Ventricular Fibrillation (VF) Detection

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Detection of Ventricular Fibrillation Using Random Forest Classifier

Detection of Ventricular Fibrillation Using Random Forest Classifier

Ventricular fibrillation (VF) is one of the most serious life-threatening cardiac arrhythmia diseases. VF is the most commonly identified arrhythmia in cardiac arrest patients [2]. VF carries high risk since it usually ends in death within minutes unless prompt corrective measures are instituted. Once a patient has suffered a VF attack, accurate detection and quick first aid treatment are essential for improving the chance of survival. Weaver et al. [3] report that the survival rate of a patient, who experiences a VF attack outside the hospital, varies from 7% to 70%, depending on how quickly the patient receives first aid. Thus, solving the problem of a quick and reliable detection is an emergent research topic.

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Ventricular Fibrillation Detection using Empirical Mode Decomposition and Approximate Entropy

Ventricular Fibrillation Detection using Empirical Mode Decomposition and Approximate Entropy

Abstract— Efficient detection of ventricular fibrillation is very important for clinical purposes as it is the most serious cardiac rhythm disturbance that can be life threatening. This paper presents a new method for detection of Ventricular fibrillation by discriminating it with Ventricular tachycardia using empirical mode decomposition (EMD) and Approximate Entropy. First Intrinsic mode functions (IMFs) of each ECG signal is used to distinct between them by calculating their approximate Entropy. We have used MIT/BIH database to validate the efficiency of our method. Simulations were carried out in MATLAB environment. The result shows that this method gives good result as accuracy of 91% is achieved for detection of Ventricular fibrillation.

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Reliability of old and new ventricular fibrillation detection algorithms for automated external defibrillators

Reliability of old and new ventricular fibrillation detection algorithms for automated external defibrillators

If more than two but less than 40 QRS complexes are found within an 8 second episode, "no VF" is diagnosed. Otherwise the two spectral parameters FSMN and A 2 from the first part are investigated again. If FSMN < 2.5 and A 2 > 0.2, the considered ECG part is diagnosed as VF. The mentioned range for the number of found QRS com- plexes has the following reason: Sometimes, especially in ECGs with a high amount of noise, the DWT part makes wrong interpretations and "finds" QRS complexes also in QRS free episodes. Therefore, a minimal number of three QRS complexes is demanded to confirm the existence of QRS complexes. On the other side, if the DWT part "finds" more than 40 QRS complexes (equal to a pulse of 300 beats per minute), the signal is likely to be VF, since such high sinus rhythms do not appear. The limits of the range were chosen from experiments with data.

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Current concepts on ventricular fibrillation: A Vicious Circle of Cardiomyocyte Calcium Overload in the Initiation, Maintenance, and Termination of Ventricular Fibrillation

Current concepts on ventricular fibrillation: A Vicious Circle of Cardiomyocyte Calcium Overload in the Initiation, Maintenance, and Termination of Ventricular Fibrillation

electrical remodeling to cause re-initiation of AF and atrial contractile dysfunction after cardioversion. The experimental studies reviewed here suggest that the probability of these adverse events is best reduced by early detection and rapid termination of VF to prevent or limit Ca 2+ overload. In other words, rapid termination of VF not only reduces the risk of cerebral

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Complexity-Measure-Based Sequential Hypothesis Testing for Real-Time Detection of Lethal Cardiac Arrhythmias

Complexity-Measure-Based Sequential Hypothesis Testing for Real-Time Detection of Lethal Cardiac Arrhythmias

