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Cardiac conduction and rhythm disturbances following suicidal ingestion of mesoridazine
CASE REPORT
Cardiac Conduction and Rhythm Disturbances Following Suicidal Ingestion of Mesoridazine James T. Niemann, MD* J. Stephan Stapczynski, MD* Robert J. Rothstein, MD* Michael M. Laks, MD t Los Angeles, California
The phenothiazine derivatives, particularly chlorpromazine and thioridazine, are known to produce significant electrocardiographic abnormalities. Until now, documented life-threatening arrhythmias have not been reported following large doses of mesoridazine, the besylate salt of a metabolite of thioridazine and a relatively recent addition to the phenothiazine group. We describe such a case in which alterations in both impulse conduction (first-degree atrioventricular block, prolonged QRS duration, and right axis deviation) and impulse formation (supraventricular and ventricular tachycardia) were noted following a suicidal ingestion of mesoridazine. The electrophysiologic mechanisms underlying phenothiazine-induced arrhythmogenesis are reviewed. Niemann JT, Stapczynski JS, Rothstein RJ, Laks MM: Cardiac conduction and rhythm disturbances following suicidal ingestion of mesoridazine. Ann Emerg Med 10:585-588, November 1981.
arrhythmias; drug-induced cardiotoxicity; phenothiazines INTRODUCTION Clinical cardiac toxicity related to phenothiazine use, whether in accidental overdose or following suicidal ingestions, remains a significant and, perhaps, frequently unrecognized and underrated problem. Abnormal electrocardiograms (ECG) and sudden death of patients receiving standard, therapeutic doses of phenothiazines have been previously reported. 1 The incidence of sudden death in this group of patients remains to be determined, and an association between the electrocardiographic findings and sudden death of presumed cardiac origin also remains to be established. 2 Suicides with phenothiazines, particularly chlorpromazine and thioridazine, have also been reported, with death being ascribed in many instances to a lethal arrhythmia despite minimal documenration? Experimental studies using isolated perfused rat hearts have demonstrated variable potency among the phenothiazine derivatives with respect to alterations in coronary blood flow and prolongation of the QT interval and QRS duration. 4 The phenothiazine most frequently responsible for clinical cardiac complications has been thioridazine. From the Departments of Emergency Medicine* and Medicine, Division of Cardiology,t Los Angeles County Harbor-UCLA Medical Center, Torrance; and the UCLA School of Medicine, Los Angeles, California, Address for reprints: James T Niemann, MD, Director, Acute Adult Care, Department of Emergency Medicine, Los Angeles County Harbor-UCLA Medical Center, 1000 West Carson Street, Torrance, California 90509.
10:11 November) 1981
Ann Emerg Med
585/61
Mesoridazine is the besylate salt of a metabolite of thioridazine and, in therapeutic doses, produces ECG effects similar to those described in patients taking thioridazine, ie, alterations in T wave, amplitude and polarity. 5 Despite the obvious similarity in structure and implied (but as yet undocumented) similarity in c a r d i a c e l e c t r o p h y s i o l o g i c effects, t h e r e has been only one r e p o r t e d death thought to have been of cardiac etiology related to the ingestion of mesoridazine. 6 The purpose of this report is to describe a case of documented meso r i d a z i n e - i n d u c e d d i s t u r b a n c e s in atrioventricular and intraventricular conduction with associated ventricul a r and s u p r a v e n t r i c u l a r a r r h y t h mias.
