Effects of abciximab on postresuscitation microcirculatory dysfunction after experimental cardiac arrest in rats

Background

The term “postresuscitation syndrome” includes among other pathophysiology impaired microcirculation and endothelial leakage. GPIIb/IIIa receptor antagonists like abciximab have been shown to reduce endothelial leakage and to improve microcirculatory disturbances during experimental endotoxaemia where comparably similar endothelial dysfunction has been observed. Previous investigations on postresuscitation endothelial leakage have indicated a possible role of platelets. Therefore, we investigated effects of abciximab on postresuscitation microcirculation applying in vivo microscopy of postcapillary mesenteric venules after experimentally induced cardiac arrest and cardiopulmonary rescuscitation in rats.

Methods

After 6 min of cardiac arrest (CA) and cardiopulmonary resuscitation (CPR), male Wistar rats were randomised into two groups (n = 10) to receive abciximab (1 mg/kg i.v.) or placebo (0.9% NaCl). Sham operated animals (n = 10) served as non-ischaemic controls. At 360, 420 and 480 min after return of spontaneous circulation (ROSC) in vivo microscopy was performed to assess venular wall shear rate (WSR) and plasma extravasation (PE).

Results

Besides typical signs of severe endothelial leakage in both CA groups, no significant differences between the treatment groups were observed with regard to WSR and PE.

Conclusion

In our study, a distinct postresuscitation microcirculatory splanchnic impairment after CA and successful CPR was observed. However, abciximab had no effects on WSR and PE. Our data does not support a valid resemblance between postresuscitation microcirculatory dysfunction observed in connection with experimental endotoxaemia. Furthermore, our data indicate that mechanisms other than GPIIb/IIIa mediated platelet activation play a role in postresuscitation syndrome. A better understanding of “postresuscitation disease” should enable the development of future therapeutic strategies for cardiac arrest survivors.     

Periodic acceleration (pGz) CPR in a swine model of asphyxia induced cardiac arrest. Short-term hemodynamic comparisons

BACKGROUND: Asphyxia is one of the most common causes of pediatric cardiac arrest, and becoming a more frequently recognized cause in adults. Periodic acceleration (pGz) is a novel method of cardiopulmonary resuscitation (CPR). pGz is achieved by rapid motion of the supine body headward-footward that generates adequate perfusion and ventilation during cardiac arrest. In a swine ventricular fibrillation cardiac arrest model, pGz produced a higher return of spontaneous circulation (ROSC), superior neurological outcome, less echocardiography evidence of post resuscitation myocardial stunning, and decreased indices of tissue injury. In contrast to standard chest compression CPR, pGz does not produce rib fractures. We investigated the feasibility of pGz in severe asphyxia cardiac arrest and assessed whether beneficial effects seen in the VF model of cardiac arrest could be realized. METHODS AND RESULTS: Sixteen swine weight 4+/-1 kg were anesthetized, tracheally intubated, and instrumented to measure, hemodynamics and echocardiography. Asphyxia was induced by occlusion of the tracheal tube. After loss of aortic pulsations (median time 10 min) animals were observed for three additional minutes following which all were in cardiac arrest. The animals were then randomized to receive 10 min of pGz or standard chest compression ventilation performed with a commercial device (Thumper). A single dose of epinephrine (adrenaline) and sodium bicarbonate were given and defibrillation attempted if appropriate for a maximum of 10 min. Both groups received fractional inspired O2 concentration of 100% during CPR and after resuscitation. Four animals in each group (50%) had an initial ROSC, however only two of the four initial survivors remained alive 3h after ROSC. There were no significant differences in blood pressure, coronary perfusion pressure during CPR and after early ROSC between groups. pGz treated animals had significantly lower pulmonary artery pressure; 20+/-4 mmHg compared to Thumper 46+/-5 mmHg, 30 min after ROSC (p<0.01). Surviving animals in both groups had severe myocardial dysfunction at 30 min after ROSC. At necropsy, 25% of the Thumper treated animals had rib fractures, while none occurred in the pGz group. CONCLUSIONS: In a lethal model of asphyxia cardiac arrest, pGz is equivalent to standard CPR, with respect to acute outcomes and resuscitation survival rates but is associated with significantly lower pulmonary artery pressures and does not produce traumatic rib fractures.     

