Successful use of emergency transthoracic pacing in bradyasystolic cardiac arrest

Successful use of emergency transthoracic pacing in bradyasystolic cardiac arrest

CASE REPORT cardiac arrest, pacing; pacing, transthoracic Successful Use of Emergency Transthoracic Pacing in BradyasystoUc Cardiac Arrest We present...

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CASE REPORT cardiac arrest, pacing; pacing, transthoracic

Successful Use of Emergency Transthoracic Pacing in BradyasystoUc Cardiac Arrest We present the documented successful resuscitation of six patients using emergency transthoracic pacing. Two patients were resuscitated from asystole, one had a slow supraventricular bradycardia following head trauma and spinal shock, and three patients had cardiovascular collapse secondary to complete A-V dissociation. One patient developed a non-fatal pericardial tamponade, but there were no cases of pneumothorax. All patients failed to respond to standard medical therapy. We believe that the initially successful resuscitation of these patients was related directly to the pacing procedure. Three patients had underlying pathology that did not allow longterm survival. Three patients were discharged from the hospital without neurologic sequelae. Although emergency transthoracic pacing has a relatively low success rate in bradyasystolic cardiac arrest and may be associated with serious complications, the procedure may be life-saving in selected cases. [Roberts JR, Greenberg MI, Crisanti J~, Gayle SW: Successful use of emergency transthoracic pacing in bradyasystolic cardiac arrest. Ann Emerg Med April 1984;13:277-283.]

James R Roberts, MD* Michael I Greenberg, MD* Philadelphia, Pennsylvania John W Crisanti, MDt Point Pleasant, New Jersey Sigsby W Gayle, MD:~ Richmond, Virginia From the Division of Emergency Medicine, Medical College of Pennsylvania, Philadelphia;* the Division of Emergency Medicine, Point Pleasant Hospital, Point Pleasant, New Jersey;I- and Chippenham Hospital, Richmond, Virginia:l: Received for publication August 31, 1982. Revision received May 23, 1983. Accepted for publication September 27, 1983.

INTRODUCTION

Despite sophisticated advances in mechanical resuscitation devices, the deployment of mobile intensive care units, the introduction of potent cardioactive drugs, and unraveling the vagaries of the mechanics of cardiopulmonary resuscitation {CPR), the percentage of successful resuscitations from cardiac arrest has remained relatively constant. Most centers report survival rates in the 15% to 20% range 1 for all types of cardiac arrest with standard advanced cardiac life support (ACLS) regimens. However, the majority of successful resuscitations involve patients with ventricular fibrillation who have access to immediate CPR and defibrillation or who suffer cardiac arrest in a hospital environment. Survival rates for patients with asystole or pulseless idioventricular rhythm are quite low, and the mortality rate associated with these rhythms approaches 100%.z-4 Obviously any technique or therapy that would improve these dismal statistics would be highly desirable. In the 1960s a popular clinical technique was developed that was termed "transthoracic pacing." The procedure involved the percutaneous placement of cardiac pacing wires into the ventricular cavity or ventricle wall by a transthoracic needle.s,6 In early clinical trials, transthoracic pacing was generally successful in treating bradycardia and A-V dissociation. Forty-four successful cases of transthoracic pacing for various types of bradycardia and heart block appear in the medical literatureff However, successful use of the procedure in bradyasystolic arrest has been mostly anecdotal. With the development of reliable transvenous pacemakers in the 1970s, the technique was largely forgotten. In the past few years, efforts to reduce the high mortality rates associated with bradyasystolic cardiac arrest have led to the revival of the procedure and to the sporadic use of transthoracic pacing in the emergency department. In our report, the term "transthoracic pacing" applies only to the percutaneous placement of wires by a trocar needle, and is not to be covdalsed with the implantation of pacing wires under direct vision through a thoracotomy. The equipment used in all cases was a 37-cm, J-shaped bipolar pacing

13:4 April 1984

Annals of Emergency Medicine

Presented at the Scientific Assembly of the American College of Emergency Physicians in San Francisco, September 1982. Address for reprints: James R Roberts, ME), Division of Emergency Medicine, Medical College of Pennsylvania,3300 Henry Avenue, Philadelphia, Pennsylvania 19129.

