Biomedical subjects
Publications and source records attributed to T J Cohen.
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This article reviews the ability of innovative rescue defibrillation techniques for the treatment of refractory ventricular fibrillation. These data were obtained in a variety of hospital settings at the University of California, San Francisco, from 1986 to 1992. Innovative rescue defibrillation techniques were applied to 15 patients with refractory ventricular fibrillation having failed > or = 2 high-energy transthoracic shocks in a variety of hospital settings. Intracardiac defibrillation was performed from a right ventricular catheter to a posterior patch in nine patients who had refractory ventricular fibrillation in the course of invasive electrophysiologic testing. Emergency simultaneous transthoracic and epicardial defibrillation was successfully performed with standard paddles placed over the thorax in contact with epicardial patch or pacing lead connectors in two patients in the operating room who underwent implantable cardioverter-defibrillator insertion and failed standard rescue defibrillations. Transesophageal defibrillation was performed in four patients in the emergency department who had a refractory ventricular fibrillation in the field. Intracardiac defibrillation successfully terminated refractory ventricular fibrillation in 9 of 9 patients in the electrophysiology laboratory. Similarly, emergency simultaneous transthoracic and epicardial defibrillation restored sinus rhythm in two patients in the operating room. Transesophageal defibrillation performed after 50 minutes of cardiac arrest successfully terminated ventricular fibrillation in each patient. Thus alternative methods now exist that permit rescue defibrillation in a variety of hospital emergency settings. These techniques are performed with simple-to-use equipment that is compatible with standard defibrillators.
Ventricular fibrillation (VF) that fails to respond to transthoracic defibrillation leaves the clinician with few alternatives. The purpose of this study was to develop a technique of rescue defibrillation by use of transesophageal electrodes. Fourteen anesthetized dogs (20-30 kg) were investigated in this study. Two electrodes (300 mm2) were mounted 8 cm apart on an esophageal probe and inserted approximately 40 cm from the mouth. VF was induced using AC current delivered to the myocardium. Defibrillation was then performed between the distal electrode (anode) and anterior skin patch (cathode). After 15 seconds of induced VF, transesophageal and transthoracic defibrillation thresholds (DFTs) were determined in random order. The esophageal DFT (90 +/- 15 joules) tended to be lower than the transthoracic DFT (115 +/- 35 joules), though this difference was not statistically significant. One dog could not be defibrillated by transthoracic defibrillation but responded to transesophageal defibrillation. Esophageal electrodes were also useful for arrhythmia discrimination and ventricular pacing (pacing threshold of 38 +/- 5 mA at a pulse duration of 2.5 msec). Following transesophageal DFT determination, in ten dogs (total energy of 600 +/- 150 joules), acute esophageal histopathology demonstrated mild to severe focal injury to the mucosa and/or muscular layers. However, esophagi in four chronic dogs (total energy of 470 +/- 110 joules) showed no gross evidence of mucosal damage, perforation, or stricture 4 weeks following defibrillation. Histopathology showed only focal myocyte atrophy and repair. As a last resort, transesophageal defibrillation was performed in the emergency room on four patients with out-of-hospital refractory VF who failed > 6 high energy transthoracic shocks.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: There are two competing theories of the mechanism of blood flow during cardiopulmonary resuscitation. The "cardiac pump" theory postulates that blood flows because the heart is squeezed between the sternum and the spine. The "thoracic pump" theory postulates that blood flows from the thorax because intrathoracic pressure exceeds extrathoracic vascular pressure and that flow is restricted to the venous-to-arterial direction because of venous valves that prevent retrograde flow at the thoracic inlet. To determine which mechanism is operative during actual cardiopulmonary resuscitation, 20 patients were imaged with transesophageal echocardiography during resuscitation. METHODS AND RESULTS: Transesophageal two-dimensional and pulse Doppler echocardiography was begun within 7 minutes of initiation of cardiopulmonary resuscitation. In the 18 patients who could be analyzed, the mitral valve opened during the release phase (diastole) and closed during the compression phase (systole) of cardiopulmonary resuscitation. Mitral velocity-time integral measured 8 +/- 3 cm during diastole. There was compression of right and left ventricular cavities with significant reduction in measured left ventricular volume during cardiopulmonary resuscitation. In five patients, mitral regurgitation was present. CONCLUSIONS: Transesophageal echocardiography performed during actual cardiopulmonary resuscitation showing mitral valve opening during cardiac release, reduction of ventricular cavity size with compression, and atrioventricular regurgitation support the cardiac pump theory of cardiopulmonary resuscitation. This study demonstrates the feasibility and usefulness of transesophageal echocardiography during cardiopulmonary resuscitation.
