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Renal dysfunction is associated with increased morbidity and mortality in intensive care patients. In most cases the glomerular filtration rate (GFR) is estimated based on serum creatinine and the Modification of Diet in Renal Disease (MDRD) formula, but cystatin C-estimated GFR is being used increasingly. The aim of this study was to compare creatinine and MDRD and cystatin C-estimated GFR in intensive care patients.Retrospective observational study was performed, on patients treated within the general intensive care unit (ICU) during 2004-2006, in a Swedish university hospital.GFR markers are frequently ordered in the ICU; 92% of the patient test results had cystatin C-estimated GFR (eGFR(cystatinC)) ≤ 80 mL/min/1.73 m(2), 75% had eGFR ≤ 50 mL/min/1.73 m(2), and 30% had eGFR ≤ 20 mL/min/1.73 m(2). In contrast, only 46% of the patients had reduced renal function assessed by plasma creatinine alone, and only 47% had eGFR(MDRD) ≤ 80 mL/min/1.73 m(2). The mean difference between eGFR(MDRD) and eGFR(cystatinC) was 39 mL/min/1.73 m(2) for eGFR(cystatinC) values ≤ 60 mL/min/1.73 m(2).GFR is commonly assessed in the ICU. Cystatin C-estimated GFR yields markedly lower GFR results than plasma creatinine and eGFR(MDRD). Many pharmaceuticals are eliminated by the kidney, and their dosage is adjusted for kidney function. Thus, the differences in GFR estimates by the methods used indicate that the GFR method used in the intensive care unit may influence the treatment.

Background Laparoscopic liver surgery is evolving rapidly. Carbon dioxide embolism is a potential complication. The aim of this work was to study the frequency and severity of gas embolism (GE) during laparoscopic liver lobe resection in a pig model and the resulting cardiovascular and respiratory changes. Methods Fifteen anaesthetized piglets underwent laparoscopic left liver lobe resection. Haemodynamic and respiratory variables were monitored, including systemic and pulmonary arterial pressures, end-tidal CO2, and pulmonary dead space. Online blood gas monitoring and a transoesophageal echocardiography (TOE) were used. GE was graded semi-quantitatively as grade 0 (none), grade 1 (minor), or grade 2 (major), depending on the TOE results. Results In 10 of 15 piglets, GE occurred. In total, 33 separate episodes of GE were recorded. All 13 episodes of grade 2 and three of grade 1 were serious enough to cause mainly respiratory, but also haemodynamic effects. Mostly, grade 1 GE caused only minor respiratory or haemodynamic changes. Most variables were affected during grade 2 GE; the most important were Pa o 2, Pa co 2, end-tidal CO2, Vd/Vt, and mean pulmonary arterial pressure. Conclusions GE occurred frequently during laparoscopic liver resection in this experimental study. Approximately half of the embolisms were serious enough to cause respiratory or haemodynamic disturbances or both. Pending further human studies, a combination of several monitoring techniques, with narrow limits for the alarm settings, will ensure correct interpretation of the complex physiological response to GE and reveal it early enough to alert the anaesthetist and the surgeon to the ongoing problem.

PURPOSE: To estimate absolute brain temperature using proton MR spectroscopy ((1)H-MRS) and mean brain-body temperature difference of healthy human volunteers. MATERIALS AND METHODS: Chemical shift difference between temperature-dependent water spectral line position and temperature-stable metabolite spectral reference was used for the estimations of absolute brain temperature. Temperature calibrations constants were obtained from the spectra of the N-acetyl aspartate (NAA line at approximately 2.0 ppm), glycero-phosphocholine (GPC line at approximately 3.2 ppm), and creatine (Cr line at approximately 3.0 ppm) aqueous solutions with pH values within physiologically pertinent ranges. Single-voxel PRESS sequence (TR/TE 2000/80 ms) was used for this purpose. Brain temperature was determined by averaging the temperatures computed from water-Cho, water-Cr, and water-NAA chemical shift differences. RESULTS: The mean brain temperature of 18 healthy volunteers was 38.1 +/- 0.4 degrees C and mean brain-body (rectal) temperature difference was 1.3 +/- 0.4 degrees C. CONCLUSION: Improved accuracy of the temperature constants and averaging the temperatures computed from water-Cho, water-Cr, and water-NAA chemical shift differences increased the reliability of the brain temperature estimations.

