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Pressures were measured in the heart and great vessels of 52 patients who underwent coronary revascularization. In 25 patients the left ventricle was vented during fibrillation; in the others a vent was not used. Samples for blood gas analysis were obtained twice during fibrillation from the aorta, left atrium, pulmonary artery, and right atrium. Left ventricular venting was found to be effective in keeping mean left heart pressure below 10 mm Hg, although temporary incompetence of the aortic valve or malfunction of the vent occasionally caused higher pressures. Vent use led to air embolism in the aorta in 16% of the patients. In the nonvented patients mean left heart pressures remained between 10 and 20 mm Hg. However, higher values were frequently observed. Blood gas analysis demonstrated that without venting, retrograde pulmonary flow occurred during fibrillation. No abnormality was encountered that could be related to nonventing.
Direct mechanical ventricular assistance (DMVA) is a method of biventricular circulatory support that employs a pneumatic device to apply both systolic and diastolic forces directly to the ventricular myocardium. This study investigated the effects of DMVA on myocardial hemodynamics when applied after a prolonged cardiopulmonary arrest. Seven swine weighting 28.3 +/- 2.5 kg were instrumented for regional myocardial blood flow (MBF) measurements using tracer microspheres. Ventricular fibrillation was then induced. After 10 min of ventricular fibrillation, CPR was initiated for 3 min. DMVA was then applied through median sternotomy. Defibrillation was attempted after 3.5 min of DMVA. If unsuccessful, DMVA was instituted for another 17.5 min and a subsequent defibrillation attempt was made. Arterial oxygen content (CaO2), coronary sinus oxygen content (CcSO2), myocardial oxygen delivery/consumption (mDO2/mVO2), extraction ratio (ER), and endocardial/epicardial blood flow ratio (EN/EP) were determined during CPR, during the initial application of DMVA (DMVA1), and after the subsequent 17.5 min of DMVA in those animals not initially defibrillated (DMVA2). Three of the seven animals were successfully defibrillated during DMVA1. After the additional 17.5 min of DMVA, only one other animal was defibrillated. There was a significant improvement in CaO2, CcSO2, MBF, mDO2, mVO2, ER, and EN/EP after DMVA1 compared to CPR. Only mVO2 and ER improved significantly after DMVA2. These findings support the concept that physical diastolic augmentation may improve myocardial hemodynamics when DMVA is applied during cardiac arrest.
This report reviews the electrophysiological mechanisms involved in the initiation, maintenance, and termination of ventricular fibrillation. Ventricular fibrillation may be defined as chaotic, random, asynchronous electrical activity of the ventricles due to repetitive re-entrant excitation and/or rapid focal discharge. The capacity to fibrillate is inherent in ventricular muscle because the electrophysiological properties of the various segments of the ventricle are not uniform. Factors that enhance electrical asynchrony facilitate, while factors that decrease electrical asynchrony hinder, the development of fibrillation. Ventricular fibrillation may result following stimulation during the vulnerable period; under certain circumstances, rapid ventricular rates produced by ventricular or supraventricular arrhythmias may provoke ventricular fibrillation. Once fibrillation is initiated, a large mass, brief refractory period, and slow conduction velocity favor perpetuation. Reducing the excitable ventricular mass to a value less than the amount necessary to support spontaneous fibrillation causes fibrillation to terminate. Depolarization of every cell in both ventricles is not necessary to terminate ventricular fibrillation in the entire heart.
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Countershock of prolonged ventricular fibrillation is usually followed by asystole or a nonperfusing rhythm. Data from three laboratory investigations indicate that administration of epinephrine and cardiopulmonary resuscitation (CPR) preceding countershock of prolonged ventricular fibrillation significantly improves cardiac resuscitation outcome compared with immediate countershock (relative risk reduction of failed resuscitation, 0.61). Preliminary investigations indicate that a similar improvement is not observed when the ventricular fibrillation period is of shorter duration, e.g., 5 mins. This time interval is probably at the lower limit at which CPR preceding shock of ventricular fibrillation provides benefit in terms of cardiac resuscitation. A single clinical trial of "CPR first" supports the use of a brief period of CPR before countershock of prolonged ventricular fibrillation. Additional trials with and without epinephrine are anticipated.
