Effects of early amiodarone administration during and immediately after cardiopulmonary resuscitation in a swine model.

BACKGROUND: Aim of this experimental study was to compare haemodynamic effects and outcome with early administration of amiodarone and adrenaline vs. adrenaline alone in pigs with prolonged ventricular fibrillation (VF). METHODS: After 8 min of untreated VF arrest, bolus doses were administered of adrenaline (0.02 mg/kg) and either amiodarone (5 mg/kg) or saline (n = 8 per group) after randomisation. Cardiopulmonary resuscitation (CPR) was commenced immediately after drug administration, and defibrillation was attempted 2 min later. CPR was resumed for another 2 min after each defibrillation attempt, and the same dose of adrenaline was given every 4th minute during CPR. Haemodynamic monitoring and mechanical ventilation continued for 6 h after return of spontaneous circulation (ROSC), and the pigs were euthanised at 48 h. Researchers were blinded for drug groups throughout the study. RESULTS: There was no difference in rates of ROSC and 48-h survival with amiodarone vs. saline (5/8 vs. 7/8 and 0/8 vs. 3/8, respectively). Diastolic aortic pressure and coronary perfusion pressure were significantly lower with amiodarone during CPR and 1 min after ROSC (P < 0.05). The number of electric shocks required for terminating VF, time to ROSC and adrenaline dose were significantly higher with amiodarone (P < 0.01). The incidence of post-resuscitation tachyarrhythmias tended to be higher in the saline group (P = 0.081). CONCLUSION: Early administration of amiodarone did not improve ROSC or 48-h survival rates, and was associated with worse haemodynamics in this swine model of cardiac arrest.

Minimum alveolar concentration (MAC) for sevoflurane and xenon at normothermia and hypothermia in newborn pigs.

BACKGROUND: Neuroprotection from therapeutic hypothermia increases when combined with the anaesthetic gas xenon in animal studies. A clinical feasibility study of the combined treatment has been successfully undertaken in asphyxiated human term newborns. It is unknown whether xenon alone would be sufficient for sedation during hypothermia eliminating or reducing the need for other sedative or analgesic infusions in ventilated sick infants. Minimum alveolar concentration (MAC) of xenon is unknown in any neonatal species. METHODS: Eight newborn pigs were anaesthetised with sevoflurane alone and then sevoflurane plus xenon at two temperatures. Pigs were randomised to start at either 38.5°C or 33.5°C. MAC for sevoflurane was determined using the claw clamp technique at the preset body temperature. For xenon MAC determination, a background of 0.5 MAC sevoflurane was used, and 60% xenon added to the gas mixture. The relationship between sevoflurane and xenon MAC is assumed to be additive. Xenon concentrations were changed in 5% steps until a positive clamp reaction was noted. Pigs' temperature was changed to the second target, and two MAC determinations for sevoflurane and 0.5 MAC sevoflurane plus xenon were repeated. RESULTS: MAC for sevoflurane was 4.1% [95% confidence interval (CI): 3.65-4.50] at 38.5°C and 3.05% (CI: 2.63-3.48) at 33.5°C, a significant reduction. MAC for xenon was 120% at 38.5°C and 116% at 33.5°C, not different. CONCLUSION: In newborn swine sevoflurane, MAC was temperature dependent, while xenon MAC was independent of temperature. There was large individual variability in xenon MAC, from 60% to 120%.

Detection of carbon dioxide in expired air after oesophageal intubation; the role of bystander mouth-to-mouth ventilation.

BACKGROUND: The identification of a correctly placed tube during anaesthesia routinely depends on the detection of carbon dioxide (CO2) in the expired air. RESULTS: We describe a previously unreported cause of false-positive prediction in two patients with high initial values of CO2 in expired air after oesophageal intubation. Both patients had received bystander cardiopulmonary resuscitation with mouth-to-mouth ventilation, and the CO2 from the rescuers' expired air was trapped and subsequently detected after oesophageal intubation.

Standard basic life support vs. continuous chest compressions only in out-of-hospital cardiac arrest.

