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Therapeutic and diagnostic efficacy of adenosine in wide-complex tachycardia
CASE REPORT
adenosine wide-complex tachycardia
Therapeutic and Diagnostic Efficacy of Adenosine in Wide-Complex Tachycardia From the Department of Emergency Medicine,* and Division of Emergency Medicine,* Mercy Hospital, Pittsburgh,Pennsylvania; Division of Emergency Medicine, University of California, Irvine;~ and Division of EmergencyMedicine, Texas A&M University Health Sciences Center, Temple, Texas.~ Receivedfor publication June 19, 1992. Revision received November 20,- 1992. Acceptedfor publication December 17, 1992.
Kaveh Ilkhanipour, MD *t Ronn Berrol, MD* Donald M Yealy, MD t§
Wide-complex tachycardia is one of the most challenging problems faced by emergency physicians. Adenosine is an endogenous nucleoside that has gained recent popularity as an antiarrhythmic drug in the setting of supraventricular tachycardia. We present the cases of two patients with stable wide-complex tachycardia in which adenosine was administered for therapeutic and diagnostic effects. Both patients quickly converted into sinus rhythm with subsequent diagnoses of atrioventricular reciprocating tachycardia secondary to Wolff-Parkinson-White syndrome. The role of adenosine in the acute management of wide-complex tachycardia is discussed. [llkhanipour K, Berrol R, Yealy DM: Therapeutic and diagnostic efficacy of adenosine in wide-complex tachycardia. Ann Emerg Med August 1993;22:1360-1364.] INTRODUCTION Adenosine has become a popular drug for the treatment of supraventricular tachycardias in the emergency department. Its rapid onset of action and short half-life allow for safe and effective termination of most supraventricular tachycardias. Most reports have described the role of adenosine m the treatment of narrow-complex tachycardias. However, recent attention has been redirected at its safety and efficacy in the treatment of wide-complex tachycardias. 1-3 We present two cases of patients presenting to the ED with wide-complex tachycardia successfully treated with adenosine. The role of adenosine in the therapeutic and diagnostic management of stable wide-complex tachycardia also is discussed.
CASE REPORTS Case 1 A 59-year-old woman with a history of WolffParkinson-White syndrome presented to the ED complaining of palpitations, light-headedness, and chest pressure. The patient's symptoms began while she was making her bed at home approximately one hour before
152/ 1360
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22:8
AUGUST 1993
ADENOSINE Ilkhanipour, Berrol & Yealy
ED arrival. The patient had been discharged from the hospital early in the day after an unsuccessful attempt at radiofrequency catheter ablation of her bypass tract in the cardiac catheterization laboratory. The palpitations and chest discomfort were of sudden onset. There was no associated loss of consciousness, shortness of breath, diaphoresis, nausea, or vomiting. The patient was diagnosed with Woiff-Parkinson-White syndrome two years earlier and had been managed medically with oral procainamide initially and subsequently switched to oral flecainide. A previous radiofrequency catheter ablation attempt also had failed in January 1991. The patient had a history of hypertension but no other cardiovascular disorders. Current medications included flecainide, nifedipine, and metoprolol. The patient had no allergies. Physical examination revealed a pleasant, well-nourished woman who appeared slightly anxious. Her initial vital signs were blood pressure of 126/90 mm Hg; pulse, 200 and regular; oral temperature, 37.1 C; and respirations, 20. The skin was warm and d® There was no jugular venous distension, and carotid pulses were 2+ bilaterally. Lung sounds were clear to auscultation. Heart sounds demonstrated regular rate and rhythm without any murmurs, rubs, or gallops. The remainder of the physical examination was unremarkable. The patient was on 2 L of oxygen through nasal prongs with a reading of 100% saturation by pulse oximeter. Peripheral IV access was established, and a 12-lead ECG revealed a wide-complex tachycardia with a QRS duration of 180 msec and ventricular rate of 200 (Figure 1). A 6-mg bolus of adenosine was given with no clinically significant Figure 1. Patient 1: Initial rhythm strip showing patient in widecomplex tachycardia at a rate of 200 before adenosine administration
