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Background: Utstein-style guidelines use an established consensus process, endorsed by the international resuscitation community, to facilitate and structure resuscitation research and publication. The first "Guidelines for Uniform Reporting of Data From Drowning" were published over a decade ago. During the intervening years, resuscitation science has advanced considerably, thus making revision of the guidelines timely. In particular, measurement of cardiopulmonary resuscitation elements and neurological outcomes reporting have advanced substantially. The purpose of this report is to provide updated guidelines for reporting data from studies of resuscitation from drowning., Methods: An international group with scientific expertise in the fields of drowning research, resuscitation research, emergency medical services, public health, and development of guidelines met in Potsdam, Germany, to determine the data that should be reported in scientific articles on the subject of resuscitation from drowning. At the Utstein-style meeting, participants discussed data elements in detail, defined the data, determined data priority, and decided how data should be reported, including scoring methods and category details., Results: The template for reporting data from drowning research was revised extensively, with new emphasis on measurement of quality of resuscitation, neurological outcomes, and deletion of data that have proved to be less relevant or difficult to capture., Conclusions: The report describes the consensus process, rationale for selecting data elements to be reported, definitions and priority of data, and scoring methods. These guidelines are intended to improve the clarity of scientific communication and the comparability of scientific investigations., (Copyright © 2017 European Resuscitation Council, American Heart Association, Inc. Published by Elsevier B.V. All rights reserved.)

Background and Aim: The majority of avalanche victims who sustain complete burial die within 35min due to asphyxia and injuries. After 35min, survival is possible only in the presence of a patent airway, and an accompanying air pocket around the face may improve survival. At this stage hypothermia is assumed to be an important factor for survival because rapid cooling decreases oxygen consumption; if deep hypothermia develops before cardiac arrest, hypothermia may be protective and prolong the time that cardiac arrest can be survived. The aim of the study was to investigate the combined effects of hypoxia, hypercapnia and hypothermia in a porcine model of avalanche burial., Methods: Eight piglets were anaesthetised, intubated and buried under snow, randomly assigned to an air pocket (n=5) or ambient air (n=3) group., Results: Mean cooling rates in the first 10min of burial were -19.7±4.7°Ch(-1) in the air pocket group and -13.0±4.4°Ch(-1) in the ambient air group (P=0.095); overall cooling rates between baseline and asystole were -4.7±1.4°Ch(-1) and -4.6±0.2°Ch(-1) (P=0.855), respectively. In the air pocket group cardiac output (P=0.002), arterial oxygen partial pressure (P=0.001), arterial pH (P=0.002) and time to asystole (P=0.025) were lower, while arterial carbon dioxide partial pressure (P=0.007) and serum potassium (P=0.042) were higher compared to the ambient air group., Conclusion: Our results demonstrate that hypothermia may develop in the early phase of avalanche burial and severe asphyxia may occur even in the presence of an air pocket., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Background: Prior meta-analyses-reported results of randomised controlled trials (RCTs) published between 1997 and 2004 failed to show any vasopressin-related benefit in cardiac arrest. Based on new RCT-data and a hypothesis of a potentially increased vasoconstricting efficacy of vasopressin, we sought to determine whether the cumulative, current evidence supports or refutes an overall and/or selective benefit for vasopressin regarding sustained restoration of spontaneous circulation (ROSC), long-term survival, and neurological outcome., Methods: Two reviewers independently searched PubMed, EMBASE, and Cochrane Database for RCTs assigning adults with cardiac arrest to treatment with a vasopressin-containing regimen (vasopressin-group) vs adrenaline (epinephrine) alone (control-group) and reporting on long-term outcomes. Data from 4475 patients in 6 high-methodological quality RCTs were analyzed. Subgroup analyses were conducted according to initial cardiac rhythm and time from collapse to drug administration (T(DRUG))<20 min., Results: Vasopressin vs. control did not improve overall rates of sustained ROSC, long-term survival, or favourable neurological outcome. However, in asystole, vasopressin vs. control was associated with higher long-term survival {odds ratio (OR)=1.80, 95% confidence interval (CI)=1.04-3.12, P=0.04}. In asystolic patients of RCTs with average T(DRUG)<20 min, vasopressin vs. control increased the rates of sustained ROSC (data available from 2 RCTs; OR=1.70, 95% CI=1.17-2.47, P=0.005) and long-term survival (data available from 3 RCTs; OR=2.84, 95% CI=1.19-6.79, P=0.02)., Conclusions: Vasopressin use in the resuscitation of cardiac arrest patients is not associated with any overall benefit or harm. However, vasopressin may improve the long-term survival of asystolic patients, especially when average T(DRUG) is <20 min., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Introduction: In a model of severe simulated upper airway haemorrhage, we compared two techniques of performing endotracheal intubation: (1) suctioning via the endotracheal tube during laryngoscopy with subsequently advancing the endotracheal tube, and (2) the standard intubation strategy with performing laryngoscopy, and performing suction with subsequently advancing the endotracheal tube., Methods: Forty-one emergency medical technicians intubated the trachea of a manikin with severe simulated airway haemorrhage using each technique in random order., Results: There was no significant difference in the number of oesophageal intubations between suctioning via the tube and the standard intubation strategy [8/41 (20%) vs. 6/41 (15%); P = 0.688], but suctioning via the endotracheal tube needed significantly more time [median (IQR, CI 95%): 42 (20, 39-60) vs. 33 (15, 35-48)s; P = 0.015]., Conclusions: Suctioning via the endotracheal tube showed no benefit regarding the number of oesophageal intubations and needed more time when compared to the standard intubation strategy., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Aims: Inexperienced health-care-providers may encounter severe problems to ventilate an unconscious child. Designing a ventilating device that could indicate how to open an upper airway correctly may be beneficial. Neutral position in young children and slight head extension in older children is recommended, although the optimal head angle is not clear. Thus, we compared effects of neutral head position and extension, measuring head-position angles and ventilation parameters., Methods: Sixty-one children scheduled for tonsillectomy were enrolled, and were ventilated with pressure-controlled ventilation after anaesthesia induction., Results: Children were divided into two groups: 1-5 years old (pre-school children, n=38) and 6-10 years old (school children, n=23). In neutral (mean+/-SD: 1.3+/-6.0) vs. head-extension position (13.2+/-6.0; P<0.001) in pre-school children, tidal volumes (132+/-44,137+/-49 ml), peak-expiratory flow (300+/-90 vs. 310+/-100 mls(-1)) and expiratory airway resistance (20+/-8 vs. 18+/-6c mH(2)O s l(-1)) were comparable (P=NS). In neutral (-0.4+/-5.4) vs. head-extension position (15.7+/-6.4; P<0.001) in school children, expiratory airway resistance (17+/-7 vs. 13+/-5 cmH(2)O s l(-1); P=0.048) differed, while tidal volume (224+/-93 vs. 230+/-92 ml) and peak-expiratory flow (427+/-181 vs. 381+/-144 ml s(-1)) were comparable (P=NS)., Conclusions: Head-extension and neutral head-position angles differed in pre-school and school children. In pre-school children, neutral head position or head extension with an angle of -1 degrees or 13 degrees , and in school children head extension of 16 degrees , may be used to achieve optimal ventilation of an unprotected airway., (Copyright 2010 Elsevier Ireland Ltd. All rights reserved.)

Aims: To review anaesthesia in prehospital emergencies and in the emergency room, and to discuss guidelines for anaesthesia indication; pre-oxygenation; anaesthesia induction and drugs; airway management; anaesthesia maintenance and monitoring; side effects and training., Methods: A literature search in the PubMed database was performed and 87 articles were included in this non-systematic review., Conclusions: For pre-oxygenation, high-flow oxygen should be delivered with a tight-fitting face-mask provided with a reservoir. In haemodynamically unstable patients, ketamine may be the induction agent of choice. The rocuronium antagonist sugammadex may have the potential to make rocuronium a first-line neuromuscular blocking agent in emergency induction. An experienced health-care provider may consider prehospital anaesthesia induction. A moderately experienced health-care provider should optimise oxygenation, fasten hospital transfer and only try to intubate a patient in extremis. If intubation fails twice, ventilation should be resumed with an alternative supra-glottic airway or a bag-valve-mask device. A lesser experienced health-care provider should completely refrain from intubation, optimise oxygenation, fasten hospital transfer and only in extremis ventilate with an alternative supra-glottic airway or a bag-valve-mask device. With an expected difficult airway, the patient should be intubated awake. With an unexpected difficult airway, bag-valve-mask ventilation should be resumed and an alternative supra-glottic airway device inserted. Senior help should be called early. In a "can-not-ventilate, can-not-intubate" situation an alternative airway should be tried and if unsuccessful because of severe upper airway pathology, a surgical airway should be performed. Ventilation should be monitored continuously with capnography. Clinical training is important to increase airway management skills., (Copyright 2009 Elsevier Ireland Ltd. All rights reserved.)

