An Electrophysiologic Study of Swallowing-lnduced Tachycardia

coronary arterial constriction seems to be secondary to external pressure from the aneurysm of the left sinus of Valsalva. During systole the greater distending pressure within the aneurysm could "entrap" and constrict the circumflex coronary artery, while diastolic pressure (re duced because of aortic insufficiency) may not be suffi cient to create arterial constriction. During exercise, electrocardiographic changes and exertional angina suggest that the coronary constriction had physiologic significance. The mechanism for produc tion of myocardial ischemia by systolic coronary arterial compression is not clear. Catecholamines, excitement, tachycardia, and exercise have been shown to shorten the diastolic filling period and also increase systolic coronary flow proportionately more than diastolic flow.8'9 We hypothesize that the potential for myocar dial ischemia to develop in the distribution of the circum flex coronary artery could increase with exercise, possibly due to limitations of this systolic reserve mechanism. This unusual cause of dynamic coronary arterial con striction with manifestation of ischemia represents both a rare acquired anatomic defect and a rare cause of myo cardial ischemia.

REFERENCES 1 Kerber RE, Ridges JD, Kriss JP, et al: Unruptured aneu rysm of the sinus of Valsalva producing right ventricular outflow obstruction. Am J Med 53:775-783, 1972 2 Fishbein MC, Obma R, Roberts WM: Unruptured sinus of Valsalva aneurysm. Am J Cardiol 35:919-922, 1975 3 Buchbinder NA, Roberts WC: Left-sided valvular active infective endocarditis: A study of 45 necropsy patients. Am J Med 53:21-35, 1972 4 Zaret BL, Conti CR: Infundibular pulmonic stenosis with intact ventricular septum in the adult. Johns Hopkins Med J 132:50-60, 1973 5 Garcia-Rinaldi R, Von Koch L, Hovvell JF: Aneurysm of the sinus of Valsalva producing obstruction of the left main coronary artery. J Thorac Cardiovasc Surg 72:123-126, 1976 6 Eliot RS, Wolbrink A, Edwards JE: Congenital aneurysm of the left aortic sinus: A rare lesion and a rare cause of coronary insufficiency. Circulation 28:951-956, 1963 7 Noble J, Bourassa MG, Petitclerc R, et al: Myocardial bridging and milking effect of the left anterior descending coronary artery: Normal variant or obstruction. Am J Cardiol 37:993-999, 1976 8 Khouri EM, Gregg DE, Rayford CR: Effect of exercise on cardiac output, left coronary flow and myocardial metabo lism in the unanesthetized dog. Circ Res 17:427-437, 1965 9 Gregg DE, Fisher LC: Blood supply to the heart. In Hamilton WF, Dow P (eds): Handbook of Physiology and Respiration: Circulation (sec 2, vol 2). Baltimore, Waverly Press, 1963, pp 1517-1584

314 SCHROEDER, WOOLEY, LEIER

An Electrophysiologic Study of Swallowing-lnduced Tachycardia* David P. Schroeder, M.D.;"

Charky

F. Wooleij, M.D.;t

and Carl V. Leier, M.D.I Electrophysiologic studies were performed on a 73-yearold man with swallowing-induced supraventricular tachycardia, in order to define the characteristics of this unique dysrhythmia in this patient Swallowing reliably provoked an automatic atrial focus type of atrial tachy cardia, which usually changed into an atrioventricular nodal reentrant tachycardia when a critical delay in atrioventricular nodal conduction (atrio-His interval > 340 msec) was achieved. The atrioventricular nodal reentrant form of tachycardia did not occur spontane ously. The ease of induction and the duration of the episodes of supraventricular tachycardia were facilitated with the intravenous administration of atropine and ouabain and were decreased with administration of procainamide hydrochloride.

Only

eight case reports1'8 of deglutition-induced tachycardia have appeared since Sakai and Mori9 first described the entity in 1926. The proposed theoretic mechanisms range from a vagovagal reflex arc to mechanical stimulation of the left atrium by a transiently distended esophagus. An electrophysiologic study (with pharmacologic manipulations) performed on a patient with deglutition-induced tachycardia forms the basis of this report.