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OBJECTIVE: To describe and compare with standard cardiopulmonary resuscitation (CPR) in humans a new form of CPR that involves both active compression and active decompression of the chest. DESIGN: Patients in cardiac arrest in whom standard advanced cardiac life support failed were randomized to receive 2 minutes of either standard or active compression-decompression (ACD) CPR using a custom, hand-held suction device, followed by 2 minutes of the alternate technique. The ACD device was applied midsternum and used to perform CPR according to the guidelines of the American Heart Association: 80 compressions per minute, compression depth of 3.8 to 5 cm, 50% duty cycle, and constant-volume ventilation. Mechanical Thumper CPR was also compared in five patients. End-tidal carbon dioxide (ETCO2) concentrations and hemodynamic variables were measured. Transesophageal Doppler echocardiography was used to assess contractility, the velocity time integral (an analogue of cardiac output), and diastolic myocardial filling times. RESULTS: Ten patients were enrolled. The mean +/- SD ETCO2 was 4.3 +/- 3.8 mm Hg with standard CPR and 9.0 +/- 3.9 mm Hg with ACD CPR (P less than .0001). Systolic arterial pressure with standard CPR was 52.5 +/- 14.0 mm Hg and with ACD CPR, 88.9 +/- 24.7 mm Hg (P less than .003). The velocity time integral increased from 7.3 +/- 2.6 cm with standard CPR to 17.5 +/- 5.6 cm with ACD CPR (P less than .0001), and diastolic filling times increased from 0.23 +/- .09 seconds with standard CPR to 0.37 +/- .12 seconds with ACD CPR (P less than .004). Mechanical Thumper CPR consistently underperformed both standard and ACD CPR. Minute ventilation obtained in four patients during ACD CPR without endotracheal ventilation was 6.6 +/- 0.9 L/min. After 1 hour of standard CPR failed, three of 10 patients randomized to ACD CPR rapidly converted to a hemodynamically stable rhythm following 2 minutes of ACD CPR. CONCLUSION: ACD CPR is a simple manual technique that improved cardiopulmonary circulation in 10 patients during cardiac arrest. Although ACD CPR may have produced a return of spontaneous circulation in three patients refractory to standard measures, its impact on survival when used early in cardiac arrest remains to be determined.
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Adenosine was administered to test the hypothesis that it would maximize preexcitation and facilitate noninvasive localization of accessory pathways in 22 patients with suspected accessory pathway-mediated tachycardias. Twelve-lead electrocardiograms and 2-dimensional echocardiograms were recorded at baseline and during adenosine-augmented ventricular preexcitation to localize the accessory pathway. Phase analysis was performed on digitized 4-chamber and short-axis views using a first harmonic Fourier transformation. At baseline, 15 patients had manifest preexcitation. In 14 of these patients (93.3%), preexcitation became more prominent after adenosine. Four patients without preexcitation at baseline clearly had it after adenosine. In patients who had preexcitation in response to adenosine, the electrocardiogram correctly identified the accessory pathway locations in 18 of 19 patients at a regional level and was incorrect in 1 of 19 patients. Echocardiographic phase analysis correctly identified the accessory pathway location in all 17 patients, who had technically adequate studies, at a regional level. In conclusion, administration of adenosine accentuates preexcitation, allowing for more accurate electrocardiographic and echocardiographic accessory pathway localization.