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TRANSTHORACIC PACING Roberts et am

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Fig. 1. Original rhythm in the patient in case number one. Note the presence of complete A-V dissociation and premature ventricular contractions. The patient developed ventricular fibrillation shortly after this strip was obtained. Fig. 2. After the third episode of ventricular fibrillation in case number one, a transthoracic pacemaker was placed with immediate capture. Ventricular fibrillation did not recur. wire introduced through a 6-inch, 18gauge blunt-end steel cannula with a pointed inner trocar needle (Elecath ll-KTM, Electrocatheter Corporation, Rahway, NJ). Recently the procedure has been reviewed extensively and clinical guidelines have been presented, z but controlled prospective trials of emergency transthoracic pacing in bradyasystolic cardiac arrest have not been forthcoming. We present the cases of six patients in whom transthoracic pacing was thought to be beneficial in initial resuscitation from bradyasystolic cardiac arrest. One case of cardiac tamponade directly related to the procedure is reported.

CASE REPORTS Case Number One A 65-year-old woman was brought 102/278

to the emergency department after collapsing at home. Her husband stated that she had become acutely confused, had collapsed to the floor, and became pale and diaphoretic. On admission she had a palpable systolic blood pressure of 80 to 90 m m Hg and an apical heart rate of 35 to 45/min. An ECG demonstrated an acute inferior-posterior myocardial infarction and complete A-V dissociation with multiple premature ventricular contractions (Figure 1). Shortly after arrival she developed ventricular fibrillation (VF) but was quickly converted to the original complete A-V dissociation with a single 200-watt-second defibrillation. Despite intravenous lidocaine, atropine, isoproterenol and bicarbonate, she suffered VF two more times. Each episode of fibrillation was quickly converted with countershock, but the A-V dissociation remained. After the third episode of VF, a transthoracic pacemaker was placed. Ventricular capture was immediate and the patient became stable with a blood pressure of 80 to 90 m m Hg (Figure 2). A chest film demonstrated the pacemaker wire to be in the fight ventricle {Figure 31. The patient was transferred to the coronary care unit {CCU), where a transvenous pacemaker was passed under fluoroscopic control. The transAnnals of Emergency Medicine

thoracic pacemaker was removed. The patient remained hypotensive but stable until eight hours after admission, when she died suddenly. An echocardiogram shortly before death revealed a large pericardial effusion and probable posterior wall myocardial rupture. No autopsy was obtained.

Case N u m b e r Two A 56-year-old woman was brought to the emergency department in cardiorespiratory arrest. The paramedic unit had been called to the patient's home, where she was found to be pulseless and apneic. In the field an esophageal obturator airway ® (EOA ®) was inserted. A peripheral intravenous line |IV I was established, bicarbonate and epinephrine were given, and CPR was initiated and continued en route to the hospital. On presentation the patient was noted to be putseless without CPR but had palpable carotid pulses with CPR. She was apneic and slightly cyanotic. Endotracheal.intubation was performed, followed by EOA ~ removal. Quicklook paddles appliedi to the anterior chest revealed VF. Following IV bicarbonate and epinephrine, the patient was defibrillated with 400 watt-seconds. Immediately following electrical c o u n t e r s h o c k , the ECG demonstrated asystole (straight line). CPR was reinstituted and a trans13:4 April 1984

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myocardial pacemaker was inserted by the subxiphoid route. Immediate capture of the pacemaker was noted. The paced beats produced a systolic blood pressure determined by Doppler ultrasound to be approximately 44 m m Hg. The patient was then transported to the radiology department, where a t e m p o r a r y transvenous p a c e m a k e r was placed by the right internal jugular route. The transmyocardial pacemaker was removed w h e n transvenous capture was established. At this time, the patient was noted to have radiographic evidence of congestive heart failure. The patient's vital signs remained stable and she recovered consciousness in 48 hours, at which time she was extubated. There was no evidence of pneumothorax or pericardial effusion and the congestive heart failure had resolved. The patient was noted to have normal sinus r h y t h m w i t h o u t evidence of heart block, and the transvenous pacemaker was removed on the eighth hospital day. She was discharged on the 21st day following admission. At the time of discharge, she was alert and oriented without evidence of neurologic deficit. She renamed to her prehospital occupation.