CASEREPORT A 73-year-old man described a 30-year history of infre quent palpitations, which were documented to be secondary to paroxysms of supraventricular tachycardia and were gen erally well controlled with therapy with quinidine sulfate. More recently, the tachyarrhythmia was precipitated only by swallowing solids or liquids. The therapy with quinidine sulfate was changed to oral administration of propranolol (40 mg every six hours), with little or no improvement. The cardiac physical findings were a nonejection midsystolic click and a grade 2/6 mid to late systolic apical murmur. On admission, the chest x-ray film, electrocardiogram, and echocardiogram were within normal limits. Continuous 24hour ambulatory electrocardiographic monitoring performed prior to admission demonstrated premature atrial contractions with varying coupling intervals between the P wave and the premature atrial contraction and paroxysms of supraven tricular tachycardia consistently initiated by swallowing solids or liquids. The results of cardiac fluoroscopic studies with a barium esophagogram were normal. The patient noticed a short period of palpitations five seconds after the 'From the Department of Medicine, Ohio State University School of Medicine, Columbus. Supported by a research grant from the Central Ohio Heart Chapter of the American Heart Association. 00 Clinical Instructor of Medicine. tProfessor of Medicine. ^Assistant Professor of Medicine and Pharmacology and Investigator for the Central Ohio Heart Chapter of the American Heart Association. Reprint requests: Dr. Leier, Division of Cardiology, 466 West Tenth Avenue, Columbus, Ohio 43210

CHEST,74: 3, SEPTEMBER, 1978

PAC coupling interval range of 400 to 750 msec initiated the type 1 tachycardia. This tachycardia was further character ized by a "warm-up" period and by an A-A interval of 370 msec. The P waves of type 1 supraventricular tachycardia (P' in Fig 1 and 2) were upright in leads 1, aVF, and Vjj

Ad)

LRA

FIGURE 1. Intracardiac and esophageal electrograms, scalar leads 1, aVF, and Vi of ECG, direct blood pressure record ing, and diagram of type 1 supraventricular tachycardia. Tachycardia was initiated by premature atrial contraction occurring 750 msec after previous atrial beat. After three beats of progressively decreasing A-A intervals, A-A interval of the supraventricular tachycardia (paroxysmal atrial tachy cardia ) becomes 370 msec HRA, LA, and HBE, Electrograms of high right atrium, left atrium, and His bundle, respectively; H, His bundle; P and P', P waves of sinus rhythm and of type-1 supraventricular tachycardia, respectively; A and A(I), A waves of sinus rhythm and of type-1 supraventricular tachycardia, respectively; LRA, low right atrium; and V, ventricle. barium cleared the esophagus. Cardiac catheterization dem onstrated normal coronary arteries and left ventricle, with mild prolapse of the mitral leaflets. Electrophysiologic studies were performed using standard techniques.10"14 Simultaneous recordings of high and low right atrial and left atrial electrical events, bundle of His and ventricular deflections, three scalar electrocardiographic leads, and a direct measurement of blood pressure (right femoral artery) were obtained throughout the period of study. Times for atrial conduction were slightly prolonged, with a right intra-atrial conduction time of 55 msec and an interatrial conduction time of 75 msec.12 The atrio-His (AH) and His-ventricle intervals were normal. The times for sinoatrial conduction and for recovery were within normal limits. The effective atrial refractory period (A-A interval = 800 to 900 msec) was 220 msec. Plots of the atrioventricular nodal conduction time and the refractory period15 did not demonstrate the presence of dual atrioventricular nodal path ways. Two types of paroxysmal supraventricular tachycardia were found and will be arbitrarily designated as type 1 and type 2. Type 1 (Fig 1) started 10 to 15 seconds after swallowing 5 ml of liquid or more and occasionally started after dry swallowing. This type did not occur spontaneously. A premature atrial contraction (PAC) occurring in the A-