Ventricular fibrillation during reperfusion after aortic cross-clamping for coronary artery bypass grafting may cause subendocardial injury. We investigated the use of lidocaine to prevent ventricular fibrillation during this period. In a blind, prospective, randomized trial, 91 consecutive patients undergoing elective coronary artery bypass graft procedures were given lidocaine (2 mg/kg) or normal saline immediately before removal of the aortic cross-clamp. The groups were similar with respect to demographic, clinical, and intraoperative variables. Myocardial preservation techniques were similar in both groups. Of 47 patients receiving lidocaine, 38 recovered a supraventricular rhythm without ventricular fibrillation, compared with only 5 of 44 patients in the control group (p less than .001). When ventricular fibrillation occurred, patients in the control group required a greater number of direct-current countershocks (2.31 versus 1.86) to convert to sinus rhythm. Transient heart block, requiring temporary pacing, developed in 3 patients in the lidocaine group, compared with 1 patient in the control group. There was no significant difference between the groups in the requirement for perioperative inotropic support (6 of 47 versus 6 of 44) or the number of myocardial infarctions (2 of 47 versus 1 of 44), and there were no deaths in either group. Lidocaine infusion immediately before removal of the aortic cross-clamp significantly reduces the incidence of ventricular fibrillation during the reperfusion period after cardiopulmonary bypass.
Ventricular fibrillation (VF) is a major cause of sudden cardiac death in which myocardial ischemia plays a leading role. During ischaemia activation of ATP-sensitive potassium channels (K(ATP)) occurs, leading to potassium efflux from cardiomyocytes and shortening of the action potential favoring the genesis of ventricular fibrillation. In confirmation of this concept the sulfonylurea glibenclamide, which stimulates insulin release by inhibition of pancreatic K(ATP) channels, has been shown to inhibit VF in different models of ischaemia by inhibition of myocardial K(ATP) channels. HMR 1883 (1-[15-12-(5-chloro-o-anisamido)ethyl]-methoxyphenyl]sulfonyl]-3-m ethylthiourea) was designed as a cardioselective K(ATP) channel blocker. The aim of this study was to show that with this compound it is possible to separate the antifibrillatory from the insulin-releasing effect for the treatment of patients at risk of ischaemia-induced arrhythmias and sudden death. In the present study HMR 1883 reduced VF in Sprague-Dawley rats during prolonged ischaemia and also diminished mortality and the duration of VF in a separate reperfusion experiment at 3 mg/kg and 10 mg/kg with no effect on blood glucose or insulin. Glibenclamide, which was antifibrillatory at 0.3 mg/kg and 1 mg/kg, increased plasma insulin and lowered blood glucose already at a dose as low as 0.01 mg/kg. In conclusion, based on its antifibrillatory action and the absence of significant pancreatic effects at therapeutic doses, HMR 1883 is of potential clinical utility for the prevention of severe arrhythmias in patients with ischaemic heart disease.
Ventricular fibrillation is the final event in the majority of cases of sudden death. The ECG and clinical precursors of ventricular fibrillation are discussed in this article. Ventricular fibrillation usually appears as a consequence of a chain of events that leads to the appearance of this lethal arrhythmia. We review the markers of the vulnerable myocardium prone to ventricular fibrillation, the triggers and modulators that act on this vulnerable myocardium, and the event(s) that constitute the final step preceding this arrhythmia. The final step may be as unique as a sudden waterfall or present as a cascade of successive phenomena.
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The incidence of ventricular fibrillation with various contrast media (CM) was assessed by canine right coronary arteriography. After the catheter was impacted into the right coronary artery, it was infused continuously with CM for 25 seconds or until fibrillation occurred. The incidences of ventricular fibrillation were significantly higher with high-osmolality CM and low-osmolality CM without sodium ions than with low-osmolality CM containing a physiologic amount of sodium ions. The incidence of ventricular fibrillation was suggested to be related to hyperosmolality and the absence of sodium ions even in low-osmolality CM.