Case Number Three A 2V2-year-old girl was hit by a car and suffered multiple injuries. The 13:4 April 1984

paramedic team at the scene reported no spontaneous respiration, no detectable blood pressure, and a totally unresponsive patient with fixed and dilated pupils. They were unable to start an IV and could not innabate the patient successfully, CPR was initiated and 2 mL 1:10,000 epinephrine was given at the base of the tongue. The patient arrived in the emergency department 20 to 30 minutes following the accident. Her pupils were fixed and dilated, and no blood pressure or spontaneous respiration was noted. An ECG demonstrated a slow, narrow QRS complex rhythm, probably junctional bradycardia, at a rate of 20/rain. The patient was innabated and given intravenously a total of three ampules of sodium bicarbonate, 2 mL hl0,000 epinephrine, and 0.25 mg atropine. CPR produced palpable pulses, but no blood pressure was obtainable. The ECG remained unchanged. A transmyocardial pacemaker was inserted by the left subxiphoid approach. Within 15 seconds capture was noted, and a systolic blood pressure of 60 m m Hg was m e a s u r e d s h o r t l y thereafter. With blood replacement the blood pressure stabilized at 90 m m Hg. After half an hour, the pacer was named to the demand mode and an intrinsic sinus tachycardia was noted. While she was on a respirator, the patient's blood pressure remained stable. Annals of Emergency Medicine

Later that evening the patient was pronounced clinically brain-dead and life support efforts were ceased. Although no autopsy was performed, the patient's death was attributed to severe closed head injury and a fracnaredislocation of the cervical spine. A postmortem chest film demonstrated the pacing wire to be in the right ventricle. No pneumothorax or pericardial effusion was seen.

Case Number Four A 48-year-old chronic alcoholic suffered a cardiac arrest in an automobile in the parking lot of the emergency department. Resuscitation was begun within five minutes following arrest. During intubation the patient vomited and aspirated stomach contents. He was found initially to be in VF, and defibrillation produced a straight line on the ECG. Because this rhythm did not respond to CPR and intravenous medications that included 2 ampules of bicarbonate, 1 mg atropine, and 10 cc epinephrine (1:10,000), a transthoracic pacemaker was inserted by the subxiphoid route. CPR was continued during the placement of the pacemaker. Capture of the pacemaker occurred immediately, and within five minutes the patient was awake and a systolic blood pressure of 100 m m Hg was obtained. The patient developed a sinus tachycardia and the pacemaker 279/103

TRANSTHORACIC PACING Roberts et al

Fig. 3. Chest film from case number one demonstrates the presence of a transthoracic pacemaker wire in the right ventricle.

was placed in the demand mode. During the next hour the patient developed a severe resistant metabolic acidosis and was successfully resuscitated twice from VF. During the resuscitation CPR was continued for a total of 30 minutes. The patient was stabilized, but a systolic blood pressure of 70 to 80 m m Pig persisted. At this t i m e the central venous pressure was noted to be 19 cm H20, the QRS complex developed low voltage, the heart sound could not be heard, and a pulsus paradoxus was felt on palpation of the femoral artery. An ECG did not demonstrate an acute injury pattem. Pericardiocentesis was performed and 140 cc of non-clotting blood was obtained. The pacing wire was rem o v e d at this time. An echocardiogram demonstrated a residual pericardial effusion, and a subxiphoid pericardiotomy was performed at the bedside. An additional 200 cc of blood was obtained. A repeat echocardiogram failed to demonstrate any residual fluid. The patient died the next day. No autopsy was performed, and the cause of death was listed as a hemorrhagic pancreatitis and sepsis.

Case Number Five A 78-year-old man presented complaimng of an acute onset of dizziness, vomiting, and sweating. He had a history of a myocardial infarction, congestive heart failure, and a transient episode of complete heart block. On examination the patient was diaphoretic and pale, with a blood pressure of 138/98 m m Hg; pulse, 28; and a respiratory rate of 24. The chest was clear, and there were no murmurs, gallops, clicks, or robs. An ECG showed complete A-V dissociation with a ventricular rate of 28/ min. The patient's rate dropped to 16, and his blood pressure was palpable at 80 m m Hg. Intravenous atropine and an Isuprel drip increased his heart rate to 40, and he was transferred to the radiology department for fluoroscopic insertion of a transvenous pacemaker. While he was in the radiology department, the ventricular rate fell to less than 20/rain with no palpable blood 104/280