Ventricular fibrillation (VF) and ventricular tachycardia (VT) are life-threatening cardiac arrhythmias [1]. Reduction of mortality from such cardiac causes depends on rapid detec- tion and accurate classification of these arrhythmias. Thus, the development of accurate noninvasive techniques for identifying patients at risk of lethal arrhythmias is essential to reducing mortality from cardiac deaths. For this reason, a number of quantitative analysis techniques for electrocar- diogram (ECG) arrhythmia recognition have been proposed previously [1–9]. While all these algorithms show advan- tages in versatile aspects of performance evaluation, some of them are still too difficult to implement and compute for defibrillators. On the other hand, for computational con- venience, some algorithms utilized in either surface ECG monitoring-based automated external defibrillators (AEDs) or in implantable cardiovertor/defibrillators relied only on simple heart rate for arrhythmia detection. In fact, this might be problematic since it has been indicated that simply using heart rate as the sole feature might always unavoidably lead to a certain error rate in the detection since while both VF and VT have significantly higher rates than normal sinus rhythm, the rate range of VF overlaps with that of VT. Therefore,

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Ventricular Arrhythmias Detection using Wavelet Decomposition

Ventricular Arrhythmias Detection using Wavelet Decomposition

The ventricular fibrillation and ventricular flutter is easily identified by seeing the ECG signal, but in automatic analysis, the detection of ventricular fibrillation and ventricular flutter in the ECG signal is more important. If QRS is not available in the signal there may be chance for ventricular fibrillation (VFIB) or ventricular Flutter (VFL). The peak value of VFIB and VFL are much lower than VT, SVT and normal one in the 2 4 level as shown in the Fig. 2. Both ventricular flutter (VFL) and ventricular fibrillation (VFIB) have dominant frequencies in the 2-5 Hz band [25],[44], and the major portion of this range is contained in D5 (2.875-5.75 Hz). The VFIB and VFL consist of several continuous cycles. By energy distribution in the frequency domain VFIB and VFL can be easily identified. The energy ratio of D4 to D6 for VFL is larger than VFIB. By this energy variation VFIB and VFL can be classified. Frequency response and energy distribution for each scale is shown in table 2.

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The dynamic pattern of end tidal carbon dioxide during cardiopulmonary resuscitation: difference between asphyxial cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest

The dynamic pattern of end tidal carbon dioxide during cardiopulmonary resuscitation: difference between asphyxial cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest

Capnometry and capnography have gained a crucial role in monitoring critically ill patients in the pre-hospital setting [1-5]. They can be used as a detector for correct endotracheal tube placement, to monitor the adequacy of ventilation, ensure a proper nasogastric tube place- ment, recognize changes in alveolar dead space, help describe a proper emptying pattern of alveoli, help esti- mate the deepness of sedation and relaxation in criti- cally ill, help in diagnostics of severe pulmonary embolism, and can be used in cardiac arrest patients as a prognostic determinant of outcome and in monitoring the effectiveness of cardiopulmonary resuscitation (CPR) [6-11]. In our previous study [12], we found that initial values of partial pressure of end-tidal carbon dioxide (PetCO2) in asphyxial arrest were significantly higher than in ventricular fibrillation/pulseless ventricular tachycardia (VF/VT) arrest. In asphyxial arrest there was also no significant difference in initial values of PetCO2 in patients with and without return of spontaneous cir- culation (ROSC). In asphyxial arrest the initial values of PetCO2 cannot be used as a prognostic factor of out- come of CPR, as they can be in VF/VT arrest [13-16]. This difference, together with other criteria, can there- fore be useful for differentiating between the causes of cardiac arrest in the pre-hospital setting [17]. In this study we sought to evaluate the pattern of PetCO2 changes in cardiac arrest caused by VF/VT and asphyx- ial cardiac arrest in patients who were resuscitated according to new 2005 guidelines [18-20].