change in the rate, rhythm, or vital signs. A second 12-rag bolus was given with a three-second period of sinus arrest followed by restoration of sinus rhythm at a rate of 90. The patient experienced a transient period of feeling warm with mild facial flushing approximately 15 seconds after adenosine administration. Blood pressure after treatment remained stable, and she experienced no further chest discomfort. A repeat 12-lead ECG revealed a sinus rhythm with shortened PR interval and delta waves (Figure 2). Serum electrolyte measurements were within normal limits, with a potassium concentration of 4.4 mEq/L and magnesium of 2.2 mEq/L. The patient was admitted to the cardiac arrhythmia monitoring unit for 72 hours, where adjustments in flecainide dosage were made. There was no recurrence of the tachyarrhythmia. Case 2 A 28-year-old man with a history of WolffParkinson-White syndrome presented to the ED complaining of palpitations, mild chest discomfort, and light-headedness. His symptoms began suddenly 90 minutes before arrival. The patient described the chest discomfort as a "pressure-type pain" localized to his anterior chest wall without radiation. There was no associated loss of consciousness, diaphoresis, nausea, vomiting, or shortness of breath. The patient was diagnosed with Wolff-Parkinson-White syndrome in 1986 and had had no palpitations while taking oral flecainide during the past four years. The patient stated that he had been experiencing a large amount of stress during the past week and had taken only half of his daily dose of flecainide over the past three days. He had no other medical history and was on no other medication. Figure 2. Patient 2: 12-lead ECG after conversion of wide-complex tachycardia into normal sinus rhythm
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Physical examination revealed a pleasant, heahhyappearing young man who appeared comfortable. His initial vital signs were blood pressure of 136/88 mm Hg; pulse, 180; oral temperature, 37.4 C; and respirations, 16. His skin was warm and d U. There was no evidence of jugular venous distention. Carotid pulses were 2+ bilaterally with good upstrokes. Lung sounds were clear to auscultation. Cardiac auscultation revealed a regular rate and rhythm without any murmurs, rubs, or gallops. The abdomen was soft and nontender with no palpable hepatosplenomegaly. There was no peripheral clubbing, cyanosis, or edema. The remainder of the physical examination was unremarkable. Figure 3. Patient 2: Initial rhythm strip showing patient in widecomplex tachycardia at a rate of 180 before adenosine administration
The ECG monitor revealed a regular wide-complex tachycardia at a rate of 180 (Figure 3). The QRS width was 120 msec. The patient was placed on 2 L of oxygen through nasal cannula, and peripheral IV access was established. A 6-mg bolus of adenosine was administered with no clinically significant change in rate, rhythm, or vital signs. A second 12-mg dose was given, which terminated the wide-complex rhythm and restored a normal sinus rhythm at a rate of 97 (Figure 4). The patient experienced a transient period of facial flushing shortly after adenosine administration. Blood pressure remained stable, and he denied any further chest pressure or lightheadedness. A 12-lead ECG revealed a sinus rhythm with shortened PR intervals and delta waves (Figure 5). Serum electrolytes were within normal limits. The patient's private cardiologist was contacted, and a single 100-mg oral dose of flecainide was recommended before discharge and resumption of the previous dosing schedule. The patient was discharged approximately two hours after conversion into sinus rhythm with no further ectopy or complaints. DISCUSSION
When faced with a wide-complex tachycardia, ventricular tachycardia always should be first in the differential diagnosis, especially in individuals with a history of heart disease. 4 Other causes include paroxysmal supraventricular tachycardia and atrial flutter or fibrillation with either fixed or rate-related bundle branch block, pre-excited reciprocating tachycardia, 5 and reciprocating tachycardia through a Mahaim fiber. 6 Immediate electrical cardioversion is the standard of care for unstable wide-complex Figure 4. Patient 2: Rhythm strip illustrating conversion of widecomplex tachycardia into a normal sinus rhythm shortly after administration of 12 rag adenosine. Patient remained hemodynamically stable during and after conversion with adenosine.