CASE REPORT A 23-year-old schizophrenic white man was brought to the emergency department one hour after ingesting 6 gm of mesoridazine (Serentil v) concentrate. The p a t i e n t ' s m o t h e r reported that on the day of admission she and her son had become involved in a heated a r g u m e n t , following which the p a t i e n t became irate, broke several household articles, and informed her that he was going to kill himself. He ingested two 4-oz bottles (6 gm) of mesoridazine and refused to accompany his mother to the hospital. One hour later the patient became drowsy and d y s a r t h r i c , and was brought to the emergency department for evaluation. The p a t i e n t ' s h i s t o r y was remarkable for a three-year history of p a r a n o i d s c h i z o p h r e n i a , a b u s e of multiple drugs, and previous hospit a l i z a t i o n s for drug overdoses and psychiatric decompensation. Initial evaluation revealed a regular pulse at 140 beats per minute; blood pressure (supine), 120/70 mm Hg; and respiratory rate, 16/min and regular. The general physical examination was unremartfable except for lethargy, mydriasis, and slurred speech. E m e s i s was induced w i t h syrup of ipecac. Approximately 30 minutes after presentation and 20 m i n u t e s after vomiting, the patient was comatose with shallow respirations. An endotracheal tube was inserted and the patient was connected to a cardiac monitor. The i n i t i a l r h y t h m strip showed broad QRS complexes at a regular rate of 130/min to 140/min. The rhythm was interpreted as ven-
62/586
Fig. 1. Admission 12-lead ECG demonstrating underlying sinus rhythm with 1 ° A - V block (P-R interval 0.30 sec) and markedly prolonged QRS duration. Mean frontal plane QRS axis is directed superiorly and rightward (+ 185°).
Fig. 2. Three-channel rhythm strip (leads I, H, III) obtained on admission shows sinus rhythm with short runs of supraventricular and ventricular (open arrow) tachycardia.
tricular tachycardia and the patient was given 100 mg lidocaine as an int r a v e n o u s bolus w i t h o u t effect on QRS morphology or rate. Electrical cardioversion was attempted. Following countershock, the QRS morphology was considered unchanged but the rate had decreased to 110/min to 120/ min and P waves were seen. A standard 12-lead ECG revealed a sinus r h y t h m with broad QRS complexes and short runs of s u p r a v e n t r i c u l a r and ventricular tachycardia (Figures 1 and 2).
Ann Emerg Med
Admission laboratory data were remarkable only for a serum potassium of 2.9 mEq/L. During controlled v e n t i l a t i o n with 100% oxygen, the a r t e r i a l PO2, PCO2, and pH were 203, 38, and 7.38, respectively. Intravenous potassium replacement was begun. Four hours after admission, the patient's blood pressure fell to 80/60 mm Hg with no change in c a r d i a c r h y t h m or r a t e noted on a r e p e a t ECG. A normal blood p r e s s u r e was r e e s t a b l i s h e d with one liter of normal saline in-
10:11 (November) 1981
fused over one hour. D u r i n g the e n s u i n g 24 hours, the patient's mental status improved and he was extubated the day after admission. Repeat serum potassium obtained 36 hours after admission was n o r m a l . S e r i a l e l e c t r o c a r d i o grams revealed only U waves and T wave c h a n g e s w i t h i n 72 h o u r s of admission (Figure 3). The QRS duration a n d QT i n t e r v a l r e m a i n e d slightly prolonged. A urine specimen obtained on admission was submitted for a qualitative drug screen which is capable of detecting chlorpromazine, thioridazine, and trifluoperazine. A substance was d e t e c t e d which crossreacted in the v a r i o u s a s s a y s b u t could not be definitely identified.
DISCUSSION To our knowledge, t h i s is the first reported case of massive mesoridazine i n g e s t i o n a s s o c i a t e d with documented p o t e n t i a l l y lethal ventricular arrhythmias and conduction d i s t u r b a n c e s . The o n l y o t h e r reported case of massive ingestion in which electrocardiographic findings are alluded to was obtained from a review of coroner's records. 6 In that case, an ECG obtained following a grand m a l s e i z u r e a n d a c a r d i a c a r r e s t is s a i d to h a v e s h o w n an %gonal rhythm." Although a quantitative serum, urine, or tissue level of the drug was not obtained for our patient, the ingestion was witnessed, the amount ingested was known, and 0nly a ~ p h e n o t h i a z i n e - l i k e " compound was noted on urine toxicologic analysis. The patient's intercurrent hypokalemia is thought to have played a facilitating and not a primary role in a r r h y t h m o g e n e s i s , a speculation supported by previous reports of r h y t h m d i s t u r b a n c e s with phenothiazine use. 7 Our p a t i e n t ' s i n i t i a l 12-lead ECG ( F i g u r e 1) a n d 3 - c h a n n e l rhythm strip (Figure 2) demonstrate an u n d e r l y i n g sinus r h y t h m w i t h short runs of s u p r a v e n t r i c u l a r and ventricular tachycardia. Altered atrioventricular conduction is present in the form of a 1° A-V block. Disturbed intraventricular conduction is manifested by m a r k e d prolongation of QRS duration, and marked rightward and superior shift of the mean frontal plane QRS vector, particularly the t e r m i n a l component. These changes resolved within 72 hours of hospitalization (Figure 3), at which time only alterations in T wave amplitude and polarity and slight pro-
10:11 (November) 1981
Fig. 3. Twelve-lead ECG obtained 72 hours after admission. PR interval has returned to normal. QRS duration (0.10 sec) and QRc interval (0.620 sec) remain prolonged. Mean frontal and horizontal plane QRS vectors have returned to normal. Terminal 0.04 sec. QRS vector has shifted leftward when compared with admission ECG. Alterations in T wave polarity and amplitude and U waves are evident.