Aim: Ventilation of a non-intubated emergency patient by inexperienced rescuers with a standard bag-valve device may result in high inspiratory flow rates and subsequently high airway pressures with stomach inflation. Therefore, a self-inflating bag has been developed that requires lay rescuers to blow up a single-use balloon inside an adult bag-valve device, which, in turn, displaces air within the bag towards the patient. This concept has been compared to standard adult bag-valve devices earlier in bench models but not in patients., Methods: An anaesthetist who was blinded to all monitor tracings ventilated the lungs of 40 apnoeic patients during routine anaesthesia induction either with a standard bag-valve device or with the mouth-to-bag resuscitator in a random order. Study endpoints were peak inspiratory flow rates, peak airway pressure, tidal volumes and inspiratory time., Results: Peak inspiratory flow was 40+/-10lmin(-1) for the standard bag-valve device versus 33+/-13lmin(-1) for the mouth-to-bag resuscitator (P<0.0001); peak airway pressure was 17+/-5cmH(2)O versus 14+/-5cmH(2)O (P<0.0001); inspiratory tidal volume was 477+/-133ml versus 644+/-248ml (P<0.001) and inspiratory time was 1.1+/-0.3s versus 1.9+/-0.6s (P<0.0001)., Conclusion: Employing the mouth-to-bag resuscitator during simulated ventilation of a non-intubated patient in respiratory arrest significantly decreased peak inspiratory flow and peak airway pressure and increased inspiratory tidal volume and inspiratory times compared to a standard bag-valve device.

Introduction: We developed a suction laryngoscope, which enables simultaneous suction and laryngoscopy in cases of airway haemorrhage and evaluated its potential benefits in physicians with varying emergency medical service experience., Methods: Eighteen physicians with regular and 24 physicians with occasional emergency medical service experience intubated the trachea of a manikin with severe simulated airway haemorrhage using the suction laryngoscope and the Macintosh laryngoscope in random order., Results: In physicians with regular emergency medical service experience, there was neither a difference in time needed for intubation [median (IQR, CI 95%)]: 34 (18, 30-46) vs. 34 (22, 30-52) s; P=0.52, nor in the number of oesophageal intubations [0/18 (0%) vs. 3/18 (16.7%); P=NS] when using the suction vs. the Macintosh laryngoscope. In physicians with occasional emergency medical service experience, there was no difference in time needed for intubation [median (IQR, CI 95%)]: 42 (25, 41-57) vs. 45 (33, 41-65) s; P=0.56, but the number of oesophageal intubations was significantly lower when using the suction laryngoscope [4/24 (16.7%) vs. 12/24 (50.0%); P=0.04]., Conclusions: In a model of severe simulated airway haemorrhage, employing a suction laryngoscope significantly decreased the likelihood of oesophageal intubations in physicians with occasional emergency medical service experience.

Aim: Stomach inflation during mask ventilation is frequent, but the effects on haemodynamic and pulmonary function are unclear. We evaluated the effects of stomach inflation on haemodynamic and pulmonary function during spontaneous circulation in a porcine model., Methods: Randomised prospective animal study. After randomisation, in 23 domestic pigs the stomach was inflated every 90s with 0L (control; n=8), 0.5L (n=7) or 1L (n=8) ambient air., Results: After 22.5min, i.e. 8.5L in the 0.5L and 17L in the 1L stomach inflation group, stomach inflation increased central venous pressure (median) (control: 10mmHg vs. 1L: 23mmHg, P<0.05) and mean pulmonary artery pressure (control: 24mmHg vs. 1L: 45mmHg, P<0.05). As a result stroke volume index decreased (control: 135mL/kg vs. 0.5L: 90mL/kg, P<0.05; vs. 1L: 72mL/kg, P<0.05). Stomach inflation also decreased static pulmonary compliance (control: 24mL/cmH(2)O vs. 0.5L: 8mL/cmH(2)O, P<0.05; vs. 1L: 3mL/cmH(2)O, P<0.05), which increased peak airway pressure (control: 28cmH(2)O vs. 0.5L: 69cmH(2)O, P<0.05; vs. 1L: 73cmH(2)O, P<0.05). Additionally, arterial oxygen partial pressure (control: 305mmHg vs. 0.5L: 140mmHg, P<0.05; vs. 1L: 21mmHg, P<0.05) and systemic oxygen delivery (control: 53mLO(2)/min vs. 1L: 19mLO(2)/min, P<0.05) decreased. Stomach inflation increased mortality (control: 0/8 vs. 1L: 5/8, P<0.05)., Conclusions: Stomach inflation with 1L when compared to 0.5L increments resulted in faster haemodynamic and pulmonary failure and increased mortality. Stomach inflation may cause a hyper-acute abdominal compartment syndrome.

Background: Most studies investigating cardiopulmonary resuscitation (CPR) interventions or functionality of mechanical CPR devices have been performed using porcine models. The purpose of this study was to identify differences between mechanical characteristics of the human and porcine chest during CPR., Material and Methods: CPR data of 90 cardiac arrest patients was compared to data of 14 porcine from two animal studies. Chest stiffness k and viscosity mu were calculated from acceleration and pressure data recorded using a Laerdal Heartstart 4000SP defibrillator during CPR. K and mu were calculated at chest compression depths of 15, 30 and 50mm for three different time periods., Results: At a depth of 15mm porcine chest stiffness was comparable to human chest stiffness at the beginning of resuscitation (4.8 vs. 4.5N/mm) and clearly lower after 200 chest compressions (2.9 vs. 4.5N/mm) (p<0.05). At 30 and 50mm porcine chest stiffness was higher at the beginning and comparable to human chest stiffness after 200 chest compressions. After 200 chest compressions porcine chest viscosity was similar to human chest viscosity at 15mm (108 vs. 110Ns/m), higher for 30mm (240 vs. 188Ns/m) and clearly higher for 50mm chest compression depth (672 vs. 339Ns/m) (p<0.05)., Conclusion: In conclusion, human and porcine chest behave relatively similarly during CPR with respect to chest stiffness, but differences in chest viscosity at medium and deep chest compression depth should at least be kept in mind when extrapolating porcine results to humans.

Aim: Stomach inflation during cardiopulmonary resuscitation (CPR) is frequent, but the effect on haemodynamic and pulmonary function is unclear. The purpose of this study was to evaluate the effect of clinically realistic stomach inflation on haemodynamic and pulmonary function during CPR in a porcine model., Methods: After baseline measurements ventricular fibrillation was induced in 21 pigs, and the stomach was inflated with 0L (n=7), 5L (n=7) or 10L air (n=7) before initiating CPR., Results: During CPR, 0, 5, and 10L stomach inflation resulted in higher mean pulmonary artery pressure [median (min-max)] [35 (28-40), 47 (25-50), and 51 (49-75) mmHg; P<0.05], but comparable coronary perfusion pressure [10 (2-20), 8 (4-35) and 5 (2-13) mmHg; P=0.54]. Increasing (0, 5, and 10L) stomach inflation decreased static pulmonary compliance [52 (38-98), 19 (8-32), and 12 (7-15) mL/cmH(2)O; P<0.05], and increased peak airway pressure [33 (27-36), 53 (45-104), and 103 (96-110) cmH(2)O; P<0.05). Arterial oxygen partial pressure was higher with 0L when compared with 5 and 10L stomach inflation [378 (88-440), 58 (47-113), and 54 (43-126) mmHg; P<0.05). Arterial carbon dioxide partial pressure was lower with 0L when compared with 5 and 10L stomach inflation [30 (24-36), 41(34-51), and 56 (45-68) mmHg; P<0.05]. Return of spontaneous circulation was comparable between groups (5/7 in 0L, 4/7 in 5L, and 3/7 in 10L stomach inflation; P=0.56)., Conclusions: Increasing levels of stomach inflation had adverse effects on haemodynamic and pulmonary function, indicating an acute abdominal compartment syndrome in this CPR model.

