Cerebral Resuscitation Research Articles

From control of airway and breathing to cardiopulmonary-cerebral resuscitation. 1958.

Background: For respiratory resuscitation without devices, the author hypothesized that providing upper airway patency requires lifting the base of the tongue off the posterior pharyngeal wall and that artificial ventilation with intermittent positive pressure using exhaled air, i.e., direct mouth-to-mouth ventilation (MMV), is more effective than back or chest pressure with or without arm lift. MMV leaves the operator's hands free for backward tilt of the head, forward displacement of the mandible, or both. Methods: The author studied 25 sedated, nonintubated adult human volunteers under neuromuscular blockade with succinylcholine for 1-3 h each. One hundred sixty-seven untrained lay persons performed various direct MMV methods after one demonstration. Eighteen trained ambulance rescuers performed back or chest pressure arm-lift methods. Ventilation volumes were recorded during MMV from a calibrated pneumograph and during the manual methods from a taped face mask on a spirometer. Arterial oxygen saturation was monitored by an ear oximeter, and end-tidal carbon dioxide was measured by an infrared analyzer. Results: With the head in the mid position or flexed, airway obstruction occurred in all volunteers, equally in the supine or prone position. With the head tilted backward and the mouth held open, one half to two thirds of the volunteers had an open airway; the remaining volunteers required additional forward displacement of the mandible or a pharyngeal tube. Ninety percent of the lay persons performed MMV effectively. Moderate hyperventilation by the operator achieved normoxemia and normocapnia in the volunteer and moderate hypocapnia in the operator. Apnea-induced moderate hypoxemia was reversed with 5-9 MMVs. In the majority of volunteers, the manual methods caused no ventilation (mostly because of neck flexion), and in others, it caused progressive airway obstruction. In some volunteers, there was valve-like nasopharyngeal obstruction. Conclusions: In coma without a tracheal tube, direct MMV is effective because of the ability of the rescuer to support the head and jaw for upper airway patency and because of controllable high inflation pressures and volumes, whereas manual methods frequently fail to ventilate, mainly because of upper airway obstruction. The author recommends that backward tilt of the head plus exhaled air inflation methods be taught for general use in adults and children.

Vladimir A. Negovsky the father of ‘reanimatology’

Vladimir A. Negovsky of Moscow (Figs. 1 and 2) created the science of resuscitation medicine [1,2]. This he calls ‘reanimatology’ [3], which includes the prevention and treatment of critical terminal states and post-resuscitation disease. This term makes more sense than our terms ‘resuscitation’ and ‘intensive care’ for two reasons: First, it focuses on ‘anima’ the mind or spirit, indicating that resuscitation efforts must aim for survival without brain damage. Secondly it focuses on science (‘--ology’) while our terms mean methods. Americans, however, may think of ‘anima'as animation for Disney movies. A compromise would be to equate ‘critical care medicine’ (CCM) with ‘resuscitology’ [4] and to identify CPR as methods of basic, advanced, and prolonged life support, i.e. ‘cardiopulmonary–cerebral resuscitation’ (CPCR) [5].

Brain energetics of cardiopulmonary cerebral resuscitation.

Recovery of normal brain energetic conditions during and after resuscitation from cardiac arrest is critical for survival and good neurologic outcome. This review emphasizes the glucose-driven metabolic processes during and after ischemia and on the post-resuscitation development of secondary energy derangements. It also explores some potential therapeutic interventions designed to attenuate these energy derangements. The article summarizes some bench research and is not intended to provide treatment strategies for clinical application.

Perioperative Stroke Prevention

The definitions of commonly used terms are given in Table 1 (1–8). Stroke has been simply defined as any form of cerebral infarction (2), which includes those attributable to hemorrhage. The latter group is more likely to occur as a complication of specific surgical procedures (e.g., carotid endarterectomy) or the use of anticoagulants and is otherwise rare in the perioperative period (3). Hence, much of the information in this review pertains to ischemic cerebral events.

