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P Safar

Publications and source records attributed to P Safar.

At least 73 records · Page 4Linked to original sources
PubMed1996

A comparison of prolonged manual and mechanical external chest compression after cardiac arrest in dogs.

The effects of manual and a new mechanical chest compression device (Heartsaver 2000) during prolonged CPR with respect to haemodynamics and outcome were tested in a prospective, randomized, controlled experimental trial during ventricular fibrillation in 12 dogs of 9-13 kg body weight after 1 min of cardiac arrest. During the first 10 min of CPR the dogs were resuscitated according to the Basic Life Support (BLS) algorithm, followed by 20 min of Advanced Life Support (ALS) algorithm. After 30 min of CPR both manual and mechanical CPR groups were resuscitated following a standardized ALS protocol. During CPR, coronary perfusion pressure and end tidal CO2 were greater with mechanical CPR. All animals were successfully resuscitated and neurological deficit scores were not different. The CPR trauma score was less in the mechanical group. Mechanical external chest compression provided better haemodynamics than the manual technique, though outcome did not differ. Both optimally performed manual and mechanical techniques produce flow sufficient to maintain organ viability for 30 min of CPR after a 1 min arrest interval.

Animals↗
PubMed1996

Utstein-style guidelines for uniform reporting of laboratory CPR research: a statement for health care professionals from a Task Force of the American Heart Association, the American College of Emergency Physicians, the American College of Cardiology, the European Resuscitation Council, the Heart and Stroke Foundation of Canada, the Institute of Critical Care Medicine, the Safar Center for Resuscitation Research, and the Society for Academic Emergency Medicine.

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Animals↗
PubMed1996

Resuscitation medicine research: quo vadis.

Laboratory research should have clinical relevance. Topics should be selected according to need, gaps in knowledge, and opportunities; the investigator's background, expertise, interests, and ambitions; scientific, clinical, and socioeconomic importance; and feasibility of successful performance and conclusion. The current explosion of knowledge and sophistication of methods will require research by multidisciplinary teams. Systematic goal-oriented studies should be conducted in environments that encourage serendipitous discoveries. Mechanism- and outcome-oriented research, in laboratories and on patients, is needed. In cardiac arrest research, hearts and brains "too good to die" offer many challenges. In trauma research, particular challenges include protection-preservation during uncontrolled hemorrhagic shock, suspended animation for delayed resuscitation in exsanguination, and prevention of brain swelling after traumatic brain injury. Emergency physicians have the unique opportunity to initiate clinical resuscitation research in unexplored territory: the prehospital arena.

Animals↗
PubMed1996

Utstein-style guidelines for uniform reporting of laboratory CPR research. A statement for healthcare professionals from a Task Force of the American Heart Association, the American College of Emergency Physicians, the American College of Cardiology, the European Resuscitation Council, the Heart and Stroke Foundation of Canada, the Institute of Critical Care Medicine, the Safar Center for Resuscitation Research, and the Society for Academic Emergency Medicine.

Explore the source record for details and available documents.

Animals↗
PubMed1996

Sodium bicarbonate in cardiac arrest: a reappraisal.

The routine use of sodium bicarbonate in patients with cardiac arrest has been discouraged, with the benefit of outcome evaluation. Current recommendations include an elaborate stratification of circumstances in which bicarbonate is to be used. The physiological and clinical aspects of bicarbonate administration during cardiopulmonary resuscitation in animal and human studies were reviewed. The onset of significant acidemia or alkalemia is associated with adverse system specific effects. The administration of bicarbonate may mitigate the adverse physiological effects of acidemia, improve response to exogenously administered vasopressor agents, or simply increase venous return due to an osmolar effect, resulting in increased coronary perfusion pressure. Likewise, bicarbonate may have adverse effects in each of these areas. The preponderance of evidence suggests that bicarbonate is not detrimental and may be helpful to outcome from cardiac arrest. An objective reappraisal of the empirical use of bicarbonate or other buffer agents in the appropriate "therapeutic window" for cardiac patients may be warranted.

Acid-Base Equilibrium↗
PubMed1996

Complete recovery after normothermic hemorrhagic shock and profound hypothermic circulatory arrest of 60 minutes in dogs.

