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At least 937 records · Page 52Linked to original sources
PubMed1998

Right and left ventricular interaction in ventricular fibrillation with mechanical maintenance of the circulation.

OBJECTIVE: To investigate the possible mechanisms of right and left ventricular interaction during ventricular fibrillation (VF) with mechanical maintenance of the circulation. EXPERIMENTAL DESIGN: In this experimental study, two para-aortic counterpulsation devices (PACDs) were implanted in 14 mongrel dogs. SETTING: The PACD is a spheroid, valveless, with one opening, 100 ml stroke volume assisting device. After midsternotomy and pericardiotomy, two PACDs were implanted on the ascending aorta and the pulmonary artery, respectively. Catheters were placed into the aortic arch, and the left and right ventricles. An electromagnetic probe was placed on the descending aorta. INTERVENTIONS: After the completion of the experimental preparation, VF was induced and the two devices were synchronized and pumped simultaneously for 10 minutes (A). Subsequently, the left sided PACD pumped alone for the same period of time (B). This sequence was repeated 1-10 times in each experiment. MEASURES: The aortic pressures, the left and right ventricular pressures and the cardiac index were obtained at the end of each intervention. RESULTS: The simultaneous pumping of the two devices (A) compared with the pumping of that implanted on the ascending aorta (B) resulted in: higher peak aortic pressure 119.1+/-32.1 mmHg (A) vs 105.7+/-36.4 mmHg (B), p<0.001, mean aortic pressure 42.1+/-13.2 mmHg vs 27.8+/-10.5 mmHg, p<0.001, mean left ventricular pressure 18.4+4.0 mmHg vs 11.7+/-3.6 mmHg, p<0.001, and cardiac index 105.7+/-40.1 ml/kg/min vs 82.0+/-39.9 ml/kg/mm, p<0.001, and lower right ventricular pressure 10.1+/-3.2 mmHg vs 13.3+/-2.6 mmHg, p<0.001. CONCLUSIONS: Maintenance of the circulation during VF with the PACD implanted on the ascending aorta results in equalization of the right and left ventricular pressures. In contrast, when both devices are pumping simultaneously, the left ventricular pressure is significantly higher than the right one and the assistance is more effective.

Animals↗
PubMed1978

Carbon monoxide and ventricular fibrillation threshold in dogs with acute myocardial injury.

In a blind, randomized study, the effect of breathing 100 p.p.m. of CO versus compressed, purified air for 2 hours on ventricular fibrillation threshold (VFT) was investigated in 21 dogs with acute myocardial injury. The mean arterial carboxyhemoglobin was 1.16 per cent in the air control period, 1.07 per cent after air, 1.08 per cent in the CO control period, and 6.34 per cent after CO. In comparison to air, CO increased the mean arterial carboxyhemoglobin (P less than 0.001). One dog developed spontaneous ventricular fibrillation 100 minutes after CO. Mean VFTs in the other 20 dogs were 12.8 +/- 6.8 milliamperes after CO, 11.2 +/- 6.0 milliamperes in the air control period, and 15.0 +/- 5.1 milliamperes after air. In comparison to air, CO decreased the VFT (P less than 0.001). These data show that breathing 100 p.p.m. of CO for 2 hours reduces the VFT in dogs with acute myocardial injury.

Acute Disease↗
PubMed2006

Predictive impact of the inducibility of ventricular fibrillation in patients with Brugada-type ECG.

The natural history of asymptomatic individuals with a Brugada-type electrocardiogram (ECG) is still controversial. In this study, we evaluated ventricular fibrillation (VF) inducibility in Brugada-type ECG patients and compared it with other risk factors to clarify the significance of these data on their prognosis. The study population consisted of 38 patients who presented with a typical ST-segment elevation in the precordial leads and underwent an electrophysiological study (EPS). The patients were divided into 3 groups; group A: patients with spontaneous ventricular fibrillation (VF) (n = 5), group B: patients without clinical VF but with inducible VF in EPS (n = 16), and group C: patients with neither clinical nor inducible VF (n = 17). The clinical features, diagnostic results, and prognosis were compared among these groups. During the follow-up period of 26 +/- 19 months, 2/5 (group A), 1/16 (group B), and 0/17 (group C) patients suffered fatal arrhythmic events. None of the clinical features showed any significant difference, although the incidence of positive results in a drug challenge test was higher in groups A and B than in group C (P < 0.05). On the other hand, VF inducibility was higher in patients with positive results in the drug challenge test than in patients with negative results (59% versus 13%; P < 0.05). No VF episodes were observed in patients without VF induction, although one was observed in 1 of 16 patients with VF induction in asymptomatic Brugada syndrome. The drug challenge test appears to be useful for predicting VF inducibility even though it is a noninvasive test.

