ECG diagnosis of native heart ventricular tachycardia in a heterotopic heart transplant recipient. (1/1256)

A case is reported of haemodynamic collapse in a 51 year old male heterotopic heart transplant recipient caused by native heart ventricular tachycardia. An accurate diagnosis was made by selective right and left sided electrocardiography. Synchronised electrical cardioversion of the native heart (200 J) resulted in restoration of sinus rhythm with prompt relief of symptoms and amelioration of the clinical situation.  (+info)

Repeated administration of vasopressin but not epinephrine maintains coronary perfusion pressure after early and late administration during prolonged cardiopulmonary resuscitation in pigs. (2/1256)

BACKGROUND: It is unknown whether repeated dosages of vasopressin or epinephrine given early or late during basic life support cardiopulmonary resuscitation (CPR) may be able to increase coronary perfusion pressure above a threshold between 20 and 30 mm Hg that renders defibrillation successful. METHODS AND RESULTS: After 4 minutes of cardiac arrest, followed by 3 minutes of basic life support CPR, 12 animals were randomly assigned to receive, every 5 minutes, either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 U/kg, respectively; n=6) or epinephrine (early epinephrine: 45, 45, and 200 microg/kg, respectively; n=6). Another 12 animals were randomly allocated after 4 minutes of cardiac arrest, followed by 8 minutes of basic life support CPR, to receive, every 5 minutes, either vasopressin (late vasopressin: 0.4 and 0.8 U/kg, respectively; n=6), or epinephrine (late epinephrine: 45 and 200 microg/kg, respectively; n=6). Defibrillation was attempted after 22 minutes of cardiac arrest. Mean+/-SEM coronary perfusion pressure was significantly higher 90 seconds after early vasopressin compared with early epinephrine (50+/-4 versus 34+/-3 mm Hg, P<0.02; 42+/-5 versus 15+/-3 mm Hg, P<0.0008; and 37+/-5 versus 11+/-3 mm Hg, P<0. 002, respectively). Mean+/-SEM coronary perfusion pressure was significantly higher 90 seconds after late vasopressin compared with late epinephrine (40+/-3 versus 22+/-4 mm Hg, P<0.004, and 32+/-4 versus 15+/-4 mm Hg, P<0.01, respectively). All vasopressin animals survived 60 minutes, whereas no epinephrine pig had return of spontaneous circulation (P<0.05). CONCLUSIONS: Repeated administration of vasopressin but only the first epinephrine dose given early and late during basic life support CPR maintained coronary perfusion pressure above the threshold that is needed for successful defibrillation.  (+info)

Predictors of atrial rhythm after atrioventricular node ablation for the treatment of paroxysmal atrial arrhythmias. (3/1256)

OBJECTIVE: To assess the natural history of the atrial rhythm of patients with paroxysmal atrial arrhythmias undergoing atrioventricular node ablation and permanent pacemaker implantation. DESIGN AND SETTING: A retrospective cohort study of consecutive patients identified from the pacemaker database and electrophysiology records of a tertiary referral hospital. PATIENTS: 62 consecutive patients with paroxysmal atrial arrhythmias undergoing atrioventricular node ablation and permanent pacemaker implantation between 1988 and July 1996. MAIN OUTCOME MEASURES: (1) Atrial rhythm on final follow up ECG, classified as either ordered (sinus rhythm or atrial pacing) or disordered (atrial fibrillation, atrial flutter or atrial tachycardia). (2) Chronic atrial fibrillation, defined as a disordered rhythm on two consecutive ECGs (or throughout a 24 hour Holter recording) with no ordered rhythm subsequently documented. RESULTS: Survival analysis showed that 75% of patients progressed to chronic atrial fibrillation by 2584 days (86 months). On multiple logistic regression analysis a history of electrical cardioversion, increasing patient age, and VVI pacing were associated with the development of chronic atrial fibrillation. A history of electrical cardioversion and increasing patient age were associated with a disordered atrial rhythm on the final follow up ECG. CONCLUSIONS: Patients with paroxysmal atrial arrhythmias are at high risk of developing chronic atrial fibrillation. A history of direct current cardioversion.  (+info)

Differential effects of defibrillation on systemic and cardiac sympathetic activity. (4/1256)