The cycle length dependence of the action potential duration and the effective refractory period of the right ventricular endocardium were investigated in 24 patients undergoing electrophysiologic studies for suspected ventricular tachycardia. The action potential duration at 90% repolarization and the effective refractory period at twice diastolic threshold strength were measured at the same catheter site at steady state cycle lengths of 350 to 600 ms. Both measurements decreased linearly with decreasing cycle length, maintaining a parallel relation. When the relation between action potential duration and effective refractory period was expressed as the effective refractory period-action potential duration difference, nearly constant values (range -12 to -15 ms) were obtained at all cycle lengths. To determine whether sodium channel blocking drugs influence the effective refractory period-action potential duration relation in humans, measurements of these two variables were obtained in 15 patients before and during the infusion of procainamide. Procainamide prolonged the action potential duration at each cycle length by a near constant amount over baseline values (p less than 0.001). Procainamide also increased the effective refractory period at each cycle length but with a greater incremental increase at the shorter cycle lengths. The rate-dependent increase in the effective refractory period-action potential duration difference became significant at cycle lengths less than or equal to 400 ms; at these high rates, the effective refractory period-action potential duration difference became positive (1.6 ms, p less than 0.01 compared with baseline). Thus, in the human ventricle, the action potential duration and the effective refractory period have a close relation that remains fixed over a wide range of cycle lengths.(ABSTRACT TRUNCATED AT 250 WORDS)
From November 1982 through April 1989, 111 patients with refractory sustained ventricular tachycardia/fibrillation had the automatic cardioverter-defibrillator implanted at our institution, the first community hospital involved in implantation of such a device. We have reviewed our long-term clinical experience to assess the feasibility, learning curve, and efficacy of device implantation in a facility with cardiac electrophysiology expertise but without open-heart surgery facilities. All patients were considered inoperable or at high risk for other concomitant surgery. Eighty-six patients (77%) underwent uneventful implantation. Nine patients (8%) died prior to hospital discharge. Operative mortality declined from 10.9% to 5.4% during the first half (55 patients; November 1982 through September 1986) and second half (56 patients; October 1986 through April 1989) of the experience. Other postoperative complications occurred in 16 patients (14%), 12 of whom experienced complications during the first half of the experience. At 22 +/- 20 (mean +/- SD) months' follow-up, 78 (76%) of 102 patients discharged were alive, and 24 patients (24%) had died. Fifty patients (49%) had experienced at least one automatic cardioverter-defibrillator discharge associated with hypotensive symptoms. The actuarial incidence of sudden death at 1, 2, and 3 years was 1.2%, 5.5%, and 6.2%, respectively. We concluded that the automatic implantable cardioverter-defibrillator is an effective therapy for refractory ventricular tachycardia/fibrillation and that device implantation at community hospitals with an experienced cardiac electrophysiology team is both feasible and practical.
Chest compression is an important part of cardiopulmonary resuscitation (CPR), but it only aids circulation during a portion of the compression cycle and has been shown to only minimally increase blood flow to vital organs. The purpose of this study was to quantitate the short-term hemodynamic effects of CPR with a hand-held suction device that incorporates both active compression and decompression of the chest. The suction device was applied to the middle of the sternum and compared with standard manual CPR in eight nonventilated anesthetized dogs. Coronary perfusion pressure, systolic and diastolic aortic pressures, right atrial diastolic pressure, and the velocity time integral (an analog of cardiac output), which were obtained by means of transesophageal pulsed wave Doppler echocardiography from the main pulmonary artery, were measured every 30 seconds during CPR. Minute ventilation was measured over the last minute of each CPR technique. Both active compression-decompression CPR and standard CPR were sequentially performed for 2 minutes in random order 30 seconds after induced ventricular fibrillation. The CPR techniques consisted of 100 compressions per minute, with a compression depth of 1.5 to 2 inches and a 50% duty cycle. Coronary perfusion pressure, velocity time integral (cardiac output analog), minute ventilation, and systolic arterial pressure were all significantly improved by active compression-decompression CPR when compared with standard CPR. We conclude that active compression-decompression CPR is a simple technique that appears to improve coronary perfusion pressure, systolic arterial pressure, cardiac output, and minute ventilation in nonventilated animals when compared with standard CPR.(ABSTRACT TRUNCATED AT 250 WORDS)