BACKGROUND: The importance of ventilations after cardiac arrest has been much debated recently and eliminating mouth-to-mouth ventilations for bystanders has been suggested as a means to increase bystander cardiopulmonary resuscitation (CPR). Standard basic life support (S-BLS) is not documented to be superior to continuous chest compressions (CCC). METHODS: Retrospective, observational study of all non-traumatic cardiac arrest patients older than 18 years between May 2003 and December 2006 treated by the community-run emergency medical service (EMS) in Oslo. Outcome for patients receiving S-BLS was compared with patients receiving CCC. All Utstein characteristics were registered for both patient groups as well as for patients not receiving any bystander CPR by reviewing Ambulance run sheets, Utstein forms and hospital records. Method of bystander CPR as well as dispatcher instruction was registered by first-arriving ambulance personnel. RESULTS: Six-hundred ninety-five out of 809 cardiac arrests in our EMS were included in this study. Two-hundred eighty-one (40%) received S-CPR and 145 (21%) received CCC. There were no differences in outcome between the two patient groups, with 35 (13%) discharged with a favourable outcome for the S-BLS group and 15 (10%) in the CCC group (P=0.859). Similarly, there was no difference in survival subgroup analysis of patients presenting with initial ventricular fibrillation/ventricular tachycardia after witnessed arrest, with 32 (29%) and 10 (28%) patients discharged from hospital in the S-BLS and CCC groups, respectively (P=0.972). CONCLUSIONS: Patients receiving CCC from bystanders did not have a worse outcome than patients receiving standard CPR, even with a tendency towards a higher distribution of known negative predictive features.

Compression force-depth relationship during out-of-hospital cardiopulmonary resuscitation.

BACKGROUND: Recent clinical studies reporting the high frequency of inadequate chest compression depth (<38 mm) during CPR, have prompted the question if adult human chest characteristics render it difficult to attain the recommended compression depth in certain patients. MATERIAL AND METHODS: Using a specially designed monitor/defibrillator equipped with a sternal pad fitted with an accelerometer and a pressure sensor, compression force and depth was measured during CPR in 91 adult out-of-hospital cardiac arrest patients. RESULTS: There was a strong non-linear relationship between the force of compression and depth achieved. Mean applied force for all patients was 30.3+/-8.2 kg and mean absolute compression depth 42+/-8 mm. For 87 of 91 patients 38 mm compression depth was obtained with less than 50 kg. Stiffer chests were compressed more forcefully than softer chests (p<0.001), but softer chests were compressed more deeply than stiffer chests (p=0.001). The force needed to reach 38 mm compression depth (F38) and mean compression force were higher for males than for females: 29.8+/-14.5 kg versus 22.5+/-10.2 kg (p<0.02), and 32.0+/-8.3 kg versus 27.0+/-7.0 kg (p<0.01), respectively. There was no significant variation in F38 or compression depth with age, but a significant 1.5 kg mean decrease in applied force for each 10 years increase in age (p<0.05). Chest stiffness decreased significantly (p<0.0001) with an increasing number of compressions performed. Average residual force during decompression was 1.7+/-1.0 kg, corresponding to an average residual depth of 3+/-2 mm. CONCLUSION: In most out-of-hospital cardiac arrest victims adequate chest compression depth can be achieved by a force<50 kg, indicating that an average sized and fit rescuer should be able to perform effective CPR in most adult patients.

Practical issues in the evaluation of methods for the prediction of shock outcome success in out-of-hospital cardiac arrest patients.

There is a need for robust, effective predictors of the outcome from shock for out-of-hospital cardiac arrest patients. Such technology would enable the emergency responder to provide a therapy tailored to the patient's needs. Here we report our most recent findings while dwelling intentionally on the rationale behind the decisions taken during system development. Specifically, we illustrate the need for sensible data selection, fully cross-validated results and the care necessary when evaluating system performance. We analyze 878 pre-shock ECG traces, all of at least 10 s duration from 110 patients with cardiac arrest of cardiac aetiology. The continuous wavelet transform was applied to preshock segments of ECG trace. Time-frequency markers are extracted from the transform and a linear threshold derived from a training set to provide high sensitivity prediction of successful defibrillation. These systems are then evaluated on a withheld test set. All experiments are cross-validated. When compared to popular Fourier-based techniques our wavelet transform method, COP (Cardioversion Outcome Predictor), provides a 10-20% improvement in performance with values of 66 +/- 4 specificity at 95 +/- 4 sensitivity, 61 +/- 4 specificity at 97 +/- 2 sensitivity and 56 +/- 1 specificity at 98 +/- 2 sensitivity achieved for datasets limited to 3, 6, and 9 shocks per patient, respectively. Thus, the assessment of the wavelet marker was associated with a high specificity value at or above 95% sensitivity in comparison to previously reported methods. Therefore, COP could provide an optimal index for the identification of patients for whom shocking would be futile, and for whom an alternative therapy could be considered.

Post resuscitation care: what are the therapeutic alternatives and what do we know?

