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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although sudden arrhythmic death is usually unrelated to exertion, there is more than anecdotal evidence that strenuous exercise in patients with coronary heart disease carries an additional risk for sudden death. When cardiac arrest has been observed after exercise stress testing or within seconds after collapse associated with exertion, ventricular fibrillation has usually been present and has responded to the prompt application of a defibrillatory shock. Exertion-related cardiac arrest is typically a "primary" arrhythmic event not due to acute myocardial infarction. As estimated here, the additional risk of exercise for cardiac arrest may be more than 100-fold during or after a few minutes of vigorous exertion.
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PMID:Exercise: a risk for sudden death in patients with coronary heart disease. 351 Feb 34

Survival from cardiac arrest is higher when the collapse occurs outside the home. Of 781 patients collapsing at home, 101 (13%) survived to hospital discharge. This compared with 66 survivors among 248 (27%) patients arresting outside the home (P less than .001). Patients collapsing outside the home were younger and more frequently were men. Cardiac arrests outside the home were more often witnessed, more likely to have bystander CPR, less often preceded by symptoms, and the collapsing rhythm was more frequently ventricular fibrillation. Mean time to CPR was shorter. Multivariate logistic regression showed that the effect of location on survival was still statistically significant, although diminished, after adjusting for the above variables (P less than .01). We speculate that comorbidity, underlying etiology, and activity level may explain the remaining difference. Because 76% of arrests occur in the home, efforts to increase the frequency of bystander-CPR through targeted and dispatcher-assisted CPR programs are warranted.
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PMID:The location of collapse and its effect on survival from cardiac arrest. 359 34

The risk of toxic effects on the heart of bupivacaine following several kinds of locoregional anaesthesia has been investigated in the dog in situ heart by determining conduction time and effective refractory period in the various parts of the conduction system and the ventricular muscle, as well as the discharge rate of the sinus node. Bupivacaine, i.v. infused at 3 rates, 0.2, 0.3 and 0.4 mg X kg-1 X min-1, proved to have depressant effects on conduction, automatism and excitability. It slows down conduction in all the parts of the myocardium, considerably at high stimulation frequencies, but always much more in the His-Purkinje system and the ventricular contractile fibres than in the atrioventricular node, because it tends to block the sodium rather than the calcium or potassium channel. Its effect remain more moderate, indeed, on sinus automatism and atrial and mainly ventricular refractoriness. Its danger lies, therefore, in the inhibition of conduction, with atrioventricular or His bundle branch block, but more frequently reentrant arrhythmias, likely to result in ventricular fibrillation. However: these alterations are observed with very high plasma levels (about 4 to 9 micrograms X ml-1), much higher than usual peak concentrations following spinal anaesthesia (0.10 micrograms X ml-1) or even epidural anaesthesia or brachial plexus block (1.20 micrograms X ml-1); reversal of these alterations occurs rapidly (reduction by 50% within 30 min for instance), when they have not led to ventricular fibrillation or they have not been associated with circulatory collapse.
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PMID:Electrophysiological study in the dog of the risk of cardiac toxicity of bupivacaine. 363 38

Survival after out-of-hospital cardiac arrest is intimately related to the time from cardiovascular collapse to the initiation of CPR, or downtime. Furthermore, the reperfusion technique that optimizes coronary and cerebral blood flow after cardiac arrest may also be dependent on downtime. Peak blood lactate levels have been shown to be unchanged throughout resuscitation and predictive of downtime in dogs subjected to cardiopulmonary arrest and open cardiac massage. The purpose of this study was to determine the course of arterial lactate levels in dogs subjected to a fibrillatory cardiopulmonary arrest and conventional closed-chest CPR (CCPR). Fourteen dogs were subjected to five minutes of cardiopulmonary arrest and 30 minutes of CCPR. Resuscitation was performed according to a standardized protocol. Arterial lactic acid samples were collected at timed intervals throughout the experiment. Mean arterial lactic acid levels increased significantly with each sampling interval during 30 minutes of CCPR (overall P less than .05). In nine dogs successfully resuscitated, there were no significant differences in mean arterial lactic acid levels after the return of spontaneous circulation (ROSC). Open-chest resuscitation after five minutes of ventricular fibrillation in dogs results in peak lactic acid levels that do not change significantly once internal cardiac massage is initiated. In contrast, CCPR in similarly arrested dogs does not appear to provide adequate tissue oxygenation and/or perfusion to prevent continuous lactic acid accumulation.
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PMID:Lactic acidosis during closed-chest CPR in dogs. 368 90

