Precision Cardiac Arrest Resuscitation Based on Etiology

The Contraction State of Myofibrils During Global Ischemia and After Reperfusion Following Different Forms of Cardiac Arrest: Correlation with Metabolic Parameters in the Canine Heart

Extracorporeal Cardiopulmonary Resuscitation: Prehospital or In-Hospital Cannulation?

THERE WAS A TIME NOT LONG AGO WHEN THE QUALity and quantity of chest compressions did not seem that important during resuscitation—at least not in comparison with early defibrillation. A ventricular tachyarrhythmia is the initiating event in more than 80% of patients who develop out-of-hospital, primary cardiac arrest during ambulatory electrocardiographic monitoring. Survival declines rapidly if defibrillation is not performed in the first few minutes (defibrillation phase) because myocardial adenosine triphosphate (ATP) levels begin to decrease as fibrillating myocardial cells continue to consume ATP at a nearly normal rate. As a result, ventricular fibrillation (VF) is the presenting rhythm in only 22% to 35% of out-of-hospital cardiac arrest cases when emergency medical services (EMS) personnel arrive on scene. By this time, myocardial ATP stores have often declined to critical levels and a defibrillation shock will usually terminate VF but frequently results in either asystole or pulseless electrical activity as cells run out of high-energy phosphate “fuel.” During this circulatory phase, a brief period of effective chest compression before defibrillation can boost myocardial ATP stores and increase the likelihood that a perfusing rhythm will follow defibrillation. Thus, the strategy for resuscitation from cardiac arrest has evolved from “shock first and often” to a time-critical, orchestrated approach of high-quality cardiopulmonary resuscitation (CPR), defibrillation, and postresuscitation care. This new approach highlights the importance of highquality, minimally interrupted chest compressions to maximize tissue oxygen delivery and intracellular high-energy phosphate levels. Conventional, closed-chest CPR is at best imperfect, producing hemodynamic change similar to that observed in cardiogenic shock. Minimal interruption of chest compression helps to maximize tissue oxygen delivery and, hence, myocardial high-energy phosphate levels. Aufderheide et al showed that both high-quality chest compression (adequate depth, force, and duration) and complete chest wall decompression are needed to maximize stroke volume and improve venous filling during the upstroke, respectively. The odds of survival from cardiac arrest increase when continuous, or nearly continuous, high-quality chest compressions are performed during resuscitation. Abella et al used a monitor/defibrillator with additional sensing capabilities to measure CPR quality (chest compression rate and depth, ventilation rate, and the fraction of cardiac arrest time without chest compressions) during resuscitation in 67 patients who experienced in-hospital cardiac arrest. The authors found that the quality of chest compression was inconsistent and often did not meet published guideline recommendations, even when performed by well-trained hospital staff. In a follow-up study, the same authors used a handheld recording device to measure chest compression rate as a surrogate for CPR quality in 3 different hospitals and found that higher chest compression rates correlated significantly with initial return of spontaneous circulation in 97 in-hospital patients with cardiac arrest. Thus, chest compression quantity and quality are critical determinants of survival from cardiac arrest. Positive pressure ventilation may not be necessary during the first few minutes of CPR because spontaneous agonal respirations often contribute to respiratory exchange of gases. Chest compression alone with a patent airway generates significant minute ventilation and the quantity of oxygen needed is reduced significantly during low blood flow states. Chandra et al assessed the time course of change in arterial blood gases during resuscitation in a canine experimental VF model and found that chest compression alone during CPR can maintain adequate gas exchange to sustain the oxygen saturation level above 90% for at least 4 minutes. Survival from out-of-hospital cardiac arrest is as good in humans when bystanders perform only chest compressions compared with when bystanders perform both chest compressions and mouth-to-mouth ventilation. In this issue of JAMA, Bobrow and colleagues provide an analysis based on a before and after comparison as well as a protocol compliance analysis of out-of-hospital

