terfered in any way with the How of coronary blood or with the motion of the mitral valve. Coronary arteriograms were normal, and the motion of the mitral valve was normal by echocardiogram. The motion of the aneurysm of the left sinus of Valsalva is interesting. Little is known about the hemodynamic behavior of aneurysms of the sinuses of Valsalva prior to rupture. The aneurysm of the left sinus of Valsalva may arise just above or just below the leaHet of the aortic valve. 7 If it arises above the leaHet, the aneurysm will be contiguous with the aorta and expand into the left atrium, a low-pressure chamber. Thus, the aneurysm can flll in systole; however, it should not empty in diastole. Diastolic emptying could occur if left atrial pressure becomes greater than aortic diastolic pressure or if the aneurysm communicates with the left ventricle, in which case the aneurysm would be expected to fill in systole and empty in diastole. In our patient the aneurysm was visualized with the supravalvular aortogram, indicating an origin above the aortic valve. The aneurysm also filled in systole and emptied in diastole. Since the patient's pulmonary capillary pressure was less than the aortic diastolic pressure, this suggests an additional communication with the left ventricle. This could occur if there were two separate orifices or if the orifice of the aneurysm overrode the valvular leaHet to be contiguous with both the aorta and the left ventricle. The exact anatomic location of the orifice remains to be defined. The echocardiogram in this case is unique. The . aneurysm is easily distinguished from left atrial myxomas, which give a mass of echoes behind the mitral valve. 9 Ruptured chordae tendineae of the mitral valve may cause prolapse of the mitral leaHets into the left atrium, but echocardiographically, this is associated with abnormal amplitude and Buttering of the valvular leaHet. 10•11 The motion of both leaHets was normal in our patient. From a technical standpoint the echocardiogram was damped well enough to show that the line of echoes was composed of distinctly separate echoes from those of the aorta, with a distinctly different movement. The movement was similar to the motion of the mitral valve, but the echoes occurred on a different plane and persisted well above the region of the mitral valve, thus indicating that they were not part of the mitral valvular apparatus itself. Recognition of these features provides a potential noninvasive way in which to diagnose the presence of an aneurysm of the left coronary sinus of Valsalva prior to rupture. ACKNOWLEDGMENT: We appreciate the help of Keith Averill, M.D., in allowing us to review the hemodynamics and angiograms of this patient's cardiac catheterization.
1 Wright JS: Ruptured aneurysm of the sinus of Valsalva. Q J Med 39:493-513, 1970 2 Lillehei CW, Stanley PT, Varco RL : Surgical treatment of aneurysms of the sinus of Valsalva. Ann Surg 146:459472, 1957
3 Cooperburg P, Mercer En, Mulder DS, et al: Rupture of
CHEST, 73: 1, JANUARY, 1978
a sinus of Valsalva aneurysm. Radiology 113:171-172, 1974
4 Rothbaum DA, Dillon JC, Chang S, et al: Echocardiographic manifestationof right sinus of Valsalva aneurysm. Circulation 49:768-771, 1974 5 Matsumoto M, Matsuo H, Beppu S, et al: Echocardiographic diagnosis of ruptured aneurysm of sinus of Valsalva. Circulation 53:382-389, 1976 6 Sakakibara S, Konno S: Congenital aneurysm of the sinus of Valsalva: Anatomy and classification. Aiil Heart J 63:405-424, 1962
7 Eliot RS, Wolbrink A, Edwards JE: Congenital aneurysm of the left aortic sinus. Circulation 28:951-956, 1963 8 Kay JH, Anderson RM, Lewis RR, et al: Successful repair of sinus of Valsalva-left atrial fistula. Circulation 20:427429,1959
9 Finegan RE, Harrison DC: Diagnosis of left atrial myxoma by echocardiography. N Engl J Med 282:1022-
1023, .1970 10 Sweatman T, Selzer A, Karnagaki M, et al: Echocardio-
graphic diagnosis of mitral regurgitation due to ruptured chordae tendineae. Circulation 46:580-586, 1972 11 Giles TD, Burch GE, Martinez EC: Value of exploratory "scanning" in the echocardiographic diagnosis of ruptured chordae tendineae. Circulation 49:678-681, 1974
Fatal Tension Pneumopericardium Complicating Tracheostomy* Donald L. Po;thumus, M.D., •• and
Thomas H. Peirce, M.D.t
The findings in a patient who developed a fatal pneumopericardium foDowing tracheostomy are reported. This complication of tracheostomy does not appear to have been reported previously in the Hteratnre. When recognized, pneumopericardium Is a treatable lesion, and clinicians should be aware of this potential complication. induced pneumopericardium has been I atrogenically described following a wide variety of procedures,
