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Embolization is a well-established method of treatment of arteriovenous malformations. Most procedures are performed under general anesthesia due to the painful nature of some sclerosing agents, procedure duration, and need for immobilization to allow precise injection. Familiarity with the possible side effects of these agents is important for the anesthesiologist to facilitate timely and successful management of intra- and postprocedural complications. This case report describes an unusual presentation of systemic migration of glue-lipiodol mixture during embolization of a calf arteriovenous malformation in an adolescent that resulted in accelerated idioventricular rhythm and its successful management leading to complete resolution.

We describe the management of a parturient woman with hypertrophic cardiomyopathy who developed a symptomatic accelerated idioventricular rhythm who required an urgent cesarean delivery at 32 weeks. Transthoracic echocardiography helped guide anesthetic management, including epidural dosing, fluid management, and phenylephrine infusion rates. This case demonstrates the application of transthoracic echocardiography to guide anesthetic management in a parturient woman at risk for cardiovascular compromise.

Background— Accelerated idioventricular rhythm (AIVR) or ventricular tachycardia (VT) originating from the right bundle branch (RBB) is rare and published clinical data on such arrhythmia are scarce. In this study, we will describe the clinical manifestations, diagnosis, and management of a cohort of patients with this novel arrhythmia. Methods and Results— Eight patients (5 men; median age, 25 years) with RBB-AIVR/VT were consecutively enrolled in the study. Pharmacological testing, exercise treadmill testing, electrophysiological study, and catheter ablation were performed in the study patients, and ECG features were characterized. All RBB-AIVR/VTs were of typical left bundle-branch block morphology with atrioventricular dissociation. The arrhythmias, which demonstrated chronotropic variability, were often isorhythmic with sinus rhythm and were accelerated by physical exercise, stress, and intravenous isoprenaline infusion. The rate of RBB-AIVR/VT varied from 45 to 200 beats per minute. Two patients experienced syncope, and 3 had impaired left ventricular function. Metoprolol was proven to be the most effective drug to decelerate the arrhythmia rate and relieve symptoms. Electrophysiology study was performed in 5 patients and the earliest activation with a sharp RBB potential was localized in the mid or distal RBB area. Catheter ablation terminated the arrhythmia with subsequent RBB block morphology during sinus rhythm. During follow-up, patients’ symptoms were controlled with normalization of left ventricular function either on metoprolol or by catheter ablation. Conclusions— RBB-AIVR/VT is an unusual type of ventricular arrhythmia. It can result in significant symptoms and depressed ventricular function and can be successfully treated with catheter ablation.

BACKGROUND Drug-induced torsade de pointes (TdP) arrhythmias can readily be induced in anesthetized dogs with remodeled hearts [chronic complete atrioventricular block (CAVB) dogs]. Similar studies in conscious CAVB dogs reveal lower TdP incidences. Regulations forced us to reconsider our anesthetic regimen, which consist of pentobarbital followed by halothane (P + H). We investigated the relevance of anesthesia for this enhanced susceptibility (part 1) and compared 3 anesthetic regimens (part 2). METHODS Part 1-Ten CAVB dogs paced from the high septum at 1000 milliseconds were challenged with dofetilide (25 microg x kg(-1) x 5 min(-1)) twice: once under anesthesia and once awake. Anesthesia consisted of P + H (n = 5) and thiopental maintained by isoflurane (T + I). Part 2-In CAVB dogs (n = 6) with spontaneous idioventricular rhythm, the electrophysiological and arrhythmogenic consequences of different anesthetic regimens (P + H, T + I, and P + I) were serially compared. RESULTS Part 1-In paced dogs, dofetilide-induced TdP was higher under anesthetized than in conscious circumstances, with the more severe outcome seen after T + I as compared with P + H or control (2x): 5/5, 2/5, 0/5, and 0/5, respectively; P < 0.05. Part 2-Electrophysiologically, T accelerated idioventricular rhythm, increased QTc, and transiently induced polymorphic ventricular tachycardias in 2 of 6 dogs. This was not seen after P. At 120 minutes (end of the preparation), QTc increase was highest after T + I, intermediate with P + I, and the smallest after P + H. Dofetilide in combination with T + I induced the most severe arrhythmogenic outcome. CONCLUSIONS Thiopental anesthesia causes arrhythmias sec, whereas anesthesia in general predisposes for drug-induced TdP in the CAVB dog. In combination with dofetilide, T + I has a more arrhythmic outcome than P + I or P + H.

