Is all ventricular fibrillation the same? A comparison of ischemically induced with electrically induced ventricular fibrillation in a porcine cardiac arrest and resuscitation model*

Niemann, James T.; Rosborough, John P.; Youngquist, Scott T.; Thomas, Jaime; Lewis, Roger J.

doi:10.1097/01.ccm.0000261882.47616.7d

Cited by 60 publications

(36 citation statements)

References 31 publications

(29 reference statements)

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“…The poor resuscitation rates observed in this experiment with shorter untreated ventricular fibrillation and CPR times than our previous work 23,35,36 can be explained by the severity of the model and the significant postresuscitation instability derived from the ischemic and very arrhythmogenic substrate in this animal model. 37,38 Our study has several limitations. It is not possible to say whether the effect of hypothermia on myocardial ischemic injury was due to the timing of or to differences in myocardial temperatures achieved during the experiments with different methods of hypothermia induction.…”

Section: Yannopoulos Et Al Intra-cpr Hypothermia and Myocardial Infarmentioning

confidence: 99%

Intra–Cardiopulmonary Resuscitation Hypothermia With and Without Volume Loading in an Ischemic Model of Cardiac Arrest

et al. 2009

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Background-We investigated the effects of intra-cardiopulmonary resuscitation (CPR) hypothermia with and without volume loading on return to spontaneous circulation and infarction size in an ischemic model of cardiac arrest. Methods and Results-Using a distal left anterior descending artery occlusion model of cardiac arrest followed by resuscitation with a total of 120 minutes of occlusion and 90 minutes of reperfusion, we randomized 46 pigs into 5 groups and used myocardial staining to define area at risk and myocardial necrosis. Group A had no intervention. Immediately after return of spontaneous circulation, group B received surface cooling with cooling blankets and ice. Group C received intra-CPR 680Ϯ23 mL of 28°C 0.9% normal saline via a central venous catheter. Group D received intra-CPR 673Ϯ26 mL of 4°C normal saline followed by surface cooling after return of spontaneous circulation. Group E received intra-CPR and hypothermia after return of spontaneous circulation with an endovascular therapeutic hypothermia system placed in the right atrium and set at a target of 32°C. Intra-CPR volume loading with room temperature (group C) or iced saline (group D) significantly (PϽ0.05) decreased coronary perfusion pressure (group C, 12.8Ϯ4.78 mm Hg; group D, 14.6Ϯ9.9 mm Hg) compared with groups A, B, and E (20.6Ϯ8.2, 20.1Ϯ7.8, and 21.3Ϯ12.4 mm Hg). Return of spontaneous circulation was significantly improved in group E (9 of 9) compared with groups A plus B and C (10 of 18 and 1 of 8). The percent infarction to the area at risk was significantly reduced with intra-CPR hypothermia in groups D (24.3Ϯ4.2%) and E (4Ϯ3.4%) compared with groups A (72Ϯ5.1%) and B (67.3Ϯ4.2%). Conclusions-Intra-CPR hypothermia significantly reduces myocardial infarction size.

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Section: Yannopoulos Et Al Intra-cpr Hypothermia and Myocardial Infarmentioning

confidence: 99%

Intra–Cardiopulmonary Resuscitation Hypothermia With and Without Volume Loading in an Ischemic Model of Cardiac Arrest

et al. 2009

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“…31,32 There was typically no mention (9 cases) of the failure of prompt defibrillation as indicating a nonelectric source for the cardiac arrest. 16,17 Almost all cases (11 of 12) ignored the critical dart-to-heart distance, which is well established in the literature for the induction of VF. 27 The unsupported implied inclusion criterion of any chest ECD exposure (regardless of the dart-to-heart distance) was surprising in view of the negative epidemiological association found between ECD chest exposures and mortality.…”

Section: Summary Of Resultsmentioning

confidence: 97%

“…16 With any chest compressions, defibrillation has a 90% success rate after 10 minutes of electrically induced VF with ≤3 shocks. 17 Hence, the failure of prompt defibrillation tends to exculpate an electric cause for VF.…”

Section: Confusing Electrically Induced Vf With Ischemically Induced Vfmentioning

confidence: 99%

TASER Electronic Control Devices and Cardiac Arrests: Coincidental or Causal?

et al. 2014

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Being arrested is a highly emotional event and can result in a fatal, adrenergically supercharged physiological state. 1 The exertion of arrest-related struggle is several-fold greater than that seen with normal exercise and leads to numerous extreme metabolic and electrolytic derangements, including elevated levels of lactate, CO 2 , potassium, creatine kinase, and myoglobin.2 Only 1.6% of US law-enforcement interactions involve the use or threats of force, and annually there are ≈700 000 cases in which force is used or threatened.3 There are ≈700 arrest-related deaths per year in the United States, yielding a mortality rate of ≈1 in 1000 for a law-enforcement interaction associated with force. 4 Response by Zipes on p 100The electronic control device (ECD) has gained widespread acceptance as the force option for law enforcement because of its dramatic reduction in both suspect and officer injury. At the same time, advocacy groups post statements on the Internet listing the hundreds of arrest-related deaths after ECD use with the implication that the ECD involvement was causal. Studies covering a total of >48 000 forceful arrests have consistently found suspect injury rate reductions of ≈65%.5,6 Of the 250 000 annual ECD field uses in the United States, only 1 in 4000 is involved in an arrest-related death. This reduction in fatality rate is consistent with published data showing that 5.4% of ECD uses "clearly prevented the use of lethal force by police." 7Of the >3 million total ECD applications, there have been 12 published case reports suggesting a potential cardiac arrest link, giving an incidence of 4×10 −6 per application. [8][9][10][11][12][13] In most cases, those authors did not consider important factors that are now better understood. These include separating postural from cardiovascular collapse, the latency of electrically induced ventricular fibrillation (VF), the presence of significant cardiac pathology, failure of prompt defibrillation, the duration of documented breathing, the distance of the ECD electrode from the heart, and the stability of electrically induced VF. We have thoroughly investigated these cases as either TASER scientific advisors or expert witnesses. The goal of this article is to resolve the confusion about these cases by introducing more complete data and by using a consistent case-report scoring methodology. Methods Understanding the Confounders Postural Versus Cardiovascular CollapseIn the normal course of life, an exertional postural collapse is, correctly, often associated with a cardiac arrest. However, it is sometimes forgotten that the ECD design goal is to cause a postural collapse to stop aggression. A sternal rub response is often blunted by the presence of alcohol, illegal drugs, psychotic break, and endorphins from the struggle. Hence, nonresponsiveness is also more difficult to evaluate in the law-enforcement scenario.(Circulation. 2014;129:93-100)