1 5 4/ 1 362
Figure 5. Patient 2: 12-lead ECG after conversion of wide-complex tachycardia into normal sinus rhythm
ANNALS OF EMERGENCY MEDICINE
22:8
AUGUST 1993
ADENOSINE
Ilhhanipour, Berrol & Yealy
tachycardia,r Stable wide-complex tachycardia remains a diagnosti c and therapeutic challenge. Formulating a specific diagnosis for hemodynamically stable wide-complex tachycardia based on initial clinical assessment remains a difficult task for even the most astute physician. Because the diagnosis of these rhythms is challenging, it would be beneficial to have a drug that has both therapeutic and diagnostic efficacy while having minimal associated morbidity. Current therapeutic options other than adenosine for an undiagnosed stable wide-complex tachycardia are limited. Lidocaine remains the drug of choice in the initial management of stable ventricular tachycardia. Procainamide is approved and commonly available for IV administration in the United States. It is the drug of choice for stable patients with a wide-complex tachycardia of indeterminate cause, especially if an antidromic tachycardia or atrial fibrillation with Wolff-Parkinson-White syndrome is suspected.S, 9 Procainamide must be given slowly (50 mg/min up to a maximum of 18 mg/kg) and can cause hypotension. Magnesium is also useful in ventricular tachycardia, supraventricular tachycardia, and many atrial dysrhythmias but is not weil studied in WolffParkinson-White syndrome and indeterminate widecomplex tachycardias, to Many drugs effective in controlling or terminating supraventricular tachycardias are potentially dangerous in ventricular tachycardia and Wolff-Parkinson-White syndromes. Digoxin, r-blockers, and class IV agent calcium channel blockers can convert or control the ventricular response rate in most atrial flutter or fibrillation and paroxysmal supraventricular tachycardia. However, calcium channel blocking drugs, such as verapamil, and digoxin can precipitate hemodynamic collapse in patients with Wolff-Parkinson-White syndrome and antidromic tachycardia or atrial flutter or fibrillation. Our cases demonstrate the safety of adenosine as a therapeutic and/or diagnostic adjunct in the hemodynamically stable patient with a wide-complex tachycardia. The mechanism of action and side effect profile of adenosine have been described. 1i,12 To date, only two cases of brief hemodynamic collapse have been reported with adenosine administration. ~3 Both cases involved short episodes of asystole or bradycardia resulting in 15 to 20 seconds of unconsciousness followed by the return of a perfusing rhythm and patient reawakening. These reports highlight the rare potential of significant asystole, bradycardia, and hypotension associated with adenosine. It Would be prudent to have an external pacemaker available at the bedside when using adenosine.
AUGUST 1993
22:8
ANNALS OF EMERGENCY MEDICINE
In 1989, Rankin and colleagues2 evaluated the use of adenosine in the treatment of both narrow- and broadcomplex tachycardias. In their series of 24 patients with broad-complex tachycardias, six patients had their dysrhythmias terminated with adenosine, whereas atrioventricular block was induced in four patients long enough to reveal atrial or ventricular tachycardias. The tachycardias persisted in the remaining 14 patients without any ill effects related to adenosine administration. The diagnostic potential of adenosine is related to its ability to slow conduction temporarily through the atrioventricular node.Z,2,12 High-grade atrioventricular nodal block would unmask atrial activity by the temporary reduction or elimination of infranodal electrical activity, while having no adverse hemodynamic effects on ventricular tachycardia. Specific diagnosis could be facilitated in patients whose wide-complex tachycardias were secondary to atrial flutter, atrial fibrillation, intra-atrial re-entry, or accessory pathways. In a study by Rankin and associates, 2 adenosine produced atri0ventricular block with termination or diagnosis of tachycardias of supraventricular origin with a sensitivity of 90%, specificity of 93%, and predictive accuracy of 92%. Both patients presented in our case report had known Wolff-Parkinson-White syndrome. The firs[ patient's widecomplex rhythm was primarily of the orthodromic atrioventricular reciprocating type in which anterograde conduction occurs through the atrioventricular node and retrograde conduction occurs through the accessory pathway. This dysrhythmia pattern is thought to be present in more than 80% of patients with Wolff-Parkinson-White syndrome who are symptomatic. 14 Orthodromic atrioventricular reciprocating tachycardias usually present with a narrow QRS complex (less than 90 msec). Our patient had a rate-related bundle branch block, which was responsible for the wide QRS morphology. The second patient most likely demonstrated an antidromic tachycardia secondary to the shortened PR interval and delta waves present on his ECG after conversion. However, we had no access to his electrophysiologic records and can only assume that he had antidromic conduction. Antidromic tachycardias traverse the same circuit but travel in the opposite direction. The ventricles are depolarized through the accessory pathway, resulting in a wide-complex tachycardia. Antidromic tachycardias represent only 11% of tachydysrhythmias seen with Wolff-Parkinson-White syndrome. 15 Although adenosine has unclear effects on accessory pathway conduction, it may interfere with both antegrade and retrograde conduction in the atrioventricular node. 16 It is this latter effect