Cardiac mortality after stroke is common, and small studies have suggested an association of short-term cardiac mortality with insular location of cerebral infarction. Few population-based studies with long-term follow-up have evaluated the effect of stroke location on the long-term risk of cardiac death or myocardial infarction (MI) after first ischemic stroke. We sought to determine the association between stroke location and cardiac death or MI in a multiethnic community-based cohort. The Northern Manhattan Study is a population-based study designed to determine stroke incidence, risk factors, and prognosis in a multiethnic urban population. First ischemic stroke patients age 40 or older were prospectively followed up for cardiac death defined as fatal MI, fatal congestive heart failure, or sudden death/arrhythmia and for nonfatal MI. Primary brain anatomic site was determined by consensus of research neurologists. Hazard ratios (HRs) and 95% CIs were calculated by Cox proportional-hazards models and adjusted for vascular risk factors (age, sex, history of coronary disease, hypertension, diabetes, cholesterol, and smoking), stroke severity, infarct size, and stroke etiology. The study population consisted of 655 patients whose mean age was 69.7+/-12.7 years; 44.6% were men and 51.3% were Hispanic. During a median follow-up of 4.0 years, 44 patients (6.7%) had fatal cardiac events. Of these, fatal MI occurred in 38.6%, fatal congestive heart failure in 18.2%, and sudden death in 43.2%. In multivariate models, clinical diagnosis of left parietal lobe infarction was associated with cardiac death (adjusted HR=4.45; 95% CI, 1.83 to 10.83) and cardiac death or MI (adjusted HR=3.30; 95% CI, 1.45 to 7.51). When analysis of anatomic location was restricted to neuroimaging (computed tomography, magnetic resonance imaging, or both [n=447]), left parietal lobe infarction was associated with cardiac death (adjusted HR=3.37; 95% CI, 1.26 to 8.97), and both left (adjusted HR=3.49; 95% CI, 1.38 to 8.80) and right (adjusted HR=3.13; 95% CI, 1.04 to 9.45) parietal lobe infarctions were associated with cardiac death or MI. We did not find an association between frontal, temporal, or insular stroke and fatal cardiac events, although the number of purely insular strokes was small. Parietal lobe infarction is an independent predictor of long-term cardiac death or MI in this population. Further studies are needed to confirm whether parietal lobe infarction is an independent predictor of cardiac events and death. Surveillance for cardiac disease and implementation of cardioprotective therapies may reduce cardiac mortality in patients with parietal stroke.

The recommendations for electrical therapies described in this section are designed to improve survival from SCA and life-threatening arrhythmias. Whenever defibrillation is attempted, rescuers must coordinate high-quality CPR with defibrillation to minimize interruptions in chest compressions and to ensure immediate resumption of chest compressions after shock delivery. The high first-shock efficacy of newer biphasic defibrillators led to the recommendation of single shocks plus immediate CPR instead of 3-shock sequences that were recommended prior to 2005 to treat VF. Further data are needed to refine recommendations for energy levels for defibrillation and cardioversion using biphasic waveforms.

Children with cardiac disease are at a higher risk of cardiac arrest as compared to healthy children. Delivering adequate cardiopulmonary resuscitation (CPR) can be challenging due to anatomic characteristics, risk profiles, and physiologies. We aimed to review the physiological aspects of resuscitation in different cardiac physiologies, summarize the current recommendations, provide un update of current literature, and highlight knowledge gaps to guide research efforts. We specifically reviewed current knowledge on resuscitation strategies for high-risk categories of patients including patients with single-ventricle physiology, right-sided lesions, right ventricle restrictive physiology, left-sided lesions, myocarditis, cardiomyopathy, pulmonary arterial hypertension, and arrhythmias. Cardiac arrest occurs in about 1% of hospitalized children with cardiac disease, and in 5% of those admitted to an intensive care unit. Mortality after cardiac arrest in this population remains high, ranging from 30 to 65%. The neurologic outcome varies widely among studies, with a favorable neurologic outcome at discharge observed in 64%-95% of the survivors. Risk factors for cardiac arrest and associated mortality include younger age, lower weight, prematurity, genetic syndrome, single-ventricle physiology, arrhythmias, pulmonary arterial hypertension, comorbidities, mechanical ventilation preceding cardiac arrest, surgical complexity, higher vasoactive-inotropic score, and factors related to resources and institutional characteristics. Recent data suggest that Extracorporeal membrane oxygenation CPR (ECPR) may be a valid strategy in centers with expertise. Overall, knowledge on resuscitation strategies based on physiology remains limited, with a crucial need for further research in this field. Collaborative and interprofessional studies are highly needed to improve care and outcomes for this high-risk population. What is Known: • Children with cardiac disease are at high risk of cardiac arrest, and cardiopulmonary resuscitation may be challenging due to unique characteristics and different physiologies. • Mortality after cardiac arrest remains high and neurologic outcomes suboptimal. What is New: • We reviewed the unique resuscitation challenges, current knowledge, and recommendations for different cardiac physiologies. • We highlighted knowledge gaps to guide research efforts aimed to improve care and outcomes in this high-risk population.

