- Email: [email protected]
Transesophageal cardiac pacing
Transesophageal BERNARD
BURACK,
and
M.D., F.A.C.C.
Bronx,
E
Cardiac Pacing*
CARDIAC pacing has been accomplished in the past by three primary methods. One involves stimulation across the closed chest by large amounts of energy. In the second approach a transvenous electrode is passed into the right ventricle or right atrium from a peripheral vein, usually under fluoroscopic control. A third method is by direct heart puncture.’ We commenced animal experimentation in 1965 to determine the feasibility of cardiac pacing by means of an electrode passed into the esophagus through the oral cavity of dogs. Our initial attempts in the intact dog were unsuccessful. We did note that high current levels of 25 m.amp. did not appear to affect adversely the animal’s ability to swallow and eat on awakening from anesthesia. It was not until we sewed the esophagus to the back of the right ventricle that some degree of capture by means of an electrode in the esophagus was accomplished. This appeared to indicate that in the dog distance and position of the heart in relation to the esophagus was an important factor. With the electrode at the level of the esophagealgastric junction, hiccoughing was caused by diaphragmatic stimulation. We were encouraged to attempt our first clinical case because of the close relation of the human esophagus to the heart and its apparent ability to withstand large transient currents for cardioversion. B
M.D.,
F.A.C.C.
heart disease, with multiple myocardial infarctions, angina pectoris and congestive heart failure. Intermittent anticoagulation had been employed for suspected pulmonary emboli. The electrocardiogram for several years demonstrated an established left bundle branch block pattern. A ventricular aneurysm had been suspected radiographically and electrocardiographically. The patient had been receiving digoxin, quinidine, nitroglycerine, tolbutamide, isosorbide dinitrate, hydrochlorothiazide and a 500 mg. sodium diet. Physical examinntion revealed the point of maximal impulse to be in the sixth intercostal space at the mid-clavicular line. A left parasternal heave was
present. A grade 3/6 systolic ejection murmur and a friction rub were heard along the left sternal border. The lungs were clear. Palpation of the left calf revealed a localized area of tenderness on the posterior lateral aspect with a 3 cm. venous cord deep in the calf. The serum glutamic oxalactic transaminase (SGOT) was 154 units on admission and gradually fell to 39 units on September 5. The lactic dehydrogenase (LDH) on admission was 880 units and remained essentially the same. -4 presumptive diagnosis of thrombophlebitis with pulmonary embolism was made. The possibility of a fresh myocardial infarction concealed by the left bundle branch block pattern on the electrocardiogram was considered. In addition to the patient’s customary medications, treatment with heparin, bed rest, warm packs to the left leg, and elastic bandages was instituted. The hospital course was uneventful until the morning of September 6, when the patient experienced the onset of right leg pain, recurrent chest pain, nausea and retching. Respiratory arrest and coma were noted at 7:45 A.M., when the cardiac arrest team was summoned. The patient was found to be in ventricular fibrillation (Fig. 1A). Defibrillation was accomplished by D.C. electroshock, which was followed by cardiac arrest. Intracardiac administration of epinephrine resulted in a return of ventricular fibrillation.
REPORT
A woman aged 65 had her fifth admission to Montefiore Hospital and Medical Center on August 32, 1967. She entered with the chief complaint of pain in the left calf of 24 hours’ duration accompanied by left precordial was a well established
FURMAN,
New York
MERGENCY
CASE
SEYMOUR
pain for several hours. There history of arteriosclerotic
* From the Cardiology Service, Medical Division and the Cardio-Thoracic Service, Surgical Division, Monteliore Hospital and Medical Center, Bronx, N. Y. This study was supported in part by Grant No. HE 09368-03 from the LT. S. Public Health Service, Department of Health, Education, and Welfare. -Address for reprints: Bernard Burack, Cardiology Service, Montcfiore Hospital and Medical Center, 111 East 210 St., Bronx, N. Y. 10467. VOLUME
23.