This study evaluated interspecies sensitivity and ability to resuscitate pentobarbital anesthetized sheep and dogs after cardiovascular toxic doses of bupivacaine. Every minute, 3 mg/kg of bupivacaine was injected into the right atrium over the course of 10 sec until cardiovascular collapse occurred. While the bupivacaine was given, the animals were made apneic for 90 sec and then ventilated with 100% oxygen. After the bupivacaine administration, cardiovascular collapse occurred in the form of electromechanical dissociation progressing to asystole in dogs, whereas in sheep the predominant rhythm was ventricular fibrillation leading to asystole. Resuscitation was performed using open chest heart massage, bretylium for treatment of ventricular tachycardia and fibrillation, and epinephrine with atropine for treatment of electromechanical dissociation or asystole. The initial dose of bupivacaine used to cause cardiovascular collapse was 3.5 +/- 1.2 mg/kg in sheep and 24.6 +/- 8.5 mg/kg in dogs (P less than 0.01). All sheep and dogs were resuscitated from the first cardiovascular collapse. The resuscitation time was 2.1 +/- 1.0 min in dogs and 36.9 +/- 15.4 min in sheep (P less than 0.01). All dogs could be resuscitated after two additional cardiovascular collapses induced by bupivacaine, but no sheep could be resuscitated after a second cardiovascular collapse. Concentrations of bupivacaine in cardiac tissue and serum levels of bupivacaine after the last resuscitation attempt were significantly greater in the dogs than in the sheep. We conclude that sheep are more sensitive to bupivacaine than dogs, but that even sheep can be resuscitated after cardiovascular collapse produced by bupivacaine.
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PMID:Comparison of resuscitation of sheep and dogs after bupivacaine-induced cardiovascular collapse. 375 50

Almost 90% of patients resuscitated from out of hospital cardiac arrest have coronary heart disease and can be categorized in one of three groups: acute myocardial infarction, ischemic event or primary arrhythmic event. The patients who have acute myocardial infarction have the best prognosis, and those with primary arrhythmic events have the worst. Recent studies show that ventricular arrhythmias after myocardial infarction are associated with mortality independent of any association with left ventricular dysfunction. Ventricular arrhythmias that have caused cardiac arrest or hemodynamic collapse, that is, malignant arrhythmias, should be treated aggressively and evaluated carefully with one of two methods that have high predictive accuracy for outcome: 1) the Holter recording/exercise test approach, or 2) the electrophysiologic approach. It is not yet known whether treating potentially malignant ventricular arrhythmias after myocardial infarction with class I or III antiarrhythmic drugs will reduce mortality, but two clinical trials are under way in the United States to address this question. Beta-adrenergic blocking drugs do reduce mortality, probably as a result of both antiischemic and antiarrhythmic effects. Calcium channel blocking agents, various antiplatelet drugs and alpha-adrenergic blocking drugs are under investigation to determine their value in secondary prevention of ventricular fibrillation.
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PMID:Patients with malignant or potentially malignant ventricular arrhythmias: opportunities and limitations of drug therapy in prevention of sudden death. 388 10

The authors retrospectively studied victims of sudden cardiac death who experienced cardiac arrest before and after arrival of emergency personnel in order to define possible etiologic factors. There were 265 patients in the arrest-after-arrival (AAA) group and 414 patients in the arrest-before-arrival (ABA) group. All patients in the AAA group had symptoms prior to cardiac arrest. Approximately half the patients in the ABA group had symptoms. The presence or absence of symptoms prior to cardiac arrest appeared strongly associated with the cardiac rhythm at time of collapse and with discharge. Of patients with symptoms, 61% were in ventricular fibrillation or ventricular tachycardia, as compared with 93% of patients without symptoms (P less than 0.001); 32% of patients with symptoms were discharged, as compared with 57% of patients without symptoms (P less than 0.001). These data suggest two potential etiologies for sudden cardiac arrest; thrombosis/ischemia (associated with symptoms) and electrical (associated with no symptoms). Inasmuch as the AAA group represented 14% of witnessed cardiac arrests, patients with symptoms of myocardial ischemia or infarction should be aggressively treated.
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PMID:Out-of-hospital cardiac arrest: significance of symptoms in patients collapsing before and after arrival of paramedics. 394 38