Background: Countershock outcome prediction using ventricular fibrillation (VF) feature analysis needs undisturbed electrocardiogram (ECG) signals and therefore requires interruption of cardiopulmonary resuscitation (CPR). Features that originate from higher frequency bands of the VF power spectrum may be less affected by CPR artefacts and as such reduce cumulative hands-off intervals., Materials and Methods: From 192 patients with in-hospital and out-of-hospital cardiac arrest, four countershock outcome prediction features (peak-peak amplitude, mean slope, median slope, power spectrum analysis) were analysed in 550 short time ECG records, each including a CPR corrupted and a subsequent undisturbed sequence. ECG features calculated from the main frequency band (0-26Hz) and from bandpass-filtered subbands (>10-26Hz) were compared using the similarity level method and differences in shock advice numbers., Results: The feature similarity between ECG periods with and without CPR artefacts was higher in bandpass-filtered (Sim=0.79, 0.8, 0.78, 0.66) than in unfiltered ECG traces (Sim=0.58, 0.69, 0.68, 0.47). For the features evaluated, the difference in number of shock advices between subsequent traces with and without CPR artefact was significantly reduced using VF analysis from higher frequency bands., Conclusion: The accuracy of shock outcome prediction during CPR could be increased by using filtered ECG features from higher ECG subbands instead of features derived from the main ECG spectrum.

Background: The 2005 revised guidelines for cardiopulmonary resuscitation (CPR) suggest a universal compression-to-ventilation (C:V) ratio of 30:2. The effects of this ratio in a realistic CPR scenario have not been investigated completely., Material and Methods: After 4 min of untreated ventricular fibrillation (VF), 24 pigs were randomly assigned to 6 min of basic-life support (BLS) CPR with 21% oxygen, and either (1) chest compressions only ("CC" group, n=8), or (2) cycles of 30 compressions followed by two breaths with a self-inflating bag (Fio2 0.21, C:V ratio 30:2; "30:2" group, n=8), or (3) 15 compressions followed by two breaths (C:V ratio 15:2; "15:2" group, n=8), all followed by advanced life support., Results: Arterial PO2 during BLS-CPR was higher in the 15:2 group compared to the 30:2 and CC groups (74+/-3 vs. 59+/-2 and 33+/-4 mmHg, respectively; p<0.05). Both mixed-venous PO2 and SO2 were higher in the 15:2 and 30:2 groups, compared to the CC group ( PO2 : 23+/-2 and 25+/-1 vs. 17+/-1 mmHg; SO2: 21+/-6 and 19+/-3 vs. 8+/-1 %, respectively; p<0.05). Arterial pH decreased in the 30:2 and CC groups compared to the 15:2 group (7.33+/-0.03 and 7.25+/-0.02 vs. 7.51+/-0.04, respectively; p<0.001). 4/8, 2/8, and 0/8 animals in the 15:2, 30:2, and CC groups, respectively, had ROSC at the end of the study period (p=ns)., Conclusions: Increasing the chest compression ratio from 15:2 to 30:2 resulted in changes in arterial, but not mixed-venous, blood gases; therefore, the advantages of more chest compressions may outweigh a decrease in gas exchange.

Background: The present study was designed to evaluate the effect of conventional fluid resuscitation and small volume resuscitation alone and combined with arginine vasopressin (AVP) on cerebral perfusion pressure (CPP) and protein S100B during experimental haemorrhagic shock., Material and Methods: Thirty anaesthetised pigs underwent a penetrating liver trauma. Following haemodynamic decompensation, pigs received either (1) a combination of crystalloid (40 mL kg(-1)) and colloid (20 mL kg(-1)) solutions (fluid, n=10), (2) hypertonic-hyperoncotic solution (HHS; 4 mL kg(-1)) combined with normal saline (HHS+NS; n=10) or (3) HHS combined with AVP (0.2 U kg(-1) followed by an infusion of 2 U kg(-1)h(-1); HHS+AVP; n=10)., Results: Compared to baseline, CPP decreased and S100B levels increased significantly at haemodynamic decompensation (S100B: fluid, 0.52+/-0.23 microg L(-1) vs. 0.85+/-0.37 microg L(-1), p<0.05; HHS+NS, 0.47+/-0.18 microg L(-1) vs. 0.90+/-0.33 microg L(-1), p<0.05; HHS+AVP, 0.53+/-0.18 microg L(-1) vs. 0.90+/-0.39 microg L(-1), p<0.01). During the initial 10 min of therapy, CPP of HHS+NS was significantly higher compared to the fluid group, increased more rapidly in the HHS+AVP group, but was not significantly different thereafter. S100B levels decreased close to baseline values (p<0.001), and did not differ between groups., Conclusion: HHS+AVP resulted in higher CPP compared to fluid and HHS+NS in the initial phase of therapy, but did not differ thereafter. Haemorrhage-induced hypotension yielded increased S100B levels that were comparable in groups throughout the study period.

Up to 90% of cardiac arrests are due to acute myocardial infarction or severe myocardial ischaemia. Thrombolysis is an effective treatment for ST-elevation myocardial infarction (STEMI), but there is no evidence or guideline to put forward a thrombolysis strategy during cardiopulmonary resuscitation (CPR). In two physician-manned emergency medical service (EMS) units in Berlin, Germany, using thrombolysis is based on an individual judgment of the EMS physician managing the CPR attempt. In this retrospective analysis over 3 years (total 22.164 scene calls), thrombolysis was started at the scene in 50 patients during brief intermittent phases of spontaneous circulation, and in 3 patients during ongoing CPR. On-scene diagnosis of myocardial infarction was established in 45 patients (85%) by a 12-lead ECG, 5 (9%) patients had a left bundle branch block. Sixteen patients (30%) died at the scene, 37 patients (70%) were admitted to a hospital. In-hospital mortality was 35% (13 of 37 patients), with cause of death being cardiogenic shock in nine patients, hypoxic cerebral coma in two and acute haemorrhage in two other patients. All 24 of 53 (45%) survivors were discharged with an excellent neurological recovery. CPR was started by an EMS physician in 18 of the 24 survivals (75%) and emergency medical technicians who arrived first in six (25%). Duration of CPR until return of spontaneous circulation was <10 min in 13 of 24 (54%) of the survivors. Thrombolysis was initiated during intermittent phases of spontaneous circulation in 50 (94%) of all patients and in 23 (96%) of the 24 survivors. In conclusion, this retrospective analysis shows excellent survival rates and neurological outcome in selected patients with a high likelihood of myocardial infarction, who develop cardiac arrest and are treated with thrombolysis.

Background: Synergistic effects of adrenaline (epinephrine) and vasopressin may be beneficial during cardiopulmonary resuscitation. However, it is unknown whether either adrenaline alone or an alternating administration of adrenaline and vasopressin is better for restoring vital organ perfusion following basic life support (BLS) according to the revised algorithm with a compression-to-ventilation (c/v) ratio of 30:2., Material and Methods: After 4min of ventricular fibrillation, and 6min of BLS with a c/v ratio of 30:2, 16 pigs were randomised to receive either 45microg/kg adrenaline, or alternating 45microg/kg adrenaline and 0.4U/kg vasopressin, respectively., Results: Coronary perfusion pressure (mean+/-S.D.) 20 and 25min after cardiac arrest was 7+/-4 and 5+/-3mm Hg after adrenaline, and 25+/-2 and 14+/-3mm Hg after adrenaline/vasopressin (p<0.001 and <0.01 versus adrenaline), respectively. Cerebral perfusion pressure was 23+/-7 and 19+/-9mm Hg after adrenaline, and 40+/-10 and 33+/-7mm Hg after adrenaline/vasopressin (p<0.001 and <0.01 versus adrenaline), and cerebral blood flow was 30+/-10 and 27+/-11% of baseline after adrenaline, and 65+/-40 and 50+/-31% of baseline after adrenaline/vasopressin (p<0.05 versus adrenaline), respectively. Return of spontaneous circulation (ROSC) did not differ significantly between the adrenaline group (0/8) and the adrenaline/vasopressin group (3/8)., Conclusion: Adrenaline/vasopressin resulted in higher coronary and cerebral perfusion pressures, and cerebral blood flow, while ROSC was comparable.