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Catheter Ablation versus Thoracoscopic Surgical Ablation in Long Standing Persistent Atrial Fibrillation (CASA AF): study protocol for a randomised controlled trial

Catheter Ablation versus Thoracoscopic Surgical Ablation in Long Standing Persistent Atrial Fibrillation (CASA AF): study protocol for a randomised controlled trial

Routine haematology and biochemistry assessments include full blood count, electrolytes, renal function tests, coagulation profile, liver function tests, thyroid function tests, C-reactive protein, tests for diabetes (haemoglobin A1C) and lipid profile (high-density lipopro- tein, low-density lipoprotein). Transthoracic echocardio- gram (TTE) and cMRI assessment will ensure that patients do not have poor left ventricular (LV) function, valvular dis- ease or other pathologies that meet the exclusion criteria. Additional clinical and study data collected at baseline, as well as at other study time points, are shown in Fig. 2 (SPIRIT figure). A detailed study codebook contains a complete list of all the variables, including type of data and reference values where appropriate.

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The Role of Cyclic Adenosine Monophosphate in Adrenergic Effects on Ventricular Vulnerability to Fibrillation in the Isolated Perfused Rat Heart

The Role of Cyclic Adenosine Monophosphate in Adrenergic Effects on Ventricular Vulnerability to Fibrillation in the Isolated Perfused Rat Heart

The relation between myocardial tissue cyclic AMP (cAMP) and the vulnerability to ventricular fibrillation was assessed in the isolated perfused rat heart by measurement of ventricular fibrillation threshold (VFT) and vulnerable period duration (VP). Exogenous dibutyryl cyclic AMP (DBcAMP) reduced VFT and increased VP by a concentration-related action whereas exogenous cAMP did not. Theophylline (1.0 mmol/liter) increased the tissue content of cAMP by 58% (P < 0.001) and caused a leftward shift in the concentration-

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Reduction of CPR artifacts in the ventricular fibrillation ECG by coherent line removal

Reduction of CPR artifacts in the ventricular fibrillation ECG by coherent line removal

Methods: For the reduction of CPR-related artifacts in ventricular fibrillation ECG we use a localized version of the coherent line removal algorithm developed by Sintes and Schutz. This method can be used for removal of periodic signals with sufficiently coupled harmonics, and can be adapted to specific situations by optimal choice of its parameters (e.g., the number of harmonics considered for analysis and reconstruction). Our testing was done with 14 different human ventricular fibrillation (VF) ECGs, whose fibrillation band lies in a frequency range of [1 Hz, 5 Hz]. The VF-ECGs were mixed with 12 different ECG-CPR-artifacts recorded in an animal experiment during asystole. The length of each of the ECG-data was chosen to be 20 sec, and testing was done for all 168 = 14 × 12 pairs of data. VF-to-CPR ratio was chosen as -20 dB, -15 dB, -10 dB, -5 dB, 0 dB, 5 dB and 10 dB. Here -20 dB corresponds to the highest level of CPR-artifacts. Results: For non-optimized coherent line removal based on signals with a VF-to-CPR ratio of -20 dB, -15 dB, -10 dB, -5 dB and 0 dB, the signal-to-noise gains (SNR-gains) were 9.3 ± 2.4 dB, 9.4 ± 2.4 dB, 9.5 ± 2.5 dB, 9.3 ± 2.5 dB and 8.0 ± 2.7 (mean ± std, n = 168), respectively. Characteristically, an original VF-to-CPR ratio of -10 dB, corresponds to a variance ratio var(VF):var(CPR) = 1:10. An improvement by 9.5 dB results in a restored VF-to-CPR ratio of -0.5 dB, corresponding to a variance ratio var(VF):var(CPR) = 1:1.1, the variance of the CPR in the signal being reduced by a factor of 8.9.

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Original Article Effect of autophagy on cardiomyocyte membrane Cx43 acute remodeling in rats with ischemia-reperfusion

Original Article Effect of autophagy on cardiomyocyte membrane Cx43 acute remodeling in rats with ischemia-reperfusion

used to block the fusion of autophagosomes and lyso- somes. It was found that Beclin-1 protein expression was decreased, p-Cx43 pro- tein degradation was reduced, p-Cx43 and Cx43 levels were upregulated, the spatial distri- bution of Cx43 tended to be normal by increasing its distri- bution on the end-to-end side, and the severity of reperfu- sion arrhythmia was alleviated in ventricular myocytes after MI/IR treated by chloroquine. It was indicated that inhibition of autophagy may improve the acute remodeling of cell mem- brane Cx4 to reduce the occurrence of malignant rhy- thm in MI/RI.