1363/ 155
ADENOSINE
IIkhanipour, Berrol & Yealy
that may be responsible for termination of the reciprocating tachycardia. Based on our experience, we believe a therapeutic and diagnostic trial of adenosine in stable patients with
A d d r e s s for reprints:
Kaveh Ilkhanipour, MD Mercy Hospital Department of Emergency Medicine
regular wide-complex tachycardias is reasonable. Its
1400 Locust Street
use in patients with atrial fibrillation or flutter and Wolff-
Pittsburgh, Pennsylvania 15219-5166
Parkinson-White syndrome is not recommended currently. Immediate cardioverting capabilities should always be available in case of hemodynamic deterioration. SUMMARY
We report two cases of Wolff-Parkinson-White syndrome in which adenosine was given as a therapeutic and diagnostic adjunct in the setting of stable wide-complex tachycardia. We believe that this experience illustrates the safety and effectiveness of adenosine in wide-complex tachycardia. REFERENCES 1. SharmaAD, Klein GJ, Yea R: Intravenous adenosine triphosphate during wide QRS complex tachycardia: Safety, therapeutic efficacy, and diagnostic utility. Am J Mad 1990;88:337-342. 2. RankinA, Oldroyd KG, Chong E, et al: Value and limitations of adenosine in the diagnosis and treatment of narrow and broad complex tachycardias. Br HeartJ 1989;62:195-203. 3. Johe RL, GallagherJJ: Use of adenosine during hypotension in the Wolff-Parkinson-WKte syndromewith supraventricular tachycardia. Am HeartJ 1991;121:1239-1240. 4. Faitelson L, GordonAE: Clinical algorithm: Treatment ef supraventriculartachycardia. Hosp Mad 1991;Nov:37-40. 5. Akhtar M, ShenasaM, JazayeFiM, et aL Wide QRS complex tachycardia: Reappraisalof a common clinical problem. Ann InternMad 1988;109:905-912. 6. Bardy GH, PackerDL, GermanLD, et al: Preexeitedreciprocating tachycardia in patients with Wolff-Parkinson-White syndrome: Incidenceand mechanisms, Circulation1984;70:377-391. 7. Bardy GH, FaderGM, German LD, et al: Surface electrocardiographicclues suggesting presence of a nedofasicular Mahaim fiber. J Am Coil Cardio11984;3:1161-1168. 8. Wellens HJJ, 9rugada P, Penn OC: The management of,preexcitation syndromes. JAMA 1987;257:2325-2333.
ERRATA In the article "Upper-Extremity Deep-Vein Thrombosis: Thrombolytic Therapy With Anistrepalase" [April 1993;22:748-750], the sentence at the bottom of page 749 and top of page 750 should read "APSAC has been used to treat acute myocardial infarction,17, ~s seems to be as effective as tissue plasminogen activator and streptokinase,2o and causes no more serious side effects such as hemorrhage.17,20 In the article "Needle Thoracostomy FaiIs to Detect a Fatal Tension Pneumothorax" [May 1993;22:863-866], arrows 1 and 2 in the Figure were reversed. The figure shouId appear as shown below.
9. Arai A, Kron J: Current management of the Wolff-Parkinson-White syndrome, WestJ Mad 1990;152:383-391. 10. KerenA, Tzeivoni D: Magnesium therapy in ventricular arrhythmias. PACE1990;7:937-945. 11. Vidt DG, Bakst AW: Adenosine: A new drug for acute termination of supraventricular tachycardia. CleveClinJ Mad 1990;57:383-388. 12. DiMarco JP, Sellers TD, Berne RM, et al: Adenosine: Electrophysiologiceffects and therapeutic use for terminating paroxysmaltachycardia. Circulation1983;68:1254-1263. 13. Reed R, FalkJL, O'Brien J: Untoward raactien to adenosine therapy for supraventricular tachycardia. Am J EmergMad 1991;9:566-570. 14. GallagherJJ, Pritchett ELC,Scaly WC, et ah The preexcitation syndromes. ProgCaldiovasc Dis 1978;20:285-327. 15. Atie J, BrugadaP, BrugadaJ, et ah Clinical and electrophysiologic characteristics of patients with antidromic circus movementtachycardia in the Walff-Parkinson-White syndrome. Am J Cardiol1990;66:1082-1091:.
Figure.
Autopsy photograph of the thoracic structures after the anterior chest wall was removed. Although the right middle and lower lobes (arrow 2) are collapsed as expected, the right upper lobe (arrow 2) is still inflated because of air trapped in bullae. A chest tube is present i n the left hemithorax.
16. DimarcoJP: Adenosine and suprayentricu/artachycardia, in Peileg A, Michelson EL, Dreifus LS (eds): CardiacElectrophysiologyand Pharmacologyof Adenosine andA TP:Basicand Clinical" Aspects. New York, Alan R Liss, 1887, p 271-281.
