Duration Of Cardiac Arrest Research Articles

Extracorporeal cardiopulmonary resuscitation.

To discuss the role of extracorporeal membrane oxygenation (ECMO) in patients with cardiac arrest. Return to spontaneous circulation dramatically decreases with the duration of cardiopulmonary resuscitation (CPR). In this context, it has been proposed to implement venoarterial ECMO in order to assist CPR (ECPR) both in inhospital cardiac arrest (IHCA) and in out-of-hospital cardiac arrest (OHCA). This review highlights that ECPR is feasible for both IHCA and OHCA. In the recent series, the outcome of ECPR in IHCA is satisfactory, with survival rates good with neurologic outcome reaching the 40-50% range. All series converge in highlighting that time from cardiac arrest to ECMO flow is a critical determinant of outcome, with survival rates of 50% when initiated within 30 min of IHCA, 30% between 30 and 60 min, and 18% after 60 min. Results of ECPR in OHCA are more challenging. Recent series suggest that good outcome can be obtained in 15-20% of the patients, provided that time from arrest to ECMO is shorter than 60 min. Duration of cardiac arrest seems to be more important than location of cardiac arrest. ECPR thus seems to be a valuable option in selected cases.

Management of Cardiac Arrest Caused by Acute Massive Pulmonary Thromboembolism

Cardiac arrest caused by acute pulmonary embolism is associated with high patient mortality. We reviewed patients who had cardiac arrest caused by acute pulmonary embolism. Between January 2001 and September 2013, we identified 20 patients at our institution with a confirmative diagnosis of acute pulmonary thromboembolism and cardiac arrest. Percutaneous cardiopulmonary support (PCPS) and surgical embolectomy are the standard course of care for patients with shock or cardiac arrest caused by pulmonary thromboembolism at our institution. Patients were divided into two groups (PCPS group and non-PCPS group). Percutaneous cardiopulmonary support was used in 60% of patients. Surgical embolectomy was performed for 85% of patients. Overall in-hospital and surgical mortalities were 35% and 29%, respectively. On the basis of the multivariate analysis, both cardiopulmonary resuscitation more than 15 minutes and absence of PCPS were significant risk factors affecting survival (p = 0.001 and 0.049, respectively). When the duration of cardiac arrest is short, surgical embolectomy is a viable option after cardiac arrest caused by pulmonary thromboembolism. Percutaneous cardiopulmonary support may be a useful tool for both stabilizing the patient and providing a bridge when deciding on further management options.

Post-resuscitation intestinal microcirculation: Its relationship with sublingual microcirculation and the severity of post-resuscitation syndrome

ObjectivePost-resuscitation syndrome has been recognized as one of the major causes of the poor outcomes of cardiopulmonary resuscitation. The aims of this study were to investigate the intestinal microcirculatory changes following cardiopulmonary resuscitation and relate those changes to sublingual microcirculation and the severity of post-resuscitation syndrome as measured by myocardial function and serum inflammatory cytokine levels. MethodsTwenty-five rats were randomized into three groups: (1) short duration of cardiac arrest (n=10): ventricular fibrillation (VF) was untreated for 4min prior to 6min of cardiopulmonary resuscitation (CPR); (2) long duration of cardiac arrest (n=10): VF was untreated for 8min followed by 8min of CPR; (3) sham control group (n=5): a sham operation was performed without VF induction and CPR. Intestinal and sublingual microcirculatory blood flow was visualized by a sidestream dark-field (SDF) imaging device at baseline and 1, 2, 4, 6, 8h post-resuscitation. Myocardial function was measured by echocardiography and serum cytokine levels (TNF-α and IL-6) were measured by enzyme-linked immunosorbent assay (ELISA). ResultsBoth intestinal and sublingual microcirculatory blood flow decreased significantly with increasing duration of cardiac arrest and resuscitation. The decreases in intestinal microcirculatory blood flow were closely correlated with the reductions of sublingual microcirculatory blood flow (perfused small vessels density: r=0.772, p<0.01; microcirculatory flow index: r=0.821, p<0.01). The decreased microcirculatory blood flow was closely correlated with weakened myocardial function and elevated inflammatory cytokine levels. ConclusionsThe severity of post-resuscitation intestinal microcirculatory dysfunction is closely correlated with that of myocardial function and inflammatory cytokine levels. The measurement of sublingual microcirculation reflects changes of intestinal microcirculation and may therefore provide a new option for post-resuscitation monitoring.

