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PubMed1995

Peritoneal cooling for mild cerebral hypothermia after cardiac arrest in dogs.

After normothermic cardiac arrest in dogs, we found that mild hypothermia (34 degrees C) of 1-2 h reduced brain damage, providing that hypothermia was achieved within 15 min of reperfusion. A clinically feasible rapid brain-cooling method is needed. As head-neck surface cooling alone in dogs was found to be too slow (0.1 degrees C/min), we reviewed peritoneal cooling in the Introduction and Discussion sections. PRELIMINARY EXPERIMENTS WITHOUT CARDIAC ARREST: In 5 dogs with spontaneous circulation and IPPV, 2 L of Ringer's solution at 10 degrees C were instilled into the peritoneal cavity, left for 5 min, and drained. Brain (tympanic membrane) temperature (Tty) decreased by a mean of 0.3 degrees C/min (12 min to 34 degrees C). Core (pulmonary artery) temperature (Tpa) decreased by a mean of 0.8 degrees C/min (5 min to 34 degrees C). COOLING AFTER CARDIAC ARREST: In our reproducible dog model of normothermic ventricular fibrillation cardiac arrest of 11 min (no flow), brief low-flow normothermic cardiopulmonary bypass (CPB) was used for reperfusion and restoration of spontaneous circulation (ROSC) within 2 min. In 24 dogs, mild hypothermia was induced by head-neck surface cooling with ice bags, starting with reperfusion, plus peritoneal lavage as above, starting with ROSC. All 24 dogs were resuscitated. Initial head-neck surface cooling alone over 2 min decreased Tty by only 0.15 degrees C/min. Subsequent additional peritoneal lavage decreased Tty by a mean of 0.3 degrees C/min (11 min to 34 degrees C); and Tpa 0.6 degrees C/min (7 min to 34 degrees C). There were no significant physiologic effects. We conclude that peritoneal instillation of cold Ringer's solution is more rapidly effective than other non-intravascular cooling methods reported previously. Peritoneal cooling should be tried in patients during CPR.

Animals↗
PubMed1998

Increased serum levels of the S-100 protein are associated with hypoxic brain damage after cardiac arrest.

BACKGROUND AND PURPOSE: Patients resuscitated from cardiac arrest have a high early mortality rate. Prognostic evaluation based on clinical observations is uncertain and would benefit from the use of biochemical markers of hypoxic brain damage. The astroglial protein S-100 is an established biochemical marker of central nervous system injury. The purpose of the present study was to validate the use of serum determinations of S-100 with regard to outcome after cardiac arrest. METHODS: Levels of serum S-100 were measured with a radioimmunoassay in 41 patients the first 3 days after out-of-hospital cardiac arrest. The main outcome variable was fatal outcome within 14 days. RESULTS: S-100 levels were increased after cardiac arrest compared with controls with the highest levels observed the first day. S-100 levels day 1 and 2 correlated to the degree of coma as well as to the time of anoxia. Seventeen patients died within 14 days after the cardiac arrest. The deceased patients had increased S-100 levels on days 1 through 3 compared with survivors. All patients (100%) with an S-100 level of > or =0.2 on day 2 after the cardiac arrest died within 14 days, and 89% of the patients with levels below this limit value survived (positive and negative predictive values). The corresponding predictive values on day 1 were 71% and 85%, respectively. CONCLUSIONS: The present study shows that hypoxic brain damage after cardiac arrest can be estimated by measurement of serum S-100 concentrations. The method can be used in early prognostic evaluation of short-term outcome after cardiac arrest.

Adult↗
PubMed2006

New approaches to out-of-hospital cardiac arrest.