longation of the QRS duration and QT i n t e r v a l w e r e noted. S i m i l a r ECG findings are encountered in pat i e n t s on c h r o n i c p h e n o t h i a z i n e therapy, s Chlorpromazine has been shown in vitro to d e c r e a s e cardiac excitability, contractility, and conduction velocity via alterations in potassium efflux, presumably during phase 3 of d e p o l a r i z a t i o n . 9 It s h a r e s t h e s e effects with other drugs (including propranolol and quinidine) 9 commonly referred to as membrane stabilizers, membrane depressants, or ~local anesthetics." Thioridazine has been shown in vivo to produce a dose-dependent increase in diastolic threshold, effective refractory period, and conduction in time. 1° Repetitive responses can be induced by p r e m a t u r e stimulation following high doses. This induced r e p e t i t i v e response is considered 1° to be an indicator of the presence of a mechanism for.the production of ventricular tachycardia or v e n t r i c u l a r fibrillation, and implicates a r e - e n t r a n t p a t h w a y ( s ) . In addition to the direct cardiac effect of the phenothiazines, a combination of autonomic changes produced by a n t i c h o l i n e r g i c and a n t i a d r e n e r g i c pharmacologic actions may serve to enhance the induction of cardiac arr h y t h m i a s . 11 The p h e n o t h i a z i n e s
Ann Emerg Med
vary considerably in their anticholinergic and antiadrenergic effects. 11 This variability may account for the more frequent clinical cardiotoxicity associated with the use of thioridazine, which possesses potent anticholinergic effects. Mesoridazine would be expected to exhibit the same electrophysiologic effects as the other phenothiazine compounds (particularly thioridazine, from which it is derived). The severity of the electrocardiographic aberrations noted during chronic phenothiazine therapy do not appear to be related to the duration of the therapy, therapeutic dose employed, or serum level of the drug. s Following massive ingestions, ventricular tachycardia, premature ventricular depolarizations, and marked widening o f the QRS complex have been d e s c r i b e d . 12 C h a n g e s in the direction of the mean QRS vector or production of conventional bundle branch blocks have been infrequently reported. 12
CONCLUSION The s u i c i d a l p a t i e n t who h a s ingested an unknown medication is a diagnostic and therapeutic problem, p a r t i c u l a r l y when s e r u m or u r i n e toxicologic screens are not r e a d i l y a v a i l a b l e . The e l e c t r o c a r d i o g r a m
587/63
may be of diagnostic v a l u e i n this setting, as only a few of the drugs commonly used in suicide a t t e m p t s produce primary ECG abnormalities. Sinus tachycardia a n d a prolonged QRS d u r a t i o n are f r e q u e n t l y seen following ingestion of tricyclic antidepressants. Rightward shift of the t e r m i n a l QRS vector a n d a n t e r i o r and r i g h t w a r d d i s p l a c e m e n t of the ST segment vector also m a y be seen. S i m i l a r electrocardiographic abnormalities may be noted following ingestion of phenothiazines, as demonstrated by our patient, and m u s t be c o n s i d e r e d i n t h e d i f f e r e n t i a l diagnosis.