The effect of levosimendan combined with 20% lipid emulsion treatment on survival from bupivacaine induced toxicity in experiment.

Recent reports demonstrated that levosimendan improved post-resuscitation myocardial function in rat and pig models. Rabbits were randomized into 4 groups as 12 rabbits in each group. Bupivacaine 10 mg/kg was injected as an intravenous bolus to all groups. Basic life support was performed by mechanical ventilation and manual external chest compressions. After 1 min, animals in the group 1 received 1.5 ml/ kg saline 0.9% solution, and animals in the groups 2 and 4 received 5 ml/kg 20% lipid emulsion for 1 min through the ear vein followed by continuous infusion at 0.25 ml/kg/min. Three additional boluses of 1.5 ml/ kg lipid emulsion were repeated at 5-min intervals. The group 3 received fluid resuscitation plus levosimendan (3 µg/kg/min) 1 min after asystole and the group 4 received both levosimendan and lipid emulsion treatment. Return of spontaneous circulation and hemodynamic metrics were obtained in 20 minutes. The number of rabbits that survived after cardiac resuscitation was lower in the Groups 1 (0%) and 3 (33.3%) than in the Group 4 (91.7%) with a statistically significant difference (p < 0.001). The number of rabbits that survived resuscitation was higher in the Group 4 than in the Group 2 (66.7%), though not with a statistically significant difference (p = 0.317). The median duration of cardiac arrest in the Group 4 was significantly shorter than that in the other three groups (p < 0.001). In this rabbit model of bupivacaine-induced cardiac arrest, resuscitation with combined iv lipid emulsion and levosimendan was more efficacious than lipid alone (Tab. 3, Ref. 24).

Abstract 183: Appropriate Prolongation of Therapeutic Hypothermia Reduces Myocardial Damage After Prolong Cardiac Arrest

Background: Therapeutic hypothermia improves myocardial dysfunction and survival in cardiac arrest survivors. However, whether the duration of hypothermia should be prolonged in according to the duration of cardiac arrest to mitigate excess myocardial damage has not been clarified. Hypothesis: Appropriate prolongation of therapeutic hypothermia can mitigates excess myocardial damage after prolong cardiac arrest. Methods: The animals were equally randomized to NormoT(normothermia), 5H1, 5H2, 7H1, 7H2 and 7H4 groups. VF was induced and untreated for 5 minutes (NormoT, 5H1, 5H2) or 7 minutes (7H1, 7H2, 7H4), followed by 1 minutes of CPR, and then one electric shock of 5 J. Therapeutic hypothermia was initiated at simultaneously at the start of CPR with intravenous administration of 4°C saline and fan. After ROSC, hypothermia was maintained for 1hour (5H1, 7H1), 2 hours (5H2, 7H2) and 4 hours (7H4), respectively. Results: The plasma Troponin-I and FABP concentration at 2 nd hour following ROSC was significantly lower in the 5H2 and 7H4 groups than in the other groups (except the 7H2 group) (Figure). At 4 th hour after ROSC, The 5H2 and 7H4 groups showed less myocytolysis and apoptosis (Tunel staining) in the myocardium when compared with the other groups. Six out of 12 animals in both the 5H2 and 7H4 groups survived 72 hours after ROSC, whereas only 3 out of 12 animals in the 5H1 and 7H2 groups, and only 1 out of 12 animals in the 7H1 and NormoT groups. At the 72 nd hour, the 5H2 and 7H4 groups showed less myocardial fibrosis when compared with the groups. Conclusion: Appropriate prolongation of therapeutic hypothermia can mitigates excess myocardial damage in prolong cardiac arrest.