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Development of the probability of return of spontaneous circulation in intervals without chest compressions during out-of-hospital cardiac arrest: an observational study

Development of the probability of return of spontaneous circulation in intervals without chest compressions during out-of-hospital cardiac arrest: an observational study

Recent evidence indicates that cardiopulmonary resusci- tation (CPR) during both in- and out-of-hospital cardiac arrest is characterised by frequent and long interruptions in chest compressions [1, 2]. This reduces vital organ perfusion [3], and in animal experiments, increased length of chest compression pause before shock correlates with reduced rates of return of spontaneous circulation (ROSC) and survival [4-6]. Edelson et al. [7] reported that successful defibrillation, defined as removal of ventricular fibrillation (VF) for at least 5 seconds, was associated with shorter pre-shock pauses in man. Eilevstjønn et al. [8] reported a similar association for shocks with ROSC outcome but only reported the median length of pre- shock pauses for ROSC and no-ROSC shocks. Identifying in detail how pausing in chest compressions affects the vitality of the myocardium, and thereby the probability of ROSC (P ROSC ) after defibrillation, is important because it

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A simulation study of the effects of cardiac anatomy in ventricular
                    fibrillation

A simulation study of the effects of cardiac anatomy in ventricular fibrillation

These dynamical instabilities interact synergistically with fixed heterogeneities to facilitate wavebreak. In computational studies in 3D rectangular slabs, some waves that remain intact in homoge- neous tissue can break up into a fibrillation-like state when anisotropic conduction is introduced (11, 17, 18). It is therefore unclear how important ventricular geometry and anisotropic con- duction are in generating wavebreak. The recent availability of an anatomically realistic computer model of the ventricles, coupled with an ionic model of the cardiac action potential, provides an opportunity to examine the role of cardiac anatomical properties in perpetuating VF. We find that the steepness of the APD restitution slope remains a major determinant of wave instability in the anatomical heart, but that the threshold of steepness required to induce wave breakup is significantly reduced by anatomical features, such as the ventricular cavities, and by the presence of anisotropic conduction, which causes waves to fold and drift.

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Key words

Key words

Results. In 31 patients (60.8%) atrial fibrillation disappeared during the first 24 hours after cardiac surgery. A sig- nificant prolongation of the QT interval after the surgery was found in Group 2 that was not observed in Group 1. Multiple regression analysis revealed that QT interval duration after surgery is related to the resolution of atrial fibrillation independently from the duration of the R-R interval duration and the need for cardiac pacing. Conclusions. Spontaneous temporary resolution of atrial fibrillation is a common finding after cardiac surgery in patients with chronic atrial fibrillation. This phenomenon is related to a prolonged QT interval, therefore it may have an electrophysiological basis rather than a hemodynamic background. Further studies are required to assess the clinical importance of the prolongation of the QT interval after cardiac surgery (Adv Clin Exp Med 2013, 22, 4, 519–527).

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Ventricular Fibrillation and the Use of Automated External Defibrillators on Children

Ventricular Fibrillation and the Use of Automated External Defibrillators on Children

1. Although the incidence of VF in children is far less than that in adults, the outcome for VF is better than that for other nonperfusing rhythms and is improved with early defibrillation. Therefore, strategies and equipment availability for treatment of pediatric arrest should be focused on shortening the intervals from collapse to recognition of VF and to defibrillation. 2. Although most data available on the correct energy for

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Prophylaxis of early ventricular fibrillation by inhibition of acylcarnitine accumulation