Hypothermia treatment with cold intravenous infusion and ice packs after cardiac arrest has been described and used in clinical practice. We hypothesised that with this method a target temperature of 32-34 degrees C could be achieved and maintained during treatment and that rewarming could be controlled.Thirty-eight patients treated with hypothermia after cardiac arrest were included in this prospective observational study. The patients were cooled with 4 degrees C intravenous saline infusion combined with ice packs applied in the groins, axillae, and along the neck. Hypothermia treatment was maintained for 26 h after cardiac arrest. It was estimated that passive rewarming would occur over a period of 8h. Body temperature was monitored continuously and recorded every 15 min up to 44 h after cardiac arrest.All patients reached the target temperature interval of 32-34 degrees C within 279+/-185 min from cardiac arrest and 216+/-177 min from induction of cooling. In nine patients the temperature dropped to below 32 degrees C during a period of 15 min up to 2.5h, with the lowest (nadir) temperature of 31.3 degrees C in one of the patients. The target temperature was maintained by periodically applying ice packs on the patients. Passive rewarming started 26 h after cardiac arrest and continued for 8+/-3h. Rebound hyperthermia (38 degrees C) occurred in eight patients 44 h after cardiac arrest.Intravenous cold saline infusion combined with ice packs is effective in inducing and maintaining therapeutic hypothermia, with good temperature control even during rewarming.

Aim To study haemodynamic effects and changes in intravascular volume during hypothermia treatment, induced by ice-cold fluids and maintained by ice-packs followed by rewarming in patients after resuscitation from cardiac arrest. Materials and methods In 24 patients following successful restoration of spontaneous circulation (ROSC), hypothermia was induced with infusion of 4 °C normal saline and maintained with ice-packs for 26 h after ROSC. This was followed by passive rewarming. Transthoracic echocardiography was performed at 12, 24 and 48 h after ROSC to evaluate ejection fraction and intravascular volume status. Central venous pressure (CVP), central venous oxygen saturation (ScvO 2 ) and serum lactate were measured. Fluid balance was calculated. Results Twelve hours after ROSC, two separate raters independently estimated that 10 and 13 out of 23 patients had a decreased intravascular volume using transthoracic echocardiography. After 24 and 48 h this number had increased further to 14 and 13 out of 19 patients and 13 and 12 out of 21 patients. Calculated fluid balance was positive (4000 ml the day 1 and 2500 ml day 2). There was no difference in ejection fraction between the recording time points. Serum lactate and ScvO 2 were in the normal range when echocardiography exams were performed. CVP did not alter over time. Conclusions Our results support the hypothesis that inducing hypothermia following cardiac arrest, using cold intravenous fluid infusion does not cause serious haemodynamic side effects. Serial transthoracic echocardiographic estimation of intravascular volume suggests that many patients are hypovolaemic during therapeutic hypothermia and rewarming in spite of a positive fluid balance.

Aim To assess the regional vulnerability to ischemic damage and perfusion/metabolism mismatch of reperfused brain following restoration of spontaneous circulation (ROSC) after cardiac arrest. Method We used positron emission tomography (PET) to map cerebral metabolic rate of oxygen (CMRO 2 ), cerebral blood flow (CBF) and oxygen extraction fraction (OEF) in brain of young pigs at intervals after resuscitation from cardiac arrest. After obtaining baseline PET recordings, ventricular fibrillation of 10min duration was induced, followed by mechanical closed-chest cardiopulmonary resuscitation (CPR) in conjunction with i.v. administration of 0.4U/kg of vasopressin. After CPR, external defibrillatory shocks were applied to achieve restoration of spontaneous circulation (ROSC). CBF and CMRO 2 were mapped and voxelwise maps of OEF were calculated at times of 60, 180, and 300min after ROSC. Results There was hypoperfusion throughout the telencephalon at 60min, with a return towards baseline values at 300min. In contrast, there was progressively increasing CBF in cerebellum throughout the observation period. The magnitude of CMRO 2 decreased globally after ROSC, especially in cerebral cortex. The magnitude of OEF in cerebral cortex was 60% at baseline, tended to increase at 60min after ROSC, and declined to 50% thereafter, thus suggesting transition to an ischemic state. Conclusion The cortical regions tended most vulnerable to the ischemic insult with an oligaemic pattern and a low CMRO 2 whereas the cerebellum instead showed a pattern of luxury perfusion.

