Cardiac arrest management.

Approximately 1,000 people in the United States suffer cardiac arrest each day, most often as a complication of acute myocardial infarction (AMI) with accompanying ventricular fibrillation or unstable ventricular tachycardia. Increasing the number of patients who survive cardiac arrest and minimizing the clinical sequelae associated with cardiac arrest in those who do survive are the objectives of emergency medical personnel. In 1990, the American Heart Association (AHA) suggested the chain of survival concept, with four links--early access, cardiopulmonary resuscitation (CPR), defibrillation, and advanced care--as the way to approach cardiac arrest. The recently published International Resuscitation Guidelines 2000 of the AHA have addressed advances in our understanding of the chain of survival. While the chain of survival concept has withstood a decade of scrutiny, there are only a few scientifically rigorous research studies that support changes in prehospital patient care. Additional research efforts carried out in the prehospital setting are needed to support the concepts included in the chain of survival for cardiac arrest patients. Participants at the second Turtle Creek Conference, a meeting of experts in the field of emergency medicine held in Dallas, Texas, on March 29-31, 2000, discussed these and other issues associated with prehospital emergency care in the cardiac arrest patient. This paper addresses a number of the issues associated with each of the links of the chain of survival, the evidence that exists, and what should be done to achieve the clinical evidence needed for true clinical significance. Also included in this paper are the consensus statements developed from small discussion groups held after the main presentation. These comments provide another perspective to the problems and to possible approaches to deal with them.

Intravenous antiarrhythmic drug therapy in the resuscitation from refractory ventricular arrhythmias.

Prompt cardiopulmonary resuscitation (CPR) and early defibrillation significantly improve the likelihood of successful resuscitation from cardiac arrest and are the key components in the American Heart Association's "chain of survival." Although representing current clinical practice in the United States, there is limited evidence supporting the benefit of acute administration of such antiarrhythmic medications as lidocaine, bretylium, magnesium, and procainamide to a victim of cardiac arrest. There has been only 1 published case-controlled clinical trial in which shock-refractory victims of out-of-hospital ventricular fibrillation were stratified into those who received lidocaine and those who did not. In this trial, no significant differences were observed between treatment groups in the return of an organized rhythm, admission to the hospital, or survival to hospital discharge. In the recently published ARREST trial, a significant improvement in admission alive to the hospital was observed in recipients of intravenous amiodarone, compared with placebo (44% vs 34%, respectively, p = 0.03). With the possible exception of intravenous amiodarone, available evidence of definitive benefit from antiarrhythmic drugs in cardiac arrest is inconclusive. Due to regulatory issues, clinical trials in cardiac arrest are extremely difficult to design and perform.

Pharmacologic treatment of cardiac arrest.

Antiarrhythmic drugs currently recommended in the American Heart Association's Advanced Cardiac Life Support (ACLS) guidelines for the treatment of cardiac arrest have not been proved in controlled clinical trials to improve survival in patients with ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT). Intravenous amiodarone is a promising agent for the treatment of VF and VT. Based on available evidence, amiodarone should be considered for use in patients with shock-refractory ventricular arrhythmias.

Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation.

