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PubMed1992

Failure of an implantable cardioverter-defibrillator to redetect ventricular fibrillation in patients with a nonthoracotomy lead system.

BACKGROUND: Shock delivery of an implantable defibrillator may cause a change in the amplitude of endocardial electrograms and impair the detection of ventricular fibrillation. Thus, the effects of shock discharges on the amplitude of endocardial electrograms were evaluated in five patients undergoing implantation of a cardioverter-defibrillator in combination with a new nonthoracotomy lead system. METHODS AND RESULTS: At implant, bipolar endocardial electrograms were recorded before each shock application, during ventricular fibrillation, during redetection of ventricular fibrillation in case the applied shock was ineffective, and at intervals of 5, 10, 20, 30, 60, and 120 seconds after each shock delivery. The amplitude of the endocardial electrograms decreased from 10.5 +/- 3.8 mV during sinus rhythm to 6.3 +/- 1.9 mV during initial ventricular fibrillation and declined to 2.2 +/- 1.3 mV during redetection of ventricular fibrillation. After successful termination, the following bipolar electrograms could be obtained at the predetermined intervals: 1.9 +/- 1.2 mV, 3.1 +/- 1.8 mV, 4.5 +/- 1.9 mV, 6.5 +/- 2.9 mV, 9.5 +/- 3.3 mV, and 10.4 +/- 3.8 mV. At predischarge testing, failure of redetection of ventricular fibrillation could be documented in two patients, requiring rescue external defibrillation in both cases to restore sinus rhythm. CONCLUSIONS: These findings demonstrate that the implantable cardioverter-defibrillator did not ensure reliable redetection of ventricular fibrillation in patients using the implanted nonthoracotomy lead system. Thus, the potential risk of sudden cardiac death may persist in these patients despite defibrillator therapy.

Cardiomyopathy, Dilated↗

PubMed1990

Mechanical myocardial actuation during ventricular fibrillation improves tolerance to ischemia compared with cardiopulmonary bypass.

Direct mechanical ventricular actuation (DMVA) is a unique non-blood-contacting biventricular assist device that provides circulatory support during ventricular fibrillation without demonstrating adverse effects on the myocardium. The purpose of this study was to assess the preservation of myocardial energy stores and myocardial responses to ischemia after circulatory support during ventricular fibrillation with direct mechanical ventricular actuation versus cardiopulmonary bypass. Twenty adult mongrel dogs were randomized to receive circulatory support with either cardiopulmonary bypass or direct mechanical ventricular actuation. After 4 hours of ventricular fibrillation, hearts were defibrillated and left ventricular transmural biopsies were obtained. Hearts were then excised and subjected to 90 minutes of normothermic total ischemia. Serial biopsies were obtained at 15-minute intervals to determine regional depletion of high energy phosphates. The time-to-peak ischemic contracture was recorded by using needle-tipped Millar catheters placed in the left ventricular endocardium, epicardium, septum, and right ventricle. Time-to-peak ischemic contracture of the endocardium (62.6 +/- 1.4 vs. 58.8 +/- 1.0 minutes, p less than 0.05) and septum (61.1 +/- 6.9 vs. 46.9 +/- 6.2 minutes, p less than 0.004) were significantly prolonged after direct mechanical ventricular actuation versus cardiopulmonary bypass, respectively. Similar trends were noted in the epicardium and right ventricular regions; however, these differences were not statistically significant. Left ventricular adenosine triphosphate (ATP) levels were better preserved after direct mechanical ventricular actuation (22 +/- 1.5 mumols/g dry wt) compared with cardiopulmonary bypass (17 +/- 1.9 mumols/g dry wt). The depletion of left ventricular endocardium ATP during normothermic ischemia was significantly delayed after direct mechanical ventricular actuation compared with cardiopulmonary bypass.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1992

Ventricular fibrillation in hypertrophic cardiomyopathy is associated with increased fractionation of paced right ventricular electrograms.