including thoracocentesis, aspiration of bone marrow, and transthoracic surgical procedures. 1 Pneumopericardium has been reported in an adult after tracheal trauma who was receiving therapy with artificial ventilation;2 however, it is rare for pneumopericardium to actually cause cardiac tamponade. The majority of reported cases have been in children with respiratory distress syndrome who required high inspiratory pressures for adequate ventilation. We report a case where the unusual complication of pneumopericardium followed a tracheostomy. From the Sacramento Medical Center, University of California, Davis. 0 °Fellow, Pulmonary Medicine. t Assistant Professor of Medicine. 0
Reprint requests: Dr. Peirce, U.C. Davis Sacramento Med~ cal Center, 4301 X Street, Sacramento 95817
FATAL TENSION PNEUMOPERICARDIUM 107
CASE REPoRT
A 62-year-old black man was transferred to Sacramento Medical Center of the University of California, Davis, nine days after an auto accident in which he suffered a fractured pelvis, fractures of multiple ribs, and a cervical fracture with a resulting sixth cervical sensorimotor loss. Care at the referring hospital included splenectomy and · stabilization of the patient's cervical spine. Continuous ventilatory support became necessary, with the early onset of the "shock lung" syndrome. The patient's transfer to Sacramento Medical Center was for further neurosurgical care and treatment of his deteriorating respiratory status. On admission to the neurosurgical intensive care unit, the patient was awake and responsive, had a nasotracheal tube in place, and was receiving therapy with mechanical ventilation on a ventilator (Bennett MA-l) which he triggered. He was afebrile, his pulse rate was 64 beats per minute and regular, and his blood pressure was 102/74 mm Hg. Examination of the chest revealed diffuse rales and rhonchi over both lower lobes, a finding consistent with his recent injuries and subsequent operation. Laboratory data showed a white blood cell count of 17,300/cu mm, with 79 percent polymorphonuclear leukocytes; the level of hemoglobin was 10.6 gm/100 mi. The electrocardiogram showed left atrial enlargement. incomplete right bundle branch block, and nonspecific inversion of T waves on the patient's anterior chest leads. A chest x-ray film showed bilateral infiltrates in the lower lobes. A culture of sputum grew Hemophilw influenzoe. On the second day after his transfer, the patient still required respiratory support, and a decision was made to perform a tracheostomy. The operation was performed with the patient under local anesthesia in the operating room, and a No. 6 Shiley tracheostomy tube was inserted between the second and third tracheal rings. The patient was then transferred to the medical intensive care unit. where he was again placed on the ventilator. His tidal volume was 800 ml, and the respiratory rate was 12/min, with a pe~ inspiratory pressure of 40 em H20. At this point the patient's pulse rate was 70 beats per minute and regular, his blood pressure was 80/40 mm Hg, and his central venous pressure was 10 em H 2 0, which was unchanged from his previous reading prior to tracheostomy. Forty minutes after operation, the patient developed bradyCardia of 40 beats per minute, which responded to atropine. Some 15 minutes later, electrical-mechanical disassociation began, with a monitored heart rate of 76 beats per minute and an unrecordable blood pressure. The ECG showed no change from the patient's previous tracing, and there was no evidence of electrical alternans. Analysis of blood gas levels with the patient being ventilated on 100 percent oxygen showed an arterial oxygen pressure of 82 min Hg, arterial carbon dioxide of 60 mm Hg, and pH of 7.25. A portable chest x-ray film was taken at this time. Efforts at resuscitation, which included a challenge with 400 ml of normal saline solution, dopamine, calcium, and steroids, were undertaken. Cardiac massage was not performed. At one point, it was thought that the patient might have a left pneumothorax; a needle ·was inserted into the left midaxillary line, without return of air under pressure. The patient rapidly developed fixed dilated pupils, and efforts at resuscitation were terminated. Subsequent review of his chest x-ray film showed a small left pneumothorax and a large pneumopericardium ( Fig 1). At autopsy, air under tension was found in the pericardium. There was no evidence for either recent myocardial infarc-
108 POSTHUMUS, PEIRCE
FiGURE 1. Pneumopericardium, with distended pericardia! sac indicated by arrows.