Background Despite early recanalization of an occluded infarct-related artery, myocardial reperfusion may remain impaired due to microvascular injury. Reperfusion arrhythmias may indicate successful microvascular reperfusion. Methods Microvascular reperfusion was assessed prospectively in 42 consecutive patients with ST-segment elevation acute myocardial infarction (AMI) by evaluation of the resolution of ST-segment elevation (

IMPLICATIONS The rapid administration of desflurane results in transient hypertension and tachycardia, especially in the presence of sympathetic imbalance. We report a case in which rapid administration of desflurane precipitated an accelerated idioventricular rhythm in a patient. This may have been related to a period of inadequate anesthesia.

The calcium-entry blocker isradipine was tested in a closed-chest pig model for chronic myocardial infarction. Ischemia was evoked in anesthetized pigs (25-35 kg) by inflating a catheter balloon in the left anterior descending coronary artery for at least 45 min. Hemodynamic monitoring and signal averaging of X, Y, and Z electrocardiographic leads were performed (150 beats, filtered at 50 Hz). After reperfusion, all animals developed an accelerated idioventricular rhythm and high creatine kinase (CPK) plasma levels. Coronary venous purines and catecholamines increased transiently. Two hours after reperfusion, heart rate was elevated from the initial 87.5 +/- 6.3 to 126 +/- 6.4 beats/min (p less than 0.01) and the pressure-rate product (PRP, an index of oxygen demand) from 9,530 +/- 630 to 11,950 +/- 790 mm Hg/min (p less than 0.05). After 2 weeks, six surviving pigs had a decreased stroke volume (98 +/- 18 versus the initial 124 +/- 14 microliters/kg, p less than 0.05), a prolonged high-frequency signal-averaged QRS duration (81.2 +/- 6.5 versus 65.7 +/- 2.9 ms, initially; p less than 0.05), and ventricular tachycardias (VTs), inducible by programmed electrical stimulation (PES). After the infusion of isradipine (1 microgram/kg/min for 30 min), the cardiac index increased from 92 +/- 14 to 133 +/- 8.7 ml/min.kg (p less than 0.02). Even at a higher heart rate, the PRP dropped from 12,600 +/- 1,900 to 10,560 +/- 1,400 mm Hg/min (p less than 0.05). Sustained monomorphic tachycardias were inducible in five pigs before and in three pigs after isradipine, and no deterioration of the signal-averaged electrocardiogram parameters was found.(ABSTRACT TRUNCATED AT 250 WORDS)

We previously reported concentration-dependent protection of captopril against ischemia-reperfusion injury in the isolated rat heart. In order to study these effects in vivo, we developed a closed-chest pig model. Reversible occlusion of the left coronary artery was achieved with a PTCA catheter during one hour. Captopril (C) i.v. was given in two different concentrations (0.6 mg/kg/10 min + 0.3 mg/kg/2 hr and 6 mg/kg/10 min + 3.0 mg/kg/2 hr) during the experiments to 11 and 10 pigs, respectively, versus 12 controls, who received only saline. Due to malignant ventricular arrhythmias, nine pigs died during ischemia. At the end of the reperfusion period of two hours, eight pigs were alive in each group. In the C-treated pigs, maximum creatine kinase after two hours of reperfusion was significantly lowered to 6,337 +/- 709 U/L in the high dose group versus 8,285 +/- 851 U/L in the low dose group and 9,635 +/- 1,115 U/L in the saline group. A reduction of local inosine overflow in the coronary sinus was seen. Maximum noradrenaline overflow after 5 min reperfusion diminished dose-dependently to 695 +/- 284 and 3,129 +/- 1,728 pg/ml in the C treated groups versus 4,693 +/- 2,277 pg/ml in the saline group. Mean arterial blood pressure and cardiac output decreased significantly during ischemia and reperfusion, but no significant differences occurred between the treated and untreated groups. Reperfusion arrhythmias, mainly accelerated idioventricular rhythm disturbances, were comparable among the three groups. We conclude that in vivo administration of C reduces myocardial damage upon reperfusion after one hour of ischemia in a dose-dependent way.(ABSTRACT TRUNCATED AT 250 WORDS)