BACKGROUND: Intraventricular conduction in hypertrophic cardiomyopathy (HCM) has been characterized to test the hypothesis that myofibrillar disarray will cause dispersion of activation throughout the ventricular myocardium. METHODS AND RESULTS: Of 37 patients with HCM, four had spontaneous ventricular fibrillation (VF), five had nonsustained ventricular tachycardia (VT), 13 had no risk factors, and 15 had a family history of sudden death. These patients and four controls were studied by pacing one site in the right ventricle and recording electrograms from three other right ventricular sites. These electrograms were high-pass filtered to emphasize small deflections due to activation of small bundles of myocytes close to the electrode. Intraventricular conduction curves were obtained with S1S2 coupling intervals decreasing in 1-msec steps from 479 msec to ventricular effective refractory period (VERP). These curves were repeated by pacing each RV site in turn and were characterized by two parameters: the point at which latency increased by 0.75 msec/20 msec reduction of the S1S2 coupling interval and an increase in electrogram duration between an S1S2 of 350 msec and VERP. Patients with VF, VT, and family history of sudden death had a mean increase in electrogram duration of 12.8 (2.9-32.3) msec versus 4.6 (-4.2 to 14.0) msec in low-risk patients and controls. Electrogram latency increased at an S1S2 of 363 msec in the VF group (342-386), 269 msec in the controls (266-279), and 326 msec in the non-VF group (260-399). Discriminant analysis separated VF patients from the remainder (p less than 0.0001) and VF, VT, and family history of sudden death patients from the low-risk and control groups (p less than 10(-6)). CONCLUSIONS: Patients with HCM who are at risk of sudden death have increased dispersion and inhomogeneity of intraventricular conduction, and this may create the conditions for reentry and arrhythmogenesis.

Adolescent↗

PubMedDate not supplied

[Sudden death in a normal heart. Idiopathic ventricular fibrillation. Review of the literature concerning one case].

Idiopathic ventricular fibrillation is that which is produced in the absence of structural cardiac disease and of other identifiable causes of ventricular fibrillation such as cardiotoxicity, electrolytical alterations or hereditary predisposition. The case of a healthy male, aged 37, who was asymptomatic until the day he was admitted to hospital where he showed numerous episodes of ventricular fibrillation without any previous triggering, is discussed. In the examination no cause was found to explain this, and an automatic defibrillator was implanted. The requirements for its diagnosis, risk stratification and the usefulness of the tests employed, as well as the treatments proposed are discussed.

Adult↗

PubMed1975

[Electrocardiographic features and vectorial analysis of cardiac potentials in electric shock-induced ventricular fibrillation (author's transl)].

The authors examined the electrocardiographic features of ventricular fibrillation and other ventricular paroxysms induced by electric shock in the guinea pig. The analysis of the electrocardiographic patterns, as well as the vectorial study of the cardiac potentials during repeated episodes of ventricular "anarchy" induced in more than forty animals, showed the following data: 1. following electric shock, ventricular paroxysms appear, featuring paroxysmal tachycardia, typical or impure flutter, tachycardia--either "torsade de pointe" or "spindle" type, and typical ventricular fibrillation. Such different electrocardiographic patterns represent evolutive stages of electric activity disorganization, leading to a complete ventricular "anarchy". Such steps may reverse when reorganization of the electric activity and spontaneous defibrillation occur; 2. an attempt can be made at present to classify ventricualr paroxysms, thus eleminating semeiotic and semantic errors, still present in the literature, and providing a standardization of both nomenclature and electrocardiographic interpretation; 3. during fibrillation, the mean ventricular rate decays, featuring an exponential curve. This phenomenon accounts for a metabolic depletion of the myocardium: the higher the number of fibrillation episodes previously induced and subsided (either spontaneously or not) in the same animal, the faster the course of the phenomenon; 4. the vectorial analysis of the fibrillation potentials and, particularly, the graphic construction of "depolarization" and "repolarization" vectorcardiograms, in the differenttypes or variants of ventricular paroxysms, show that the basic mechanisms leading to ventricular electric activity disgregation are the multiple re-entry and the irregular spreading of the activation front; 5. on the basis of the acquired data, the authors believe that the "circus movement" theory (Wiggers) is still the most suitable for explaining the onset and the evolution of ventricualr fibrillation.

Animals↗

PubMed1978

Repolarization abnormalities in survivors of out-of-hospital ventricular fibrillation.

