Tricyclic Overdose Causing Sustained Monomorphic Ventricular Tachycardia Robert W. Peters, MD, Gregory A. Buser, MD, Hyun Joe Kim, MD, and Michael R. Gold, MD, PhD esipramine belongsto a group of psychotropic compounds called D tricyclic antidepressants that have similar chemical structures and share a variety of pharmacologic actions. They tend to be lipophilic and are found in high concentrations in the myocardium of treated patients.’ Actions responsible for most of their cardiovascular effects include anticholinergic properties, an ability to block norepinephrine reuptake and a type 1 antiarrhythmic action.‘p2 A variety of cardiac dysrhythmias have beenassociatedwith tricyclic antidepressant usage and especially with overdosage. Sustained ventricular arrhythmias are an uncommon complication of nonfatal tricyclic antidepressant overdose4and usually conFrom the Department of Medicine, Division of Cardiology of the Department of VeteransAffairs Medical Center, 3900 L.ochRaven Boulevard, and the University of Maryland, Baltimore, Maryland 21218. Manuscript received March 30, 1992;revised manuscript received and acceptedJune 3, 1992.

1226

sist of polymorphous ventricular tachycardia (or ventricular fibrillation). In the present report, we describe a young personwithout apparent organic heart diseasewho ingested a large amount of desipramine and who presented with sustained monomorphic ventricular tachycardia which persisted over a 3-day period. A 31-year-old man with a history of depression was admitted to another hospital after ingestion of an unknown amount of desipramine. On admission, he was somnolent and mildly tachypneic. Blood pressure was 100/60 mm Hg and heart rate 160 beatslmin. Electrocardiogram (Figure 1) revealed a regular rhythm at a rate of 168 beatslmin with no discernible P waves and a wide QRS complex with a right bundle branch block configuration. Initial therapy consisted of oral charcoal, milk of magnesia,intravenous furosemide and infusion of intravenous fluids containing bicarbonate.

THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 70

NOVEMBER 1, 1992

Laboratory studies were normal except for a serum desipramine concentration of 777 ngjml (therapeutic range = 75 to 300). The patient was transferred to the Baltimore VeteransAdministration Medical Center 24 hours after his overdose. At that time, blood pressure was 100160mm Hg. Electrocardiogram showed a heart rate of 180 beats/min with a right bundle branch block morphology identical to that seen earlier. Carotid sinus massagehad no effect on the cardiac rhythm, nor did a 1 mg of intravenous metoprolol although marked hypotension resulted. A Swan-Ganz catheter revealed a pulmonary capillary wedgepressureof 12 to 15 mm Hg. It was considered that the rhythm wassupraventricular (possibly sinus) tachycardia with aberrant conduction. Becausethe patient was stable, it was decided that further observation, without specific intervention, was indicated until more of the drug had beenmetabolized and excreted. The heart rate continued to increase, however, and was accompanied by signsand symptomsof hypoperfusion. He was taken to the electrophysiology laboratory where intracardiac recordings revealed atrioventricular dissociation with a

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CASE REPORTS 1227

ventricular cycle length of 270 ms and an atria1 cycle length of 630 ms (Figure 2, top). Ventricular overdrive burst pacing resulted initially in entrainment and finally in termination of the tachycardia (Figure 2, bottom). After conversionto normal sinus rhythm, a 12-lead electrocardiogram revealed T-wave inversion that gradually normalized over the next few days. Serial cardiac enzymes were not elevated. Two-dimensional echocardiography and radionuclide ventriculogram showed normal morphology and left ventricular function. Becauseof the lack of evidenceof organic heart disease,no attempt was made to reproduce the arrhythmia in the electrophysiology laboratory. The remainder of his

convalescencewas uneventful and the patient was discharged several days later. We are not aware of previous reports of sustainedmonomorphicventricular tachycardia occurring as a complication of tricyclic antidepressant overdose.The lack of underlying heart diseaseand the extendedduration of the dysrhythmia (>72 hours) led us to believethat we were dealing with a supraventricular mechanism. The reason for the gradual increase in tachycardia rate from 168 to 230 beats/min is not apparent but may be related to an increasein catecholamines associatedwith systemic hypoperfusion. In conclusion,our experiencesuggests that sustained ventricular