BACKGROUND: Whether antiarrhythmic drugs improve the rate of successful resuscitation after out-of-hospital cardiac arrest has not been determined in randomized clinical trials. METHODS: We conducted a randomized, double-blind, placebo-controlled study of intravenous amiodarone in patients with out-of-hospital cardiac arrest. Patients who had cardiac arrest with ventricular fibrillation (or pulseless ventricular tachycardia) and who had not been resuscitated after receiving three or more precordial shocks were randomly assigned to receive 300 mg of intravenous amiodarone (246 patients) or placebo (258 patients). RESULTS: The treatment groups had similar clinical profiles. There was no significant difference between the amiodarone and placebo groups in the duration of the resuscitation attempt (42+/-16.4 and 43+/-16.3 minutes, respectively), the number of shocks delivered (4+/-3 and 6+/-5), or the proportion of patients who required additional antiarrhythmic drugs after the administration of the study drug (66 percent and 73 percent). More patients in the amiodarone group than in the placebo group had hypotension (59 percent vs. 48 percent, P=0.04) or bradycardia (41 percent vs. 25 percent, P=0.004) after receiving the study drug. Recipients of amiodarone were more likely to survive to be admitted to the hospital (44 percent, vs. 34 percent of the placebo group; P=0.03). The benefit of amiodarone was consistent among all subgroups and at all times of drug administration. The adjusted odds ratio for survival to admission to the hospital in the amiodarone group as compared with the placebo group was 1.6 (95 percent confidence interval, 1.1 to 2.4; P=0.02). The trial did not have sufficient statistical power to detect differences in survival to hospital discharge, which differed only slightly between the two groups. CONCLUSIONS: In patients with out-of-hospital cardiac arrest due to refractory ventricular arrhythmias, treatment with amiodarone resulted in a higher rate of survival to hospital admission. Whether this benefit extends to survival to discharge from the hospital merits further investigation.

Utility of the prehospital electrocardiogram in diagnosing acute coronary syndromes: the Myocardial Infarction Triage and Intervention (MITI) Project.

OBJECTIVES: We sought to determine whether the prehospital electrocardiogram (ECG) improves the diagnosis of an acute coronary syndrome. BACKGROUND: The ECG is the most widely used screening test for evaluating patients with chest pain. METHODS: Prehospital and in-hospital ECGs were obtained in 3,027 consecutive patients with symptoms of suspected acute myocardial infarction, 362 of whom were randomized to prehospital versus hospital thrombolysis and 2,665 of whom did not participate in the randomized trial. Prehospital and hospital records were abstracted for clinical characteristics and diagnostic outcome. RESULTS: ST segment and T and Q wave abnormalities suggestive of myocardial ischemia or infarction were more common on both the prehospital and hospital ECGs of patients with as compared with those without acute coronary syndromes (p < or = 0.00001). Those with prehospital thrombolysis were more likely to show resolution of ST segment elevation by the time of hospital admission (14% vs. 5% in patients treated in the hospital, p = 0.004). In patients not considered for prehospital thrombolysis, both persistent and transient ST segment and T or Q wave abnormalities discriminated those with from those without acute coronary ischemia or infarction. Compared with ST segment elevation on a single ECG, added consideration of dynamic changes in ST segment elevation between serial ECGs improved the sensitivity for an acute coronary syndrome from 34% to 46% and reduced specificity from 96% to 93% (both p < 0.00004). Overall, compared with abnormalities observed on a single ECG, consideration of serial evolution in ST segment, T or Q wave or left bundle branch block (LBBB) abnormalities between the prehospital and initial hospital ECG improved the diagnostic sensitivity for an acute coronary syndrome from 80% to 87%, with a fall in specificity from 60% to 50% (both p < 0.000006). CONCLUSIONS: ECG abnormalities are an early manifestation of acute coronary syndromes and can be identified by the prehospital ECG. Compared with a single ECG, the additional effect of evolving ST segment, T or Q waves or LBBB between serially obtained prehospital and hospital ECGs enhanced the diagnosis of acute coronary syndromes, but with a fall in specificity.

Biphasic transthoracic defibrillation causes fewer ECG ST-segment changes after shock.