tion or massive pulmonary embolism, which might have accounted for the patient's death. DISCUSSION
Tracheostomy is commonly regarded as a simple operation, with serious complication occurring only rarely. These usually have been associated with prolonged inflation of cuffs in patients receiving mechanical ventilation and included erosion of the innominate artery and the development of tracheoesophageal fistulae. To our knowledge, tension pneumopericardium as a complication has not been described previously, although pneumothorax, pneumomediastinum, and subcutaneous emphysema occur frequently following tracheostomy.a In this patient, it is somewhat difficult to explain how air entered the pericardium without significant mediastinal air also being present. The pericardium is usually regarded as a closed compartment without direct contact with other fascial planes; however, Marchand4 has clearly demonstrated that fluid injected into the peritracheal subfascial region could dissect between the serosal and fibrous layers of the parietal pericardium. Pneumopericardium usually does not cause tamponade. To do so, both human and animal experiments would suggest that the intrapericardial pressure must exceed atrial filling pressure by at least 20 to 25 em H 20 in normovolemic subjects. 5 •6 This is most likely to happen if the patient is receiving therapy. with posi~ tive-pressure ventilation, although recently, tension pneumopericardium secondary to blunt trauma of the chest has been described 7 where the patient was not receiving artificial ventilation. Here, the mechanisin of a one-way valve was postulated. Pericardia} tamponade from any cause will usually show some response to
CHEST, 73: 1, JANUARY, 1978
infusion of fluids or pressor agents, or both. The failure of this patient to respond to these treatments may have been due to dysfunction of the autonomic nervous system secondary to his initial cervical injury Tension pneumopericardium would appear to be a very rare complication of tracheostomy; if recognized, this complication should be readily amenable to treatment by aspiration with a needle. Tension pneumopericardium should be suspected particularly in those patients receiving positive-pressure ventilation if there is evidence of damage to the trachea in the setting of unexplained hypotension with electromechanical dis-
sociation of the heart. Although a loud precordial splashing with mufBed heart sound has been described as characteristic, 7 these findings were not present in our patient.
1 Toledo TM, Moore WL Jr. Nash DA, et al: Spontaneous pneumopericardium in acute asthma: Case report and review of the literature. Chest 62:118-120, 1972 2 McCaughery W, King R: Pneumopericardium associated with tracheal rupture. Anesthesia 30: 199-205, 1975 3 Padovan IF, Dawson CA, Henschel EO, et al: Pathogenesis of mediastinal emphysema and pneumothorax following tracheostomy. Chest 66:553-556, 1974 ~ Marchand P: The anatomy and applied anatomy of the mediastinal fascia. Thorax 6:359-368, 1951 5 Maurer ER, Mendez FL Jr, Finklestein M: Cardiovascular dynamics in pneumopericardium and hydropericardium. Angiology 9:176-179, 1958 6 Adcock JD, Lyons RH, Barnwell JB: The circulatory effects produced in a patient with pneumopericardium by artificially varying the intrapericardial pressure. Am Heart J 19:283-296, 1940 7 Westaby S: Pneumopericardium and tension pneumopericardium after cloud chest injury. Thorax 32:91-97, 1977.
Anterograde and Retrograde Bradycardiac Block in the His-Purkinje System* Finding in a Patient with Acute Myocardial Infarction Jose A. Sobrino, M.D.; Ale;andro del Rio, M.D.; Isabel Mate, M.D.; Javier Pasalodos, M.D.; and Nicolas Sobrlno, M.D.
