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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. [ABSTRACT FROM AUTHOR]

Quinidine gluconate (total dose 4-4 to 9-1 mg/kg) was infused intravenously over 22 minutes in 20 patients with either frequent premature ventricular contractions or supraventricular arrhythmias, 16 of whom had bundle-branch block. Therapeutic plasma quinidine levels (3 to 7 mg/l) were achieved in 15. Heart rate, atrioventricular nodal, and infranodal conduction times did not change significantly. The QRS duration increased significantly from 128+/-30 to 134+/-29 ms at peak plasma quinidine levels (P less than 0.01). Mild hypotension occurred during infusion in most patients. Two patients had a severe but transient toxic response characterised by hypotension, nausea, vomiting, and diaphoresis. Atrioventricular dissociation with escape His bundle or fascicular rhythm occurred in 1 patient with sinus bradycardia. Bundle-branch block does not contraindicate administration of quinidine. Quinidine gluconate administered intravenously (0-3 to 0-4 mg/kg per min) is frequently associated with hypotenstion and should be used only in an intensive care setting and with careful monitoring of blood pressure. [ABSTRACT FROM PUBLISHER]

Objective: To assess the short- and long-term safety and efficacy of oral flecainide therapy in patients with symptomatic tachycardia and an extranodal accessory pathway.Design: Open-label, uncontrolled trial with a mean follow-up of 24 months.Setting: Referral-based, teaching medical center.Patients: Sixty-three patients with symptomatic tachycardia and an extranodal accessory pathway.Interventions: Patients had electrophysiologic testing before and after the initiation of oral flecainide therapy and were followed long-term for the presence of symptoms, new physical limitations, and adverse effects of therapy.Measurements and Main Results: Flecainide therapy prevented or slowed (324 +/- 59 ms to 398 +/- 55 ms; P less than 0.001) inducible sustained atrioventricular reciprocating tachycardia in 44 of 63 patients (70%). Of the 44 patients discharged from the hospital, 33 (75%) have continued to receive flecainide therapy and have shown no adverse effects (mean follow-up, 24 +/- 10 months). Adverse cardiac reactions (proarrhythmia or sinus node suppression) attributable to flecainide occurred in 11 of 63 patients (17%); in 9 (82%) of these 11 patients, events were detected during either in-hospital monitoring or the electrophysiologic study done before discharge. Structural heart disease was detected by two-dimensional echocardiography in 8 of 11 patients who had adverse cardiac events and in 6 of 52 patients who did not have such events (P less than 0.001). Isoproterenol reversed the effects of flecainide therapy in 11 of 21 patients; 7 of the 11 patients had spontaneous clinical recurrences of tachycardia or palpitations during the follow-up period, but these symptoms occurred in only 1 of 10 patients who did not show isoproterenol-induced reversal (P = 0.02).Conclusions: Oral flecainide therapy was effective in 33 of 63 patients who had tachycardia and an extranodal accessory connection. Hospital monitoring during initial therapy is recommended, and flecainide should be used with caution, if at all, in patients with structural heart disease. An isoproterenol challenge appears to be helpful in predicting late recurrence of tachycardia. [ABSTRACT FROM AUTHOR]

Objective: To assess the efficacy of encainide and flecainide in treating patients with sustained ventricular arrhythmias.Design: Patients were treated with encainide or flecainide. Efficacy was assessed by comparing the results of programmed ventricular stimulation while patients received therapy with the results while they were drug free.Setting: The electrophysiology laboratory of the University of California at San Francisco.Patients: Forty-nine patients with spontaneous or inducible sustained ventricular tachycardia or ventricular fibrillation for whom treatment with at least one class IA antiarrhythmic agent had failed.Interventions: Patients were treated with encainide, 35 to 50 mg three or four times daily, or flecainide, 100 to 200 mg twice daily.Results: Arrhythmia worsened early in 5 of 16 patients receiving encainide and 3 of 33 patients receiving flecainide. Patients with poor left ventricular function were more likely to exhibit proarrhythmia (P = 0.02). Nine of eleven patients receiving encainide and 23 of 28 patients receiving flecainide who had repeat programmed ventricular stimulation while receiving drug therapy still had inducible, poorly tolerated ventricular tachycardia.Conclusion: Encainide and flecainide have a low efficacy rate and a high incidence of worsening of arrhythmia in patients with sustained ventricular arrhythmias, particularly when this condition is associated with poor left ventricular function. [ABSTRACT FROM AUTHOR]