Sex differences in cardiac injury after severe haemorrhage and ventricular fibrillation in pigs

Aim of the study

Experimental studies have shown sex differences in haemodynamic response and outcome after trauma and haemorrhagic shock. We recently reported that female sex protects against cerebral injury after exsanguination cardiac arrest (CA), independent of sexual effects of hormones. The current study examines if female sex is also cardioprotective.

Methods

In this study 21 sexually immature piglets (12 males and 9 females) were subjected to 5 min of haemorrhagic shock followed by 2 min of ventricular fibrillation and 8 min of cardiopulmonary resuscitation (CPR). Volume resuscitation was started during CPR with intravenous administration of 3 ml kg⁻¹ hypertonic saline-dextran (HSD) solution for 20 min. Sexually immature animals were used to differentiate innate sex differences from the effects of sexual hormones. Sex differences in haemodynamics, myocardial injury (troponin I), and short-term survival (3-h) were evaluated.

Results

After resuscitation female animals had a higher blood pressure, lower heart rate, lower troponin I concentrations, and higher survival rate (100% and 63% in 3 h) despite comparable sex hormone levels.

Conclusions

After resuscitation from haemorrhage and circulatory arrest, haemodynamic parameters are better preserved and myocardial injury is smaller in female piglets. This difference in outcome is independent of sexual hormones.     

Distribution of potassium levels on admission for CPR--severe hypokalaemia with dysmorphophobic eating disorders

Aim

To evaluate the prevalence and cause of severe hypokalaemia in patients administered for cardiopulmonary resuscitation (CPR) for non-traumatic cardiac arrest.

Methods

We conducted a retrospective database review in the setting of a University hospital on 281 consecutive adult patients admitted to emergency admission, cardiac catheterization laboratory or intensive care units for resuscitation from non-traumatic cardiac arrest. The first available potassium value was evaluated.

Results

The mean potassium level was 3.9 ± 0.9 mmol/l and thus within the reference range of 3.5-5.0 mmol/l, but the overall prevalence of hypokalaemia was high (31.0%). Moderate rather than severe hypokalaemia was typically observed, with 95% of patients exhibiting potassium levels above 2.7 mmol/l. Among those six patients with extreme hypokalaemia defined as a potassium levels below the 2.5 percentile, two adult females were identified to suffer from previously untreated body scheme disorder with furosemide abuse (potassium 1.1 and 1.4 mmol/l). Another patient (potassium 2.1 mmol/l) suffered from poorly controlled bulimia nervosa and acute diarrhoea due to GI infection and one (potassium 2.4 mmol/l) from untreated bulimic anorexia.

Conclusions

In contrast to moderately reduced potassium which is a frequent finding in adult patients at the time of admission for non-traumatic cardiac arrest, severe hypokalaemia is uncommon. The high prevalence of patients with body dysmorphophobic eating disorders in this group underscores accidental self-induced hypokalaemia may evolve as an important differential diagnosis in cardiac arrest in young female patients.     

Post-resuscitation myocardial microcirculatory dysfunction is ameliorated with eptifibatide

Background

The post-cardiac arrest syndrome includes a decline in myocardial microcirculation function. Inhibition of the platelet IIb/IIIa glycoprotein receptor has improved myocardial microvascular function post-percutaneous coronary intervention. Therefore, we evaluated such inhibition with eptifibatide for its effect on myocardial microcirculation function post-cardiac arrest and resuscitation.

Methods

Four groups of swine were studied in a prospective, randomized, blinded, placebo-controlled protocol including; eptifibatide administered during CPR (Group 1, n = 5), after resuscitation (Group 2, n = 4), during and after resuscitation (Group 3, n = 5), or placebo (Group 4, n = 10). CPR was initiated following 12 min of untreated VF. Those successfully resuscitated were studied during a 4-h post-resuscitation period. Coronary flow reserve, a measure of microcirculation function (in the absence of coronary obstruction), as well as parameters of left ventricular systolic and diastolic function, were measured pre-arrest and serially post-resuscitation.

Results

Coronary flow reserve was preserved during the post-resuscitation period, indicating normal microcirculatory function in the eptifibatide-treated animals, but not in the placebo-treated group. However, LV function declined equally in both groups during the first 4 h after cardiac arrest.

