An unexpected case of ventricular fibrillation cardiac arrest in a Caucasian female.
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ABSTRACT:
SUBMITTER: O'Neill L
PROVIDER: S-EPMC4216881 | biostudies-literature | 2014 Oct
REPOSITORIES: biostudies-literature
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An unexpected case of ventricular fibrillation cardiac arrest in a Caucasian female.
O'Neill Louisa L O'Hanlon Rory R Owens Patrick P Maree Andrew A
BMJ case reports 20141031
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Project description:IntroductionBesides therapeutic hypothermia or targeted temperature management no novel therapies have been developed to improve outcomes of patients after cardiac arrest (CA). Recent studies suggest that nitrite reduces neurological damage after asphyxial CA. Nitrite is also implicated as a new mediator of remote post conditioning produced by tourniquet inflation-deflation, which is under active investigation in CA. However, little is known about brain penetration or pharmacokinetics (PK). Therefore, to define the optimal use of this agent, studies on the PK of nitrite in experimental ventricular fibrillation (VF) are needed. We tested the hypothesis that nitrite administered after resuscitation from VF is detectable in cerebrospinal fluid (CSF), brain and other organ tissues, produces no adverse hemodynamic effects, and improves neurologic outcome in rats.MethodsAfter return of spontaneous circulation (ROSC) of 5 min untreated VF, adult male Sprague-Dawley rats were given intravenous nitrite (8 μM, 0.13 mg/kg) or placebo as a 5 min infusion beginning at 5 min after CA. Additionally, sham groups with and without nitrite treatment were also studied. Whole blood nitrite levels were serially measured. After 15 min, CSF, brain, heart and liver tissue were collected. In a second series, using a randomized and blinded treatment protocol, rats were treated with nitrite or placebo after arrest. Neurological deficit scoring (NDS) was performed daily and eight days after resuscitation, fear conditioning testing (FCT) and brain histology were assessed.ResultsIn an initial series of experiments, rats (n = 21) were randomized to 4 groups: VF-CPR and nitrite therapy (n = 6), VF-CPR and placebo therapy (n = 5), sham (n = 5), or sham plus nitrite therapy (n = 5). Whole blood nitrite levels increased during drug infusion to 57.14 ± 10.82 μM at 11 min post-resuscitation time (1 min after dose completion) in the VF nitrite group vs. 0.94 ± 0.58 μM in the VF placebo group (p < 0.001). There was a significant difference between the treatment and placebo groups in nitrite levels in blood between 7.5 and 15 min after CPR start and between groups with respect to nitrite levels in CSF, brain, heart and liver. In a second series (n = 25 including 5 shams), 19 out of 20 animals survived until day 8. However, NDS, FCT and brain histology did not show any statistically significant difference between groups.ConclusionsNitrite, administered early after ROSC from VF, was shown to cross the blood brain barrier after a 5 min VF cardiac arrest. We characterized the PK of intravenous nitrite administration after VF and were able to demonstrate nitrite safety in this feasibility study.