3-Iodobenzylguanidine↗
PubMed1990

The use of an implantable left ventricular assist device following irreversible ventricular fibrillation secondary to massive myocardial infarction.

A TCI1 rough surface left ventricular assist device (LVAD) was implanted in a 47-year-old man who had sustained a recent massive myocardial infarction complicated by ventricular failure which remained unresponsive to intra-aortic balloon pump therapy and which was further complicated by irreversible ventricular fibrillation. Following implantation of the device and while awaiting a suitable donor organ for transplantation, further extension of the previous infarct resulted in left ventricular rupture and massive haemorrhage which led to his death. We report the successful use of the device in providing haemodynamic support, but caution against inordinate delay in bridging to transplantation patients who are at risk of extension of infarction.

Heart-Assist Devices↗
PubMed1996

Electrosurgery-induced ventricular fibrillation during pacemaker replacement--a unique mechanism.

Arrhythmias and pacemaker malfunction are known to occur from the use of an electrosurgical device. The present case report describes a patient with sick sinus syndrome who experienced ventricular fibrillation while undergoing surgery. During replacement of his non-functioning cardiac pacemaker under general anesthesia, electrosurgery was used to ensure hemostasis. Electric current may have stimulated myocardial leads present in the surrounding tissue, leading to ventricular fibrillation. The patient was resuscitated from the episode without any residual sequelae. Microshock and possible mechanisms that can lead to ventricular arrhythmias in patients with pacemakers during electrosurgery are discussed.

Adult↗
PubMed1985

[Risk profile and prognosis after myocardial infarct complicated by ventricular fibrillation].

In a prospective series of 190 patients under the age of 70 with a first myocardial infarction, the risk profile for ischemia, heart function and arrhythmias was investigated at the time of hospital discharge. Fifteen of these 190 patients had had ventricular fibrillation within 24 hours after admission which could be converted into sinus rhythm. In comparison, patients with ventricular fibrillation had a significantly larger infarct as estimated with the thallium-defect score (11.0 +/- 5.8 vs. 7.3 +/- 5.4; p less than 0.02)). In addition, left ventricular ejection fraction at rest was lower, at 42.7 +/- 17.4% compared to 50.0 +/- 14.0, but the p-value reached only 0.07. Persistent arrhythmias and ischemia were not significantly different in the two groups. In the first year after infarction none of these 15 patients died, compared to 8/175 patients.

Adult↗
PubMed1994

Ventricular fibrillation related to coronary spasm in patients without significant coronary or other structural heart disease.

We present three patients without significant coronary or other structural heart disease who were resuscitated after ventricular fibrillation attributed to coronary spasm. Angina pectoris was present in two of the cases and silent myocardial ischemia in the third. All patients were given calcium antagonists at discharge. A defibrillator was also implanted in the patient with silent myocardial ischemia because further episodes of ischemia would probably have occurred without premonitory symptoms. Coronary spasm might be a mechanism of ventricular fibrillation in patients without significant structural heart disease. Diagnostic tests should therefore be performed to confirm or exclude coronary spasm in such cases. The implantation of an automatic defibrillator seems justified in selected patients with documented coronary spasm, silent myocardial ischemia, and associated sustained ventricular tachyarrhythmia, although prospective studies are not yet available.

Adult↗
PubMed2001

Prevention of ventricular fibrillation during acute myocardial ischemia: control of free fatty acids.

Fatal ventricular fibrillation is a common complication of acute coronary syndromes. Effective preventive measures are not available. Immediate restriction of free fatty acid availability should optimize ischemic myocardial metabolism, reduce ventricular vulnerability, and increase glucose utilization. Rapid inhibition of lipoprotein lipase activity will achieve this. The clinical effects of antilipolytic treatment require further study.

Acute Disease↗
PubMed1985

Carbachol and dibutyryl cyclic GMP on the vulnerability to ventricular fibrillation in rat isolated hearts.

