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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although recent clinical reports have noted hypokalemia after resuscitation from cardiac arrest, extensive animal work indicates that potassium is released from cells during ischemia. This study was undertaken to define the changes that occur in serum potassium ion during cardiac arrest and resuscitation in a canine model. Fourteen dogs were subjected to 5 min of cardiac arrest followed by 30 min of closed-chest CPR (CCPR). Resuscitation was performed according to a standardized protocol. Serum potassium increased significantly (p less than .001) from baseline, remained elevated 5 min after return of spontaneous circulation (ROSC), but declined to baseline levels at 15 min post-ROSC. Increases in interstitial potassium would be expected to be even greater due to the poor exchange between interstitial and intravascular compartments during CCPR. Interstitial hyperkalemia may play a role in the genesis of wide-complex electromechanical dissociation and may explain the reported success of calcium chloride in treating this problem.
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PMID:Hyperkalemia during cardiac arrest and resuscitation in the canine model. 395 20

There is a type of cerebral lesion, which kills neuronal cells at a later stage (greater than 48 hrs) post CA, while the systemic circulation is functioning normally. Although this lesion is probably dependent on multiple factors (----multiple therapies), a keyfactor in the pathogenesis is the loss of autoregulation and "finetuning" of the cerebral bloodflow according to local tissue metabolic needs. Although beneficial effect of almost none of the following therapies has been documented in randomised clinical studies, the following suggestions are made: a) In the CA-CPR phase: efficient respiratory care and external cardiac compressions (ECC), especially during bicarbonate administration; consider open chest CPR early, especially in cases of long arrest time and ineffective ECC. The socalled new CPR does not improve neurological outcome. b) In the post CPR phase: The non-autoregulated brain (cfr. focal ischemia) is kept preferentially at pCO2 values 25-30 mmHg, pO2 values greater than 100 mmHg, and normotension. Some form of stress, seizure and hyperthermia control prevents further imbalance metabolism/bloodflow. Relative dehydration, oncotic balance, steroids, early control of sepsis and uremia, early CT scan and measurement/control of ICP. All the above is currently grouped under "standard neuro-intensive therapy". Some other therapies, presently suggested by animal research are not very obvious, need first randomised clinical studies and are not suggested at this stage for clinical use: barbiturate coma, diphantoine, streptokinase, multifaceted therapy including hemodilution-brainflushing, Ca++ influx blocking drugs (lidoflazine). One such "innovative" therapy, barbiturate coma, has already been proven to be relatively ineffective (BRCT I) (Acta anaesth. belg., 1984, 25, suppl., 219-226).
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PMID:Brain protection in the immediate post-resuscitation phase. 651 33

The cerebrovascular resistance (CVR) of rat, and its dependence on stagnant blood or endothelial capillary swelling, was studied after 10 min of total ischemia by 10 s single carotid infusion of [14C]butanol in saline. The regional saline flow (CPR) was calculated from the uptake of [14 C]butanol. CVR was estimated at infusion pressures ranging from 8--25 kPa (60--190 mm Hg). At 14.7 kPa (110 mm Hg) infusion pressure, the regional CVR of the non-ischemic group varied between 0.21 and 0.40 kPa 100 g min ml-1. After 10 min of complete global cerebral ischemia, it increased to values between 0.82 and 1.95. Removal of blood from the brain by rinsing prior to ischemia did not change the CVR in ischemia. Increasing the plasma osmolality by 8% with mannitol before ischemia attenuated the CVR increase in ischemia. Thus, although osmotic swelling of endothelial cells contributed, the main cause of the CVR increase in ischemia was constriction of arterioles.
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PMID:Cerebrovascular resistance in ischemia. 678 47

