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

Extracorporeal membrane oxygenation (ECMO) can be set up quickly at the bedside and provides reliable temporary mechanical circulatory support for severe heart failure. We report the case of a 56-year-old female with circulatory collapse due to sustained ventricular tachycardia and ventricular fibrillation (VT/Vf) after coronary artery bypass grafting (CABG) who was successfully resuscitated using ECMO. The sustained VT/Vf might have been secondary to myocardial stunning, ischemia, infarction, or reperfusion. There were 40 cardioversions within the first 5 postoperative days. The patient improved after 8 days of ECMO in addition to use of an intraaortic balloon pump and administration of inotropic agents for profound heart failure. Left ventricular ejection fraction improved from 28% preoperatively to 54.5% on the 20th postoperative day. Cardiogenic shock due to sustained VT/Vf after CABG may be an indication for ECMO support. Immediate establishment of circulatory support using ECMO provides valuable time for spontaneous and interventional correction of reversible causes of sustained VT/Vf.
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PMID:Successful rescue of sustained ventricular tachycardia/ventricular fibrillation after coronary artery bypass grafting by extracorporeal membrane oxygenation. 1210 65

Survival of cardiac arrest is improved by basic life support (BLS). This study investigated the relationship between ventricular fibrillation (VF) characteristics and survival. In a 2-year prospective study out-of-hospital witnessed non-traumatic cardiac arrests were observed. The probabilities of recording VF, asystole or other rhythms in relation to BLS and the time to the rhythm recording were analyzed with logistic regression. Amplitude and baseline crossings of VF were related to survival, using linear regression analysis. In 873 patients, the probability to record VF decreased per minute (OR 0.92, 95%CI 0.89-0.95) and of asystole increased (OR 1.13, 95%CI 1.09-1.18) as time from collapse elapsed. BLS reduced these trends significantly for VF (OR 0.97, 95%CI 0.94-0.99) and asystole (OR 1.09, 95%CI 1.05-1.13). This effect was not observed for other rhythms. The amplitude of VF decreased in time; significantly less for patients who received BLS than for those who did not (p=0.009). Survival significantly decreased with lower amplitude of VF (OR 0.23 per mV, 95%CI 0.07-0.79) and with less baseline crossings (OR 0.80 per baseline crossings per second, 95%CI 0.71-0.91). Our study demonstrated that BLS and VF as initial rhythm, considered being "baseline" predictors in survival models, were proved not independent of each other. The decrease of VF amplitude and increase in prevalence of asystole is slowed significantly by BLS. Predicting survival from VF amplitude and baseline crossings alone is limited.
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PMID:Prevention of deterioration of ventricular fibrillation by basic life support during out-of-hospital cardiac arrest. 1210 6

The present study addressed the incidence of unpredicted hemodynamic collapse in off-pump coronary artery bypass grafting (OPCAB). Since 1999, OPCAB was attempted in 114 patients without preoperative hemodynamic collapse to date. 95% patients of OPCAB were completed without percutaneous cardiopulmonary support (PCPS) and all patients were discharged. In this study, patients are divided into a prophase of 60 patients and an anaphase of 50 patients, in consideration of learning curve. As for the trouble in procedures, 12 patients of ventricular fibrillation, 6 patients of conversion to PCPS, 19 patients of bradycardia which were evaded in temporary pacing were observed. Patients with conversion to PCPS decreased in 5 patients (8%) in prophase and 1 patient (1.8%) in anaphase. Avoidance of hemodynamic collapse were prevention of ischemia by positive use of coronary perfusion, prophylactic intra-aortic balloon pumping (IABP) use for decrease of blood pressure, apical evacuation heart positioner for visual field security.
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PMID:[Hemodynamic collapse during off-pump coronary artery bypass grafting and optimization]. 1291 Sep 42