A patient with an acute inferior myocardial infarction developed a complete atrioventricular block and intermittent periods of atrioventricular conduction with QRS complexes showing right bundle bnnch block associated with left anterior hemiblock. Recordings of the His bundle electrogram showed that the atrioventricular block •From the Department of Cardiovascular Surgery, Cardiology Unit, ''La Paz," Madrid, Spain. Reprint requests: Dr. Sobrino, Hilarlon Eslova 55, Madrid
15, Spain
CHEST, 73: 1, JANUARY, 1978
Wl8 infrlhlllan and dud ID pcdoda of I'CIUIDcd lllrlovcntricular conduction, the His-ventricle (H-V) Interval was long. Ventricular escape beats showed concealed conduction to the atrioventricular node. Anterograde atrioventricular conduction was always resumed throulh the left posterior division when the preceding Intervals between ventricular escape beats and the atrium (V--A Intervals) were shorter than 580 msec. Tbe same phenomenon occurred with right ventricular pacing. A retrograde His potential conld be observed. Retrograde conduction of ventricular escape beats and ventricular paced beats was blocked if the H-V- interval and the interval between the His bundle aod tbe veotritular J*ed beat (H·V· interval) were long (more than 600 msec and 550 msec, respectively). The existence of an Intermittent anterograde and retrograde bradycardiac infrabisian block was inferred from the previously mentioned data; a fb:ed retrograde atrial nodal block was also present. is known that in the presence of complete atriovenI t tricular block, atrioventricular conduction is sometimes resumed when the atrial impulse is generated following a fixed period after the ventricular escape beat. There are several explanations for this phenomenon, such as ( 1) the existence of a short period of supernormal conduction originated by the ventricular escape beat, 1 (2) facilitation and Wedensky's effect, 2 and ( 3) ventriculophasic supernormality induced by vagal reflexes. 3 Bradycardia-dependent blocks also explain intermittent atrioventricular block;H however, these phenomena are not known to be related to retrograde conduction in man. We report the findings in a patient with complete infrahisian block and intermittent atrioventricular conduction through the left posterior division of the left bundle branch conditioned by the ventricular impulse. This phenomenon was observed at the same level, but with ventriculoatrial conduction in a retrograde sense conditioned by the atrial impulse. CASE REPoRT
A 62-year-old woman was admitted to the coronary care unit with acute myocardial infarction. Her electrocardiogram showed sinus rhythm, signs of acute inferior myocardial infarction, a P-R interval of 0.24 second, and the features of right bundle branch block and left anterior hemiblock. One day after admission to the hospital, the patient developed complete atrioventricular block with ventricular escape beats showing features of right bundle branch block plus left posterior hemiblock. Occasionally, atrioventricular conduction was resumed following a ventricular escape beat. The conducted beats had aP-R interval of 0.24 second and a QRS complex indicative of right bundle branch block and left anterior hemiblock ( Fig 1 ) . A transvenous demand pacemaker was inserted into the right ventricle; during the procedure a His bundle electrogram was recorded, A permanent demand pacemaker was implanted, and the patient was discharged from the hospital 15 days later. In subsequent examinations the patient showed regular sinus rhythm, right bundle branch block, and left anterior hemiblock.