The hypothesis that elevation of intracellular guanosine 3':5' cyclic monophosphate (cyclic GMP) concentrations may increase electrical stability of the myocardium was examined by determination of ventricular fibrillation thresholds (VFT) on isolated perfused hearts of the rat. Hearts were paced to circumvent any complicating effects of bradycardia. Using this system, carbachol produced a concentration-related reduction in VFT. The reduction in VFT produced by carbachol was not significantly modified by a high concentration of atenolol (10(-5)M), indicating that the increased vulnerability to ventricular fibrillation was not an indirect consequence of catecholamine release from intramyocardial stores. Atropine (10(-6)M) blocked the carbachol-induced reduction in VFT. At the concentrations of carbachol used to reduce VFT, myocardial cyclic GMP concentrations were also elevated. The dibutyryl analogue of cyclic GMP (10(-4)M) mimicked the effect of carbachol in reducing VFT. Carbachol potentiated the adrenaline (3 X 10(-7)M)-induced reduction in VFT.

Animals↗
PubMed1976

Basis for recurring ventricular fibrillation in the absence of coronary heart disease and its management.

A 39-year-old man twice experienced ventricular fibrillation and exhibited numerous ventricular premature beats. Coronary arteries were normal, and no impaired cardiac function was found upon catheterization. Evidence was adduced that the ventricular premature beats were related to higher nervous activity. The patient had serious psychiatric problems; the ventricular premature beats were provoked by psychophysiologic stress, increased during REM sleep, were reduced by meditation, and were controlled by beta-adrenergic blockade, phenytoin and digitalization. We conclude that psychologic and neurophysiologic factors may predispose to life-threatening cardiac arrhythmia in the absence of organic heart disease. Effective management of the recurrent ventricular arrhythmia involved; acute drug testing for assessing antiarrhythmic efficacy; use of programmed trendscription to provide on-line information on drug action; a treatment program involving more than one agent; and use of measures to reduce sympathetic nervous activity.

Adult↗
PubMed1984

[Modification of a model of ventricular fibrillation by a combination of ligation of the interventricular artery and ultraviolet irradiation of autoblood].

The combination of interventricular artery ligation and extracorporeal intensive ultraviolet irradiation of autoblood enabled the researchers to bring down the threshold and to increase the frequency of ventricular fibrillations. The above finding has served as a basis for creating a new experimental model of delayed ventricular fibrillation with a higher possibility of its development.

Animals↗
PubMed1987

Determinants of induced sustained arrhythmias in survivors of out-of-hospital ventricular fibrillation.

We prospectively studied 196 consecutive survivors of out-of-hospital ventricular fibrillation (VF) not associated with acute myocardial infarction and 46 consecutive, control patients without prior ventricular arrhythmias. Programmed stimulation included two extrastimuli (S3 protocol) in all patients and three extrastimuli (S4 protocol) in the last 140 study patients and in all control patients. Sustained ventricular tachycardia (VT) or VF was not induced in any control patient. In study patients, logistic regression identified two independent predictors of induced, sustained VT for both S3 and S4 protocols: prior spontaneous, sustained VT (37 patients; p less than or equal to .001) and prior myocardial infarction (113 patients; p = .005). With the S3 protocol, sustained VT was induced in 54% of patients with both prior myocardial infarction and prior sustained VT vs 4% without either; with the S4 protocol, sustained VT was induced in 91% vs 13%, respectively. Eighty-three percent of induced VT episodes had a cycle length less than 300 msec, and all required termination by cardioversion or pacing. VF was induced only in survivors of out-of-hospital VF without prior, spontaneous, sustained VT (S3 protocol, 9%; S4 protocol, 24%) but not in study patients with prior sustained VT (S3, p = .10; S4, p = .05) or control patients (S3, p = .06; S4, p = .01). The mean coupling intervals of extrastimuli that induced VF were not significantly different from the intervals that induced sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1990

Mechanisms underlying the development of ventricular fibrillation during early myocardial ischemia.