In order to determine the role of the coupling interval of a premature ventricular contraction (PVC) in the development of paroxysmal ventricular tachycardia (PVT) during the early phase of acute myocardial infarction in man, 52 male patients with documented acute myocardial infarction had 24-hour Holter monitoring commenced within 24 hours of the onset of prolonged chest pain. Review of the tape recordings revealed that 27 patients had PVT documented, while 25 patients did not. Analysis of the data on the two groups showed that the frequency of PVCs, coupled PVCs, and accelerated idioventricular rhythm (AIVR) were found to be associated with a significantly increased incidence of ventricular tachycardia. The mean coupling interval of the PVCs initiating episodes of ventricular tachycardia was not significantly different from either the mean coupling interval of the isolated PVCs in the patients with PVT or the mean coupling interval of the PVCs in the patients without PVT. This suggests that the coupling interval of a ventricular ectopic is a poor predictor of ventricular tachycardia in the early phases of acute myocardial infarction.

Fifty-six patients with acute myocardial infarction complicated by sinus bradycardia (SB) were treated with intravenous atropine and monitored in a coronary care unit. Atropine decreased or completely abolished premature ventricular contractions (PVCs) and/or bouts of accelerated idioventricular rhythm in 27 of 31 patients (87%) and brought systemic blood pressure up to normal in 15 of 17 patients (88%) with hypotension. In addition, atropine administration was associated with improved atrioventricular conduction in 11 of 13 patients (85%) with acute inferior myocardial infarction associated with 2 degrees or 3 degrees atrioventricular block. Seven patients developed ten significant adverse effects: ventricular tachycardia or fibrillation in three, sustainedsinus tachycardia in three, increased PVCs in three, and toxic psychosis in one. These major adverse effects correlated with either a higher initial dose of atropine (i.e., 1.0 mg aa compared with the usual 0.5 or 0.6 mg) or a total cumulative dose exceeding 2.5 mg over 21/2 hours. Atropine is the drug of choice for management of patients with SB and hypotension and is effective in the treatment of ventricular arrhythmias as well as conduction disturbances in patients with inferior myocardial infarction. Serious adverse effects, however, preclude use of atropine without careful medical supervision.

Epicardial mapping technics were used to locate the origin of ventricular ectopic beats produced by pacing and by the administration of ouabain and acetylstrophanthidin in pentobarbital-anesthetized open-chest dogs. The sequence of epicardial depolarization was determined with close bipolar reference and roving electrodes. The wave of excitation spread in concentric manner from driven points with the origin having the earliest time. Nonparasystolic unifocal ventricular tachycardia (UVT) was then aroused in nine dogs with ouabain or acetylstrophanthidin. Plunge electrodes were inserted for recording and stimulating of bundle of His and Purkinje fibers. Earliest epicardial ventricular activation of the UVT beats always occurred at or near the apex of the left ventricle. Purkinje fiber (PF) spikes from the region of earliest epicardial depolarization appeared just prior to ventricular activation. Pacing at this point produced QRS configuration almost identical to that during UVT. His bundle pacing normalized QRS configuration and suppressed UVT. Isolated right ventricular and left ventricular PF were perfused in the same tissue bath for microelectrode impalement. Infusion of ouabain increased the rate of automatic discharge of left ventricular PF before those from the right ventricle in each of five preparations. These studies suggest that digitalis-induced unifocal ventricular tachycardia originates below the His bundle from Purkinje tissue supplying the left ventricle and demonstrate that automaticity of canine PF from the left ventricle is preferentially enhanced by ouabain.

We report the case of a patient who developed severe hypoxemia and an unusual arrhythmia, accelerated idioventricular rhythm, during flexible fiberoptic bronchoscopy. Coronary artery disease was subsequently suspected despite an unremarkable history and physical examination, and confirmed by a thallium 201 imaging. The appearance of accelerated idioventricular rhythm during fiberoptic bronchoscopy should raise the possibility of underlying coronary artery disease.