Since the 1985 Emergency Cardiac Care Conference, numerous controversies about the pharmacology of CPR have arisen (eg, questions about the pharmacokinetics and pharmacodynamics of drugs during CPR, the optimal vehicle for delivery of medications, and the dose of atropine in brady-asystolic cardiac arrest). This article has three objectives: 1) to critically explore these controversies, 2) to provide recommendations for clinical practice, and 3) to identify areas for future study. The ideal route is one which combines rapid access with quick delivery of drug to the central circulation. Because of hemodynamic changes during CPR, administration of drugs into the central circulation is preferable when compared with peripheral venous injection. Whenever drugs are administered from a peripheral i.v. site, the extremity should be elevated, and a 20-mL bolus of i.v. fluid should be given to facilitate access of the agent to the central circulation. If there is a delay in obtaining venous access, epinephrine, lidocaine, and atropine may be administered through the endotracheal tube at 2.5 times the i.v. dose. When administering these drugs through the endotracheal tube, dilute the drug in 10 mL of saline or water and inject it through a long catheter beyond the tip of the endotracheal tube. Dextrose 5% water is the primary vehicle for drug delivery during CPR. However, the administration of glucose during CPR is controversial because of the potentially detrimental effects of hyperglycemia on neuronal function during periods of ischemia. Data are inconclusive regarding the effects of glucose levels on neurologic outcome following resuscitation. Hyperglycemia may be a marker for prolonged resuscitation with subsequent impairment in insulin release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacologic controversies in CPR. 843 31

To improve emergency cardiac care (ECC) on the national or international level, we must translate to the rest of our communities the successes found in cities with high survival rates. In recent years, important developments have evolved in our understanding of the treatment and evaluation of cardiac arrest. Some of the most important of these developments include 1) recognition of the chain of survival, which is necessary to achieve high survival rates; 2) widespread acceptance that survival rates must be assessed routinely to ensure continuous quality improvements in the emergency medical services (EMS) system; and 3) development of improved methods for performing survival rate studies that will maximize the effectiveness of information gathering and analysis. While each community should determine how to optimize their own ECC services, some general guidelines are useful. Successful treatment of cardiac arrest starts in the community with prevention and education, including early recognition of the signs and symptoms of cardiovascular ischemia. Obtaining 911 service (and preferably enhanced 911) should be a top priority for all communities. EMS dispatchers should dispatch the unit to the scene in less than one minute, provide critical information to the responders regarding the type of emergency, and offer the caller telephone-assisted CPR instructions. The EMS first-responders should strive to arrive at the patient's side in less than four minutes, be able to immediately defibrillate if necessary, and begin basic CPR. An excellent strategy to accomplish this is to equip and train all fire-fighting units in the operation of automatic external defibrillators and dispatch them as a first-responder team. To manage the cardiac arrest patient, a minimum of two rescuers trained in advanced cardiac life support plus two or more rescuers trained in basic life support are needed. Furthermore, an EMS system is not complete without on-going evaluation. Therefore, the 1992 National Conference on CPR and ECC strongly endorses the position that all ECC systems assess their survival rates through an ongoing quality improvement process and that all members of the chain of providers should be represented in the outcome assessment team. We still have much to discover regarding optimal techniques of CPR, methods for data collection, and optimal structure of an EMS system. Research in these areas will provide the foundation for future changes in EMS systems development.
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PMID:Ensuring the effectiveness of community-wide emergency cardiac care. 843 34

