Perfluorocarbon induced intra-arrest hypothermia does not improve survival in a swine model of asphyxial cardiac arrest

Background

Pulseless electrical activity is an important cause of cardiac arrest. Our purpose was to determine if induction of hypothermia with a cold perfluorocarbon-based total liquid ventilation (TLV) system would improve resuscitation success in a swine model of asphyxial cardiac arrest/PEA.

Methods

Twenty swine were randomly assigned to control (C, no ventilation, n = 11) or TLV with pre-cooled PFC (n = 9) groups. Asphyxia was induced by insertion of a stopper into the endotracheal tube, and continued in both groups until loss of aortic pulsations (LOAP) was reached, defined as a pulse pressure less than 2 mmHg. The TLV animals underwent asphyxial arrest for an additional 2 min after LOAP, followed by 3 min of hypothermia, prior to starting CPR. The C animals underwent 5 min of asphyxia beyond LOAP. Both groups then underwent CPR for at least 10 min. The endpoint was the resumption of spontaneous circulation maintained for 10 min.

Results

Seven of 9 animals achieved resumption of spontaneous circulation (ROSC) in the TLV group vs. 5 of 11 in the C group (p = 0.2). The mean pulmonary arterial temperature was lower in total liquid ventilation animals starting 4 min after induction of hypothermia (TLV 36.3 ± 0.2 °C vs. C 38.1 ± 0.2 °C, p < 0.0001). Arterial pO₂ was higher in total liquid ventilation animals at 2.5 min of CPR (TLV 76 ± 12 mmHg vs. C 44 ± 2 mmHg; p = 0.03).

Conclusion

Induction of moderate hypothermia using perfluorocarbon-based total liquid ventilation did not improve ROSC success in this model of asphyxial cardiac arrest.     

Comparison of non-calibrated pulse-contour analysis with continuous thermodilution for cardiac output assessment in patients with induced hypothermia after cardiac arrest

Aim

Induced mild hypothermia after cardiac arrest interferes with clinical assessment of the cardiovascular status of patients. In this situation, non-invasive cardiac output measurement could be useful. Unfortunately, arterial pulse contour is altered by temperature, and the performance of devices using arterial blood pressure contour analysis to derive cardiac output may be insufficient.

Methods

Mild hypothermia (32-34 °C) was induced in eight patients after out-of-hospital cardiac arrest and successful resuscitation. Cardiac output (CO) was measured simultaneously by continuous thermodilution using a pulmonary artery catheter and a cardiac output monitor (Vigilance II, Edwards Lifesciences) and by pulse contour analysis using an arterial line and the Vigileo monitor (Edwards Lifesciences) during both normothermia (>36 °C) and hypothermia. Continuous CO from both monitors was compared (Bland-Altman) and concordance of changes measured in consecutive 8-min intervals was measured.

Results

Mean cardiac output was 3.9 ± 1.2 l/min during hypothermia and 6.1 ± 2.6 l/min during normothermia (p < 0.001). During hypothermia (normothermia), bias was 0.23 (0.77) l/min, precision (1 SD) was 0.6 (0.72) l/min, and the limits of agreement were −1.06 to 1.51 (−0.64 to 2.18) l/min, corresponding to a percentage error of ±34% (±24%). Concordance of directional CO changes >10% was 53.9% in hypothermia and 51.4% in normothermia.

Conclusion

Induced hypothermia was not associated with increased bias or limits of agreement for the comparison of Vigileo and continuous thermodilution, but percentage error was high during normothermia and increased further during hypothermia. Less than 50% of clinically relevant CO changes during hypothermia were concordant.     

Outcome after resuscitation using controlled rapid extracorporeal cooling to a brain temperature of 30 °C, 24 °C and 18 °C during cardiac arrest in pigs

Aim of the study

To identify the optimal level of hypothermia during cardiac arrest, just prior to resuscitation with an extracorporeal cooling system and without fluid overload, for neurological outcome at day 9 in pigs.