Sudden cardiac death is the leading cause of death in the US and most developed nations. Ventricular fibrillation (VF) is the most common initial rhythm in survivors of cardiac arrest. The most important factor in determining survival from VF is the time from collapse to administration of the first defibrillation shock. Automatic external defibrillators (AEDs) have been developed and widely deployed in an attempt to reduce the time to defibrillation. Data on early defibrillation using AEDs has led to a number of public access defibrillator placements in the US and ongoing studies of public access AED use. The safety of lay person AED use is clear. Clearly some concentrated captive populations (e.g. airports, airplanes) may benefit from public access AEDs. Therefore, widespread AED education as a means of increasing public acceptance of lay person AED use must be a priority. As technology evolves costs will decline, however, the current economic reality requires careful consideration of the cost effectiveness of specific AED placement.
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PMID:Treatment of cardiac arrest with automatic external defibrillators: impact on outcome. 1472 79

The main survival factor in cardiac arrest secondary to ventricular fibrillation (VF) is the interval between collapse and defibrillation; consequently, this treatment constitutes one of the most important links in the survival chain in adults. Although VF is a rare cause of out-of-hospital cardiac arrest in children, its detection and treatment is essential because in the pediatric cardiac arrest scenario, VF is the dysrhythmia with the best prognosis. Automated external defibrillators (AED) are simple devices that allow cardiac rhythm to be analyzed; they can also determine whether it is shockable or not with high sensitivity and specificity in adults and children. Currently available evidence has prompted the recommendation of AED use in children older than 1 year without signs of circulation, mainly in the pre-hospital setting and ideally with a dose-limiting device.
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PMID:[Semiautomatic defibrillation in children]. 1527 83

Few minutes of suspended malignant ventricular arrhythmia may be permitted for the patient with left ventricular assist system (LVAS). However, longer and continuous ventricular arrhythmia, especially ventricular fibrillation (Vf), may induce the low output of LVAS, which leads circulatory collapse immediately. Our presenting case is a female dilated cardiomyopathy patient who has been supported with LVAS. Four months after the LVAS installation, her electrocardiogram has changed to Vf without any symptoms. Her ventricular function has never recovered, even ventricular tachycardia. She has been a candidate of heart transplantation for more than 19 months with this rare hemodynamic condition (LVAS+Vf), like the Fontan circulation. Her performance status is limited due to deceasing of the LVAS flow, which caused by the change of her position: 2.5-2.9 l/min (lie down) to 2.0 l/min (rise). Her peak VO2/W is 6.9 ml/min/kg measured by the cardio-pulmonary exercise test. However, she has developed her general status by doing rehabilitation program and is able to walk for more than 100-150 meters.
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PMID:[Long survival with chronic ventricular fibrillation under support of uni-left-ventricular assist system]. 1546 41

Exercise-induced ventricular tachycardia (VT) is rare in children and young adults without structural heart disease. Catecholaminergic polymorphic VT (CPVT) is among the possible causes and carries a poor prognosis. The QRS morphology of CPVT can be bidirectional, polymorphic or even ventricular fibrillation. We report a case of CPVT initially presenting as sudden collapse in an 18-year-old Taiwanese woman. Family history was negative for arrhythmias and sudden death. Laboratory analyses, transthoracic echocardiography, magnetic resonance imaging, electrophysiological study including procainamide and isoproterenol test were all negative. Bidirectional VT was induced by treadmill exercise test. She responded well to beta-blocker therapy. Some cases of CPVT are sporadic and some occur in patients with a family history. The treatment of choice for this disease is beta-blocker and implantation of an internal cardioverter defibrillator.
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PMID:Exercise-provoked bidirectional ventricular tachycardia in a young woman. 1549 29

From April 2000 to November 2002, the Department of Health (England) placed 681 automated external defibrillators (AEDs) in 110 public places for use by volunteer lay first responders. An audit has been undertaken of the first 250 deployments, of which 182 were for confirmed cardiac arrest. Of these, 177 were witnessed whilst 5 occurred in situations that were remote or initially inaccessible to the responders. The response interval between collapse and the initiation of CPR or AED placement was estimated to be 3-5 min in most cases. Ventricular fibrillation or rapid ventricular tachycardia (one case) was the first recorded rhythm in 146 cases (82%). In all, 44 of the 177 witnessed cases are known to have survived to hospital discharge (25%). Complete downloads are available for 173 witnessed cases and of these 140 were shocked: first-shock success, defined as termination of the fibrillatory waveform for 5 s or more, was achieved in 132 of them. When data quality permitted, the downloads were analysed with special reference to the numbers of compressions given and also to interruptions in compression sequences for ventilations, for rhythm analysis by the AED, for clinical checks, and for unexplained operator delays. The average rate of compressions during sequences was 120 min(-1), but because of interruptions, the actual number administered over a full minute from the first CPR prompt was a median of only 38. The speed of response by the lay first responders in relation to AED use was similar to that reported for healthcare professionals.
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PMID:The Department of Health National Defibrillator Programme: analysis of downloads from 250 deployments of public access defibrillators. 1573 53