Unlabelled: We have shown previously that arginine vasopressin (AVP) given during sinus rhythm increases mean arterial blood pressure (MAP) and left anterior descending (LAD) coronary artery cross sectional area. AVP was assumed to result in vasodilatation via activation of the endothelial nitric oxide system. The purpose of the present study was to assess the effects of AVP before and after NO-inhibition. Nine domestic pigs were instrumented for measurement of haemodynamic variables using micromanometer-tipped catheters, and measurement of LAD coronary artery cross sectional area employing intravascular ultrasound (IVUS). Haemodynamic variables, LAD coronary artery cross sectional area and cardiac output were measured at baseline, 90 s and 5, 15, and 30 min after AVP (0.4 U kg (-1) IV) before and after blockade of nitric oxide synthase with N(G)-nitro L-arginine methyl ester (L-NAME). Compared with baseline, AVP significantly increased MAP after 90 s (89+/-4 versus 160+/-5 mm Hg), increased LAD coronary artery cross sectional area (11.3+/-1 versus 11.8+/-1 mm(2)) and decreased cardiac index (138+/-6 versus 53+/-6 mL/min kg(-1)). After blockade of nitric oxide synthase, AVP significantly increased MAP after 90 s (135+/-4 versus 151+/-3 mm Hg), increased LAD coronary artery cross sectional area (8.7+/-1 versus 8.9+/-1 mm(2)), and significantly decreased cardiac index (95+/-6 versus 29+/-4 mL/min kg (-1))., Implications: During sinus rhythm, AVP increased MAP and LAD coronary artery cross sectional area, but decreased cardiac index.

The duration of untreated ventricular fibrillation (VF) is of paramount importance for CPR success. Moreover, therapeutic interventions taking into account the interval between cardiac arrest onset and initiation of CPR improve outcome. This study was performed to investigate whether VF feature analysis could be used to estimate the duration of VF in patients with out-of-hospital cardiac arrest. Demographic data recorded according to the Utstein guidelines and ECG recordings of 376 cardiac arrest patients from three European areas were analysed. Ten features in the time and frequency domain derived from different sub-bands of the initial VF ECG (n=127) were evaluated. The correlation between VF ECG features and cardiac arrest times was investigated using Pearson's correlation coefficient in a subset of 40 patients with reliably estimated downtimes and artefact-free initial VF tracings. No significant correlation (p<.05) between any of the VF ECG features and downtime could be found. The duration of cardiac arrest could not be estimated reliably from human VF ECG single feature analysis.

Targeted defibrillation therapy is needed to optimise survival chances of ventricular fibrillation (VF) patients, but at present VF analysis strategies to optimise defibrillation timing have insufficient predictive power. From 197 patients with in-hospital and out-of-hospital cardiac arrest, 770 electrocardiogram (ECG) recordings of countershock attempts were analysed. Preshock VF ECG features in the time and frequency domain were tested retrospectively for outcome prediction. Using band pass filters, the ECG spectrum was split into various frequency bands of 2-26 Hz bandwidth in the range of 0-26 Hz. Neural networks were used for single feature combinations to optimise prediction of countershock success. Areas under curves (AUC) of receiver operating characteristics (ROC) were used to estimate prediction power of single and combined features. The highest ROC AUC of 0.863 was reached by the median slope in the interval 10-22 Hz resulting in a sensitivity of 95% and a specificity of 50%. The best specificity of 55% at the 95% sensitivity level was reached by power spectrum analysis (PSA) in the 6-26 Hz interval. Neural networks combining single predictive features were unable to increase outcome prediction. Using frequency band segmentation of human VF ECG, several single predictive features with high ROC AUC>0.840 were identified. Combining these single predictive features using neural networks did not further improve outcome prediction in human VF data. This may indicate that various simple VF features, such as median slope already reach the maximum prediction power extractable from VF ECG.

Introduction: Although the concept of intermittent airway occlusion with the inspiratory impedance threshold valve (ITV) is a well-recognised strategy for improving efficiency of cardiopulmonary resuscitation (CPR), little is known about possible pulmonary side effects., Methods: After a baseline chest CT-scan, 24 pigs with beating hearts undergoing apnoeic oxygenation received an injection of a contrast medium and were then assigned randomly to either active compression-decompression CPR with ITV (ACD ITV CPR), ACD CPR alone, or standard-CPR with ITV (standard-ITV CPR), or standard-CPR alone. After a maximum of 5 min of chest compressions or if oxygen saturation dropped below 70%, the experiment was stopped, haemodynamic variables and blood gas values were measured, and another CT-scan was performed; all animals underwent a 30 min recovery-period and a third subsequent CT-scan., Results: At baseline arterial oxygen saturation by pulse oxymetry was 99% in all four groups; in both the ACD ITV CPR and the standard-ITV CPR groups, arterial oxygen saturation dropped below 70% within 126+/-9s, whereas chest compressions in all ACD CPR and standard-CPR pigs were performed over 5 min (P<0.001). Before stopping chest compressions arterial oxygen pressure decreased in the ACD ITV CPR group from 426+/-96 to 42+/-8 mmHg while it decreased in the ACD CPR group only from 415+/-116 to 197+/-127 mmHg (P<0.001 between groups); in the standard-ITV CPR group arterial oxygen partial pressure decreased from 427+/-109 to 34+/-5 mmHg while oxygen partial pressure decreased only from 467+/-44 to 144+/-98 mmHg in the standard-CPR group (P<0.004 between groups). After the second CT scan arterial oxygen partial pressure decreased further to 19+/-2 mmHg in the ACD ITV CPR versus 210+/-41 mmHg in the ACD CPR group; to 20+/-2 mmHg in the standard-ITV CPR versus 148+/-33 mmHg in the standard-CPR group. Lung-density values (Hounsfield units) were significantly higher in the ACD ITV CPR versus ACD CPR group (-134+/-54 versus -330+/-77) and standard-ITV CPR versus standard-CPR group (-98+/-50 versus -387+/-42). After a 30 min recovery-period, there were no significant differences in arterial oxygen partial pressure (ACD ITV CPR 275+/-110 mmHg versus ACD CPR 379+/-111 mmHg and standard-ITV CPR 265+/-138 mmHg versus standard CPR 367+/-55 mmHg). Furthermore, there were no differences in lung density values between groups after 30 min of recovery., Conclusion: In this animal model with a beating heart, intermittent airway obstruction through an ITV combined with apnoeic oxygenation and without active ventilation resulted in hypoxaemia due to transiently impaired lung function.

Aim of Study: To report the management of cardiovascular failure refractory to standard catecholamine therapy with terlipressin in a patient with tricyclic antidepressant (TCA) intoxication., Case Report: A 41-year-old woman, with suicidal ingestion of 11.25 g amitriptyline and 1500 mg diclofenac, was admitted to the emergency department. After 30 min in ventricular fibrillation, with ongoing CPR, she regained a potentially perfusing rhythm, but with hypotension refractory to standard catecholamine therapy with adrenaline, 2 microg/kg/min (norepinephrine); adrenaline, 1 microg/kg/min (epinephrine) until 55 min after admission. An injection of 1 mg terlipressin restored mean arterial blood pressure >65 mmHg within 10 min. Ten hours after admission to the intensive care unit, catecholamine support could be withdrawn because of a stable haemodynamic state. Within 7 days, all organ function recovered, and the patient regained full neurological function., Conclusions: Successful management of cardiovascular failure with terlipressin after TCA intoxication refractory to catecholamines suggests a potential role for terlipressin as an adjunct vasopressor in severely hypotensive patients.