Methods

In a prospective randomised laboratory investigation, 24 female Large White pigs (31-38 kg) underwent ventricular-fibrillation cardiac arrest for 15 min, followed by 1 min, 3 min or 5 min (n = 8 per group) of 4 °C cooling with an extracorporeal cooling system via an aortic balloon catheter and resuscitation with cardiopulmonary bypass. Sixty minutes following induction of cardiac arrest, defibrillation attempts were started. Mild hypothermia (34.5 °C) and intensive care were continued for 20 h and final outcome was evaluated after 9 days.

Results

Brain temperature decreased from 38.5 °C to 30.4 ± 1.6 °C within 221 ± 81 s in the 1-min group; to 24.2 ± 4.6 °C within 375 ± 127 s in the 3-min group; and to 18.8 ± 4.0 °C within 450 ± 121 s in the 5-min group. Restoration of spontaneous circulation was achieved in seven (1-min group), six (3-min group) and six (5-min group) animals (p = 0.78), whereas survival to 9 days was only achieved in six, three and three animals in each group (p = 0.22), respectively.

Conclusions

An extracorporeal cooling system rapidly induced brain hypothermia following prolonged normovolaemic cardiac arrest in pigs. Difference in outcome was not statistically significant amongst the three groups with various levels of hypothermia (30 °C, 24 °C and 18 °C) during cardiac arrest prior to resuscitation; however, the animals with the least temperature reduction showed a trend to better survival at 9 days. Further studies are necessary to investigate optimised methods for induction, as well as level, of cerebral hypothermia.     

Cold saline infusion and ice packs alone are effective in inducing and maintaining therapeutic hypothermia after cardiac arrest

Aim of the study

Hypothermia treatment with cold intravenous infusion and ice packs after cardiac arrest has been described and used in clinical practice. We hypothesised that with this method a target temperature of 32-34 °C could be achieved and maintained during treatment and that rewarming could be controlled.

Materials and methods

Thirty-eight patients treated with hypothermia after cardiac arrest were included in this prospective observational study. The patients were cooled with 4 °C intravenous saline infusion combined with ice packs applied in the groins, axillae, and along the neck. Hypothermia treatment was maintained for 26 h after cardiac arrest. It was estimated that passive rewarming would occur over a period of 8 h. Body temperature was monitored continuously and recorded every 15 min up to 44 h after cardiac arrest.

Results

All patients reached the target temperature interval of 32-34 °C within 279 ± 185 min from cardiac arrest and 216 ± 177 min from induction of cooling. In nine patients the temperature dropped to below 32 °C during a period of 15 min up to 2.5 h, with the lowest (nadir) temperature of 31.3 °C in one of the patients. The target temperature was maintained by periodically applying ice packs on the patients. Passive rewarming started 26 h after cardiac arrest and continued for 8 ± 3 h. Rebound hyperthermia (>38 °C) occurred in eight patients 44 h after cardiac arrest.

Conclusions

Intravenous cold saline infusion combined with ice packs is effective in inducing and maintaining therapeutic hypothermia, with good temperature control even during rewarming.     

Clinical predictors of survival in patients treated with therapeutic hypothermia following cardiac arrest

Introduction

Therapeutic hypothermia has been shown to provide neuroprotection and improved survival in patients suffering a cardiac arrest. We report outcomes of consecutive patients receiving therapeutic hypothermia for cardiac arrest and describe predictors of short and long-term survival.

Methods

Eighty patients receiving therapeutic hypothermia between January 2005 and December 2008 were identified and categorized as those who survived and died. Outcomes and predictors of survival were determined.

Results

Forty-five patients (56%) survived to hospital discharge and were alive at 30 days and among survivors 41 (91%) were alive 1 year after discharge. Survivors were younger, were more likely to present with VF, required less epinephrine during resuscitation, were more likely to have preserved renal function, and were less likely to be taking beta-blockers and ACE inhibitors. Predictors of survival included VF on presentation (OR 14.9, CI 2.7-83.2, p = 0.002), pre-cardiac arrest aspirin use (OR 9.7, CI 1.6-61.1, p = 0.02), return of spontaneous circulation <20 min (OR 9.4, CI 2.2-41.1, p = 0.003), absence of coronary artery disease (OR 5.3, CI 1.1-24.7, p = 0.002) and preserved renal function.

Conclusion

Therapeutic hypothermia is useful in the treatment of patients suffering a cardiac arrest. Several clinical factors may aid in predicting patients who are likely to survive after a cardiac arrest.     