A large proportion of deaths in the Western World are caused by ischaemic heart disease. Among these patients a majority die outside hospital due to sudden cardiac death. The prognosis among these patients is in general, poor. However, a significant proportion are admitted to a hospital ward alive. The proportion of patients who survive the hospital phase of an out of hospital cardiac arrest varies considerably. Several treatment strategies are applicable during the post resuscitation care phase, but the level of evidence is weak for most of them. Four treatments are recommended for selected patients based on relatively good clinical evidence: therapeutic hypothermia, beta-blockers, coronary artery bypass grafting, and an implantable cardioverter defibrillator. The patient's cerebral function might influence implementation of the latter two alternatives. There is some evidence for revascularisation treatment in patients with suspected myocardial infarction. On pathophysiological grounds, an early coronary angiogram is a reasonable alternative. Further randomised clinical trials of other post resuscitation therapies are essential.

Predicting outcome of defibrillation by spectral characterization and nonparametric classification of ventricular fibrillation in patients with out-of-hospital cardiac arrest.

BACKGROUND: In 156 patients with out-of-hospital cardiac arrest of cardiac cause, we analyzed the ability of 4 spectral features of ventricular fibrillation before a total of 868 shocks to discriminate or not between segments that correspond to return of spontaneous circulation (ROSC). METHODS AND RESULTS: Centroid frequency, peak power frequency, spectral flatness, and energy were studied. A second decorrelated feature set was generated with the coefficients of the principal component analysis transformation of the original feature set. Each feature set was split into training and testing sets for improved reliability in the evaluation of nonparametric classifiers for each possible feature combination. The combination of centroid frequency and peak power frequency achieved a mean+/-SD sensitivity of 92+/-2% and specificity of 27+/-2% in testing. The highest performing classifier corresponded to the combination of the 2 dominant decorrelated spectral features with sensitivity and specificity equal to 92+/-2% and 42+/-1% in testing or a positive predictive value of 0.15 and a negative predictive value of 0.98. Using the highest performing classifier, 328 of 781 shocks not leading to ROSC would have been avoided, whereas 7 of 87 shocks leading to ROSC would not have been administered. CONCLUSIONS: The ECG contained information predictive of shock therapy. This could reduce the delivery of unsuccessful shocks and thereby the duration of unnecessary "hands-off" intervals during cardiopulmonary resuscitation. The low specificity and positive predictive value indicate that other features should be added to improve performance.

Have the implementation of a new specialised emergency medical service influenced the pattern of general practitioners involvement in pre-hospital medical emergencies? A study of geographic variations in alerting, dispatch, and response.

OBJECTIVES: Emergency medical service systems in Norway are based on equity and equality. A toll free number (113) and criteria based dispatch are crucial components. The establishment of an emergency medical system (EMS) manned by an air and ground emergency physician (EP) has challenged the role of the general practitioner (GP) in emergency medical care. We investigated whether there were any geographical differences in the use of 113, alerts to GPs by the emergency medical dispatch centres (EMDCs), and of the presence of GPs on scene in medical emergencies leading to a turnout of the EP manned EMS. METHODS: This was a prospective, observational cohort study of 385,000 inhabitants covered by the two EMDCs of Rogaland county, Norway, including 1035 on scene missions of the EP manned EMS during the period 1998-99. RESULTS: The proportion of emergency calls routed through 113 was significantly lower, the proportion of alerts to GPs significantly higher, and the proportions of GPs on scene significantly higher in rural than urban areas. CONCLUSION: We found geographical differences in the involvement of GPs in pre-hospital emergency medical situations, probably caused by a specialised emergency medical service system including an EMDC and an air and ground EP manned EMS. There were geographical differences in public use of the toll free 113, and alerts to GPs by the EMDCs, which is likely to result from geographical conditions and proximity to medical resources. Future organisation of the EMS has to reflect this to prevent unplanned and unwanted autonomously emerging EMS systems.

The effects of nimodipine on cerebral blood flow and metabolism.

Nimodipine, a calcium entry blocker, was administered in increasing doses of 0.1-3.0 micrograms kg-1 min-1 to six dogs after they had recovered consciousness from a surgical preparation that was conducted under general anesthesia and while they were under the influence of total spinal anesthesia. CBF was measured with a sagittal sinus outflow technique and CMRO2 was calculated as the product of CBF and the arteriovenous O2 difference. Nimodipine did not influence either CBF or CMRO2. There was a decrease in the cortical pyruvate level at the end of the study, but no significant change in phosphocreatine, ATP, lactate, or energy charge when compared with six control dogs. It has previously been reported that nimodipine increases the CBF in global ischemia with a potentially beneficial effect on the neurological outcome. With no effect on normal CBF or metabolism, this suggests that nimodipine may be useful in a variety of ischemic situations without fear of either a steal phenomenon or untoward effects on intracranial pressure.