OBJECTIVE: To assess the effect of defibrillation shocks on cardiac and circulating catecholamines. DESIGN: Prospective examination of myocardial catecholamine balance during dc shock by simultaneous determination of arterial and coronary sinus plasma concentrations. Internal countershocks (10-34 J) were applied in 30 patients after initiation of ventricular fibrillation for a routine implantable cardioverter defibrillator test. Another 10 patients were externally cardioverted (50-360 J) for atrial fibrillation. MAIN OUTCOME MEASURES: Transcardiac noradrenaline, adrenaline, and lactate gradients immediately after the shock. RESULTS: After internal shock, arterial noradrenaline increased from a mean (SD) of 263 (128) pg/ml at baseline to 370 (148) pg/ml (p = 0.001), while coronary sinus noradrenaline fell from 448 (292) to 363 (216) pg/ml (p = 0.01), reflecting a shift from cardiac net release to net uptake. After external shock delivery, there was a similar increase in arterial noradrenaline, from 260 (112) to 459 (200) pg/ml (p = 0.03), while coronary sinus noradrenaline remained unchanged. Systemic adrenaline increased 11-fold after external shock (p = 0.01), outlasting the threefold rise following internal shock (p = 0.001). In both groups, a negative transmyocardial adrenaline gradient at baseline decreased further, indicating enhanced myocardial uptake. Cardiac lactate production occurred after ventricular fibrillation and internal shock, but not after external cardioversion, so the neurohumoral changes resulted from the defibrillation process and not from alterations in oxidative metabolism. CONCLUSIONS: A dc shock induces marked systemic sympathoadrenal and sympathoneuronal activation, but attenuates cardiac sympathetic activity. This might promote the transient myocardial depression observed after electrical discharge to the heart.  (+info)

Effect of biphasic shock duration on defibrillation threshold with different electrode configurations and phase 2 capacitances: prediction by upper-limit-of-vulnerability determination. (5/1256)

BACKGROUND: The defibrillation threshold (DFT) may be affected by biphasic shock duration (BSD), electrode configuration, and capacitance. The upper limit of vulnerability (ULV) may be used to estimate the DFT. For different lead configurations and phase 2 capacitances, we investigated in 18 pigs whether the use of ULV may predict waveforms with lowest DFT. METHODS AND RESULTS: -DFT and ULV were determined by up-down protocols for 10 BSDs. ULVs were measured by T-wave scanning during ventricular pacing (cycle length 500 ms). In protocol 1 (n=6), a pectoral "active can" was combined with an electrode in the superior vena cava as common cathode and a right ventricle electrode as anode (AC+SVC). In protocol 2 and protocol 3 (n=6 each), only the "active can" was used as proximal electrode (AC). Capacitance was 150 microF during both phases in protocol 1 and protocol 3 but 150 microF (phase 1) and 300 microF (phase 2) in protocol 2. ULV and DFT demonstrated a linear correlation in each protocol (r=0.78 to 0.84). Lowest DFTs were found at 10 ms for AC+SVC and at 14 ms for AC (P<0.001). At optimal BSDs, voltage DFTs did not differ significantly between AC (527+/-57 V) and AC+SVC (520+/-70 V). Switching capacitors for phase 2 in a way that reduced leading-edge voltage by 50% while doubling capacity did not change BSD for optimal voltage DFT but increased minimum DFT from 527+/-57 V to 653+/-133 V (P=0.04). CONCLUSIONS: The BSD with lowest DFT is shorter for AC+SVC than for AC. There is no significant difference in voltage DFT between both at optimal BSD. A lower phase 2 capacitance reduces DFTs irrespective of BSD. Because strength-duration curves for DFT and ULV correlate for different BSDs, lead systems, and phase 2 capacitances, ULV determination may allow the prediction of waveforms with lowest DFT.  (+info)

The cost-effectiveness of ibutilide versus electrical cardioversion in the conversion of atrial fibrillation and flutter to normal rhythm. (6/1256)

Atrial fibrillation and atrial flutter are cardiac rhythm disorders that are often symptomatic and may interfere with the heart's function, limiting its effectiveness. These arrhythmias are responsible for a large number of hospitalizations at a significant cost to the healthcare system. Electrical cardioversion (EC) is the most common nonpharmacologic intervention used to convert atrial fibrillation and atrial flutter to normal rhythm. Electrical cardioversion is highly successful in converting patients to normal rhythm; however, it is more traumatic and resource intensive than pharmacologic treatment. Recently, a new rapid-acting drug, ibutilide, was approved for the conversion of atrial fibrillation and atrial flutter. Ibutilide is administered through intravenous infusion and does not require anesthetization of the patient, as is required for EC. A decision-tree model was developed to estimate the cost-effectiveness of ibutilide therapy compared with EC therapy. Clinical outcomes were based on a phase III trial of ibutilide, and resource use was based on the literature and physician clinical judgment. A stepped conversion regimen of first-line ibutilide followed by EC for patients who fail to convert is less expensive and has a higher conversion rate than first-line EC. Sensitivity analysis shows that our results are robust to changes in cost and effectiveness estimates.  (+info)