Whether ventricular fibrillation occurring within 48 h after acute myocardial infarction is associated with particular clinical features and poor prognosis, especially in patients with anterior myocardial infarction, is still debated. Therefore, clinical variables and in-hospital and 1 year mortality rates were analyzed in 2,088 patients, aged 18 to 95 years (mean +/- SD 64 +/- 12), admitted to the hospital with acute myocardial infarction between 1979 and mid 1984. One hundred forty-seven patients (7%) had at least one episode of ventricular fibrillation occurring within 48 h of hospital admission. Of these, 25% died during their initial hospitalization compared with 13% of patients without early ventricular fibrillation (p less than 0.001). In greater than 50% of patients with early ventricular fibrillation, the immediate cause of death was left ventricular failure or cardiogenic shock. In contrast, the 1 year mortality rate after hospital discharge was not significantly greater in patients with than in those without early ventricular fibrillation (15 versus 11%, respectively), particularly in the subgroup of patients with anterior myocardial infarction in which the mortality rate tended to be lower in patients with early ventricular fibrillation (8 versus 14%, respectively). Similar mortality results were found when only primary (not associated with left ventricular failure) ventricular fibrillation was analyzed. The left ventricular ejection fraction and the incidence of complex ventricular arrhythmias from 24 h ambulatory electrocardiographic monitoring obtained at hospital discharge were not different in survivors with or without early ventricular fibrillation (0.45 +/- 0.13 versus 0.49 +/- 0.14 and 41 versus 41%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Ventricular fibrillation following release of the aortic cross clamp is not uncommon. In 38 patients undergoing aortic valve replacement we investigated if this disturbance of rhythm is due to perioperative myocardial ischemia or due to deterioration of myocardial function prior to surgery. In all cases hypothermic cardioplegic arrest (Bretschneider) was used. The mean duration of ischemia was 49.39 +/- 10.46 minutes. After release of the aortic cross clamp in 17 of 38 patients ventricular fibrillation occurred. To find out which factors are responsible for the occurrence of ventricular fibrillation we performed a statistical analysis. Thereby we found out that the occurrence of ventricular fibrillation did not correlate with ischemia, the maximal level of myocardium-bound creatine kinase, the NYHA stage, or the left ventricular end diastolic pressure. The left-ventricular concentration of noradrenaline determined just before release of the aortic cross clamp showed a significant negative correlation with the occurrence of ventricular fibrillation. From our results we conclude that ischemic injury was not the determining factor for the occurrence of ventricular fibrillation in our study. We suggest that the significant correlation with reduced myocardial noradrenaline content demonstrates that myocardial deterioration prior to surgery is the determining factor for the occurrence of ventricular fibrillation.
We report the case of a 42-year-old female, affected by mitral valve prolapse and ventricular arrhythmias, who died suddenly from ventricular fibrillation recorded during Holter monitoring. The lethal arrhythmia initiated with late diastolic couplets followed by a ventricular tachycardia that eventually degenerated into ventricular fibrillation. The patient had experienced four orthostatic and stress-related syncopal episodes, associated with nausea and diaphoresis, and a positive tilt test. Holter monitoring documented ventricular arrhythmias, consisting of both isolated monomorphic and sporadic repetitive beats. Her standard ECG and exercise test were normal, but signal-averaged study findings were significantly positive. QT prolongation in the absence of arrhythmias was observed during the Valsalva manoeuvre and isoproterenol infusion. 2D echo showed a remarkable mitral valve prolapse without regurgitation and localized structural abnormalities of the right ventricle. Postmortem study confirmed mitral valve prolapse, and also disclosed pulmonary infundibulum dilatation, massive adipose infiltration of the right ventricular free wall, patchy fibrosis and scattered myocardial inflammatory infiltrates in the left ventricle; these features are all consistent with arrhythmogenic right ventricular cardiomyopathy.
Malignant ventricular arrhythmias can result from isolated right ventricular infarction, and reports of this phenomenon in the literature are rare. We present a case of a 46-year-old man with acute onset of chest pain angiographically confirmed to be a result of isolated occlusion of a right ventricular branch artery. He developed ventricular fibrillation within 5 hours of symptom onset. This case highlights the point that despite its benign clinical appearance and preserved left ventricular function, necrosis of right ventricular tissue can have life-threatening consequences.
Ventricular fibrillation has been observed in association with the administration of haloperidol. This study was designed to determine the effect of intravenous haloperidol on ventricular fibrillation threshold (VFT). VFT's were determined prior to and 15 min. following an intravenous infusion of haloperidol (50 mg administered over 10 min.) in five pigs anaesthetized with alpha-chloralose. VFT's were determined using a single stimulus method. Mean arterial pressure (MAP), heart rate (HR), and electrocardiogram (ECG) were monitored continuously. Mean VFT (mA) at baseline and following haloperidol infusion was 50.2 +/- 4.6 and 65.1 +/- 12.8, respectively (P less than 0.05). Mean MAP (mmHg) at baseline and following haloperidol infusion was 127 +/- 32 and 107 +/- 23, respectively (P less than 0.05). Haloperidol infusion did not significantly influence mean HR, QRS duration or corrected QT interval. Intravenous haloperidol increases VFT and decreases MAP in pigs. In this model, haloperidol may offer protection against ventricular fibrillation. Further study is required to determine the clinical significance of the antifibrillatory effect of haloperidol.