STUDY OBJECTIVE: Electrocardiographic abnormalities are common after transthoracic defibrillation. ECG ST-segment changes are especially problematic after defibrillation and may indicate ischemic or shock-induced cardiac dysfunction after resuscitation. Biphasic defibrillation waveforms, compared with monophasic waveforms, diminish shock-induced cardiac dysfunction in laboratory preparations. This effect has not been validated in human subjects. We therefore evaluated in a prospective, blinded fashion the effect of biphasic and monophasic transthoracic defibrillation on the ECG ST segment in 30 consecutive patients during surgery for the implantation of a cardioverter-defibrillator. METHODS: In each patient two low-energy truncated biphasic transthoracic defibrillation shocks (115 and 130 J) were compared with a standard clinical 200 J monophasic damped-sine wave shock. The biphasic shocks and the damped-sine wave shock have been demonstrated to have equal defibrillation efficacy of 97%. Fifteen-second ECG signals recorded across transthoracic defibrillation electrodes were digitized before ventricular fibrillation induction and immediately after each defibrillation attempt. The ST segments 80 msec after the J point were analyzed in a blinded fashion by two reviewers. The ST-segment deflection, QRS-interval duration, QT interval, and heart rate after each therapy were compared with baseline values. RESULTS: ECG ST-segment elevation was significantly greater with the 200-J damped-sine waveform than with either biphasic waveform. The ECG ST-segment levels were -.55 +/- .36 at baseline, -.76 +/- .36 mm after internal shock, -.02-.36 mm after 115-J biphasic shock, .21 +/- .38 mm after 130-J biphasic shock, and 2.09 +/- .37 mm after 200-J damped-sine wave shock (P<.0001). QRS-interval duration, QT interval, and heart rate did not change significantly with any waveform. CONCLUSION: Transthoracic defibrillation with biphasic waveforms results in less postshock ECG evidence of myocardial dysfunction (injury or ischemia) than standard monophasic damped sine waveforms without compromise of defibrillation efficacy.

Association of gender and survival in patients with acute myocardial infarction.

BACKGROUND: During the last 5 years, many studies have produced conflicting results concerning the survival of women hospitalized with acute myocardial infarction (AMI). OBJECTIVE: To determine if gender is associated with hospital mortality and long-term survival in individuals with AMI. METHODS: This prospective study included 4255 consecutive women (34%) and 8076 (66%) men who developed AMI in 19 Seattle, Wash, area hospitals between January 1988 and June 1994. Key information was abstracted from hospital records and entered in the Myocardial Infarction Triage and Intervention registry database. In addition, data concerning survival and rehospitalization were obtained from the state of Washington and linked to the Myocardial Infarction Triage and Intervention registry. RESULTS: In comparison with men, women were 8 years older, more often had history of congestive heart failure, hypertension, or diabetes mellitus, and less often had history of myocardial infarction or coronary surgery. During hospitalization, women were less likely to undergo coronary angiography, thrombolytic therapy, coronary angioplasty, or bypass surgery. After adjustment for covariates, women were 20% more likely to die in the hospital (odds ratio, 1.22; 95% confidence interval, 1.06-1.39), yet long-term survival was similar in the 2 groups (hazard ratio, 0.97; 95% confidence interval, 0.90-1.05). The use of thrombolytic therapy or revascularization during the index hospitalization did not change the association between gender and survival. CONCLUSIONS: All things being equal, women with AMI were more likely to die in the hospital, yet survival after hospital discharge did not differ according to gender. Appropriate treatment to reduce hospital mortality in women is needed.

Prospective evaluation of the effect of biphasic waveform defibrillation on ventricular pacing thresholds.

INTRODUCTION: Significant increases in ventricular pacing threshold have been observed following monophasic waveform ventricular defibrillation shocks. High-output pacing is recommended to ensure consistent capture, particularly in pacemaker-dependent patients who are likely to be defibrillated. Whether biphasic waveform defibrillation compounds this problem is not known. The purpose of this prospective study was to examine serial changes in ventricular pacing thresholds following single, multiple, low- and high-energy biphasic defibrillation shocks from an implanted defibrillator. METHODS AND RESULTS: Bipolar pacing thresholds before and after defibrillation, and the adequacy of pacing capture at three times preshock threshold in the immediate aftermath of ventricular defibrillation, were prospectively evaluated in 67 consecutively tested recipients of a biphasic implanted cardioverter defibrillator. Overall, serial pacing thresholds following successful defibrillation were completely unchanged after 141 of 177 (80%) ventricular fibrillation inductions. In no case did the threshold pulse width increment > 0.06 msec from its baseline value after shock, nor did pacing at a pulse width of three times preshock threshold from dedicated bipolar pacing electrodes fail to result in successful ventricular capture. Changes in threshold were not related to when measured from the time of shock, defibrillation energy, number of shocks, electrode system, chronicity of leads, shock orientation, or to clinical factors. CONCLUSIONS: No clinically important changes in pacing threshold were observed after biphasic waveform defibrillation. Bradycardia pacing at conventional pacemaker outputs of three times baseline pulse width threshold from bipolar electrodes dedicated exclusively to pacing or sensing (but not defibrillation) consistently allowed for an adequate safety margin following defibrillation.