Prophylaxis of early ventricular fibrillation by inhibition of acylcarnitine accumulation

ischemia in vivo. The present study was performed to determine whether POCA could prevent accumulation of both LCA and LPC induced by ischemia in vivo and if so, whether attenuation of early arrhythmogenesis would result. LAD coronary artery occlusions were induced for 5 min in chloralose-anesthetized cats. Coronary occlusion in untreated control animals elicited prompt, threefold increases of LCA (73 +/- 8 to 286 +/- 60 pmol/mg protein) and twofold increase of LPC (3.3 +/- 0.4 to 7.5 +/- 0.9 nmol/mg protein) selectively in the ischemic zone, associated with ventricular tachycardia (VT) or ventricular fibrillation (VF) occurring within the 5-min interval before acquisition of myocardial samples in 64% of the animals. POCA prevented the increase of both LCA and LPC. It also prevented the early occurrence of VT or VF (within 5 min of occlusion) in all animals studied. The antiarrhythmic effect of POCA was […]

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Ventricular Fibrillation Caused by Traumatic Coronary Artery Dissection

Ventricular Fibrillation Caused by Traumatic Coronary Artery Dissection

resolved via conservative treatment, or may spontaneously heal during follow-up observation, and it has been argued that aggressive early intervention is unnecessary unless there is ongoing myocardial ischemia, involve- ment of proximal left coronary artery, or involvement of a large area of the myocardium [5]-[7]. Unfortunately, once TCAD develops into VF, the likelihood of survival is very low [8].

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Upstream therapeutic strategies of Valsartan and Fluvastatin on Hypertensive patients with non permanent Atrial Fibrillation (VF HT AF): study protocol for a randomized controlled trial

Upstream therapeutic strategies of Valsartan and Fluvastatin on Hypertensive patients with non permanent Atrial Fibrillation (VF HT AF): study protocol for a randomized controlled trial

Methods/design: The VF-HT-AF study is a multicenter, randomized, open-label, four-arm parallel group study with comparative evaluation of valsartan and fluvastatin as upstream therapies for the treatment of non-permanent AF complicated by hypertension. The primary outcome measure is change in the development of paroxysmal AF into persistent or permanent AF, the development of persistent AF to permanent AF, and change in incidence of overall and persistent AF recurrence, as evaluated by 7-days ambulatory electrocardiograph monitoring (Holter) and patients ’ diaries during 2 years ’ follow-up. Secondary outcome measures of this study include the occurrence of: (1) fatal and nonfatal myocardial infarction; (2) heart failure (New York Heart Association stage III or IV); (3) cardiogenic shock; (4) serious bleeding necessitating hospitalization; (5) malignant ventricular arrhythmia; (6) revascularization therapy; (7) radiofrequency catheter ablation of AF; (8) changes of left atrial dimension, as measured by ultrasound echocardiography; (9) stroke; (10) cardiovascular mortality; and (11) all-cause mortality. A total of 1879 patients will be investigated from 15 medical centers throughout China to obtain the relevant information.

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Original Article Cardiac characteristics in the premature ventricular contraction patients with or without ventricular tachycardia

Original Article Cardiac characteristics in the premature ventricular contraction patients with or without ventricular tachycardia

The premature ventricular contractions (PVCs) are early depolarization of the myocardium caused by an electrical impulse or ectopic rhythm from any part of the ventricles, includ- ing the ventricular septum, before the sinoatrial impulse has reached the ventricles. According to the frequency of ventricular premature beats (VPB), PVCs can be divided into sporadic and frequent [1]. Sporadic PVCs are, also called functional premature beats, defined as less than 6 pules/min, which can occur in healthy people; while frequent PVCs, defined as more than 6 pules/min, can occur in patients with

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Electrophysiological Mechanisms of Ventricular Fibrillation Induction

Electrophysiological Mechanisms of Ventricular Fibrillation Induction

Although reentry has been proposed in most hypotheses as the mechanism responsible for VF induction, recent VF induction studies in pigs have demonstrated different findings. Chattipakorn et al have shown that following near ULV shocks, the first few post-shock activations arose on the epicardium in a focal manner before degenerating into VF. 46,47 No

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