Survivors of out-of-hospital ventricular fibrillation (VF) are at high risk for recurrent VF, probably reflecting continued myocardial electrical instability. In this study 12-lead ECGs of 125 VF survivors with coronary heart disease were examined and compared to those of 98 ambulatory post-MI patients. The study was part of an effort to define clinical identifiers of patients likely to develop sudden cardiac death. Ventricular fibrillation survivors were commonly had premature ventricular complexes (PVCs):30% versus 13% (P less than 0.01). In addition, ECGs of VF survivors showed a significantly greater prevalence of ST-segment depression (46% versus 10%), T wave flattening (52% versus 26%), and QTc prolongation (35% versus 18%). It is proposed that these repolarization abnormalities represent asynchronous repolarization, which together with frequent PVCs, may set the stage for re-entrant ventricular dysrhythmias and ultimately VF. It is also possible that repolarization abnormalities together with premature ventricular contractions might serve as markers of patients with coronary heart disease who are at increased risk for sudden cardiac death.

Aged↗

PubMed1993

Hypothermic ventricular fibrillation with pulsatile coronary perfusion during repair of ventricular septal perforation following infarction.

Emergency or urgent surgery for ventricular septal perforation (VSP) following acute myocardial infarction still carries a high operative mortality rate. Hypothermic fibrillatory arrest studies without aortic cross-clamping and using continuous pulsatile coronary flow were performed to improve this result. Of 19 patients suffering from VSP, 12 underwent hypothermic (mean(s.d.) blood temperature 23.5(1.7) degrees C) ventricular fibrillation with concomitant pulsatile systemic and continuous coronary perfusion (group 1), and seven underwent deep hypothermic cardioplegic ischaemic arrest with systemic pulsatile perfusion alone (group 2). The two groups were comparable in terms of age, sex, location of infarction, number of coronary arteries involved, interval between infarction and surgery, and preoperative maximum enzyme levels and haemodynamics. Pulsatile flow with a mean(s.d.) pulse pressure of 48(13) mmHg was produced by an intra-aortic balloon pumping device in both groups. Operative exposure in the two groups was comparable. In group 1, mean(s.d.) cardiac output in the early postoperative period (within 3 h of procedure) was significantly higher than in group 2 (4.2(0.9) versus 2.6(0.7)lmin-1m-2, P < 0.01). The 30-day operative mortality rate was significantly lower in group 1 (8% (80% confidence interval 1-29%)) than in group 2 (57% (80% confidence interval 28-83%)) (P < 0.05). On the basis of these results, hypothermic fibrillatory arrest with continuous pulsatile coronary perfusion can be recommended for myocardial protection during surgery for VSP associated with severe heart failure or cardiogenic shock.

Aged↗

PubMed2005

Enhanced coagulation activation by in vitro lipopolysaccharide challenge in patients with ventricular fibrillation complicating acute myocardial infarction.

BACKGROUND: Indicators of coagulation and inflammation are elevated in patients with coronary heart disease. A role of coagulation activation in ventricular fibrillation during acute myocardial infarction has not been described. METHODS AND RESULTS: Whole blood samples of 21 patients with a history of acute myocardial infarction complicated by ventricular fibrillation and whole blood samples of 18 patients without ventricular fibrillation were incubated with lipopolysaccharide (LPS). In both groups, the in vitro blood coagulation time was measured with the ReoRox, a viscometric whole blood coagulometer. CD62P expression on platelets, tissue-factor binding on monocytes, and platelet-monocyte aggregates were measured with flow cytometry. Without LPS, no difference in the coagulation times were observed in both patient groups. After incubation with LPS, patients with a history of ventricular fibrillation showed a significantly decreased coagulation time compared to patients without ventricular fibrillation. The decrease of coagulation time after incubation with LPS also differed significantly in both groups. Expression of CD62P on platelets was significantly higher in patients with a history of ventricular fibrillation after incubation with LPS. Although in each patient group incubation with LPS induced a significantly increased amount of tissue factor on monocytes and a significantly increased the number of platelet-monocyte aggregates, the two groups did not differ significantly concerning tissue factor binding on monocytes and the amount of platelet-monocyte aggregates. CONCLUSIONS: After in vitro LPS challenge, patients with a history of ventricular fibrillation during myocardial infarction show an enhanced coagulation activation, which may partly be due to an enhanced platelet activation.