Aim This was an experimental study performed to investigate cerebral metabolism during hypothermia treatment and rewarming after resuscitation from cardiac arrest (CA). Materials and methods Sixteen pigs underwent CA followed by cardiopulmonary resuscitation (CPR). After randomisation into one hypothermic ( n =8) and one normothermic group ( n =8) the animals received infusion of 4 or 38°C saline, respectively. Following restoration of spontaneous circulation (ROSC) both groups were observed for 360min. The hypothermic group was cooled for 180min and then rewarmed. Temperature was not modulated in the normothermic group. Cerebral microdialysis was conducted and lactate/pyruvate (L/P)-ratio and glutamate were analysed. Intracranial pressure probe was inserted. Oxygen saturation in venous jugular bulb blood (SjO 2 ) was analysed. Results All animals initially had increased L/P-ratio (>30). A total of nine animals developed secondary increase. In the hypothermic group this was observed in 2/7 animals and in the normothermic group in 7/8 ( p =0.04). Glutamate increased initially in all animals with secondary increases in two animals in each group. No differences in L/P-ratio or glutamate were detected during the rewarming phase compared to the hypothermic phase. The hypothermic group had higher SjO 2 ( p =0.04). In both groups intracranial pressure increased after ROSC. Conclusion After resuscitation from CA there was a risk of cerebral secondary energy failure (reflected as an increased L/P-ratio) but hypothermia treatment seemed to counteract this effect. Cerebral oxygen extraction, measured by SjO 2, was increased in the hypothermic group probably due to reduced metabolism. Rewarming did not reveal any obvious harmful events.

Hypothermia treatment with cooling to a body temperature of 32-34°C has been shown to be an effective way of improving neurological outcome and survival in unconscious patients successfully resuscitated after cardiac arrest (CA). The method is used clinically but there are still many questions on the biological mechanisms and on how the treatment is best performed. This thesis focuses on cerebral and haemodynamic effects of hypothermia and rewarming. A porcine model of CA was used. To shorten time to reach target temperature, induction of hypothermia, by means of infusion of 4°C cold fluid, was started already during ongoing cardiopulmonary resuscitation. The temperature was satisfactorily reduced without obvious haemodynamic disturbances. Cerebral effects of hypothermia and rewarming were studied. Microdialysis monitoring showed signs of cerebral energy failure (increased lactate/pyruvate-ratio) and excitotoxicity (increased glutamate) immediately after CA. There was a risk of secondary energy failure that was reduced by hypothermia. Intracranial pressure (ICP) increased gradually after CA irrespectively of if hypothermia was used or not. There were no indications of increasing cerebral disturbances during rewarming. Haemodynamic effects of hypothermia treatment and rewarming were examined in a study of patients successfully resuscitated after CA. Hypothermia was induced by means of cold intravenous infusion. No negative effects on the cardiovascular system were revealed. There were indications of decreased intravascular volume in spite of a positive fluid balance. Cerebral microdialysis and ICP recording were performed in four patients. All patients had signs of energy failure and excitotoxicity following CA. ICP was only exceptionally above 20 mmHg. In contrast to the experimental study indications of increasing ischemia were seen during rewarming. Glycerol had a biphasic pattern, perhaps due to an overspill of metabolites from the general circulation. As most patients become extensively anti-coagulated following CA, intracranial monitoring is not suitable to be used in routine care.