Post-resuscitation therapies

This chapter provides a review of recent developments in pathophysiology and treatment of post-resuscitation disease. The emphasis is on those organs that are most affected by cardiac arrest, namely the heart and the brain. Post-resuscitation ventricular dysrhythmias and heart failure, and post-resuscitation myocardial dysfunction, are the leading causes of the high post-resuscitation mortality rate. The mechanisms, including the effects of defibrillation and epinephrine, are discussed and new effective therapeutic options for improving outcomes are defined. Although post-resuscitation neurological dysfunction is complex and multifactorial, both controversial and well-known mechanisms are described. Novel cerebral resuscitation measures, especially brain cooling, are fully presented with the awareness that they are somewhat difficult to apply in clinical practice.

Cardiopulmonary cerebral resuscitation using emergency cardiopulmonary bypass, coronary reperfusion therapy and mild hypothermia in patients with cardiac arrest outside the hospital

OBJECTIVESThe purpose of this study was to evaluate the efficacy of an alternative cardiopulmonary cerebral resuscitation (CPCR) using emergency cardiopulmonary bypass (CPB), coronary reperfusion therapy and mild hypothermia.BACKGROUNDGood recovery of patients with out-of-hospital cardiac arrest is still inadequate. An alternative therapeutic method for patients who do not respond to conventional CPCR is required.METHODSA prospective preliminary study was performed in 50 patients with out-of-hospital cardiac arrest meeting the inclusion criteria. Patients were treated with standard CPCR and, if there was no response, by emergency CPB plus intra-aortic balloon pumping. Immediate coronary angiography for coronary reperfusion therapy was performed in patients with suspected acute coronary syndrome. Subsequently, in patients with systolic blood pressure above 90 mm Hg and Glasgow coma scale score of 3 to 5, mild hypothermia (34°C for at least two days) was induced by coil cooling. Neurologic outcome was assessed by cerebral performance categories at hospital discharge.RESULTSThirty-six of the 50 patients were treated with emergency CPB, and 30 of 39 patients who underwent angiography suffered acute coronary artery occlusion. Return of spontaneous circulation and successful coronary reperfusion were achieved in 92% and 87%, respectively. Mild hypothermia could be induced in 23 patients, and 12 (52%) of them showed good recovery. Factors related to a good recovery were cardiac index in hypothermia and the presence of serious complications with hypothermia or CPB.CONCLUSIONSThe alternative CPCR demonstrated an improvement in the incidence of good recovery. Based upon these findings, randomized studies of this hypothermia are needed.

Part 8: Advanced Challenges in Resuscitation

Part 8: Advanced Challenges in Resuscitation

Part 6: Advanced Cardiovascular Life Support

Part 6: Advanced Cardiovascular Life Support

Thiopental combination treatments for cerebral resuscitation after prolonged cardiac arrest in dogs. Exploratory outcome study

We postulate that mitigating the multifactorial pathogenesis of postischemic encephalopathy requires multifaceted treatments. In preparation for expensive definitive studies, we are reporting here the results of small exploratory series, compared with historic controls with the same model. We hypothesized that the brain damage mitigating effect of mild hypothermia after cardiac arrest can be enhanced with thiopental loading, and even more so with the further addition of phenytoin and methylprednisolone. Twenty-four dogs (four groups of six dogs each) received VF 12.5 min no-flow, reversed with brief cardiopulmonary bypass (CPB), controlled ventilation to 20 h, and intensive care to 96 h. Group 1 with normothermia throughout and randomized group 2 with mild hypothermia (from reperfusion to 2 h) were controls. Then, group 3 received in addition, thiopental 90 mg/kg i.v. over the first 6 h. Then, group 4 received, in addition to group 2 treatment, thiopental 30 mg/kg i.v. over the first 90 min (because the larger dose had produced cardiopulmonary complications), plus phenytoin 15 mg/kg i.v. at 15 min after reperfusion, and methylprednisolone 130 mg/kg i.v. over 20 h. All dogs survived. Best overall performance categories (OPC) achieved (OPC 1=normal, OPC 5=brain death) were better in group 2 than group 1 (<0.05) and numerically better in groups 3 or 4 than in groups 1 or 2. Good cerebral outcome (OPC 1 or 2) was achieved by all six dogs only in group 4 ( P<0.05 group 4 vs. 2). Best NDS were 44±3% in group 1; 20±14% in group 2 ( P=0.002); 21±15% in group 3 (NS vs. group 2); and 7±8% in group 4 ( P=0.08 vs. group 2). Total brain histologic damage scores (HDS) at 96 h were 156±38 in group 1; 81±12 in group 2 ( P<0.001 vs. group 1); 53±25 in group 3 ( P=0.02 vs. group 2); and 48±5 in group 4 ( P=0.02 vs. group 2). We conclude that after prolonged cardiac arrest, the already established brain damage mitigating effect of mild immediate postarrest hypothermia might be enhanced by thiopental, and perhaps then further enhanced by adding phenytoin and methylprednisolone.