| S-EPMC6957908 | biostudies-literature
Project description:BackgroundQuantitative measures of the ventricular fibrillation (VF) ECG waveform can assess myocardial physiology and predict cardiac arrest outcomes, making these measures a candidate to help guide resuscitation. Chest compressions are typically paused for waveform measure calculation because compressions cause ECG artifact. However, such pauses contradict resuscitation guideline recommendations to minimize cardiopulmonary resuscitation interruptions. We evaluated a comprehensive group of VF measures with and without ongoing compressions to determine their performance under both conditions for predicting functionally-intact survival, the study's primary outcome.MethodsFive-second VF ECG segments were collected with and without chest compressions before 2755 defibrillation shocks from 1151 out-of-hospital cardiac arrest patients. Twenty-four individual measures and 3 combination measures were implemented. Measures were optimized to predict functionally-intact survival (Cerebral Performance Category score ≤2) using 460 training cases, and their performance evaluated using 691 independent test cases.ResultsMeasures predicted functionally-intact survival on test data with an area under the receiver operating characteristic curve ranging from 0.56 to 0.75 (median, 0.73) without chest compressions and from 0.53 to 0.75 (median, 0.69) with compressions ( P<0.001 for difference). Of all measures evaluated, the support vector machine model ranked highest both without chest compressions (area under the receiver operating characteristic curve, 0.75; 95% CI, 0.73-0.78) and with compressions (area under the receiver operating characteristic curve, 0.75; 95% CI, 0.72-0.78; P=0.75 for difference).ConclusionsVF waveform measures predict functionally-intact survival when calculated during chest compressions, but prognostic performance is generally reduced compared with compression-free analysis. However, support vector machine models exhibited similar performance with and without compressions while also achieving the highest area under the receiver operating characteristic curve. Such machine learning models may, therefore, offer means to guide resuscitation during uninterrupted cardiopulmonary resuscitation.
| S-EPMC6532650 | biostudies-literature
Project description:AimVentricular fibrillation (VF) cardiac arrest may consist of three time-sensitive phases: electrical, circulatory, and metabolic. However, the time boundaries of these phases are unclear. We aimed to determine the time boundaries of the three-phase model for VF cardiac arrest.MethodsWe reviewed 20,741 out-of-hospital cardiac arrest cases with initial VF and presumed cardiac origin from the All-Japan Utstein-style registry between 2013 and 2017. The study endpoint was 1-month neurologically intact survival. The collapse-to-shock interval was defined as the time from collapse to the first shock delivery by emergency medical service personnel. The patients were divided into the bystander cardiopulmonary resuscitation (CPR, n = 11,606) and non-bystander CPR (n = 9135) groups.ResultsIn the bystander CPR group, the collapse-to-shock times that were associated with increased adjusted 1-month neurologically intact survival, compared with those in the non-bystander CPR group, ranged from 7 min (42.9% [244/4999] vs. 26.0% [119/458], adjusted odds ratio [aOR], 1.95; 95% confidence interval [CI], 1.44-2.63; P < 0.0001) to 17 min (17.1% [70/410] vs. 7.3% [21/288], aOR, 2.82; 95% CI, 1.62-4.91; P = 0.0002). However, the neurologically intact survival rate of the bystander CPR group was statistically insignificant compared with that of the non-bystander CPR group when the collapse-to-shock time was outside this range.ConclusionsThe time boundaries of the three-phase time-sensitive model for VF cardiac arrest may be defined as follows: electrical phase, from collapse to <7 min; circulatory phase, from 7 to 17 min; and metabolic phase, from >17 min onward.
| S-EPMC8244403 | biostudies-literature
Project description:BackgroundDiaphragmatic pacemakers are used to assist respiration in ventilator-dependent patients. Electromagnetic interference with intrinsic cardiac electrical activity is a theoretical risk but has never been reported in the literature. This case highlights a serious complication of cardiac arrest as a result of diaphragmatic pacing.Case summaryWe report a quadriplegic patient with recent diaphragmatic pacemaker implantation who presented with ventricular tachycardia leading to cardiac arrest. Extensive workup was negative for other aetiologies for ventricular arrhythmias. Reduction of the left-sided diaphragmatic pacemaker voltage resulted in cessation of ventricular ectopy.DiscussionDiaphragmatic pacing at high voltages can cause unwanted transmission of impulses to the cardiac myocytes as a rare complication. This should be noted as a possible complication of intramuscular diaphragmatic pacing, and efforts should be taken to circumvent this risk in the future.