The effects of vasopressin on the gut in a porcine uncontrolled haemorrhagic shock model are described. In eight anaesthetised pigs, a liver laceration was performed; when haemorrhagic shock was decompensated, all animals received 0.4 IU/kg vasopressin, followed by 0.08 IU/kg min over 30 min, which maintained a mean arterial blood pressure >40 mmHg. Subsequent surgical intervention, infusion of whole blood and fluids resulted in a stable cardiocirculatory status. Three hours after stabilisation, all pigs developed non-bloody diarrhoea which converted into normal bowel movements within 24 h. All histological samples retained 7 days after the experiment revealed no histopathological changes. In conclusion, in this small observational study of uncontrolled porcine haemorrhagic shock, a resuscitation strategy that included high dose vasopressin was associated with transient diarrhoea and good long term survival.

Arginine vasopressin (AVP) has been employed successfully during cardiopulmonary resuscitation, but there exist only few data about the effects of AVP infusion for cardiovascular failure during the post-cardiac arrest period. Cardiovascular failure is one of the main causes of death after successful resuscitation from cardiac arrest. Although the "post-resuscitation syndrome" has been described as a "sepsis-like" syndrome, there is little information about the haemodynamic response to AVP in advanced cardiovascular failure after cardiac arrest. In this retrospective study, haemodynamic and laboratory variables in 23 patients with cardiovascular failure unresponsive to standard haemodynamic therapy during the post-cardiac arrest period were obtained before, and 30 min, 1, 4, 12, 24, 48, and 72 h after initiation of a supplementary AVP infusion (4 IU/h). During the observation period, AVP significantly increased mean arterial blood pressure (58+/-14 to 75+/-19 mmHg, p < 0.001), and decreased noradrenaline (norepinephrine) (1.31+/-2.14 to 0.23+/-0.3 microg/kg/min, p = 0.03), adrenaline (epinephrine) (0.58+/-0.23 to 0.04+/-0.03 microg/kg/min, p = 0.001), and milrinone requirements (0.46+/-0.15 to 0.33+/-0.22 microg/kg/min, p < 0.001). Pulmonary capillary wedge pressure changed significantly (p < 0.001); an initial increase being followed by a decrease below baseline values. While arterial lactate concentrations (95+/-64 to 21+/-18 mg/dL, p < 0.001) and pH (7.27+/-0.14 to 7.4+/-0.14, p < 0.001) improved significantly, total bilirubin concentrations (1.12+/-0.95 to 3.04+/-3.79 mg/dL, p = 0.001) increased after AVP. There were no differences in the haemodynamic or laboratory response to AVP between survivors and non-survivors. In this study, advanced cardiovascular failure that was unresponsive to standard therapy could be reversed successfully with supplementary AVP infusion in >90% of patients surviving cardiac arrest.

Objective: Direct measurement of brain tissue oxygenation (PbtO2) is established during spontaneous circulation, but values of PbtO2 during and after cardiopulmonary resuscitation (CPR) are unknown. The purpose of this study was to investigate: (1) the time-course of PbtO2 in an established model of CPR, and (2) the changes of cerebral venous lactate and S-100B., Methods: In 12 pigs (12-16 weeks, 35-45 kg), ventricular fibrillation (VF) was induced electrically during general anaesthesia. After 4 min of untreated VF, all animals were subjected to CPR (chest compression rate 100/min, FiO2 1.0) with vasopressor therapy after 7, 12, and 17 min (vasopressin 0.4, 0.4, and 0.8 U/kg, respectively). Defibrillation was performed after 22 min of cardiac arrest. After return of spontaneous circulation (ROSC), the pigs were observed for 1h., Results: After initiation of VF, PbtO2 decreased compared to baseline (mean +/- SEM; 22 +/- 6 versus 2 +/- 1 mmHg after 4 min of VF; P < 0.05). During CPR, PbtO2 increased, and reached maximum values 8 min after start of CPR (25 +/- 7 mmHg; P < 0.05 versus no-flow). No further changes were seen until ROSC. Lactate, and S-100B increased during CPR compared to baseline (16 +/- 2 versus 85 +/- 8 mg/dl, and 0.46 +/- 0.05 versus 2.12 +/- 0.40 microg/l after 13 min of CPR, respectively; P < 0.001); lactate remained elevated, while S-100B returned to baseline after ROSC., Conclusions: Though PbtO2 returned to pre-arrest values during CPR, PbtO2 and cerebral lactate were lower than during post-arrest reperfusion with 100% oxygen, which reflected the cerebral low-flow state during CPR. The transient increase of S-100B may indicate a disturbance of the blood-brain-barrier.

The aim of this report is to establish recommendations for reviewing, reporting, and conducting research during the post-resuscitation period in hospital. It defines data that are needed for research and more specialised registries and therefore supplements the recently updated Utstein template for resuscitation registries. The updated Utstein template and the out-of-hospital "Chain of Survival" describe factors of importance for successful resuscitation up until return of spontaneous circulation (ROSC). Several factors in the in-hospital phase after ROSC are also likely to affect the ultimate outcome of the patient. Large differences in survival to hospital discharge for patients admitted alive are reported between hospitals. Therapeutic hypothermia has been demonstrated to improve the outcome, and other factors such as blood glucose, haemodynamics, ventilatory support, etc., might also influence the result. No generally accepted, scientifically based protocol exists for the post-resuscitation period in hospital, other than general brain-oriented intensive care. There is little published information on this in-hospital phase. This statement is the result of a scientific consensus development process started as a symposium by a task force at the Utstein Abbey, Norway, in September 2003. Suggested data are defined as core and supplementary and include the following categories: pre-arrest co-morbidity and functional status, cause of death, patients' quality of life, in-hospital system factors, investigations and treatment, and physiological data at various time points during the first three days after admission. It is hoped that the publication of these recommendations will encourage research into the in-hospital post-resuscitation phase, which we propose should be included in the chain-of-survival as a fifth ring. Following these recommendations should enable better understanding of the impact of different in-hospital treatment strategies on outcome.

Hypothermia < 28 degrees C is rarely compatible with life, with only a few cases described surviving such low temperatures. We present a case of a man who survived with a core body temperature below 21.0 degrees C after spending a night in a snowbank with an ambient temperatures as low as -20.0 degrees C. Prolonged CPR and early initiation of extracorporeal membrane oxygenation enabled survival without neurological deficit at hospital discharge. Frostbite was limited to both hands and all toes only; although the entire upper and lower extremity appeared to be deeply frozen on admission, amputation of both hands was inevitable and resulted in permanent disability.

During CPR, an inspiratory time of 2 s is recommended when the airway is unprotected; indicating that approximately 30% of the resuscitation attempt is spent on ventilation, but not on chest compressions. Since survival rates may not decrease when ventilation levels are relatively low, and uninterrupted chest compressions with a constant rate of approximately 100/min have been shown to be lifesaving, it may be beneficial to cut down the time spent on ventilation, and instead, increase the time for chest compressions. In an established bench model of a simulated unprotected airway, we evaluated if inspiratory time can be decreased from 2 to 1 s at different lower oesophageal sphincter pressure (LOSP) levels during ventilation with a bag-valve-mask device. In comparison with an inspiratory time of 2 s, 1 s resulted in significantly (p < 0.001) higher peak airway pressure and peak inspiratory flow rate, while lung tidal volumes at all LOSP levels were clinically comparable. Neither ventilation strategy produced stomach inflation at 20 cmH2O LOSP, and 1 s versus 2 s inspiratory time did not produce significantly higher (mean +/- S.D.) stomach inflation at 15 (8 +/-9 ml versus 0 +/- 0 ml; p < 0.01) and 10 cmH2O LOSP (69 +/- 20 ml versus 34 +/- 18 ml; p < 0.001), and significantly lower stomach inflation at 5 cmH2O LOSP (219 +/- 16 ml versus 308 +/- 21 ml; p < 0.001) per breath. Total cumulative stomach inflation volume over constantly decreasing LOSP levels with an inspiratory time of 2 s versus 1 s was higher (6820 ml versus 5920 ml). In conclusion, in this model of a simulated unprotected airway, a reduction of inspiratory time from 2 to 1 s resulted in a significant increase of peak airway pressure and peak inspiratory flow rate, while lung tidal volumes remained clinically comparable (up to approximately 15% difference), but statistically different due to the precise measurements. Theoretically, this may increase the time available for, and consequently the actual number of, chest compressions during CPR by approximately 25% without risking an excessive increase in stomach inflation.