Conclusion

Inhibition of platelet IIb/IIIa glycoprotein receptors with eptifibatide post-resuscitation prevented myocardial microcirculation dysfunction. Left ventricular dysfunction post-resuscitation was not improved with eptifibatide, and perhaps transiently worse at 30 min post-resuscitation. Post-cardiac arrest ventricular dysfunction may require a multi-modality treatment strategy for successful prevention or amelioration.     

How accurately can the aetiology of cardiac arrest be established in an out-of-hospital setting? Analysis by "concordance in diagnosis crosscheck tables"

Introduction

Several previous studies have focused on establishing the cause of cardiac arrest (CA) during cardiopulmonary resuscitation (CPR) provided in an out-of-hospital setting.

Objectives

To analyze the ability of professional advanced life support providers to correctly establish the aetiology of cardiac arrest during out-of-hospital CPR.

Study design

A retrospective cohort study analysing 211 cases of out-of-hospital cardiac arrest.

Method

The aetiology assumed by out-of-hospital physicians was compared with the diagnosis that was later established by clinicians or pathologists.

Results

Cases were sorted into five diagnostic groups and the overall diagnostic concordance was 74.4% (157 of 211 cases). The cardiac aetiology was presumed in 132 out of 211 patients and confirmed in 135 out of 211 patients.However, an analysis of individual cases of the cardiac causes of cardiac arrest revealed diagnostic matches in only 112 cases. Acute myocardial infarction (AMI) or pulmonary embolism (PE), both of which represent cases that can be potentially influenced by thrombolytic therapy, were presumed in 74 (53 + 21) and confirmed in 97 (77 + 20) cases, however with individual diagnostic matches in only 55 cases.

Conclusion

This study demonstrates the importance of analysing concordance in presumed and definitive diagnosis of individual cases, since an overall comparison in a cohort of cases may be highly misleading. It introduces the method of the crosscheck table for visualization and comparison of presumed and final diagnoses. The two alternative approaches of inclusion rule for applying the thrombolytic therapy in out-of-hospital care were discussed with regard to the recent TROICA study.     

Reducing the duration of 100% oxygen ventilation in the early reperfusion period after cardiopulmonary resuscitation decreases striatal brain damage

Purpose

Previous data indicate that 100% O₂ ventilation during early reperfusion after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) increases neuronal death. However, current guidelines encourage the use of 100% O₂ during resuscitation and for an undefined period thereafter. We retrospectively analyzed data from a porcine CA model and hypothesized that prolonged hyperoxic reperfusion would be associated with increased neurohistopathological damage and impaired neurological recovery.

Methods

Fifteen male pigs underwent 8 min of CA and 5 min of CPR. After resuscitation animals were ventilated with either 100% oxygen for 60 min (hyperoxia; n = 8) or 10 min (normoxia; n = 7). Physiological variables were obtained at baseline and 10, 60 and 240 min after resuscitation. Daily functional performance was assessed using an established neurocognitive test in parallel to a neurological deficit score (NDS). On day 5, brains of the re-anaesthetized pigs were harvested for neurohistopathological analyses.

Results

At baseline there were no differences in hemodynamics and neurological status between groups. Post-arrest only PaO₂, as a result of the different inspired oxygen fractions, was significantly higher in the hyperoxia group.There was a numerical trend towards improved clinical recovery in both the NDS and the neurocognitive testing for animals exposed to 10 min of 100% oxygen. However, hyperoxic animals showed a significantly greater degree of necrotic neurons and perivascular inflammation in the striatum in comparison to normoxic animals.

Conclusion

In this retrospective analysis prolonged hyperoxia after CA aggravated necrotic brain damage and perivascular inflammation in the striatum of pigs.     

The feasibility of measuring joint angular velocity with a gyro-sensor

Arai T, Obuchi S, Shiba Y, Omuro K, Nakano C, Higashi T. The feasibility of measuring joint angular velocity with a gyro-sensor.

Objectives

To determine the reliability of an assessment of joint angular velocity using a gyro-sensor and to examine the relationship between ankle angular velocity and physical functions.

Design

Cross-sectional.

Setting

Kinesiology laboratory.