OBJECTIVE: We hypothesize that during severe normothermic hemorrhagic shock (HS), induction of profound hypothermic circulatory arrest (PHCA) of 60 minutes to allow repair of otherwise lethal injuries in a bloodless field, can be survived without brain damage. In previous dog studies, normothermic HS with mean arterial pressure (MAP) of 40 mm Hg for 30 minutes, followed by PHCA of 2 hours at brain (tympanic membrane) temperature of 5 to 10 degrees C and core temperature of 10 degrees C, induced and reversed with cardiopulmonary bypass, resulted in survival with mild histopathologic brain damage. This study was designed to determine the severity of HS that can safely allow 1 hour of PHCA. In pilot studies with HS at MAP 30 mm Hg for 90 minutes with or without subsequent PHCA of 60 minutes there were no survivors. METHODS: In the definitive study, outcomes in four groups of five dogs each were compared: group I, HS at MAP 30 mm Hg for 60 minutes and normothermic fluid resuscitation; group II, HS at MAP 30 mm Hg for 60 minutes, PHCA for 60 minutes, and resuscitation; group III, HS at MAP 40 mm Hg for 60 minutes and normothermic fluid resuscitation; and group IV, HS at MAP 40 mm Hg for 60 minutes, PHCA for 60 minutes, and resuscitation. Controlled ventilation was maintained for at least 20 hours and intensive care for 72 hours. RESULTS: In groups I and II, two of five dogs in each group survived to 72 hours. In groups III and IV, all ten dogs survived. All survivors were functionally normal, with neurologic deficit scores (0% = normal, 100% = brain dead) of < 10%. Light microscopic scoring of 18 brain regions revealed no ischemic changes. All nonsurvivors had a severe metabolic acidemia after HS and developed multiple organ failure, including pulmonary edema, pneumonia, and intestinal necrosis. CONCLUSIONS: The critical level of hypotension during 60 minutes normothermic HS that is compatible with survival in dogs is a MAP of between 30 and 40 mm Hg. After otherwise survivable severe normothermic HS of 60 minutes, PHCA of 60 minutes does not add brain damage or mortality, and may allow survival from injuries that would otherwise be irreparable.

Animals↗
PubMed1996

Mild resuscitative hypothermia and outcome after cardiopulmonary resuscitation.

Recovery without residual neurological damage after cardiac arrest with global cerebral ischemia is still a rare event. Severe impairment of bodily or cognitive functions is often the result. The individual, emotional, and social aspects of brain damage and rehabilitation are seldom taken into account. Efforts to improve the prevention of brain damage immediately after successful resuscitation of patients are missing. The efficacy of hypothermia in preserving neurologic function when instituted before and during certain no-flow cardiovascular states has been well documented both clinically and experimentally since the 1950s. Most studies have used moderate (28-33 degrees C) to deep (20-28 degrees C) hypothermia to demonstrate these protective effects. Considering the use of hypothermia for preservation and resuscitation, the lack of controlled outcome trials, the long period of time required to reach therapeutic hypothermia, and the incidence of rewarming complications such as infection, arrhythmia, and coagulopathy have made it difficult to apply these methods to emergency situations such as cardiac arrest. Recent experimental evidence in dogs has shown that hypothermia induced after cardiac arrest does indeed mitigate the effects of the postresuscitation syndrome and improves neurologic function and reduces histologic brain damage. More importantly, such benefits can be demonstrated with mild (34-36 degrees C) hypothermia, thus minimizing complications and requiring less time for induction of hypothermia. Ice water nasal lavage, direct carotid infusion of cold fluids, use of a cooling helmet, and peritoneal cooling are promising techniques for clinical cerebral cooling. External auditory canal temperature (e.g., tympanic membrane temperature changes) could provide an approximation to brain temperatures. For accurate temperature monitoring, however, a central pulmonary artery thermistor probe should be inserted. Temperature monitoring is needed to avoid temperature < 30 degrees C. Mild hypothermia may prove to be an important and secure component for cerebral preservation and resuscitation during and after global ischemia; it may also prove to be a useful method of cerebral resuscitation after global ischemic states, thereby promoting the prevention of neuromental diseases.