Out-of-hospital cardiac arrest (OOH-CA) is a leading cause of mortality and the focus of significant research. Recent studies provide new evidence that may change our management of OOH-CA and improve outcomes. The findings of two recently published studies of OOH-CA are reviewed in this article. The first, the Public Access Defibrillation Trial, was a randomized, controlled trial of public access defibrillation in 993 community facilities in the U.S. and Canada . It demonstrated that a community strategy to train laypersons to respond to cardiac arrests significantly increased survival to hospital discharge following OOH-CA in nonresidential community units with community members trained and equipped to provide public access defibrillation, compared to community units with community members trained to provide cardiopulmonary resuscitation (CPR) without any capacity for defibrillation. The second, the European Resuscitation Council Vasopressor during Cardiopulmonary Resuscitation Study, was a randomized, controlled, double-blinded trial that compared vasopressin to epinephrine as the initial pharmacological therapy for 1,219 patients who sustained OOH-CA. The study demonstrated that vasopressin is similar to epinephrine for OOH-CA due to ventricular fibrillation or pulseless electrical activity, and superior to epinephrine for the initial treatment of asystolic arrest; it also demonstrated that the combination of vasopressin and epinephrine is superior to epinephrine alone in the treatment of refractory, out-of-hospital cardiac arrest. Studies on alternative CPR techniques and adjunctive devices for CPR were also reviewed. We conclude that pre-hospital access to defibrillators and the use of vasopressin in the management of asystole hold promise for improving survival for patients with out-of-hospital cardiac arrest.

Antidiuretic Agents↗
PubMed1992

Role of electrophysiologic testing and coronary spasm provocation test in survivors of cardiac arrest.

Twenty-one patients were successfully resuscitated from cardiac arrest. Electrocardiograms (ECG) during cardiac arrest were recorded in 14 patients with ventricular fibrillation in 7, ventricular tachycardia in 4, cardiac standstill in three, Torsade de Points in one and atrial fibrillation with rapid ventricular response in 1. Thirteen patients (group I) had structural heart disease or primary ECG abnormality and 8 patients (group II) had no apparent heart disease. Electrophysiologic study (EPS) was performed in 12 patients of group I and 5 of group II. In group I, ventricular tachycardia was induced in 7, and His-ventricular conduction disturbance was demonstrated in 2, and 2 patients with Wolff-Parkinson-White (WPW) syndrome had an effective refractory period of the antegrade accessory pathway less than 250 msec. No patients in group II showed abnormal EPS findings. Spasm provocation test was performed in 8 patients (2 in group I and 6 in group II). Coronary spasm was induced in 5 patients (1 in group I and 4 in group II). Two patients in group II had positive results of upright-tilt testing. During the follow-up period, 2 patients died suddenly in group I and 1 patient whose cause of cardiac arrest was unknown had a recurrence of cardiac arrest. In group II, all patients whose etiology could be demonstrated by serial examinations had good prognosis. In conclusion, EPS is useful in evaluation of the cause of cardiac arrest especially when patients have structural heart disease, and coronary spasm may be involved in patients with cardiac arrest without apparent heart disease.

Adolescent↗
PubMed2003

Impact of percutaneous coronary intervention or coronary artery bypass grafting on outcome after nonfatal cardiac arrest outside the hospital.

Survivors of cardiac arrest due to ventricular arrhythmias are at risk for recurrent events. The role of revascularization in secondary prevention for survivors of cardiac arrest has been addressed in various studies with conflicting results. A total of 142 survivors of cardiac arrest with coronary artery disease were evaluated according to a standardized protocol, including 2-dimensional echocardiography, myocardial perfusion scintigraphy, coronary angiography, and electrophysiologic testing. Revascularization of scintigraphically documented ischemic myocardial regions was performed in 44 patients (31%). Final therapy was based on the results of electrophysiologic testing. Four-year survival rates were 100% for revascularized noninducible patients, 84% for revascularized inducible patients, 91% for nonrevascularized noninducible patients, and 72% for nonrevascularized inducible patients. Only 1 patient (<1% of study population) died suddenly. Recurrences were much more frequent in patients without revascularization (38% vs 7%, p <0.001) and the recurrence rate was 0% in the revascularized noninducible patients. Thus, revascularization of ischemically jeopardized myocardium in survivors of cardiac arrest resulted in excellent survival; moreover, in absence of inducible ventricular arrhythmias, the recurrence rate was 0%. Systematic evaluation of survivors of cardiac arrest due to ventricular arrhythmias allows risk stratification and guidance of subsequent antiarrhythmic therapy.