Objectives: To compare the long term prognosis of patients having silent versus symptomatic ischaemia during dobutamine stress echocardiography (DSE). Design: Observational study. Setting: Tertiary referral centre. Patients: 931 patients who...

Biochemical markers of cerebral damage

Part 12.1: Cardiac Arrest Associated With AsthmaAsthma is responsible for more than 2 million visits to the emergency department (ED) in the United States each year, with 1 in 4 patients requiring admission to a hospital. 1Annually there are 5,000 to 6,000 asthma-related deaths in the United States, many occurring in the prehospital setting. 2 Severe asthma accounts for approximately 2% to 20% of admissions to intensive care units, with up to one third of these patients requiring intubation and mechanical ventilation. 3This section focuses on the evaluation and treatment of patients with near-fatal asthma.Several consensus groups have developed excellent guidelines for the management of asthma that are available on the World Wide Web

Therapeutic hypothermia (TH), which prevents and ameliorates the cascade of secondary neurologic injury after the return of spontaneous circulation, is the most effective neuroprotective therapy for encephalopathic survivors of cardiac arrest. Despite the compelling efficacy of TH, most patients who survive cardiac arrest long enough to be hospitalized will nonetheless suffer a poor neurologic outcome. Attention to the details of therapy and an integrated approach involving emergency medicine, neurology, cardiology, critical care medicine, and palliative care are likely to yield the best results. This effort is complex, and broad implementation of TH has been slow in the United States and Europe. Given that most cardiac arrest mortality in patients who survive long enough to be hospitalized is due to brain injury rather than circulatory collapse, neurologists should recognize their primary role as advocates for neuroprotective therapy at all stages of the evaluation. In the emergency department, hemodynamic stabilization must be achieved and a rapid neurologic and cardiac evaluation performed, with patients efficiently triaged to hypothermia and cardiac revascularization. Cardiologists should be aware that it is safe and desirable to induce TH, even when urgent coronary angiography and percutaneous revascularization procedures are required. In the intensive care unit, cerebral perfusion must be optimized, metabolic homeostasis achieved, and neuromonitoring used during the dangerous decooling phase. Cardiac arrest is always a life-altering event for patients and their families. Even after cardiac arrest survivors have been stabilized and treated, physicians must recogonize and embrace their role in facilitating a variety of difficult transitions: to organ donation, end-of-life care, nursing or rehabilitation placement, or home.

Background Among women the incidence of sudden cardiac death (SCD) is significant, but lower than in men. During the last decades the proportion of nonischemic SCD seems to have increased in both sexes. Coronary artery disease (CAD) have changed to be sickness of elderly women rather than middle-aged men as in women the prevalence and incidence of CAD starts to increase after the menopause. Purpose The aim of this study was to illustrate how the amount and the proportions of ischemic and nonischemic SCD vary between women and men in different age groups. Methods The Fingesture study has systematically collected clinical and autopsy data from SCD victims in Northern Finland between 1998 and 2017. The cohort consists of 5,869 SCD victims. Results Approximately one fifth of the SCD victims were women (21.1%; P<0.001). Three out of four SCDs were ischemic (74.8%; P<0.001) and majority of the ischemic SCD victims were men (79.8%; P=0.005). The mean age of female victims was 70.1±13.1 years and 63.5±11.8 years among male victims (P<0.001). Amongst women one SCD out of 15 occurred to the subject under 50 years of age (6.7%; P<0.001) whereas in men one SCD victim out of nine was under 50 years old (11.4%; P<0.001). A nonischemic SCD was observed in 350 women and in 1,127 men (P<0.001). The proportion of nonischemic death was higher among women than in men in every age group from under 30 years of age to subjects of 84 years old studied in five year periods (Figure 1). Only age group of 65-69 years in women and 60-64 years in men were not statistically significant, otherwise all the P-values were ≤0.003. The difference in proportion of ischemic and non-ischemic SCD was the smallest among subjects of 40-49 years of age amongst the proportion of ischemic SCD increased rapidly both in women and in men as the prevalence of non-ischemic SCD started to decrease (Figure 1). Amongst SCD victims aged 40-44 years 47.9% of the deaths of men (P<0.001) and 41.7% of the deaths of women (P<0.001) were ischemic etiology. Among women aged 50-54 years over half of the SCDs were ischemic (53.1%; P<0.001). The gender difference in proportion of ischemic SCD was actually the smallest in age groups 40-49 years and after 70 years of age, and its largest in the middle in favor of men. (Figure 1). After the age of 70 years the total amount of SCDs started to plateau in men and decrease in the amount of SCDs was seen in men after the age of 75 years as in women the plateau phase was not reached until the age of 80 years (Figure 2). Conclusion Minority of the SCDs occur under the age of 50 years, especially among women. The proportion of nonischemic SCD was higher in women than in men despite the age. However, already in pre- and perimenopausal age the proportion of ischemic SCD in women was remarkable and the amount of ischemic SCD increased until the age of 80 years emphasizing the need of early primary and secondary prevention of CAD also in women not only in men.Figure 1.Figure 2.