Malignant sustained ventricular tachyarrhythmias in women: characteristics and outcome of treatment with an implantable cardioverter defibrillator.

Clinical rhythm, heart disease, ejection fraction, defibrillation threshold, recurrent arrhythmias, and mortality were compared in 268 consecutive recipients (213 men and 55 women) of their first implantable cardioverter defibrillator for life-threatening ventricular tachycardia or fibrillation. Women were younger than men, less likely to have structural heart disease, and more likely to have clinical ventricular fibrillation, a higher ejection fraction, and a lower defibrillation threshold. Complications of defibrillator placement were similar in both sexes. Unadjusted survival tended to be higher in women than in men (97% vs 90%, respectively, at 2 years, P = 0.08), largely due to fewer deaths from noncardiac causes or cardiac causes other than arrhythmia (P = 0.04). Women also tended to be at lower, albeit still substantial, risk for recurrent arrhythmias during follow-up (37% vs 52% in men at 2 years, P = 0.11). After adjustment for baseline differences, overall survival, arrhythmia death-free survival, nonarrhythmia death-free survival, and frequency of recurrent arrhythmias were not found to be gender related. Despite their apparent "lower risk" status on initial presentation, women remained at substantial risk for recurrent arrhythmias. This underscores the need to avoid being unduly biased by the "appearance" of health in managing women with malignant arrhythmias. That survival and other clinical endpoints were all ultimately independent of gender emphasizes the importance of other clinical variables in assessing risk from ventricular tachyarrhythmias.

Comparison of presentation, treatment, and outcome of acute myocardial infarction in men versus women (the Myocardial Infarction Triage and Intervention Registry)

This study compared the presentation (symptoms and signs), treatment, and outcome of 1,097 consecutive patients (851 men and 246 women) from the Myocardial Infarction Triage and Intervention (MITI) Project Registry with confirmed acute myocardial infarction (AMI), all of whom were initially evaluated in the prehospital setting, met clinical criteria for possible thrombolysis, and were followed throughout their hospital course. Women were older than men and had a higher prevalence of known cardiovascular risk factors, including systemic hypertension and congestive heart failure. The presentation of AMI with respect to symptoms, delay, and hemodynamic and electrocardiographic findings was for the most part indistinguishable between mean and women. Women appeared "undertreated" early in the course of AMI and were half as likely as men to undergo acute catheterization, angioplasty, thrombolysis, or coronary bypass surgery (odds ratio 0.5 [0.3 to 0.7]). The risk for hospital mortality in women was almost twice that for men (odds ratio 1.95 [1.01 to 3.8]). Hospital mortality after AMI was also independently predicted by older age, early evidence of hemodynamic instability, and an intraventricular conduction abnormality on the initial electrocardiogram. Although similar in its presentation, AMI in women is not as aggressively treated, and results in a less favorable outcome than in men. Gender as well as nongender-specific risk factors are important in assessing risk and the likelihood of early intervention after AMI.

Atrial fibrillation pearls and perils of management.