Although arginine vasopressin (AVP) has been shown to be a promising drug during cardiopulmonary resuscitation (CPR), concern has been raised about the potential for AVP-mediated vasoconstriction of the coronary arteries. In a prospective, randomized laboratory investigation employing an established porcine model, the effects of AVP on haemodynamic variables, left anterior descending (LAD) coronary artery cross sectional area employing intravascular ultrasound (IVUS), and return of spontaneous circulation were studied. During sinus rhythm, the LAD coronary artery cross sectional area was measured by IVUS at baseline, and 90 s and 5 min after AVP (0.4 U/kg IV). Following a 60 min recovery, ventricular fibrillation was induced. At 4 min, chest compressions were initiated; AVP (0.4 U/kg IV) was injected at 5.5 min, and defibrillation performed at 8 min. LAD coronary artery cross sectional area was measured by IVUS at the pre-arrest baseline, 90 s after drug injection during CPR, and 5 min after return of spontaneous circulation. Compared with baseline, the mid-LAD coronary artery cross sectional area increased significantly (P<.05) 90 s and 5 min after AVP administration (9.2+/-.5mm2 versus 10.7+/-.6mm2 versus 11.7+/-.6mm2, respectively) during normal sinus rhythm. Similarly during ventricular fibrillation and CPR plus AVP, the mid-LAD coronary artery cross sectional area increased at 90 s after AVP compared with baseline (9.5+/-.6mm2 versus 11.0+/-.7mm2; P<.05). Moreover, the cross sectional area increased further 5 min after return of spontaneous circulation (9.5+/-.6mm2 versus 14.0+/-.8mm2, P<.05). In conclusion, in this experimental model with normal coronary arteries, AVP resulted in significantly increased LAD coronary artery cross sectional area during normal sinus rhythm, during ventricular fibrillation with CPR, and after return of spontaneous circulation.

Reducing inspiratory flow rate and peak airway pressure may be important in order to minimise the risk of stomach inflation when ventilating an unprotected airway with positive pressure ventilation. This study was designed to yield enough power to determine whether employing an inspiratory gas flow limiting bag-valve device (SMART BAG, O-Two Medical Technologies Inc., Ontario, Canada) would also decrease the likelihood of stomach inflation in an established bench model of a simulated unintubated respiratory arrest patient. The bench model consists of a training lung (lung compliance, 50 ml/cm H2O; airway resistance, 4 cm H2O/l/s) and a valve simulating lower oesophageal sphincter opening at a pressure of 19 cm H(2)O. One hundred and ninety-one emergency medicine physicians were requested to ventilate the manikin utilising a standard single-person technique for 1 min (respiratory rate, 12/min; Vt, 500 ml) with both a standard adult bag-valve-mask and the SMART BAG. The volunteers were blinded to the experimental design of the model until completion of the experimental protocol. The SMART BAG versus standard bag-valve-mask resulted in significantly (P < 0.001) lower (mean +/- S.D.) mean airway pressure (14 +/- 2 cm H2O versus 16 +/- 3 cm H2O), respiratory rates (13 +/- 3 breaths per min versus 14 +/- 4 breaths per min), incidence of stomach inflation (4.2% versus 38.7%) and median stomach inflation volumes (351 [range, 18-1211 ml] versus 1426 [20-5882 ml]); lung tidal volumes (538 +/- 97 ml versus 533 +/- 97 ml) were comparable. Inspiratory to expiratory ratios were significantly (P < 0.001) increased (1.7 +/- 0.5 versus 1.5 +/- 0.6). In conclusion, the SMART BAG reduced inspiratory flow, mean airway pressure and both the incidence and actual volume of stomach inflation compared with a standard bag-valve-mask device while maintaining delivered lung tidal volumes and increasing the inspiratory to expiratory ratio.

Unlabelled: Because of the possibility of vasopressin-mediated coronary vasospasm, this study was designed to assess effects of vasopressin compared to saline placebo on left anterior descending (LAD) coronary artery blood flow. Twelve anaesthetized domestic swine were prepared for LAD coronary artery blood flow measurement with ultrasonic flow probes, using cardiopulmonary by-pass adjusted to 10% of the prearrest cardiac output. This 10% value approximates that reported for cardiac output during conventional closed-chest CPR. After 4 min of untreated ventricular fibrillation, and 3 min of cardiopulmonary by-pass blood flow, 12 pigs were randomly assigned to receive intravenously, every 5 min, either vasopressin (0.4, 0.4, and 0.8 U/kg; n = 6) or saline placebo (n = 6). The mean +/- S.D. LAD coronary artery blood flow in the vasopressin and placebo pigs was comparable before cardiac arrest, and during cardiopulmonary by-pass low flow; but increased significantly (P < 0.05) 90 s after each of three vasopressin injections compared to placebo (78 +/- 1 versus 42 +/- 2 ml/min; 62 +/- 2 versus 36 +/- 1 ml/min; and 54 +/- 1 versus 27 +/- 1 ml/min), respectively. Coronary vascular resistance decreased significantly (P < 0.05 ) 90 s after each of three vasopressin and placebo injections. In this model, repeated bolus administration of vasopressin, given during simulated extremely low cardiac output improved LAD coronary artery blood flow to prearrest levels without affecting coronary vascular resistance., Conclusions: during extremely low blood flow using cardiopulmonary by-pass, vasopressin improves LAD coronary artery blood flow without affecting coronary vascular resistance.

When ventilating an unintubated patient with a standard adult self-inflating bag, high peak inspiratory flow rates may result in high peak airway pressures with subsequent stomach inflation. In a previous study we have tested a newly developed mouth-to-bag-resuscitator (max. volume, 1500 ml) that limits peak inspiratory flow, but the possible advantages were masked by excessive tidal volumes. The mouth-to-bag-resuscitator requires blowing up a balloon inside the self-inflating bag that subsequently displaces air, which then flows into the patient's airway. Due to this mechanism, gas flow and peak airway pressures are reduced during inspiration when compared with a standard bag-valve-mask-device. In addition, the device allows the rescuer to use two hands instead of one to seal the mask on the patient's face. The purpose of the present study was to assess the effects of the mouth-to-bag-resuscitator, which was modified to produce a maximum tidal volume of 500 ml, compared with a paediatric self-inflating bag (max. volume, 380 ml), and a standard adult self-inflating bag (max. volume, 1500 ml) in an established bench model simulating an unintubated patient with respiratory arrest. The bench model consisted of a face mask, manikin head, training lung (lung compliance, 100 ml/0.098 kPa (100ml/cm H2O); airway resistance, 0.39 kPa/(l s) (4 cm H2O/(l s)), and a valve simulating lower oesophageal sphincter pressure, 1.47 kPa (15 cm H2O). Twenty critical care nurses volunteered for the study and ventilated the manikin for 1 min with a respiratory rate of 20 min(-1) with each ventilation device in random order. The mouth-to-bag-resuscitator versus paediatric self-inflating bag resulted in significantly (P < 0.05) higher lung tidal volumes (302 +/- 41 ml versus 233 +/- 22 ml), and peak airway pressure (10 +/- 1 cm H2O versus 9 +/- 1 cm H2O), but comparable inspiratory time fraction (28 +/- 5% versus 27 +/- 5%, Ti/Ttot), peak inspiratory flow rate (0.6 +/- .01 l/s versus 0.6 +/- 0.2 l/s), and stomach inflation (149 +/- 495 ml/min versus 128 +/- 278 ml/min). In comparison with the adult self-inflating bag, there was significantly (P < 0.05) less gastric inflation (3943 +/- 4896 ml/min versus 149 +/- 495 ml/min versus 128 +/- 278 ml/min, respectively) with both devices, but the standard adult self-inflating bag had significantly higher lung tidal volumes (566 +/- 77 ml), peak airway pressure (13 +/- 1 cm H2O), and peak inspiratory flow rate (0.8 +/- 0.11 l/s). In conclusion, comparing the mouth-to-bag-resuscitator with small tidal volumes versus the paediatric self-inflating-bag during simulated ventilation of an unintubated patient in respiratory arrest resulted in comparable marginal stomach inflation, but significantly reduced the likelihood of gastric inflation compared to the adult self-inflating-bag. Lung tidal volumes were improved from approximately 250 ml with the paediatric self-inflating-bag to approximately 300 ml with the mouth-to-bag-resuscitator.