Background: Special clinical situations where general hypothermia cannot be recommended but can be a useful treatment demand a new approach, selective brain cooling. The purpose of this study was to selectively cool the brain with cold saline circulating in balloon catheters introduced into the nasal cavity in pigs. Material and methods: Twelve anaesthetised pigs were subjected to selective cerebral cooling for a period of 6 h. Cerebral temperature was towered by means of bilaterally introduced nasal balloon catheters perfused with saline cooled by a heat exchanger to 8-10 degrees C. Brain temperature was measured in both cerebral hemispheres. Body temperature was measured in rectum, oesophagus and the right atrium. The pigs were normoventilated and haemodynamic variables were measured continuously. Acid-base and electrolyte status was measured hourly. Results: Cerebral hypothermia was induced rapidly and within the first 20 min of cooling cerebral temperature was lowered from 38.1 +/- 0.6 degrees C by a mean of 2.8 +/- 0.6 to 35.3 +/- 0.6 degrees C. Cooling was maintained for 6 h and the final brain temperature was 34.7 +/- 0.9 degrees C. Concomitantly, the body temperature, as reflected by oesophageal temperature was decreased from 38.3 +/- 0. 5 to 36.6 +/- 0.9 degrees C. No circulatory or metabolic disturbances were noted. Conclusions: Inducing selective brain hypothermia with cold saline via nasal balloon catheters can effectively be accomplished in pigs, with no major disturbances in systemic circulation or physiological variables. The temperature gradients between brain and body can be maintained for at least 6 h. (Less)

Bleeding is a known and CO2 embolization a suggested risk factor for increased morbidity after laparoscopic liver resection. Devices for laparoscopic liver parenchymal transection must be evaluated for safety in this context. Twelve piglets underwent laparoscopic surgery during CO2 pneumoperitoneum, each animal receiving three 6 cm long transections into the liver parenchyma made with ultrasonic dissector, ultrasonic shears and vessel sealing system, respectively. Endpoints were bleeding, operation time and gas embolization. The transections and embolization events, evaluated with transesophageal echocardiography, were video recorded. Bleeding and embolization were also assessed on video tapes and operating time measured. Arterial blood gases were recorded on line. The ultrasonic dissector was least advantageous in terms of bleeding and operation time. Gas embolization was more frequent with the vessel sealing system than with the ultrasonic dissector and ultrasonic shears. During two episodes of gas embolization, pCO2 increased and pO2 and pH decreased. Use of all three devices is feasible. Bleeding and operation time are greatest with the ultrasonic dissector. Gas embolization occurs during transection, though in most instances it is completely harmless. Laparoscopic liver surgery with these techniques used may pose a risk of gas embolization with clinical implications. Monitoring for such events is probably to be recommended.

Automatic mechanical chest compressions during cardiopulmonary resuscitation : What is the evidence for its use?

Objective To perform two predefined sub-group analyses within the LINC study and evaluate if the results were supportive of the previous reported intention to treat (ITT) analysis. Methods Predefined subgroup analyses from the previously published LINC study were performed. The Per-Protocol population (PPP) included the randomized patients included in the ITT-population but excluding those with violated inclusion or exclusion criteria and those that did not get the actual treatment to which the patient was randomized. In the Pre-Defined population (PDP) analyses patients were also excluded if the dispatch time to ambulance arrival at the address exceeded 12min, there was a non-witnessed cardiac arrest, or if it was not possible to determine whether the arrest was witnessed or not, and those cases where LUCAS was not brought to the scene at the first instance. Results After exclusion from the 2589 patients within the ITT-population, the Per-Protocol analysis was performed in 2370 patients and the Pre-Defined analysis within 1133 patients. There was no significant difference in 4-h survival of patients between the mechanical-CPR group and the manual-CPR group in the Per-Protocol population; 279 of 1172 patients (23.8%) versus 281 of 1198 patients (23.5%) (risk difference −0.35%, 95% C.I. −3.1 to 3.8, p =0.85) or in the Pre-Defined population; 176 of 567 patients (31.0%) versus 192 of 566 patients (33.9%) (risk difference −2.88%, 95% C.I. −8.3 to 2.6, p =0.31). There was no difference in any of the second outcome variables analyzed in the Pre-Protocol or Pre-Defined populations. Conclusions The results from these predefined sub-group analyses of the LINC study population did not show any difference in 4h survival or in secondary outcome variables between patients treated with mechanical-CPR or manual-CPR. This is consistent with the previously published ITT analysis.