REFERENCES 1. Hollister LE, Kosek JC: Sudden death during treatment with phenothiazine de-
64/588
rivatives. J A M A 192:1035-1038, 1965. 2. Leetstma JE, Koenig KL: Sudden death and phenothiazines: A current controversy. Arch Gen Psychiatr 18:137-148, 1968. 3. Davis JN, Bartlett E, Termini BA: Overdosage of psychotropic drugs: A review. Dis Nerv Syst 29:157-164, 1968. 4. Langslet A: Changes in coronary flow and ECG in the isolated perfused rat heart induced by phenothiazine drugs. Acta P h a r m a c o l et Toxicol 27:183-192, 1969. 5. Dellenkoffer RL, Gallant DM, Phillips JH: Electrocardiographic evaluation of mesoridazine (Serentil). Curr Therap Res 14:71-72, 1971. 6. Donlon PT, Tupin JP: Successful suicides with thioridazine and mesoridazine. A result of probable cardiotoxicity. Arch Gen Psychiatr 34:955-957, 1977. 7. Rosenquist RJ, Brauer WW, Mork JN:
Ann Emerg Med
Recurrent major ventricular arrhythmias associated with thioridazine therapy. Minnesota Med 54:877-881, 1971. 8. Huston JR, Bell GE: The effects of thioridazine hydrochloride and chlorpromazine on the electrocardiogram. J A M A 198:134-138, 1966. 9. Langslet A: Membrane stabilization and cardiac effects of d,l-propranolol, dpropranolol, and chlorpromazine. E u r J Pharmacol 13:6-14, 1970. 10. Yoon MS, Han J, Dersham GH, et al: Effects of thioridazine (Mellaril) on ventricular electrophysiologic properties. A m J Cardiol 43:1155-1158, 1979. 11. Snyder SH, Banerjie SP, Yamamura H: Drugs, neurotransmitters, and schizophrenia. Science 184:1243-1253, 1974. 12. Alexander CS, Nino A: Cardiovascular complications in young patients taking psychotropic drugs. A m H e a r t J 78:757-769, 1969.
10:11 (November) 1981
Cardiac Conduction and Rhythm Disturbances Following Suicidal Ingestion of Mesoridazine James T. Niemann, MD* J. Stephan Stapczynski, MD* Robert J. Rothstein, MD* Michael M. Laks, MD t Los Angeles, California
The phenothiazine derivatives, particularly chlorpromazine and thioridazine, are known to produce significant electrocardiographic abnormalities. Until now, documented life-threatening arrhythmias have not been reported following large doses of mesoridazine, the besylate salt of a metabolite of thioridazine and a relatively recent addition to the phenothiazine group. We describe such a case in which alterations in both impulse conduction (first-degree atrioventricular block, prolonged QRS duration, and right axis deviation) and impulse formation (supraventricular and ventricular tachycardia) were noted following a suicidal ingestion of mesoridazine. The electrophysiologic mechanisms underlying phenothiazine-induced arrhythmogenesis are reviewed. Niemann JT, Stapczynski JS, Rothstein RJ, Laks MM: Cardiac conduction and rhythm disturbances following suicidal ingestion of mesoridazine. Ann Emerg Med 10:585-588, November 1981.
arrhythmias; drug-induced cardiotoxicity; phenothiazines INTRODUCTION Clinical cardiac toxicity related to phenothiazine use, whether in accidental overdose or following suicidal ingestions, remains a significant and, perhaps, frequently unrecognized and underrated problem. Abnormal electrocardiograms (ECG) and sudden death of patients receiving standard, therapeutic doses of phenothiazines have been previously reported. 1 The incidence of sudden death in this group of patients remains to be determined, and an association between the electrocardiographic findings and sudden death of presumed cardiac origin also remains to be established. 2 Suicides with phenothiazines, particularly chlorpromazine and thioridazine, have also been reported, with death being ascribed in many instances to a lethal arrhythmia despite minimal documenration? Experimental studies using isolated perfused rat hearts have demonstrated variable potency among the phenothiazine derivatives with respect to alterations in coronary blood flow and prolongation of the QT interval and QRS duration. 4 The phenothiazine most frequently responsible for clinical cardiac complications has been thioridazine. From the Departments of Emergency Medicine* and Medicine, Division of Cardiology,t Los Angeles County Harbor-UCLA Medical Center, Torrance; and the UCLA School of Medicine, Los Angeles, California, Address for reprints: James T Niemann, MD, Director, Acute Adult Care, Department of Emergency Medicine, Los Angeles County Harbor-UCLA Medical Center, 1000 West Carson Street, Torrance, California 90509.