| S-EPMC8440889 | biostudies-literature
Project description:AimWhile previous studies have shown that the initial documented rhythm is associated with clinical outcomes in out-of-hospital cardiac arrest (OHCA), little is known about the difference in clinical outcomes between pulseless ventricular tachycardia (p-VT) and ventricular fibrillation (VF).MethodsFrom a nationwide, prospective population-based database of OHCA from 2011 to 2015, we selected bystander-witnessed adult patients who were not treated with a public automated external defibrillator. The outcomes examined were favorable 30-day neurological survival rates, 30-day survival rates, and prehospital return of spontaneous circulation (ROSC) rates. To determine the association of the initial documented rhythm with outcome, we used a logistic regression model while adjusting for patient factors and prehospital care-related factors.ResultsA total of 19,594 bystander-witnessed OHCA patients who had a shockable rhythm were included: 454 (2.3%) were p-VT and 19,140 (97.7%) were VF. Compared to VF patients, p-VT patients were older, less likely to have a cardiogenic cause, and had shorter resuscitation-related time intervals (collapse to bystander cardiopulmonary resuscitation, collapse to emergency medical services contact, collapse to first ROSC, and first defibrillation to first ROSC). After adjustment for covariates, p-VT was associated with high favorable 30-day neurological survival rates (adjusted odds ratio [OR], 1.85; 95% confidence interval [CI], 1.30-2.64, p = 0.001), 30-day survival rates (adjusted OR, 1.41; 95% CI, 1.03-1.95, p = 0.037), and prehospital ROSC rates (adjusted OR, 1.90; 95% CI, 1.42-2.55, p < 0.001).ConclusionIn this study, patients with p-VT as the initial documented rhythm had significantly better outcomes than those with VF.
| S-EPMC8244523 | biostudies-literature
Project description:BackgroundAtrial fibrillation (AF) has been linked to an increased risk of ventricular arrhythmias (VAs) and sudden death. We investigated this association in hospitalised patients in France.MethodsAll hospitalised patients from 2013 were identified from the French National database and included if they had at least 5 years of follow-up data.ResultsOverall, 3,381,472 patients were identified. After excluding 35,834 with a history of VAs and cardiac arrest, 3,345,638 patients were categorised into two groups: no AF (n = 3,033,412; mean age 57.2 ± 21.4; 54.3% female) and AF (n = 312,226; 78.1 ± 10.6; 44.0% female). Over a median follow-up period of 5.4 years (interquartile range (IQR) 5.0-5.8 years), the incidence (2.23%/year vs. 0.56%/year) and risk (hazard ratio (HR) 3.657 (95% confidence interval (CI) 3.604-3.711)) of VAs and cardiac arrest were significantly higher in AF patients compared to non-AF patients. This was still significant after adjusting for confounders, with a HR of 1.167 (95% CI 1.111-1.226) and in the 1:1 propensity score-matched analysis (n = 289,332 per group), with a HR of 1.339 (95% CI 1.313-1.366). In the mediation analysis, the odds of cardiac arrest were significantly mediated by AF-associated VAs, with an OR of 1.041 (95% CI 1.040-1.042).ConclusionIn hospitalised French patients, AF was associated with an increased risk of VAs and sudden death.
| S-EPMC9917986 | biostudies-literature
Project description:The risk of having atrial fibrillation (AF) is associated with alcohol intake. However, it is not clear whether sudden cardiac arrest (SCA) and ventricular arrhythmia (VA) including ventricular tachycardia, flutter, or fibrillation have similar associations with alcohol. We aimed to evaluate the association of alcohol intake with all-cause death, new-onset AF, VA, and SCA using single cohort with a sufficient sample size. A total of 3,990,373 people without a prior history of AF, VAs, or SCA was enrolled in this study based on nationwide health check-up in 2009. We classified the participants into four groups according to weekly alcohol consumption, and evaluated the association of alcohol consumption with each outcome. We observed a significant association between mild (hazard ratio [HR] = 0.826; 95% confidence interval [CI] = 0.815-0.838) to moderate (HR = 0.930; 95% CI = 0.912-0.947) drinking with decreased risk of all-cause mortality. However heavy drinking (HR = 1.108; 95% CI = 1.087-1.129) was associated with increased all-cause death. The risk of new-onset AF was significantly associated with moderate (HR = 1.129; 95% CI = 1.097-1.161) and heavy (HR = 1.298; 95% CI = 1.261-1.337) drinking. However, the risk of SCA showed negative association with all degrees of alcohol intake: 20% (HR = 0.803; 95% CI = 0.769-0.839), 15% (HR = 0.853; 95% CI = 0.806-0.902), and 8% (HR = 0.918; 95% CI = 0.866-0.974) lower risk for mild, moderate, and heavy drinkers, respectively. Mild drinking was associated with reduced risk of VA with moderate and heavy drinking having no associations. In conclusion, the association between alcohol and various outcomes in this study were heterogeneous. Alcohol might have different influences on various cardiac disorders.