Association between a quantitative CT scan measure of brain edema and outcome after cardiac arrest

Background

Cerebral edema is one physical change associated with brain injury and decreased survival after cardiac arrest. Edema appears on computed tomography (CT) scan of the brain as decreased X-ray attenuation by gray matter. This study tested whether the gray matter attenuation to white matter attenuation ratio (GWR) was associated with survival and functional recovery.

Methods

Subjects were patients hospitalized after cardiac arrest at a single institution between 1/1/2005 and 7/30/2010. Subjects were included if they had non-traumatic cardiac arrest and a non-contrast CT scan within 24 h after cardiac arrest. Attenuation (Hounsfield Units) was measured in gray matter (caudate nucleus, putamen, thalamus, and cortex) and in white matter (internal capsule, corpus callosum and centrum semiovale). The GWR was calculated for basal ganglia and cerebrum. Outcomes included survival and functional status at hospital discharge.

Results

For 680 patients, 258 CT scans were available, but 18 were excluded because of hemorrhage (10), intravenous contrast (3) or technical artifact (5), leaving 240 CT scans for analysis. Lower GWR values were associated with lower initial Glasgow Coma Scale motor score. Overall survival was 36%, but decreased with decreasing GWR. The average of basal ganglia and cerebrum GWR provided the best discrimination. Only 2/58 subjects with average GWR < 1.20 survived and both were treated with hypothermia. The association of GWR with functional outcome was completely explained by mortality when GWR < 1.20.

Conclusions

Subjects with severe cerebral edema, defined by GWR < 1.20, have very low survival with conventional care, including hypothermia. GWR estimates pre-treatment likelihood of survival after cardiac arrest.     

Repeated magnetic resonance imaging and cerebral performance after cardiac arrest--a pilot study

Aim of the study

Prognostication may be difficult in comatose cardiac arrest survivors. Magnetic resonance imaging (MRI) is potentially useful in the prediction of neurological outcome, and it may detect acute ischemia at an early stage. In a pilot setting we determined the prevalence and development of cerebral ischemia using serial MRI examinations and neurological assessment.

Methods

Ten witnessed out-of-hospital cardiac arrest patients were included. MRI was carried out approximately 2 h after admission to the hospital, repeated after 24 h of therapeutic hypothermia and 96 h after the arrest. The images were assessed for development of acute ischemic lesions. Neurophysiological and cognitive tests as well as a self-reported quality-of-life questionnaire, Short Form-36 (SF-36), were administered minimum 12 months after discharge.

Results

None of the patients had acute cerebral ischemia on MRI at admission. Three patients developed ischemic lesions after therapeutic hypothermia. There was a change in the apparent diffusion coefficient, which significantly correlated with the temperature (p < 0.001). The neurophysiological tests appeared normal. The patients scored significantly better on SF 36 than the controls as regards both bodily pain (p = 0.023) and mental health (p = 0.016).

Conclusions

MRI performed in an early phase after cardiac arrest has limitations, as MRI performed after 24 and 96 h revealed ischemic lesions not detectable on admission. ADC was related to the core temperature, and not to the volume distributed intravenously. Follow-up neurophysiologic tests and self-reported quality of life were good.     

Changes in interleukin-10 mRNA expression are predictive for 9-day survival of pigs in an emergency preservation and resuscitation model

Aim of the study

This study aimed at evaluating (I) the impact of different intra-arrest hypothermia levels on the expression of selected cytokines and (II) their prognostic value for 9-day survival.

Methods

Female Large White pigs (n = 21, 31-38 kg) were subjected to 15 min of ventricular fibrillation, followed by intra-arrest cardiopulmonary bypass cooling for 1, 3, or 5 min achieving brain temperatures (Tbr) of 30.4 ± 1.6, 24.2 ± 4.6 and 18.8 ± 4.0 °C. After 40 min of controlled rewarming, pigs were defibrillated and kept at Tbr of 34.5 °C for 20 h, survival was for 9 days. Plasma samples were analysed for interleukin (IL)-6, tumor necrosis factor-α (TNF-α), and IL-10 levels by ELISA. Total RNA out of peripheral blood mononuclear cells was analysed by real-time PCR for IL-1, IL-2, IL-4, IL-10, TNF-α, interferon-γ, inducible NO synthase, and heme oxygenase-1 gene expressions.