Atrial fibrillation, a common arrhythmia, is responsible for considerable cardiovascular morbidity. Its management demands more than antiarrhythmic therapy alone, but must address the causes and consequences of the arrhythmia. Although remediable causes are infrequently found, a thorough search for associated heart disease or its risk factors results in better-informed patient management. Controlling the ventricular response and protecting from thromboembolic complications are important initial goals of therapy and may include the administration of aspirin in younger, low-risk patients. Older patients and those with risk factors for systemic embolism are not adequately protected from stroke complications by aspirin therapy alone. It remains controversial whether all high-risk patients should receive warfarin and at what intensity. Whether and how sinus rhythm should be restored and maintained poses the greatest therapeutic controversy for atrial fibrillation. The mortal risk of antiarrhythmic therapy is substantially greater in patients with evidence of heart failure. In such persons, the risks and benefits of maintaining normal sinus rhythm with antiarrhythmic medications should be weighted carefully. A definitive cure for atrial fibrillation remains elusive, but promising surgical and catheter ablation therapies are being developed.

Management of ventricular fibrillation with transvenous defibrillators without baseline electrophysiologic testing or antiarrhythmic drugs.

INTRODUCTION: Baseline electrophysiologic study (EPS) is routinely performed in patients resuscitated from ventricular fibrillation (VF) to risk stratify and select patients for chronic antiarrhythmic drug therapy. The role of EP testing prior to insertion of a multiprogrammable implantable cardioverter defibrillator (ICD), however, is unclear. METHODS AND RESULTS: This study was a retrospective review of outcome in 66 survivors of an initial episode of out-of-hospital VF not associated with a Q wave myocardial infarction or reversible causes, treated with transvenous ICDs as first-line therapy. Patients were excluded from the study if they had a previous history of monomorphic ventricular tachycardia (VT), a clinical history suggestive of supraventricular tachycardia, or had undergone preoperative EP testing. Fifty-two of the patients (79%) were male with an average age of 58 +/- 11 years. Coronary artery disease was present in 43 patients (66%), cardiomyopathy in 15 patients (23%), and valvular heart disease in 1 patient (1.5%). Seven patients (11%) had no detectable structural heart disease. The mean left ventricular ejection fraction was 0.40 +/- 0.16. With an average follow-up of 25 +/- 12 months, survival free of death from any cause was 100%. Twenty-three patients (35%) experienced 48 episodes of recurrent rapid VT or VF (average cycle length: 236 +/- 47 msec) treated by their device. The mean time to first therapy was 223 +/- 200 days. Only one of these patients also received antitachycardia pacing for two episodes of VT. One patient (1.5%) temporarily received amiodarone after removal of an infected device that was subsequently replaced. No other patient received antiarrhythmic drug therapy. CONCLUSION: After a cardiac arrest due to primary VF, select patients treated with multiprogrammable ICDs can be managed successfully without baseline EPS or antiarrhythmic drug therapy.

A prospective randomized comparison in humans of 90-mu F and 120-mu F biphasic pulse defibrillation using a unipolar defibrillation system.

INTRODUCTION: Capacitance is known to influence defibrillation. Optimal biphasic waveform capacitance for transvenous unipolar defibrillation systems in man is currently being defined. In an effort to improve defibrillation efficacy, we examined the relative defibrillation efficacy of a 65% tilt biphasic pulse from a 90-mu F capacitor compared to a 65% tilt biphasic pulse from a 120-mu F capacitor in a prospective, randomized fashion in 16 consecutive cardiac arrest survivors undergoing defibrillator surgery. METHODS AND RESULTS: The transvenous unipolar pectoral defibrillation system uses a single endocardial RV anodal defibrillation coil and the shell of an 80-cc volume (88 cm2 surface area) pulse generator (Medtronic Model 7219C PCD "active CAN") as the cathode for the first phase of the biphasic shock: RV+ --> CAN-. Defibrillation thresholds for each capacitance were determined prospectively in a randomized fashion. The defibrillation threshold results for the 90-mu F capacitance were: leading edge voltage 383 +/- 132 V; stored energy 7.4 +/- 5.0 J; and resistance 57 +/- 10 omega. The results for the 120-mu F capacitance were: leading edge voltage 315 +/- 93 V (P = 0.002); stored energy 6.5 +/- 3.7 J (P = 0.21); and resistance 57.0 +/- 11 omega (P = 0.87). CONCLUSIONS: We conclude that 90-mu F, 65% tilt biphasic pulses used with unipolar pectoral defibrillation systems have equivalent stored energy defibrillation efficacy compared to 120-mu F, 65% tilt pulses. Use of lower capacitance is possible in present implantable defibrillators without compromising defibrillation.