Adult↗

PubMed1983

Hypokalaemia and ventricular fibrillation in acute myocardial infarction.

Serum potassium concentrations obtained on admission to hospital were inversely related to the incidence of ventricular fibrillation in 289 women and 785 men with acute myocardial infarction, 92 of whom developed ventricular fibrillation. Hypokalaemia (serum potassium concentration less than or equal to 3.5 mmol/l) was found in 122 patients (11.4%). The incidence of ventricular fibrillation was significantly greater in patients with hypokalaemia compared with those classified as normokalaemic (serum potassium concentration greater than or equal to 3.6 mmol/l) (17.2% v 7.4%). The increased risk of ventricular fibrillation in the hypokalaemic group was about the same for women and men. While they were in hospital patients with hypokalaemia developed ventricular fibrillation significantly earlier than did normokalaemic patients (median 0.3 hours v 7 hours). Hypokalaemia was more common in women (17.3%) than in men (9.2%), and 55% of the hypokalaemic patients had been treated with diuretics before admission compared with 22% of the normokalaemic group. Hypokalaemia on admission to hospital predicts an increased likelihood and early occurrence of ventricular fibrillation in patients with acute myocardial infarction.

Aged↗

PubMed2000

Time dependent variability of QT dispersion after acute myocardial infarction and its relation to ventricular fibrillation: a prospective study.

OBJECTIVE: To show whether increased QT dispersion on admission predicts ventricular fibrillation after acute myocardial infarction, and to determine the nature of time related changes in QT dispersion. DESIGN: Prospective cohort study. SETTING: Coronary care units of three teaching hospitals in Newcastle-upon-Tyne over an eight month period. PATIENTS: All had acute myocardial infarction according to World Health Organization criteria. INTERVENTIONS: For all patients, QT dispersion (QTd) and Bazett rate corrected QTc dispersion (QTcd) were measured from a high quality 12 lead ECG recorded on admission at a paper speed of 50 mm/s. In a subset, serial ECGs were recorded regularly to show time related changes in QTcd following acute myocardial infarction. MAIN OUTCOME MEASURES: Occurrence of ventricular fibrillation within the first 24 hours after myocardial infarction. RESULTS: Data collected from 201 patients, 12 of whom (6%) developed ventricular fibrillation within 24 hours. Neither QTd nor QTcd differed between those developing ventricular fibrillation and those who did not: QTd mean (SD), 74 (24) ms (95% confidence interval (CI) 59 to 89) v 66 (24) ms (95% CI 62 to 70), respectively; QTcd, 86 (26) ms(0.5) (95% CI 70 to 102) v 77 (29) ms(0.5) (95% CI 72 to 82), respectively. Significant QTcd changes occurred early after myocardial infarction. CONCLUSIONS: Admission QTd and QTcd do not predict ventricular fibrillation after acute myocardial infarction. There are significant changes in QTcd with time, which may account for this measured lack of correlation.

Aged↗

PubMed1997

Lidocaine in out-of-hospital ventricular fibrillation. Does it improve survival?

BACKGROUND: A large proportion of cardiac arrests outside hospital are caused by ventricular fibrillation. Although it is frequently used, the exact role for treatment with lidocaine in these patients remains to be determined. AIM: To describe the proportion of patients with witnessed out-of-hospital cardiac arrest found in ventricular fibrillation who survived and were discharged from hospital in relation to whether they were treated with lidocaine prior to hospital admission. PATIENTS AND TREATMENT: All the patients with out-of-hospital cardiac arrest found in ventricular fibrillation in Göteborg between 1980 and 1992 in whom cardiopulmonary resuscitation (CPR) was initiated by our emergency medical service (EMS). During the observation period, some of the EMS staff were authorized to give medication and some were not. RESULTS: In all, 1,360 patients were found in ventricular fibrillation, with detailed information being available in 1,212 cases (89%). Lidocaine was given in 405 of these cases (33%). Among patients with sustained ventricular fibrillation, those who received lidocaine had a return of spontaneous circulation (ROSC) more frequently (P < 0.001) and were hospitalized alive more frequently (38% vs. 18%, P < 0.01). However, the rate of discharge from hospital did not significantly differ between the two groups. Among patients who were converted to a pulse-generating rhythm, those who received lidocaine on that indication were more frequently alive than those who did not receive such treatment (94% vs. 84%; P < 0.05). However, the rate of discharge did not significantly differ between the two groups. CONCLUSION: In a retrospective analysis comparing patients who received lidocaine with those who did not in sustained ventricular fibrillation and after conversion to a pulse-generating rhythm, such treatment was associated with a higher rate at ROSC and hospitalization but was not associated with an increased rate of discharge from hospital.