MARCH
1969
469
470
Burack and Furman
Figure 1. Electrocardiogramduring and after respiratoryarrest. A, spontaneous ventricular fibrillation; B, idioventricular rhythm; C, transesophageal cardiac pacing; arrows point to pacer impulses.
She was defibrillated seven more times, subjected to continuous cardiac compression, endotracheand transferred to the intensive ally intubated, care unit in coma with idioventricular cardiac rhythm (Fig. 1B). An attempt at passage of a Flexible Platinum Probe (Davis and Geck) to the right ventricle to establish cardiac pacing8 was unsuccessful. In the absence of sustained cardiac contractions, the ability to pass the Flexible PIatinum Probe into the right ventricle has been disappointing in our hands, and we have abandoned the use of that instrument. Esophageal Pacing: A transvenous bipolar electrode, 58 cm. long, was then passed its entire length through the nose into the esophagus. It was connected to the internal output of an American Optical Co. Pacer
Figure
2.
trode catheter
Chest roentgenograms.
A, portable
Monitor, and gradually withdrawn until pacing occurred (Fig. 1C). Complete capture was not accomplished until the fixed rate of the pacer was raised to 110 impulses/min. This rate was required to eliminate ventricular irritability. The amperage and voltage applied at threshold were measured by a Tektronix 567 oscilloscope and found to be 15 m.amp. and 10 v., respectively, with a resistance of 660 ohms. The esophageal electrode was firmly attached to the external nares with adhesive tape. A portable roentgenogram of the chest revealed the electrode catheter to be in the esophagus at the level of D9-DlO, posterior to the left ventricle and 5 cm. above the diaphragm (Fig. 2). The patient was given lidocaine hydrochloride, bicarbonate sodium, intravenous fluids, and she was
anteroposterior
film; B, lateral
views of the elec-
in the esophagus. THE
AMERICAN
,JOURNAL
OF CARDIOLOGY
Transesophageal \.rntilated wirh a respirator. The central venous l)ressurt’ was monitored, and adequate urinary output was maintained. She was paced in this manner for 36 hours. At that time an electrocardiogram taken through the esophageal electrode revealed spontaneous atria1 activity. ‘I’he mode of pacing was then changed from asynchronous fixed-rate pacing to demand pacing utilizing the same esophageal electrode. Triggering of the pacemaker in the demand mode in the American Optical unit is mediated through the limb leads of the electrocardiogram and not by the stimulating eiectrode.4 On September 8 a tracheostomy was performed. The patient remained in deep coma and an electroencephelogram two hours before death showed no cerebral activity. Respiratory arrest occurred during a change of the tracheostomy tube. Widening of the QRS complex on the monitor immediately followed, with no response to the esophageal pacing. The patient died at 6 P.M. on September 8. The esophageal electrode had been in place 60 hours. Of this total 36 hours were spent in continuous fixedrate pacing and the remainder in demand pacing. NECKOPSY
FINDINGS
The postmortem examination was performed two hours after death. * A longitudinal section of the esophagus revealed the pacer catheter in the collapsed esophagus just posterior to the left ventricle and 4 cm. above the esophageal-gastric junction (Fig. 3). The immediate overlying pericardium was normal. The esophagus appeared grossly normal, without evidence of mucosal lesions. The distal end of the bipolar electrode was carefully located in situ, and two sutures were placed in the wall of the esophagus corresponding to the levels of the positive and negative poles (Fig. 4). The esophageal mucosa appeared normal histologically throughout, except for two small areas of mucosal erosions with acute inflammation found in the upper third of the esophagus where the bipolar electrode was located (Fig. 5). This was interpreted as pressure necrosis of the mucosa, commonly seen with any esophageal intubation. No areas of coagulative necrosis of the mucosa were present, as would be anticipated with mucosal burns. There was hemorrhage in the soft tissues of the neck surrounding the tracheostomy with a blood clot occluding the left main stem bronchi. The heart was enlarged, weighing 600 gm., due to predominant left ventricular hypertrophy and dilatation. ‘I‘here were two discrete areas of healed infarction, each measuring about 3.0 cm. in their greatest diameter, in the upper and lower portions of the posterior wall of the left ventricle. An almost completely organized infarct, measuring about 2 cm. in diameter, was located in the upper anterior portion of the interventricular septum. The myocardium elsewhere showed focal myocardial scars on micro* Necropsy VOLUME
23,
performed MARCH
1969
by Dr. Lazaro
Completo.
