Reversible “cardiomyopathy” after accidental adrenaline overdose

other adverseeffects include gastro intestinal (gingivitis, stomatitis, excessive salivation, vomiting, diarrhea) and renal impairment. The toxic effects reflect the slow oxida tion of metallic mercury to the soluble mercuric ion, which interacts with protein sulfhydryl groups and interferes with cellular enzyme ac tion. Oxidation of metallic mercury to the toxic ion is slow (in contrast to chronic inhalation); this may account for the rarity with which mercuri-

alism is seen. With time, however, continued absorption occurs, documented by decreasing radiographic evidence of mercury over the years following intravenousinjection.6,7Intermittent or long-term drug therapy with penicillamine or dimercaprol should therefore be considered. 1. Giombetti JR, Rosen DH, Kuczmierczyk AR, Marsh DO. Repeatedsuicide attempts by the intravenousinjection of elementalmercury.In? J Psychiutry h4ed 1988;18:153-167. 2 Celli B, Khan MA. Mercury embolization of the

Reversible Wardiomyopathy” After Accidental Adrenaline Overdose

lung. N Engl J Med 1976;295:883-885. 3. Burton EM, Weaver DL. Repeatedsystemicmercury embolization. South Med J 1988;81:11901192. 4. Vas W, Tuttle RJ, Zylak CJ. Intravenous selfadministration of metallic mercury. Radiology 1980;

137:313-315. 5. Oliver RM, ThomasMR. Cornaby AJ, Neville E. Mercury pulmonary emboli following intravenous self-injection. Br J Dis Chest 1987;81:76-79. 6. Walter E. [Long-term observation of a case of intravenousinjection of elemental mercuryl. Radiologe 1986;26:&46.

7. Gulden JW, Christ F, Hauser E, Kramer HJ. [Circulatory distribution of intravenously injected metallic mercury]. Rontgenblatter 1987;40401405.

withdrawn, while noradrenaline and phentolamine infusions and intraaortic balloon pump support were instituted. On this regimen her systemic vascular resistance stabilized at 1,I 00 to 1,500dynes-s-cm-5with a cardiac index of I .9 to 2.8 liters/min/ m2. Mild metabolic acidosis was seenwithin thefirst 24 hours with 17 mmol of bicarbonate and creatine kinase increasedto 615 U/liter (normal
Al&air I. Fvfe. MBBS, Paul A. Daly, MD, Paul Dorian, MD, and Judith-Tough, MD

Hg systolic after a peak of 152/l 10 mm Hg. Over the following 4 to 6 hours, hypotension progressed and report a case of severe ventricular she was treated with intravenous sadysfunction due to inadvertent ad- line solution and dopamine. A pulministration of a large doseof adren- monary artey catheter was inserted; aline with subsequentnear complete the initial cardiac index was 1.8 lirecovery of ventricular function. ters/min/m2, and systemic vascular A previously healthy 30-year-old resistance 2,100 dynes-s-em-5.Niwoman was admittedfor conebiopsy troprusside was temporarily added. of the cervix. After intravenous in- The electrocardiogramshowedsinus duction, anesthesia was maintained tachycardia, incomplete right bunwith isoflurane, nitrous oxide and dle branch block and left anterior oxygen through a face mask. Cervi- hemiblock. Echocardiography cal injection of what was thought to showedsevereglobal left ventricular be 2% lidocaine was undertaken af- dysfunction with normal ventricular ter confirming that the needle was size. Moderate hypokinesia of the not intravenous. Ventricular prema- right ventricle was seen.The patient ture complexes were immediately became increasingly hypotensive noted, followed by bigeminy and with arterial blood pressuresas low sustained ventricular tachycardia. as 55125mm Hg; nitroprusside was She was given 100%oxygen and lidocaine; the rhythm reverted to sinus tachycardia. Pulmonary edemarapTABLE I Adrenaline Overdose-Cardiovascular Hemodynamic Support idly ensued requiring intubation. It was subsequently noted that the DAY HR BP SVR Cl IABP DA drug injected was l:l,OOO epineph1 130 78/44 2,100 1.8 0 + rine, to a total dose of 7 mg. Blood 1 140 78/58 1,300 2.4 + -Ipressure decreasedto 80 to 120 mm 2 125 78/60 1,400 2.1 + + ardiotoxic effectsof excesscatecholamines have been docuC mented since their discovery.’ We

From the Division of Cardiology, Department of Medicine and Department of Anesthesia, The Toronto Hospital, 200 Elizabeth Street, 13 Eaton North 224, University of Toronto, Toronto, Ontario, Canada MSG 2C4. Manuscript received April 23, 1990, revised manuscript received September 4, 1990, and accepted September 6.

318

3 4 5 6 7 8

120 105

84/56 76/52

100

84/46

89 98 80

KM/54 110/64 112/66

Status and NA

P

EF(%)

0 0

0 +

<20 <20

+

+

1,200

2.5

+

+

+

+

l.ooO 1,coo

2.7 3.1

+ +

+ +

0 0

0 0

20-39

900 750

3.4 4.6 -

0 0 0

0 0 0

0 0 0

0 0 0

-59

-

All values are average for 24 hours. BP = bleed pressure (mm Hg); Cl - cardiacindex (liters/min/mz); DA = dopamine; EF = ejection fraction (echocardiogram); HR = heart rate (beats/mink IABP = intraaortic balloon pump; NA - noradrenaln?; P = phentolamme; SVR = systemic vascular resistance (dynerrcm-5).

THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 67

left ventricular size. On day 6 the intraaortic balloon pump and dopamine were withdrawn and she was extubated. A repeat echocardiogram on day 10 showed that global left ventricularjiinction had improved to normal. A blood pool scan performed at rest before discharge on day 23 showed an ejection fraction of 49%. She is asymptomatic 1 year later. Table I summarizes the cardiovascular status and hemodynamic support used during the ftrst 9 days in the hospital.