CHEST,74: 3, SEPTEMBER, 1978

and the sequence of atrial activation was high right atrium (HRA), left atrium ( LA), and low right atrium ( LRA), with conduction times for HRA-LA interval of 10 msec and for the HRA-LRA interval of 45 msec (Fig 2). The type 1 su praventricular tachycardia could not be initiated by the placement of atrial premature depolarizations (extrastimulus) and either ended spontaneously after a short salvo of five to ten beats or evolved into type 2 supraventricular tachycardia. Type 2 supraventricular tachycardia was initiated by type 1 when the A-H interval increased to 340 msec or greater (Fig 2). The A-A interval of type 2 was 400 msec, with a constant A-H interval (360 msec). The sequence of atrial activation of this dysrhythmia was low right atrium to left atrium and high right atrium (conduction interval of 40 msec), with the left atrial and high right atrial deflections occurring at the same time. Type 2 supraventricular tachy cardia did not develop spontaneously and was related to swallowing only by evolving from type 1. Placement of atrial premature depolarizations in an A-S] range of 380 to 400 msec (with an A-H interval > 340 msec) also initiated type 2. In contrast to type 1 supraventricular tachycardia (which either stopped spontaneously or evolved into type 2), type 2 persisted until it was converted to sinus rhythm with carotid massage, atrial pacing, or the placement of atrial premature depolarizations. The electrophysiologic studies were repeated after the intravenous administration of each of the following three drugs: atropine (1 mg); procainamide hydrochloride (350 mg); and ouabain (0.5 mg). Administration of atropine dramatically increased the frequency of supraventricular tachycardia (type 1 to type 2) and, in fact, the supraven tricular tachycardia occasionally began spontaneously (ie, without swallowing). After the basic cycle length returned to baseline values (45 minutes), procainamide was adminis tered. Within three to five minutes, the frequency of type 1 supraventricular tachycardia (hence, type 2) decreased dramatically; and over the ensuing hour, only one episode of three successive atrial beats of type 1 were noted. Swallow ing increasing amounts of liquids did not elicit the supraven tricular tachycardia. Administration of ouabain (90 minutes after administration of procainamide) significantly increased the frequency and ease of induction of type 1 supraventricu lar tachycardia, which evolved into type 2 in most instances.

DISCUSSION The electrophysiologic study demonstrated that this patient's swallowing-induced tachycardia was a com posite of two types of supraventricular tachycardia. The mechanism of type 1 supraventricular tachycardia is most compatible with an automatic atrial focus on the basis of (1) a variable coupling interval between the A wave and the premature atrial contractions, (2) the presence of a "warm-up" period of the first two to three beats, and (3) the inability to initiate or terminate the tachycardia with the placement of premature atrial de polarizations. In addition, the atrioventricular nodal echo beats (type 2) depolarized the automatic focus (type 1), causing a reset of the focus (compensatory SWALLOWING-INDUCED TACHYCARDIA315

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FIGURE2. Recordings taken during episode of supraventricular tachycardia, showing type-1 supraventricular tachycardia evolving into type 2 after attaining A-H interval of 340 msec. Sequence of atrial activation is high right atrium (HRA) to left atrium (LA) to low right atrium (LRA) in type 1 and is LRA to HRA and LA in type 2. Left atrial deflection of type 1 follows HRA deflection by 10 msec and occurs simultaneously with HRA deflection in type 2. Blood pressure drops to low levels after three to four beats of supraventricular tachycardia. HRA, LA, HBE, and LRA, Electrograms or high right atrium, left atrium, His bundle, and low right atrium, respectively; H, His bundle; V, ventricle; P and P', P waves of sinus rhythm and of type 1 supraventricular tachycardia, respectively; and A, A(I), and A(II), A waves of sinus rhythm and of type 1 and type 2 supraventricular tachycardia, respectively. pause), accounting for the total suppression of the focus during the type 2 supraventricular tachycardia (despite the longer cycle length of the reentrant dysrhythmia). The sequence of atrial activation, the atrial conduction intervals, and the P-wave configuration of type 1 supraventricular tachycardia suggest that the focus was in the high right atrium or high interatrial septum. Exploration with the esophageal catheter during type 1 supraven tricular tachycardia did not reveal a left atrial deflection occurring earlier than 10 msec after the high right atrial depolarization. The type 2 supraventricular tachycardia fulfills the criteria for an atrioventricular nodal reentrant mechanism,16'17 with induction and termination by a single premature atrial depolarization, initiation only after a critically prolonged A-H interval, a constant and prolonged A-H interval during the supraventricular tachycardia, and a sequence of atrial activation of low right atrium to high right atrium and left atrium. The potential mechanisms by which deglutition may provoke supraventricular tachycardia have been re viewed in other reports.1-4-6 In contrast to the case reported by Engel and colleagues,1 mechanical stimula tion of the left atrium by transient distention of the esophagus is an unlikely mechanism in our patient for the following reasons: (1) the focus appeared to be located in the high right atrium or interatrial septum (areas usually not adjacent to the esophagus); (2) the left atrium was of normal size, and no atrial indentation 316 SCHROEDER, WOOLEY, LEIER