10:11 November) 1981
Ann Emerg Med
585/61
Mesoridazine is the besylate salt of a metabolite of thioridazine and, in therapeutic doses, produces ECG effects similar to those described in patients taking thioridazine, ie, alterations in T wave, amplitude and polarity. 5 Despite the obvious similarity in structure and implied (but as yet undocumented) similarity in c a r d i a c e l e c t r o p h y s i o l o g i c effects, t h e r e has been only one r e p o r t e d death thought to have been of cardiac etiology related to the ingestion of mesoridazine. 6 The purpose of this report is to describe a case of documented meso r i d a z i n e - i n d u c e d d i s t u r b a n c e s in atrioventricular and intraventricular conduction with associated ventricul a r and s u p r a v e n t r i c u l a r a r r h y t h mias.
CASE REPORT A 23-year-old schizophrenic white man was brought to the emergency department one hour after ingesting 6 gm of mesoridazine (Serentil v) concentrate. The p a t i e n t ' s m o t h e r reported that on the day of admission she and her son had become involved in a heated a r g u m e n t , following which the p a t i e n t became irate, broke several household articles, and informed her that he was going to kill himself. He ingested two 4-oz bottles (6 gm) of mesoridazine and refused to accompany his mother to the hospital. One hour later the patient became drowsy and d y s a r t h r i c , and was brought to the emergency department for evaluation. The p a t i e n t ' s h i s t o r y was remarkable for a three-year history of p a r a n o i d s c h i z o p h r e n i a , a b u s e of multiple drugs, and previous hospit a l i z a t i o n s for drug overdoses and psychiatric decompensation. Initial evaluation revealed a regular pulse at 140 beats per minute; blood pressure (supine), 120/70 mm Hg; and respiratory rate, 16/min and regular. The general physical examination was unremartfable except for lethargy, mydriasis, and slurred speech. E m e s i s was induced w i t h syrup of ipecac. Approximately 30 minutes after presentation and 20 m i n u t e s after vomiting, the patient was comatose with shallow respirations. An endotracheal tube was inserted and the patient was connected to a cardiac monitor. The i n i t i a l r h y t h m strip showed broad QRS complexes at a regular rate of 130/min to 140/min. The rhythm was interpreted as ven-
62/586
Fig. 1. Admission 12-lead ECG demonstrating underlying sinus rhythm with 1 ° A - V block (P-R interval 0.30 sec) and markedly prolonged QRS duration. Mean frontal plane QRS axis is directed superiorly and rightward (+ 185°).
Fig. 2. Three-channel rhythm strip (leads I, H, III) obtained on admission shows sinus rhythm with short runs of supraventricular and ventricular (open arrow) tachycardia.
tricular tachycardia and the patient was given 100 mg lidocaine as an int r a v e n o u s bolus w i t h o u t effect on QRS morphology or rate. Electrical cardioversion was attempted. Following countershock, the QRS morphology was considered unchanged but the rate had decreased to 110/min to 120/ min and P waves were seen. A standard 12-lead ECG revealed a sinus r h y t h m with broad QRS complexes and short runs of s u p r a v e n t r i c u l a r and ventricular tachycardia (Figures 1 and 2).