Background and Purpose: Microdialysis is an established tool to analyse tissue biochemistry, but the value of this technique to monitor cardiopulmonary resuscitation (CPR) effects on cerebral metabolism is unknown. The purpose of this study was to assess the effects of active-compression-decompression (ACD) CPR in combination with an inspiratory threshold valve (ITV) (=experimental CPR) vs. standard CPR on cerebral metabolism measured with microdialysis., Methods: Fourteen domestic pigs were surfaced-cooled to a body core temperature of 26 degrees C and ventricular fibrillation was induced, followed by 10 min of untreated cardiac arrest; and subsequently, standard (n=7) CPR vs. experimental (n=7) CPR. After 8 min of CPR, all animals received 0.4 U/kg vasopressin IV, and CPR was maintained for an additional 10 min in each group; defibrillation was attempted after a total of 28 min of cardiac arrest, including 18 min of CPR., Results: In the standard CPR group, microdialysis measurements showed a 13-fold increase of the lactate-pyruvate ratio from 7.2+/-1.3 to 95.5+/-15.4 until the end of CPR (P<0.01), followed by a further increase up to 138+/-32 during the postresuscitation period. The experimental group developed a sixfold increase of the lactate-pyruvate ratio from 7.1+/-2.0 to 51.1+/-8.7 (P<0.05), and a continuous decrease after vasopressin. In the standard resuscitated group, but not during experimental CPR, a significant increase of cerebral glucose levels from 0.6+/-0.1 to 2.6+/-0.5 mM was measured (P<0.01)., Conclusion: Using the technique of microdialysis we were able to measure changes of brain biochemistry during and after the very special situation of hypothermic cardiopulmonary arrest. Experimental CPR improved the lactate-pyruvate ratio, and glucose metabolism.

The mechanism of forward blood flow due to external chest compressions during cardiopulmonary resuscitation (CPR) remains controversial, with the main theories being based on either a cardiac, or thoracic pump mechanism. Both potential mechanisms are well investigated by echocardiographic assessment. In the present case, a postoperative complication of cardiac tamponade that was detected by a thoracoabdominal CT-scan, led to cardiac arrest with subsequent successful CPR over 15 min until definitive surgical management was performed. This observation suggests that the thoracic pump mechanism may have been the predominant mechanism of forward blood flow in the present case of a pericardial tamponade.

Reducing inspiratory flow rate and peak airway pressure may be important in order to minimise the risk of stomach inflation when ventilating an unprotected airway with positive pressure ventilation. The purpose of this study was to assess the effects of a newly developed bag-valve-mask device (SMART BAG), O-Two Systems International, Ont., Canada) that limits peak inspiratory flow. A bench model simulating a patient with an unintubated airway was used consisting of a face mask, manikin head, training lung (lung compliance, 100 ml/cm H(2)O, airway resistance 4 cm H(2)O/l/s, lower oesophageal sphincter pressure 20 cm H(2)O and simulated stomach). Twenty nurses were randomised to each ventilate the manikin using a standard single person technique for 1 min (respiratory rate, 12/min) with either a standard adult self-inflating bag, or the SMART BAG. The volunteers were blinded to the experimental design of the model until completion of the experimental protocol. The SMART BAG vs. standard self-inflating bag resulted in significantly (P<0.05) lower mean+/-S.D. peak inspiratory flow rates (32+/-2 vs. 61+/-13 l/min), peak inspiratory pressure (12+/-2 vs. 17+/-2 cm H(2)O), lung tidal volumes (525+/-111 vs. 680+/-154 ml) and stomach tidal volumes (0+/-0 vs. 17+/-36 ml), longer inspiratory times (1.9+/-0.3 vs. 1.5+/-0.3 s), but significantly higher mask leakage (26+/-13 vs. 14+/-8%); mask tidal volumes (700+/-104 vs. 785+/-172 ml) were comparable. The mask leakage observed is not an uncommon factor in bag-valve-mask ventilation with leakage fractions of 25-40% having been previously reported. The differences observed between the standard BVM and the SMART BAG are due more to the anatomical design of the mask and the non-anatomical shape of the manikin face than the function of the device. Future studies should remove the mask to manikin interface and should introduce a standardized mask leakage fraction. The use of a two-person technique may have removed the problem of mask leakage. In conclusion, using the SMART BAG during simulated ventilation of an unintubated patient in respiratory arrest significantly decreased inspiratory flow rate, peak inspiratory pressure, stomach tidal volume, and resulted in a significantly longer inspiratory time when compared to a standard self-inflating bag.

The Dörges universal laryngoscope blade has several features designed to facilitate tracheal intubation. The number of laryngoscope blades may be reduced from four to two, or even one, which indicate less space requirement and costs. This new universal laryngoscope blade, has a lower profile (height 15 vs. 22 mm) than a Macintosh laryngoscope blade size 3 and 4, which may facilitate manoeuvring of the laryngoscope in the mouth. In random order, 40 non-anaesthesia senior house officers used a Macintosh laryngoscope blade size 3 or 4 in an adult airway management trainer, a Macintosh laryngoscope blade size 2 in a paediatric airway management trainer, and the Dörges universal laryngoscope blade for both airway management trainers to perform orotracheal intubation. The number of intubation attempts and failures was counted. Participants reported the laryngoscopic view according to Cormack and Lehane. The time from touching the laryngoscope to the first adequate lung insufflation was measured, and subjective assessment regarding handling of both blades was recorded. Number of intubation failures, the laryngoscopic view according to Cormack and Lehane, and subjective assessment was comparable between groups. Orotracheal intubation of the adult airway management trainer with the Dörges universal laryngoscope blade took significantly less time compared to the Macintosh laryngoscope blades (14 (7-57) vs. 20 (8-43) s; P<0.001); all other intubating times were comparable. In conclusion, in this model, the Dörges universal laryngoscope blade was comparable to the Macintosh laryngoscope blades size 2-4, and may save time, cost and space.

When ventilating an unintubated patient with a self-inflating bag, high peak inspiratory flow rates may result in high peak airway pressure with subsequent stomach inflation; this may occur frequently when rescuers without daily experience in bag-valve-mask ventilation need to perform advanced airway management. The purpose of this study was to assess the effects of a newly developed self-inflating bag (mouth-to-bag resuscitator; Ambu, Glostrup, Denmark) that limits peak inspiratory flow. A bench model simulating a patient with an unintubated airway was used, consisting of a face mask, manikin head, training lung (lung compliance, 100 ml/0.098 kPa (100 ml/cm H(2)O)); airway resistance, 0.39 kPa/l per second (4 cm H(2)O/l/s), oesophagus (LESP, 1.96 kPa (20 cm H(2)O)) and simulated stomach. Twenty nurses were randomised to ventilate the manikin for 1 min (respiratory rate: 12 per minute) with either a standard self-inflating bag or the mouth-to-bag resuscitator, which requires the rescuer to blow up a single-use balloon inside the self-inflating bag, which in turns displaces air towards the patient. When supplemental oxygen is added, ventilation with up to 100% oxygen may be obtained, since expired air is only used as the driving gas. The mouth-to-bag resuscitator therefore allows two instead of one hand sealing the mask on the patient's face. The volunteers were blinded to the experimental design of the model until completion of the experimental protocol. The mouth-to-bag resuscitator versus standard self-inflating bag resulted in significantly (P<0.05) higher mean+/-S.D. mask tidal volumes (1048+/-161 vs. 785+/-174 ml) and lung tidal volumes (911+/-148 vs. 678+/-157 ml), longer inspiratory times (1.7+/-0.4 vs. 1.4+/-0.4 s), but significantly lower peak inspiratory flow rates (50+/-9 vs. 62+/-13 l/min) and mask leakage (10+/-4 vs. 15+/-9%); peak inspiratory pressure (17+/-2 vs. 17+/-2 cm H(2)O) and stomach tidal volumes (16+/-30 vs. 18+/-35 ml) were comparable. In conclusion, employing the mouth-to-bag resuscitator during simulated ventilation of an unintubated patient in respiratory arrest significantly decreased inspiratory flow rate and improved lung tidal volumes, while decreasing mask leakage.