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adenosine wide-complex tachycardia
Therapeutic and Diagnostic Efficacy of Adenosine in Wide-Complex Tachycardia From the Department of Emergency Medicine,* and Division of Emergency Medicine,* Mercy Hospital, Pittsburgh,Pennsylvania; Division of Emergency Medicine, University of California, Irvine;~ and Division of EmergencyMedicine, Texas A&M University Health Sciences Center, Temple, Texas.~ Receivedfor publication June 19, 1992. Revision received November 20,- 1992. Acceptedfor publication December 17, 1992.
Kaveh Ilkhanipour, MD *t Ronn Berrol, MD* Donald M Yealy, MD t§
Wide-complex tachycardia is one of the most challenging problems faced by emergency physicians. Adenosine is an endogenous nucleoside that has gained recent popularity as an antiarrhythmic drug in the setting of supraventricular tachycardia. We present the cases of two patients with stable wide-complex tachycardia in which adenosine was administered for therapeutic and diagnostic effects. Both patients quickly converted into sinus rhythm with subsequent diagnoses of atrioventricular reciprocating tachycardia secondary to Wolff-Parkinson-White syndrome. The role of adenosine in the acute management of wide-complex tachycardia is discussed. [llkhanipour K, Berrol R, Yealy DM: Therapeutic and diagnostic efficacy of adenosine in wide-complex tachycardia. Ann Emerg Med August 1993;22:1360-1364.] INTRODUCTION Adenosine has become a popular drug for the treatment of supraventricular tachycardias in the emergency department. Its rapid onset of action and short half-life allow for safe and effective termination of most supraventricular tachycardias. Most reports have described the role of adenosine m the treatment of narrow-complex tachycardias. However, recent attention has been redirected at its safety and efficacy in the treatment of wide-complex tachycardias. 1-3 We present two cases of patients presenting to the ED with wide-complex tachycardia successfully treated with adenosine. The role of adenosine in the therapeutic and diagnostic management of stable wide-complex tachycardia also is discussed.
CASE REPORTS Case 1 A 59-year-old woman with a history of WolffParkinson-White syndrome presented to the ED complaining of palpitations, light-headedness, and chest pressure. The patient's symptoms began while she was making her bed at home approximately one hour before
152/ 1360
ANNALS OF EMERGENOY MEDICINE
22:8
AUGUST 1993
ADENOSINE Ilkhanipour, Berrol & Yealy
ED arrival. The patient had been discharged from the hospital early in the day after an unsuccessful attempt at radiofrequency catheter ablation of her bypass tract in the cardiac catheterization laboratory. The palpitations and chest discomfort were of sudden onset. There was no associated loss of consciousness, shortness of breath, diaphoresis, nausea, or vomiting. The patient was diagnosed with Woiff-Parkinson-White syndrome two years earlier and had been managed medically with oral procainamide initially and subsequently switched to oral flecainide. A previous radiofrequency catheter ablation attempt also had failed in January 1991. The patient had a history of hypertension but no other cardiovascular disorders. Current medications included flecainide, nifedipine, and metoprolol. The patient had no allergies. Physical examination revealed a pleasant, well-nourished woman who appeared slightly anxious. Her initial vital signs were blood pressure of 126/90 mm Hg; pulse, 200 and regular; oral temperature, 37.1 C; and respirations, 20. The skin was warm and d® There was no jugular venous distension, and carotid pulses were 2+ bilaterally. Lung sounds were clear to auscultation. Heart sounds demonstrated regular rate and rhythm without any murmurs, rubs, or gallops. The remainder of the physical examination was unremarkable. The patient was on 2 L of oxygen through nasal prongs with a reading of 100% saturation by pulse oximeter. Peripheral IV access was established, and a 12-lead ECG revealed a wide-complex tachycardia with a QRS duration of 180 msec and ventricular rate of 200 (Figure 1). A 6-mg bolus of adenosine was given with no clinically significant Figure 1. Patient 1: Initial rhythm strip showing patient in widecomplex tachycardia at a rate of 200 before adenosine administration