BRADYCARDIAC BLOCK IN HIS.PURIUNJE SYSTEM 109
1 Wright JS: Ruptured aneurysm of the sinus of Valsalva. Q J Med 39:493-513, 1970 2 Lillehei CW, Stanley PT, Varco RL : Surgical treatment of aneurysms of the sinus of Valsalva. Ann Surg 146:459472, 1957
3 Cooperburg P, Mercer En, Mulder DS, et al: Rupture of
CHEST, 73: 1, JANUARY, 1978
a sinus of Valsalva aneurysm. Radiology 113:171-172, 1974
4 Rothbaum DA, Dillon JC, Chang S, et al: Echocardiographic manifestationof right sinus of Valsalva aneurysm. Circulation 49:768-771, 1974 5 Matsumoto M, Matsuo H, Beppu S, et al: Echocardiographic diagnosis of ruptured aneurysm of sinus of Valsalva. Circulation 53:382-389, 1976 6 Sakakibara S, Konno S: Congenital aneurysm of the sinus of Valsalva: Anatomy and classification. Aiil Heart J 63:405-424, 1962
7 Eliot RS, Wolbrink A, Edwards JE: Congenital aneurysm of the left aortic sinus. Circulation 28:951-956, 1963 8 Kay JH, Anderson RM, Lewis RR, et al: Successful repair of sinus of Valsalva-left atrial fistula. Circulation 20:427429,1959
9 Finegan RE, Harrison DC: Diagnosis of left atrial myxoma by echocardiography. N Engl J Med 282:1022-
1023, .1970 10 Sweatman T, Selzer A, Karnagaki M, et al: Echocardio-
graphic diagnosis of mitral regurgitation due to ruptured chordae tendineae. Circulation 46:580-586, 1972 11 Giles TD, Burch GE, Martinez EC: Value of exploratory "scanning" in the echocardiographic diagnosis of ruptured chordae tendineae. Circulation 49:678-681, 1974
Fatal Tension Pneumopericardium Complicating Tracheostomy* Donald L. Po;thumus, M.D., •• and
Thomas H. Peirce, M.D.t
The findings in a patient who developed a fatal pneumopericardium foDowing tracheostomy are reported. This complication of tracheostomy does not appear to have been reported previously in the Hteratnre. When recognized, pneumopericardium Is a treatable lesion, and clinicians should be aware of this potential complication. induced pneumopericardium has been I atrogenically described following a wide variety of procedures,
including thoracocentesis, aspiration of bone marrow, and transthoracic surgical procedures. 1 Pneumopericardium has been reported in an adult after tracheal trauma who was receiving therapy with artificial ventilation;2 however, it is rare for pneumopericardium to actually cause cardiac tamponade. The majority of reported cases have been in children with respiratory distress syndrome who required high inspiratory pressures for adequate ventilation. We report a case where the unusual complication of pneumopericardium followed a tracheostomy. From the Sacramento Medical Center, University of California, Davis. 0 °Fellow, Pulmonary Medicine. t Assistant Professor of Medicine. 0
Reprint requests: Dr. Peirce, U.C. Davis Sacramento Med~ cal Center, 4301 X Street, Sacramento 95817
FATAL TENSION PNEUMOPERICARDIUM 107
CASE REPoRT
A 62-year-old black man was transferred to Sacramento Medical Center of the University of California, Davis, nine days after an auto accident in which he suffered a fractured pelvis, fractures of multiple ribs, and a cervical fracture with a resulting sixth cervical sensorimotor loss. Care at the referring hospital included splenectomy and · stabilization of the patient's cervical spine. Continuous ventilatory support became necessary, with the early onset of the "shock lung" syndrome. The patient's transfer to Sacramento Medical Center was for further neurosurgical care and treatment of his deteriorating respiratory status. On admission to the neurosurgical intensive care unit, the patient was awake and responsive, had a nasotracheal tube in place, and was receiving therapy with mechanical ventilation on a ventilator (Bennett MA-l) which he triggered. He was afebrile, his pulse rate was 64 beats per minute and regular, and his blood pressure was 102/74 mm Hg. Examination of the chest revealed diffuse rales and rhonchi over both lower lobes, a finding consistent with his recent injuries and subsequent operation. Laboratory data showed a white blood cell count of 17,300/cu mm, with 79 percent polymorphonuclear leukocytes; the level of hemoglobin was 10.6 gm/100 mi. The electrocardiogram showed left atrial enlargement. incomplete right bundle branch block, and nonspecific inversion of T waves on the patient's anterior chest leads. A chest x-ray film showed bilateral infiltrates in the lower lobes. A culture of sputum grew Hemophilw influenzoe. On the second day after his transfer, the patient still required respiratory support, and a decision was made to perform a tracheostomy. The operation was performed with the patient under local anesthesia in the operating room, and a No. 6 Shiley tracheostomy tube was inserted between the second and third tracheal rings. The patient was then transferred to the medical intensive care unit. where he was again placed on the ventilator. His tidal volume was 800 ml, and the respiratory rate was 12/min, with a pe~ inspiratory pressure of 40 em H20. At this point the patient's pulse rate was 70 beats per minute and