| S-EPMC10904378 | biostudies-literature
Project description:BackgroundEvidence of the association between AMplitude Spectral Area (AMSA) of ventricular fibrillation and outcome after out-of-hospital cardiac arrest (OHCA) is limited to short-term follow-up. In this study, we assess whether AMSA can stratify the risk of death or poor neurological outcome at 30 days and 1 year after OHCA in patients with an initial shockable rhythm or with an initial non-shockable rhythm converted to a shockable one.MethodsThis is a multicentre retrospective study of prospectively collected data in two European Utstein-based OHCA registries. We included all cases of OHCAs with at least one manual defibrillation. AMSA values were calculated after data extraction from the monitors/defibrillators used in the field by using a 2-s pre-shock electrocardiogram interval. The first detected AMSA value, the maximum value, the average value, and the minimum value were computed, and their outcome prediction accuracy was compared. Multivariable Cox regression models were run for both 30-day and 1-year deaths or poor neurological outcomes. Neurological cerebral performance category 1-2 was considered a good neurological outcome.ResultsOut of the 578 patients included, 494 (85%) died and 10 (2%) had a poor neurological outcome at 30 days. All the AMSA values considered (first value, maximum, average, and minimum) were significantly higher in survivors with good neurological outcome at 30 days. The average AMSA showed the highest area under the receiver operating characteristic curve (0.778, 95% CI: 0.7-0.8, p < 0.001). After correction for confounders, the highest tertiles of average AMSA (T3 and T2) were significantly associated with a lower risk of death or poor neurological outcome compared with T1 both at 30 days (T2: HR 0.6, 95% CI: 0.4-0.9, p = 0.01; T3: HR 0.6, 95% CI: 0.4-0.9, p = 0.02) and at 1 year (T2: HR 0.6, 95% CI: 0.4-0.9, p = 0.01; T3: HR 0.6, 95% CI: 0.4-0.9, p = 0.01). Among survivors at 30 days, a higher AMSA was associated with a lower risk of mortality or poor neurological outcome at 1 year (T3: HR 0.03, 95% CI: 0-0.3, p = 0.02).DiscussionLower AMSA values were significantly and independently associated with the risk of death or poor neurological outcome at 30 days and at 1 year in OHCA patients with either an initial shockable rhythm or a conversion rhythm from non-shockable to shockable. The average AMSA value had the strongest association with prognosis.