tachycardia should be consideredin the differential diagnosis of a wide QI2S complex tachycardia in the setting of tricyclic antidepressantoverdose.Wide QRS tachycardia in this clinical setting should be promptly investigatedwith intracardiac or esophageal recordings. 1. Marshall JB, Forker AD. Cardiovascular effects of tricyclic antidepressantdrugs: therapeutic usage, overdose and managementof complications. Am Heart J 1982;103:401-414. 2. Burckhardt D, Raeder E, Muller V, Lmhof P, Preabanner H. Cardiovascular effects of tricyclic and t&acyclic antidepressants.JAMA 1978;239: 213-216. 3. Groleau G, Jotte R, Barish R. The ekxtrwardiographic manifestationsof cyclic antidepressanttherapy and overdose:a review. J Emerg Med 1990;8: 591-605. 4. Langou RA, Van Dyke CV, Tahan SR, Cohen

LS. Cardiovascular manifestationsof tricyclic antidepressantoverdose.Am Hear? J 1980;100:458-464.

Myocardial Respiratory Chain Enzyme Activities in Anomalous Origin of the Left Main Coronary Artery from the Pulmonary Trunk (Bland-White-Garland Syndrome) and Comparison with Atherosclerotic Coronary Artery Disease

the anomalousorigin of the left main coronary artery from the pulmonary trunk is gradual in onsetowing to the high pulmonary artery pressurethat limits blood flow through the anomalous left coronary artery in the postnatal period. Survival to adulthood dependson the development of colIris Maurer, MD, and Stephan Zierz, MD lateral circulation from the right coronary or may eventually be related to 0th anomalous origin of the left a marked right coronary artery domFrom the Department of CardiovascularSurmain coronary artery from the inance.* In contrast to atherosclerotgery, University of Kiel, Kiel; and the Neuromuscular Laboratory, Department of Neurol- pulmonary trunk and atherosclerotic ic coronary artery disease,left venogy, University of Bonn, Sigmund-Freud- coronary artery disease are condi- tricular ejection fraction is only modStrasse 25, 5300 Bonn 1, Germany. Manuscript received April 1, 1992; revised tions associatedwith myocardial is- erately depressedor normal in most manuscript received and accepted June 8, chemia. In contrast to atherosclerotic patients with anomalousorigin of the coronary artery disease,ischemia in left main coronary artery from the 1992.

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TABLE I individual Hemodynamic Data of the Patient with Anomalous Origin of the Left Main Coronary Artery from the Pulmonary Trunk and of Seven Patients with Atherosclerotic Coronary Artery Disease Atherosclerotic LMCA from PT Pressures (mm Hg) Left ventricle (s/d) Aorta (s/d) Right ventricle (s/d) Pulmonary artery (s/d) Pulmonary artery wedge pressure (mean) Cardiac output (liters/min) Cardiac index (liters/min/m2) Heart rate (beatslmin) Left ventricular end-diastolic volume index (ml/m2) End-systolic volume index (ml/m2) Ejection fraction (%) Oxygen saturation (%I Aorta Pulmonary artery LMCA = left main coronayartery:

1228

PT = pulmonary

Coronary Artery Disease

Pt. 1

Pt. 2

Pt. 3

Pt. 4

1 lo/25 105/50 3017 30/15 12

95/20 92162 2817 24115 12

92122 86158 2719 28117 17

96127 96/70 2214 25116 12

104133 104187 2717

5.6 2.9

3.9

3.1

4.6

1.9

1.6

2.1

102

89

Pt. 5

Pt. 6

Pt. 7

108119

140/10

141/23

17

110184 3219 40 27

140/90 2812 28112 12

135491 2919 30/21 16

2.6 1.2 106 220

2.8 1.4 94 174

4.2 2.2 9% 182

3.6 1.8 168

29117

100

106

76 141

169

90 139

48 53

112 20

145 15

90 35

177 20

124 32

80 25

98 30

96 77

98 64

91 55

98 61

97 68

96 62

99 66

98 63

trunk; s/d = systolic/diastolic.

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Tricyclic overdose causing sustained monomorphic ventricular tachycardia.

Tricyclic Overdose Causing Sustained Monomorphic Ventricular Tachycardia Robert W. Peters, MD, Gregory A. Buser, MD, Hyun Joe Kim, MD, and Michael R...
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