Subarachnoid Hemorrhage after Resuscitation from Out-of-hospital Cardiac Arrest

This study was undertaken to retrospectively investigate clinical features of subarachnoid hemorrhage (SAH) with cardiopulmonary arrest in patients achieving return of spontaneous circulation (ROSC) in order to explore the possibility of long-term survival. Of 143 SAH patients with cardiopulmonary arrest in our hospital between April 2004 and June 2012, data on 59 (41%) patients who attained ROSC were analyzed to determine the predictive factors for neurologic recovery and outcome. Recovery of brainstem reflexes and improvement of Glasgow Coma Scale (GCS) motor score were noted (postresuscitation neurologic restorative assessment, grade I) in 5, and 2 of these patients survived. By-grade analysis of patient background characteristics revealed a significantly shorter duration of cardiac arrest (P = .001) and a significantly smaller adrenaline dose (P = .011) for grade I patients. A logistic analysis of 1-week survival data revealed significant differences in duration of cardiac arrest (P = .022) and adrenaline dose (P = .019), with odds ratios of 0.89 and 0.25, respectively. Cox regression analysis of mortality data revealed significant differences in the duration of cardiac arrest (P = .012), adrenaline dose (P < .0001), and location of ROSC (P = .016), with hazard ratios of 1.03, 1.43, and 1.98, respectively. Cardiac arrest caused by SAH is a disease state with a grave prognosis, but there is the possibility of a good survival outcome when the administration of a small dose of adrenaline results in the rapid recovery of brainstem reflexes.

Effect of valproic acid on survival and neurologic outcomes in an asphyxial cardiac arrest model of rats

Aim of the studyValproic acid (VPA) has been known to reduce neuronal injury, has anti-inflammatory and anti-apoptotic effects as a histone deacetylase (HDAC) inhibitor. Thus, this study was performed to investigate the effects of VPA on survival and neurological outcomes in an asphyxial cardiac arrest model of rats. MethodsMale Sprague-Dawley rats were subjected to asphyxial cardiac arrest. For survival study, rats were subjected to 450s of asphyxial cardiac arrest. Cardiopulmonary resuscitation (CPR) was performed and then rats were blindly allocated to one of two groups (control group, n=10; VPA group, n=10). Valproic acid (300mgkg−1) or vehicle (normal saline) was administered via tail vein immediately after return of spontaneous circulation (ROSC) and observed for 72h. For neurological outcome study, rats (n=7 for each group) were subjected to same experimental procedures except duration of cardiac arrest of 360s. Neurological deficit scale (NDS) score was measured every 24h after ROSC for 72h and was ranged from 0 (brain dead) to 80 (normal). Brain tissues were harvested at 72h for evaluation of apoptotic injury and acetylation status of histone H3. ResultsIn survival study, 2 rats in VPA group were excluded because cardiac arrest was not achieved in predetermined time. Thus, 10 rats were allocated to control group and 8 rats were allocated to VPA group. The survival rates at 72h after cardiac arrest were significantly higher in VPA group than in control group (6/8 in VPA group, 3/10 rats in control group; log rank test, p<0.05). In neurological outcome study, all rats survived for 72h and NDS at 72h were significantly higher in VPA group than in control group (p<0.05). In brain tissues, expressions of acetylated histone H3 were not significantly different. However, expressions of cleaved caspase-3 were significantly lower in VPA group than in control group (p<0.05). ConclusionVPA increased survival rates and improved neurologic outcome in asphyxial cardiac arrest model of rats while decreasing expressions of cleaved caspase-3.