pressure. The patient was intubated and CPR was initiated. A transthoracic pacemaker was inserted by the subxiphoid approach, with immediate capture and stabilization of vital signs. A transvenous pacemaker was then inserted into the fight internal jugular vein, also with capture. Both the t r a n s t h o r a c i c and the transvenous pacemakers were left in place and the patient was transferred to the CCU. Because the transvenous pacemaker showed intermittent failure to capture, both pacemakers were left in place. The transthoracic pacer was used as a stand-by with consistent capture during the episode of transvenous pacemaker failure. Three days after the pacemaker insertions, the patient developed a pericardial rub that subsided a f t e r 48 hours. Six days post insertion, the transthoracic pacemaker was withAnnals of Emergency Medicine

drawn and a cardiac ultrasound at that time showed no evidence of pericardial effusion. The transvenous pacemaker was replaced by a permanent pacemaker on day nine, and the patient was discharged from the hospital on day 17 with no significant neurologic or cardiovascular compromise.

Case Number Six An 80-year-old man with a longstanding history of coronary artery disease, hypertension, myocardial infarction, and congestive heart failure had the sudden onset of e x t r e m e weakness, shortness of breath and vertigo, almost to the point of syncope. He was walking in his yard and "almost passed out." Emergency department evaluation revealed an elderly man who was slightly dyspneic at rest, with vital signs as follows: blood pressure, 68 to 40/0 m m Hg; pulse, 34 13:4 April 1984

and irregularly irregular; and respirations, 26/rain. Initial ECG revealed idioventricular rhythm at a rate of 30 to 32/min, with complete heart block. He was given 0.5 mg atropine sulfate W, and the pulse rate increased to 74/min. After one minute the pulse rate slowed to 40/min. The patient then c o m p l a i n e d of s h o r t n e s s of breath and was quite lethargic and dyspneic. An Isuprel drip with 1 mg Isuprel in 1,000 cc D5W was initiated. Pulse rate increased to 50/min. However, there was a drop in systolic blood pressure to 40 m m Hg. A transthoracic pacing catheter was inserted by a left subxiphoid approach, and pacing was initiated i m m e d i a t e l y without difficulty at a rate of 70/min at m_A of 2.0, with threshold 0.2 mA. After a few minutes the blood pressure was 100/70 m m Hg with pacing and a titrated infusion of dopamine. Other studies obtained shortly after arrival included a chest film that revealed cardiomegaly with congestive heart failure. The transthoracic pacing catheter was noted to be present within the heart and was thought to be in the right ventricular cavity, A temporary transvenous pacing catheter was inserted from a cutdown site over the left basilic vein under fluoroscopy. Threshold for the transvenous pacing catheter was 0.2 mA. The transthoracic pacer was left in place and the patient was admitted to the CCU. After several hours there was failure of the temporary transvenous pacing catheter, at which time pacing was r e i n s t i t u t e d using the transthoracic pacing catheter, which functioned well. The temporary transvenous pacing catheter was repositioned and functioned satisfactorily for the next several days. His overall condition slowly improved and he stabilized. He subsequently was taken to the surgical suite to have a permanent transvenous pacemaker implanted in the right pectoral region with a catheter introduced into the right cephalic vein. Both temporary pacing catheters were removed at that time without difficulty, There was no evidence of pneumothorax or pericardial tamponade. The patient continued to improve slowly and was discharged w i t h no neurologic sequelae.

DISCUSSION Although earlier reports of successful transthoracic pacing for drug-resistant bradycardia and heart block 13:4 April 1984