Participants

Twenty healthy young adults (mean age, 22.5y) and 113 community-dwelling older adults (mean age, 75.1y).

Interventions

Not applicable.

Main Outcome Measures

Maximal ankle joint velocity was measured using a gyro-sensor during heel-rising and jumping with knee extended. The intraclass correlation coefficient (ICC) was used to determine the intertester and intratester reliability. The Pearson correlation coefficient was used to examine the relationships between maximal ankle joint velocity and isometric muscle strength and isokinetic muscle power in young adults and also to examine the relationships between maximal ankle joint velocity and functional performance measurements such as walking time in older adults.

Results

High reliability was found for intertester (ICC=.96) and intratester reliability (ICC=.96). The data from the gyro-sensor highly correlated with muscle strength (r range, .62−.68; P<.01) and muscle power (r range, .45−.79; P range, .01−.05). In older subjects, mobility functions significantly correlated with the angular velocity of ankle plantarflexion.

Conclusions

Measurement of ankle angular velocity using a gyro-sensor is both reliable and feasible, with the results representing a significant correlation to muscle power and performance measurements.     

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.     

Use of cyst fluid CEA, CA19-9, and amylase for evaluation of pancreatic lesions

Objectives

The study goals were development of reference intervals and an interpretive algorithm for pancreatic cyst fluid tumor markers.

Design and methods

442 pancreatic cyst fluids were tested for CEA, CA19-9, and amylase.

Results

CEA > 30 ng/mL discriminates mucinous from non-mucinous cysts. After CEA analysis, amylase and CA19-9 segregate non-mucinous and mucinous subtypes, respectively.

Conclusions

Pancreatic cyst fluid tumor markers supplement other diagnostic measures. This study provides estimated reference intervals and an algorithm for interpretation.     

A novel hands-free carotid ultrasound detects low-flow cardiac output in a swine model of pulseless electrical activity arrest

Objective

To determine if a hands-free, noninvasive Doppler ultrasound device can reliably detect low-flow cardiac output by measuring carotid artery blood flow velocities. We compared the ability of observers to detect carotid artery flow velocity differences between pseudo-pulseless electrical activity (PEA) and true-PEA cardiac arrest.

Methods

Five swine were instrumented with aortic (Ao) and right atrial pressure-transducing catheters. The Doppler ultrasound device was adhered to the neck over the carotid artery. Continuous electrocardiogram, pressure readings, and Doppler signal were recorded. Each swine underwent multiple episodes of fibrillation and resuscitation. Episodes of true-PEA and pseudo-PEA were retrospectively identified from all resuscitation attempts by examination of electrocardiogram and Ao waveforms. The sensitivity and specificity of the device to detect pseudo-PEA was obtained using observers blinded to Ao waveform recordings.

Results

There was good interobserver reliability related to identification of pseudo- and true-PEA (κ = 0.873). The observers blinded to Ao waveform recordings agreed on 8 of the 9 episodes of pseudo-PEA, whereas 4 false positives of 26 true-PEA events were reported (sensitivity, 0.89; specificity, 0.85). The Doppler device was able to detect carotid flow velocity over a wide range of Ao blood pressures.

Conclusions

This hands-free, noninvasive Doppler ultrasound device can reliably differentiate pseudo-PEA from true-PEA during resuscitation from cardiac arrest, detecting pressure gradient changes of less than 5 mm Hg through to normotension. This device distinguishes conditions of no cardiac output from low cardiac output and may have applications for use during resuscitation from various etiologies of arrest and shock.     

Transpulmonary cardiac output measurement in a rat model of cardiac arrest and CPR: Impact of vascular access

Objective

The present study investigated the impact of the vascular access site for cardiac output (CO) measurement by thermodilution on survival and neurohistopathological injury in a rat model of cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Secondary the influence of the vascular access site on cardiac output measurements was examined.

Methods

Rats underwent asphyxial CA and CPR. Thermocouple probes were either placed via the femoral artery into the bifurcation of abdominal aorta/iliac artery (Femoral) or via the carotid artery into the aortic arch (Carotid). CPR was initiated after 9 min CA. Local cerebral blood flow (lCBF) and CO were assessed for 120 min after restoration of spontaneous circulation. Neurohistopathological injury was determined using Fluoro-Jade B staining.