The mechanisms underlying the development of ventricular fibrillation (VF) during early myocardial ischemia were assessed by use of a computerized three-dimensional mapping system capable of recording simultaneously from 232 intramural recording sites throughout the entire feline heart in vivo. Occlusion of the proximal left anterior descending coronary artery led to ventricular tachycardia (VT), which degenerated to VF in 1-5 minutes in four of 15 animals. Normal sinus beats immediately preceding the initiation of VT leading to VF demonstrated delayed activation (total activation time 133 +/- 14 msec), which was not significantly different from the activation time for normal sinus beats immediately preceding nonsustained VT (149 +/- 7 msec). Most of the conduction delay occurred in the subendocardial and midmyocardial regions in both groups. Initiation of VT leading to VF occurred by intramural reentry in three of the four cases. In one case, a mechanism responsible for the initiation of VT could not be assigned. The coupling interval of the initiating beats of VT ultimately leading to VF (210 +/- 15 msec) did not differ from that of nonsustained VT. Maintenance of the VT that led to VF was due primarily to intramural reentry (84% of cases) involving multiple activation sites in and around the border region of the ischemic zone. Nonreentrant mechanisms, arising in the subendocardium and subepicardium, also contributed to the maintenance of VT before development of VT. The transition from VT to VF was due exclusively to intramural reentry with initiation of the reentrant beats in the subendocardium and, occasionally, the subepicardium. Acceleration of the tachycardia by intramural reentry, along with very rapid and inhomogeneous recovery of excitability (as low as 50-60 msec), led to increased functional block and conduction delay. As a result, the total activation time for a given beat exceeded the coupling interval for that beat and led to the multiple reentrant circuits and multiple simultaneous activations characteristic of VF. Thus, the initiation and maintenance of VT leading to VF during early ischemia is due to intramural reentry, although nonreentrant mechanisms also contribute. However, the development of VF is due to continued intramural reentry and rapid recovery of excitability.

Animals↗
PubMed1984

Ventricular fibrillation threshold in the three-toed sloth (Bradypus tridactylus).

The ventricular fibrillation threshold (VFT) can be defined as the minimum electrical value able to trigger fibrillation. The objective was to determine the threshold fibrillatory current in the three-toed sloth, animal which may show spontaneous defibrillation. Ten specimens were used (average weight 3.9 kg, SD 0.28). Two electrodes of the spoon type were laterally applied to the ventricles, stimulating with a nonsynchronized train of rectangular pulses, variable amplitude, until fibrillation was established. Applied voltage and current were displayed on a storage oscilloscope. The average VFT current was 2.3 mA/g of heart (SD 0.4). Each threshold was obtained as the mid-range value between the maximum current which did not fibrillate and the minimum one which did fibrillate. Out of 98 fibrillations, 40% showed spontaneous reversal before 60 sec of fibrillation were completed. Beyond that time, electrical defibrillation was instituted. Three puppies (average weight 5.2 kg, SD 1.4) yielded an average VFT of 0.59 mA/g of heart (SD 0.14) using the same procedure. When the two VFT were compared (unpaired "t"-test), a significant difference was found (t 6.35; p less than 0.001), concluding that sloths would appear as more difficult to fibrillate than dogs of comparable body size.

Animals↗
PubMed2006

Delayed ventricular fibrillation following blunt chest trauma in a 4-year-old child.

A 4-year-old boy who was involved in a motor vehicle accident as a pedestrian and suffered blunt chest trauma was admitted to the emergency room. Unpredictable delayed ventricular fibrillation was diagnosed and treated successfully 2 h later. This case cannot be classified as commotio cordis as the ventricular fibrillation (VF) developed so long after the sustained chest injury. At the same time, other possible etiologies of VF such as cardiac pathology or electrolyte and metabolic disorders had been ruled out. Thus, an etiological link between the chest trauma and the subsequent VF could not be ruled out and is in fact plausible despite the late onset.

Accidents, Traffic↗
PubMed1987

Fat-free diet and myocardial excitability, refractoriness and ventricular fibrillation.

The lipid composition of the sarcolemma influences its function. The purpose of this study is to investigate the electrophysiological alterations induced in the rat's heart by dietary manipulation of cardiac fatty-acid composition. Strength-duration and strength-interval relationships were used to study excitability and refractoriness respectively. Ventricular fibrillation threshold measured by short bursts of rapid stimulation was used to indicate ventricular vulnerability. Gas liquid chromatography was used to analyse cardiac fatty-acid-composition. We used two-week-old rats fed with fat-free diet and 5% and 10% soya bean oil-supplemented diets for 6-9 weeks. Fat-free diet only was associated with increased eicosatrienoic acid content, a marker of essential fatty-acid deficiency. A decrease in poly-unsaturated to saturated (P:S) fatty-acid ratio was also observed. Five percent oil supplementation was associated with a delay and attenuation of this effect. Fat-free diet was associated with increased excitability, decreased refractoriness and reduced ventricular fibrillation threshold. Ten percent oil supplementation prevented these effects while 5% oil supplementation had only a temporary protective effect. We conclude that manipulation of dietary fat content can affect cardiac fatty-acid composition and electrophysiology.

Animals↗