Objective: To assess the safety and efficacy of intravenous adenosine in terminating acute episodes of paroxysmal supraventricular tachycardia.Design: Two prospective, double-blind, randomized, placebo-controlled trials to evaluate dose response in patients receiving adenosine and to compare the effects of adenosine with those of verapamil.Patients: A total of 359 patients with a tachycardia electrocardiographically consistent with paroxysmal supraventricular tachycardia were entered into the two protocols. Patients subsequently found to have arrhythmias other than paroxysmal supraventricular tachycardia were excluded from the efficacy analysis.Interventions: The first protocol compared sequential intravenous bolus doses of 3, 6, 9, and 12 mg of adenosine to equal volumes of saline. In the second protocol, patients received either 6 mg and, if necessary, 12 mg of adenosine or 5 mg and, if necessary, 7.5 mg of verapamil.Measurements and Main Results: When data are expressed in terms of cumulative response in eligible patients, intravenous adenosine terminated acute episodes of paroxysmal supraventricular tachycardia in 35.2%, 62.3%, 80.2%, and 91.4% of patients who received maximum doses of 3, 6, 9, and 12 mg, respectively, in a four-dose sequence, whereas 8.9%, 10.7%, 14.3%, and 16.1% of patients responded to four sequential placebo doses (P less than 0.0001). In the second trial, cumulative response rates after 6 mg followed, if necessary, by 12 mg of adenosine were 57.4% and 93.4%, and after 5 mg followed, if necessary, by 7.5 mg of verapamil were 81.3% and 91.4%. The average time after injection to termination of tachycardia by adenosine was 30 seconds. Adenosine caused adverse effects in 36% of patients, but they lasted less than 1 minute and were usually mild.Conclusions: Adenosine in graded doses up to 12 mg rapidly and effectively terminates acute episodes of paroxysmal supraventricular tachycardia in which the atrioventricular node is an integral part of the re-entrant circuit. The overall efficacy of adenosine is similar to that of verapamil, but its onset of action is more rapid. Adverse reactions to adenosine are common but are minor and brief. [ABSTRACT FROM AUTHOR]

Since disopyramide was introduced 5 years ago, the therapeutic spectrum of this drug in treating patients with ventricular and atrial arrhythmias has been found to be similar to that of the other type I antiarrhythmic drugs, quinidine and procainamide. Disopyramide has the potential to suppress sinus node function and, therefore, must be used cautiously in patients with the sick sinus syndrome. The available data indicate that it can be used safely in patients with bundle branch block and first-degree or type I second-degree atrioventricular block. Disopyramide has been found at times to precipitate ventricular tachycardia or ventricular fibrillation. Because this drug often causes decompensation in patients with congestive heart failure, it must be used very cautiously, if at all, in such patients. [ABSTRACT FROM AUTHOR]

Seven patients with either recurrent paroxysmal supraventricular tachycardia (five), alternatinng bradycardiatachycardia (one), or ventricular tachycardia (one) underwent insertion of permanent radiofrequency-triggered pacemakers. Follow-up evaluation (36 +/- 24 months, mean +/- SD) revealed that arrhythmias were well controlled in five of seven patients, although three of the five required medication to decrease frequency of arrhythmias. Overdrive pacing was ineffective in one patient with Wolff-Parkinson-White syndrome who had recurrent bouts of atrial fibrillation or atrial flutter. One additional patient with ventricular tachycardia became refractory to overdrive atrial pacing. These studies document the long-term effectiveness of radiofrequency pacemakers in some patients with recurrent refractory arrhythmias. Careful patient selection and electrophysiologic studies are mandatory before implantation of a permanent radiofrequency pacemaker. Physicians must be aware of both the benefits and possible limitations of radiofrequency pacemakers in order to choose between pacemaker versus surgical intervention in patients with cardiac arrhythmias refractory to standard drug therapy. [ABSTRACT FROM AUTHOR]