Training non-surgeons to perform resuscitative thoracotomy

Training non-surgeons to perform resuscitative thoracotomy

The effects of a newly developed miniaturized mechanical chest compressor on outcomes of cardiopulmonary resuscitation in a porcine model*

When the duration of cardiac arrest is prolonged, reperfusion of the vital organs by effective chest compression is the most important intervention for successful resuscitation. We investigated the effects of a newly developed miniaturized chest compressor on the outcomes of cardiopulmonary resuscitation. Prospective, randomized, controlled experimental study. University-affiliated animal research laboratory. Thirty male domestic pigs. Ventricular fibrillation was induced in 30 male domestic pigs weighing 35 ± 2 kg. Cardiopulmonary resuscitation was initiated after 7 mins of untreated ventricular fibrillation. The animals were randomized to receive mechanical chest compression with a miniaturized chest compressor, a LUCAS device or a Thumper device. After 5 mins of cardiopulmonary resuscitation, a 150-J defibrillation was delivered. If resuscitation was not successful, cardiopulmonary resuscitation was continued for 2 mins before the next defibrillation. The protocol was continued until successful resuscitation or for a total of 15 mins of cardiopulmonary resuscitation. The animals were observed for 72 hrs after resuscitation. The miniaturized chest compressor generated significantly greater coronary perfusion pressure, end-tidal PCO2, carotid blood flow, and intrathoracic negative pressure, with significantly lower compression depth and fewer rib fractures when compared with both the LUCAS and Thumper devices. Both the miniaturized chest compressor and LUCAS devices required lower numbers of defibrillation for successful resuscitation when compared with the Thumper device. This was associated with lower prevalence of recurrent ventricular fibrillation and better postresuscitation myocardial and neurological function when compared with the Thumper device. The miniaturized chest compressor improves hemodynamic efficacy and the success of cardiopulmonary resuscitation with significantly less injury, which is as effective as the LUCAS device. It may provide a new option for cardiopulmonary resuscitation.

Regional systems of care after out-of-hospital cardiac arrest in the UK: premier league care saves lives

Regional systems of care after out-of-hospital cardiac arrest in the UK: premier league care saves lives

In-Hospital Cardiac Arrest

A cardiac arrest is classified as ‘in-hospital’ (IHCA) if it occurs in a hospitalized patient who had a pulse at the time of admission. Unfortunately, the majority of patients resuscitated successfully from IHCA die before hospital discharge, and their prognosis has changed little over the past 30 years. Recent data indicate that survival to hospital discharge after in-hospital cardiac arrest is approximately 20%. A variety of factors have been proposed as determinants of poor outcomes associated with IHCA, which include first monitored rhythm, time to first shock, duration of cardiac arrest, hospital location of cardiac arrest and time of day of cardiac arrest occurrence. According to current guidelines for prevention of in-hospital cardiac arrest, hospitals should provide a system of care that includes staff education for rapid response, appropriate and regular patient vital sign monitoring, clear and uniform system of timely calling for assistance. Finally, after cardiac arrest has occurred, the quality of resuscitation and early defibrillation are crucial factors for improving survival.

A feasibility study evaluating the role of cerebral oximetry in predicting return of spontaneous circulation in cardiac arrest

To date there has been no reliable noninvasive real time monitoring available to determine cerebral perfusion during cardiac arrest. ObjectivesTo investigate the feasibility of using a commercially available cerebral oximeter during in-hospital cardiac arrest, and determine whether this parameter predicts return of spontaneous circulation (ROSC). MethodsCerebral oximetry was incorporated in cardiac arrest management in 19 in-hospital cardiac arrest cases, five of whom had ROSC. The primary outcome measure was the relationship between rSO2 and ROSC. ResultsThe use of cerebral oximetry was found to be feasible during in hospital cardiac arrest and did not interfere with management. Patients with ROSC had a significantly higher overall mean±SE rSO2 (35±5 vs. 18±0.4, p<0.001). The difference in mean rSO2 between survivors and non-survivors was most pronounced in the final 5min of cardiac arrest (48±1 vs. 15±0.2, p<0.0001) and appeared to herald imminent ROSC. Although spending a significantly higher portion of time with an rSO2>40% was found in survivors (p<0.0001), patients with ROSC had an rSO2 above 30% for >50% of the duration of cardiac arrest, whereas non-survivors had an rSO2 that was below 30%>50% of their cardiac arrest. Patients with ROSC also had a significantly higher change in rSO2 from baseline compared to non-survivors (310%±60% vs. 150%±27%, p<0.05). ConclusionCerebral oximetry may have a role in predicting ROSC and the optimization of cerebral perfusion during cardiac arrest.