of the esophagus was noted during fluoroscopic examina tion via a barium swallow; (3) the supraventricular tachycardia developed five seconds or more after the barium cleared the esophagus; and (4) the tachyarrhythmia could occasionally be precipitated by a dry swallow and occurred spontaneously after administra tion of atropine. A complete vagovagal reflex arc is also an unlikely mechanism in our patient, since administration of atro pine dramatically increased the frequency of supraven tricular tachycardia, indicating that efferent vagal stimu lation was not necessary for the initiation of the tachyarrhythmia and, in fact, may have played an inhibiting role. On the other hand, the importance of the influence of the sympathetic nervous system is also in question because of the failure of our patient's condition (and those in other reports) to respond to administration of varying doses of propranolol. While it is apparent that the mechanism of deglutitioninduced tachycardia remains elusive, it is noteworthy that administration of quinidine and procainamide pro vides the most successful control of this unique dis turbance in rhythm (six of nine patients) in the few reports available, 1>2'5>esuggesting a common mecha nism in these patients. An ectopic atrial focus (probably automatic) easily provoked by "autonomic imbalance," a pharmacologic effect, or mechanical stimulation is a favorable hypothesis. Additional electrophysiologic studCHEST,74: 3, SEPTEMBER, 1978

ies will have to be performed in patients with deglutitioninduced tachycardia in order to determine whether this hypothetic mechanism is correct.

Cleft Tongue and Ulceration Palate*

ACKNOWLEDGMENT: We thank Mrs. Marlene Griffin and Ms. Barbara Metzner for their technical assistance.

John L. Statiffer, M.D.;"

REFERENCES 1 Engel TR, Laporte SM, Meister SG, et al: Tachycardia upon swallowing: Evidence for a left atrial automatic focus. J Electrocardiol 9:69-73, 1976 2 Forsberg CW: Paroxysmal premature ventricular con tractions induced by swallowing: Case report. Lancet 53:298-302, 1930 3 Kramer P, Harris L, Kaplan R, et al: Recurrent supraventricular paroxysmal tachycardia precipitated by swallow ing. Proc N EngI Cardiovasc Soc 21:21, 1962-63 4 Lindsay AE: Tachycardia Mechanisms and treatment.

caused by swallowing: Am Heart J 85:679-684,

1973 5 Bajaj SC, Ragaza EP, Silva H, et al: Deglutition tachy cardia. Gastroenterology 62:632-635, 1972 6 Mirvis DM, Bandura JP, Brody DA: Symptomatic swallowing-induced paroxysmal supraventricular tachycardia. Am J Cardiol 39:741-743, 1977 7 Gallavardin L, Froment R: Tachycardie paroxystique de deglutition (avec accidents syncopaux). Lyon Med 145: 456-459, 1930 8 Clerc A: A propos de la tachycardie de deglutition. Arch Mai Coeur 34:73-80, 1941 9 Sakai D, Mori F: Uber einen Fall von sog "Schlucktachykardie". Z Gesamte Exp Med 50:106-109, 1926 10 Barold S: Filtered bipolar esophageal phy. Am Heart J 83:431-436, 1972