Defibrillation-guided radiofrequency ablation of atrial fibrillation secondary to an atrial focus. (7/1256)

OBJECTIVES: Our aim was to evaluate a potential focal source of atrial fibrillation (AF) by unmasking spontaneous early reinitiation of AF after transvenous atrial defibrillation (TADF), and to describe a method of using repeated TADF to map and ablate the focus. BACKGROUND: Atrial fibrillation may develop secondary to a rapidly discharging atrial focus that the atria cannot follow synchronously, with suppression of the focus once AF establishes. Focus mapping and radiofrequency (RF) ablation may be curative but is limited if the patient is in AF or if the focus is quiescent. Early reinitiation of AF has been observed following defibrillation, which might have a focal mechanism. METHODS: We performed TADF in patients with drug-refractory lone AF using electrodes in the right atrium (RA) and the coronary sinus. When reproducible early reinitiation of AF within 2 min after TADF was observed that exhibited a potential focal mechanism, both mapping and RF ablation were performed to suppress AF reinitiation. Clinical and ambulatory ECG monitoring was used to assess AF recurrence. RESULTS: A total of 44 lone AF patients (40 men, 4 women; 32 persistent, 12 paroxysmal AF) with a mean age of 58+/-13 years underwent TADF. Sixteen patients had early reinitiation of AF after TADF, nine (20%; 5 paroxysmal) exhibited a pattern of focal reinitiation. Earliest atrial activation was mapped to the right superior (n = 4) and the left superior (n = 3) pulmonary vein, just inside the orifice, in the seven patients who underwent further study. At the onset of AF reinitiation, the site of earliest activation was 86+/-38 ms ahead of the RA reference electrogram. The atrial activities from this site were fragmented and exhibited progressive cycle-length shortening with decremental conduction to the rest of the atrium until AF reinitiated. Radiofrequency ablation at the earliest activation site resulted in suppression of AF reinitiation despite pace-inducibility. Improved clinical outcome was observed over 8+/-4 months' follow-up. CONCLUSIONS: Transvenous atrial defibrillation can help to unmask, map, and ablate a potential atrial focus in patients with paroxysmal and persistent AF. A consistent atrial focus is the cause of early reinitiation of AF in 20% of patients with lone AF, and these patients may benefit from this technique.  (+info)

Effect of butorphanol tartrate on shock-related discomfort during internal atrial defibrillation. (8/1256)

BACKGROUND: In patients with atrial fibrillation, intracardiac atrial defibrillation causes discomfort. An easily applicable, short-acting analgesic and anxiolytic drug would increase acceptability of this new treatment mode. METHODS AND RESULTS: In a double-blind, placebo-controlled manner, the effect of intranasal butorphanol, an opioid, was evaluated in 47 patients with the use of a step-up internal atrial defibrillation protocol (stage I). On request, additional butorphanol was administered and the step-up protocol continued (stage II). Thereafter, if necessary, patients were intravenously sedated (stage III). After each shock, the McGill Pain Questionnaire was used to obtain a sensory (S), affective (A), evaluative (E), and total (T) pain rating index (PRI) and a visual analogue scale analyzing pain (VAS-P) and fear (VAS-F). For every patient, the slope of each pain or fear parameter against the shock number was calculated and individual slopes were averaged for the placebo and butorphanol group. All patients were cardioverted at a mean threshold of 4.4+/-3.3 J. Comparing both patient groups for stage II, the mean slopes for PRI-T (P=0.0099), PRI-S (P=0.019), and PRI-E (P=0.015) became significantly lower in the butorphanol group than in the placebo group. Comparing patients who received the same shock intensity ending stage I and going to stage II, in those patients randomized to placebo the mean VAS-P (P=0.023), PRI-T (P=0. 029), PRI-S (P=0.030), and PRI-E (P=0.023) became significantly lower after butorphanol administration. CONCLUSIONS: During a step-up internal atrial defibrillation protocol, intranasal butorphanol decreased or stabilized the value of several pain variables and did not affect fear. Of the 3 qualitative components of pain, only the affective component was not influenced by butorphanol. The PRI evaluated pain more accurately than the VAS.  (+info)