Despite the vagus nerve stimulator (VNS) being used in neuroscience, it has recently been highlighted that it has cardioprotective functions. However, many studies related to VNS are not mechanistic in nature. This systematic review aims to focus on the role of VNS in cardioprotective therapy, selective vagus nerve stimulators (sVNS), and their functional capabilities. A systemic review of the current literature was conducted on VNS, sVNS, and their ability to induce positive effects on arrhythmias, cardiac arrest, myocardial ischemia/reperfusion injury, and heart failure. Both experimental and clinical studies were reviewed and assessed separately. Of 522 research articles retrieved from literature archives, 35 met the inclusion criteria and were included in the review. Literature analysis proves that combining fiber-type selectivity with spatially-targeted vagus nerve stimulation is feasible. The role of VNS as a tool for modulating heart dynamics, inflammatory response, and structural cellular components was prominently seen across the literature. The application of transcutaneous VNS, as opposed to implanted electrodes, provides the best clinical outcome with minimal side effects. VNS presents a method for future cardiovascular treatment that can modulate human cardiac physiology. However, continued research is needed for further insight.

Part 6: Defibrillation

Local anesthetic (LA) intoxication with cardiovascular arrest is a potential fatal complication of regional anesthesia. Lipid resuscitation has been recommended for the treatment of LA-induced cardiac arrest. Aim of the study was to compare four different rescue regimens using epinephrine and/or lipid emulsion and vasopressin to treat cardiac arrest caused by bupivacaine intoxication. Twenty-eight piglets were randomized into four groups (4 × 7), anesthetized with sevoflurane, intubated, and ventilated. Bupivacaine was infused with a syringe driver via central venous catheter at a rate of 1 mg·kg(-1)·min(-1) until circulatory arrest. Bupivacaine infusion and sevoflurane were then stopped, chest compression was started, and the pigs were ventilated with 100% oxygen. After 1 min, epinephrine 10 μg·kg(-1) (group 1), Intralipid(®) 20% 4 ml·kg(-1) (group 2), epinephrine 10 μg·kg(-1) + Intralipid(®) 4 ml·kg(-1) (group 3) or 2 IU vasopressin + Intralipid(®) 4 ml·kg(-1) (group 4) were administered. Secondary epinephrine doses were given after 5 min if required. Survival was 71%, 29%, 86%, and 57% in groups 1, 2, 3, and 4. Return of spontaneous circulation was regained only by initial administration of epinephrine alone or in combination with Intralipid(®). Piglets receiving the combination therapy survived without further epinephrine support. In contrast, in groups 2 and 4, return of spontaneous circulation was only achieved after secondary epinephrine rescue. In cardiac arrest caused by bupivacaine intoxication, first-line rescue with epinephrine and epinephrine + Intralipid(®) was more effective with regard to survival than Intralipid(®) alone and vasopressin + Intralipid(®) in this pig model.

Rates of survival from out-of-hospital cardiac arrest (OHCA) have been notoriously poor (NEJM JW Gen Med Apr 16 1999). However, the past decade has seen a shift in resuscitative strategies, with increased emphasis on high-quality cardiopulmonary resuscitation, early defibrillation, and prevention of hyperthermia. Two large cohort studies, one from the U.S. (Cardiac Arrest Registry to Enhance …