Adult↗
PubMed2004

Witnessed arrest, but not delayed bystander cardiopulmonary resuscitation improves prehospital cardiac arrest survival.

INTRODUCTION: This study correlated the effect of witnessing a cardiac arrest and instituting bystander CPR (ByCPR), as a secondary end point in a study evaluating the effect of bicarbonate on survival. METHODS: This prospective, randomised, double blinded clinical intervention trial enrolled 874 prehospital cardiopulmonary arrest patients encountered in a prehospital urban, suburban, and rural regional emergency medical service (EMS) area. This group underwent conventional advanced cardiac life support intervention followed by empiric early administration of sodium bicarbonate (1 mEq/l), monitoring conventional resuscitation parameters. Survival was measured as presence of vital signs on emergency department (ED) arrival. Data were analysed using chi(2) with Pearson correlation and odds ratio where appropriate. RESULTS: The overall survival rate was 13.9% (110 of 792) of prehospital cardiac arrest patients. The mean (SD) time until provision of bystander cardiopulmonary resuscitation (ByCPR) by laymen was 2.08 (2.77) minutes, and basic life support (BLS) by emergency medical technicians was 6.62 (5.73) minutes. There was improved survival noted with witnessed cardiac arrest-a 2.2-fold increase in survival, 18.9% (76 of 402) versus 8.6% (27 of 315) compared with unwitnessed arrests (p<0.001) with a decreased risk ratio of mortality of 0.4534 (95% CI, 0.0857 to 0.1891). The presence of ByCPR occurred in 32% (228 of 716) of patients, but interestingly did not correlate with survival. The survival rate was 18.2% (33 of 181) if ByCPR was performed within two minutes and 12.8% (6 of 47), if performed >two minutes (p = 0.3752). CONCLUSIONS: Survival after prehospital cardiac arrest is more likely when witnessed, but not necessarily when ByCPR was performed by laymen.

Adult↗
PubMed1982

Cardiac arrest and jogging.

Cardiac arrest related to jogging usually occurs in the setting of a structural cardiac abnormality. The patients often have no prodromal symptoms. Certain aspects of these cases, such as delayed entrance into the medical care system and exercise-induced lactic acidosis, make successful resuscitation difficult. We describe three such patients under the age of 36 who died after running.

Acidosis↗
PubMed1990

Mitral valve prolapse: cardiac arrest with long-term survival.

Cardiac arrest has been reported in patients with mitral valve prolapse; however, clinical characteristics and survival information are limited since most of the cases reported include autopsy data. Nine patients (2 male, 7 female) with mitral valve prolapse were identified who had cardiac arrest; ventricular fibrillation was documented in 8 patients; resuscitation was unsuccessful in 2. Eight had a history of palpitations (months to 15 years duration) and ventricular arrhythmias, 3 had a history (5-15 years) of recurrent syncope, and 1 was totally asymptomatic. Cardiac catheterization-angiographic studies in 8 patients demonstrated normal coronary artery anatomy and mitral valve prolapse. All 9 patients had auscultatory and echocardiographic evidence of mitral valve prolapse. Seven survivors (6 still alive) were followed from 3 to 14 years after cardiac arrest. A subset of patients with mitral valve prolapse and cardiac arrest is described in whom past medical history is compatible with cardiac arrhythmias or syncope, and whose long-term prognosis appears better than patients with other causes of cardiac arrest.

Adult↗
PubMed2006

Adenosine treatment delays postischemic hippocampal CA1 loss after cardiac arrest and resuscitation in rats.

