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Query: KEGG:D01401 (CPR)
 1,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The empiric administration of 50% dextrose to all patients presenting to the ED with altered mental status is a standard of care predicated on the assumption that glucose administration is harmless to nonhypoglycemic patients. Considerable evidence now disputes this assumption. Glucose administration before complete cerebral ischemia in experimental animals worsens neurologic and histologic outcome. Administration of glucose during severe incomplete ischemia has a similar detrimental effect. The translation of these experimental findings into clinical practice has been slow, perhaps hindered by the frequent use of rodent models and large bolus doses of glucose. However, evidence is now provided by primate and human studies and by experimental designs using clinically relevant doses of glucose. These clinical and experimental findings in conjunction with the wide availability of a rapid bedside screen for hypoglycemia provide the rationale for an alteration in the standard of care. The empiric administration of glucose should be avoided in patients at risk of cerebral ischemia, such as those with acute stroke, impending cardiac arrest, or severe hypotension or receiving CPR. A bedside fingerstick blood glucose estimation should be performed immediately on all patients presenting with altered mental status. The administration of 50% dextrose should be reserved for those patients in whom hypoglycemia is demonstrated; this practice will uphold Hippocrates' most basic principle of clinical medicine, "The physician must...do no harm."
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PMID:50% dextrose: antidote or toxin? 212 May 1

The empiric administration of 50% dextrose to all patients presenting to the ED with altered mental status is a standard of care predicated on the assumption that glucose administration is harmless to non-hypoglycemic patients. Considerable evidence now disputes this assumption. Glucose administration before complete cerebral ischemia in experimental animals worsens neurologic and histologic outcome. Administration of glucose during severe incomplete ischemia has a similar detrimental effect. The translation of these experimental findings into clinical practice has been slow, perhaps hindered by the frequent use of rodent models and large bolus doses of glucose. However, evidence is now provided by primate and human studies and by experimental designs using clinically relevant doses of glucose. These clinical and experimental findings in conjunction with the wide availability of a rapid bedside screen for hypoglycemia provide the rationale for an alteration in the standard of care. The empiric administration of glucose should be avoided in patients at risk for cerebral ischemia, such as those with acute stroke, impending cardiac arrest, or severe hypotension or receiving CPR. A bedside fingerstick blood glucose estimation should be performed immediately on all patients presenting with altered mental status. The administration of 50% dextrose should be reserved for those patients in whom hypoglycemia is demonstrated; this practice will uphold Hippocrates' most basic principle of clinical medicine, "The physician must ... do no harm."
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PMID:50% dextrose: antidote or toxin? 218 38

Animal and human studies have suggested that higher doses of epinephrine than currently recommended may improve resuscitation rates after prolonged cardiac arrest. Because of our failure to resuscitate four patients with the standard American Heart Association protocol for cardiac arrest, we used a larger dose of epinephrine in an attempt to enhance resuscitative efforts. All patients required CPR and had nonperfusing rhythms for at least 20 minutes. The four patients received from 0.12 to 0.22 mg/kg epinephrine. Within five minutes of high-dose epinephrine, all four patients developed perfusing rhythms with maximum systolic blood pressures ranging from 134 to 220 mm Hg. Cardiac dysrhythmias did not occur after these doses of epinephrine. Only one of four patients had ECG evidence of an acute myocardial infarction. In this patient, the history suggested that the myocardial infarction was a primary event, not the consequence of epinephrine. All four patients sustained severe brain injury leading to their demise. This injury was probably due to prolonged cardiopulmonary arrest and global brain ischemia. Pharmacologic and potential pathophysiologic mechanisms of high-dose epinephrine are reviewed.
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PMID:Four case studies: high-dose epinephrine in cardiac arrest. 231 72

Neurologic impairment remains a serious consequence of cardiac arrest. While current investigations are difficult to compare due to their lack of standardization, our understanding of the pathophysiology of CNS ischemia has been greatly increased. Ion fluxes, especially K and Ca, may contribute to injury by initiating a cascade of events culminating in free fatty acid, prostaglandin, and free radical formation, with their related pathogenetic potential. Treatment measures currently consist of CPR (although disagreement exists as to which form of CPR), standard supportive measures, and attention to intracranial pressure control. There is some experimental evidence to support the use of calcium channel-blockers, phenytoin, prostaglandin inhibitors, and free-radical scavengers or inhibitors; however, no human trials have been performed. Steroids and barbiturates have been investigated in human trials and do not appear to be efficacious in ameliorating CNS injury after cardiac arrest.
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PMID:Cerebral function and preservation during cardiac arrest. 264 72

