a