Resuscitation from cardiac arrest results in reperfusion injury that leads to increased postresuscitation mortality and delayed neuronal death. One of the many consequences of resuscitation from cardiac arrest is a derangement of energy metabolism and the loss of adenylates, impairing the tissue's ability to regain proper energy balance. In this study, we investigated the effects of adenosine (ADO) on the recovery of the brain from 12 min of ischemia using a rat model of cardiac arrest and resuscitation. Compared to the untreated group, treatment with adenosine (7.2 mg/kg) initiated immediately after resuscitation increased the proportion of rats surviving to 4 days and significantly delayed hippocampal CA1 neuronal loss. Brain blood flow was increased significantly in the adenosine-treated rats 1 h after cardiac arrest and resuscitation. Adenosine-treated rats exhibited less edema in cortex, brainstem and hippocampus during the first 48 h of recovery. Adenosine treatment significantly lowered brain temperature during recovery, and a part of the neuroprotective effects of adenosine treatment could be ascribed to adenosine-induced hypothermia. With this dose, adenosine may have a delayed transient effect on the restoration of the adenylate pool (AXP = ATP + ADP + AMP) 24 h after cardiac arrest and resuscitation. Our findings suggested that improved postischemic brain blood flow and ADO-induced hypothermia, rather than adenylate supplementation, may be the two major contributors to the neuroprotective effects of adenosine following cardiac arrest and resuscitation. Although adenosine did not prevent eventual CA1 neuronal loss in the long term, it did delay neuronal loss and promoted long-term survival. Thus, adenosine or specific agonists of adenosine receptors should be evaluated as adjuncts to broaden the window of opportunity in the treatment of the reperfusion injury following cardiac arrest and resuscitation.

Adenosine↗
PubMed2001

Serum levels of the brain-derived proteins S-100 and NSE predict long-term outcome after cardiac arrest.

BACKGROUND AND PURPOSE: patients with cardiac arrest have a high mortality and the long-term outcome is doubtful. The prognosis is mainly dependent on clinical parameters. S-100 and neurone specific enolase (NSE) are established biochemical markers of central nervous system (CNS) injury. The purpose of this study was to validate the use of serum determinations of S-100 and NSE with neurological investigations in regard to brain damage and long-term outcome after cardiac arrest. METHODS: neurological examinations were performed on 66 patients after cardiac arrest. Serum levels of S-100 and NSE were determined during the first 3 days of post arrest, using commercial luminescent immunoassays (LIAs). The main outcome variable was the Glasgow Outcome Scale (GOS), while secondary variables were the activity of daily living (ADL) index and mini mental state examination (MMSE). Outcome was determined at 1 year. RESULTS: the serum levels of S-100 and NSE were increased during the first 3 days after the arrest and were related to coma depth, time of anoxia and abnormal brain stem reflexes. High levels predicted a poor outcome, according to the GOS (death, vegetative state and severe disability). The prognostic value of the brain damage markers was comparable with that of traditional clinical parameters. None of the secondary outcome variables (ADL and MMSE) was strongly associated with S-100 or NSE. DISCUSSION: the serum levels of S-100 and NSE increased after cardiac arrest due to the anoxic brain damage. The determination of S-100 and NSE can be used as an adjunct to predict long-term outcome after cardiac arrest.

Activities of Daily Living↗
PubMed2005

Use of vasopressors in the treatment of cardiac arrest.

Intervention for cardiac arrest may require intervention for electrical abnormalities or hemodynamic instability. These actions can result in ineffective cardiac functioning and systemic hypotension. Vasopressors are capable of improving severe hypotension that can result from reduced cardiovascular contractility or heart rate. These vasopressor actions are critical to successful resuscitation efforts for patients.

Cardiopulmonary Resuscitation↗
PubMed1989

Plasma catecholamines and resuscitation from prolonged cardiac arrest.