Adenosine by aortic flush fails to augment the brain preservation effect of mild hypothermia during exsanguination cardiac arrest in dogs — an exploratory study

Most trauma cases with rapid exsanguination to cardiac arrest (CA) in the field, as well as many cases of normovolemic sudden cardiac death are ‘unresuscitable’ by standard cardiopulmonary–cerebral resuscitation (CPCR). We are presenting a dog model for exploring pharmacological strategies for the rapid induction by aortic arch flush of suspended animation (SA), i.e. preservation of cerebral viability for 15 min or longer. This can be extended by profound hypothermic circulatory arrest of at least 60 min, induced and reversed with (portable) cardiopulmonary bypass (CPB). SA is meant to buy time for transport and repair during pulselessness, to be followed by delayed resuscitation to survival without brain damage. This model with exsanguination over 5 min to CA of 15-min no-flow, is to evaluate rapid SA induction by aortic flush of normal saline solution (NSS) at room temperature (24°C) at 2-min no-flow. This previously achieved normal functional recovery, but with histologic brain damage. We hypothesized that the addition of adenosine would achieve recovery with no histologic damage, because adenosine delays energy failure and helps repair brain injury. This dog model included reversal of 15-min no-flow with closed-chest CPB, controlled ventilation to 20 h, and intensive care to 72 h. Outcome was evaluated by overall performance, neurologic deficit, and brain histologic damage. At 2 min of CA, 500 ml of NSS at 24°C was flushed (over 1 min) into the brain and heart via an aortic balloon catheter. Controls ( n=5) received no drug. The adenosine group ( n=5) received 2-chloro-adenosine (long acting adenosine analogue), 30 mg in the flush solution, and, after reperfusion, adenosine i.v. over 12 h (210 μg/kg per min for 3 h, 140 μg/kg per min for 9 h). The 24°C flush reduced tympanic membrane temperature ( T ty) within 2 min of CA from 37.5 to ≈36.0°C in both groups. At 72 h, final overall performance category (OPC) 1 (normal) was achieved by all ten dogs of the two groups. Final neurologic deficit scores (NDS; 0–10% normal, 100% brain death) were 5±3% in the control group versus 6±5% in the adenosine group (NS). Total brain histologic damage scores (HDS) at 72 h were 74±9 (64–80) in the control group versus 68±19 (40–88) in the adenosine group (NS). In both groups, ischemic neurons were as prevalent in the basal ganglia and neocortex as in the cerebellum and hippocampus. The mild hypothermic aortic flush protocol is feasible in dogs. The adenosine strategy used does not abolish the mild histologic brain damage.

On the future of reanimatology.