Results

Plasma IL-6 and TNF-α levels significantly (p = 0.0001 and 0.0003) increased in all animals within 1 h after resuscitation with no significant differences between groups. Pigs surviving exhibited a decrease in IL-10 expression between baseline and intra-arrest values as compared to non-surviving animals, which showed a slight increase (p = 0.0078). ROC curve analysis revealed that changes in IL-10 expression had a good prognostic power for survival to day 9 (area under the curve = 0.882).

Conclusion

The systemic inflammatory response syndrome after cardiac arrest was reflected by a remarkable increase of plasma IL-6 and TNF-α levels. Intra-arrest hypothermia levels did not influence the expression of selected cytokines. As prognostic marker for survival IL-10 was identified with decreasing mRNA levels during cardiac arrest in survivors.     

Quality of closed chest compression on a manikin in ambulance vehicles and flying helicopters with a real time automated feedback

Context

Automated verbal and visual feedback improves quality of resuscitation in out-of-hospital cardiac arrest and was proven to increase short-term survival. Quality of resuscitation may be hampered in more difficult situations like emergency transportation. Currently there is no evidence if feedback devices can improve resuscitation quality during different modes of transportation.

Objective

To assess the effect of real time automated feedback on the quality of resuscitation in an emergency transportation setting.

Design

Randomised cross-over trial.

Setting

Medical University of Vienna, Vienna Municipal Ambulance Service and Helicopter Emergency Medical Service Unit (Christophorus Flugrettungsverein) in September 2007.

Participants

European Resuscitation Council (ERC) certified health care professionals performing CPR in a flying helicopter and in a moving ambulance vehicle on a manikin with human-like chest properties.

Interventions

CPR sessions, with real time automated feedback as the intervention and standard CPR without feedback as control.

Main outcome measures

Quality of chest compression during resuscitation.

Results

Feedback resulted in less deviation from ideal compression rate 100 min⁻¹ (9 ± 9 min⁻¹, p < 0.0001) with this effect becoming steadily larger over time. Applied work was less in the feedback group compared to controls (373 ± 448 cm × compression; p < 0.001). Feedback did not influence ideal compression depth significantly. There was some indication of a learning effect of the feedback device.

Conclusions

Real time automated feedback improves certain aspects of CPR quality in flying helicopters and moving ambulance vehicles. The effect of feedback guidance was most pronounced for chest compression rate.     

Improving outcome after out-of-hospital cardiac arrest by strengthening weak links of the local Chain of Survival; quality of advanced life support and post-resuscitation care

Background

Survival after out-of-hospital cardiac arrest (OHCA) depends on a well functioning Chain of Survival. We wanted to assess if targeted attempts to strengthen the weak links of our local chain; quality of advanced life support (ALS) and post-resuscitation care, would improve outcome.

Materials and methods

Utstein data from all OHCAs in Oslo during three distinct 2-year time periods 1996-1998, 2001-2003 and 2004-2005 were collected. Before the second period the local ALS guidelines changed with increased focus on good quality chest compressions with minimal pauses, while standardized post-resuscitation care including goal directed therapy with therapeutic hypothermia and percutaneous coronary intervention was added in the third period. Additional a priori sub-group analyses of arrests with cardiac aetiology as well as bystander witnessed ventricular fibrillation/tachycardia (VF/VT) arrests with cardiac aetiology were performed.

Results

ALS was attempted in 454, 449, and 417 patients with OHCA in the first, second and last time period, respectively. From the first to the third period VF/VT arrests declined (40% vs. 33%, p = 0.039) and fewer arrests were witnessed (80% vs. 72%, p = 0.022) and response intervals increased (7 ± 4 to 9 ± 4 min, p < 0.001). Overall survival increased from 7% (first period) to 13% (last period), p = 0.002, and survival in the sub-group of bystander witnessed VF/VT arrests with cardiac aetiology increased from 15% (first period) to 35% (last period), p = 0.001.

Conclusions

Survival after OHCA was increased after improving weak links of our local Chain of Survival, quality of ALS and post-resuscitation care.     