Cardiac
Pacing
3. Longitudinal section of the esophqus at postexamination demonstrating the position of the c~lectroclt~catheter just posterior to thr heart. Figure
mortem
scopic examination. The anterior descending and circumflex branches of the left coronary artery showed focal marked narrowing of their lumina by arteriosclerosis. There were no fresh thrombi in the coronary arteries. 7’he lungs weighed 900 gm. There was some atelectasis of the lower pulmonary lobes. No evidence of pulmonary emboli was found. The liver had severe
The opened esopha,ps with the electrode in situ. Figure 4. The sutures and arrows correspond to the lcvrls of the positive
and negative
poles.
472
Burack and Furman pletely avoided by esophageal pacing. In addition, interruption of anticoagulation therapy is no longer required. Of greatest importance is the speed with which this method can be employed, since time is often the most important single element in survival and morbidity. The esophageal electrode was employed in our patient for both fixed pacing and demand pacing. The identification of atria1 activity can readily be accomplished with use of the esophageal electrode. There was no evidence of burn damage to the esophagus despite the presence of the electrode for sixty consecutive hours. The limited microscopic pressure necrosis of the mucosa is to be anticipated with any prolonged intubation. SUMMARY
Figure 5. Microscopic section of the esophagus at the levels of electrode contact revealing mucosal erosions and inflammation secondary to pressure. acute centrilobular necrosis, associated with shock. The kidneys showed arterial and arteriolar nephrosclerosis. The left popliteal vein was thickened with both fresh and old thrombi.
Our initial clinical experience with human transesophageal pacing is described. We were successful in pacing the heart of this patient at a fixed rate for 36 hours and on demand pacing for 24 additional hours, with no significant adverse effects to the esophagus. This was accomplished after unsuccessful attempts to pass a flexible cardiac probe into the right ventricle. Transesophageal cardiac pacing may be a simple, effective and safe method for temporary emergency cardiac pacing. ACKNOWLEDGMENT We are indebted to Dr. Jacob Halperin of the Medical Division, who was this patient’s physician, and to Dr. Jack Hasson of the Laboratory Division, who reviewed the pathologic material.
DISCUSSION Transesophageal cardiac pacing may have clinical advantages for short-term emergency pacing. It may be readily accomplished by a physician or nurse in an emergency room, coronary or intensive care unit, or general hospital setting. The passing of an esophageal electrode is comparable to the usual nasogastric intubation. Transesophageal pacing should circumvent the dangers of bleeding, cardiac perforation,5 thrombus formation and direct myocardial irritability which can occur with present pacing methods. Anesthesia and surgical trauma are com-
REFERENCES 1. FURMAN, S. Fundamentals 2.
3.
4.
5.
of cardiac pacing. Am. Heart J., 73~261, 1966. SCHATMAN, .J., CRAIG, S. D., BERKOVITS,B. V., FIELDS, J. and ROGER, A. Special electrode device for transesophageal cardioversion, p. 77. Digest of 7th Internat. Conf. Med. &o. Engr., 1967. KIMBALL, J. T. and KILLIP, T. A simple bedside method for transvenous intracardiac pacing. Am. Heart J., 70~35, 1965. LEMBERG. L., CASTELLANOS, A. and BERKOVITS,B. V. Pacemaking on demand in A-V block. J.A.M.A., 191:12, 1965. NATHAN, D. A., CENTER, S., PINA, R. E., MEDOW, A. and KELLER, W. Perforation during indwelling catheter pacing. Circulation, 33:128, 1966.
