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As is known, hypoxia leads to an increase in microcirculatory blood flow of the skin in healthy volunteers. In this pilot study, we investigated microcirculatory blood flow and reactive hyperemia of the skin in healthy subjects in normobaric hypoxia. Furthermore, we examined differences in microcirculation between hypoxic subjects with and without short-term acclimatization, whether or not skin microvasculature can acclimatize. Fourty-six healthy persons were randomly allocated to either short-term acclimatization using intermittent hypoxia for 1 h over 7 days at an FiO 2 0.126 (treatment, n = 23) or sham short-term acclimatization for 1 h over 7 days at an FiO 2 0.209 (control, n = 23). Measurements were taken in normoxia and at 360 and 720 min during hypoxia (FiO 2 0.126). Microcirculatory cutaneous blood flow was assessed with a laser Doppler flowmeter on the forearm. Reactive hyperemia was induced by an ischemic stimulus. Measurements included furthermore hemodynamics, blood gas analyses and blood lactate. Microcirculatory blood flow increased progressively during hypoxia (12.3 ± 7.1-19.0 ± 8.1 perfusion units; p = 0.0002) in all subjects. The magnitude of the reactive hyperemia was diminished during hypoxia (58.2 ± 14.5-40.3 ± 27.4 perfusion units; p = 0.0003). Short-term acclimatization had no effect on microcirculatory blood flow. When testing for a hyperemic response of the skin's microcirculation we found a diminished signal in hypoxia, indicative for a compromised auto-regulative circulatory capacity. Furthermore, hypoxic short-term acclimatization did not affect cutaneous microcirculatory blood flow. Seemingly, circulation of the skin was unable to acclimatize using a week-long short-term acclimatization protocol. A potential limitation of our study may be the 7 days between acclimatization and the experimental test run. However, there is evidence that the hypoxic ventilatory response, an indicator of acclimatization, is increased for 1 week after short-term acclimatization. Then again, 1 week is what one needs to get from home to a location at significant altitude.

Objective: We examined the effects of systemic ETX on jejunal mucoal microcirculatory parameters in anesthetized pigs., Methods: Jejunal mucosal tissue PO 2 was measured employing Clark-type surface oxygen electrodes. Oxygen saturation of jejunal microvascular hemoglobin was determined by tissue reflectance spectrophotometry. Jejunal microcirculatory blood flow was assessed by laser Doppler flowmetry. Microvascular conductance and rhythmical oscillation of the tissue PO 2 were calculated. Systemic hemodynamic variables, mesenteric venous and systemic acid base and blood gas variables, and lactate measurements were recorded. Measurements were taken at BL and after Escherichia coli LPS administration in 20 minutes intervals for 110 minutes., Results: ETX infusion led to a significant (P<.05) decrease of PO 2 muc (from 24±4 to 8±4 mm Hg) and microvascular HbO 2 (from 41±13 to 24±12%). Microcirculatory conductivity increased in ETX animals, microvascular blood flow remained unchanged (PU; from 228±45 to 232±58). ETX induced an increase in oscillation frequency of mucosal tissue oxygenation., Conclusions: Endotoxinemia resulted in a significant depression of mucosal tissue oxygenation despite a constant microcirculatory blood flow. This impairment of tissue oxygenation resulted in an increase in the vasomotion pattern in a futile attempt to counteract the undersupply of oxygen to the jejunal tissue., (© 2017 John Wiley & Sons Ltd.)

This report describes a case of sudden cardiac arrest and subsequent attempted cardiopulmonary resuscitation of an 11-year-old child on the shores of a swimming lake. Reports of eyewitnesses excluded the obviously suspected diagnosis of a drowning accident. The result of the autopsy was sudden cardiac death due to a congenital coronary anomaly (abnormal left coronary artery, ALCA). Favored by vigorous physical activity, this anomaly can lead to malignant arrhythmias because the ectopic coronary artery with its intramural course through the aortic wall is compressed during every systole. This pathology was not known to the boy or his family; in fact he liked sports but had suffered of a syncope once which was not followed up. Without a strong suspicion it is difficult to diagnose a coronary artery anomaly and it is often missed even in college athletes. Tragically, sudden cardiac arrest may be the first symptom of an undiagnosed abnormal coronary artery. Following syncope or chest pain during exercise with a normal electrocardiogram (ECG) cardiac imaging, such as computed tomography (CT) or angiography should be initiated in order to enable surgical repair of an abnormal coronary artery.

Objective: Locoregional anesthesia is an effective method for evaluating cerebral function during carotid endarterectomy (CEA). Landmark-guided regional anesthesia (RA) is currently used for CEA and can provoke substantial perioperative hypertension. Ultrasound-guided RA (US-RA) is a new method for performing RA in CEA; however, the effect on sympathetic activity and blood pressure is uncertain. This study assessed early sympathetic activity during CEA in US-RA compared with general anesthesia (GA)., Methods: Patients were prospectively randomized to receive US-RA (n = 32) or GA (n = 28) for CEA. The primary end point was the change in systolic arterial blood pressure after induction of anesthesia (just before starting surgery) comparing US-RA with GA. We also recorded heart rate and analyzed concentrations of plasma blood hormones, including cortisol, metanephrine, and normetanephrine at five different times. Creatinine kinase, troponin I, and N-terminal pro-B-type natriuretic peptide were analyzed to detect potential changes in cardiac biomarkers during the procedure., Results: Systolic arterial blood pressure (mean ± standard deviation) increased significantly in US-RA patients compared with GA patients even before surgery was initiated (180 ± 26 mm Hg vs 109 ± 24 mm Hg; P < .001), then remained elevated during the entire surgery and returned to baseline values 1 hour after admission to the postoperative anesthesia care unit. Heart rate (US-RA: 78 ± 16 beats/min, GA: 52 ± 12 beats/min; P < .001) and cortisol levels (US-RA: 155 ± 97 μg/L, GA: 99 ± 43 μg/L; P = .006) were also significantly higher in the US-RA group after induction of anesthesia. Other values did not differ., Conclusions: The US-RA technique for CEA induces temporary intraoperative hypertension and an increase in stress hormone levels. Nevertheless, US-RA is a feasible, effective, and safe form of locoregional for CEA that enables targeted placement of low volumes of local anesthesia under direct visualization., (Copyright © 2015 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.)