Nimodipine improves cerebral blood flow and neurologic recovery after complete cerebral ischemia in the dog.

Ten minutes of complete ischemia was produced in 11 dogs by temporary ligation of the aorta. Immediately before the ischemic episode, the dogs received nimodipine, a new calcium entry blocker, 10 micrograms kg-1, i.v., followed by an infusion of 1 microgram kg-1 min-1 for 2 h. Post-ischemic cerebral blood flow and metabolism were measured for 120 min in six dogs. Neurologic recovery was evaluated 48 h post-ischemia in five dogs. The results were compared to previously determined controls. Nimodipine nearly doubled cerebral blood flow in the delayed post-ischemic hypoperfusion period, compared to untreated dogs (approximately 45% versus 25% of pre-ischemic control values), but had no significant effect on metabolism. Nimodipine also improved neurologic recovery. Four of five treated dogs were normal and one was moderately damaged, whereas six of seven controls were either severely damaged or dead. This suggests that the delayed hypoperfusion state occurring after complete cerebral ischemia probably does contribute to the ultimate neurologic damage, and that nimodipine offers a potential protective effect.

Cerebral blood flow and neurologic outcome when nimodipine is given after complete cerebral ischemia in the dog.

Ten minutes of complete cerebral ischemia was produced in 26 dogs by temporary ligation of the aorta and the venae cavae. Twenty dogs received nimodipine, a calcium entry blocker, 10 micrograms kg-1 i.v. 2 min after the ischemic period, followed by 1 microgram kg-1 min-1 for 2-3 h. Six dogs received only the solvent used for nimodipine. Fourteen dogs received nimodipine for 3 h and were subsequently evaluated neurologically up to 48 h postischemia. In the 12 other dogs, CBF and metabolism were followed for 2 h postischemia while either nimodipine or the solvent only was infused. The results were compared to previously published results for untreated dogs and dogs given nimodipine before the ischemic event. Nimodipine had the same effect on postischemic CBF whether started before or after the ischemic event, nearly doubling the flow when compared with untreated controls, whereas the solvent alone caused only a slight increase in CBF over control. By contrast, nimodipine initiated in the preischemic period significantly improved the neurologic outcome, but when initiated in the postischemic period the results were equivocal, such that the outcome was not significantly different from either the untreated group or the group in which nimodipine was initiated preischemia. Metabolic measurements did not give any indication of a specific effect of nimodipine, nor could the metabolic results be used as an indicator of neurologic outcome. The results are consistent with a beneficial effect of nimodipine following complete cerebral ischemia; however, evaluation of neurologic functional effects will require a more sensitive model.

Effects of the chiral isomers of erythro- and threo-9-(2-hydroxy-3-nonyl)adenine on purine metabolism in sarcoma 180 cells.

The effects of the chiral isomers of erythro- and threo-9-(2-hydroxy-3-nonyl)adenines (EHNA and THNA) on purine metabolism in Sarcoma 180 cells have been determined. At concentrations of 10-80 microM [10- to 1000-fold greater than their Ki values with adenosine deaminase (ADA)], all isomers inhibited purine salvage and biosynthesis de novo. Although (+)-EHNA, the most potent ADA inhibitor, exerted the greatest effects, there was no direct correlation between the potency of ADA inhibition and the secondary effects on purine metabolism, e.g. (+)-EHNA is about 2-fold more inhibitory than (-)-EHNA in blocking purine base incorporation but about 250-fold more potent as an inhibitor of ADA (Ki of (+)-EHNA = 2 nM; Ki of (-)-EHNA = 500 nM [Bessodes et al., Biochem. Pharmac. 31, 879 (1982)]). All the isomers inhibited the incorporation of radiolabeled purine bases (adenine, guanine and hypoxanthine) and nucleosides (guanosine and inosine) into acid-soluble nucleotides and of glycine into 5'-phosphoribosyl-formylglycineamide. Unlike the results of Henderson et al. [Biochem. Pharmac. 26, 1967 (1977)] with Ehrlich ascites cells, the incorporation of adenosine into nucleotides was only slightly inhibited in Sarcoma 180 cells. (+)-EHNA did not inhibit the activities of 5-phosphoribosyl-1-pyrophosphate (PRPP) synthetase, purine phosphoribosyltransferases or nucleotide kinases in cell extracts. Accumulation of PRPP was inhibited only under conditions that fostered rapid synthesis.