Introduction Previous studies have suggested an effect of gender on outcome after out-of-hospital cardiac arrest (OHCA), but the results are conflicting. We aimed to investigate the association of gender to outcome, coronary angiography (CAG) and adverse events in OHCA survivors treated with mild induced hypothermia (MIH). Methods We performed a retrospective analysis of prospectively collected data from the International Cardiac Arrest Registry. Adult patients with a non-traumatic OHCA and treated with MIH were included. Good neurological outcome was defined as a cerebral performance category (CPC) of 1 or 2. Results A total of 1,667 patients, 472 women (28%) and 1,195 men (72%), met the inclusion criteria. Men were more likely to receive bystander cardiopulmonary resuscitation, have an initial shockable rhythm and to have a presumed cardiac cause of arrest. At hospital discharge, men had a higher survival rate (52% vs. 38%, P

Therapeutic hypothermia after resuscitation has been shown to improve the outcome regarding neurological state and to reduce mortality. The earlier hypothermia therapy is induced probably the better. We studied the induction of hypothermia with a large volume of intravenous ice-cold fluid after cardiac arrest during ongoing cardiopulmonary resuscitation (CPR).Twenty anaesthetised piglets were subjected to 8 min of ventricular fibrillation, followed by CPR. They were randomized into two groups. The hypothermic group was given an infusion of 4 degrees C acetated Ringer's solution 30 ml/kg at an infusion rate of 1.33 ml/kg/min, starting after 1 min of CPR. The control group received the same infusion at room temperature. All pigs received a bolus dose of vasopressin after 3 min of CPR. After 9 min, defibrillatory shocks were applied to achieve restoration of spontaneous circulation (ROSC). Core temperature and haemodynamic variables were measured at baseline and repeatedly until 180 min after ROSC. Cortical cerebral blood flow was measured, using Laser-Doppler flowmetry.All pigs had ROSC, except one animal in the hypothermic group. Only one animal in the hypothermic group died during the observation period. The calculated mean temperature reduction was 1.6+/-0.35 degrees C (S.D.) in the hypothermic group and 1.1+/-0.37 degrees C in the control group (p=0.009). There was no difference in cortical cerebral blood flow and haemodynamic variables.Inducing hypothermia with a cold infusion seems to be an effective method that can be started even during ongoing CPR. This method might warrant consideration for induction of early therapeutic hypothermia in cardiac arrest victims.

Feeding tubes are used frequently in the intensive care unit to provide enteral nutrition. For critically ill patients, enteral nutrition is preferable to parenteral in terms of cost, complication and gut mucosal maintenance. Fine bore feeding tubes are always preferred because their soft, flexible construction and narrow diameter enables these tubes to be well tolerated by patients and they rarely contribute to sinus infections or obstruction of breathing. On the other hand it is not uncommon that these tubes are misplaced in the tracheobronchial tree or the pleural cavity, especially in high-risk patients, i.e. sedated patients, patients with weak cough reflex, endotracheally intubated patients and agitated patients (1–3). Malpositioning in the peritoneal cavity or the mediastinum through gastric or esophageal perforation is also possible ( 1, 4–7); even intravascular ( 8, 9) and intracranial misplacement have been reported (10–13). The incidence of misplacement of a feeding tube is difficult to estimate because few studies have been performed. The largest study of 1100 such tubes revealed an overall malposition rate of 1.3% ( 1), but it should be mentioned that this study included only radiographically detected misplacements. Other researchers estimate the occurrence of accidental misplacement and migration out of position as high as 13% to 20% in high-risk patients ( 14, 15).