Background: Only randomized clinical trials can improve the outcome of life-threatening injuries or diseases but observations from England and North America suggest that the number of such randomized clinical trials is decreasing. In this study contributions from German speaking countries with regards to randomized clinical trials in emergency medicine over the last 22 years were investigated., Methods: The Medline database was searched from January 1990 to December 2012 for prospective randomized clinical trials in the prehospital setting using the criteria "cardiac arrest", "cardiopulmonary resuscitation", "multiple trauma", "hemorrhagic shock", "head trauma", "stroke" as well as myocardial infarction and emergency medical service. Only studies originating from Germany, Austria or Switzerland were included., Results: A total of 474 studies were found and 25 studies (5.3 %) fulfilled the inclusion criteria. In the last 22 years German speaking countries have published approximately one prospective, randomized, clinical trial per year on prehospital emergency medicine. The median number of patients included in the trials was 159 (minimum 16, maximum 1,219). Most (80 %) studies originated from Germany and most (64 %) studies were conducted by anesthesiology departments. Cardiac arrest was the most frequent subject of the investigated studies. Approximately 50 % of the studies had financial support from industrial companies., Conclusion: A significant increase or decrease in the number of prospective randomized clinical trials in the out-of-hospital setting could not be found in German speaking countries despite the fact that the absolute numbers of studies had increased. Only about one prospective, randomized clinical trial with an emergency medicine core tracer diagnosis originated from Germany, Austria and Switzerland per year.

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.

Background: We created a prediction model to be used in cardiopulmonary resuscitation (CPR) attempts as a decision tool to omit futile CPR attempts and to save resources., Methods: In this post hoc analysis, we assessed predictive parameters for neurological recovery after successful CPR. The original study was designed as a blinded, randomized, prospective, controlled, multicenter clinical trial., Results: We identified 1166 prehospital cardiac arrest patients being treated with advanced cardiac life support. Seven hundred eighty-six of 1166 patients (67.4%) died at the scene and 380 of 1166 (32.6%) were brought to the hospital. Two hundred sixty-five of 1166 patients (22.7%) died in the hospital. One hundred fifteen of 1166 (9.8%) were discharged from the hospital and 92 of the 115 patients (80%) could be followed-up. Good cerebral performance was regained by 54% of discharged patients (50 of 92 patients). In 46% of patients (42/92), unconsciousness or severe disability remained. Ventricular fibrillation was more likely to have occurred in patients with good neurological recovery (42/50 = 84.0%), whereas asystole was more likely in patients with poor neurological recovery (9/42 = 21.4%). A score was developed to predict the probability of death using logistic regression analysis. Predicting death in the hospital revealed a sensitivity of 99.8% (953/955), but only a specificity of 2.9% (3/104; threshold 0.5). Predicting survival until discharge from the hospital revealed a sensitivity of 99% (103/104), but only a specificity of 8% (72/955; threshold 0.99). A receiver operating characteristic curve yielded an area under the curve of 0.795 (0.751-0.839) at a confidence interval of 95%., Conclusion: For out-of-hospital patients with cardiac arrest, parameters documented in the field did not allow accurate prediction of hospital survival.

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.

Background: We compared three techniques for insertion of the laryngeal mask airway ProSeal (PLMA) in patients with simulated difficult laryngoscopy using a rigid neck collar., Methods: Ninety-nine anesthetized healthy female patients aged 19-68 yr were randomly allocated for PLMA insertion using the digital, introducer tool (IT) or guided techniques. Difficult laryngoscopy was simulated using a rigid neck collar. The laryngoscopic view was graded before PLMA insertion. The digital and IT techniques were performed according to the manufacturer's instructions. The guided technique involved priming the drain tube with an Eschmann tracheal tube introducer, placing the introducer in the esophagus under direct vision and railroading the PLMA into position. Failed insertion was defined by any of the following criteria: 1) failed pharyngeal placement, 2) malposition, and 3) ineffective ventilation., Results: The median laryngoscopic view was 3 and the mean interincisor distance was 3.3 cm. Insertion was more frequently successful with the guided technique at the first attempt (guided 100%, digital 64%, IT 61%; P<0.0001), but success after three attempts was similar (guided 100%, digital 94%, IT 91%). The time taken for successful placement was similar among groups at the first attempt, but was shorter for the guided technique after three attempts (guided 31+/-8 s, digital 49+/-28 s, IT 54+/-37 s; P<0.02)., Conclusion: The guided insertion technique is more frequently successful than the digital or IT techniques in patients with simulated difficult laryngoscopy using a rigid neck collar.

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.