Variable effects of high-dose adrenaline relative to standard-dose adrenaline on resuscitation outcomes according to cardiac arrest duration

Aim of the studyAdjustment of adrenaline (epinephrine) dosage according to cardiac arrest (CA) duration, rather than administering the same dose, may theoretically improve resuscitation outcomes. We evaluated variable effects of high-dose adrenaline (HDA) relative to standard-dose adrenaline (SDA) on resuscitation outcomes according to CA duration. MethodsTwenty-eight male domestic pigs were randomised to the following 4 groups according to the dosage of adrenaline (SDA 0.02mg/kg vs. HDA 0.2mg/kg) and duration of CA before beginning cardiopulmonary resuscitation (CPR): 6min SDA, 6min HDA, 13min SDA, or 13min HDA. After the predetermined duration of untreated ventricular fibrillation, CPR was provided. ResultsAll animals in the 6min SDA, 6min HDA, and 13min HDA groups were successfully resuscitated, while only 4 of 7 pigs in the 13min SDA group were successfully resuscitated (p=0.043). HDA groups showed higher right atrial pressure, more frequent ventricular ectopic beats, higher blood glucose, higher troponin-I, and more severe metabolic acidosis than SDA groups. Animals of 13min groups showed more severe metabolic acidosis and higher troponin-I than animals of 6min groups. All successfully resuscitated animals, except two animals in the 13min HDA group, survived for 7 days (p=0.121). Neurologic deficit score was not affected by the dose of adrenaline. ConclusionHDA showed benefit in achieving restoration of spontaneous circulation in 13min CA, when compared with 6min CA. However, this benefit did not translate into improved long-term survival or neurologic outcome.

Impact of cardiac arrest duration on extravascular lung water and pulmonary vascular permeability in patients with postcardiac arrest syndrome: a prospective observational study

Pulmonary dysfunction after cardiac arrest is a common phenomenon. Evidence appears to support the usefulness of quanti-tative assessment of pulmonary dysfunction using extravascular lung water (EVLW) and the pulmonary vascular permeability index (PVPI). We hypothesized that the duration of cardiac arrest (CPA TIME) would impact the pulmonary dysfunction in patients with postcardiac arrest syndrome. The aim of the present study was to investigate the lung dysfunction quantitatively using EVLW and PVPI in successfully resuscitated patients after cardiac arrest (CPA).

