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Effect of methylene blue on the genomic response to reperfusion injury induced by cardiac arrest and cardiopulmonary resuscitation in porcine brain
Cécile Martijn, Lars Wiklund
BMC Medical Genomics , 2010, DOI: 10.1186/1755-8794-3-27
Abstract: Pigs underwent either untreated cardiac arrest (CA) or CA with subsequent cardiopulmonary resuscitation (CPR) accompanied with an infusion of saline or an infusion of saline with MB. Genome-wide transcriptional profiling using the Affymetrix porcine microarray was performed to 1) gain understanding of delayed neuronal death initiation in porcine brain during ischemia and after 30, 60 and 180 min following reperfusion, and 2) identify the mechanisms behind the neuroprotective effect of MB after ischemic injury (at 30, 60 and 180 min).Our results show that restoration of spontaneous circulation (ROSC) induces major transcriptional changes related to stress response, inflammation, apoptosis and even cytoprotection. In contrast, the untreated ischemic and anoxic insult affected only few genes mainly involved in intra-/extracellular ionic balance. Furthermore, our data show that the neuroprotective role of MB is diverse and fulfilled by regulation of the expression of soluble guanylate cyclase and biological processes accountable for inhibition of apoptosis, modulation of stress response, neurogenesis and neuroprotection.Our results support that MB could be a valuable intervention and should be investigated as a therapeutic agent against neural damage associated with I/R injury induced by cardiac arrest.Despite recent advances in out-of-hospital cardiac arrest (CA) resuscitation, hypoxic-ischemic brain damage still causes considerable mortality and morbidity. Of the patients who survive to discharge, only 20% or fewer will have good neurologic function at the end of 1 year [1] After successful CPR and restoration of spontaneous circulation (ROSC) neuronal death initiated by ischemia during CA is increased also during reperfusion leading to secondary postischemic-anoxic encephalopathy [2], part of the so-called postresuscitation syndrome [3,4]. Cerebral recovery is dependent on duration of arrest and cardiopulmonary resuscitation (CPR), and numerous factors related to bas
CARDIAC ARREST
LIAQUAT ALI
The Professional Medical Journal , 2006,
Abstract: We present hereby a case report of 65 years old female scheduled for laparotomy for excision ofhydatid cyst liver diagnosed on ultrasonography and CT scan, but on laparotomy unexpectedly it turned out to bepheochromocytoma right adrenal and was further complicated by rupture of tumour, avulsion of inferior vena cava,massive haemorrhage, leading to cardiac arrest. Detailed in this report is the management of unexpectedpheochromocytoma, treatment of acute severe haemorrhage with massive transfusion and resuscitation and revivalof patient from cardiac arrest with CPR.
Does anesthetic provide similar neuroprotection to therapeutic hypothermia after cardiac arrest?