Austria↗
PubMed1996

[Delivery from breech presentation with the delivery chair. Initial experiences with a new obstetric method].

OBJECTIVE: To prove safety and practicability of birth from breech presentation on a delivery chair. METHOD: In a retrospective study (1990-1995) all fetuses with breech presentation and those born using a delivery chair were collected. RESULTS: Out of a total of 2,925 fetuses 138 (4.7%) had breech presentation; 82 of them were born on a delivery chair. CONCLUSIONS: Since 1992 all fetuses with breech presentation were born on the delivery chair. The frequency of cesarean sections was roughly the same in both collectives (25.5%). We could not identify any disadvantages with this new technique.

Adult↗
PubMed1996

Improved cerebral resuscitation from cardiac arrest in dogs with mild hypothermia plus blood flow promotion.

BACKGROUND AND PURPOSE: In past studies, cerebral outcome after normothermic cardiac arrest of 10 or 12.5 minutes in dogs was improved but not normalized by resuscitative (postarrest) treatment with either mild hypothermia or hypertension plus hemodilution. We hypothesized that a multifaceted combination treatment would achieve complete cerebral recovery. METHODS: With our established dog outcome model, normothermic ventricular fibrillation of 11 minutes (without blood flow) was followed by controlled reperfusion (with brief normothermic cardiopulmonary bypass simulating low flow and low PaO2 of external cardiopulmonary resuscitation) and defibrillation at < 2 minutes. Controlled ventilation was provided to 20 hours and intensive care to 96 hours. Control group 1 (n = 8) was kept normothermic (37.5 degrees C), normotensive, and hypocapnic throughout. Experimental group 2 (n = 8) received mild resuscitative hypothermia (34 degrees C) from about 10 minutes to 12 hours (by external and peritoneal cooling) plus cerebral blood flow promotion with induced moderate hypertension, mild hemodilution, and normocapnia. RESULTS: All 16 dogs in the protocol survived. At 96 hours, all 8 dogs in control group 1 achieved overall performance categories 3 (severe disability) or 4 (coma). In group 2, 6 of 8 dogs achieved overall performance category 1 (normal); 1 dog achieved category 2 (moderate disability), and 1 dog achieved category 3 (P < .001). Final neurological deficit scores (0% [normal] to 100% [brain death]) at 96 hours were 38 +/- 10% (22% to 45%) in group 1 versus 8 +/- 9% (0% to 27%) in group 2 (P < .001). Total brain histopathologic damage scores were 138 +/- 22 (110 to 176) in group 1 versus 43 +/- 9 (32 to 56) in group 2 (P < .001). Regional scores showed similar group differences. CONCLUSIONS: After normothermic cardiac arrest of 11 minutes in dogs, resuscitative mild hypothermia plus cerebral blood flow promotion can achieve functional recovery with the least histological brain damage yet observed with the same model and comparable insults.

Animals↗
PubMed1996

Resuscitation from severe hemorrhage.

The potential to be successfully resuscitation from severe traumatic hemorrhagic shock is not only limited by the "golden 1 hr", but also by the "brass (or platinum) 10 mins" for combat casualties and civilian trauma victims with traumatic exsanguination. One research challenge is to determine how best to prevent cardiac arrest during severe hemorrhage, before control of bleeding is possible. Another research challenge is to determine the critical limits of, and optimal treatments for, protracted hemorrhagic hypotension, in order to prevent "delayed" multiple organ failure after hemostasis and all-out resuscitation. Animal research is shifting from the use of unrealistic, pressure-controlled, hemorrhagic shock models and partially realistic, volume-controlled hemorrhagic shock models to more realistic, uncontrolled hemorrhagic shock outcome models. Animal outcome models of combined trauma and shock are needed; a challenge is to find a humane and clinically realistic long-term method for analgesia that does not interfere with cardiovascular responses. Clinical potentials in need of research are shifting from normotensive to hypotensive (limited) fluid resuscitation with plasma substitutes. Topics include optimal temperature, fluid composition, analgesia, and pharmacotherapy. Hypotensive fluid resuscitation in uncontrolled hemorrhagic shock with the addition of moderate resuscitative (28 degrees to 32 degrees C) hypothermia looks promising in the laboratory. Regarding the composition of the resuscitation fluid, despite encouraging results with new preparations of stroma-free hemoglobin and hypertonic salt solutions with colloid, searches for the optimal combination of oxygen-carrying blood substitute, colloid, and electrolyte solution for limited fluid resuscitation with the smallest volume should continue. For titrating treatment of shock, blood lactate concentrations are of questionable value although metabolic acidemia seems helpful for prognostication. Development of devices for early noninvasive monitoring of multiple parameters in the field is indicated. Molecular research applies more to protracted hypovolemic shock followed by the systemic inflammatory response syndrome or septic shock, which were not the major topics of this discussion.