regular, his blood pressure was 80/40 mm Hg, and his central venous pressure was 10 em H 2 0, which was unchanged from his previous reading prior to tracheostomy. Forty minutes after operation, the patient developed bradyCardia of 40 beats per minute, which responded to atropine. Some 15 minutes later, electrical-mechanical disassociation began, with a monitored heart rate of 76 beats per minute and an unrecordable blood pressure. The ECG showed no change from the patient's previous tracing, and there was no evidence of electrical alternans. Analysis of blood gas levels with the patient being ventilated on 100 percent oxygen showed an arterial oxygen pressure of 82 min Hg, arterial carbon dioxide of 60 mm Hg, and pH of 7.25. A portable chest x-ray film was taken at this time. Efforts at resuscitation, which included a challenge with 400 ml of normal saline solution, dopamine, calcium, and steroids, were undertaken. Cardiac massage was not performed. At one point, it was thought that the patient might have a left pneumothorax; a needle ·was inserted into the left midaxillary line, without return of air under pressure. The patient rapidly developed fixed dilated pupils, and efforts at resuscitation were terminated. Subsequent review of his chest x-ray film showed a small left pneumothorax and a large pneumopericardium ( Fig 1). At autopsy, air under tension was found in the pericardium. There was no evidence for either recent myocardial infarc-
108 POSTHUMUS, PEIRCE
FiGURE 1. Pneumopericardium, with distended pericardia! sac indicated by arrows.
tion or massive pulmonary embolism, which might have accounted for the patient's death. DISCUSSION
Tracheostomy is commonly regarded as a simple operation, with serious complication occurring only rarely. These usually have been associated with prolonged inflation of cuffs in patients receiving mechanical ventilation and included erosion of the innominate artery and the development of tracheoesophageal fistulae. To our knowledge, tension pneumopericardium as a complication has not been described previously, although pneumothorax, pneumomediastinum, and subcutaneous emphysema occur frequently following tracheostomy.a In this patient, it is somewhat difficult to explain how air entered the pericardium without significant mediastinal air also being present. The pericardium is usually regarded as a closed compartment without direct contact with other fascial planes; however, Marchand4 has clearly demonstrated that fluid injected into the peritracheal subfascial region could dissect between the serosal and fibrous layers of the parietal pericardium. Pneumopericardium usually does not cause tamponade. To do so, both human and animal experiments would suggest that the intrapericardial pressure must exceed atrial filling pressure by at least 20 to 25 em H 20 in normovolemic subjects. 5 •6 This is most likely to happen if the patient is receiving therapy. with posi~ tive-pressure ventilation, although recently, tension pneumopericardium secondary to blunt trauma of the chest has been described 7 where the patient was not receiving artificial ventilation. Here, the mechanisin of a one-way valve was postulated. Pericardia} tamponade from any cause will usually show some response to
CHEST, 73: 1, JANUARY, 1978
infusion of fluids or pressor agents, or both. The failure of this patient to respond to these treatments may have been due to dysfunction of the autonomic nervous system secondary to his initial cervical injury Tension pneumopericardium would appear to be a very rare complication of tracheostomy; if recognized, this complication should be readily amenable to treatment by aspiration with a needle. Tension pneumopericardium should be suspected particularly in those patients receiving positive-pressure ventilation if there is evidence of damage to the trachea in the setting of unexplained hypotension with electromechanical dis-
sociation of the heart. Although a loud precordial splashing with mufBed heart sound has been described as characteristic, 7 these findings were not present in our patient.
1 Toledo TM, Moore WL Jr. Nash DA, et al: Spontaneous pneumopericardium in acute asthma: Case report and review of the literature. Chest 62:118-120, 1972 2 McCaughery W, King R: Pneumopericardium associated with tracheal rupture. Anesthesia 30: 199-205, 1975 3 Padovan IF, Dawson CA, Henschel EO, et al: Pathogenesis of mediastinal emphysema and pneumothorax following tracheostomy. Chest 66:553-556, 1974 ~ Marchand P: The anatomy and applied anatomy of the mediastinal fascia. Thorax 6:359-368, 1951 5 Maurer ER, Mendez FL Jr, Finklestein M: Cardiovascular dynamics in pneumopericardium and hydropericardium. Angiology 9:176-179, 1958 6 Adcock JD, Lyons RH, Barnwell JB: The circulatory effects produced in a patient with pneumopericardium by artificially varying the intrapericardial pressure. Am Heart J 19:283-296, 1940 7 Westaby S: Pneumopericardium and tension pneumopericardium after cloud chest injury. Thorax 32:91-97, 1977.