Results

Survival was reduced in the Carotid group compared to the Femoral group (p < 0.01). Fluoro-Jade B staining in the hippocampus showed no difference between CA groups. CO measurements were comparable between femoral and carotid artery access sites. lCBF revealed a delayed hyperperfusion in the Carotid group only.

Conclusions

The present study demonstrates the influence of the vascular access site for placing thermocouple probes for CO measurement on animal survival after CA/CPR. CO did not differ between the two access sites with consequential different detection sites. Use of the femoral access for CO measurement is recommended for long-term survival after CA/CPR.     

A model of survival from out-of-hospital cardiac arrest using the Boston EMS arrest registry

Objectives

To characterize the survival rate for out-of-hospital arrests of cardiac aetiology and predictor variables associated with survival in Boston, MA, and to develop a composite multivariate logistic regression model for projecting survival rates.

Methods

This is a retrospective analysis of all arrests of presumed cardiac aetiology (from January 1, 2004 to December 31, 2007) where resuscitation was attempted (n = 1156) by 911 emergency responders.

Results

The survival-at-hospital discharge rate was 11% (vs. 1-10% often reported). The coefficients and odds ratios in the first equation of the model show that joint presence of presenting rhythm of ventricular fibrillation/tachycardia (VF/VT) and return of spontaneous circulation in the pre-hospital setting (ROSC) is a substantial direct predictor of survival (e.g., 54% of such cases survive). Response time, public location, witnessed, and age are significant but less sizable direct predictors of survival. A second equation shows that these four variables make an additional indirect contribution to survival by affecting the probability of joint presence of VF/VT and ROSC; bystander CPR also makes such an indirect contribution but no significant direct one as shown in the first equation. The projected survival rate if cases had always experienced bystander CPR and rapid response time of less than four minutes is 21%.

Conclusions

The unique model describes the major contribution of VF/VT and ROSC, and key relationships among predictors of survival. These connections may have otherwise gone underreported using standard approaches and should be considered when allocating scarce resources to impact cardiac arrest survival.     

Correlations between hemodynamic, oxygenation and tissue perfusion parameters during asphyxial cardiac arrest and resuscitation in a pediatric animal model

Aim

To analyze the correlations between hemodynamic, oxygenation and tissue perfusion values in an infant animal model of asphyctic cardiac arrest (ACA).

Methods

A prospective observational animal study was performed in seventy one, two month-old piglets. CA was induced by removal of mechanical ventilation and was followed by advanced life support after at least 10 min. Correlations between hemodynamic [heart rate (HR), mean arterial pressure (MAP), cardiac index (CI), stroke volume index (SVI) and intrathoracic blood index (ITBI) measured by PiCCO method], blood gas values (arterial and central venous saturation), and tissue perfusion values [intramucosal gastric pH (pHi), and tissue oxygenation (cerebral and renal saturation)] were analyzed during asphyxia, resuscitation and after return of spontaneous circulation (ROSC).

Results

Among global hemodynamic parameters, the only moderate significant correlation observed was between CI and ITBI (r = .551). Among tissue oxygenation/perfusion values, a moderate to good significant correlation (r = .460-.763) between arterial oxygen saturation, central venous, renal and cerebral oxygen saturation was observed. Lactic acid, potassium (K) and pHi were correlated (r = .561-.639), but no correlation was found between them and tissue oxygenation parameters. Global hemodynamic parameters (CI, HR, MAP) did not correlate with renal and cerebral saturations and tissue perfusion parameters.

Conclusions

During ACA and after ROSC global hemodynamic parameters do not correlate with oxygenation and tissue perfusion values. Additional studies which assess the potential usefulness of tissue oxygenation/perfusion parameters during cardiac arrest and ROSC are needed.     

Glucagon-like peptide-1 (GLP-1) attenuates post-resuscitation myocardial microcirculatory dysfunction

Aim of the study

Post-resuscitation syndrome leads to death in approximately 2 out of every 3 successfully resuscitated victims, and myocardial microcirculatory dysfunction is a major component of this syndrome. The aim of this study was to determine if glucagon-like peptide-1 (GLP-1) improves post-resuscitation myocardial microcirculatory function.