Editorial The role of the immunoinflammatory response after cardiac arrest

Cardiac arrest is a good (experimental) model for research in ischaemic tolerance [1], so it has been used often during the last 20 years in animal models. The (global) ischaemic event induced by cardiac arrest is followed by a phase of ischaemic preconditioning if the initial phase was of shorter or even stroke/complete ischaemia if the initial phase was of longer duration [2]. During the last years, there has been great effort in different research groups all over the world to find out the underlying pathophysiological mechanisms involved after these events or at least to find out some risk factors either in the brain or in the whole body [3, 4]. In the present issue of Archives of Medical Science, Anna Samborska-Sablik et al. present an interesting manuscript that deals with the role of the immunoinflammatory response after cardiac arrest in humans [5]. It is one of the very few studies in humans after cardiac arrest and is therefore of special interest [6]. The authors could find a significant correlation of the post-cardiac-arrest immunoinflammatory response (hs-CRP and IL-6) with the patients’ clinical state and also with the prediction of survival [5]. Such data are in line with previous research in the brain [7, 8] and open the door to so-called “immunomodulatory therapy”. In the brain such research is advanced, but we need a better understanding of the brain and immune system after such ischaemic events [9]. For the whole body, nearly no data exist so far. However, Anna Samborska-Sablik et al. have now provided a better insight into the clinical relevance of such research [5]: They show the relevance of this immunoinflammatory response for Glasgow Coma Scale (GCS) and Acute Physiology and Chronic Health Evaluation II (APACHE II) score: two of the major scores used in clinical daily practice. Therefore the immunoinflammatory response after ischaemic events is not only an experimental phenomenon (as many others), but also of great clinical importance [10, 11]. What are now the therapeutic implications of these findings? In experimental studies, preventive antibiotic treatment dramatically improved survival and outcome after ischaemic events, and even reduced the organ’s infarct size area [9, 12]. Apart from these experimental studies there are several clinical trials with promising results in this direction [12]. Smaller events of shorter duration can be protective – for example in the postoperative period – for further ischaemic events [7]. In this context, the oxygen-conserving reflex has gained more interest [13, 14] and can explain – at least partly – why the brain is only damaged after a very long duration of cardiac arrest. Nevertheless, the article of Samborska-Sablik et al. [5] goes deep into the pathophysiology of different organs. Further clinical research on this topic will open widely the doors to interesting therapeutic modalities and will help to resolve one of the great problems in internal medicine. Let’s go on this way!

Usefulness of Cooling and Coronary Catheterization to Improve Survival in Out-of-Hospital Cardiac Arrest

Survival rates after out-of-hospital cardiac arrest (OHCA) continue to be poor. Recent evidence suggests that a more aggressive approach to postresuscitation care, in particular combining therapeutic hypothermia with early coronary intervention, can improve prognosis. We performed a single-center review of 125 patients who were resuscitated from OHCA in 2 distinct treatment periods, from 2002 to 2003 (control group) and from 2007 to 2009 (contemporary group). Patients in the contemporary group had a higher prevalence of cardiovascular risk factors but similar cardiac arrest duration and prehospital treatment (adrenaline administration and direct cardioversion). Rates of cardiogenic shock (48% vs 41%, p = 0.2) and decreased conscious state on arrival (77% vs 86%, p = 0.2) were similar in the 2 cohorts, as was the incidence of ST-elevation myocardial infarction (33% vs 43%, p = 0.1). The contemporary cohort was more likely to receive therapeutic hypothermia (75% vs 0%, p <0.01), coronary angiography (77% vs 45%, p <0.01), and percutaneous coronary intervention (38% vs 23%, p = 0.03). This contemporary therapeutic strategy was associated with better survival to discharge (64% vs 39%, p <0.01) and improved neurologic recovery (57% vs 29%, p <0.01) and was the only independent predictor of survival (odds ratio 5.5, 95% confidence interval 1.2 to 26.2, p = 0.03). Longer resuscitation time, presence of cardiogenic shock, and decreased conscious state were independent predictors of poor outcomes. In conclusion, modern management of OHCA, including therapeutic hypothermia and early coronary angiography is associated with significant improvement in survival to hospital discharge and neurologic recovery.

Transient Adenosine-Induced Asystole During the Surgical Treatment of Anterior Circulation Cerebral Aneurysms: Technical Note

Transient adenosine-induced asystole is a reliable method for producing a short period of relative hypotension during surgical and endovascular procedures. Although the technique has been described in the endovascular treatment of brain arteriovenous malformations, aortic aneurysms, and posterior circulation cerebral aneurysms, little description of its use in anterior circulation aneurysms is available. To assess the benefits of adenosine-induced transient asystole in complex anterior circulation aneurysms, to describe our experience in selected cases, and to provide the first experience of the use of adenosine in anterior circulation aneurysms. The adenosine-induced cardiac arrest protocol allows us to titrate the duration of cardiac arrest on the basis of individual patient responses. The operative setup is the same as with all aneurysm clippings, with the addition of the placement of transcutaneous pacemakers as a precaution for prolonged bradycardia or asystole. Escalating doses of adenosine are given to determine the approximate dose that results in 30 seconds of asystole. When requested by the surgeon, the dose of adenosine is administered for definitive dissection and clipping. We present 6 cases in which this technique was used. The use of transient adenosine-induced asystole provided excellent circumferential visualization of the aneurysm neck and safe clip application. All patients did well neurologically and suffered no evidence of perioperative cerebral ischemia or delayed complication from the use of adenosine itself. Transient adenosine-induced asystole is a safe and effective technique in select circumstances that may aid in safe and effective aneurysm clipping. Along with the traditional techniques of brain relaxation, skull base approaches, and temporary clipping, adenosine-induced asystole facilitates circumferential visualization of the aneurysm neck and is another technique available to cerebrovascular surgeons.