In 1961, in Pittsburgh, PA, "cerebral" was added to the cardiopulmonary resuscitation system (CPR --> CPCR). Cerebral recovery is dependent on arrest and cardiopulmonary resuscitation times, and numerous factors related to basic, advanced, and prolonged life support. Postischemic-anoxic encephalopathy (the cerebral postresuscitation disease or syndrome) is complex and multifactorial. The prevention or mitigation of this syndrome requires that there be development and trials of special, multifaceted, combination treatments. The selection of therapies to mitigate the postresuscitation syndrome should continue to be based on mechanistic rationale. Therapy based on a single mechanism, however, is unlikely to be maximally effective. For logistic reasons, the limit for neurologic recovery after 5 mins of arrest must be extended to achieve functionally and histologically normal human brains after 10 to 20 mins of circulatory arrest. This goal has been approached, but not quite reached. Treatment effects on process variables give clues, but long-term outcome evaluation is needed for documentation of efficacy and to improve clinical results. Goals have crystallized for clinically relevant cardiac arrest-intensive care outcome models in large animals. These studies are expensive, but essential, because positive treatment effects cannot always be confirmed in the rat forebrain ischemia model. Except for a still-elusive breakthrough effect, randomized clinical trials of CPCR are limited in their ability to statistically document the effectiveness of treatments found to be beneficial in controlled outcome models in large animals. Clinical studies of feasibility, side effects, and acceptability are essential. Hypertensive reperfusion overcomes multifocal no-reflow and improves outcome. Physical combination treatments, such as mild resuscitative (early postarrest) hypothermia (34 degrees C) plus cerebral blood flow promotion (e.g., with hypertension, hemodilution, and normocapnia), each having multiple beneficial effects, achieved complete functional and near-complete histologic recovery of the dog brain after 11 mins of normothermic, ventricular fibrillation cardiac arrest. Calcium entry blockers appear promising as a treatment for postischemic-anoxic encephalopathy. However, the majority of single or multiple drug treatments explored so far have failed to improve neurologic outcome. Assembling and evaluating combination treatments in further animal studies and determining clinical feasibility inside and outside hospitals are challenges for the near future. Treatments without permanent beneficial effects may at least extend the therapeutic window. All of these investigations will require coordinated efforts by multiple research groups, pursuing systematic, multilevel research--from cell cultures to rats, to large animals, and to clinical trials. There are still many gaps in our knowledge about optimizing extracerebral life support for cerebral outcome.
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PMID:Cerebral resuscitation from cardiac arrest: treatment potentials. 860 8

We report two patients with out-of-hospital cardiac arrest who recovered after hypothermia therapy. A 25-year-old man and a 16-year-old boy were transferred to our hospital after cardiopulmonary arrest due to idiopathic ventricular fibrillation and hypertrophic cardiomyopathy, respectively. We carried out hypothermia therapy using cooling blankets, and the patients were maintained at 32-33 degrees C for 96 and 36 h, respectively. After slow rewarming, they regained consciousness and recovered. During hypothermia, hypokalemia and arrhythmia occurred. Their arrest times (no spontaneous circulation and no CPR) were 10 min and 8 min, and CPR times (no spontaneous circulation while CPR was being performed) were 24 min and 20 min, respectively. In cases where the duration of ischemia is prolonged, the prognosis is expected to be poor. Therefore, we believe that hypothermia therapy is beneficial for such patients.
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PMID:[Recovery from out-of-hospital cardiac arrest after mild hypothermia: report of two cases]. 969 97

Up to 10% of patients who arrive at the hospital with acute myocardial infarction (AMI) present with or develop cardiogenic shock. Some patients, despite inotropes and intra-aortic balloon pump (IABP) placement, are not hemodynamically stable enough to undergo emergent revascularization. The use of percutaneous extracorporeal life support (ECLS) can stabilize patients to allow effective therapy. In a retrospective review of the first 100 patients emergently placed on ECLS by a nurse-supported physician insertion technique at Sharp Memorial Hospital, 10 patients underwent placement of ECLS after out-of hospital AMI. All AMI patients required intubation for respiratory failure and temporary CPR for cardiovascular collapse before initiation of ECLS. Of the 10 AMI patients placed on ECLS, four (40%) are currently long-term survivors (5.1 +/- 4.2 years; range, 6 months to 11 years). All survivors underwent successful revascularization after placement on ECLS. The cause of death in the other six patients was neurologic insufficiency in two, ineffective ECLS in two, and recurrent cardiovascular collapse after weaning from bypass in two. Total CPR time before initiation of cardiopulmonary bypass was 17 +/- 10.3 minutes for the survivors and 54.2 +/-11.1 minutes for the nonsurvivors (p < 0.001). The average time on ECLS was 29 +/- 26 hours for the survivors and 30 +/-67 hours for the nonsurvivors (p = NS). Leg complications were common among long-term survivors, associated with the use of ECLS (three ischemia, one infection). After AMI and cardiovascular collapse, insertion of ECLS may permit long-term patient survival.
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PMID:Long-term survival with use of percutaneous extracorporeal life support in patients presenting with acute myocardial infarction and cardiovascular collapse. 1059 95