were encouraging, S the technique did not gain much popularity in the cardiac arrest situation. Most textbooks only briefly mention the transthoracic route of pacing, vaguely stating that it should be used in an emergency situation,9 or fail to reference the technique at all.lo, 11 Anecdotal clinical experience with emergency transthoracic pacing in bradyasystolic cardiac arrest generally has not been favorable, and a consensus on its value cannot be gleaned from the sparse medical literature. Generally the technique has been used in a final effort to resuscitate a patient after all other regimens have failed. Often the severity of the underlying pathology or the length of time w i t h o u t adequate prehospital CPR preclude successful resuscitation by any means, and the t r a n s t h o r a c i c pacer is placed merely as a terminal gesture. Indeed previous attempts to pace an asystolic heart after other standard methods of resuscitation have failed have been fruitless.3,12. Recently Tintinalli and White 12 reported a retrospective series of 21 unsuccessful resuscitations in which the transthoracic pacer was used in bradyasystolic cardiac arrest. Transient capture occurred in eight of 21 cases in their series, but there were no longterm survivors. Cardiac tamponade occurred in one patient, and it was suggested that this complication was a direct result of the procedure. They concluded that the pacer does not alter outcome in bradyasystolic arrest if standard ACLS therapy has been unsuccessful. White 3 retrospectively reviewed 139 patients who presented with asystole or developed asystole following defibrillation and received delayed transthoracic pacing. He found no longterm survivors. He also concluded that transthoracic pacing provides no benefit if the procedure is delayed for more than a few minutes following the onset of asystole, and advocated a study that investigates the benefit of immediate pacing. Edhag et a113 reported a series of 20 patients who developed asystole in the CCU and had t r a n s t h o r a c i c pacemaker wires placed rapidly. This small series had one patient survive to eventual hospital discharge. Baksi 14 likewise reported 20 cases in which immediate transthoracic pacing was used to treat asystole and had one survivor. However, retrospectively, only four of the 20 patients had potentially reversAnnals of Emergency Medicine

ible pathology. It is very difficult indeed to assess the benefit of one therapeutic intervention in a situation in which a number of procedures, medications, and other variables are employed simultaneously. Likewise it would be very difficult to design a clinical trial that would define precisely the role of emergency pacing in cardiac arrest. It has been our experience, however, that transthoracic pacing can be a valuable adjunctive therapy in the proper clinical situation. We directly attribute the initial successful resuscitation of our six patients to transthoracic pacing. Unfortunately, as is often the case in cardiac arrest, the severity of the underlying clinical condition did not predispose to long-term survival in three patients. With the current state of knowledge, it is impossible to speculate on possible changes in survival rates if transthoracic pacing were used roufinely in the initial treatment of bradyasystolic cardiac arrest. It is our opinion that the procedure has a real, albeit relatively low, success rate. Although it is commonplace in our institution to attempt pacing in bradyasystolic cardiac arrest, specific criteria and time of insertion vary among physicians and no controlled statistics are available. As a very rough estimate of success rate, these six cases are compared to approximately 40 to 60 unsuccessful attempts at transthoracic pacing in cardiac arrest. A detailed discussion of the clinical indications for transthoracic pacing and the specifics of the actual procedure has been published recently,7 and our report will not attempt to summarize that discussion. Emergency pacing is not a panacea for cardiac arrest, and not all causes of sudden death may be amenable to pacing. However, one may speculate under what circumstances pacing might be beneficial. Because pacing would have little to offer in the treatment of VF, its use cannot be advocated in this arrhythmia. Electromechanical dissociation (EMD}, which Can result from primary cardiac disease, hypovolemia or cardiac tamponade, can be defined as electrical activity in the absence of blood pressure, pulse, or audible heart sounds. 15 Occasionally this condition is associated with a relatively normal QRS complex at an acceptable rate. In such cases the addition of another 281/105

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electrical stimulation in the form of a pacemaker would not be beneficial. However, if the EMD is associated with an u n a c c e p t a b l y slow supraventricular rate or if the EMD is associated with a slow, bizarre QRS complex idioventricular rhythm, we advocate the use of a pacer. As demonstrated in our cases, asystole or severe ventricular bradycardia are r h y t h m s for which pacing would most likely be useful. Obviously, vigorous correction of hypoxia and electrolyte and acidbase disturbances must be instituted simultaneously. Complete heart block with a slow ventricular response is a well-accepted indication for emergency pacing. 1° Some patients may be stabilized with medication long enough to allow the placement of a transvenous pacer. However, the presence of lethal escape rhythms, cardiogenic shock, or inadequate cerebral perfusion requires immediate therapy and one does not have the luxury of time, fluoroscopy, ECG guidance, or blood flow to float a transvenous pacemaker. As noted in this report, these unstable patients are candidates for transthoracic pacing. We believe that pacing would be most effective following cardiac arrest from primary heart disease, although such events as asphyxia or neardrowning may also be responsive to pacing. Asystole may occur secondary to such a catastrophic event as cardiac rupture, and no form of therapy can be expected to alter the mortality rate from such an event. Often asystole is not a primary event, but rather it is the end result of m a n y minutes of untreated ventricular tachycardia or ventricular fibrillation. Asystole on presentation to the emergency department is almost universally terminal with current therapy. Similarly cardiac collapse secondary to hypovolemia, sepsis, severe acidosis or electrolyte abnormalities, or drug intoxication would be less likely to respond to pacing. 16 Millikan et a117 reported life-saving benefit from emergency pacing in two trauma arrest victims. Emergency epicardial pacing was used in two patients with penetrating thoracic injuries with bradycardia unresponsive to cardiac medication and volume replacement. One does not u s u a l l y think of pacing the trauma victim but, as our third case report demonstrates, it may be a valuable technique to consider if standard trauma resuscitation therapy is unsuccessful. 106/282