Effect of smoking habits on limb loss rates and cumulative patency rates of 136 arterial reconstructions performed for lower limb ischemia were analyzed in a five year follow-up retrospective study. Of 121 patients, 103 (85%) smoked before the operation and 43 of the smokers (42%) discontinued smoking postoperatively. Patients who continued to smoke more than 15 cigarettes per day (34 patients) increased the probability of losing their limb approximately five times at two years and three times at five years postoperatively, compared with nonsmokers and smokers of up to 15 cigarettes per day (87 patients) (p = 0.013). Cumulative patency rates of nonsmokers and smokers of up to five cigarettes per day (Group A, 66 patients) were not significantly influenced (p = 0.518) by preoperative symptoms (claudication versus limb salvage). However, for smokers of more than five cigarettes per day (Group B, 55 patients), at five years claudicants had a cumulative patency rate of 62.9% compared to 38.3% for limb salvage patients (p = 0.015). In group A at five years, autologous saphenous vein grafts had a cumulative patency rate of 74.2%, compared to 24% for prosthetic grafts (P = 0.013). In group B the CPR differences between autologous saphenous vein and prosthetic grafts were not significantly different (p = 0.394). Multiple interactions between smoking and variables like age, preoperative symptoms, and graft material demonstrate the complexity of the effects of smoking on cumulative patency rate and the need for sub-grouping and removal of confounding factors. In view of the adverse affects of continued smoking on postrevascularization prognosis, patients should be strongly advised to discontinue smoking.
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PMID:The effect of postoperative smoking on femoropopliteal bypass grafts. 271 28

Although hypokalemia has been reported after cardiac arrest and successful resuscitation, experimental data indicate that potassium is released from cells during ischemia. The purpose of this investigation was to study serum potassium concentration ([K+]) during closed chest cardiopulmonary resuscitation (CC-CPR) in humans. Twenty-two patients presenting to the emergency department (ED) in cardiopulmonary arrest had simultaneous measurement of central venous and arterial [K+] and blood gases during CC-CPR utilizing current advanced cardiac life support protocols and a pneumatic chest compressor and ventilator. Mean arterial and central venous [K+] were 5.0 +/- 1.3 and 5.6 +/- 2.9 mEq/L, respectively, (p greater than .05) with 7 patients having [K+] of greater than 6 mEq/L. Significant hyperkalemia does occur in some patients during cardiac arrest and CC-CPR. Because poor tissue perfusion during CC-CPR impairs exchange between the interstitial and intravascular compartments, increases in interstitial [K+] would be expected to be even greater. Interstitial hyperkalemia may play a role in the genesis of wide complex electromechanical dissociation (EMD) seen after prolonged cardiac arrest. Since calcium has long been known to be beneficial in the treatment of hyperkalemia-induced dysrhythmias, the success of calcium chloride in treating wide complex EMD may be on the basis of this phenomenon.
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PMID:Hyperkalemia during human cardiopulmonary resuscitation: incidence and ramifications. 278 2

Since its introduction in 1960, CPR has evolved into a complex program involving not only the medical community but also the lay public. Currently, program activities include instruction of the lay public in basic life support techniques, development and deployment of emergency medical systems, recommendations for drug protocols for advanced cardiac life support and, most recently, introduction of new methods for tissue protection following resuscitation. After 25 years of experience, we are beginning to understand the pathophysiology of tissue ischemia during cardiac arrest and the interventions required to improve chances of survival and quality of life of the cardiac arrest victim. Recent data in the literature suggest that modification of certain interventions in the resuscitation program may be needed. The poor neurologic outcomes with prolonged standard CPR show that it is not protective after 4 to 6 minutes of cardiac arrest. Modifications to this technique, including SVC-CPR or IAC-CPR, have not been shown to increase resuscitability or hospital discharge rates. Human studies of open-chest cardiac massage are needed to evaluate this option. Defibrillation is the definitive treatment for ventricular fibrillation. Greater emphasis should be placed on the earliest possible delivery of this treatment modality. Computerized defibrillators may provide greater and earlier access to defibrillation in the homes of patients at high risk of ventricular fibrillation. They may also be applicable by untrained public service personnel (police and firemen), individuals in geographically inaccessible areas (aircraft), or emergency medical technicians in rural areas where skill retention is a significant problem. Calcium has no proved benefit in cardiac resuscitation. There is biochemical evidence that it may be harmful in brain resuscitation. Its use in resuscitation should be discontinued. The dose of epinephrine currently advocated in the ACLS protocols may be inadequate to increase aortic diastolic pressure and coronary and cerebral perfusion pressures and thus aid resuscitation. Animal studies indicate that substantial increases in the current dosage are needed to achieve these effects. Human studies are needed to verify these results. A role for calcium antagonists in the treatment of postarrest encephalopathy has been demonstrated in animals and is currently undergoing clinical trials. Iron-dependent lipid peroxidative cell membrane injury may be important in the pathogenesis of postarrest encephalopathy. Animal studies suggest that the iron chelator deferoxamine may have a significant therapeutic role in the treatment of postarrest encephalopathy.
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PMID:Ischemia, resuscitation, and reperfusion: mechanisms of tissue injury and prospects for protection. 351 7