Hong Zhang
Critical Care , 2010, DOI: 10.1186/cc8923
Abstract: Therapeutic hypothermia has been shown to provide neuroprotection against ischemic injury after cardiac arrest in in vitro and in vivo models. In the previous issue of Critical Care, Meybohm and colleagues [1] demonstrate that cardiac arrest triggers the release of cerebral inflammatory cytokines in pigs' cerebral cortex. Therapeutic hypothermia alters inflammatory response in cardiac arrest and subsequent cardiopulmonary resuscitation. The combination of hypothermia with sevoflurane post-conditioning does not confer additional anti-inflammatory effects compared with hypothermia alone.Cardiac arrest remains the leading cause of death in the US and Europe, with an out-of-hospital cardiac arrest survival-to-discharge rate of less than 10%. In-hospital cardiac arrest presents a dismal prognosis. According to a large in-hospital registry, the survival-to-discharge rate is 18%, whereas that of a developing country is 6.9% [2,3]. Without prompt care, the chance for meaningful survival falls dramatically within minutes of arrest onset. When immediate care is available and victims are successfully resuscitated, the majority of these initial survivors subsequently suffer crippling neurologic injury or die in the few days following the cardiac arrest event. Thus, improving survival and brain function after initial resuscitation from cardiac arrest remains a critical challenge. Therapeutic hypothermia, introduced more than six decades ago, remains an important neuroprotective factor in cardiac arrest. Laboratory studies have demonstrated that cooling after resuscitation from cardiac arrest improves both survival as well as subsequent neurologic and cardiac function and has few side effects. these findings have been reproduced using a variety of cooling techniques in different species, including rats, dogs, and pigs.However, physician use of hypothermia induction in patients resuscitated from cardiac arrest is low. In 2003, Abella and colleagues [4] reported that 87% of US phys
Hypothermia and pediatric cardiac arrest  [cached]
Schlunt Michelle,Wang Lynn
Journal of Emergencies, Trauma and Shock , 2010,
Abstract: The survival outcome following pediatric cardiac arrest still remains poor. Survival to hospital discharge ranges anywhere from 0 to 38% when considering both out-of-hospital and in-hospital arrests, with up to 50% of the survivors having neurologic injury. The use of mild induced hypothermia has not been definitively proven to improve outcomes following pediatric cardiac arrest. This may be due to the lack of consensus regarding target temperature, best method of cooling, optimal duration of cooling and identifying the patient population who will receive the greatest benefit. We review the current applications of induced hypothermia in pediatric patients following cardiac arrest after searching the current literature through Pubmed and Ovid journal databases. We put forth compiled recommendations/guidelines for initiating hypothermia therapy, its maintenance, associated monitoring and suggested adjunctive therapies to produce favorable neurologic and survival outcomes.
Cardiac arrest in children  [cached]
Tress Erika,Kochanek Patrick,Saladino Richard,Manole Mioara
Journal of Emergencies, Trauma and Shock , 2010,
Abstract: Major advances in the field of pediatric cardiac arrest (CA) were made during the last decade, starting with the publication of pediatric Utstein guidelines, the 2005 recommendations by the International Liaison Committee on Resuscitation, and culminating in multicenter collaborations. The epidemiology and pathophysiology of in-hospital and out-of-hospital CA are now well described. Four phases of CA are described and the term "post-cardiac arrest syndrome" has been proposed, along with treatment goals for each of its four phases: immediate post-arrest, early post-arrest, intermediate and recovery phase. Hypothermia is recommended to be considered as a therapy for post-CA syndrome in comatose patients after CA, and large multicenter prospective studies are underway. We reviewed landmark articles related to pediatric CA published during the last decade. We present the current knowledge of epidemiology, pathophysiology and treatment of CA relevant to pre-hospital and acute care health practitioners.
Cardiac arrest and pregnancy  [cached]
Campbell Tabitha,Sanson Tracy
Journal of Emergencies, Trauma and Shock , 2009,
Abstract: Cardiopulmonary arrest in pregnancy is rare occurring in 1 in 30,000 pregnancies. When it does occur, it is important for a clinician to be familiar with the features peculiar to the pregnant state. Knowledge of the anatomic and physiologic changes of pregnancy is helpful in the treatment and diagnosis. Although the main focus should be on the mother, it should not be forgotten that there is another potential life at stake. Resuscitation of the mother is performed in the same manner as in any other patient, except for a few minor adjustments because of the changes of pregnancy. The specialties of obstetrics and neonatology should be involved early in the process to ensure appropriate treatment of both mother and the newborn. This article will explore the changes that occur in pregnancy and their impact on treatment. The common causes of maternal cardiac arrest will be discussed briefly.