Intraosseous infusion of ice cold saline is less efficacious than intravenous infusion for induction of mild therapeutic hypothermia in a swine model of cardiac arrest

Background

Intravenous (IV) infusion of ice cold saline is an effective method to initiate induction of mild therapeutic hypothermia (MTH) following resuscitation from out-of-hospital cardiac arrest (OOHCA). Intraosseous (IO) infusion of cold saline may be an alternative method to induce MTH.

Objective

The goal of this study was to determine if IO infusion of cold saline is a comparable alternative to IV infusion for inducing MTH in a laboratory swine model of cardiac arrest.

Methods

Ten mixed breed swine were resuscitated from cardiac arrest and randomized post-resuscitation to infusion with ice cold saline using either IO (n = 5) or IV (n = 5) access. The study endpoints were either a goal esophageal temperature of 34 °C or the elapse of a 30 min time period, simulating a long prehospital transport.

Results

Four of five pigs in the IV infusion group achieved goal temperature within 30 min compared to 0/5 in the IO infusion group (p = 0.048). The mean esophageal temperature change was significantly higher in the IV group when compared to the IO group (p < 0.001). Post-arrest hemodynamic parameters were similar between the two groups.

Conclusions

IV infusion of ice cold saline is an efficacious method to achieve MTH in this swine model of cardiac arrest. Furthermore, IO infusion of cold saline is not sufficient to induce MTH in the time routinely available in the prehospital setting following OOHCA.     

Usefulness of routine laboratory parameters in the decision to treat refractory cardiac arrest with extracorporeal life support

Aim

To evaluate the usefulness of routine laboratory parameters in the decision to treat refractory cardiac arrest patients with extracorporeal life support (ECLS).

Methods

Sixty-six adults with witnessed cardiac arrest of cardiac origin unrelated to poisoning or hypothermia undergoing cardiopulmonary resuscitation without return of spontaneous circulation (duration: 155 min [120-180], median, [25-75%-percentiles]) were included in a prospective cohort-study. ECLS was implemented under cardiac massage, using a centrifugal pump connected to a hollow-fiber membrane-oxygenator, aiming to maintain ECLS flow ≥2.5 l/min and mean arterial pressure ≥60 mm Hg.

Results

Forty-seven of 66 patients died within 24 h from multiorgan failure and massive capillary leak. Of 19/66 patients who survived ≥24 h with stable circulatory conditions permitting neurological evaluation, four became conscious and were transferred for further cardiac assistance, while three became organ donors. Ultimately, one patient survived without neurologic sequelae after cardiac transplantation. Using multivariate analysis, only pre-cannulation peripheral venous oxygen saturation (SpvO₂, 28% [15-52]) independently predicted inability to maintain targeted ECLS conditions ≥24 h (odds ratio for each 10%-decrease [95%-confidence interval]: 1.65 [1.21; 2.25], p = 0.002). The area under the receiver-operating-characteristics curve was 0.78 [0.63; 0.93]. SpvO₂ cut-off value of 33% was associated with a sensitivity of 0.68 [0.50; 0.83] and specificity of 0.81 [0.54; 0.96]. SpvO₂ ≤8%, lactate concentration ≥21 mmol/l, fibrinogen ≤0.8 g/l, and prothrombin index ≤11% predicted premature ECLS discontinuation with a specificity of 1.

Conclusion

SpvO₂ is useful to predict the inability of maintaining refractory cardiac arrest victims on ECLS without detrimental capillary leak and multiorgan failure until neurological evaluation.     

Coagulopathy during cardiac arrest and resuscitation in a swine model of electrically induced ventricular fibrillation

Aims

Coagulopathy is often present after resuscitation from cardiac arrest but plays an undefined role in the post cardiac arrest syndrome. The aim of this study was to characterize coagulation changes during cardiac arrest and post-resuscitation care in order to direct further focused study.

Methods

Ventricular fibrillation (VF) was induced electrically in immature male swine, followed by normothermic American Heart Association Advanced Cardiac Life Support and a uniform post-resuscitation goal-directed resuscitation protocol. PT, aPTT, fibrinogen, Thrombelastography (TEG), platelet contractile force (PCF), clot elastic modulus (CEM), and collagen-induced platelet aggregation were compared at baseline, at 8 min of VF, during the 3rd round of chest compressions (CPR), and at 15, 90, 180, and 360 min after return of circulation using repeated measures ANOVA.