change in the rate, rhythm, or vital signs. A second 12-rag bolus was given with a three-second period of sinus arrest followed by restoration of sinus rhythm at a rate of 90. The patient experienced a transient period of feeling warm with mild facial flushing approximately 15 seconds after adenosine administration. Blood pressure after treatment remained stable, and she experienced no further chest discomfort. A repeat 12-lead ECG revealed a sinus rhythm with shortened PR interval and delta waves (Figure 2). Serum electrolyte measurements were within normal limits, with a potassium concentration of 4.4 mEq/L and magnesium of 2.2 mEq/L. The patient was admitted to the cardiac arrhythmia monitoring unit for 72 hours, where adjustments in flecainide dosage were made. There was no recurrence of the tachyarrhythmia. Case 2 A 28-year-old man with a history of WolffParkinson-White syndrome presented to the ED complaining of palpitations, mild chest discomfort, and light-headedness. His symptoms began suddenly 90 minutes before arrival. The patient described the chest discomfort as a "pressure-type pain" localized to his anterior chest wall without radiation. There was no associated loss of consciousness, diaphoresis, nausea, vomiting, or shortness of breath. The patient was diagnosed with Wolff-Parkinson-White syndrome in 1986 and had had no palpitations while taking oral flecainide during the past four years. The patient stated that he had been experiencing a large amount of stress during the past week and had taken only half of his daily dose of flecainide over the past three days. He had no other medical history and was on no other medication. Figure 2. Patient 2: 12-lead ECG after conversion of wide-complex tachycardia into normal sinus rhythm
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AUGUST 1993
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ANNALS 0F EMERGENCY MEDICINE
1 3 6 1/ 153
ADENOSINE
Ilkhanipour, Berrol & Yealy
Physical examination revealed a pleasant, heahhyappearing young man who appeared comfortable. His initial vital signs were blood pressure of 136/88 mm Hg; pulse, 180; oral temperature, 37.4 C; and respirations, 16. His skin was warm and d U. There was no evidence of jugular venous distention. Carotid pulses were 2+ bilaterally with good upstrokes. Lung sounds were clear to auscultation. Cardiac auscultation revealed a regular rate and rhythm without any murmurs, rubs, or gallops. The abdomen was soft and nontender with no palpable hepatosplenomegaly. There was no peripheral clubbing, cyanosis, or edema. The remainder of the physical examination was unremarkable. Figure 3. Patient 2: Initial rhythm strip showing patient in widecomplex tachycardia at a rate of 180 before adenosine administration
The ECG monitor revealed a regular wide-complex tachycardia at a rate of 180 (Figure 3). The QRS width was 120 msec. The patient was placed on 2 L of oxygen through nasal cannula, and peripheral IV access was established. A 6-mg bolus of adenosine was administered with no clinically significant change in rate, rhythm, or vital signs. A second 12-mg dose was given, which terminated the wide-complex rhythm and restored a normal sinus rhythm at a rate of 97 (Figure 4). The patient experienced a transient period of facial flushing shortly after adenosine administration. Blood pressure remained stable, and he denied any further chest pressure or lightheadedness. A 12-lead ECG revealed a sinus rhythm with shortened PR intervals and delta waves (Figure 5). Serum electrolytes were within normal limits. The patient's private cardiologist was contacted, and a single 100-mg oral dose of flecainide was recommended before discharge and resumption of the previous dosing schedule. The patient was discharged approximately two hours after conversion into sinus rhythm with no further ectopy or complaints. DISCUSSION
When faced with a wide-complex tachycardia, ventricular tachycardia always should be first in the differential diagnosis, especially in individuals with a history of heart disease. 4 Other causes include paroxysmal supraventricular tachycardia and atrial flutter or fibrillation with either fixed or rate-related bundle branch block, pre-excited reciprocating tachycardia, 5 and reciprocating tachycardia through a Mahaim fiber. 6 Immediate electrical cardioversion is the standard of care for unstable wide-complex Figure 4. Patient 2: Rhythm strip illustrating conversion of widecomplex tachycardia into a normal sinus rhythm shortly after administration of 12 rag adenosine. Patient remained hemodynamically stable during and after conversion with adenosine.