Background: Patients with uncontrolled hemorrhage may benefit if resuscitation with large amounts of fluids is replaced by a small volume or vasopressor until surgery. Norepinephrine (NE) is commonly used as a vasopressor to control hypotension. The purpose of this study was to compare the effects of hypertonic-hyperoncotic saline starch solution (HHS) either alone or combined with NE on brain tissue oxygen pressure (PbtO2) and brain oxygen saturation (rSO2) in a model of uncontrolled hemorrhage., Methods: After approval of the animal investigation committee, 22 anesthetized pigs underwent simulated penetrating liver trauma. At hemodynamic decompensation, animals were randomly assigned to receive HHS (Hyperhaes; 4 mL/kg; n = 8) with normal saline placebo, low-dose NE (low NE; 500 microg, and 1 microg/kg/min; n = 7), or high-dose NE (high NE; 1,000 microg, and 1 microg/kg/min; n = 7). Bleeding was controlled manually 30 minutes after drug administration., Results: Cerebral perfusion pressure (CePP), PbtO2, and rSO2 decreased with hemorrhage in all groups (baseline vs. decompensation, CePP-HHS, 83 +/- 5 mm Hg vs. 9 +/- 1 mm Hg; low NE, 67 +/- 6 mm Hg vs. 16 +/- 2 mm Hg; high NE, 77 +/- 7 mm Hg vs. 15 +/- 1 mm Hg. PbtO2-HHS, 100% vs. 29%; low NE, 100% vs. 33%; high NE, 100% vs. 27%. rSO2-HHS, 100% vs. 70%; low NE, 100% vs. 76%; high NE, 100% vs. 63%). Therapy with HHS, low NE, and high NE resulted in a comparable increase of CePP, PbtO2, and rSO2, respectively (5 minutes after therapy, CePP-HHS, 29 +/- 3 mm Hg; low NE, 27 +/- 3 mm Hg; high NE, 28 +/- 3 mm Hg. PbtO2-HHS, 207%; low NE, 129%; high NE, 170%. rSO2-HHS, 94%; low NE, 83%; high NE, 87%). Overall survival was six of eight, four of seven, and six of seven, respectively., Conclusion: After uncontrolled hemorrhagic shock, addition of different dosages of NE to HHS, compared with HHS alone, showed no beneficial effect on CePP, rSO2, or PbtO2.

Endogenous arginine vasopressin (AVP) levels in multiple trauma patients are unknown. Arginine vasopressin is considered to play an important role in severe hemorrhage. In this prospective study, 87 multiple trauma patients (Injury Severity Score >15) and 50 healthy volunteers were enrolled. On admission to the emergency department (ED), demographic, clinical, and laboratory data were documented, and blood was sampled for determination of AVP (radioimmunosassay) and copeptin, a stable fragment of the AVP precursor (immunoluminometric assay). In patients requiring intensive care unit (ICU) therapy, blood and data sampling were repeated at 4, 6, and 24 h after ED admission. Linear logistic and mixed-effects regression analyses were used for statistical analysis. On ED admission, AVP plasma concentrations (43.2 +/- 84.9 pM) were significantly increased when compared with controls (0.92 +/- 0.44 pM, P < 0.001). Plethysmographic oxygen saturation was the only parameter independently associated with AVP (regression coefficient, -0.126; 95% confidence interval, -0.237 to -0.014; P = 0.03). No correlation was observed between AVP and survival (P = 0.62), hemodynamic variables (systolic arterial pressure, P = 0.24; MAP, P = 0.59; diastolic arterial pressure, P = 0.74; central venous pressure, P = 0.36), or brain trauma (P = 0.46). In ICU patients, AVP decreased during the first 24 h (P < 0.001) and was independently associated with heart rate (P = 0.02) and blood glucose (P = 0.009). Copeptin concentrations were correlated with AVP (r2 = 0.718, P < 0.001). In conclusion, AVP was significantly increased in multiple trauma patients and seems to be an integral part of the neuroendocrine response to severe injury. In ICU patients, AVP decreased to moderately elevated levels within 24 h after ED admission.

Background: Optimal prehospital and clinical management of patients with severe pelvic trauma is controversial. Prospective evaluations of different treatment strategies have not been performed and treatment is currently not evidence-based. The purpose of the present study was to develop a porcine model of reproducible severe pelvic trauma for subsequent laboratory trials., Methods: The study was performed on 13 juvenile porcine cadavers. Pelvic fractures were created by applying a pure anterior-posterior compression load to the pelvic ring using a servohydraulic material testing machine. Fracture patterns were classified according to the Young-Burgess classification and the Tile classification using postfracture CT scans including 3D-reconstructions., Results: Disruptions of the posterior pelvic ring segment were unilateral in 12 cases and bilateral in one case transforaminal vertical sacrum fractures. Injuries of the anterior ring segment were obturator ring fractures bilateral, ipsilateral or contralateral to the injury of the posterior ring segment. According to the Tile classification this resulted in 12 type C1 and 1 type C3 fractures. In the Young classification all injuries were classified as type APC III. In six cases transverse process fractures were found ipsilateral to the posterior ring disruption. Initial force drops indicating bony or ligamentous injuries occurred at mean forces of 4030 +/- 269N (range, 3617-4374N)., Conclusion: The present model was able to create reproducible unstable pelvic fractures and can be used for controlled laboratory trials to study the management of patients with pelvic fractures.

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.

Background: Microcirculatory dysfunction has been hypothesized to play a key role in the pathophysiology of multiple organ failure and, consequently, patient outcome. The objective of this study was to investigate the differences in reactive hyperemia response and oscillation frequency in surviving and non-surviving patients with multiple organ dysfunction syndrome., Methods: Twenty-nine patients (15 survivors; 14 non-survivors) with two or more organ failures were eligible for study entry. All patients were hemodynamically stabilized, and demographic and clinical data were recorded. A laser Doppler flowmeter was used to measure the cutaneous microcirculatory response. Reactive hyperemia and oscillatory changes in the Doppler signal were measured during 3 min before and after a 5-min period of forearm ischemia., Results: Non-survivors demonstrated a significantly higher multiple organ dysfunction score when compared with survivors (P= 0.004). Norepinephrine administration was higher in non-survivors (P= 0.018). Non-survivors had higher arterial lactate levels (P= 0.046), decreased arterial pH levels (P= 0.001) and decreased arterial Po(2) values (P= 0.013) when compared with survivors. A higher oscillation frequency of the skin microvasculature at rest (P= 0.033) and after an ischemic stimulus (P= 0.009) was observed in non-survivors. The flow motion frequency observed in reactive hyperemia was associated with the severity of multiple organ dysfunction (P= 0.009) and, although not statistically significant, with the arterial lactate concentration (P= 0.052)., Conclusion: Increased skin microvascular oscillation frequency at rest and in the hyperemic state after an ischemic stimulus is associated with increased mortality in patients suffering from multiple organ dysfunction. The underlying mechanism could be a response of the skin microvasculature to an impaired oxygen utilization of the skin tissue.