Cerebral neurons can tolerate at least 20 min of normothermic ischemic anoxia. Cerebral recovery from more than 5 min of cardiac arrest is hampered by complex secondary derangements of multiple organ systems after reperfusion. There is increasing support of our hypothesis that this "postresuscitation syndrome" includes the following: secondary cerebral perfusion failure, cerebral reoxygenation injury (cell-necrotizing cascades), and cerebral "intoxication" from derangements of extracerebral organs. To be optimal for the brain, CPR with optimal perfusion pressure must be started as promptly as possible. Significant though inconsistent mitigation of permanent brain damage after prolonged complete global brain ischemia has been achieved in animal outcome preparations with the use of the following treatments initiated at the start of reperfusion: brain-oriented extracerebral life support by protocol, intra-arterial hemodilution, hypertension, and artificial circulation, barbiturates, calcium-entry blockers, free-radical scavengers, and multifaceted treatments. We currently recommend treatment 1 for patient care and treatment 2 for clinical feasibility trials. Treatment 3, thiopental loading (starting 10 to 50 min after restoration of spontaneous circulation), was tested in a randomized clinical trial and was not shown to confer a statistically significant benefit. A calcium-entry blocker is under clinical investigation. Many other novel treatments appear promising but further animal studies are required. The complex multifactorial pathogenesis of postcardiac arrest encephalopathy requires systematic multicenter development of etiology-specific combination therapies.
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PMID:Cerebral resuscitation after cardiac arrest: a review. 353 60

Although in vitro studies have demonstrated functional recovery of neurons after prolonged ischemia, in vivo experience with patients resuscitated from cardiopulmonary arrest demonstrates much less cerebral resistance to global ischemia. The purpose of our investigation was to compare the effectiveness of femoro-femoral veno-arterial cardiopulmonary bypass (CPB) to standard cardiopulmonary resuscitation in the treatment of prolonged cardiopulmonary arrest. Ten mongrel dogs were electrically fibrillated and left in cardiopulmonary arrest without any therapy for 12 minutes. Subsequently, either CPB (n = 5) or CPR (n = 5) was initiated and resuscitation attempted according to a standardized protocol that included administration of the calcium channel blocker lidoflazine in an effort to optimize cerebral and myocardial recovery. If there was return of spontaneous circulation, the animal was managed in an intensive care setting with invasive hemodynamic monitoring and ventilatory support for up to nine hours. Neurologic function was graded using a standardized neurologic deficit scoring (NDS) system at 12 hours after insult and daily for one week or until death. Prearrest hemodynamic and metabolic parameters were comparable in both groups (P greater than .05). All CPB animals were resuscitated successfully and alive at 24 hours after insult as opposed to none in the CPR group (P less than .005). In addition, three of the CPB animals were neurologically normal at final grading with NDS scores of zero. The other two CPB animals had persistent severe neurologic impairment and a mean NDS score of 51%. Thus CPB is more effective than CPR in the treatment of prolonged cardiopulmonary arrest. The improved outcome probably results primarily from improvement in blood flow with CPB.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiopulmonary bypass vs CPR as treatment for prolonged canine cardiopulmonary arrest. 357 65

Controlled clinically relevant animal models are essential in the ongoing search for increasingly cost-effective methods to reverse clinical death. Acute (up to 12 h) and short-term (up to 24 h) experiments are useful for the study of dying mechanisms and restoration of spontaneous circulation. Although long-term models are difficult and expensive, they are essential to permit lesions to mature, treatments to take effect, secondary deterioration to be recognized, and survival and brain damage to be quantified and compared between treatment groups. The insults studied include temporary complete global head ischemia in monkeys, ventricular fibrillation cardiac arrest in dogs, asphyxial cardiac arrest in rats and dogs, and exsanguination arrest in dogs. Standard external CPR combined with advanced life support is less successful than open-chest CPR or emergency cardiopulmonary bypass after prolonged ventricular fibrillation. Postinsult monitoring of multiple organ systems can be used to explore the postresuscitation syndrome and evaluate novel treatment potentials. Outcome measurements include brain enzyme leakage into the cerebrospinal fluid, neurologic deficit scoring, overall performance categorization, incidence of secondary deterioration, and histopathologic damage scoring of brain and viscera.
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PMID:Long-term animal outcome models for cardiopulmonary-cerebral resuscitation research. 393 81


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