Plasma catecholamine levels rise markedly with cardiac arrest and attempted resuscitation. We examined whether epinephrine (EPI) or norepinephrine (NE) plasma concentrations could predict resuscitation outcome. In nine mongrel dogs, EPI and NE levels were drawn before cardiac arrest and after 8 and 14 min of cardiac arrest and CPR. Intravenous EPI (1 mg) was given 1 min before the last plasma level was drawn. Catecholamines were quantitated by high-performance liquid chromatography with triple-electrode coulometric electrochemical detection. Plasma catecholamines increased significantly with cardiac arrest, EPI levels increased from a control level of 15.9 +/- 3.0 to 396.0 +/- 63.3 pmol/ml after 8 min of cardiac arrest (p less than .05), and NE levels similarly increased from 4.4 +/- 1.7 to 66.5 +/- 12.0 pmol/ml (p less than .01). Neither the absolute catecholamine plasma concentration nor the response to cardiac arrest of the endogenous catecholamine concentrations could predict outcome, but catecholamine responses to exogenous EPI did correlate with outcome. Animals which were subsequently resuscitated had a greater increase in the plasma EPI concentrations after exogenous EPI than animals that were not resuscitated, a 53-fold vs. a 23-fold increase (p less than .05). Successfully resuscitated animals also had increased NE levels after exogenous EPI, while unsuccessfully resuscitated animals had either no change or a decrease (p less than .02). Successfully resuscitated animals had an increase in coronary perfusion pressure (p less than .01) in response to exogenous EPI, in contrast to those that were not resuscitated. This suggests that the exogenous administration of EPI during prolonged CPR is beneficial despite markedly elevated endogenous catecholamine levels.

Animals↗
PubMed1992

High prevalence of coronary artery spasm in survivors of cardiac arrest with no apparent heart disease.

The pathogenesis of cardiac arrest in the absence of any apparent heart disease remains unclear. Based on the hypothesis that coronary spasm may be a cause of cardiac arrest in the absence of apparent heart disease, ergonovine testing and/or electrophysiologic studies (EPS) were performed to evaluate the cause of cardiac arrest. Fourteen patients resuscitated from cardiac arrest had no apparent heart disease. A spontaneous episode of angina with ST-segment elevation occurred in 4 patients while under observation. Ergonovine testing was performed in 9 patients, and coronary spasm was induced in 5. EPS were performed in 8 patients, including 3 patients with coronary spasm. No electrophysiologic abnormalities were found in the 3 patients with coronary spasm. Ventricular fibrillation was induced by programmed ventricular stimulation in 2 patients with documented ventricular fibrillation at the time of resuscitation. All but one of the patients with coronary spasm had chest pain preceding cardiac arrest or at least a history of chest pain at rest, while 4 of 5 patients without coronary spasm had no prodromal symptoms. Patients with coronary spasm had a good prognosis when treated with a Ca-antagonist and/or long-acting nitrate. In conclusion, coronary spasm is the most frequent cause of cardiac arrest in cardiac arrest survivors with no apparent heart disease. Ergonovine testing should be performed to evaluate the cause of cardiac arrest when patients have no apparent heart disease.

Cardiac Pacing, Artificial↗
PubMed2005

Therapeutic hypothermia after cardiac arrest.

PURPOSE OF REVIEW: Most patients who suffer a cardiac arrest die after the event. Full neurological recovery occurs in only 6-23%. Until recently no specific post-arrest therapy was available to improve outcome. Application of therapeutic hypothermia (32-34 degrees C for 12-24 h) applied after cardiac arrest could help to improve this dreadful situation. This review covers the background of and recent clinical studies into hypothermia after cardiac arrest, and gives some insights into the future of resuscitation, namely suspended animation. RECENT FINDINGS: Two randomized clinical trials of mild therapeutic hypothermia applied after successful resuscitation from cardiac arrest showed that hypothermia after cardiac arrest improves neurological outcome as well as overall mortality. SUMMARY: The introduction of therapeutic hypothermia after cardiac arrest into routine intensive care practice could save thousands of lives worldwide, because only six patients must be treated to yield one additional patient with favourable neurological recovery. New developments in cooling techniques will make early induction of therapeutic hypothermia simple and convenient. The optimal duration and depth of hypothermia will be determined by future trials. Suspended animation is cooling during cardiac arrest to preserve the organism under conditions of prolonged controlled clinical death, followed by delayed resuscitation, resulting in survival without brain damage. This concept was initially introduced for trauma victims who rapidly bleed to death, and proved to be feasible in studies evaluating outcomes following exsanguination cardiac arrest in large animals. Whether the concept of suspended animation is applicable to normovolemic cardiac arrest is under investigation.