A prospective randomized evaluation of implantable cardioverter-defibrillator size on unipolar defibrillation system efficacy.

BACKGROUND: The active can unipolar implantable cardioverter-defibrillator (ICD) has been shown to defibrillate efficiently, but its current 80-cc size limits use in the pectoral position in many patients. Decreasing can size will facilitate pectoral insertion and will soon be feasible as an inevitable consequence of technological advancements. However, decreasing the can size has the potential to compromise unipolar defibrillation efficacy. It is the purpose of this study, therefore, to prospectively and randomly compare unipolar defibrillation efficacy with 80-cc, 60-cc, and 40-cc can sizes in patients immediately before ICD surgery in anticipation of advances in technology that will make smaller ICDs possible. METHODS AND RESULTS: Twenty-four consecutive patients underwent prospective, randomized evaluation of the effect of ICD can size on defibrillation efficacy during standard ICD surgery. Each patient had the unipolar defibrillation threshold (DFT) measured with 80-cc, 60-cc, or 40-cc active can placed in the left subcutaneous infraclavicular region. The system included a 10.5F tripolar right ventricular electrode that served as the shock anode. The shock waveform used in each instance was a single capacitor biphasic 65% pulse delivered from a 120-microF capacitor. Stored energy at the DFT for the 80-cc, 60-cc, and 40-cc cans were 8.1 +/- 4.7 J, 8.7 +/- 5.8 J, and 9.5 +/- 4.8 J, respectively. There was no statistical significant difference between the DFTs for the three unipolar can electrodes (P = 39). Leading edge voltage also did not differ significantly among the three unipolar cans (356 +/- 92 V, 365 +/- 110 V, and 387 +/- 94 V, respectively, P = .29). There was, however, a slight progressive increase in resistance with decreasing can size (57 +/- 7 omega, 60 +/- 9 omega, and 65 +/- 9 omega, respectively, P < .001). CONCLUSIONS: Decreasing can volume from 80 cc to 60 cc to 40 cc does not compromise unipolar defibrillation efficacy despite a slight rise in shock resistance. These findings indicate that technological advances that allow for smaller-volume ICDs will not compromise defibrillation efficacy for unipolar systems.

Anatomical findings in patients having had a chronically indwelling coronary sinus defibrillation lead.

The purpose of this report is to review the gross and histological cardiac anatomical findings in patients with chronically indwelling coronary sinus leads at the time of autopsy or cardiac transplantation. Transvenous cardioverter defibrillators offer effective protection against sudden death. The use of a coronary sinus electrode has been shown in some patients to decrease the defibrillation threshold. The anatomical consequences of chronically indwelling coronary sinus cardioversion/defibrillation electrodes in patients having transvenous implantable cardioverter defibrillators is unknown. The hearts of seven patients with chronically indwelling coronary sinus electrodes were evaluated following autopsy (n = 2) or cardiac transplantation (n = 5). The coronary sinus electrode in each case was a 6.5 French silicone lead with a 5-cm long defibrillation coil (Medtronic CS lead model 6933) that was positioned as distally as possible within the coronary sinus at the time of implantable cardioverter defibrillator surgery. The seven hearts examined were derived from patients whose age ranged between 49 and 69 (mean 56 +/- 7 years). Six had coronary artery disease and one had idiopathic dilated cardiomyopathy. The time from implant to death or cardiac transplantation was 8 +/- 6 months, range 1-18 months. In all seven patients, there was no evidence of any significant damage from the presence of the coronary sinus lead. The only finding in each case was the scattered presence of a thin white fibrous sheath over the lead that intermittently adhered to the coronary sinus endothelium and, in the two patients transplanted 1-3 months after implantable cardioverter defibrillator insertion, a mild inflammation reaction adjacent to the leads in the coronary sinus endothelium. There was no evidence of coronary sinus occlusion, adjacent coronary artery injury, coronary sinus perforation, coronary sinus burn, or myocardial injury adjacent to the lead. Cause of death was due to end-stage congestive heart failure and thrombotic stroke, respectively, in the two patients examined at autopsy. Coronary sinus defibrillation leads can be used safely without harmful anatomical effect.