Results

8/18 (44%) animals were resuscitated after 10.9 ± 0.9 min of VF and 7.6 ± 3.4 min of CPR. TEG revealed a significant impairment in clot strength (MA) and clot formation kinetics (K, alpha angle) arising during CPR, followed by a brief prolongation of clot onset times (R) after return of circulation. Both PCF and CEM fell significantly during CPR (PCF by 50%, CEM by 47% of baseline) and platelet aggregation was significantly decreased during CPR. Coagulation changes were partially recovered by 3 h of post-resuscitation care.

Conclusion

Whole blood coagulation was rapidly impaired during CPR after electrically induced VF in this swine model by impaired platelet aggregation/contractile function and clotting kinetics. Further platelet-specific study is indicated.     

A rapid, safe, and low-cost technique for the induction of mild therapeutic hypothermia in post-cardiac arrest patients

Aim of study

The benefits of inducing mild therapeutic hypothermia (MTH) in cardiac arrest patients are well established. Timing and speed of induction have been related to improved outcomes in several animal trials and one human study. We report the results of an easily implemented, rapid, safe, and low-cost protocol for the induction of MTH.

Methods

All in-hospital cardiac arrest (IHCA) and out-of-hospital cardiac arrest (OHCA) patients admitted to an intensive care unit meeting inclusion criteria were cooled using a combination modality of rapid, cold saline infusion (CSI), evaporative surface cooling, and ice water gastric lavage. Cooling tasks were performed with a primary emphasis on speed. The main endpoints were the time intervals between return of spontaneous circulation (ROSC), initiation of hypothermia (IH), and achievement of target temperature (TT).

Results

65 patients underwent MTH during a 3-year period. All patients reached target temperature. Median ROSC-TT was 134 min. Median ROSC-IH was 68 min. Median IH-TT was 60 min. IH-TT cooling rate was 2.6 °C/h. Complications were similar to that of other large trials. 31% of this mixed population of IHCA and OHCA patients recovered to a Pittsburgh cerebral performance score (CPC) of 1 or 2.

Conclusion

A protocol using a combination of core and surface cooling modalities was rapid, safe, and low cost in achieving MTH. The cooling rate of 2.6 °C/h was superior to most published protocols. This method uses readily available equipment and reduces the need for costly commercial devices.     

Mild therapeutic hypothermia is associated with favourable outcome in patients after cardiac arrest with non-shockable rhythms

Aim

Mild therapeutic hypothermia (32-34 °C) improves neurological recovery and reduces the risk of death in comatose survivors of cardiac arrest when the initial rhythm is ventricular fibrillation or pulseless ventricular tachycardia. The aim of the presented study was to investigate the effect of mild therapeutic hypothermia (32-34 °C for 24 h) on neurological outcome and mortality in patients who had been successfully resuscitated from non-ventricular fibrillation cardiac arrest.

Methods

In this retrospective cohort study we included cardiac arrest survivors of 18 years of age or older suffering a witnessed out-of-hospital cardiac arrest with asystole or pulseless electric activity as the first documented rhythm. Data were collected from 1992 to 2009. Main outcome measures were neurological outcome within six month and mortality after six months.

Results

Three hundred and seventy-four patients were analysed. Hypothermia was induced in 135 patients. Patients who were treated with mild therapeutic hypothermia were more likely to have good neurological outcomes in comparison to patients who were not treated with hypothermia with an odds ratio of 1.84 (95% confidence interval: 1.08-3.13). In addition, the rate of mortality was significantly lower in the hypothermia group (odds ratio: 0.56; 95% confidence interval: 0.34-0.93).

Conclusion

Treatment with mild therapeutic hypothermia at a temperature of 32-34 °C for 24 h is associated with improved neurological outcome and a reduced risk of death following out-of-hospital cardiac arrest with non-shockable rhythms.     

The influence of time on the accuracy of healthcare personnel to diagnose paediatric cardiac arrest by pulse palpation

Aim

To determine time and accuracy diagnosing paediatric cardiac arrest (CA) by pulse palpation.