Journal Article↗
PubMed1979

Prevalence and prognostic significance of coma after cardiac arrest outside intensive care and coronary units.

In 181 patients resuscitated from cardiac arrest, the prevalence and duration of coma were registered and related to the site of occurrence of cardiac arrest, cardiac rhythm during arrest, age and clinical outcome of the patients. Coma was most frequent after cardiac arrest outside the hospital, as 84% of these patients were comatose for more than 1 h and 56% for more than 24 h; the corresponding values for patients with cardiac arrest in general wards were 63% and 30%, respectively, and for patients with cardiac arrest during ambulance transport, 80% and 44%. Permanent brain damage was extremely rare if the coma lasted less than 6 h (1 out of 62 patients), and relatively rare with a coma duration between 6 and 24 h (5 out of 34 patients). Of the patients, 85 remained comatose for more than 24 h and only 7 of them were discharged alive, all with cerebral impairment of a severity increasing with the duration of the coma. None regained consciousness after more than 7 days' coma, and a total of 80 patients died in coma, 20 with signs of cerebral death. Older patients were more vulnerable to coma than younger ones, but coma as such was not more frequent. We found no differences in coma after asystole and ventricular fibrillation. Problems concerning the selection of patients who have a chance of survival, although comatose after cardiac arrest, are discussed.

Adolescent↗
PubMed1986

Transcutaneous and transvenous cardiac pacing for early bradyasystolic cardiac arrest.

Emergency transcutaneous cardiac pacing was studied prospectively in 19 patients presenting to the emergency department with a bradyasystolic cardiopulmonary arrest of 20 minutes duration or less. Pacing was initiated when conventional advanced cardiac life support (including atropine administration) and a fluid challenge failed to restore a pulse. Seventeen patients also had placement of transvenous pacemaker electrodes for cardiac pacing. Transcutaneous cardiac pacing rapidly established a blood pressure in the two patients who for clinical reasons did not receive a transvenous pacemaker. Five patients were transcutaneously paced within five minutes of cardiac arrest (Group 1) and the remaining 14 were paced between five and 20 minutes following cardiac arrest (Group 2). Two of the Group 1 patients were admitted and subsequently recovered full neurological and prearrest cardiac function. Fewer Group 2 patients developed a blood pressure (P = .04), and there were no patients with full neurologic recovery in this group (P = .06). Similar results were found for transvenous cardiac pacing; there was a greater incidence of a palpable pulse and measurable blood pressure (P = .05 for both) in the Group 1 patients than in the Group 2 patients. No difference in clinical outcome was noted between the two pacing techniques. These results support the concept that cardiac pacing must be initiated early if the outcome of bradyasystolic cardiac arrest is to be altered.

Aged↗
PubMed1988

Incomplete global myocardial ischemia during cardiac arrest and resuscitation.

During cardiac arrest (no flow) and CPR (low flow), the onset of myocardial ischemia is followed by myocardial respiratory acidosis. Myocardial contractility is more decreased by respiratory than by metabolic acidosis. We demonstrated in a porcine model of cardiac arrest and in human patients increases in mixed venous PCO2 during CPR, whereas PaCO2 was decreased. Consequently, there was a striking increase in the venoarterial gradients for both [H+] and CO2. Both cardiac output (pulmonary blood flow) and the concentration of expired CO2 were simultaneously decreased. In great cardiac vein blood, even more profound respiratory acidosis with only minor decreases in bicarbonate and only moderate increases in lactate were observed. Intramyocardial pH was profoundly decreased. The severity of respiratory acidosis as a determinant of resuscitability and survival should be further investigated.

Animals↗