THE AMERICANJOURNAL OF CARDIOLOGY
BURACK,
and
M.D., F.A.C.C.
Bronx,
E
Cardiac Pacing*
CARDIAC pacing has been accomplished in the past by three primary methods. One involves stimulation across the closed chest by large amounts of energy. In the second approach a transvenous electrode is passed into the right ventricle or right atrium from a peripheral vein, usually under fluoroscopic control. A third method is by direct heart puncture.’ We commenced animal experimentation in 1965 to determine the feasibility of cardiac pacing by means of an electrode passed into the esophagus through the oral cavity of dogs. Our initial attempts in the intact dog were unsuccessful. We did note that high current levels of 25 m.amp. did not appear to affect adversely the animal’s ability to swallow and eat on awakening from anesthesia. It was not until we sewed the esophagus to the back of the right ventricle that some degree of capture by means of an electrode in the esophagus was accomplished. This appeared to indicate that in the dog distance and position of the heart in relation to the esophagus was an important factor. With the electrode at the level of the esophagealgastric junction, hiccoughing was caused by diaphragmatic stimulation. We were encouraged to attempt our first clinical case because of the close relation of the human esophagus to the heart and its apparent ability to withstand large transient currents for cardioversion. B
M.D.,
F.A.C.C.
heart disease, with multiple myocardial infarctions, angina pectoris and congestive heart failure. Intermittent anticoagulation had been employed for suspected pulmonary emboli. The electrocardiogram for several years demonstrated an established left bundle branch block pattern. A ventricular aneurysm had been suspected radiographically and electrocardiographically. The patient had been receiving digoxin, quinidine, nitroglycerine, tolbutamide, isosorbide dinitrate, hydrochlorothiazide and a 500 mg. sodium diet. Physical examinntion revealed the point of maximal impulse to be in the sixth intercostal space at the mid-clavicular line. A left parasternal heave was
present. A grade 3/6 systolic ejection murmur and a friction rub were heard along the left sternal border. The lungs were clear. Palpation of the left calf revealed a localized area of tenderness on the posterior lateral aspect with a 3 cm. venous cord deep in the calf. The serum glutamic oxalactic transaminase (SGOT) was 154 units on admission and gradually fell to 39 units on September 5. The lactic dehydrogenase (LDH) on admission was 880 units and remained essentially the same. -4 presumptive diagnosis of thrombophlebitis with pulmonary embolism was made. The possibility of a fresh myocardial infarction concealed by the left bundle branch block pattern on the electrocardiogram was considered. In addition to the patient’s customary medications, treatment with heparin, bed rest, warm packs to the left leg, and elastic bandages was instituted. The hospital course was uneventful until the morning of September 6, when the patient experienced the onset of right leg pain, recurrent chest pain, nausea and retching. Respiratory arrest and coma were noted at 7:45 A.M., when the cardiac arrest team was summoned. The patient was found to be in ventricular fibrillation (Fig. 1A). Defibrillation was accomplished by D.C. electroshock, which was followed by cardiac arrest. Intracardiac administration of epinephrine resulted in a return of ventricular fibrillation.
REPORT
A woman aged 65 had her fifth admission to Montefiore Hospital and Medical Center on August 32, 1967. She entered with the chief complaint of pain in the left calf of 24 hours’ duration accompanied by left precordial was a well established
FURMAN,
New York
MERGENCY
CASE
SEYMOUR
pain for several hours. There history of arteriosclerotic
* From the Cardiology Service, Medical Division and the Cardio-Thoracic Service, Surgical Division, Monteliore Hospital and Medical Center, Bronx, N. Y. This study was supported in part by Grant No. HE 09368-03 from the LT. S. Public Health Service, Department of Health, Education, and Welfare. -Address for reprints: Bernard Burack, Cardiology Service, Montcfiore Hospital and Medical Center, 111 East 210 St., Bronx, N. Y. 10467. VOLUME
23.