Methods

Ventricular fibrillation (VF) was induced electrically in 20 anesthetized domestic swine (30-35 kg). Following 8 min of untreated VF, animals were resuscitated with aggressive advanced cardiac life support (ACLS). Animals were blindly randomized to receive a continuous infusion of either GLP-1 (10 pM/kg/min) or equal volume saline as placebo (PBO) for 4 h, beginning 1 min after return of spontaneous circulation (ROSC). Left ventricular (LV) haemodynamics, LV ejection fraction, cardiac output, and coronary flow reserve (CFR) [using a standard technique of intracoronary Doppler flow measurements before and after intracoronary administration of 60 μg adenosine] were performed pre-arrest and at 1 and 4 h post-resuscitation. In the present study, CFR is a measure of myocardial microcirculatory function since these swine had no obstructive coronary artery disease. Twenty-four hour post-resuscitation survival and neurological functional scores were also determined.

Results

CFR was significantly increased in GLP-1-treated animals, 1 h (1.79 ± 0.13 in control animals vs. 2.05 ± 0.12 in GLP-1-treated animals, P = < 0.05) and 4 h (1.82 ± 0.16 in control animals vs. 2.31 ± 0.13 in GLP-1-treated animals, P = < 0.05) after ROSC. In addition, compared to PBO-treated animals, GLP-1 increased cardiac output 1 h after ROSC (2.1 ± 0.1 in control animals vs. 2.7 ± 0.2 in GLP-1-treated animals, P = < 0.05). There was no statistically significant difference in survival between GLP-1-treated (100%) and PBO-treated animals (78%).

Conclusions

In this swine model of prolonged VF followed by successful resuscitation, myocardial microcirculatory function was enhanced with administration of GLP-1. However, GLP-1 treatment was not associated with a clinically significant improvement in post-resuscitation myocardial function.     

Quality management in resuscitation--towards a European cardiac arrest registry (EuReCa)

Background

Knowledge about the epidemiology of cardiac arrest in Europe is inadequate.

Aim

To describe the first attempt to build up a Common European Registry of out-of-hospital cardiac arrest, called EuReCa.

Methods

After approaching key persons in participating countries of the European Resuscitation Council, five countries or areas within countries (Belgium, Germany, Andalusia, North Holland, Sweden) agreed to participate. A standardized questionnaire including 28 items, that identified various aspects of resuscitation, was developed to explore the nature of the regional/national registries. This comprises inclusion criteria, data sources, and core data, as well as technical details of the structure of the databases.

Results

The participating registers represent a population of 35 million inhabitants in Europe. During 2008, 12,446 cardiac arrests were recorded. The structure as well as the level of complexity varied markedly between the 5 regional/national registries. The incidence of attempted resuscitation ranged between registers from 17 to 53 per 100,000 inhabitants each year whilst the number of patients admitted to hospital alive ranged from 5 to 18 per 100,000 inhabitants each year. Bystander CPR varied 3-fold from 20% to 60%.

Conclusion

Five countries agreed to participate in an attempt to build up a common European Registry for out-of-hospital cardiac arrest. These regional/national registries show a marked difference in terms of structure and complexity. A marked variation was found between countries in the number of reported resuscitation attempts, the number of patients brought to hospital alive, and the proportion that received bystander CPR. At present, we are unable to explain the reason for the variability but our first findings could be a ‘wake-up-call’ for building up a high quality registry that could provide answers to this and other key questions in relation to the management of out-of-hospital cardiac arrest.     

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

Aim of the study

Adjustment 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.

Methods

Twenty-eight male domestic pigs were randomised to the following 4 groups according to the dosage of adrenaline (SDA 0.02 mg/kg vs. HDA 0.2 mg/kg) and duration of CA before beginning cardiopulmonary resuscitation (CPR): 6 min SDA, 6 min HDA, 13 min SDA, or 13 min HDA. After the predetermined duration of untreated ventricular fibrillation, CPR was provided.

Results

All animals in the 6 min SDA, 6 min HDA, and 13 min HDA groups were successfully resuscitated, while only 4 of 7 pigs in the 13 min 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 13 min groups showed more severe metabolic acidosis and higher troponin-I than animals of 6 min groups. All successfully resuscitated animals, except two animals in the 13 min HDA group, survived for 7 days (p = 0.121). Neurologic deficit score was not affected by the dose of adrenaline.