Sudden cardiac death accounts for more than half of all cardiovascular deaths in the US, and a large proportion of these deaths are attributed to ischemia-induced ventricular fibrillation. As such, the mechanisms underlying the initiation and maintenance of these lethal rhythms are of significant clinical and scientific interest. In large animal hearts, regional ischemia induces two phases of ventricular arrhythmia. The first phase (1A) occurs between 5 and 7 min after arrest of perfusion. This phase is associated with membrane depolarization, a mild intracellular and extracellular acidification and a small membrane depolarization. A second phase (1B) of ventricular arrhythmia occurs between 20 and 30 minutes after arrest of perfusion. This phase occurs at a time when ischemia-induced K+ and pH changes are relatively stable. The arrhythmia is presumed to relate to the process of cell-to-cell electrical uncoupling because a rapid increase of tissue impedance precedes the onset of the arrhythmia. Of note is that tissue resistance is primarily determined by the conductance properties of the gap junctions accounting for cell-to-cell coupling. Impulse propagation in heart is determined by active and passive membrane properties. An important passive cable property that is modulated by ischemia is intercellular resistance and is determined primarily by gap junctional conductance. As such changes in Impulse propagation during myocardial ischemia are determined by contemporaneous changes in active and passive membrane properties. Cellular K loss, intracellular and extracellular acidosis and membrane depolarization are important factors decreasing excitatory currents, while the collapse of the extracellular compartment and cell-to-cell electrical uncoupling increase the resistance to current flow. The time-course of cellular coupling is closely linked to a number of physiological processes including depletion of ATP, and accumulation of intracellular Ca2+. Hence, interventions such as ischemic preconditioning attenuate the effect of subsequent ischemia, delay the onset of cell-to-cell electrical uncoupling and likewise delay the onset of ischemia-induced arrhythmia.
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PMID:Ischemia-induced arrhythmia: the role of connexins, gap junctions, and attendant changes in impulse propagation. 1622 75

Recovery of the mitochondrial inner membrane potential (DeltaPsi(m)) is a key determinant of postischemic functional recovery of the heart. Mitochondrial ROS-induced ROS release causes the collapse of DeltaPsi(m) and the destabilization of the action potential (AP) through a mechanism involving a mitochondrial inner membrane anion channel (IMAC) modulated by the mitochondrial benzodiazepine receptor (mBzR). Here, we test the hypothesis that this mechanism contributes to spatiotemporal heterogeneity of DeltaPsi(m) during ischemia-reperfusion (IR), thereby promoting abnormal electrical activation and arrhythmias in the whole heart. High-resolution optical AP mapping was performed in perfused guinea pig hearts subjected to 30 minutes of global ischemia followed by reperfusion. Typical electrophysiological responses, including progressive AP shortening followed by membrane inexcitablity in ischemia and ventricular fibrillation upon reperfusion, were observed in control hearts. These responses were reduced or eliminated by treatment with the mBzR antagonist 4'-chlorodiazepam (4'-Cl-DZP), which blocks depolarization of DeltaPsi(m). When applied throughout the IR protocol, 4'-Cl-DZP blunted AP shortening and prevented reperfusion arrhythmias. Inhibition of ventricular fibrillation was also achieved by bolus infusion of 4'-Cl-DZP just before reperfusion. Conversely, treatment with an agonist of the mBzR that promotes DeltaPsi(m) depolarization exacerbated IR-induced electrophysiological changes and failed to prevent arrhythmias. The effects of these compounds were consistent with their actions on IMAC and DeltaPsi(m). These findings directly link instability of DeltaPsi(m) to the heterogeneous electrophysiological substrate of the postischemic heart and highlight the mitochondrial membrane as a new therapeutic target for arrhythmia prevention in ischemic heart disease.
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PMID:The mitochondrial origin of postischemic arrhythmias. 1628 48


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