Materials and methods

Blinded rescuers (82 nurses, 71 doctors) palpated for a brachial pulse in 17 children (1 day-11 years) with non-pulsatile extracorporeal circulation for CA or cardiac failure. Timed rescuer decisions (pulse present/absent) were compared with non-blinded investigator decisions.

Results

CA on 55 occasions was diagnosed by 42 (76%) rescuers in mean (±SD) time 30 ± 19 s. Experienced rescuers diagnosed CA in 25 ± 14 s, inexperienced rescuers in 37 ± 24 s (p = 0.042). CA absent on 98 occasions was confirmed by 77 (79%) rescuers in 13 ± 13 s. Experienced rescuers confirmed absent CA in 9 ± 5 s, inexperienced rescuers in 21 ± 19 s (p = 0.0001). Diagnosis of CA compared to confirmation of absence took longer by all rescuers (p < 0.0001), experienced rescuers (p < 0.0001) and inexperienced rescuers (p = 0.018). Twenty-eight of 33 (85%) experienced doctors diagnosed CA or confirmed absence in 13 ± 9 s, 49 of 61 (80%) experienced nurses in 15 ± 12 s, 11 of 21 (52%) inexperienced nurses in 18 ± 15 s and 31 of 38 (82%) inexperienced doctors in 30 ± 24 s. Overall accuracy was 78% (95%CI 71-84%), sensitivity 0.76 (95%CI 0.64-0.86) and specificity 0.79 (95%CI 0.69-0.86). Experienced doctors were 85% accurate, inexperienced doctors 82%, experienced nurses 80%, inexperienced nurses 52%. Rescuers diagnosing quickly (<10 s) had 90% accuracy, in 11-20 s 77% accuracy and in 21-30 s 62.5% accuracy (p = 0.015).

Conclusions

Diagnosis of cardiac arrest by pulse palpation alone is unreliable. At least 30 s is required but accuracy and speed are related to clinical experience.     

Early selective trans-nasal cooling during CPR improves success of resuscitation in a porcine model of prolonged pulseless electrical activity cardiac arrest

Aim of study

In the present study, we investigated trans-nasal cooling in settings of pulseless electrical activity (PEA). We hypothesized that early trans-nasal cooling during CPR improves outcomes when cardiac arrest is associated with PEA.

Methods

Ventricular fibrillation (VF) was electrically induced in 16 domestic male pigs weighing 40 ± 3 kg. After 14 min of untreated VF, PEA was induced following delivery of one or more electrical shocks. One min after onset of PEA, CPR was started, including chest compression and ventilation. Each animal received 5 min of CPR prior to defibrillation attempt. CPR and resuscitation efforts were discontinued at 15 min unless return to spontaneous circulation was achieved. In 8 animals, selective trans-nasal cooling was begun coincident with start of CPR and 8 randomized controls were identically treated except for trans-nasal cooling. Mean aortic pressure was continuously measured together with aortic and right atrial pressure and nasal, body and right jugular vein temperatures. Coronary perfusion pressure (CPP) was computed from measured data.

Results

Six of eight animals were resuscitated after early trans-nasal cooling, while only one untreated control was resuscitated (p = 0.012). Nasal, body and jugular vein temperatures decreased after cooling. At PC (precordial compression) 5 min, the cooled group recorded a higher CPP (25 ± 5 mmHg) than the non-cooled group (15 ± 4 mmHg, p = 0.001).

Conclusion

When selective trans-nasal cooling was initiated during CPR in the animal model of prolonged cardiac arrest with PEA, CPP was higher and the likelihood of return of spontaneous circulation was improved.     

S-100B is superior to NSE, BDNF and GFAP in predicting outcome of resuscitation from cardiac arrest with hypothermia treatment

Objective

To conduct a pilot study to evaluate the blood levels of brain derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), neuron specific enolase (NSE) and S-100B as prognostic markers for neurological outcome 6 months after hypothermia treatment following resuscitation from cardiac arrest.

Design

Prospective observational study.

Setting

One intensive care unit at Uppsala University Hospital.

Patients

Thirty-one unconscious patients resuscitated after cardiac arrest.