Conclusion

HDA showed benefit in achieving restoration of spontaneous circulation in 13 min CA, when compared with 6 min CA. However, this benefit did not translate into improved long-term survival or neurologic outcome.     

Evolution of somatosensory evoked potentials after cardiac arrest induced hypoxic-ischemic injury

Aim

We tested the hypothesis that early recovery of cortical SEP would be associated with milder hypoxic-ischemic injury and better outcome after resuscitation from CA.

Methods

Sixteen adult male Wistar rats were subjected to asphyxial cardiac arrest. Half underwent 7 min of asphyxia (Group CA7) and half underwent 9 min (Group CA9). Continuous SEPs from median nerve stimulation were recorded from these rats for 4 h immediately following CA, and at 24, 48, and 72 h. Clinical recovery was evaluated using the Neurologic Deficit Scale.

Results

All rats in group CA7 survived to 72 h, while only 50% of rats in group CA9 survived to that time. Mean NDS values in the CA7 group at 24, 48, and 72 h after CA were significantly higher than those of CA9. The N10 (first negative potential at 10 ms) amplitude was significantly lower within 1 h after CA in rats that suffered longer CA durations. SEPs were also analyzed by separating the rats into good (NDS ≥ 50) vs. bad (NDS < 50) outcomes at 72 h, again showing significant difference in N10 and peak-to-peak amplitudes between the two groups. In addition, a smaller N7 potential was consistently observed to recover earlier in all rats.

Conclusions

The diminished recovery of N10 is associated with longer CA times in rats. Higher N10 and peak-to-peak amplitudes during early recovery are associated with better neurologic outcomes. N7, which may represent thalamic activity, recovers much earlier than cortical responses (N10), suggesting failure of thalamocortical conduction during early recovery.     

Non-selective cyclooxygenase inhibition before periodic acceleration (pGz) cardiopulmonary resuscitation (CPR) in a porcine model of ventricular fibrillation

Whole body periodic acceleration (pGz) along the spinal axis is a novel method of cardiopulmonary resuscitation (CPR). Oscillatory motion of the supine body in a horizontal fashion provides ventilation and blood flow to vital organs during cardiac arrest and pulsatile shear stress to the vascular endothelium. We previously showed in pigs that pGz–CPR affords better overall survival, post resuscitation myocardial function, and neurological outcomes compared to conventional chest compression CPR. pGz through pulsatile shear stress on the vascular endothelium elicits acute production of prostaglandins and endothelial-derived nitric oxide (eNO) in whole animal models and in vitro preparations. The salutary effects associated with pGz–CPR compared to chest compression CPR are in part related to endothelial-derived nitric oxide. Both eNO and prostaglandins are cardioprotective in ischemia reperfusion models. To differentiate between the roles of these mediators, indomethacin a non-selective cyclooxygenase inhibitor (COX) was used as a tool to investigate prostaglandin effects during pGz–CPR by acute outcomes of survival, cardioprotection and regional blood flows (RBF). Two groups of anesthetized, intubated pigs weighing 25–36 kg were studied. Prior to electrical induction of ventricular fibrillation (VF) animals received equal volumes of either saline placebo Control (CONT) (n = 9) or indomethacin (INDO), (n = 8), (2 mg/kg). After 3 min of unsupported VF, both groups received 15 min of pGz–CPR followed by pharmacologic and electrical attempts for resuscitation. Return of circulation (ROSC) to 3 h occurred in (78%) in CONT and (63%) in INDO pretreated animals. There was no statistically significant difference in hemodynamics between groups at baseline or during the protocol. At baseline, INDO caused a decrease in brain RBF. Two hours after ROSC, INDO blunted the hyperemia response to brain and heart. Echocardiographic evidence of myocardial dysfunction was most notable for the INDO group in the wall motion score index (WMSI). After 3 h of ROSC there was a 4-fold difference in both creatine phosphokinase (CPK) and Troponin I concentration between INDO and CONT. Therefore, non-specific acute inhibition of COX in part blunts the salutary effects of pGz–CPR. These data suggest that prostaglandins in part are involved in the cardio protection induced by pGz during CPR.