Adult↗

PubMed2006

[Time-frequency analysis of ventricular fibrillation. An experimental study].

INTRODUCTION AND OBJECTIVES: The analysis of frequency variability during ventricular fibrillation has yielded inconsistent results. We used an experimental model of ventricular fibrillation, with a short timescale, to analyze variations in frequency and their associated spatial distribution. METHODS: Epicardial recordings of ventricular fibrillation were made in 10 perfused isolated rabbit heart preparations using a multiple electrode system (i.e., 240 unipolar electrodes). Both spectral and time-frequency analysis were used to derive the dominant frequency in the anterolateral wall of the left ventricle. RESULTS: Linear regression analysis showed that there was a good correlation between the dominant frequency obtained using the two signal analysis methods: frequency (spectral analysis) = 1.01 x frequency (time-frequency analysis) -- 0.4 (r=0.9; P< .0001; standard error of the estimate, 2.2 Hz). In all cases except one, the dominant frequency exhibited a significant temporal variation on a short timescale (time-frequency analysis); the coefficient of variation was between 0.19 (0.06) and 0.24 (0.07) (NS). In all cases, there were significant differences between regions. The location at which the frequency was highest varied according to the timepoint considered, though it was predominantly in the apical or anterior zone. CONCLUSIONS: In the absence of external modulating factors, the frequency of ventricular fibrillation exhibits temporal and spatial variations which can be observed at short timescales. In the free wall of the left ventricle, the dominant frequency is highest in the apical and anterior zones, and the maximum frequencies are most often found in these zones.

Animals↗

PubMed1992

Ventricular fibrillation is not an anodally induced phenomenon in open-chest dogs.

It is generally assumed that ventricular fibrillation evoked by electrical stimulation depends on anodal excitation. To test this hypothesis, six open-chest dogs were studied with computerized mapping techniques. A plaque electrode array containing 56 closely (2.5-5 mm) spaced bipolar electrodes was placed on the right ventricle. The patterns of activation after premature stimulation and at the onset of multiple responses or ventricular fibrillation were determined when the baseline driving stimuli (S1) were given to the center, and when a 5-ms bipolar single premature stimulus (S2) was given via two electrodes (one anodal and one cathodal) at the opposite edges of the plaque electrode array. The results showed that the classical anodal and cathodal strength-interval curves could be demonstrated by this method. A relatively supernormal period was observed only in the anodal strength-interval curve and coincided with the most vulnerable phase of the cardiac cycle. Although a supernormal period was found only at the anodal site, the origins of excitation at the onset of multiple responses or ventricular fibrillation could be anodal, cathodal, or both. When the S2 polarity was reversed, the origin of multiple responses or ventricular fibrillation stayed at the same site and did not change according to the polarity of the S2. These findings indicate that ventricular fibrillation is not an anodally induced phenomenon. The preexisting electrophysiological state at the site of stimulation determines the initiation and maintenance of multiple responses or ventricular fibrillation.

Animals↗

PubMed1983

Resuscitation time in ventricular fibrillation--a prognostic indicator.

Length of resuscitation in prehospital ventricular fibrillation patients was studied to define its relationship to survival. Five hundred sixty-five patients presenting with the initial rhythm of ventricular fibrillation to the Milwaukee County Paramedic System between January 1978 and April 1982 were resuscitated successfully. Pediatric patients and patients with trauma, poisoning, and drowning were excluded. Of the 565 resuscitated patients, 262 (46%) were discharged alive and 303 (54%) died during hospitalization. For all 565 patients the resuscitation time and times from arrival of paramedics until the first sustained pulse were plotted against survival to define a curve. The curve demonstrated rapidly declining survival rates for resuscitation time up to 20 minutes; thereafter, survival declined more gradually with respect to resuscitation time. The mean resuscitation time for those eventually discharged alive was 12.6 minutes, which was statistically shorter (P less than .0001) than the mean resuscitation time of 23.9 minutes for those who eventually died. The overall survival curve of witnessed arrest patients was not statistically different from that of unwitnessed patients. The survival curve of those patients receiving bystander cardiopulmonary resuscitation (CPR) was similar to the curve of those who received no CPR. We conclude that resuscitation time is a heretofore undefined significant predictor of survival of resuscitated prehospital ventricular fibrillation patients.