Perioperative myocardial infarction in patients with coronary artery disease with and without aorta--coronary artery bypass grafts.

The incidence of perioperative myocardial infarction (MI) was examined in 148 patients with known coronary artery disease (CAD) who underwent 226 noncardiac surgical procedures. In 168 operations in 99 patients who had prior coronary artery bypass grafting (CABG) there were no perioperative MI's whereas in the 49 patients who had not undergone prior CABG who underwent 58 noncardiac operations, there were three MI's (5 percent). The lower (p less than 0.02) incidence of perioperative MI in patients with CAD who had had prior CABG suggests a protective effect for subsequent noncardiac operation, which could not be explained by other differences in cardiac status between the groups. All three MI's occurred in patients with three-vessel CAD, evidence that this should be added to prior MI as a significant risk factor. The study indicates also that patients with prior CABG have less risk of MI during and following anesthesia and noncardiac operation than do patients without CABG who have had a previous MI.

Post-hypoxic hypothermia reduces cerebrocortical release of NO and excitotoxins.

Hypothermia applied after hypoxia offers neuroprotection in neonatal animals, but the mechanisms involved remain unknown. Hypoxia was induced in newborn piglets and changes in excitatory amino acids (EAAs) and the citrulline:arginine ratio (CAR) were followed by microdialysis for 5 h. After the 45 min hypoxic insult, the animals were randomized to receive normothermia (39 degrees C; n=7) or hypothermia (35 degrees C; n = 7). After reoxygenation, extracellular glutamate, aspartate and the excitotoxic index were significantly lower in the cerebral cortex of hypothermic animals than in normothermic animals. A progressive rise of the CAR occurred during reoxygenation in the normothermic group whereas the ratio tended to decrease in the hypothermic group. In conclusion, post-hypoxic hypothermia attenuated NO production and overflow of EAAs.

The ventilation/compression ratio influences the effectiveness of two rescuer advanced cardiac life support on a manikin.

Time is of crucial importance during advanced cardiac life support (ACLS). Several parallel tasks have to be performed more or less simultaneously. The guidelines recommend a ventilation/ compression ratio of 1:5 in two-rescuer ACLS. This was compared with respect to time and CPR quality to an alternative method of a 2:15 ratio performed by one of the two rescuers freeing one rescuer to concentrate on other tasks than ventilation and chest compression. Seventeen paramedic students were trained in pairs in ACLS according to the European Resuscitation Council guidelines using an Ambu Mega Code trainer manikin. From a starting point of asystole paramedics were required to perform ECG analysis, intubation, i.v. access, adrenalin and atropine injection, flushing of the drug bolus before conversion to ventricular fibrillation followed by defibrillation in addition to ventilation and chest compression. Unpaired two-tailed Student t-test and the Fisher's exact test were used for statistical analysis, with a P-value less than 0.05 regarded as significant. It took significantly less time to perform successful CPR with the 2:15 ratio compared to the 1:5 ratio. The quality of the ventilations and compressions performed were not significantly different between 2:15 and 1:5 ratio. When two rescuers are performing ACLS, the 2:15 ratio method appears to be time saving vs. the 1:5. This could potentially improve the outcome after cardiac arrest.

Arterial blood gases with 700 ml tidal volumes during out-of-hospital CPR.

The optimal tidal and minute ventilation during cardiopulmonary resuscitation (CPR) is not known. In the present study seven adult, non-traumatic, out-of-hospital cardiac arrest patients were intubated and mechanically ventilated at 12 min(-1) with 100% oxygen and a tidal volume of 700 ml (10 +/- 2 ml kg(-1)). Arterial blood gas samples were analysed after 6-8 min of unsuccessful resuscitation and mechanical ventilation. Mean PaCO2 was 5.2 +/- 1.3 kPa and mean PaO2 30.7 +/- 17.2 kPa. The patient with the highest (14 ml kg(-1)) and lowest (8 ml kg(-1)) tidal volumes per kg had the lowest and highest PaCO2 values of 2.6 and 6.8 kPa, respectively. Linear regression analysis confirmed a significant correlation between arterial pCO2 and tidal volume in ml/kg, r2 = 0.87. We conclude that aiming for an estimated ventilation of 10 ml kg(-1) tidal volume at frequency of 12 min(-1) might be expected to achieve normocapnia during ALS.