MARCH
1969
469
470
Burack and Furman
Figure 1. Electrocardiogramduring and after respiratoryarrest. A, spontaneous ventricular fibrillation; B, idioventricular rhythm; C, transesophageal cardiac pacing; arrows point to pacer impulses.
She was defibrillated seven more times, subjected to continuous cardiac compression, endotracheand transferred to the intensive ally intubated, care unit in coma with idioventricular cardiac rhythm (Fig. 1B). An attempt at passage of a Flexible Platinum Probe (Davis and Geck) to the right ventricle to establish cardiac pacing8 was unsuccessful. In the absence of sustained cardiac contractions, the ability to pass the Flexible PIatinum Probe into the right ventricle has been disappointing in our hands, and we have abandoned the use of that instrument. Esophageal Pacing: A transvenous bipolar electrode, 58 cm. long, was then passed its entire length through the nose into the esophagus. It was connected to the internal output of an American Optical Co. Pacer
Figure
2.
trode catheter
Chest roentgenograms.
A, portable
Monitor, and gradually withdrawn until pacing occurred (Fig. 1C). Complete capture was not accomplished until the fixed rate of the pacer was raised to 110 impulses/min. This rate was required to eliminate ventricular irritability. The amperage and voltage applied at threshold were measured by a Tektronix 567 oscilloscope and found to be 15 m.amp. and 10 v., respectively, with a resistance of 660 ohms. The esophageal electrode was firmly attached to the external nares with adhesive tape. A portable roentgenogram of the chest revealed the electrode catheter to be in the esophagus at the level of D9-DlO, posterior to the left ventricle and 5 cm. above the diaphragm (Fig. 2). The patient was given lidocaine hydrochloride, bicarbonate sodium, intravenous fluids, and she was
anteroposterior
film; B, lateral
views of the elec-
in the esophagus. THE
AMERICAN
,JOURNAL
OF CARDIOLOGY
Transesophageal \.rntilated wirh a respirator. The central venous l)ressurt’ was monitored, and adequate urinary output was maintained. She was paced in this manner for 36 hours. At that time an electrocardiogram taken through the esophageal electrode revealed spontaneous atria1 activity. ‘I’he mode of pacing was then changed from asynchronous fixed-rate pacing to demand pacing utilizing the same esophageal electrode. Triggering of the pacemaker in the demand mode in the American Optical unit is mediated through the limb leads of the electrocardiogram and not by the stimulating eiectrode.4 On September 8 a tracheostomy was performed. The patient remained in deep coma and an electroencephelogram two hours before death showed no cerebral activity. Respiratory arrest occurred during a change of the tracheostomy tube. Widening of the QRS complex on the monitor immediately followed, with no response to the esophageal pacing. The patient died at 6 P.M. on September 8. The esophageal electrode had been in place 60 hours. Of this total 36 hours were spent in continuous fixedrate pacing and the remainder in demand pacing. NECKOPSY
FINDINGS
The postmortem examination was performed two hours after death. * A longitudinal section of the esophagus revealed the pacer catheter in the collapsed esophagus just posterior to the left ventricle and 4 cm. above the esophageal-gastric junction (Fig. 3). The immediate overlying pericardium was normal. The esophagus appeared grossly normal, without evidence of mucosal lesions. The distal end of the bipolar electrode was carefully located in situ, and two sutures were placed in the wall of the esophagus corresponding to the levels of the positive and negative poles (Fig. 4). The esophageal mucosa appeared normal histologically throughout, except for two small areas of mucosal erosions with acute inflammation found in the upper third of the esophagus where the bipolar electrode was located (Fig. 5). This was interpreted as pressure necrosis of the mucosa, commonly seen with any esophageal intubation. No areas of coagulative necrosis of the mucosa were present, as would be anticipated with mucosal burns. There was hemorrhage in the soft tissues of the neck surrounding the tracheostomy with a blood clot occluding the left main stem bronchi. The heart was enlarged, weighing 600 gm., due to predominant left ventricular hypertrophy and dilatation. ‘I‘here were two discrete areas of healed infarction, each measuring about 3.0 cm. in their greatest diameter, in the upper and lower portions of the posterior wall of the left ventricle. An almost completely organized infarct, measuring about 2 cm. in diameter, was located in the upper anterior portion of the interventricular septum. The myocardium elsewhere showed focal myocardial scars on micro* Necropsy VOLUME
23,
performed MARCH
1969
by Dr. Lazaro
Completo.