Ann Emerg Med
Admission laboratory data were remarkable only for a serum potassium of 2.9 mEq/L. During controlled v e n t i l a t i o n with 100% oxygen, the a r t e r i a l PO2, PCO2, and pH were 203, 38, and 7.38, respectively. Intravenous potassium replacement was begun. Four hours after admission, the patient's blood pressure fell to 80/60 mm Hg with no change in c a r d i a c r h y t h m or r a t e noted on a r e p e a t ECG. A normal blood p r e s s u r e was r e e s t a b l i s h e d with one liter of normal saline in-
10:11 (November) 1981
fused over one hour. D u r i n g the e n s u i n g 24 hours, the patient's mental status improved and he was extubated the day after admission. Repeat serum potassium obtained 36 hours after admission was n o r m a l . S e r i a l e l e c t r o c a r d i o grams revealed only U waves and T wave c h a n g e s w i t h i n 72 h o u r s of admission (Figure 3). The QRS duration a n d QT i n t e r v a l r e m a i n e d slightly prolonged. A urine specimen obtained on admission was submitted for a qualitative drug screen which is capable of detecting chlorpromazine, thioridazine, and trifluoperazine. A substance was d e t e c t e d which crossreacted in the v a r i o u s a s s a y s b u t could not be definitely identified.
DISCUSSION To our knowledge, t h i s is the first reported case of massive mesoridazine i n g e s t i o n a s s o c i a t e d with documented p o t e n t i a l l y lethal ventricular arrhythmias and conduction d i s t u r b a n c e s . The o n l y o t h e r reported case of massive ingestion in which electrocardiographic findings are alluded to was obtained from a review of coroner's records. 6 In that case, an ECG obtained following a grand m a l s e i z u r e a n d a c a r d i a c a r r e s t is s a i d to h a v e s h o w n an %gonal rhythm." Although a quantitative serum, urine, or tissue level of the drug was not obtained for our patient, the ingestion was witnessed, the amount ingested was known, and 0nly a ~ p h e n o t h i a z i n e - l i k e " compound was noted on urine toxicologic analysis. The patient's intercurrent hypokalemia is thought to have played a facilitating and not a primary role in a r r h y t h m o g e n e s i s , a speculation supported by previous reports of r h y t h m d i s t u r b a n c e s with phenothiazine use. 7 Our p a t i e n t ' s i n i t i a l 12-lead ECG ( F i g u r e 1) a n d 3 - c h a n n e l rhythm strip (Figure 2) demonstrate an u n d e r l y i n g sinus r h y t h m w i t h short runs of s u p r a v e n t r i c u l a r and ventricular tachycardia. Altered atrioventricular conduction is present in the form of a 1° A-V block. Disturbed intraventricular conduction is manifested by m a r k e d prolongation of QRS duration, and marked rightward and superior shift of the mean frontal plane QRS vector, particularly the t e r m i n a l component. These changes resolved within 72 hours of hospitalization (Figure 3), at which time only alterations in T wave amplitude and polarity and slight pro-
10:11 (November) 1981
Fig. 3. Twelve-lead ECG obtained 72 hours after admission. PR interval has returned to normal. QRS duration (0.10 sec) and QRc interval (0.620 sec) remain prolonged. Mean frontal and horizontal plane QRS vectors have returned to normal. Terminal 0.04 sec. QRS vector has shifted leftward when compared with admission ECG. Alterations in T wave polarity and amplitude and U waves are evident.