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.

Introduction: We sought to determine and compare the effects of vasopressin, fluid resuscitation and saline placebo on haemodynamic variables and short-term survival in an abdominal vascular injury model with uncontrolled haemorrhagic shock in pigs., Methods: During general anaesthesia, a midline laparotomy was performed on 19 domestic pigs, followed by an incision (width about 5 cm and depth 0.5 cm) across the mesenterial shaft. When mean arterial blood pressure was below 20 mmHg, and heart rate had declined progressively, experimental therapy was initiated. At that point, animals were randomly assigned to receive vasopressin (0.4 U/kg; n = 7), fluid resuscitation (25 ml/kg lactated Ringer's and 25 ml/kg 3% gelatine solution; n = 7), or a single injection of saline placebo (n = 5). Vasopressin-treated animals were then given a continuous infusion of 0.08 U/kg per min vasopressin, whereas the remaining two groups received saline placebo at an equal rate of infusion. After 30 min of experimental therapy bleeding was controlled by surgical intervention, and further fluid resuscitation was performed. Thereafter, the animals were observed for an additional hour., Results: After 68 +/- 19 min (mean +/- standard deviation) of uncontrolled bleeding, experimental therapy was initiated; at that time total blood loss and mean arterial blood pressure were similar between groups (not significant). Mean arterial blood pressure increased in both vasopressin-treated and fluid-resuscitated animals from about 15 mmHg to about 55 mmHg within 5 min, but afterward it decreased more rapidly in the fluid resuscitation group; mean arterial blood pressure in the placebo group never increased. Seven out of seven vasopressin-treated animals survived, whereas six out of seven fluid-resuscitated and five out of five placebo pigs died before surgical intervention was initiated (P < 0.0001)., Conclusion: Vasopressin, but not fluid resuscitation or saline placebo, ensured short-term survival in this vascular injury model with uncontrolled haemorrhagic shock in sedated pigs.

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.

Background and Objective: The present study was designed to compare cerebral oxygenation measured with near infrared spectroscopy and local brain tissue oxygen partial pressure, respectively, in pigs during cardiopulmonary resuscitation. Since tissue overlying the brain may have an impact on near infrared spectroscopy readings, we tested whether optode placement on intact skin or on the skull yielded comparable results., Methods: Twelve healthy pigs were anaesthetized and subjected to continuous haemodynamic, near infrared spectroscopy and brain tissue oxygen partial pressure monitoring. After 4 min of untreated ventricular fibrillation, cardiopulmonary resuscitation was started and arginine vasopressin was administered repeatedly three times. Near infrared spectroscopy values recorded were both the tissue oxygenation index and the tissue haemoglobin index as well as relative changes of chromophores (haemoglobin and cytochrome oxidase). Four animals served as control and were measured with both near infrared spectroscopy optodes mounted on the intact skin of the forehead, while in the remaining eight animals, one near infrared spectroscopy optode was implanted directly on the skull., Results: Near infrared spectroscopy readings at the skin or at the skull differed consistently throughout the study period. After arginine vasopressin administration, near infrared spectroscopy values at the different locations showed a transient dissociation. In contrast to near infrared spectroscopy measured on intact skin, near infrared spectroscopy readings obtained from skull showed a significant correlation to brain tissue oxygen partial pressure values (r = 0.67, P < 0.001)., Conclusion: Near infrared spectroscopy readings obtained from skin and skull differed largely after vasopressor administration. Near infrared spectroscopy optode placement therefore may have an important influence on the tissue region investigated.

In this post hoc analysis, we assessed effects of thrombolysis during out-of-hospital cardiopulmonary resuscitation. The original study was designed as a double-blinded, prospective, multicenter, randomized, controlled clinical trial. In this report, 1,219 patients were randomized, but 33 patients were excluded due to missing study drug codes. Thus, 1,186 patients were analyzed based on receipt (n = 99) versus nonreceipt (n = 1,087) of thrombolysis; the primary end point was hospital admission, and the secondary end point was hospital discharge. Patients who received thrombolysis versus those who did not were significantly younger (mean +/- SD 62.7 +/- 13.3 vs 66.5 +/- 14.3 years of age, p = 0.01) and more likely to have had an acute myocardial infarction (75.3% vs 54.6%, p < 0.01) or pulmonary embolism (20.2% vs 12.0%, p = 0.03) as the suspected underlying cause for cardiac arrest. In patients who underwent thrombolysis versus those who did not, cardiac arrest was more often witnessed (86.9% vs 77.5%, p = 0.03), initial ventricular fibrillation was more likely (59.6% vs 38.0%, p < 0.01), and a short estimated interval (0 to 5 minutes) between collapse and initiation of basic life support was more likely (51.3% vs 29.2%, p < 0.01). In patients who received thrombolysis, sodium bicarbonate (45.5% vs 33.0%, p = 0.01), lidocaine (32.3% vs 18.1%, p < 0.01), and amiodarone (30.3% vs 12.2%, p < 0.01) were administered significantly more often. Hospital admission rates were significantly higher in patients who underwent thrombolysis than in patients who did not (45.5% vs 32.7%, p = 0.01), and there was a trend to higher hospital discharge rates (14.1% vs 9.5%, p = 0.14). In patients who had suspected myocardial infarction, hospital admission and discharge rates were significantly higher in patients who underwent thrombolysis than in patients who did not. In logistic regression models after adjusting for confounding variables (e.g., age, initial electrocardiographic rhythm, and initiation of basic life support), hospital admission and discharge rates did not differ significantly. In conclusion, even when being employed in patients with a potentially better chance to survive, thrombolysis in patients with cardiac arrest resulted in an increased hospital admission but not discharge rate in this post hoc analysis.