This article is adapted from a presentation given at the 1999 SAEM annual meeting by Dr. Peter Safar. Dr. Safar has been involved in resuscitation research for 44 years, and is a distinguished professor and past initiating chairman of the Department of Anesthesiology and Critical Care Medicine at the University of Pittsburgh. He is the founder and director of the Safar Center for Resuscitation Research at the University of Pittsburgh, and has been the research mentor of many critical care and emergency medicine research fellows. Here he presents a brief history of past accomplishments, recent findings, and future potentials for resuscitation research. Additional advances in resuscitation, from acute terminal states and clinical death, will build upon the lessons learned from the history of reanimatology, including optimal delivery by emergency medical services of already documented cardiopulmonary cerebral resuscitation, basic-advanced-prolonged life support, and future scientific breakthroughs. Current controversies, such as how to best educate the public in life-supporting first aid, how to restore normotensive spontaneous circulation after cardiac arrest, how to rapidly induce mild hypothermia for cerebral protection, and how to minimize secondary insult after cerebral ischemia, are discussed, and must be resolved if advances are to be made. Dr. Safar also summarizes future technologies already under preliminary investigation, such as ultra-advanced life support for reversing prolonged cardiac arrest, extending the "golden hour" of shock tolerance, and suspended animation for delayed resuscitation.

Effect of arrest time and cerebral perfusion pressure during cardiopulmonary resuscitation on cerebral blood flow, metabolism, adenosine triphosphate recovery, and pH in dogs.

To test the hypothesis that greater cerebral perfusion pressure (CPP) is required to restore cerebral blood flow (CBF), oxygen metabolism, adenosine triphosphate (ATP), and intracellular pH (pHi) levels after variable periods of no-flow than to maintain them when cardiopulmonary resuscitation (CPR) is started immediately. Prospective, randomized, comparison of three arrest times and two perfusion pressures during CPR in 24 anesthetized dogs. University cerebral resuscitation laboratory. We used radiolabeled microspheres to determine CBF and magnetic resonance spectroscopy to derive ATP and pHi levels before and during CPR. Ventricular fibrillation was induced, epinephrine administered, and thoracic vest CPR adjusted to provide a CPP of 25 or 35 mm Hg after arrest times of O, 6, or 12 mins. When CPR was started immediately after arrest with a CPP of 25 mm Hg, CBF and ATP were 57 +/- 10% and 64 +/- 14% of prearrest (at 10 mins of CPR). In contrast, CBF and ATP were minimally restored with a CPP at 25 mm Hg after a 6-min arrest time (23 +/- 5%, 16 +/- 5%, respectively). With a CPP of 35 mm Hg, extending the no-flow arrest time from 6 to 12 mins reduced reflow from 71 +/- 11% to 37 +/- 7% of pre-arrest and reduced ATP recovery from 60 +/- 11% to 2 +/- 1% of pre-arrest. After 6- or 12-min arrest times, brainstem blood flow was restored more than supratentorial blood flow, but cerebral pHi was never restored. A CPP of 25 mm Hg maintains supratentorial blood flow and ATP at 60% to 70% when CPR starts immediately on arrest, but not after a 6-min delay. A higher CPP of 35 mm Hg is required to restore CBF and ATP when CPR is delayed for 6 mins. After a 12-min delay, even the CPP of 35 mm Hg is unable to restore CBF and ATP. Therefore, increasing the arrest time at these perfusion pressures increases the resistance to reflow sufficient to impair restoration of cerebral ATP.

Cerebral protection and resuscitation in the liver transplant recipient.