Patients with accessory pathway-mediated supraventricular tachycardia have typically been treated with drugs or surgery. Although catheter ablation using high voltage direct current shocks has been used to treat patients with drug-refractory supraventricular tachycardia, there are associated disadvantages, including damage due to barotrauma as well as the need for general anesthesia. Recently, transcatheter radiofrequency energy has evolved as an alternative to direct current shock or surgery to ablate accessory pathways. Percutaneous catheter ablation of 109 accessory pathways with use of radiofrequency energy was attempted in 100 consecutive patients. Patient age ranged from 3 to 67 years. The patients had been treated for recurrent tachycardia with a mean of 2.7 +/- 0.2 antiarrhythmic agents that either proved ineffective or caused unacceptable side effects. In seven patients previous attempts at accessory pathway ablation with use of direct current shock had been unsuccessful. Forty-five (41%) of the pathways were left free wall, 43 (40%) were septal and 21 (19%) were right free wall. Eighty-nine (89%) of the 100 patients had successful radiofrequency ablation at the time of hospital discharge. In all but 12 patients the ablation was accomplished in a single session. Complications attributable to the procedure, but not to the ablation itself, occurred in four patients (4%). No patient developed atrioventricular block or other cardiac arrhythmias. Over a mean follow-up period of 10 months, nine patients had some return of accessory pathway conduction; a repeat ablation procedure was successful in all five patients in whom it was attempted. It is concluded that a catheter ablation procedure using radiofrequency energy can be performed on accessory pathways in all locations. The procedure is effective and safer, less costly and more convenient than cardiac surgery and can be considered as an alternative to lifelong medical therapy in any patient with symptomatic accessory pathway-mediated tachycardia.
Eight of 120 consecutive patients with inducible sustained ventricular tachycardia who were studied at our institution from September 1, 1988 to January 1, 1991, were found to have reentry within the His-Purkinje System as the mechanism of their tachycardias. Two of the eight patients (25%) required the recording of the right bundle branch potential to elucidate the tachycardia circuits. The electrophysiological findings of these two patients are described. In both instances, the diagnosis of supraventricular tachycardia with aberrancy was excluded. In patient 1, a His-bundle electrogram preceded each QRS complex during tachycardia and the His-to-His interval variation preceded changes in QRS intervals. However, recordings from the right bundle branch allowed for exclusion of bundle branch reentry and evidence was found for reentry restricted to the left fascicles. In patient 2, despite instances of dissociation of the His-bundle deflection from the tachycardia, a right bundle branch potential preceded each QRS and spontaneous changes in the interval between successive activation of the right bundle branch preceded changes in ventricular activation. Catheter ablation of the right bundle branch eliminated the tachycardia. It is concluded that the recording of a right bundle branch potential should be included in electrophysiology study of patients in whom there is suspicion of reentry within the His-Purkinje System. Clinically, recognizing these forms of tachycardias can be important because they can be effectively treated with catheter ablation.
BACKGROUND: The permanent form of junctional reciprocating tachycardia (PJRT) commonly presents as recurrent drug-refractory, narrow-complex tachycardia. We studied the efficacy and safety of catheter ablation in treating these patients. METHODS AND RESULTS: Six patients with the diagnosis of PJRT were treated at our institution with direct-current catheter ablation. The study cohort comprised three men and three women with a mean age of 33.8 +/- 4.5 years. The mean time from onset of symptoms to ablation was 129 +/- 44.7 months. All failed multiple drug therapy (mean number of drugs failed was 5.3 +/- 0.5). The left ventricular ejection fractions were calculated by echocardiography and were greater than 60% in all except two patients, whose ejection fractions were 25% and 32%. Symptom duration was significantly longer in those with depressed ejection fraction compared with normal patients (258 versus 64.5 months, p less than 0.01). Electrophysiological findings revealed evidence of an atrioventricular reciprocating tachycardia involving retrograde decremental conduction over an accessory pathway localized to the posteroseptal area. Five patients received two direct-current shocks (250 +/- 16.7 J per shock) via paired electrodes from a catheter positioned just outside the coronary sinus os to a patch placed between the scapulae or on the anterior chest wall. One patient received a single direct-current shock of 300 J. The only complication was the development of complete atrioventricular block in one patient. This patient had previously undergone permanent pacemaker insertion for the sick sinus syndrome. The mean hospital stay after ablation was 2.2 days. Mean peak creatinine phosphokinase after ablation was 352 +/- 58.1 units/l and the MB fraction was 12 +/- 2%. Follow-up echocardiograms or gated nuclear studies showed improvement of ejection fraction in the two patients who presented with depressed ejection fractions. After a mean follow-up of 35.8 +/- 10.3 months, all patients remained free of tachycardia without antiarrhythmic drugs. CONCLUSIONS: We conclude that catheter ablation by using direct current energy appears to be an effective treatment in patients with PJRT.