Therapeutic hypothermia and neurological outcome after cardiac arrest  [PDF]
Petrovi? Milovan,Pani? Gordana,Joveli? Aleksandra,?anji Tibor
Vojnosanitetski Pregled , 2011, DOI: 10.2298/vsp1106495p
Abstract: Introduction/Aim. The most important clinically relevant cause of global cerebral ischemia is cardiac arrest. Clinical studies showed a marked neuroprotective effect of mild hypothermia in resuscitation. The aim of this study was to evaluate the impact of mild hypothermia on neurological outcome and survival of the patients in coma, after cardiac arrest and return of spontaneous circulation. Methods. The prospective study was conducted on consecutive comatose patients admitted to our clinic after cardiac arrest and return of spontaneous circulation, between February 2005 and May 2009. The patients were divided into two groups: the patients treated with mild hypothermia and the patients treated conservatively. The intravascular in combination with external method of cooling or only external cooling was used during the first 24 hours, after which spontaneous rewarming started. The endpoints were survival rate and neurological outcome. The neurological outcome was observed with Cerebral Performance Category Scale (CPC). Follow-up was 30 days. Results. The study was conducted on 82 patients: 45 patients (age 57.93 ± 14.08 years, 77.8% male) were treated with hypothermia, and 37 patients (age 62.00 ± 9.60 years, 67.6% male) were treated conservatively. In the group treated with therapeutic hypothermia protocol, 21 (46.7%) patients had full neurological restitution (CPC 1), 3 (6.7%) patients had good neurologic outcome (CPC 2), 1 (2.2%) patient remained in coma and 20 (44.4%) patients finally died (CPC 5). In the normothermic group 7 (18.9%) patients had full neurological restitution (CPC 1), and 30 (81.1%) patients remained in coma and finally died (CPC 5). Between the two therapeutic groups there was statistically significant difference in frequencies of different neurologic outcome (p = 0.006), specially between the patients with CPC 1 and CPC 5 outcome (p = 0.003). In the group treated with mild hypothermia 23 (51.1%) patients survived, and in the normothermic group 30 (81.1%) patients died, while in the group of survived patients 23 (76.7%) were treated with mild hypothermia (p = 0.003). Conclusion. Mild therapeutic hypothermia applied after cardiac arrest improved neurological outcome and reduced mortality in the studied group of comatose survivors.
Metoclopramide-induced cardiac arrest  [cached]
Martha M. Rumore,Spencer Evan Lee,Steven Wang,Brenna Farmer
Clinics and Practice , 2011, DOI: 10.4081/cp.2011.e83
Abstract: The authors report a case of cardiac arrest in a patient receiving intravenous (IV) metoclopramide and review the pertinent literature. A 62-year-old morbidly obese female admitted for a gastric sleeve procedure, developed cardiac arrest within one minute of receiving metoclopramide 10 mg via slow intravenous (IV) injection. Bradycardia at 4 beats/min immediately appeared, progressing rapidly to asystole. Chest compressions restored vital function. Electrocardiogram (ECG) revealed ST depression indicative of myocardial injury. Following intubation, the patient was transferred to the intensive care unit. Various cardiac dysrrhythmias including supraventricular tachycardia (SVT) associated with hypertension and atrial fibrillation occurred. Following IV esmolol and metoprolol, the patient reverted to normal sinus rhythm. Repeat ECGs revealed ST depression resolution without pre-admission changes. Metoclopramide is a non-specific dopamine receptor antagonist. Seven cases of cardiac arrest and one of sinus arrest with metoclopramide were found in the literature. The metoclopramide prescribing information does not list precautions or adverse drug reactions (ADRs) related to cardiac arrest. The reaction is not dose related but may relate to the IV administration route. Coronary artery disease was the sole risk factor identified. According to Naranjo, the association was possible. Other reports of cardiac arrest, severe bradycardia, and SVT were reviewed. In one case, five separate IV doses of 10 mg metoclopramide were immediately followed by asystole repeatedly. The mechanism(s) underlying metoclopramide’s cardiac arrest-inducing effects is unknown. Structural similarities to procainamide may play a role. In view of eight previous cases of cardiac arrest from metoclopramide having been reported, further elucidation of this ADR and patient monitoring is needed. Our report should alert clinicians to monitor patients and remain diligent in surveillance and reporting of bradydysrrhythmias and cardiac arrest in patients receiving metoclopramide.