Liver Transplantation and SurgeryVolume 5, Issue 4 p. 351-352 ProceedingsFree Access Cerebral protection and resuscitation in the liver transplant recipient David J. Plevak, Corresponding Author David J. Plevak Department of Anesthesiology, Mayo Clinic, Rochester, MNAddress reprint requests to David J. Plevak, MD, Department of Anesthesiology, Mayo Clinic, 200 First St SW, Rochester, MN 55905Search for more papers by this author David J. Plevak, Corresponding Author David J. Plevak Department of Anesthesiology, Mayo Clinic, Rochester, MNAddress reprint requests to David J. Plevak, MD, Department of Anesthesiology, Mayo Clinic, 200 First St SW, Rochester, MN 55905Search for more papers by this author First published: 30 December 2003 https://doi.org/10.1002/lt.500050415AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat References 1 Rehncrona S, Rosén I, Siesjö BK. Brain lactic acidosis and ischemic cell damage: 1. Biochemistry and neurophysiology. J Cereb Blood Flow Metab 1981; 1: 297– 311. MEDLINE 2 Staub F, Baethmann A, Peters J, Weigt H, Kempski O. Effects of lactacidosis on glial cell volume and viability. J Cereb Blood Flow Metab 1990; 10: 866– 876. MEDLINE 3 Freeman B, Crapo J. Biology of disease: Free radicals and tissue injury. Lab Invest 1982; 47: 412– 426. MEDLINE 4 Donovan JP, Schafer DF, Shaw BW, Sorrell MF. Cerebral oedema and increased intracranial pressure in chronic liver disease. Lancet 1998; 351: 719– 721. MEDLINE 5 Hindfelt B, Plum F, Duffy TE. Effect of acute ammonia intoxication on cerebral metabolism in rats with portacaval shunts. J Clin Invest 1977; 59: 386– 396. MEDLINE 6 Aggarwal S, Kramer D, Yonas H, Obrist W, Kang Y, Martin M, Policare R. Cerebral hemodynamic and metabolic changes in fulminant hepatic failure: A retrospective study. Hepatology 1994; 19: 80– 87. MEDLINE 7 Strauss G, Hansen BA, Kirkegaard P, Rasmussen A, Hjortrup A, Larsen FS. Liver function, cerebral blood flow autoregulation, and hepatic encephalopathy in fulminant hepatic failure. Hepatology 1997; 25: 837– 839. MEDLINE 8 Livingstone AS, Potvin M, Goresky CA, Finlayson MH, Hinchey EJ. Changes in the blood-brain barrier in hepatic coma after hepatectomy in the rat. Gastroenterology 1977; 73: 697– 704. MEDLINE 9 Lidofsky SD, Bass NM, Prager MC, Washington DE, Read AE, Wright TL, et al. Intracranial pressure monitoring and liver transplantation for fulminant hepatic failure. Hepatology 1992; 16: 1– 7. MEDLINE 10 Ridenour TR, Warner DS, Todd MM, et al. Comparative effects of propofol and halothane on outcome from temporary middle cerebral artery occlusion in the rat. Anesthesiology 1992; 76: 807– 812. MEDLINE Volume5, Issue4July 1999Pages 351-352 ReferencesRelatedInformation

Cardiopulmonary cerebral resuscitation--present and future perspectives.

Acta Anaesthesiologica ScandinavicaVolume 43, Issue 5 p. 526-535 Cardiopulmonary cerebral resuscitation – present and future perspectives S. Rubertsson, S. Rubertsson Department of Anesthesiology and Intensive Care, Uppsala University Hospital, Uppsala, SwedenSearch for more papers by this author S. Rubertsson, S. Rubertsson Department of Anesthesiology and Intensive Care, Uppsala University Hospital, Uppsala, SwedenSearch for more papers by this author First published: 19 January 2002 https://doi.org/10.1034/j.1399-6576.1999.430507.xCitations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume43, Issue5May 1999Pages 526-535 RelatedInformation

Twelfth Annual Meeting of the Society for Pediatric Anesthesia, Orlando, Florida, October 16, 1998

Twelfth Annual Meeting of the Society for Pediatric Anesthesia, Orlando, Florida, October 16, 1998

Cardiopulmonary resuscitation: update, controversies and new advances.

Cardiopulmonary arrest is a medical emergency in which the lapse of time between event onset and the initiation of measures of basic and advanced support, as well as the correct care based on specific protocols for each clinical situation, constitute decisive factors for a successful therapy. Cardiopulmonary arrest care cannot be restricted to the hospital setting because of its fulminant nature. This necessitates the creation of new concepts, strategies and structures, such as the concept of life chain, cardiopulmonary resuscitation courses for professionals who work in emergency medical services, the automated external defibrillator, the implantable cardioverter-defibrillator, and mobile intensive care units, among others. New concepts, strategies and structures motivated by new advances have also modified the treatment and improved the results of cardiopulmonary resuscitation in the hospital setting. Among them, we can cite the concept of cerebral resuscitation, the application of the life chain, the creation of the universal life support algorithm, the adjust-ment of drug doses, new techniques--measure of the end-tidal carbon dioxide levels and of the coronary perfusion pressure--and new drugs under research.