longation of the QRS duration and QT i n t e r v a l w e r e noted. S i m i l a r ECG findings are encountered in pat i e n t s on c h r o n i c p h e n o t h i a z i n e therapy, s Chlorpromazine has been shown in vitro to d e c r e a s e cardiac excitability, contractility, and conduction velocity via alterations in potassium efflux, presumably during phase 3 of d e p o l a r i z a t i o n . 9 It s h a r e s t h e s e effects with other drugs (including propranolol and quinidine) 9 commonly referred to as membrane stabilizers, membrane depressants, or ~local anesthetics." Thioridazine has been shown in vivo to produce a dose-dependent increase in diastolic threshold, effective refractory period, and conduction in time. 1° Repetitive responses can be induced by p r e m a t u r e stimulation following high doses. This induced r e p e t i t i v e response is considered 1° to be an indicator of the presence of a mechanism for.the production of ventricular tachycardia or v e n t r i c u l a r fibrillation, and implicates a r e - e n t r a n t p a t h w a y ( s ) . In addition to the direct cardiac effect of the phenothiazines, a combination of autonomic changes produced by a n t i c h o l i n e r g i c and a n t i a d r e n e r g i c pharmacologic actions may serve to enhance the induction of cardiac arr h y t h m i a s . 11 The p h e n o t h i a z i n e s
Ann Emerg Med
vary considerably in their anticholinergic and antiadrenergic effects. 11 This variability may account for the more frequent clinical cardiotoxicity associated with the use of thioridazine, which possesses potent anticholinergic effects. Mesoridazine would be expected to exhibit the same electrophysiologic effects as the other phenothiazine compounds (particularly thioridazine, from which it is derived). The severity of the electrocardiographic aberrations noted during chronic phenothiazine therapy do not appear to be related to the duration of the therapy, therapeutic dose employed, or serum level of the drug. s Following massive ingestions, ventricular tachycardia, premature ventricular depolarizations, and marked widening o f the QRS complex have been d e s c r i b e d . 12 C h a n g e s in the direction of the mean QRS vector or production of conventional bundle branch blocks have been infrequently reported. 12
CONCLUSION The s u i c i d a l p a t i e n t who h a s ingested an unknown medication is a diagnostic and therapeutic problem, p a r t i c u l a r l y when s e r u m or u r i n e toxicologic screens are not r e a d i l y a v a i l a b l e . The e l e c t r o c a r d i o g r a m
587/63
may be of diagnostic v a l u e i n this setting, as only a few of the drugs commonly used in suicide a t t e m p t s produce primary ECG abnormalities. Sinus tachycardia a n d a prolonged QRS d u r a t i o n are f r e q u e n t l y seen following ingestion of tricyclic antidepressants. Rightward shift of the t e r m i n a l QRS vector a n d a n t e r i o r and r i g h t w a r d d i s p l a c e m e n t of the ST segment vector also m a y be seen. S i m i l a r electrocardiographic abnormalities may be noted following ingestion of phenothiazines, as demonstrated by our patient, and m u s t be c o n s i d e r e d i n t h e d i f f e r e n t i a l diagnosis.
REFERENCES 1. Hollister LE, Kosek JC: Sudden death during treatment with phenothiazine de-
64/588
rivatives. J A M A 192:1035-1038, 1965. 2. Leetstma JE, Koenig KL: Sudden death and phenothiazines: A current controversy. Arch Gen Psychiatr 18:137-148, 1968. 3. Davis JN, Bartlett E, Termini BA: Overdosage of psychotropic drugs: A review. Dis Nerv Syst 29:157-164, 1968. 4. Langslet A: Changes in coronary flow and ECG in the isolated perfused rat heart induced by phenothiazine drugs. Acta P h a r m a c o l et Toxicol 27:183-192, 1969. 5. Dellenkoffer RL, Gallant DM, Phillips JH: Electrocardiographic evaluation of mesoridazine (Serentil). Curr Therap Res 14:71-72, 1971. 6. Donlon PT, Tupin JP: Successful suicides with thioridazine and mesoridazine. A result of probable cardiotoxicity. Arch Gen Psychiatr 34:955-957, 1977. 7. Rosenquist RJ, Brauer WW, Mork JN:
Ann Emerg Med
Recurrent major ventricular arrhythmias associated with thioridazine therapy. Minnesota Med 54:877-881, 1971. 8. Huston JR, Bell GE: The effects of thioridazine hydrochloride and chlorpromazine on the electrocardiogram. J A M A 198:134-138, 1966. 9. Langslet A: Membrane stabilization and cardiac effects of d,l-propranolol, dpropranolol, and chlorpromazine. E u r J Pharmacol 13:6-14, 1970. 10. Yoon MS, Han J, Dersham GH, et al: Effects of thioridazine (Mellaril) on ventricular electrophysiologic properties. A m J Cardiol 43:1155-1158, 1979. 11. Snyder SH, Banerjie SP, Yamamura H: Drugs, neurotransmitters, and schizophrenia. Science 184:1243-1253, 1974. 12. Alexander CS, Nino A: Cardiovascular complications in young patients taking psychotropic drugs. A m H e a r t J 78:757-769, 1969.
10:11 (November) 1981