Mechanical complications after implantation of multiple-lead nonthoracotomy defibrillator systems: implications for management and future system design.

Nonthoracotomy lead system (NTL) implantable cardioverter defibrillators (ICDs) provide excellent protection against sudden death from ventricular tachyarrhythmias. However, these devices have unique mechanical complications and management issues. We reviewed the major complications occurring in 159 patients who underwent attempted implantation of a multilead NTL system. Successful implantation was obtained in 98% of patients. Two-year, all-cause actuarial survival on an intention-to-treat basis was 94%. Major complications occurred in 28 (17.6%) patients over a follow-up period of 21 +/- 10 months. Complications included 11 (6.9%) lead dislodgements, 10 (5.7%) lead fractures in 9 patients, 2 (1.3%) pocket infections, 1 frozen shoulder, 1 right ventricular perforation, 1 pneumothorax, 1 bleed requiring transfusion, 1 thromboembolism, and 1 "twiddle"-induced torsion of leads. Most of the lead dislodgements and fractures were identified by routine x-ray surveillance. Single-lead systems may significantly reduce complication rates in the future and maintain excellent survival rates.

Prospective randomized comparison of biphasic waveform tilt using a unipolar defibrillation system.

BACKGROUND: A unipolar defibrillation system using a single right ventricular (RV) electrode and the active shell or container of an implantable cardioverter defibrillator situated in a left infraclavicular pocket has been shown to be as efficient in defibrillation as an epicardial lead system. Additional improvements in this system would have favorable practice implications and could derive from alterations in pulse waveform shape. The specific purpose of this study is to determine whether defibrillation efficacy can be improved further in humans by lowering biphasic waveform tilt. METHODS: We prospectively and randomly compared the defibrillation efficacy of a 50% and a 65% tilt asymmetric biphasic waveform using the unipolar defibrillation system in 15 consecutive cardiac arrest survivors prior to implantation of a presently available standard transvenous defibrillation system. The RV defibrillation electrode has a 5-cm coil located on a 10.5 French lead and was used as the anode. The system cathode was the active 108 cm2 surface area shell (or "CAN") of a prototype titanium alloy pulse generator placed in the left infraclavicular pocket. The defibrillation pulse derived from a 120-microF capacitor and was delivered from RV-->CAN, with RV positive with respect to the CAN during the initial portion of the cycle. Defibrillation threshold (DFT) stored energy, delivered energy, leading edge voltage and current, pulse resistance, and pulse width were measured for both tilts examined. RESULTS: The unipolar single lead system, RV-->CAN, using a 65% tilt biphasic pulse resulted in a stored energy DFT of 8.7 +/- 5.7 J and a delivered energy DFT of 7.6 +/- 5.0 J. In all 15 patients, stored and delivered energy DFTs were < 20 J. The 50% tilt biphasic pulse resulted in a stored energy DFT of 8.2 +/- 5.4 J and a delivered energy DFT of 6.1 +/- 4.0 J; P = 0.69 and 0.17, respectively. As with the 65% tilt pulse, all 15 patients had stored and delivered energy DFTs < 20 J. CONCLUSION: The unipolar single lead transvenous defibrillation system provides defibrillation at energy levels comparable to that reported with epicardial lead systems. This system is not improved by use of a 50% tilt biphasic waveform instead of a standard 65% tilt biphasic pulse.