Introduction: Disturbances in microcirculatory homeostasis have been hypothesized to play a key role in the pathophysiology of multiple organ dysfunction syndrome and vasopressor-associated ischemic skin lesions. The effects of a supplementary arginine vasopressin (AVP) infusion on microcirculation in vasodilatory shock and postoperative multiple organ dysfunction syndrome are unknown., Method: Included in the study were 18 patients who had undergone cardiac or major surgery and had a mean arterial blood pressure below 65 mmHg, despite infusion of more than 0.5 microg/kg per min norepinephrine. Patients were randomly assigned to receive a combined infusion of AVP/norepinephrine or norepinephrine alone. Demographic and clinical data were recorded at study entry and after 1 hour. A laser Doppler flowmeter was used to measure the cutaneous microcirculatory response at randomization and after 1 hour. Reactive hyperaemia and oscillatory changes in the Doppler signal were measured during the 3 minutes before and after a 5-minute period of forearm ischaemia., Results: Patients receiving AVP/norepinephrine had a significantly higher mean arterial pressure (P = 0.047) and higher milrinone requirements (P = 0.025) than did the patients who received norepinephrine only at baseline. Mean arterial blood pressure significantly increased (P < 0.001) and norepinephrine requirements significantly decreased (P < 0.001) in the AVP/norepinephrine group. Patients in the AVP/norepinephrine group exhibited a significantly higher oscillation frequency of the Doppler signal before ischaemia and during reperfusion at randomization. During the study period, there were no differences in either cutaneous reactive hyperaemia or the oscillatory pattern of vascular tone between groups., Conclusion: Supplementary AVP infusion in patients with advanced vasodilatory shock and severe postoperative multiple organ dysfunction syndrome did not compromise cutaneous reactive hyperaemia and flowmotion when compared with norepinephrine infusion alone.

Vasopressin administration may be a promising therapy in the management of various shock states. In laboratory models of cardiac arrest, vasopressin improved vital organ blood flow, cerebral oxygen delivery, the rate of return of spontaneous circulation, and neurological recovery compared with epinephrine (adrenaline). In a study of 1219 adult patients with cardiac arrest, the effects of vasopressin were similar to those of epinephrine in the management of ventricular fibrillation and pulseless electrical activity; however, vasopressin was superior to epinephrine in patients with asystole. Furthermore, vasopressin followed by epinephrine resulted in significantly higher rates of survival to hospital admission and hospital discharge. The current cardiopulmonary resuscitation guidelines recommend intravenous vasopressin 40 IU or epinephrine 1mg in adult patients refractory to electrical countershock. Several investigations have demonstrated that vasopressin can successfully stabilize hemodynamic variables in advanced vasodilatory shock. Use of vasopressin in vasodilatory shock should be guided by strict hemodynamic indications, such as hypotension despite norepinephrine (noradrenaline) dosages >0.5 mug/kg/min. Vasopressin must never be used as the sole vasopressor agent. In our institutional routine, a fixed vasopressin dosage of 0.067 IU/min (i.e. 100 IU/50 mL at 2 mL/h) is administered and mean arterial pressure is regulated by adjusting norepinephrine infusion. When norepinephrine dosages decrease to 0.2 microg/kg/min, vasopressin is withdrawn in small steps according to the response in mean arterial pressure. Vasopressin also improved short- and long-term survival in various porcine models of uncontrolled hemorrhagic shock. In the clinical setting, we observed positive effects of vasopressin in some patients with life-threatening hemorrhagic shock, which had no longer responded to adrenergic catecholamines and fluid resuscitation. Clinical employment of vasopressin during hemorrhagic shock is experimental at this point in time.

Nerve stimulators are widely used to assist with peripheral nerve blocks but do not eliminate the risk of nerve injury. We evaluated the histologic findings 6 h after sciatic nerve block with bupivacaine in pigs. When a motor response was still obtained with a current <0.2 mA (n = 10), the postmortem microscopic evaluation revealed lymphocytes and granulocytes sub-, peri-, and intraneurally in 5 (50%) of 10 pigs. No signs of inflammation were observed when the muscle contraction was achieved with a current between 0.3 and 0.5 mA (P = 0.03). In conclusion, the current required to elicit a motor response, the position of the needle tip, and the subsequent likelihood of nerve damage merit further evaluation.

Study Objective: Although a moderate positive end-expiratory pressure (PEEP) level is widely recommended, it is unknown whether moderate PEEP during mechanical ventilation has adverse effects during severe hemorrhagic shock. Therefore, the purpose of our study was to evaluate the effects of 0 cm H2O PEEP versus 5 cm H2O PEEP versus 10 cm H2O PEEP on short-term survival in a porcine model of severe hemorrhagic shock. Secondary study endpoints were hemodynamic variables and blood gases., Methods: Twenty-four anesthetized pigs were bled approximately 45 mL/kg, randomized into 3 groups, and then ventilated with 0, 5, or 10 cm H2O PEEP. Survival rates were compared using Kaplan-Meier methods with log rank (Mantel Cox) comparison of cumulative survival by treatment group., Results: Seven of 8 0 cm H2O PEEP animals survived the 120-minute study period, but 8 of 8 5 cm H2O PEEP animals died within 30 minutes, and 8 of 8 10 cm H2O PEEP animals were dead within 20 minutes (P<.0001). Ventilation with 0 cm H2O PEEP prevented a further reduction of mean arterial blood pressure and cardiac output. When compared with the 0 cm H2O PEEP group, end-tidal CO2 declined in the 5 cm H2O PEEP and 10 cm H2O PEEP animals. Compared with the 0 cm H2O PEEP animals, those ventilated with 5 or 10 cm H2O PEEP had higher lactate levels after 10 minutes., Conclusion: When compared with pigs ventilated with either 5 or 10 cm H2O PEEP, those ventilated with 0 cm H2O PEEP during untreated, severe hemorrhagic shock had significantly improved short-term survival.