| S-EPMC10876863 | biostudies-literature
Project description:IntroductionDespite decades of improved strategy in conventional cardiopulmonary resuscitation (CCPR), survival rates of favorable neurological outcome after cardiac arrest (CA) remains poor. It is indicated that the survival rate of successful resuscitation of extracorporeal membrane oxygenation (ECMO) is superior to that of CCPR. But the effect of ECMO in heart is unclear. We aimed to investigate whether ECMO produces cardiac protection by ameliorating post-ischemia reperfusion myocardial injury and myocardial apoptosis.MethodsAfter undergoing 8-min untreated ventricle fibrillation (VF) and 6-min basic life support, 20 male pigs were ultimately used in this study and randomly divided into two groups: CCPR group (n = 10) and extracorporeal CPR (ECPR) group (n = 10). Hemodynamics and blood samples were obtained at baseline and 1, 2, 4, and 6 h during resuscitation. The successfully resuscitated pigs were sacrificed at 6 h after return of spontaneous circulation (ROSC), and the hearts were removed and analyzed under electron microscopy, and immunohistochemistry, quantitative real-time polymerase chain reaction, and immunofluorescence staining assay were performed to evaluate myocardial injury and myocardial apoptosis.ResultsThere were no significant differences at basic hemodynamic status between the two groups. The survival rate of ECPR was significantly higher than CCPR group (10/10 [100%] vs. 4/10 [40%], P = 0.04). Compared to CCPR group, ECPR group exhibited a better outcome in hemodynamic function. Cardiac function was significantly impaired after ROSC in both groups, but left ventricular ejection fraction (LVEF) was significantly elevated in ECPR group than CCPR group. The expression of myocardial injury biomarkers (CK-MB, cTNI, H-FABP), endothelial injury biomarker (sP-selectin), and cardiac function biomarker (BNP) were remarkably increased after ROSC in both groups, but low levels in ECPR group than in CCPR group. Cardiomyocytes injury was attenuated in ECPR group under transmission electron microscopy (TEM). Typical apoptotic nuclei of cardiomyocytes were significantly reduced and oxidative damage were attenuated in ECPR group.ConclusionsDuring prolonged VF-induced CA, ECPR contributes to improving hemodynamics, attenuating myocardial ischemia-reperfusion injury, ameliorating myocardial ultra structure, improving cardiac function, and elevating survival rate by preventing oxidative damage, regulating energy metabolism, inhibiting cardiomyocyte apoptosis.
| S-EPMC6714103 | biostudies-literature
Project description:BackgroundHypothermia has been shown to improve survival and neurological outcomes for ventricular fibrillation (VF) cardiac arrest. The electrophysiological mechanisms of hypothermia are not well-understood, nor are the effects of beginning cooling during the resuscitation.Methods and resultsWe hypothesized that inducing hypothermia prior to the onset of VF would slow the deleterious changes seen in the ECG during VF and that inducing hypothermia at the start of resuscitation would increase the rates of ROSC and short-term survival in a porcine model of prolonged VF. We randomly assigned 42 domestic swine (27.2+/-2.3 kg) to either pretreatment with hypothermia before induction of VF (PRE), normothermic resuscitation (NORM) or intra-resuscitation hypothermia (IRH). During anesthesia, animals were instrumented via femoral cutdown. Lead II ECG was recorded continuously. PRE animals were cooled before the induction of VF, with a rapid infusion of 4 degrees normal saline (30mL/kg). VF was induced electrically, left untreated for 8min, then mechanical CPR began. During CPR the NORM animals got 30mL/kg body-temperature saline and the IRH animals got 30mL/kg 4 degrees saline. In all groups first rescue shocks were delivered after 13min of VF. We calculated the VF scaling exponent (ScE) for the entire 8min period (compared using GEE). ROSC and survival were compared with Fisher's exact test. Mean temperature in degrees C at the onset of VF was PRE=34.7 degrees (+/-0.8), NORM=37.8 (+/-0.9), and IRH=37.9 (+/-0.9). The ScE values over time were significantly lower after 8min in the PRE group (p=0.02). ROSC: PRE=10/14 (71%), NORM=6/14 (43%) and IRH=12/14 (86%); p for IRH vs. NORM=0.02. Survival: PRE=9/14 (64%), NORM=5/14 (36%), IRH 8/14 (57%).ConclusionHypothermia slowed the decay of the ECG waveform during prolonged VF. IRH improved ROSC but not short-term survival compared to NORM. It is possible to rapidly induce mild hypothermia during CPR using an IV infusion of ice-cold saline.
| S-EPMC2720166 | biostudies-literature