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“…Poor collateralization influenced the CPR-generated regional myocardial blood flow, and possibly the resuscitation rate and degree of postresuscitation myocardial dysfunction [173,174]. A model of ischemically induced VF followed by standard resuscitative interventions would have replicated more closely the conditions of patients with out-of-hospital cardiac arrest resuscitation [174] than the method of electrically induced VF. The hemodynamic response to exogenously administered arginine vasopressin may be different in humans because the vasopressin receptors in pigs (lysine vasopressin) and humans (arginine vasopressin) are different [175].…”

Section: The Experimental Model Of Cprmentioning

confidence: 99%

“…Second, the swine myocardium is poorly collateralized compared to the myocardium of patients with chronic obstructive coronary artery disease, who are likely to demonstrate collateralization [172,173]. Poor collateralization influenced the CPR-generated regional myocardial blood flow, and possibly the resuscitation rate and degree of postresuscitation myocardial dysfunction [173,174]. A model of ischemically induced VF followed by standard resuscitative interventions would have replicated more closely the conditions of patients with out-of-hospital cardiac arrest resuscitation [174] than the method of electrically induced VF.…”

Section: The Experimental Model Of Cprmentioning

confidence: 99%

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

Miclescu¹

2010

Acta Anaesthesiol Scand

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Although survival rates are increasing, brain injury continues to be a leading cause of death after cardiac arrest (CA). Permanent brain damage after CA is determined by limited tolerance to ischemia from CA and cardiopulmonary resuscitation (CPR), as well as the unique cerebral response to reperfusion after return of spontaneous circulation (ROSC). A major pathway leading to neurotoxic cascade and neuronal injury after CA involves the increased presence of reactive oxygen and nitrogen species generated during ischemia and reperfusion. The magnitude of cerebral oxidative injury induced by free radicals increased with the duration of CA (Paper I). Nitric oxide (NO), a free radical responsible for the formation of reactive nitrogen species, is increased during global ischemia from CA and reperfusion (Paper IV). Hypothetically, the administration of a drug that counteracts the overproduction of NO and also acts as a scavenger of oxygen free radicals might be warranted in order to reduce the damage caused by nitrosative and oxidative stress. For these purposes we used methylene blue (MB), an old dye that has been used in medicine for almost half a century, and an experimental pig model of 20 min of ventricular fibrillation (VF) to reflect a clinical scenario of ischemia/reperfusion injury. Administration of MB added to a hypertonic-hyperoncotic solution (MBHSD) that was started during CPR and continued for 50 min after ROSC increased short-term survival by decreasing myocardial damage, as well as cerebral peroxidation and inflammatory injury (Paper II). Immunostaining of cerebral tissue collected at different time points after CA and ROSC (Paper IV) provided experimental evidence that cortical blood-brain barrier (BBB) disruption begins as early as during the initial phase of untreated as well as treated CA. The results indicated that MB administration reduced the neurologic injury and BBB disruption considerably, but did not reverse the ongoing detrimental processes. The demonstrated positive effects of MB were related to a decrease of nitrite/nitrate tissue content, and thus to a decrease of excess NO due to the MB inhibitory effects on NOS isoforms. A mixture of MB in hypertonic sodium lactate (MBL) was investigated to facilitate administration of MB in "the field." Based on findings that MBL cardio-and neuroprotective properties were similar to those of MBHSD, there is reason to believe that the use of MBL might be extended during ongoing CPR and after ROSC (Paper III). It would therefore make sense to try using MB as a pharmacological neuroprotectant during or after clinical CPR in order to expand the temporal therapeutic window before other measures for neuroprotection such as hypothermia are available. Keywords: Cardiac arrest, cardiopulmonary resuscitation, reperfusion injury, methylene blue, nitric oxide, nitric oxide synthases, blood-brain barrier

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Is all ventricular fibrillation the same? A comparison of ischemically induced with electrically induced ventricular fibrillation in a porcine cardiac arrest and resuscitation model*

Cited by 60 publications

References 31 publications

Intra–Cardiopulmonary Resuscitation Hypothermia With and Without Volume Loading in an Ischemic Model of Cardiac Arrest

Intra–Cardiopulmonary Resuscitation Hypothermia With and Without Volume Loading in an Ischemic Model of Cardiac Arrest

TASER Electronic Control Devices and Cardiac Arrests: Coincidental or Causal?

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

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