1 5 4/ 1 362
Figure 5. Patient 2: 12-lead ECG after conversion of wide-complex tachycardia into normal sinus rhythm
ANNALS OF EMERGENCY MEDICINE
22:8
AUGUST 1993
ADENOSINE
Ilhhanipour, Berrol & Yealy
tachycardia,r Stable wide-complex tachycardia remains a diagnosti c and therapeutic challenge. Formulating a specific diagnosis for hemodynamically stable wide-complex tachycardia based on initial clinical assessment remains a difficult task for even the most astute physician. Because the diagnosis of these rhythms is challenging, it would be beneficial to have a drug that has both therapeutic and diagnostic efficacy while having minimal associated morbidity. Current therapeutic options other than adenosine for an undiagnosed stable wide-complex tachycardia are limited. Lidocaine remains the drug of choice in the initial management of stable ventricular tachycardia. Procainamide is approved and commonly available for IV administration in the United States. It is the drug of choice for stable patients with a wide-complex tachycardia of indeterminate cause, especially if an antidromic tachycardia or atrial fibrillation with Wolff-Parkinson-White syndrome is suspected.S, 9 Procainamide must be given slowly (50 mg/min up to a maximum of 18 mg/kg) and can cause hypotension. Magnesium is also useful in ventricular tachycardia, supraventricular tachycardia, and many atrial dysrhythmias but is not weil studied in WolffParkinson-White syndrome and indeterminate widecomplex tachycardias, to Many drugs effective in controlling or terminating supraventricular tachycardias are potentially dangerous in ventricular tachycardia and Wolff-Parkinson-White syndromes. Digoxin, r-blockers, and class IV agent calcium channel blockers can convert or control the ventricular response rate in most atrial flutter or fibrillation and paroxysmal supraventricular tachycardia. However, calcium channel blocking drugs, such as verapamil, and digoxin can precipitate hemodynamic collapse in patients with Wolff-Parkinson-White syndrome and antidromic tachycardia or atrial flutter or fibrillation. Our cases demonstrate the safety of adenosine as a therapeutic and/or diagnostic adjunct in the hemodynamically stable patient with a wide-complex tachycardia. The mechanism of action and side effect profile of adenosine have been described. 1i,12 To date, only two cases of brief hemodynamic collapse have been reported with adenosine administration. ~3 Both cases involved short episodes of asystole or bradycardia resulting in 15 to 20 seconds of unconsciousness followed by the return of a perfusing rhythm and patient reawakening. These reports highlight the rare potential of significant asystole, bradycardia, and hypotension associated with adenosine. It Would be prudent to have an external pacemaker available at the bedside when using adenosine.
AUGUST 1993
22:8
ANNALS OF EMERGENCY MEDICINE
In 1989, Rankin and colleagues2 evaluated the use of adenosine in the treatment of both narrow- and broadcomplex tachycardias. In their series of 24 patients with broad-complex tachycardias, six patients had their dysrhythmias terminated with adenosine, whereas atrioventricular block was induced in four patients long enough to reveal atrial or ventricular tachycardias. The tachycardias persisted in the remaining 14 patients without any ill effects related to adenosine administration. The diagnostic potential of adenosine is related to its ability to slow conduction temporarily through the atrioventricular node.Z,2,12 High-grade atrioventricular nodal block would unmask atrial activity by the temporary reduction or elimination of infranodal electrical activity, while having no adverse hemodynamic effects on ventricular tachycardia. Specific diagnosis could be facilitated in patients whose wide-complex tachycardias were secondary to atrial flutter, atrial fibrillation, intra-atrial re-entry, or accessory pathways. In a study by Rankin and associates, 2 adenosine produced atri0ventricular block with termination or diagnosis of tachycardias of supraventricular origin with a sensitivity of 90%, specificity of 93%, and predictive accuracy of 92%. Both patients presented in our case report had known Wolff-Parkinson-White syndrome. The firs[ patient's widecomplex rhythm was primarily of the orthodromic atrioventricular reciprocating type in which anterograde conduction occurs through the atrioventricular node and retrograde conduction occurs through the accessory pathway. This dysrhythmia pattern is thought to be present in more than 80% of patients with Wolff-Parkinson-White syndrome who are symptomatic. 14 Orthodromic atrioventricular reciprocating tachycardias usually present with a narrow QRS complex (less than 90 msec). Our patient had a rate-related bundle branch block, which was responsible for the wide QRS morphology. The second patient most likely demonstrated an antidromic tachycardia secondary to the shortened PR interval and delta waves present on his ECG after conversion. However, we had no access to his electrophysiologic records and can only assume that he had antidromic conduction. Antidromic tachycardias traverse the same circuit but travel in the opposite direction. The ventricles are depolarized through the accessory pathway, resulting in a wide-complex tachycardia. Antidromic tachycardias represent only 11% of tachydysrhythmias seen with Wolff-Parkinson-White syndrome. 15 Although adenosine has unclear effects on accessory pathway conduction, it may interfere with both antegrade and retrograde conduction in the atrioventricular node. 16 It is this latter effect