Clinical predictors of the defibrillation threshold with the unipolar implantable defibrillation system.

OBJECTIVES: The purpose of this study was to determine the relation between clinical variables and the defibrillation threshold by using a standardized testing protocol and a uniform implantable defibrillator system. BACKGROUND: Past studied have not revealed useful correlations between clinical variables and the energy required to terminate ventricular fibrillation. Most of these studies did not use a uniform implantable defibrillator system or a standardized protocol to measure the defibrillation threshold and, thus, did not control for the influence of these technical influences. We postulated that defibrillator and defibrillation threshold measurement-based sources of variability overshadowed important clinical predictors. METHODS: The defibrillation threshold was measured by using a standardized protocol in 101 consecutive patients. We used a transvenous unipolar pectoral defibrillation system that employed a single endocardial right ventricular defibrillation coil as the anode and the shell of an 80-cm3 pulse generator as the cathode to deliver a 65% tilt biphasic pulse. RESULTS: Several clinical variables were found to be significantly associated with the defibrillation threshold: patient gender, height, weight, body surface area, heart rate at rest, QRS and corrected QT (QTc) intervals, left ventricular mass and several measures of heart and chest size by chest roentgenogram. None of these variables had a correlation coefficient > 0.45 with the defibrillation threshold. On multivariate analysis, left ventricular mass and heart rate at rest were the only independent predictors of the defibrillation threshold and explained only 25% of the observed variability. CONCLUSIONS: Despite the use of a uniform transvenous defibrillation system and a standardized protocol to measure the defibrillation threshold, no clinically relevant correlation was found between clinical variables and the defibrillation threshold. The defibrillation threshold is probably a function of a complex interaction of anatomic, physiologic and cellular variables that are not adequately represented by easily obtainable clinical information. It is probably not possible to predict defibrillation outcome from standard clinical variables.

Comparison of monophasic and biphasic defibrillating pulse waveforms for transthoracic cardioversion. Biphasic Waveform Defibrillation Investigators.

All transthoracic defibrillators on the US market use nominally monophasic shock waveforms. However, biphasic waveforms have a lower defibrillation threshold than monophasic waveforms for transthoracic defibrillation of animals and for defibrillation of humans by implantable cardioverter defibrillators. The relative efficacies of Edmark monophasic and Gurvich biphasic transthoracic cardioversion waveforms (200 J into 50 omega) were compared for transthoracic cardioversion in 171 patients undergoing electrophysiologic study for evaluation of ventricular arrhythmias. Patients were randomized in a blinded fashion to receive either a monophasic or a biphasic waveform for the initial shock for conversion of induced ventricular arrhythmias (ventricular fibrillation [VF] = 53, monomorphic ventricular tachycardia [VT] = 80, polymorphic VT = 30, ventricular flutter = 8). Delivered energies for the Edmark and Gurvich waveforms were 215 +/- 11 and 171 +/- 11 J, respectively. There were no significant differences in patient characteristics, use of antiarrhythmic agents, arrhythmia cycle length, or duration of arrhythmia prior to shock for monophasic and biphasic waveform groups. The first shock for all arrhythmias was successful in 75 of 88 patients (85.2%) for the monophasic waveform compared with 81 of 83 patients (97.6%) for the biphasic waveform, p = 0.0054. The first shock for VF was successful in 22 of 28 patients (78.6%) for the monophasic waveform compared with 25 of 25 (100%) for the biphasic waveform, p = 0.0241. The Gurvich biphasic waveforms delivering a mean of 171 J were superior to Edmark monophasic waveforms delivering a mean of 215 J for transthoracic cardioversion of arrhythmias of short duration. This finding may have important implications for the development of future transthoracic defibrillators.