In this paper the cardiac actions of adenosine, as well as its therapeutic and diagnostic applications are reviewed. Adenosine has been demonstrated to be useful in the assessment of coronary artery disease in conjunction with perfusion SPECT scintigraphy, PET imaging and two-dimensional echocardiography. The reported sensitivities and specificities of adenosine in these settings are high and similar to those of imaging after exercise or dipyridamole induced coronary hyperemia. Minor side effects are commonly associated with adenosine infusion, however they are transient, generally well tolerated, and rarely require test termination or the administration of aminophylline. Adenosine has proven very useful in the noninvasive diagnosis of Wolff-Parkinson-White syndrome and in the localization of the ventricular insertion of the accessory pathway. As a provocative test, adenosine 12.0 mg rapid bolus has a sensitivity and specificity of 100% for identifying anterograde atrioventricular accessory pathway conduction. The use of adenosine is particularly well suited to the technique of echocardiographic phase analysis and cine-loop inspection as image acquisition is rapid and may be obtained on-line. Although the only approved therapeutic use of adenosine is in the emergency treatment of paroxysmal supraventricular tachycardia, several other clinical applications are suggested by the agents specific cardiovascular and electrophysiologic properties. These include 1. post-thrombolytic therapy to reduce reperfusion injury, 2. as an afterload reduction agent in malignant hypertension and congestive heart failure, 3. to produce controlled hypotension intraoperatively during vascular procedures, and 4. to terminate catecholamine and exercise mediated ventricular tachycardia. Furthermore, the technique of adenosine echocardiographic phase analysis offers the potential for precise subsegmental localization of accessory pathways which has never been achieved by any noninvasive technique, and adenosine augmentation of preexcitation obviates the need for invasive cardiac pacing. Future applications of adenosine scintigraphic and echocardiographic methods will undoubtedly involve newer imaging modalities, such as multiplanar transesophageal and magnetic resonance imaging, which may improve our current abilities to localize accessory pathways and noninvasively diagnose coronary artery disease.
Ventricular fibrillation refractory to cardiopulmonary resuscitation including multiple transthoracic defibrillations occurred in four patients during 1,215 consecutive ventricular tachycardia induction studies. A technique of emergency intracardiac defibrillation for management of refractory ventricular fibrillation is described. In four patients, stable monomorphic ventricular tachycardia (320 to 570 ms cycle length) was induced during the study and overdrive ventricular pacing resulted in ventricular fibrillation. These patients did not respond to prompt transthoracic defibrillations (5 to 15 attempts/patient) and cardiopulmonary resuscitation, including antiarrhythmic therapy. As a last resort, intracardiac defibrillation was performed with use of a previously inserted standard right ventricular quadripolar catheter as cathode and a posterior skin patch as anode. High energy intracardiac defibrillation pulses (100 to 500 J) delivered from a standard defibrillator successfully terminated each arrhythmia. Intracardiac defibrillation is technically simple and appears effective in terminating refractory ventricular fibrillation in the electrophysiology laboratory. However, further research is necessary to determine the safety and efficacy of this technique, as well as potential applications in other emergency settings.
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