Cardiac arrest results in immediate interruption of blood flow. The primary goal of cardiopulmonary resuscitation (CPR) is to re-establish blood flow and hence oxygen delivery to the vital organs. This thesis describes different pharmacological interventions aimed at increasing cerebral blood flow during CPR and after restoration of spontaneous circulation (ROSC).In a porcine model of cardiac arrest, continuous infusion of adrenaline generated higher cortical cerebral blood flow during CPR as compared to bolus administration of adrenaline. While bolus doses resulted in temporary peaks in cerebral blood flow, continuous infusion led to a sustained increase in this flow.Administration of vasopressin resulted in higher cortical cerebral blood flow and a lower cerebral oxygen extraction ratio as compared to continuous infusion of adrenaline during CPR. In addition, vasopressin generated higher coronary perfusion pressure during CPR and increased the likelihood of achieving ROSC.Parameters of coagulation and inflammation were measured after successful resuscitation from cardiac arrest. Immediately after ROSC, thrombin-antithrombin complex, a marker of thrombin generation, was elevated and eicosanoid levels were increased, indicating activation of coagulation and inflammation after ROSC. The thrombin generation was accompanied by a reduction in antithrombin. In addition, there was substantial haemoconcentration in the initial period after ROSC.By administration of antithrombin during CPR, supraphysiological levels of antithrombin were achieved. However, antithrombin administration did not increase cerebral circulation or reduce reperfusion injury, as measured by cortical cerebral blood flow, cerebral oxygen extraction and levels of eicosanoids, after ROSC. In a clinical study, the adrenaline dose interval was found to be longer than recommended in the majority of cases of cardiac arrest. Thus, the adherence to recommended guidelines regarding the adrenaline dose interval seems to be poor.

To determine whether antithrombin (AT) administration during cardiopulmonary resuscitation (CPR) increased cerebral circulation and reduced reperfusion injury.Ventricular fibrillation was induced in 24 anaesthetised pigs. After a 5-min non-intervention interval, CPR was started. The animals were randomised into two groups. The treatment group received AT (250 U/kg) and the control group received placebo, after 7 min of CPR. Defibrillation was attempted after 9 min of CPR. If restoration of spontaneous circulation (ROSC) was achieved, the animals were observed for 4 h. Cortical cerebral blood flow was measured using laser-Doppler flowmetry. Cerebral oxygen extraction was calculated to reflect the relation between global cerebral circulation and oxygen demand. Measurements of eicosanoids (8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha)), AT, thrombin-antithrombin complex (TAT) and soluble fibrin in jugular bulb plasma were performed to detect any signs of cerebral oxidative injury, inflammation and coagulation.There was no difference between the groups in cortical cerebral blood flow, cerebral oxygen extraction, or levels of eicosanoids, TAT or soluble fibrin in jugular bulb plasma after ROSC. In the control group reduction of AT began 15 min after ROSC and continued throughout the entire observation period (P0.05). Eicosanoids and TAT were increased compared to baseline in all animals (P0.01).In this experimental model of CPR, AT administration did not increase cerebral circulation or reduce reperfusion injury after ROSC.

To determine whether activation of coagulation and inflammation during cardiac arrest results in a reduction of antithrombin (AT) and an increase in thrombin-antithrombin (TAT) complex during reperfusion.Ventricular fibrillation (VF) was induced in ten anaesthetized pigs. After a 5-min non-intervention interval, closed-chest cardiopulmonary resuscitation (CPR) was performed for 9 min before defibrillation was attempted. If restoration of spontaneous circulation (ROSC) was achieved, the animals were observed for 4 h and repeated blood samples were taken for assay of AT, TAT and eicosanoids (8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha)).AT began to decrease 15 min after ROSC and the reduction continued throughout the observation period (P0.05). The lowest mean value (79%) occurred 60 min after ROSC. The TAT level was increased during the first 3 h after ROSC (P0.05), indicating thrombin generation. The eicosanoids were increased throughout the observation period (P0.05).AT is reduced and TAT and eicosanoids are increased after cardiac arrest, indicating activation of coagulation and inflammation.