Timing of Pacing We do not believe that pacing instituted after ACLS therapy has failed will result in any successful resuscitations, and our opinion has been bome out in the literature.a, 12, In order to be useful clinically, pacing must be introduced before irreversible brain damage has occurred and before cardiac metabolic activity has degenerated into terminal or irreversible stages. Our successful resuscitations seem to indicate that bradyasystolic cardiac arrest p e r s e is not synonymous with irreversibility. The criteria for irreversibility, however, are extremely difficult to assess within the short period of time in which the e m e r g e n c y p h y s i c i a n m u s t decide whether to even attempt resuscitation and whether to consider transthoracic pacing. Therefore resuscitation is usually initiated before other pertinent clinical or historical data are available and usually before a cause for the arrest has been identified. Retrospectively this m a y result in m a n y attempts to resuscitate uusalvageable or obviously dead patients, and it relegates to any therapy a low success rate. It is certain that e m e r g e n c y transthoracic pacing will not resuscitate irreversibly dead patients. We believe that patients who have had the benefit of prehospital life support, or who suffer bradyasystolic arrest from a treatable or reversible cause, have the best chance of initial resuscitation and long-term survival with transmyocardial pacing. Some m e d i c a l t h e r a p y was attempted in our patients before pacing was introduced. In asystole or slow idioventricular rhythm, it is our opinion that, following intubation, transthoracic pacing should be instituted before or in conjunction with initial medical therapy. One should continue efforts at pacing throughout the resuscitation, because correction of hypoxia and acidosis may alter the threshold for stimulation of the myocardium, is The use of transthoracic pacing in A-V dissociation will depend on the clinical condition of the patient.

Complications In our experience, bleeding serious enough to produce pericardial tamponade is quite rare but can occur. It has also been our experience, from autopsy findings in patients who have not been resuscitated successfully, that all patients experience some pericardial bleeding from transthoracic Annals of Emergency Medicine

p a c e m a k e r insertion. The bleeding may be limited to only a few milliliters, but it can be considerably more if the patient has a bleeding diathesis or is taking anticoagulants, or if CPR is performed for an extended period of time. Significant pericardial bleeding from the procedure has been reported in the past.6,12 One would expect that pneumothorax (or tension pneumothorax I would also be more prevalent if the pacer is combined with vigorous CPR and positive pressure ventilation, although pneumothorax from this procedure has not been reported in the literature and has not occurred in our hands when the subxiphoid approach has been used. No clotting studies were available on the patient with pericardial tamponade, but his alcoholic h i s t o r y could easily have predisposed him to bleeding tendencies. Prolonged CPR may have also contributed to the pericardial bleeding.

Future Considerations Although resuscitation from bradyasystolic cardiac arrest in the emergency department with transthoracic pacing m a y be infrequent, we have documented success. Its use as an initial mode of therapy is encouraged until valid clinical studies prove otherwise. Asystole in the e m e r g e n c y department may indeed prove to be a terminal event; however, such dismal projections were once made for VE Cardiac pacing in the field has not yet received an adequate clinical trial, and emergency pacing by paramedics may prove to be beneficial. It is interesting to speculate on the theoretical advantages of pacing equipment that can be applied quickly and easily in the prehospital care of bradyasystolic cardiac arrest.