Background: Brain tissue oxygen pressure (PbtO2) correlates to cerebral blood flow (CBF) during spontaneous circulation, with one important regulator being nitric oxide (NO). Although it is established that arginine vasopressin (AVP) improves CBF and global cerebral oxygenation during cardiopulmonary resuscitation, it is unknown whether similar beneficial effects are present during spontaneous circulation. The purpose of this study was to investigate the effects of AVP with and without pre-treatment with the NO synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) on local brain tissue oxygenation in a beating heart model., Methods: Following approval of the Animal Investigational Committee, nine healthy piglets underwent general anaesthesia, and were instrumented with a probe in the cerebral cortex to measure PbtO2. Each animal was assigned to receive AVP (0.4 U . kg(-1)), and after a wash-out period, L-NAME (25 mg x kg(-1) over 20 min) followed by AVP (0.4 U x kg(-1)). After each AVP administration, nitroglycerine (25 microg x kg(-1) over 1 min) as a NO donor was infused to test the vascular reactivity independently from NOS inhibition., Findings: Three minutes after administration of AVP, PbtO2 increased significantly (P < .05; mean +/- SEM, 31 +/- 11 versus 43 +/- 14 mm Hg, +39%), compared with baseline. After pre-treatment with L-NAME, the changes of PbtO2 after AVP were not significant (32 +/- 11 versus 28 +/- 10, -13%) when compared with the baseline., Conclusion: In this beating heart porcine model, local brain tissue oxygenation was improved after AVP alone, but not after inhibition of NO synthesis with L-NAME.

Resuscitation of patients in hemorrhagic shock remains one of the most challenging aspects of trauma care. We showed in experimental studies that vasopressin, but not fluid resuscitation, enabled short-term and long-term survival in a porcine model of uncontrolled hemorrhagic shock after penetrating liver trauma. In this case report, we present two cases with temporarily successful cardiopulmonary resuscitation (CPR) using vasopressin and catecholamines in uncontrolled hemorrhagic shock with subsequent cardiac arrest that was refractory to catecholamines and fluid replacement. In a third patient, an infusion of vasopressin was started before cardiac arrest occurred; in this case, we were able to stabilize blood pressure thus allowing further therapy. The patient underwent multiple surgical procedures, developed multi-organ failure, but was finally discharged from the critical care unit without neurological damage.

Background and Objective: The aim of the present study was to investigate the impact of arginine vasopressin (AVP), a drug currently under investigation for use during cardiopulmonary resuscitation, on cerebral oxygenation and cerebral blood volume (CBV) in pigs with intact systemic circulation using near infrared spectroscopy., Methods: Nine healthy pigs were anaesthetized and subjected to invasive haemodynamic monitoring as well as to non-invasive determination (with near infrared spectroscopy) of changes in the Tissue Oxygenation Index (TOI is the ratio of oxygenated to total tissue haemoglobin), Tissue Haemoglobin Index (THI, representing CBV) and cytochrome oxidase (deltaCytOx, representing the balance of intracellular oxygen supply)., Results: At both 3 and 5 min after AVP administration, TOI, THI and deltaCytOx were significantly (P < 0.001) reduced compared to baseline, while cerebral perfusion pressure increased significantly (P < 0.001). The effects of AVP on TOI and THI lasted longer than on deltaCytOx. There were no significant changes with respect to the intracranial pressure throughout the study period., Conclusions: No improvement of cerebral oxygenation was detected after AVP administration in swine with an intact systemic circulation. In contrast to recently published investigations, AVP provoked a sustained drop in indices of cerebral oxygenation and CBV.

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.

Experimental and clinical studies investigated whether urinary incontinence can be effectively treated with transurethral ultrasound-guided injections of autologous myoblasts and fibroblasts.This new therapy was performed in eight female pigs. It could be shown that the injected cells survived well and that new muscle tissue was formed. Next, 42 patients (29 women, 13 men) suffering from urinary stress incontinence were treated. The fibroblasts were mixed with a small amount of collagen as carrier material and injected into the urethral submucosa to treat atrophies of the mucosa. The myoblasts were directly injected into the rhabdosphincter to reconstruct the muscle and to heal morphological and functional defects. In 35 patients urinary incontinence could be completely cured. In seven patients who had undergone multiple surgical procedures and radiotherapy urinary incontinence improved. No side effects or complications were encountered postoperatively. The experimental as well as the clinical data clearly demonstrate that urinary incontinence can be treated effectively with autologous stem cells. The present data support the conclusion that this new therapeutic concept may represent a very promising treatment modality in the future.

Objective: In patients undergoing cardiopulmonary resuscitation, circulating endogenous vasopressin concentrations were significantly higher in successfully resuscitated patients than in patients who died. These observations have prompted several investigations to assess the role of vasopressin to improve cardiopulmonary resuscitation management., Design: Literature review., Results: In the cardiopulmonary resuscitation laboratory, vasopressin improved vital organ blood flow, cerebral oxygen delivery, the probability of restoring spontaneous circulation, and neurologic recovery better than epinephrine. In pediatric preparations with asphyxia, epinephrine was superior to vasopressin, whereas in both pediatric pigs with ventricular fibrillation and adult porcine models with asphyxia, combinations of vasopressin and epinephrine proved to be highly effective. In addition, vasopressin enabled short- and long-term survival in a porcine model of uncontrolled hemorrhagic shock. In a recently published European, multiple-center trial, 1,219 adult patients with out-of-hospital cardiac arrest were randomized to receive two injections of either 40 IU of vasopressin or 1 mg of epinephrine followed by additional epinephrine if needed. The clinical study did not confirm laboratory data showing vasopressin to be more effective than epinephrine in ventricular fibrillation and pulseless electrical activity, but vasopressin was superior to epinephrine in patients with asystole. Vasopressin followed by epinephrine was more effective than epinephrine alone in the treatment of refractory cardiac arrest., Conclusions: According to new data from the European vasopressin study, we suggest, first, the administration of 1 mg of epinephrine, followed alternately by 40 IU of vasopressin and 1 mg of epinephrine every 3 mins in adult cardiac arrest victims, regardless of the initial electrocardiographic rhythm.