The objective of this research was to compare the effects of an alpha- and beta-adrenergic agonist, epinephrine, a selective alpha(2)-adrenergic agonist, alpha-methylnorepinephrine (alpha-MNE), and a non-adrenergic vasopressin on post-resuscitation myocardial function and duration of survival. Epinephrine continues to be the primary adrenergic agent for advanced cardiac life support. However, its major inotropic actions and especially its beta-adrenergic and, to a lesser extent, its alpha(1)-actions increase the severity of global ischemia during cardiac arrest and adversely affect post-resuscitation myocardial function and survival. We had previously observed significantly better outcomes with a selective alpha(2)-adrenergic agonist when compared with epinephrine. Non-adrenergic vasopressin also has promise of more favorable actions. The present study was, therefore, undertaken to compare a selective alpha(2)-adrenergic vasopressor drug with vasopressin, epinephrine, and saline placebo. Ventricular fibrillation (VF) was induced in 20 Sprague-Dawley rats. Mechanical ventilation and precordial compression were initiated after 8 min of untreated VF. About 2 min later, alpha-MNE in a dose of 100 microgram/kg, vasopressin in a dose of 0.4 U/kg, epinephrine in a dose of 30 microgram/kg, or saline control was administered. Defibrillation was attempted after 6 min of CPR. Left ventricular pressure, dP/dt(40), -dP/dt, and cardiac index were measured for an interval of 240 min after resuscitation. Except for saline controls, comparable increases in coronary perfusion pressure (CPP) were observed after each drug intervention. All animals were successfully resuscitated. Post-resuscitation myocardial function and survival were significantly better in animals treated with alpha-MNE. Both post-resuscitation myocardial function and survival were most improved after administration of the selective alpha(2)-adrenergic agonist, intermediate after vasopressin and least after epinephrine and saline placebo.
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PMID:A comparison of alpha-methylnorepinephrine, vasopressin and epinephrine for cardiac resuscitation. 1266 5

The hippocampus is highly sensitive to ischemia and is one of the most extensively damaged regions of brain during cardiac arrest. Damage to hippocampus can subsequently lead to learning and memory deficits. The current study used the Morris water maze to characterize spatial learning and memory deficits elicited by 8 min of cardiac arrest with cardiopulmonary resuscitation (CA/CPR) in mice, which is associated with a 25-50% decrease in CA1 neurons. Mice were trained to navigate the water maze prior to CA/CPR or sham surgery (SHAM). They were retested in the water maze on days 7 and 8 postsurgery; both CA/CPR and SHAM groups were able to perform the task at presurgical levels. However, when the hidden platform was moved to a new location, the SHAM mice were able to adapt more quickly to the change and swam a shorter distance in search of the platform than did CA/CPR mice. Thus, CA/CPR did not affect the ability of mice to retain a previously learned platform location, but it did affect their ability to learn a new platform location. This behavioural impairment was correlated with dendritic spine density in the CA1 region of the hippocampus. Data presented here suggest that morphological changes, such as spine density, that occur in neurons that survive CA/CPR may be associated with cognitive impairments.
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PMID:Cardiac arrest with cardiopulmonary resuscitation reduces dendritic spine density in CA1 pyramidal cells and selectively alters acquisition of spatial memory. 1538 8


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