SUMMARY We have presented the cases of six patients in w h o m emergency transthoracic pacing was instituted early in their resuscitation from bradyasystolic cardiac arrest. We surmised that the initial successful resuscitation was directly related to the pacing procedure. The development of a pericardial tamponade in one patient demonstrated that the procedure is not w i t h o u t complications. The procedure should not be used indiscriminately; whenever the time and clinical situation permit, transvenous pacing should be the procedure Of choice. In addition the transthoracic route should not be 13:4 April !984

used if t h e p a t h o l o g y is q u i c k l y or easily reversed w i t h medication. Currently insufficient data are available to c o m m e n t on t h e p o s s i b l e changes in survival rates if emergency transthoracic pacing were used routinely in bradyasystolic cardiac arrest. Although the procedure cannot be exp e c t e d to r e s u s c i t a t e an o b v i o u s l y dead or unsalvageable patient, it m a y be valuable in selected cases of bradyasystolic cardiac arrest. Because the exact cause of bradyasystolic cardiac arrest is usually u n k n o w n w h e n decisions a b o u t r e s u s c i t a t i o n m u s t be made in the e m e r g e n c y department, we advocate that pacing be used as initial therapy in the resuscitation efforts. The procedure should not preclude c o n c o m i t a n t use of previously proven p r i n c i p l e s of s t a n d a r d ACLS therapy.

REFERENCES 1. Schiriver JA: Results of cardiopulmonary resuscitation: A review. Topics in Emergency Medicine 1979;1:103-t08. 2. Iseri LT, Humphrey SB, Siner EJ: Prehospital bradyasystolic cardiac arrest. Ann Intern Med 1978;88:741-745. 3. White JD: Transthoracic pacing in car-

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diac asystole. American Journal of Emergency Medicine 1983;1:264-266. 4. Myerberg RJ, Conde CA, Sung RJ, et al: Clinical electrophysiologic and hemodynamic profile of patients resuscitated from prehospital cardiac arrest. A m J Med 1980;68:568-576. 5. Thevenet A, Hodges PC, Lillehei CW: The use of myocardial electrodes inserted percutaneousty for control of complete atrioventricular block by an artificial pacemaker. Dis Chest 1958;34:621-631. 6. Kodjababian GH, Gray RE, Keenan RL, et ah Percutaneous implantation of cardiac pacemaker electrodes. A m J Cardiol 1967;19:372-376. 7. Roberts JR, Greenberg MI: Emergency transthoracic pacemaker. Ann Emerg Med 1981;10:600-612. 8. Lillehei CW, Levy MJ, Bonnabeau RC, et ah Direct wire electrical stimulation for acute post surgical and post infarction complete heart block. Ann N Y Acad Sci 1964;111:938-949. 9. Kodjababian GH, Grey RE, Keenan RL, et ah Percutaneous implantation of cardiac pacemaker electrodes. A.m J Cardiol 1967;19:372-376 10. Braunwald E: Heart Disease. Philadelphia, WB Saunders Co, 1980.

Annals of Emergency Medicine

ll. Gottlieb R, Chung EK: Technique of temporary pacing, in Chung EK (ed): Artifical Cardiac Pacing, A Practical Approach. Baltimore, Williams & Wilkins,

1978. i2. Tintinalli JE, White BC: Transthoracic pacing during CPR. A n n Emerg Med 1981;10:113-116. !3. Edhag O, Nyquist O, Orsinius E, et al: Cardiac pacing through transthoracic electrode in acute myocardial infarction. Acta Med Scand 1972;192:145-147. 14. Baksi KB, Hossain A, Chopra DS, et al: Transthoracic pacing in ventricular asystole. J Indian Med Assoc 1973;60: 134-137. 15. Raizes G, Wagner G, Hackel D: Instantaneous nonarrhythmic cardiac death in acute myocardial infarction. A m J Cardiol 1977;39:1-6. 16. Hazard PB, Benton C, Milnor JP: Transvenous cardiac pacing in cardiopulmonary resuscitation. Crit Care M e d 1981;9:666-668. 17. Millikan JS, Moore EE, Dunn EL, et al: Temporary cardiac pacing in trauma arrest victims. A n n Emerg Med 1980; 9:591-593. 18. Bartecchi CE: Effects of hypoxia on pacemaker stimulation. Rocky Mountain Medical Journal, October 1973, p 50-52.

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