Animals↗
PubMed1996

Suspended animation for delayed resuscitation.

Suspended animation is defined as the therapeutic induction of a state of tolerance to temporary complete systemic ischemia, i.w., protection-preservation of the whole organism during prolonged circulatory arrest ( > or = 1 hr), followed by resuscitation to survival without brain damage. The objectives of suspended animation include: a) helping to save victims of temporarily uncontrollable (internal) traumatic (e.g., combat casualties) or nontraumatic (e.g., ruptured aortic aneurysm) exsanguination, without severe brain trauma, by enabling evacuation and resuscitative surgery during circulatory arrest, followed by delayed resuscitation; b) helping to save some nontraumatic cases of sudden death, seemingly unresuscitable before definite repair; and c) enabling selected (elective) surgical procedures to be performed which are only feasible during a state of no blood flow. In the discussion session, investigators with suspended animation-relevant research interests brainstorm on present knowledge, future research potentials, and the advisability of a major research effort concerning this subject. The following topics are addressed: the epidemiologic facts of sudden death in combat casualties, which require a totally new resuscitative approach; the limits and potentials of reanimation research; complete reversibility of circulatory arrest of 1 hr in dogs under profound hypothermia ( < 10 degrees C), induced and reversed by portable cardiopulmonary bypass; the need for a still elusive pharmacologic or chemical induction of suspended animation in the field; asanguinous profound hypothermic low-flow with cardiopulmonary bypass; electric anesthesia; opiate therapy; lessons learned by hypoxia tolerant vertebrate animals, hibernators, and freeze-tolerant animals (cryobiology); myocardial preservation during open-heart surgery; organ preservation for transplantation; and reperfusion-reoxygenation injury in vital organs, including the roles of nitric oxide and free radicals; and how cells (particularly cerebral neurons) die after transient prolonged ischemia and reperfusion. The majority of authors believe that seeking a breakthrough in suspended animation is not utopian, that ongoing communication between relevant research groups is indicated, and that a coordinated multicenter research effort, basic and applied, on suspended animation is justified.

Animals↗
PubMed1996

On the history of modern resuscitation.

The development of modern cardiopulmonary-cerebral resuscitation (CPCR) has given every person the ability to challenge death anywhere. Despite sparks of knowledge and occasional applications of possibly effective lifesaving efforts since antiquity, the possibility to reverse acute terminal states or clinical death by modern, physiologically sound, and effective measures did not come about until around 1900 inside hospitals, and around 1960 outside hospitals. Additional potentially effective cerebral resuscitation, research since around 1970, may be taken to clinical trials before the year 2000. The history of resuscitation medicine around 1900, when many opportunities to assemble existing bits of knowledge into an effective system were missed, should be a warning for those individuals who will lead CPCR beyond the year 2000. History has shown the need for continuing communication and collaboration among investigators of different countries, and between laboratory researchers, clinicians of various disciplines, and prehospital rescuers. The lessons learned from history, for research challenges in the near future, include: a) the development of ultra-advanced life support to be initiated outside the hospital, to bridge cardiopulmonary resuscitation (CPR)-resistant cases to definitive cardiac procedures in the hospital; and b) cerebral resuscitation to complete recovery after 10 to 15 mins of normothermic cardiac arrest without blood flow. Both challenges above will require research projects at multiple levels--from the molecular and cellular levels, to the use of small and large animal models (with organs' and organisms' process and outcome evaluations), to studies of patients and communities. Beyond the year 2000, resuscitation research might become more challenging and cost-effective in the area of multiple trauma, which concerns the young and fit. Research challenges concerning brain trauma, uncontrolled hemorrhagic shock, and "suspended animation" for delayed resuscitation have their own histories, and are not covered here. The author apologizes for not having recognized many important contributors to the history of CPCR because of space constraints or lack of knowledge about such contributions. Input on this subject from readers of this paper is hereby invited.