Buffer therapy during out-of-hospital cardiopulmonary resuscitation.

The effects of infusing a buffer solution on resuscitability and outcome was tested in patients during out-of-hospital cardiac arrest. A number (502) of adults with asystole or ventricular fibrillation with failure of first defibrillation attempt were entered into a prospective, randomized, double-blind, controlled trial. Of these, 245 patients received 250 ml of sodium bicarbonate-trometamol- phosphate mixture with buffering capacity 500 mmol/l and 257 patients received 250 ml 0.9% saline. Except for the investigational infusion, all patients were resuscitated according to international guidelines. Eighty-seven patients (36%) receiving buffer were admitted to hospital ICU and 24 (10%) were discharged from hospital alive, vs. 92 (36%) and 35 (14%) receiving saline (95% confidence interval (CI) for difference between groups: -6%-6% for rate of admission and -1%-9% for rate of discharge). Using a logistic regression analysis, ventricular fibrillation as initial rhythm (odds ratio 8.06, CI 3.70-17.56) improved the outcome, whereas buffer therapy had no effect (odds ratio 0.77, CI 0.43-1.41). Mean base excess at hospital admission was -9 after Tribonat vs. -11 after saline (P = 0.04, CI for difference 0.2-3.8). Only 16 of the 502 patients had arterial alkalosis on arrival in the hospital and no patient had a positive base excess. Patients resuscitated after out-of-hospital cardiac arrest had metabolic acidosis, but buffer therapy did not improve the outcome.

Quality of bystander cardiopulmonary resuscitation influences outcome after prehospital cardiac arrest.

To evaluate the influence of quality of bystander cardiopulmonary resuscitation (CPR) on outcome in prehospital cardiac arrest we consecutively included patients with prehospital cardiac arrest treated by paramedics in a community run ambulance system in Oslo, Norway from 1985 to 1989. Good CPR was defined as palpable carotid or femoral pulse and intermittent chest expansion with inflation attempts. Outcome measure was hospital discharge rate. One hundred and forty-nine of 334 patients (45%) received bystander CPR. The discharge rate after good BCPR (23%) was higher than after no good BCPR (1%, P < 0.0005) or after no BCPR (6%, P < 0.0005). There was no difference between no good and no BCPR (P = 0.1114). There were no differences in paramedic response interval between the groups, but the mean interval from start of unconsciousness to initiation of CPR (arrest-CPR interval) was significantly shorter in the group receiving good bystander CPR (2.5 min, 95% confidence interval (CI): 1.7-3.3 min) than no good CPR (6.6 min, CI: 5.2-8.0 min) or no bystander CPR (7.8 min, CI: 7.2-8.4 min). Bystanders started CPR more frequently in public than in the patient's home (58 vs. 34%, P < 0.0005). Good bystander CPR was associated with a shorter arrest-CPR interval and improved hospital discharge rate as compared to no good BCPR or no BCPR.

Quality of mechanical, manual standard and active compression-decompression CPR on the arrest site and during transport in a manikin model.

The quality of mechanical CPR (M-CPR) was compared with manual standard CPR (S-CPR) and active compression-decompression CPR (ACD-CPR) performed by paramedics on the site of a cardiac arrest and during manual and ambulance transport. Each technique was performed 12 times on manikins using teams from a group of 12 paramedic students with good clinical CPR experience using a random cross-over design. Except for some lost ventilations the CPR effort using the mechanical device adhered to the European Resuscitation Council guidelines, with an added time requirement of median 40 s for attaching the device compared with manual standard CPR. Throughout the study, in comparison with mechanical CPR the quality of CPR with either manual method was significantly worse. In particular, there were considerable individual variations during stretcher transport. With S-CPR and ACD-CPR the median compression times were 38 and 31%, significantly lower than the recommended 50%, and 46-98% of the decompression efforts with ACD-CPR were too weak, particularly during transport on the stairs. With both manual methods, there were no significant differences in the CPR effort between the site of the arrest and the ambulance transport. However, compression rates were reduced and became more erratic during stretcher transport to the ambulance. When walking horizontally, a median of 19% of S-CPR compressions and 84% of ACD-CPR compressions were to weak. On the stairs, 68% of S-CPR compressions and 100% of ACD-CPR compressions were too weak. In conclusion, when evaluated on a manikin, in comparison with manual standard and ACD-CPR, mechanical CPR adhered more closely to ERC guidelines. This was particularly true when performing CPR during transport on a stretcher.