Unlabelled: In a porcine model of uncontrolled hemorrhagic shock, we evaluated the effects of vasopressin versus an equal volume of saline placebo versus fluid resuscitation on hemodynamic variables and short-term survival. Twenty-one anesthetized pigs were subjected to severe liver injury. When mean arterial blood pressure was <20 mm Hg and heart rate decreased, pigs randomly received either vasopressin IV (0.4 U/kg; n = 7), an equal volume of saline placebo (n = 7), or fluid resuscitation (1000 mL each of lactated Ringer's solution and hetastarch; n = 7). Thirty minutes after intervention, surviving pigs were fluid resuscitated while bleeding was surgically controlled. Mean (+/- SEM) arterial blood pressure 5 min after the intervention was significantly (P < 0.05) higher after vasopressin than with saline placebo or fluid resuscitation (58 +/- 9 versus 7 +/- 3 versus 32 +/- 6 mm Hg, respectively). Vasopressin improved abdominal organ blood flow but did not cause further blood loss (vasopressin versus saline placebo versus fluid resuscitation 10 min after intervention, 1343 +/- 60 versus 1350 +/- 22 versus 2536 +/- 93 mL, respectively; P < 0.01). Seven of 7 vasopressin pigs survived until bleeding was controlled and 60 min thereafter, whereas 7 of 7 saline placebo and 7 of 7 fluid resuscitation pigs died (P < 0.01). We conclude that vasopressin, but not saline placebo or fluid resuscitation, significantly improves short-term survival during uncontrolled hemorrhagic shock., Implications: Although IV fluid administration is the mainstay of nonsurgical management of trauma patients with uncontrolled hemorrhagic shock, the efficacy of this strategy has been discussed controversially. In this animal model of severe liver trauma with uncontrolled hemorrhagic shock, vasopressin, but not saline placebo or fluid resuscitation, improved short-term survival.

Objective: To assess the value of 2 transducer positions for measurement of finger flexor tendon thickness by sonography., Methods: Flexor tendon thickness of the third finger was measured sonographically by 2 independent investigators in 20 healthy volunteers (n = 40 fingers) and in 4 cadaveric specimens (n = 4 fingers). Flexor tendon thickness was measured at histologic examination in the cadaveric specimens. We defined the area of the A1 annular pulley as position I and the area of the A2 annular pulley as position II. Sonographic measurements were performed in transverse (dorsovolar and radioulnar) and longitudinal planes. Interobserver and intraobserver variabilities were evaluated by each investigator performing 3 measurements at each position., Results: In position I, volunteers had flexor tendon thickness of 2.7 to 4.0 mm (mean +/- SD, 3.28 +/- 0.26 mm) longitudinally; transversally the thickness was 2.5 to 4.0 mm (mean, 3.34 +/- 0.29 mm) dorsovolar and 5.5 to 8.9 mm (mean, 7.34 +/- 0.71) radioulnar in position I. Position II revealed thickness of 3.2 to 4.2 mm (mean, 3.6 +/- 0.23 mm) longitudinally; transversally the thickness was 2.7 to 4.1 mm (mean, 3.4 +/- 0.27) dorsovolar and 4.3 to 6.8 mm (mean, 5.27 +/- 0.65) radioulnar. Interobserver and intraobserver variability for position I was better than for position II (P < .01 versus P < .05). Sonographic findings correlated excellently with histologic findings (r2 = 0.94)., Conclusions: Standardized transducer positions for sonographic measurements of finger flexor tendon thickness showed good interobserver and intraobserver variability. Position I was found to be more reliable than position II.

Unlabelled: Reducing inspiratory flow rate and peak airway pressure may be important to minimize the risk of stomach inflation when ventilating an unprotected airway with positive pressure ventilation. In this study, we assessed the effects of a standard self-inflating bag compared with a new pressure-responsive, inspiratory gas flow-limiting device (SMART BAG) on respiratory mechanics in 60 adult patients undergoing routine induction of anesthesia. Respiratory variables were measured using a pulmonary monitor. The SMART BAG resulted in significantly decreased inspiratory flow rate and peak airway pressure while providing adequate tidal volume delivery., Implications: The SMART BAG, a new pressure-responsive, peak inspiratory gas flow-limiting bag-valve mask device, limits inspiratory gas flow from up to 120 L/min in a standard self-inflating bag to approximately 40 L/min. It is designed for use by all levels of health care professionals and has been proven in a clinical pilot study to effectively ventilate patients in respiratory arrest.

Background: Aim of this experimental animal study was to investigate the influence of vasopressin and amiodarone on cardiopulmonary resuscitation (CPR) outcome in a pig model of hypothermic cardiac arrest., Methods: After surface cooling to a core temperature of 26 degrees C, ventricular fibrillation was induced in 14 12-16-week-old domestic pigs. After 15 min of untreated cardiac arrest, a manual closed chest CPR was started and pigs were randomly assigned to two treatment groups: Group 1 pigs (n = 7) received vasopressin 0.4 U kg-1 as initial drug therapy, followed by a combination vasopressin (0.4 U kg-1) and amiodarone (4 mg kg-1) as subsequent drug therapy. Subsequent drug therapy was administered in animals without permanent restoration of spontaneous circulation after a first series of electrical countershocks 10 min after drug administration. Group 2 pigs (n = 7) received saline placebo as initial drug therapy and saline placebo and amiodarone (4 mg kg-1) as subsequent drug therapy., Results: Vasopressin significantly increased coronary perfusion pressure and defibrillation success (successful defibrillation in five of seven Group 1 vs. none of seven Group 2 pigs, P = 0.02). Due to refibrillation within 30-150 s, the 60-min survival rate was not improved by vasopressin. Subsequent drug therapy with amiodarone had no further effect on defibrillation success or the refibrillation rate., Conclusions: Data from this experimental animal model suggest that vasopressin and amiodarone may not be beneficial for treatment of ventricular fibrillation associated with severe hypothermia when concomitant measures at core rewarming are not applied.