著明な脳腫脹によりＣＴ上くも膜下出血が疑われた１例

A 68-year-old man who had suffered from interferon encephalopathy was admitted to our hospital due to cardiopulmonary arrest (CPA) resulting from suffocation. Immediately after recovery of spontaneous circulation, a head CT demonstrated no causative lesions in the brain. On the fifth hospital day during hypothermic cerebral resuscitation, the patient manifested dilated fixed pupils. The second head CT revealed marked brain swelling and high density regions on the falx, tent and subarachnoid space. He died on the seventh hospital day, when an autopsy showed an absence of subarachnoid hemorrhage and vascular thrombosis. We discuss here the me chanism of a high density region on the head CT after whole-brain ischemia and emphasize the importance of a head CT examination for CPA patients to evaluate the situation.

Theoretical calculation of maximum attainable benefit of public access defibrillation in Belgium

Objective: Assuming that a lay person performing cardiopulmonary resuscitation (CPR) will also use an automatic external defibrillator (AED) wherever available, we tried to estimate the maximal attainable benefit of public access defibrillation in some centres in Belgium. Methods: We analysed retrospectively the data from the Belgian Cardio Pulmonary Cerebral Resuscitation Registry collected between 1991 and June 1996. The majority of these emergency medical service (EMS) systems are two-tiered with an early defibrillation program for the first tier and a physician-staffed second tier. Results: The data show that, in 5543 registered cases, there were 1001 (18%) adults with non-traumatic ventricular fibrillation/ventricular tachycardia (VF/VT) as the first monitored rhythm. In this subgroup there were 419 (42%) cases who had lay CPR. The duration of lay CPR before the first defibrillation either by the first or the second tier is known in 357 cases. This duration was more than 5 min and 10 min, in 80% and 53% of the cases, respectively. The median (Q 1, Q 3) lay CPR duration was 11 (7, 15) min. Survival to hospital discharge in this subgroup was achieved in 80/357 (22%) patients. Using Weaver's linear model for survival after witnessed VF/VT, an estimated increase of more than 30% in survival rate was calculated. Conclusion: It is concluded that in our EMS system, laymen reach a substantial number of VF/VT victims many minutes before the arrival of the professional EMS teams. Therefore, a substantial increase in the number of survivors could be expected if lay responders were prepared to use an AED.

Mild protective and resuscitative hypothermia for asphyxial cardiac arrest in rats

It has been shown in dogs that mild hypothermia (34°C) during or immediately after ventricular fibrillation cardiac arrest can improve cerebral outcome. The effect of mild hypothermia on outcome after 8 minutes of asphyxiation (5 minutes' cardiac arrest) was studied for the first time in rats. Restoration of spontaneous circulation was with external cardiopulmonary resuscitation and observation to 72 hours. Three groups of 10 rats each were studied. At 72 hours postarrest, compared with the normothermic control group 1, final overall performance categories (OPC) and neurological deficit scores (NDS) were numerically better in the resuscitative (post-arrest) hypothermia group 2 and significantly better in the protective (pre-intra-arrest) hypothermia group 3 ( P < .05). Total brain histopathological damage scores (HDS) were 17 ± 5 in group 1, 14 ± 6 in group 2 (NS), and 6 ± 2 in group 3 ( P < .001 versus group 1). HDS correlated with OPC ( r = .6, P < .05) and NDS ( r = .7, P < .05). Mild hypothermia improved cerebral outcome after asphyxial cardiac arrest in rats, more when induced before than after arrest. The model's insult is within the therapeutic window, which makes it also suitable for screening other cerebral resuscitation potentials.

Cerebral resuscitation paper competition

The following two abstracts were the finalists for the Cerebral Resuscitation Paper Competition at the National Association of EMS Physicians Annual Meeting, January 10, 1998, Ft. Lauderdale, Florida. Names of presenters are shown in boldface type