Cardioversion of atrial tachycardia and flutter by atrial stimulation

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<ul><li><p>Cardioversion of Atrial Tachycardia and Flutter </p><p>by Atrial Stimulation </p><p>STEPHEN J. GULOTTA, MD, FACC ALFRED L. ARONSON, MD </p><p>Manhasset, New York </p><p>Electrical stimulation of the right atrium using a bipolar electrode cath- eter terminated 9 episodes of atrial flutter in 8 patients and 32 episodes of atrial tachycardia in 1 patient. Six episodes of flutter were converted directly to sinus rhythm, and 3 were converted initially to atrial fibrillation with a slower ventricular rate and then to sinus rhythm. Conversion of atrial flutter to sinus rhythm by pacing rates slower than the atrial rates implies that interruption of a reentry circuit was responsible for termination of the arrhythmia. </p><p>Two separate mechanisms were found to terminate atrial tachycardia: (1) overdrive suppression, and (2) interruption of a reentry circuit by delivery of a single appropriately timed stimulus. Attempts to convert atrial fibrillation to sinus rhythm by right atrial stimulation were unsuc- cessful. </p><p>This technique is a safe and effective method for terminating atrial tachycardia and flutter, especially in patients receiving large doses of digitalis. It may be performed repetitively at the bedside without anes- thesia and without discomfort to the patient. </p><p>Atria1 tachycardia and atria1 flutter frequently complicate or produce acute cardiac failure and unless converted or controlled can produce severe hemodynamic alterations in the presence of valvular or myo- cardial disease. Although cardioversion using transthoracic direct current countershock has been highly successful in terminating su- praventricular tachycardias, its use in patients receiving digitalis is not without danger.1-3 The development of newer, safer techniques for the treatment of rapid atria1 arrhythmias in the acutely ill, digitalized patient has significant clinical value. </p><p>In 1967, Massumi et al. and Durrer et al. reported the termination of supraventricular tachycardias in patients with Wolff-Parkinson- White syndrome by delivering a single electrical stimulus to the right atrium. Subsequently, Lister et al. terminated supraventricular tachycardias in 10 patients by applying rapid repetitive electrical stimuli to the right atrium, and Zeft et al. reported the conversion of atria1 flutter to sinus rhythm in 8 of 10 patients by this same technique. </p><p>From the Division of Medicine (Cardiology), North Shore Hospital, Manhasset, N.Y., and the Department of Medicine, Cornell University Medical College, New York, N.Y. Manuscript received October 29, 1969, accepted January 9, 1970. </p><p>Address for reprints: Stephen J. Gulotta, MD, FACC, North Shore Hospital, Manhasset, N.Y. 11030. </p><p>Utilizing electrical stimulation of the right atrium, 9 episodes of atria1 flutter were converted to normal sinus rhythm in 8 pa- tients, and 32 episodes of atria1 tachycardia were converted to sinus rhythm in 1 patient. All patients had received large doses of digi- talis. In addition, the effects of electrical stimulation of the right atrium on long standing atria1 fibrillation were evaluated in 2 patients. </p><p>This renort demonstrates the safetv and efhcacv of atria1 stim- I ulation in digitalized patients and discusses anisms by which this technique terminates and flutter. </p><p>the possible mech- atria1 tachycardia </p><p>262 The American Journal of CARDIOLOGY </p></li><li><p>CARDIOVERSION OF ATRIAL TACHYCARDIA AND FLUTTER </p><p>Methods Under fluoroscopic control, bipolar electrode catheters </p><p>were inserted percutaneously through the femoral vein and were positioned in the right atrium so that 1 or both electrodes would lie against the endocardium, with the tip of the catheter directed away from the tricuspid valve. Electrical stimulation was carried out by a battery-driven (Medtronics, model 607) or isolated alternating current powered (American Optical, model 10970R) pulse genera- tor. Impulses of 2 msec duration were delivered singly or repetitively at frequencies varying from 115 to 3751min. Current levels were varied from 5 to 20 ma. Stimulation rates and current amplitudes were altered independently in order to study numerous rate-current ratios. </p><p>In the 2 patients with atria1 fibrillation, stimulation rates were varied from 150 to 1200/min (Medtronics, model 1187), and the duration of impulses ranged from 0.2 to 10 msec. The bipolar electrodes were alternately spaced 1 em and 10 cm apart, and both electrodes were placed in contact with the endocardium. </p><p>Continuous monitoring of the electrocardiogram was performed during insertion of the catheter electrodes and during right atria1 stimulation. The electrocardiogram was recorded using either a standard instrument, an Elec- </p><p>TABLE I Results of Atrial Stimulation in 11 Patients </p><p>tronics for Medicine recorder or a $-channel ink jet recorder (Mingograf 34, Elema Schonander Co.). Patients and equipment were grounded so that the introduction of any undesirable current flow was prevented. </p><p>Results </p><p>The pertinent clinical data and the results of &amp;trial stimulation in the 11 patients studied are presented in Table I. </p><p>In 5 of 8 patients with stable atria1 flutter, conver- sion directly to normal sinus rhythm occurred within 3 minutes after the initiation of atria1 stimuIation. In the remaining 3 patients conversion occurred ini- tially to atria1 fibrillation and then (within 2 hours) to normal sinus rhythm. In these 3 cases the ven- tricular rate slowed considerably with the onset of atria1 fibrillation, thus permitting a prompt im- provement in hemodynamic status. </p><p>Patient 1 responded the most rapidly, with conver- sion to normal sinus rhythm after 6 seconds of elec- trical pacing (Fig. 1). The fourth impulse terminated the flutter, and the fifth, seventh, eighth, tenth and </p><p>no. - </p><p>1 </p><p>2 </p><p>3 </p><p>4 </p><p>5 </p><p>6 </p><p>7 </p><p>8 </p><p>9 </p><p>10 </p><p>11 </p><p>Age &amp; sex Diigncds </p><p>Rhythm, Duration Drug Therapy </p><p>Results of Stimulrtfon </p><p>44M Congenital heart disease; massive tricuspid re- </p><p>gurgitation 54M Rheumatic heart disease; </p><p>mitral stenosis; pul- monary edema </p><p>70M lschemic heart disease; </p><p>complete heart block (permanent pacemaker); pacer failure </p><p>58M lschemic heart disease; angina1 syndrome </p><p>52M lschemic heart disease; </p><p>acute cardiac failure </p><p>62F lschemic heart disease; </p><p>acute myocardial in- farction </p><p>54M lschemic heart disease; angina1 syndrome </p><p>73M lschemic heart disease; acute myocardial in- farction </p><p>42F No known organic heart disease </p><p>50F Rheumatic heart disease; Atrial fibrilla- mitral stenosis tion, 4 years </p><p>44M Rheumatic heart disease; Atrial fibrilla- mitral insufficiency tion, 3 years </p><p>Atrial flutter, Digoxin (2 mg i.v.), Normal sinus 12 hours quinidine rhythm </p><p>Atrial flutter, Digoxin (2.75 mg i.v.), Normal sinus 36 hours quinidine rhythm </p><p>Atrial flutter, </p><p>2% years </p><p>Atrial flutter, 2 hours </p><p>Atrial flutter, </p><p>12 hours </p><p>Atrial flutter, 18 hours </p><p>Atrial flutter, </p><p>24 hours </p><p>Atrial flutter, </p><p>14 hours </p><p>Paroxysmal atrial tachy- cardia, 4 days </p><p>Digoxin (0.5 mg/day) Normal sinus rhythm </p><p>Digoxin (0.5 mg/day) </p><p>Digoxin (1.5 mg Lv.), quinidine, lidocaine </p><p>Digoxin (2 mg i.v.), lidocaine </p><p>Digoxin (1.5 mg i.v.) </p><p>Digoxin (2 mg i.v.) </p><p>Digoxin (3 mg i.v., and p.o.), quinidine, lidocaine, propranolol </p><p>Digoxin (0.5 mg/day) </p><p>Digoxin (0.5 mg/day) </p><p>Normal sinus rhythm </p><p>Normal sinus rhythm </p><p>Atrial fibrilla- </p><p>tion to normal sinus rhythm </p><p>Atrial fibrilla- </p><p>tion to normal sinus