1363/ 155
ADENOSINE
IIkhanipour, Berrol & Yealy
that may be responsible for termination of the reciprocating tachycardia. Based on our experience, we believe a therapeutic and diagnostic trial of adenosine in stable patients with
A d d r e s s for reprints:
Kaveh Ilkhanipour, MD Mercy Hospital Department of Emergency Medicine
regular wide-complex tachycardias is reasonable. Its
1400 Locust Street
use in patients with atrial fibrillation or flutter and Wolff-
Pittsburgh, Pennsylvania 15219-5166
Parkinson-White syndrome is not recommended currently. Immediate cardioverting capabilities should always be available in case of hemodynamic deterioration. SUMMARY
We report two cases of Wolff-Parkinson-White syndrome in which adenosine was given as a therapeutic and diagnostic adjunct in the setting of stable wide-complex tachycardia. We believe that this experience illustrates the safety and effectiveness of adenosine in wide-complex tachycardia. REFERENCES 1. SharmaAD, Klein GJ, Yea R: Intravenous adenosine triphosphate during wide QRS complex tachycardia: Safety, therapeutic efficacy, and diagnostic utility. Am J Mad 1990;88:337-342. 2. RankinA, Oldroyd KG, Chong E, et al: Value and limitations of adenosine in the diagnosis and treatment of narrow and broad complex tachycardias. Br HeartJ 1989;62:195-203. 3. Johe RL, GallagherJJ: Use of adenosine during hypotension in the Wolff-Parkinson-WKte syndromewith supraventricular tachycardia. Am HeartJ 1991;121:1239-1240. 4. Faitelson L, GordonAE: Clinical algorithm: Treatment ef supraventriculartachycardia. Hosp Mad 1991;Nov:37-40. 5. Akhtar M, ShenasaM, JazayeFiM, et aL Wide QRS complex tachycardia: Reappraisalof a common clinical problem. Ann InternMad 1988;109:905-912. 6. Bardy GH, PackerDL, GermanLD, et al: Preexeitedreciprocating tachycardia in patients with Wolff-Parkinson-White syndrome: Incidenceand mechanisms, Circulation1984;70:377-391. 7. Bardy GH, FaderGM, German LD, et al: Surface electrocardiographicclues suggesting presence of a nedofasicular Mahaim fiber. J Am Coil Cardio11984;3:1161-1168. 8. Wellens HJJ, 9rugada P, Penn OC: The management of,preexcitation syndromes. JAMA 1987;257:2325-2333.
ERRATA In the article "Upper-Extremity Deep-Vein Thrombosis: Thrombolytic Therapy With Anistrepalase" [April 1993;22:748-750], the sentence at the bottom of page 749 and top of page 750 should read "APSAC has been used to treat acute myocardial infarction,17, ~s seems to be as effective as tissue plasminogen activator and streptokinase,2o and causes no more serious side effects such as hemorrhage.17,20 In the article "Needle Thoracostomy FaiIs to Detect a Fatal Tension Pneumothorax" [May 1993;22:863-866], arrows 1 and 2 in the Figure were reversed. The figure shouId appear as shown below.
9. Arai A, Kron J: Current management of the Wolff-Parkinson-White syndrome, WestJ Mad 1990;152:383-391. 10. KerenA, Tzeivoni D: Magnesium therapy in ventricular arrhythmias. PACE1990;7:937-945. 11. Vidt DG, Bakst AW: Adenosine: A new drug for acute termination of supraventricular tachycardia. CleveClinJ Mad 1990;57:383-388. 12. DiMarco JP, Sellers TD, Berne RM, et al: Adenosine: Electrophysiologiceffects and therapeutic use for terminating paroxysmaltachycardia. Circulation1983;68:1254-1263. 13. Reed R, FalkJL, O'Brien J: Untoward raactien to adenosine therapy for supraventricular tachycardia. Am J EmergMad 1991;9:566-570. 14. GallagherJJ, Pritchett ELC,Scaly WC, et ah The preexcitation syndromes. ProgCaldiovasc Dis 1978;20:285-327. 15. Atie J, BrugadaP, BrugadaJ, et ah Clinical and electrophysiologic characteristics of patients with antidromic circus movementtachycardia in the Walff-Parkinson-White syndrome. Am J Cardiol1990;66:1082-1091:.
Figure.
Autopsy photograph of the thoracic structures after the anterior chest wall was removed. Although the right middle and lower lobes (arrow 2) are collapsed as expected, the right upper lobe (arrow 2) is still inflated because of air trapped in bullae. A chest tube is present i n the left hemithorax.
16. DimarcoJP: Adenosine and suprayentricu/artachycardia, in Peileg A, Michelson EL, Dreifus LS (eds): CardiacElectrophysiologyand Pharmacologyof Adenosine andA TP:Basicand Clinical" Aspects. New York, Alan R Liss, 1887, p 271-281.
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ANNALS OF EMERGENCY MEDICINE
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AUGUST 1993