Objective: Despite the important role of the adrenal gland during cardiac arrest, little is known about changes in the adrenal medullary or cortical blood flow in this setting. This study was designed to assess regional adrenal gland perfusion in the medulla and cortex during cardiopulmonary resuscitation (CPR), and after administration of adrenaline (epinephrine) versus vasopressin versus saline placebo., Methods: After 4 min of untreated ventricular fibrillation, and 3 min of basic life support CPR, 19 animals were randomly assigned to receive either vasopressin (0.4 U/kg; n=7), adrenaline (45 microg/kg; n=6) or saline placebo (n=6), respectively. Haemodynamic variables, adrenal, and renal blood flow were measured after 90 s of CPR, and 90 s and 5 min after drug administration., Results: All values are given as mean+/-S.E.M. Blood flow in the adrenal medulla was significantly higher 90 s after adrenaline when compared with saline placebo in the right adrenal medulla (210+/-14 vs. 102+/-5 ml/min per 100 mg), and in the left adrenal medulla (218+/-14 vs. 96+/-3 ml/min per 100 mg). Blood flow in the adrenal medulla was significantly higher 90 s and 5 min after vasopressin when compared with adrenaline in the right (326+/-22 mg vs. 210+/-14 ml/min per 100 mg, and 297+/-17 vs. 103+/-5 ml/min per 100 mg), and in the left medulla (333+/-25 vs. 218+/-14 ml/min per 100 mg, and 295+/-14 vs. 111+/-7 ml/min per 100 mg). Ninety seconds and five minutes after vasopressin, and 90 s after adrenaline, adrenal cortex blood flow was significantly higher when compared with saline placebo. After 12 min of cardiac arrest, including 8 min of CPR, seven of seven pigs in the vasopressin group, one of six pigs in the adrenaline group, but none of six placebo were successfully defibrillated., Conclusion: Both vasopressin and adrenaline produced significantly higher medullary and cortical adrenal gland perfusion during CPR than did a saline placebo; but vasopressin resulted in significantly higher medullary adrenal gland blood flow when compared with adrenaline.

There is increasing evidence that the combination of epinephrine (adrenaline) with vasopressin may be superior to either epinephrine or vasopressin alone for treatment of cardiac arrest. However, the optimal combination, and dosage of cardiovascular drugs to minimize side effects, and to improve outcome has yet to be found. We therefore evaluated whether the combination of vasopressin plus epinephrine plus nitroglycerin (EVN), would improve vital organ blood flow during cardiopulmonary resuscitation (CPR) when compared with epinephrine (EPI) alone. After 4 min of ventricular fibrillation (VF) and 4 min of standard CPR, pigs were randomized to the combination of epinephrine (45 microg/kg) plus vasopressin (0.4 U/kg) plus nitroglycerin (7.5 microg/kg; n=12), or epinephrine (40 microg/kg; n=12) alone. Cerebral and myocardial blood flow was measured with radiolabeled microspheres. Defibrillation was attempted after 19 min of VF including 15 min of CPR. Mean+/-SEM coronary perfusion pressures were significantly (P < 0.01) higher 5 min after EVN vs. EPI alone (34+/-3 vs. 24+/-3 mmHg, respectively). At the same time, mean+/-SEM left ventricular, and global cerebral blood flow was also significantly (P < 0.05) higher after EVN vs. EPI alone (0.78+/-0.11 vs. 0.48+/-0.08 ml/min/g; and 0.37+/-0.05 vs. 0.22+/-0.0 3 ml/min/g, respectively). Spontaneous circulation was restored in 11 of 12 animals in the EVN group vs. 6 of 12 swine after EPI alone (P = N.S.). In conclusion, the combination of EVN significantly improved vital organ blood flow during CPR compared with EPI alone. Addition of nitroglycerin to the combination of low dose epinephrine with vasopressin during cardiac arrest may be beneficial.

If the airway of a cardiac arrest patient is unprotected, basic life support with low rather than high inspiratory flow rates may reduce stomach inflation. Further, if the inspiratory flow rate is fixed such as with a resuscitator performance may improve; especially when used by less experienced rescuers. The purpose of the present study was to assess the effect of limited flow ventilation on respiratory variables, and lung and stomach volumes, when compared with a bag valve device. After institutional review board approval, and written informed consent was obtained, 20 critical care unit registered nurses volunteered to ventilate a bench model simulating a cardiac arrest patient with an unprotected airway consisting of a face mask, manikin head, training lung [with lung compliance, 50 ml/0.098 kPa (50 ml/cmH(2)O); airway resistance, 0.39 kPa/l/s (4 cmH(2)O/l/s)] oesophagus [lower oesophageal sphincter pressure, 0.49 kPa (5 cmH(2)O)] and simulated stomach. Each volunteer ventilated the model with a self-inflating bag (Ambu, Glostrup, Denmark; max. volume, 1500 ml), and a resuscitator providing limited fixed flow (Oxylator EM 100, CPR Medical devices Inc., Toronto, Canada) for 2 min; study endpoints were measured with 2 pneumotachometers. The self-inflating bag vs. resuscitator resulted in comparable mean +/- SD mask tidal volumes (945 +/- 104 vs. 921 +/- 250 ml), significantly (P < 0.05) higher peak inspiratory flow rates (111 +/- 27 vs. 45 +/- 21 l/min), and peak inspiratory pressure (1.2 +/- 0.47 vs. 78 +/- 0.07 kPa), but significantly shorter inspiratory times (1.1 +/- 0.29 vs. 1.6 +/- 0.35 s). Lung tidal volumes were comparable (337 +/- 120 vs. 309 +/- 61 ml), but stomach tidal volumes were significantly (P < 0.05) higher (200 +/- 95 vs. 140 +/- 51 ml) with the self-inflating bag. In conclusion, simulated ventilation of an unintubated cardiac arrest patient using a resuscitator resulted in decreased peak flow rates and therefore, in decreased peak airway pressures when compared with a self-inflating bag. Limited flow ventilation using the resuscitator decreased stomach inflation, although lung tidal volumes were comparable between groups.

Objective: HMR 1883 (the free acid form of HMR 1098) selectively inactivates myocardial ATP sensitive potassium channels, which may be a potential important therapeutic approach to prevent life-threatening arrhythmias. This study was designed to assess the effects of HMR 1883 combined with adrenaline on haemodynamic variables, blood gases, and cardiac arrhythmias in a porcine cardiac arrest model., Methods: After 8 min of untreated cardiac arrest, followed by 1 min of cardiopulmonary resuscitation (CPR), 12 pigs weighing 30-40 kg were assigned randomly to receive either 45 microg/kg adrenaline alone (n=6), or 45 microg/kg adrenaline combined with 3 mg/kg HMR 1883 (n=6), followed by up to three defibrillation attempts 2 min later. Five minutes after return of spontaneous circulation, cardiac arrest was induced for 1 min, with the CPR protocol following as described above. All animals subsequently underwent four cardiac arrest intervals of 1, 2, 3, and 4 min duration which were separated by four episodes of 5 min of return of spontaneous circulation., Results: Haemodynamic variables, cardiac arrhythmias in the acute resuscitation phase between termination of chest compressions and return of spontaneous circulation, and after return of spontaneous circulation in both groups were comparable throughout the experiment. Survival rates throughout the experiment were comparable between groups. Arterial blood gases, electrolyte, glucose, and lactate levels in both groups during the experiment indicated comparable severe metabolic acidosis, with increasing levels after each episode of simulated refibrillation, and subsequent return of spontaneous circulation., Conclusion: Combining HMR 1883 with adrenaline during CPR resulted in comparable haemodynamic variables, return of spontaneous circulation rates, cardiac arrhythmias, lactate and glucose levels compared with adrenaline alone. This indicates that injection of HMR 1883 was safe under these conditions.