rhythm </p><p>Atrial fibrilla- tion to normal sinus rhythm </p><p>Temporary normal sinus rhythm </p><p>Ventricular rate slowed for 10 min </p><p>No change </p><p>i.v. = intravenously: p.0. = orally. </p><p>VOLUME 26, SEPTEMBER 1970 263 </p></li><li><p>GULOTTA AND ARONSON </p><p>ATRIA1 FLUTTER ATRIA1 STIMULATION IlS/min </p><p>AK. MM. ATRIAL FLUTTER </p><p>ATRIAL STIYULATIOW 37Wmin </p><p>Figure 1. Patient 1. Continuous electrocar- diographic recording demonstrating atrial flutter with various degrees of block. The fourth electrical impulse (black arrows) ter- minates the flutter. Impulses 5, 7, 8, 10 and 11 capture the atrium. When pacing is stopped, sinus rhythm follows. </p><p>Figure 2. Patient 2. Continuous recording of intraatrial unipolar electrogram at paper speed of 50 mm/set demonstrating atrial flutter. Short (2.3 seconds) burst of atrial stimulation (middle panel) results in prompt conversion to stable sinus rhythm. Initiation and termination of atrial stimulation are indicated by black arrows. A = atrial com- plex; AUP = atrial unipolar electrogram; NSR = normal sinus rhythm; V = ven- tricular complex. </p><p>Figure 3. Patient 3. Continuous electrocar- diographic recording showing atrial flutter, complete heart block and pacer rhythm. Atrial stimulation was begun (top panel) and the rate of stimulation was varied in a ran- dom fashion resulting in conversion to nor- mal sinus rhythm (NSR). The heart block remained unchanged. </p><p>264 The American Journal of CARDIOLOGY </p></li><li><p>CARDIOVERSION OF ATRIAL TACHYCARDIA AND FLUTTER </p><p>Figure 4. Patient 4. Top panel, atrial flutter with irregular ventricular response. Middle panel, continuous recording of atrial stimu- lation at rate of 120 impulses/min. The ventricular rate becomes regular when atrial flutter is terminated and the pacemaker captures the atrium on a 1: 1 basis (curved arrow). Lower panel, when pacing is discon tinued, sinus rhythm follows. api = atrial pacemaker impulse. </p><p>eleventh impulses produced atria1 captured beats. Abrupt cessation of electrical pacing was followed by asystole for 1 second and finally normal sinus rhythm. </p><p>Patient 2 had mitral stenosis and acute pulmonary edema. His atria1 flutter was resistant to drug ther- apy but was converted to sinus rhythm with inter- mittent right atria1 stimulation at 120 impulses/min. However, after a few beats atria1 flutter reappeared. Rapid atria1 stimulation at a rate of 375/min was then performed with prompt (2 to 3 seconds) rever- sion to normal sinus rhythm (Fig. 2). </p><p>Patient 3, an elderly man with complete heart block, had a permanent nonsynchronous fixed rate transvenous pacemaker (Medtronics, model 5870) im- planted 2% years previously and a battery replace- ment 2 months before the present admission. Atria1 flutter developed at the time of the first implanta- tion, and the patient did not respond to quinidine or procainamide therapy. He was admitted on the present occasion because of intermittent pacing fail- ure. Failure to capture the ventricles for 6 to 7 sec- onds produced dizziness and near syncope. A bipolar catheter electrode was introduced per-venously for temporary pacing. Before advancing the catheter into the right ventricle, the right atrium was stimu- lated to evaluate its effectiveness in terminating long-standing atria1 flutter. Conversion to normal sinus rhythm was prompt (Fig. 3) and persisted for the following 8 months. The patient has not dropped a single paced beat since conversion of the atria to a normal sinus mechanism. This suggests that the </p><p>VOLUME 26. SEPTEMBER 1970 265 </p><p>pacing failure was probably related to alteration of ventricular threshold by partial penetration of the ventricular conduction system by the rapid atria1 rhythm.