Cardiac Arrest during Gamete Release in Chum Salmon Regulated by the Parasympathetic Nerve System  [PDF]
Yuya Makiguchi, Shinya Nagata, Takahito Kojima, Masaki Ichimura, Yoshifumi Konno, Hideki Murata, Hiroshi Ueda
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005993
Abstract: Cardiac arrest caused by startling stimuli, such as visual and vibration stimuli, has been reported in some animals and could be considered as an extraordinary case of bradycardia and defined as reversible missed heart beats. Variability of the heart rate is established as a balance between an autonomic system, namely cholinergic vagus inhibition, and excitatory adrenergic stimulation of neural and hormonal action in teleost. However, the cardiac arrest and its regulating nervous mechanism remain poorly understood. We show, by using electrocardiogram (ECG) data loggers, that cardiac arrest occurs in chum salmon (Oncorhynchus keta) at the moment of gamete release for 7.39±1.61 s in females and for 5.20±0.97 s in males. The increase in heart rate during spawning behavior relative to the background rate during the resting period suggests that cardiac arrest is a characteristic physiological phenomenon of the extraordinarily high heart rate during spawning behavior. The ECG morphological analysis showed a peaked and tall T-wave adjacent to the cardiac arrest, indicating an increase in potassium permeability in cardiac muscle cells, which would function to retard the cardiac action potential. Pharmacological studies showed that the cardiac arrest was abolished by injection of atropine, a muscarinic receptor antagonist, revealing that the cardiac arrest is a reflex response of the parasympathetic nerve system, although injection of sotalol, a β-adrenergic antagonist, did not affect the cardiac arrest. We conclude that cardiac arrest during gamete release in spawning release in spawning chum salmon is a physiological reflex response controlled by the parasympathetic nervous system. This cardiac arrest represents a response to the gaping behavior that occurs at the moment of gamete release.
The Use of Bedside Ultrasound in Cardiac Arrest  [cached]
Shoenberger, Jan M,Massopust, Kristy,Henderson, Sean O
Western Journal of Emergency Medicine : Integrating Emergency Care with Population Health , 2007,
Abstract: BACKGROUND: The decision to terminate resuscitative measures in the setting of cardiac arrest is based on several criteria, some of which are subjective. Ultrasound in the emergency department has potentially added an objective data point to assist in this decision. OBJECTIVE: We sought to determine if emergency physicians who were trained in the use of ultrasound use it in cardiac arrest scenarios and if so, what effect they believe it has on the duration of the resuscitative event. Our hypothesis was that emergency physicians terminate resuscitative efforts sooner with visualization of cardiac standstill and feel more comfortable in doing so. METHODS: The ultrasound training program at Los Angeles County + University of Southern California Medical Center began in 1995. We surveyed all graduates of the residency program since that date about their use of ultrasound in cardiac arrest. RESULTS: Surveys were mailed to 154 practicing emergency physicians. One hundred and sixteen surveys (75%) surveys were returned. During residency, the majority of individuals (68%) reported that they had used ultrasound during at least 10 cardiac arrests. It was used to search for a reversible cause of cardiac arrest (pericardial effusion) or for documentation of cardiac standstill. Ninety-one percent of individuals used the ultrasound result as an aid in deciding when to terminate resuscitative efforts and 59% believed it shortened their resuscitation time. After graduation, only 53% of individuals in this study have ultrasound available in their daily clinical practice. For these individuals, 60% use it in more than 50% of their cardiac arrest situations. Ultrasound was used to shorten the code time (63%) as well as to reassure and confirm the presence of cardiac standstill for the physician (88%) and the resuscitation team (59%). CONCLUSION: Most emergency physicians in this cohort who have access to ultrasound use it in cardiac arrest cases and believe that it shortens code times.
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