Survival to hospital discharge was related to the clinical history and emergency care system factors in 285 patients with witnessed cardiac arrest due to ventricular fibrillation. Only the emergency care factors were associated with differences in outcome. Both the period from collapse until initiation of basic life support and the duration of basic life support before delivery of the first defibrillatory shock were shorter in patients who survived compared with those who died (3.6 +/- 2.5 versus 6.1 +/- 3.3 minutes and 4.3 +/- 3.3 versus 7.3 +/- 4.2 minutes; p less than 0.05). A linear regression model based on emergency response times for 942 patients discovered in ventricular fibrillation was used to estimate expected survival rates if the first-responding rescuers, in addition to paramedics, had been equipped and trained to defibrillate. Expected survival rates were higher with early defibrillation (38 +/- 3%; 95% confidence limits) than the observed rate (28 +/- 3%). Because outcome from cardiac arrest is primarily influenced by delays in providing cardiopulmonary resuscitation and defibrillation, factors affecting response time should be carefully examined by all emergency care systems.
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PMID:Factors influencing survival after out-of-hospital cardiac arrest. 395 32

The amplitude of ventricular fibrillation found initially in 394 patients was compared to clinical and logistical findings at the time of cardiac arrest. Peak-to-peak amplitude averaged 0.55 +/- 0.25 mV; a very low amplitude (0.2 mV or less) or "fine" fibrillation was present in 66 patients (17%). The amplitude was not found to be related to clinical histories, but depended on the length of the period from collapse until start of basic life support (p = 0.004) and the delay until assessment by paramedics (p = 0.001). Survival rates were strongly associated with amplitude: only 4 patients (6%) with fine ventricular fibrillation survived, compared to 117 or 328 patients (36%) in whom the initial amplitude was higher (p less than 0.001). Patient outcome related to amplitude even after adjusting for clinical history and logistical delays (p less than 0.005). We conclude that fine ventricular fibrillation is in part the result of delay in initiation of treatment, and that fibrillation amplitude is a powerful indicator of outcome after cardiac arrest.
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PMID:Amplitude of ventricular fibrillation waveform and outcome after cardiac arrest. 396 46

The prognostic importance of electrophysiologic studies in patients with sustained ventricular tachyarrhythmias treated with amiodarone was prospectively studied in 100 consecutive patients. Sustained ventricular tachycardia (VT)/ventricular fibrillation (VF) was inducible in all patients before amiodarone therapy. After amiodarone administration 2 groups of patients were identified. In group 1 patients the ventricular tachyarrhythmia was no longer inducible and in group 2 patients the arrhythmia remained inducible. In group 1, no recurrent arrhythmia occurred during a follow-up of 18 +/- 10 months. In group 2, 38 of 80 patients (48%) had arrhythmia recurrence during a follow-up of 12 +/- 9 months. The difference between group 1 and 2 could not be explained by clinical variables, amiodarone doses or plasma concentrations, or electrocardiographic variables. In patients in whom cardiovascular collapse or other severe symptoms where noted during electrophysiologic study after amiodarone treatment, recurrences caused sudden death (n = 12). However, in patients in whom the induced arrhythmia produced moderate symptoms, the recurrent arrhythmia was nonfatal VT (n = 26). Electrophysiologic testing provides clinical guidance and predicts prognosis in patients treated with amiodarone as it does for the evaluation of other antiarrhythmic agents.
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PMID:Usefulness of electrophysiologic testing in evaluation of amiodarone therapy for sustained ventricular tachyarrhythmias associated with coronary heart disease. 396 70


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