Interventions

None.

Measurements and main results

Unconscious patients after cardiac arrest with restoration of spontaneous circulation (ROSC) were treated with mild hypothermia to 32-34 °C for 26 h. Time from cardiac arrest to target temperature was measured. Blood samples were collected at intervals of 1-108 h after ROSC. Neurological outcome was assessed with Glasgow-Pittsburgh cerebral performance category (CPC) scale at discharge from intensive care and again 6 months later, when 15/31 patients were alive, of whom 14 had a good outcome (CPC 1-2). Among the predictive biomarkers, S-100B at 24 h after ROSC was the best, predicting poor outcome (CPC 3-5) with a sensitivity of 87% and a specificity of 100%. NSE at 96 h after ROSC predicted poor outcome, with sensitivity of 57% and specificity of 93%. BDNF and GFAP levels did not predict outcome. The time from cardiac arrest to target temperature was shorter for those with poor outcome.

Conclusions

The blood concentration of S-100B at 24 h after ROSC is highly predictive of outcome in patients treated with mild hypothermia after cardiac arrest.     

A sternal accelerometer does not impair hemodynamics during piglet CPR

Aim

To determine whether the residual weight of a 260 g sternal accelerometer/force feedback device (AFFD) adversely affects hemodynamics during cardiopulmonary resuscitation in a piglet model of ventricular fibrillation cardiac arrest.

Methods

After induction of ventricular fibrillation, cardiopulmonary resuscitation was provided to ten piglets (10.8 ± 1.9 kg) for 12 min while maintaining aortic systolic pressure of 80-90 mmHg during four 3-min periods with or without an AFFD on the chest. Cardiac output and left ventricular myocardial blood flow were determined by neutron-microsphere technique.

Results

Using a linear mixed-effect model with residual maximum likelihood estimation to control for changes in cardiopulmonary resuscitation hemodynamics over time, cardiac output and myocardial blood flow did not differ with AFFD versus without AFFD. During the first 6 min, mean (±SEM) cardiac outputs were 0.42 (±0.05) L/min with AFFD versus 0.31 (±0.04) L/min without AFFD, and median left ventricular myocardial blood flows were 40.5 (±7.3) mL/min/100 g with AFFD versus 40.4 (±5.0) mL/min/100 g without AFFD. The mean right atrial diastolic pressures and coronary perfusion pressures were also not different (8 ± 0.7 mmHg versus 8 ± 0.9 mmHg and 16 ± 2 mmHg versus 16 ± 2 mmHg, respectively, during the first 6 min of CPR).

Conclusion

The use of a 260 g accelerometer/force feedback device designed for real-time feedback to the rescuer during resuscitation efforts did not adversely affect cardiac output or left ventricular myocardial blood flow during 12 min of chest compressions in a piglet model of ventricular fibrillation cardiac arrest.     

iCPR: a new application of high-quality cardiopulmonary resuscitation training

Objectives

The present study evaluates a new CPR feedback application for the iPhone (iCPR) designed to improve chest compression performance tested in a cardiac arrest simulation to evaluate performance and acceptance by healthcare professionals and lay people.

Methods

We built an application specifically dedicated to self-directed CPR training through a tutorial that includes a simple feedback module to guide training in order to improve the quality of chest compressions. We tested it in a sample of 50 users to evaluate the effect of iCPR on performance and it is acceptance. The participants were randomly assigned to one of the study groups and were asked to perform a trial of 2 min of chest compressions (CC), to answer a predefined set of questions and then to perform two more minutes of CC. The first group performing the sequence of CC with iCPR - questions - CC without feedback, and the second the sequence CC without feedback - questions CC with iCPR.

Results

The mean compression rate was 101 ± 2.8 min⁻¹ when CC were performed with iCPR and 107.8 ± 20.5 min⁻¹ when performed without iCPR (p < 0.01). Overall, the participants considered iCPR useful to maintain CC at the desired rate of 100 compressions per minute.

Conclusions

The iCPR feedback tool was able to significantly improve the performance of chest compressions in terms of the compression rate in a simulated cardiac arrest scenario. The participants also believed that iCPR helped them to achieve the correct chest compression rate and most users found this device easy to use.