Aged↗

PubMed1997

A questionnaire survey of resuscitation equipment carried by general practitioners and their initial management of ventricular fibrillation.

BACKGROUND: The early defibrillation of patients having a cardiac arrest and who are in ventricular fibrillation has been shown to increase survival and is recommended by the European Resuscitation Council (ERC) and the American Heart Association. General practitioners (GPs) may expect to encounter a cardiac arrest in 5% of patients they attend who have a suspected acute myocardial infarction. AIM: To establish whether GPs on call were equipped to treat a patient in ventricular fibrillation, and to investigate their knowledge of the early stages of the current ERC guidelines for this cardiac rhythm. METHOD: A postal questionnaire was sent to all the 175 GPs who regularly admit patients to the West Suffolk Hospital. It asked for details of equipment and drugs carried when on call, recognition of a cardiac rhythm strip of ventricular fibrillation, and treatment to be given for this rhythm. RESULTS: A total of 105 replies were returned (representing a 60% response rate). The distribution of practice size and location reflected primary health care in this area. Fourteen GPs (13%) had attended an advanced cardiac life-support course at some time, and 44 (41.9%) had read the current ERC guidelines. The majority of GPs (60%) carried advanced airway management equipment to allow endotracheal intubation, but only 37 (35%) would have been able to administer additional oxygen. Again, most (82%) would have been able to establish intravenous access, but only 39% carried 2 mg or more of adrenaline, the only recommended drug in the initial stages of resuscitation from ventricular fibrillation. A defibrillator was carried by 37 GPs (35%) when on call, but out of these only 14 had an integral monitor screen and 3 were semi-automatic defibrillators. Ninety-five GPs (91%) successfully identified ventricular fibrillation, but only 32 (31%) were able to state correctly the initial recommended treatment, and only 17 (16%) were able to quote the first two stages of the ERC guidelines of treatment of ventricular fibrillation. However, 78 GPs (74%) would have provided treatment compatible with the guidelines by giving the patient a pre-cordial thump and two subsequent defibrillatory shocks, albeit perhaps at an incorrect energy level and only if a defibrillator was available. CONCLUSIONS: This study shows that the equipment carried by the majority of GPs in this area is inadequate to deal successfully with the victims of cardiac arrest, and that significant reliance is placed on the resources of the ambulance service. It would also appear that most GPs are not fully conversant with the current ERC guidelines. The ability of GPs to manage cardiac arrests could be enhanced by their attending courses to update their resuscitation skills, one example being the advanced life-support courses endorsed by the United Kingdom Resuscitation Council, and that the Royal College of General Practitioners could stimulate interest in this area by extending their requirement for candidates for the membership examination to include written documentation demonstrating proficiency at advanced life support, in addition to the current requirement for basic life support only.

Clinical Competence↗

PubMed1995

Comparison of initial detection and redetection of ventricular fibrillation in a transvenous defibrillator system with automatic gain control.

OBJECTIVES: The purpose of this study was to prospectively evaluate postshock redetection of ventricular fibrillation by a system that coupled an implantable cardioverter-defibrillator with an automatic gain control sense amplifier and a transvenous lead system. BACKGROUND: Redetection of ventricular fibrillation after an unsuccessful first shock has not been systematically evaluated. Previous studies have suggested that sensing performance of some lead systems may be adversely affected by the delivery of subthreshold shocks. METHODS: The time required for both initial detection and redetection of ventricular fibrillation was compared in 22 patients. These times were estimated by subtracting the capacitor charge time from the total event time. RESULTS: A total of 113 successful and 57 unsuccessful initial shocks were delivered during induced ventricular fibrillation. The mean +/- SD initial time to detection of ventricular fibrillation was 5.5 +/- 1.7 s (range 2.4 to 10.8); the time to redetection ranged from 1.5 to 18.5 s (mean 4.5 +/- 2.8, p = NS vs. detection time). Abnormal redetection episodes, defined as a redetection time > 10.2 s (i.e., > 2 SD above the mean redetection time), were observed in 4 (18%) of 22 patients. CONCLUSIONS: Redetection of ventricular fibrillation after a subthreshold first shock may be delayed. Device testing with intentional delivery of subthreshold shocks to verify successful postshock redetection of ventricular fibrillation should be performed routinely in all patients.