Cardiac
Pacing
3. Longitudinal section of the esophqus at postexamination demonstrating the position of the c~lectroclt~catheter just posterior to thr heart. Figure
mortem
scopic examination. The anterior descending and circumflex branches of the left coronary artery showed focal marked narrowing of their lumina by arteriosclerosis. There were no fresh thrombi in the coronary arteries. 7’he lungs weighed 900 gm. There was some atelectasis of the lower pulmonary lobes. No evidence of pulmonary emboli was found. The liver had severe
The opened esopha,ps with the electrode in situ. Figure 4. The sutures and arrows correspond to the lcvrls of the positive
and negative
poles.
472
Burack and Furman pletely avoided by esophageal pacing. In addition, interruption of anticoagulation therapy is no longer required. Of greatest importance is the speed with which this method can be employed, since time is often the most important single element in survival and morbidity. The esophageal electrode was employed in our patient for both fixed pacing and demand pacing. The identification of atria1 activity can readily be accomplished with use of the esophageal electrode. There was no evidence of burn damage to the esophagus despite the presence of the electrode for sixty consecutive hours. The limited microscopic pressure necrosis of the mucosa is to be anticipated with any prolonged intubation. SUMMARY
Figure 5. Microscopic section of the esophagus at the levels of electrode contact revealing mucosal erosions and inflammation secondary to pressure. acute centrilobular necrosis, associated with shock. The kidneys showed arterial and arteriolar nephrosclerosis. The left popliteal vein was thickened with both fresh and old thrombi.
Our initial clinical experience with human transesophageal pacing is described. We were successful in pacing the heart of this patient at a fixed rate for 36 hours and on demand pacing for 24 additional hours, with no significant adverse effects to the esophagus. This was accomplished after unsuccessful attempts to pass a flexible cardiac probe into the right ventricle. Transesophageal cardiac pacing may be a simple, effective and safe method for temporary emergency cardiac pacing. ACKNOWLEDGMENT We are indebted to Dr. Jacob Halperin of the Medical Division, who was this patient’s physician, and to Dr. Jack Hasson of the Laboratory Division, who reviewed the pathologic material.
DISCUSSION Transesophageal cardiac pacing may have clinical advantages for short-term emergency pacing. It may be readily accomplished by a physician or nurse in an emergency room, coronary or intensive care unit, or general hospital setting. The passing of an esophageal electrode is comparable to the usual nasogastric intubation. Transesophageal pacing should circumvent the dangers of bleeding, cardiac perforation,5 thrombus formation and direct myocardial irritability which can occur with present pacing methods. Anesthesia and surgical trauma are com-
REFERENCES 1. FURMAN, S. Fundamentals 2.
3.
4.
5.
of cardiac pacing. Am. Heart J., 73~261, 1966. SCHATMAN, .J., CRAIG, S. D., BERKOVITS,B. V., FIELDS, J. and ROGER, A. Special electrode device for transesophageal cardioversion, p. 77. Digest of 7th Internat. Conf. Med. &o. Engr., 1967. KIMBALL, J. T. and KILLIP, T. A simple bedside method for transvenous intracardiac pacing. Am. Heart J., 70~35, 1965. LEMBERG. L., CASTELLANOS, A. and BERKOVITS,B. V. Pacemaking on demand in A-V block. J.A.M.A., 191:12, 1965. NATHAN, D. A., CENTER, S., PINA, R. E., MEDOW, A. and KELLER, W. Perforation during indwelling catheter pacing. Circulation, 33:128, 1966.
THE AMERICANJOURNAL OF CARDIOLOGY