Cardiopulmonary Resuscitation↗
PubMed1996

Cerebral resuscitation from cardiac arrest: pathophysiologic mechanisms.

Both the period of total circulatory arrest to the brain and postischemic-anoxic encephalopathy (cerebral postresuscitation syndrome or disease), after normothermic cardiac arrests of between 5 and 20 mins (no-flow), contribute to complex physiologic and chemical derangements. The best documented derangements include the delayed protracted inhomogeneous cerebral hypoperfusion (despite controlled normotension), excitotoxicity as an explanation for selectively vulnerable brain regions and neurons, and free radical-triggered chemical cascades to lipid peroxidation of membranes. Protracted hypoxemia without cardiac arrest (e.g., very high altitude) can cause angiogenesis; the trigger of it, which lyses basement membranes, might be a factor in post-cardiac arrest encephalopathy. Questions to be explored include: What are the changes and effects on outcome of neurotransmitters (other than glutamate), of catecholamines, of vascular changes (microinfarcts seen after asphyxia), osmotic gradients, free-radical reactions, DNA cleavage, and transient extracerebral organ malfunction? For future mechanism-oriented studies of the brain after cardiac arrest and innovative cardiopulmonary-cerebral resuscitation, increasingly reproducible outcome models of temporary global brain ischemia in rats and dogs are now available. Disagreements exist between experienced investigative groups on the most informative method for quantitative evaluation of morphologic brain damage. There is agreement on the desirability of using not only functional deficit and chemical changes, but also morphologic damage as end points.

Altitude Sickness↗
PubMed1996

Cerebral resuscitation from cardiac arrest: treatment potentials.

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.

Animals↗
PubMed1996

Resuscitative hypothermia.

Resuscitative (postinsult) hypothermia is less well studied than protective-preservative (pre- and intra-arrest) hypothermia. The latter is in wide clinical use, particularly for protecting the brain during cardiac surgery. Resuscitative hypothermia was explored in the 1950s and then lay dormant until the 1980s when it was revived. This change occurred through the discoveries of brain damage mitigating effects after cardiac arrest in dogs, and after forebrain ischemia in rats, of mild (34 degrees C) hypothermia (which is safe), and of benefits derived from moderate hypothermia (30 degrees C) after traumatic brain injury or focal brain ischemia in various species. The idea that protection-preservation or resuscitation by hypothermia is mainly explained by its ability to reduce cerebral oxygen demand has been replaced by an increasingly documented synergism of many beneficial mechanisms. Deleterious chemical cascades during and after these insults are suppressed even by mild hypothermia. Prolonged moderate hypothermia carries some risks, e.g., arrhythmias, infection and coagulopathies. These side effects need further study. In global brain ischemia, protective-preservative mild hypothermia provides lasting mitigation of brain damage. Resuscitative mild hypothermia, however, may be beneficial in terms of long-term outcome or may merely delay the inevitable loss of selectively vulnerable neurons. Even if the latter is true, mild hypothermia may extend the therapeutic window for other interventions. This extension of the therapeutic window requires further documentation. After normothermic cardiac arrest of 11 mins in dogs, mild resuscitative hypothermia from 15 mins to 12 hours after reperfusion plus cerebral blood flow promotion normalized functional recovery with the least histologic damage seen thus far. Optimal duration of, and rewarming methods from, resuscitative hypothermia need clarification. The earliest possible induction of mild hypothermia after cardiac arrest seems desirable. Head-neck surface cooling alone is too slow. Among many clinically feasible rapid cooling methods, carotid cold flush and peritoneal cooling look promising. After traumatic brain injury or focal brain ischemia, which seem to still benefit from even later cooling, surface cooling methods may be adequate. Resuscitative hypothermia after cardiac arrest, traumatic brain injury, or focal brain ischemia should be considered for clinical trials.

Animals↗