electrocardiogra-

11 Scherlag BJ, Lau SH, Helfant RH, et al: Catheter tech nique for recording His bundle activity in man. Circula tion 39:13-18, 1969 12 Leier CV, Meacham JA, Meacham MP, et al: Atrial conduction disease in sinus node dysfunction states (ab stract). Clin Res 24:519A, 1976 13 Strauss HC, Saroff AL, Bigger JT, et al: Premature atrial stimulation as a key to the understanding of sino-atrial conduction in man. Circulation 47:86-93, 1973 14 Narula OS, Samet P, Javier RP: Significance of the sinus node recovery time. Circulation 45:140-158, 1972 15 Denes P, Wu D, Dhingra RC, et al: Demonstration of dual AV nodal pathways in patients with paroxysmal supraventricular tachycardias. Circulation 48:549-555, 1973 16 Goldreyer GN, Bigger JT: Site of re-entry in paroxysmal supraventricular tachycardia in man. Circulation 43:1526, 1971 17 Goldreyer BN, Damato AN: The essential role of atrioventricular conduction delay in the initiation of par oxysmal supraventricular tachycardia. Circulation 43: 679-687, 1971

CHEST, 74: 3, SEPTEMBER, 1978

of Hard

Complications of Oral Intubation and

Thomas L. Petty, M.D., F.C.C.P.f

In a prospective study of the complications of endotracheal intubation and tracheotomy, we encountered an unusual complication of oral intubation. This report describes a 32-year-old man who sustained laceration and cleft of the tongue and alteration of the hard palate as a result of the use of an oral airway in conjunction with oral intubation. Oral

complications of endotracheal intubation are common and include injury to the teeth, lips, gums, tongue, and mucosa.1 Most of these injuries result from traumatic insertion of the oral endotracheal tube, but some may occur after initial placement of the tube.2 Oral airways are widely used to facilitate oral care and to prevent trauma to the soft tissues of the mouth during orotracheal intubation; however, these devices may themselves be hazardous. We report a case of laceration and cleft of the tongue and ulceration of the hard palate from prolonged use of an oral airway, in order to make the reader aware of these potential complications of oral intubation.

CASEREPORT A 32-year-old man was admitted to Colorado General Hospital, Denver, after sustaining an injury to the brain stem in an automobile accident. On admission, he was comatose and decerebrate and had acute respiratory failure. An oral endotracheal tube (Portex; 9.0 mm in internal diameter) was inserted without trauma, and a curved polyethylene Bermantype oral airway (length, 9.0 cm; width, 2.1 cm; and thick ness, 0.8 cm) was placed in the mouth and secured with tape. Decerebrate rigidity with tense contraction of the jaw in creased during the first 48 hours of hospitalization. Five days after admission, brisk oral bleeding developed from a 2.5-cm through-and-through transverse laceration of the tongue, which had been trapped between the lower incisor teeth and the oral airway. A tracheostomy was imme diately performed, and the oral airway was left in place to facilitate oral care and to prevent biting of the tongue. On the 34th day of hospitalization, massive hemorrhage occurred from an erosion of the stoma of the tracheostomy into the inferior thyroid artery. An oral endotracheal tube (Portex; 9.0 mm in internal diameter) was again inserted and left in place, along with an oral airway, for eight days before cricothyroidotomy was performed. On the 45th day of hospitalization, rigidity of the jaw abated, and a 3.0-cm cleft on the left side of the tip of the tongue, distal to the previous laceration, was discovered (Fig 1A). Pressure necrosis on both sides of the cleft was apparent. The cleft coincided with the position of the oral airway "From the Division of Pulmonary Sciences, Department of Medicine, University of Colorado Medical Center, Denver. "Formerly Senior Fellow, Division of Pulmonary Sciences; presently Pulmonary Disease Section, Department of Med icine, Veterans Administration Hospital, Fresno, Calif. •¿ (•Professor of Medicine and Head, Division of Pulmonary Sciences. Reprint requests: Dr. Stauffer, Veterans Administration Hos pital, Fresno 93703

CLEFTTONGUE ANDULCERATION OFHARDPALATE317