Catecholamines are known to causea wide spectrum of cardiotoxicity.’ Animal studies have shown myocardial depressanteffects of an oxidant product of epinephrine, which causesdose and time-dependent irreversible mitochondrial and myocardial damage.2Dysfunction is initially functional becauseof adrenergic receptor-mediatedcalcium influx, which may causemyocardial injury alone or in concert with coronary vasoconstriction. Endogenous overproduction of catecholamines can cause cardiac abnormalities in patients with pheochromocytoma,a cardiomyopathy, and histologic ab-

normalities have been documented. This dysfunction is reversible with medical or surgical management of the underlying tumor.3 Patients with subarachnoid hemorrhage develop focal or diffuse left ventricular dysfunction? presumably related to the massivesympathetic discharge associated with brain injury, becausethe dysfunction is attenuated by (Yand /3 blockade5and surgical sympathectomy.6 These abnormalities are also transient in nature with completerecovery documen&14 This report is the first recorded caseof the nearly fatal consequencesof inadvertent administration of a very large dose of epinephrine, with the subsequentdevelopmentof a severecatecholamineinduced “cardiomyopathy.” Paradoxically, after the initial phase of massive catecholamine excess, this patient required exogenouscatecholamines to support the injured, dysfunctional myocardium and maintain adequate perfusion pressure to vital organs.This caseillustrates the need for aggressivesupport of patients receiving overdoses of catecholamines, with the expectation that, while cardiac function may be

extremely impaired early in the courseof the illness,recoveryis virtually complete over time. Addendum: Since preparation of this manuscript for publication, we have treated a similar caseof a 21year-old woman who received 3 mg of adrenaline intravenously for the treatment of anaphylaxis. Myocardial dysfunction persistedfor 36 hours before resolving completely.

1. Rona G. Catccholamine cardiotoxicity. J Mel Cell Cardiol 1985;17:291-306.

2. Yates JC, BeamishRE, Dhalla NS. Ventricular dysfunction and necrosisproducedby adrenochrome metaboliteof epinephrine:relation to pathogenesisof catecholaminecardiomyopathy. Am Heorf J 1981; 102:210-221. 3. Sadowski D, Cujec B, McMeekin JD, Wilson TW. Reversibility of catecholamineinducedcardiomyopathy in a woman with pheochromocytoma.Can Med Assoc J 1989;141:923-924.

4. Pollick C, Cujec B. Parker S, Tator C. Left ventricular wall motion abnormalities in subarachnoid hemorrhage:an echocardiographicstudy. J Am Co/l Cardiol 1988;12:600-605. 9. Neil-Dwyer G, Walter P, Cruickshank JM, Doshi B, O’Gorman P. Effect of propranolol and phentolamine on myocardial necrosis after subarachnoid hemorrhage.Br Med J 1978;2:990-992. 6. Novitsky D, Wicomb WN, Cooper DKC, Rose AG, Reichart B. Prevention of myocardial injury during brain death bv total cardiac svmoathectomv 1986;4(: in thechacma baboon. Ann Thorac’S& 520-524.

Persistent Left Fifth Aortic Arch with Complex Coarctation

the right arm, but diminished in the left arm and lower extremities. Heart sounds were normal. An ejecCandace L. Gibbin, MD, Frank M. Midgley, MD, Barry M. Potter, MD, tion sound and 216 systolic ejection murmur were heard at the right upand Gerard R. Martin, MD per sternal border. Echocardiograersistent fifth aortic arch is a noted to have an innocent murmur phy showed a bicommissural aortic rare anomaly, with only 22 cases and normal pulses in the legs and valve without significant stenosis or reported.lv2Its recognition and suc- arms. An electrocardiogram showed insufficiency and a coarctation of the aorta. There was aneurysmal dicessfulmanagementwhen associated findings of Wolf-Parkinson-White with coarctation is even rarer. We syndrome. At 3.5 years, echocardi- latation of the left subclavian artery. Cardiac catheterization showed a present a child with persistent left ography showed normal intracardififth aortic arch and complex coarc- ac structure and ‘buckling” of the 15mm Hg pressure difference betation successfullydiagnosedand re- aorta. At 4.5 years, a discrepancy tween the ascending and descending was noted between the upper and aorta. Ascending aortic angiography paired. lower extremity pulses. A magnetic showed a competent, bicommissural A 6-year-old girl was referredfor aortic valve and a normal ascending evaluation of pseudocoarctation of resonance imaging study was interthe aorta. At 2 years old, she was preted as showing tortuosity and aorta that gave rise to 2 anterior, elongation of the aortic arch between left-sided transverse arches. The C7 and TI and narrowing of the de- fourth aortic arch gave rise to an inFrom the Departments of Pediatrics, Cardiolscendingportion of the thoracic aor- nominate, left carotid and dilated ogy, Radiology and Cardiovascular Surgery, left subclavian artery. The fourth George Washington University School of ta at T4. Medicine, Washington, D.C., and the ChilAt presentation, she was asymp- arch joined the descending aorta at dren’s National Medical Center, 111 Michitomatic. Blood pressure was 122176 the junction of the more caudalfifth nan Avenue. N.W.. Washington. D.C. 20010. mm Hg in the right arm, I1 O/88 mm aortic arch and the descending aorta. kanuscript received Augusi22, ‘1990;revised Hg in the left arm and 90160 mm Hg Coarctations of the aorta were noted manuscript received and acceptedSeptember 25, 1990. in the left leg. Pulses were normal in just distal to the junction of the

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