Unlabelled: We assessed the effects of a calcium channel blocker versus saline placebo on ventricular fibrillation mean frequency and hemodynamic variables during prolonged cardiopulmonary resuscitation (CPR). Before cardiac arrest, 10 animals were randomly assigned to receive either nifedipine (0.64 mg/kg; n = 5) or saline placebo (n = 5) over 10 min. Immediately after drug administration, ventricular fibrillation was induced. After 4 min of cardiac arrest and 18 min of basic life support CPR, defibrillation was attempted. Ninety seconds after the induction of cardiac arrest, ventricular fibrillation mean frequency was significantly (P < 0.01) increased in nifedipine versus placebo pigs (mean +/- SD: 12.4 +/- 2.1 Hz versus 8 +/- 0.7 Hz). From 2 to 18.5 min after the induction of cardiac arrest, no differences in ventricular fibrillation mean frequency were detected between groups. Before defibrillation, ventricular fibrillation mean frequency was significantly (P < 0.05) increased in nifedipine versus placebo animals (9.7 +/- 1.2 Hz versus 7.1 +/- 1.3 Hz). Coronary perfusion pressure was significantly lower in the nifedipine than in the placebo group from the induction of ventricular fibrillation to 11.5 min of cardiac arrest; no animal had a return of spontaneous circulation after defibrillation. In conclusion, nifedipine, but not saline placebo, prevented a rapid decrease of ventricular fibrillation mean frequency after the induction of cardiac arrest and maintained ventricular fibrillation mean frequency at approximately 10 Hz during prolonged CPR; this was nevertheless associated with no defibrillation success., Implications: This study evaluates the effects of a calcium channel blocker on ventricular fibrillation mean frequency, hemodynamic variables, and resuscitability during prolonged cardiopulmonary resuscitation (CPR) in pigs. Nifedipine, but not saline placebo, prevented a rapid decrease of ventricular fibrillation mean frequency after the induction of cardiac arrest and maintained ventricular fibrillation mean frequency at approximately 10 Hz during prolonged CPR but did not improve resuscitability.

Unlabelled: We sought to determine the effects of a combination of vasopressin and epinephrine on neurologic recovery in comparison with epinephrine alone and saline placebo alone in an established porcine model of prolonged cardiopulmonary resuscitation (CPR). After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive, every 5 min, either a combination of vasopressin and epinephrine (vasopressin [IU/kg]/epinephrine [ micro g/kg]: 0.4/45, 0.4/45, and 0.8/45; n = 6), epinephrine alone (45, 45, and 200 micro g/kg; n = 6), or saline placebo alone (n = 5). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve the return of spontaneous circulation. Aortic diastolic pressure was significantly (P < 0.01) increased 90 s after each of 3 vasopressin/epinephrine injections versus epinephrine alone versus saline placebo alone (mean +/- SEM: 69 +/- 3 mm Hg versus 45 +/- 3 mm Hg versus 29 +/- 2 mm Hg, 63 +/- 4 mm Hg versus 27 +/- 3 mm Hg versus 23 +/- 1 mm Hg, and 52 +/- 4 mm Hg versus 21 +/- 3 mm Hg versus 16 +/- 3 mm Hg, respectively). Spontaneous circulation was restored in six of six vasopressin/epinephrine pigs, whereas six of six epinephrine and five of five saline placebo pigs died (P < 0.01). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait and was normal 5 days after the experiment in all vasopressin/epinephrine-treated animals. In conclusion, in this porcine model of prolonged CPR, repeated vasopressin/epinephrine administration, but not epinephrine or saline placebo alone, ensured long-term survival with full neurologic recovery., Implications: We present a study to evaluate the effects of a combination of vasopressin and epinephrine during prolonged cardiopulmonary resuscitation on neurological outcome in pigs. We found that all pigs treated with a combination of vasopressin and epinephrine could be resuscitated and had full neurologic recovery observed over an entire period of 5 days.

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.

Background: The authors compared the effects of vasopressin fluid resuscitation on survival in a liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs., Methods: A midline laparotomy was performed on 23 domestic pigs, followed by an incision, and subsequent finger fraction across the right medial liver lobe. During hemorrhagic shock, animals were randomly assigned to receive either 0.4 U/kg vasopressin (n = 9), or fluid resuscitation (n = 7), or saline placebo (n = 7), respectively. A continuous infusion of 0.08 U x kg(-1) x min(-1) vasopressin in the vasopressin group, or normal saline was subsequently administered in the fluid resuscitation and saline placebo group, respectively. After 30 min of experimental therapy, bleeding was controlled by surgical intervention, and blood transfusion and rapid fluid infusion were subsequently performed., Results: Maximum mean arterial blood pressure during experimental therapy in the vasopressin-treated animals was significantly higher than in the fluid resuscitation and saline placebo groups (mean +/- SD, 72 +/- 26 vs 38 +/- 16 vs 11 +/- 7 mmHg, respectively; P< 0.05). Subsequently, mean arterial blood pressure remained at approximately 40 mmHg in all vasopressin-treated animals, whereas mean arterial blood pressure in all fluid resuscitation and saline placebo pigs was close to aortic hydrostatic pressure (approximately 15 mmHg) within approximately 20 min of experimental therapy initiation. Total blood loss was significantly higher in the fluid resuscitation pigs compared with vasopressin or saline placebo after 10 min of experimental therapy (65 +/- 6 vs 42 +/- 4 vs 43 +/- 6 ml/kg, respectively; P< 0.05). Seven of seven fluid resuscitation, and seven of seven saline placebo pigs died within approximately 20 min of experimental therapy, while 8 of 9 vasopressin animals survived more than 7 days (P < 0.05)., Conclusions: Vasopressin, but not fluid resuscitation or saline placebo, ensured survival with full recovery in this liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs.

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.