* The complete heart block remained un- changed. </p><p>In Patient 4 atria1 flutter developed during cardiac catheterization. At the end of the procedure, the rhythm was reverted by stimulating the right atrium at 120 impulses/min (Fig. 4). Immediately after ter- mination of the atria1 flutter, 1 to 1 atria1 capture ensued, and when atria1 stimulation was discon- tinued, normal sinus rhythm occurred. </p><p>Patient 5 had acute congestive heart failure with atria1 flutter and a ventricular rate of 160 beats/min. Large doses of digoxin slowed the ventricular rate to 130/min, and attempts to terminate the flutter with quinidine and lidocaine were unsuccessful. In- termittent right atria1 stimulation produced prompt conversion to sinus rhythm (Fig. 5). </p><p>In Patients 6, 7 and 8, atria1 flutter was initially converted to atria1 fibrillation by pacing the atrium at rates of 166 to 375 beats/min (Fig. 6). In all 3 patients the ventricular rates slowed considerably (162 to 100, 150 to 94, and 150 to 100, respectively) with the onset of atria1 fibrillation. Efforts to break the newly established atria1 fibrillation by repeated stimulation of the atrium with rates up to 1,200 impulses/min in Patients 7 and 8 were unsuccessful. In all 3 cases spontaneous conversion to sinus rhythm occurred within 2 hours. </p><p>Patient 9, a 42 year old woman with no known heart disease, was admitted because of paroxysmal </p></li><li><p>GULOTTA AND ARONSON </p><p>atria1 tachycardia (140 to 180 beats/min). The P wave configuration (Fig. 7) suggested a coronary sinus or left atria1 mechanism. Since the tachycardia did not respond to digitalis, quinidine, lidocaine or proprano- 101 therapy, attempts were made to terminate the rhythm by atria1 pacing. Unipolar atria1 electrograms (Fig. 8) were obtained before stimulation. The QS pattern of the P wave recorded near the entrance of the inferior vena cava indicated that this area was the locus of the abnormal pacemaker. On 32 occasions the tachycardia was easily broken with right atria1 stimulation but recurred after short in- tervals. Two independent mechanisms appeared to terminate this patients tachycardia: (1) overdrive suppression (Fig. 9), and (2) interruption of a reentry circuit (Fig. 10). Since hospitalization the patient has been maintained successfully on digitalis and pro- pranolol therapy. </p><p>In 2 patients (Cases 10 and 11) with long standing atria1 fibrillation attempts to restore sinus rhythm were unsuccessful. The stimulating electrodes were placed 10 cm apart and positioned so that both elec- trodes contacted the atria1 endocardium. Stimulation of at least 3 different pairs of sites in the atrium, using current amplitudes of 5 to 20 ma and stimula- tion rates up to 1,200 impulses/min, was performed. The impulse duration was varied from 0.2 to 10 msec. Atria1 fibrillation persisted in both cases; however, in Patient 10 the fibrillatory waves became smaller and finer, and the ventricular rate slowed transiently from 80 to 68 beats/min. </p><p>Figure 5. Patient 5. Panel A, atrial flutter with irregular ventricular response. Panels B, C and D, continuous electrocardiographic recording at paper speed of 25 mm/set dur- ing right atrial stimulation. Both rate and amplitude were varied randomly. Panel E, the third complex is a sinus beat, and the fourth is a premature atrial beat. The fifth is sinus and is followed by a nonconducted premature atrial beat that is followed by 3 junctional beats and, finally, stable sinus rhythm. </p><p>Mechanisms responsible for terminating atria1 flutter: The electrophysiologic mechanism respon- sible for producing atria1 flutter has not been defined precisely. Most clinical and experimental data sup- port the circus movement theory.g Similarly, some supraventricular tachycardias represent reentry rhythms that are produced by circus movements in the atrioventricular conduction system.l </p><p>Our results lend support to the circus movement theory of atria1 flutter. In 5 patients with flutter conversion directly to sinus rhythm occurred after brief periods of right atria1 stimulation at ra...</p></li></ul>