Disease relevance of Heart Arrest

• Patients who had cardiac arrest with ventricular fibrillation (or pulseless ventricular tachycardia) and who had not been resuscitated after receiving three or more precordial shocks were randomly assigned to receive 300 mg of intravenous amiodarone (246 patients) or placebo (258 patients) [1].
• CONCLUSIONS: In patients with out-of-hospital cardiac arrest due to refractory ventricular arrhythmias, treatment with amiodarone resulted in a higher rate of survival to hospital admission [1].
• Hypotension and cardiac arrest in rats after infusion of mono(2-ethylhexyl) phthalate (MEHP), a contaminant of stored blood [2].
• Rapid, appropriate response to abnormal drug levels, to electrocardiographic signs of adverse drug effects, and to signs and symptoms of congestive heart failure or toxic effects from digoxin might decrease the incidence of cardiac arrest among hospitalized patients [3].
• MAIN RESULTS--For the 596 patients studied (median age, 67 years; 52% female), the primary cause of coma was cardiac arrest in 31% and cerebral infarction or intracerebral hemorrhage in 36% [4].

Psychiatry related information on Heart Arrest

• The time course of lactate appearance in ECF was found to be considerably slower than that observed in tissue following electroconvulsive shock or during ischemia following cardiac arrest [5].
• Labetalol does not lengthen asystole during electroconvulsive therapy [6].
• We report a patient with massive cocaine ingestion who developed psychomotor agitation and generalized seizures followed by asystolic cardiac arrest [7].
• PRIMARY OBJECTIVE: This paper examined the use of an atypical neuroleptic medication, risperidone, in reducing the excessive motor activity of an adolescent with an anoxic brain injury following cardiac arrest from a lightning strike [8].

High impact information on Heart Arrest

• Amiodarone in out-of-hospital cardiac arrest [9].
• Epinephrine for out-of-hospital cardiac arrest [10].
• METHODS: Patients who had cardiac arrest in the Paris metropolitan area or in Thionville, France, more than 80 percent of whom had asystole, were assigned to receive either standard CPR (377 patients) or active compression-decompression CPR (373 patients) according to whether their arrest occurred on an even or odd day of the month, respectively [11].
• High-dose epinephrine improved the rate of successful resuscitation in patients with asystole, but not in those with ventricular fibrillation [12].
• Both the dose of thiazide drugs and the addition of potassium-sparing drugs influence the risk of primary cardiac arrest [13].

Chemical compound and disease context of Heart Arrest

• High-dose epinephrine in adult cardiac arrest [14].
• Atropine and cardiac arrest [15].
• Lactate washout was therefore investigated in a porcine model of cardiac arrest due to electromechanical dissociation [16].
• Hypotension and cardiopulmonary arrest associated with concurrent haloperidol and propranolol therapy [17].
• We studied prospectively the neuropsychological sequelae of cardiac arrest and evaluated the effects of nimodipine on them [18].

Biological context of Heart Arrest

• Thomas' Hospital solution and Stanford solution and subsequently reperfused for 1 h at 35 degrees C. In other groups of hearts, basal oxygen consumption and rest intracellular calcium (Indo 1 technique) were evaluated during ethanol-, hexanol- and potassium-induced cardiac arrest [19].
• Proarrhythmia, cardiac arrest and death in young patients receiving encainide and flecainide. The Pediatric Electrophysiology Group [20].
• Two patients died after fibrinolysis (one of acute renal failure after cardiac tamponade and one of cardiac arrest after cerebral hemorrhage) and one patient in the heparin group died of recurrent pulmonary embolism [21].
• In 60 rats anesthetized with chloral hydrate and maintained at one of three body temperatures, we unilaterally ligated the left common carotid artery and placed electrodes in the striatum to measure impedance (reflecting the extracellular space) during hypoxia, recovery, and/or cardiac arrest [22].
• OBJECTIVE: To examine the utility of somatosensory evoked potential (SEP) peaks and CSF creatine kinase BB isoenzyme activity (CKBB) in predicting nonawakening from coma due to cardiac arrest [23].

Anatomical context of Heart Arrest

• Adequate oxygenation and, if this cannot be achieved, maintenance atropin should prevent the bradycardia and cardiac arrest associated with stimulation of the trachea in artificially ventilated tetraplegic patients [24].
• The relationship between cerebrospinal fluid creatine kinase and morphologic changes in the brain after transient cardiac arrest [25].
• In vivo studies further demonstrated an incapacity for male, but not female, 17-day-old rats to maintain reduced glutathione levels within cerebral cortex acutely after an 8-min asphyxial cardiac arrest [26].
• Reduced blood-brain barrier permeability after cardiac arrest by conjugated superoxide dismutase and catalase in piglets [27].
• Adenosine-induced transient cardiac asystole enhances precise deployment of stent-grafts in the thoracic or abdominal aorta [28].

Gene context of Heart Arrest

• OBJECTIVES: We investigated coagulation abnormalities in out-of-hospital cardiac arrest (OHCA) patients, with special attention to the protein C anticoagulant pathway [29].
• Hypothermic reperfusion after cardiac arrest augments brain-derived neurotrophic factor activation [30].
• We have examined the effect of global transient cerebral ischemia, evoked in rat by 10 min of cardiac arrest, upon the changes in the cellular expression of two nerve growth factor (NGF) receptors (TrkA and p75) in the hippocampus [31].
• Loss of parvalbumin immunoreactivity defines selectively vulnerable thalamic reticular nucleus neurons following cardiac arrest in the rat [32].
• Significance of elevated serum interleukin-8 in patients resuscitated after cardiopulmonary arrest [33].

Analytical, diagnostic and therapeutic context of Heart Arrest

• We randomly assigned 650 patients who had had cardiac arrest either in or outside the hospital to receive up to five doses of high-dose (7 mg) or standard-dose (1 mg) epinephrine at five-minute intervals according to standard protocols for advanced cardiac life support [14].
• BACKGROUND: Clinical trials have not shown a benefit of high doses of epinephrine in the management of cardiac arrest [12].
• METHODS: 40 patients in ventricular fibrillation resistant to electrical defibrillation were prospectively and randomly assigned epinephrine (1 mg intravenously; n = 20) or vasopressin (40 U intravenously; n = 20) as primary drug therapy for cardiac arrest [34].
• Potassium cardioplegia and the higher dose of nifedipine resulted in immediate asystole [35].
• A prospective randomized double-blind study comparing calcium chloride and saline controls in the Milwaukee Paramedic system for asystole and EMD using standard AHA protocols showed no statistically significant difference in resuscitation rates or long-term survival between the calcium and no-calcium groups for the rhythm of asystole [36].

References