Anterograde and Retrograde Bradycardiac Block in the His-Purkinje System* Finding in a Patient with Acute Myocardial Infarction Jose A. Sobrino, M.D.; Ale;andro del Rio, M.D.; Isabel Mate, M.D.; Javier Pasalodos, M.D.; and Nicolas Sobrlno, M.D.
A patient with an acute inferior myocardial infarction developed a complete atrioventricular block and intermittent periods of atrioventricular conduction with QRS complexes showing right bundle bnnch block associated with left anterior hemiblock. Recordings of the His bundle electrogram showed that the atrioventricular block •From the Department of Cardiovascular Surgery, Cardiology Unit, ''La Paz," Madrid, Spain. Reprint requests: Dr. Sobrino, Hilarlon Eslova 55, Madrid
15, Spain
CHEST, 73: 1, JANUARY, 1978
Wl8 infrlhlllan and dud ID pcdoda of I'CIUIDcd lllrlovcntricular conduction, the His-ventricle (H-V) Interval was long. Ventricular escape beats showed concealed conduction to the atrioventricular node. Anterograde atrioventricular conduction was always resumed throulh the left posterior division when the preceding Intervals between ventricular escape beats and the atrium (V--A Intervals) were shorter than 580 msec. Tbe same phenomenon occurred with right ventricular pacing. A retrograde His potential conld be observed. Retrograde conduction of ventricular escape beats and ventricular paced beats was blocked if the H-V- interval and the interval between the His bundle aod tbe veotritular J*ed beat (H·V· interval) were long (more than 600 msec and 550 msec, respectively). The existence of an Intermittent anterograde and retrograde bradycardiac infrabisian block was inferred from the previously mentioned data; a fb:ed retrograde atrial nodal block was also present. is known that in the presence of complete atriovenI t tricular block, atrioventricular conduction is sometimes resumed when the atrial impulse is generated following a fixed period after the ventricular escape beat. There are several explanations for this phenomenon, such as ( 1) the existence of a short period of supernormal conduction originated by the ventricular escape beat, 1 (2) facilitation and Wedensky's effect, 2 and ( 3) ventriculophasic supernormality induced by vagal reflexes. 3 Bradycardia-dependent blocks also explain intermittent atrioventricular block;H however, these phenomena are not known to be related to retrograde conduction in man. We report the findings in a patient with complete infrahisian block and intermittent atrioventricular conduction through the left posterior division of the left bundle branch conditioned by the ventricular impulse. This phenomenon was observed at the same level, but with ventriculoatrial conduction in a retrograde sense conditioned by the atrial impulse. CASE REPoRT
A 62-year-old woman was admitted to the coronary care unit with acute myocardial infarction. Her electrocardiogram showed sinus rhythm, signs of acute inferior myocardial infarction, a P-R interval of 0.24 second, and the features of right bundle branch block and left anterior hemiblock. One day after admission to the hospital, the patient developed complete atrioventricular block with ventricular escape beats showing features of right bundle branch block plus left posterior hemiblock. Occasionally, atrioventricular conduction was resumed following a ventricular escape beat. The conducted beats had aP-R interval of 0.24 second and a QRS complex indicative of right bundle branch block and left anterior hemiblock ( Fig 1 ) . A transvenous demand pacemaker was inserted into the right ventricle; during the procedure a His bundle electrogram was recorded, A permanent demand pacemaker was implanted, and the patient was discharged from the hospital 15 days later. In subsequent examinations the patient showed regular sinus rhythm, right bundle branch block, and left anterior hemiblock.
BRADYCARDIAC BLOCK IN HIS.PURIUNJE SYSTEM 109