Algorithms↗

PubMed1980

Role of alpha- and beta-adrenergic activation in ventricular fibrillation death of corticoid-pretreated rats.

Death in ventricular fibrillation was induced consistently in desoxycorticosterone acetate-pretreated rats by the beta-adrenergic agonist isoproterenol but not by norepinephrine or epinephrine, both of which possess alpha- as well as beta-adrenergic activity. Aminophylline, which enhances beta-adrenergic activity, and phenoxybenzamine, an alpha-receptor blocking agent, were used to study the roles of alpha- and beta-adrenergic stimulation in the production of ventricular fibrillation. With the addition of aminophylline, both norepinephrine and epinephrine produced death in ventricular fibrillation, and the existing cardiotoxicity of isoproterenol was potentiated. Similarly, in the presence of phenoxylbenzamine, doses of norepinephrine and epinephrine that had been well tolerated became lethal. Internventions that favor beta-adrenergic preponderance, either by enhancing beta-effects or by blocking protective alpha-adrenergic activation, apparently increase the arrhythmogenic propensity of norepinephrine and epinephrine in steroid-pretreated rats. The similarity of some forms of stress to the experimental protocol of chronic steroid treatment followed by acute catecholamine exposure is discussed.

Adrenergic alpha-Agonists↗

PubMed1990

Pericardial prostaglandin biosynthesis prevents the increased incidence of reperfusion-induced ventricular fibrillation produced by efferent sympathetic stimulation in dogs.

This study tested the hypothesis that sympathetic neural stimulation increases the prevalence of reperfusion-induced ventricular fibrillation and explored the mechanisms by which this occurs and how it may be prevented. In anesthetized, autonomically denervated dogs, we examined the effects of bilateral ansae subclaviae stimulation (SS) and of induction of pericardial biosynthesis of prostaglandins, an intervention that reduces SS effects by acting at presynaptic sites. A 5-minute occlusion of the left anterior descending coronary artery distal to the first or second diagonal branch was performed during SS. Heart rate was maintained constant by atrial pacing. In the absence of SS, one of 23 dogs developed ventricular fibrillation during occlusion, and three of the remaining 22 dogs developed ventricular fibrillation upon reperfusion. SS did not increase the prevalence of occlusion-induced ventricular fibrillation (four of 23 dogs) but increased the prevalence of reperfusion-induced ventricular fibrillation (12 of the remaining 19 dogs, p = 0.01). SS did not affect occlusion-induced decrease in local electrogram amplitude recorded from the ischemic myocardium or myocardial blood flow to the ischemic myocardium during occlusion or reperfusion. SS, however, prevented occlusion-induced increase in diastolic excitability threshold. Instillation into the pericardial cavity of arachidonic acid solution (3 micrograms/ml) resulted in release of prostacyclin, measured by radioimmunoassay as a stable metabolite 6-ketoprostaglandin F1 alpha (63.1 +/- 11.3 ng/ml, n = 11, mean +/- SEM), and of prostaglandin E2 (7.0 +/- 0.9 ng/ml, n = 11). This pericardial solution blunted SS-induced increase in mean arterial blood pressure and reduced the prevalence of ventricular fibrillation during reperfusion (six dogs to one dog, p less than 0.05). Blood flow to the ischemic myocardium remained unaffected. Indomethacin, when added to the solution (3 micrograms/ml), reversed the effects of prostaglandin release and arrhythmia development. These data indicate that efferent sympathetic stimulation during a coronary occlusion and reperfusion sequence increases the prevalence of reperfusion-induced ventricular fibrillation that is reduced by pericardial biosynthesis of prostaglandins. Pericardial prostaglandin synthesis may serve as a unique antiarrhythmic function by regulating efferent cardiac sympathetic nerve effects.

Animals↗