Distribution of neuropathological lesions in pig brains after different durations of cardiac arrest

Aim of the study To evaluate all brain regions reported to be selectively vulnerable to global ischaemia in a pig cardiac arrest model with different durations of no-flow by establishing a semi-quantitative brain histopathologic scoring system and to compare histological damage with neurological deficits. Methods In a prospective randomised laboratory investigation, 35 female Large White pigs weighing 35–45 kg underwent ventricular fibrillation cardiac arrest for 0, 7, 10 or 13 min. In the brains of all animals that survived until the final endpoint (72 h post-arrest), 22 distinct regions were evaluated on paraffin-embedded sections in terms of type and extent of lesions. The results of the histological examination were compared to the results of a neurological outcome evaluation after 72 h. Results Significant differences were found in all cortex regions, the caudate nucleus and putamen, the hippocampal formation, the cerebellar cortex, and the thalamus between the ischaemic groups (7- and 10-min groups) and the control group (0-min group). No 13-min group animal survived. The main findings were neuronal necrosis and oedema. In animals from the 10-min group, many neurons were reabsorbed in the cerebral cortex, caudate nucleus and cerebellar granule cell layer. There was a highly significant correlation between histological damage and neurological deficits. Conclusions The pattern of neuronal lesions in this pig model bear good resemblance to the pattern known in humans and other animal models. The amount of histological lesions in selectively vulnerable brain regions correlates to neurological outcome.

Gasping during cardiac arrest

The purpose of this study is to review the prevalence and significance of gasping in patients experiencing cardiac arrest. In a recent study by Bobrow et al., gasping was identified in 33% of patients who arrested after the arrival of emergency medical services (EMS). Patients who arrested previous to EMS arrival experienced a decreasing incidence of gasping with increasing duration of cardiac arrest: 20% if EMS arrived within 7 min, 14% if EMS arrival was between 7 and 9 min, and 7% if EMS arrived after 9 min. There was a positive association between the presence of gasping and survival: 28% of those who gasped survived compared with 8% of those who did not gasp (odds ratio, 3.4, 95% confidence interval, 2.2-5.2). Among the 481 patients who received bystander cardiopulmonary resuscitation, survival to hospital discharge occurred among 39% of patients who gasped versus 9% among those who did not gasp (adjusted odds ratio, 5.1, 95% confidence interval, 2.7-9.4). Gasping frequently occurs during cardiac arrest. Public and emergency medical dispatchers must be more aware of its presence and significance.

Oxypurine Release in Cardiac Disease

The excretion of hypoxanthine-xanthine and uric acid in urine and the concentrations in peripheral venous blood were determined in nine patients with cardiac arrest due to acute myocardial infarction (AMI), in ten control patients with AMI without cardiac arrest and in nine with angina pectoris. The patients with cardiac arrest showed a 6-fold increase in urinary excretion of hypoxanthine-xanthine 0-2 hours after cardiac arrest. No difference was observed in the uric acid excretion or the hypoxanthine-xanthine and uric acid concentrations in peripheral venous blood. The urinary excretion of hypoxanthine-xanthine increases considerably in connection with reversible cardiac arrest, indicating general tissue hypoxia. No relationship could be found between the duration of cardiac arrest and the increased hypoxanthine-xanthine excretion in the urine.