BACKGROUND: An investigation of the free radical scavenger sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) and the weak vasodilatator Tris buffer mixture (TBM) on cerebral cortical blood flow (CC ...

To explore the effects of alkaline buffers on cerebral perfusion and cerebral acidosis during and after cardiopulmonary resuscitation (CPR), 45 anaesthetized piglets were studied. The animals were subjected to 5 min non-interventional circulatory arrest followed by 7 min closed chest CPR and received either 1 mmol/kg of sodium bicarbonate, 1 mmol/kg of tris buffer mixture, or the same volume of saline (n=15 in all groups), adrenaline (epinephrine) boluses and finally external defibrillatory shocks. Systemic haemodynamic variables, cerebral cortical blood flow, arterial, mixed venous, and internal jugular bulb blood acid-base status and blood gases as well as cerebral tissue pH and PCO(2) were monitored. Cerebral tissue acidosis was recorded much earlier than arterial acidaemia. After restoration of spontaneous circulation, during and after temporary arterial hypotension, pH in internal jugular bulb blood and in cerebral tissue as well as cerebral cortical blood flow was lower after saline than in animals receiving alkaline buffer. Buffer administration during CPR promoted cerebral cortical reperfusion and mitigated subsequent post-resuscitation cerebral acidosis during lower blood pressure and flow in the reperfusion phase. The arterial alkalosis often noticed during CPR after the administration of alkaline buffers was caused by low systemic blood flow, which also results in poor outcome.

BACKGROUND: In experimental cardiopulmonary resuscitation (CPR) aortic balloon occlusion, vasopressin, and hypertonic saline dextran administration improve cerebral blood flow. Free radical scavenger alpha-phenyl-N-tert-butyl-nitrone (PBN) and cyclosporine-A (CsA) alleviate neuronal damage after global ischemia. Combining these treatments, we investigated neurological outcome after experimental cardiac arrest.METHODS: Thirty anesthetized piglets, randomly allocated into three groups, were subjected to 8 min of ventricular fibrillation followed by 5 min of closed-chest CPR. The combined treatment (CT) group received all the above-mentioned modalities; group B was treated with balloon occlusion and epinephrine; and group C had sham balloon occlusion with epinephrine. Indicators of oxidative stress (8-iso-PGF(2 alpha)), inflammation (15-keto-dihydro-PGF(2 alpha)), energy crisis (hypoxanthine and xanthine), and anoxia/hypoxia (lactate) were monitored in jugular bulb venous blood. Neurological outcome was evaluated 24 h after CPR.RESULTS: Restoration of spontaneous circulation (ROSC) was more rapidly achieved and neurological outcome was significantly better in the CT group, although there was no difference in coronary perfusion pressure between groups. The jugular venous PCO2 and cerebral oxygen extraction ratio were lower in the CT group at 5-15 min after ROSC. Jugular venous 8-iso-PGF(2 alpha) and hypoxanthine after ROSC were correlated to 24 h neurological outcomeCONCLUSIONS: A combination of cerebral blood flow promoting measures and administration of alpha-phenyl-N-tert-butyl-nitrone and cyclosporine-A improved 24 h neurological outcome after 8 min of experimental normothermic cardiac arrest, indicating an ongoing neuronal injury in the reperfusion phase.

Prophylactic antibiotics (PRO) reduce the incidence of early-onset pneumonia in comatose patients with structural brain injury, but have not been examined in cardiac arrest survivors undergoing targeted temperature management (TTM). We investigated the effect of PRO on the development of pneumonia in that population.We conducted a retrospective cohort study comparing patients treated with PRO to those not receiving PRO (no-PRO) using Northern Hypothermia Network registry data. Cardiac arrest survivors ≥ 18 years of age with a GCS8 at hospital admission and treated with TTM at 32-34 °C were enrolled in the registry. Differences were analyzed in univariate analyses and with logistic regression models to evaluate independent associations of clinical factors with incidence of pneumonia and good functional outcome.416 of 1240 patients (33.5%) received PRO. Groups were similar in age, gender, arrest location, initial rhythm, and time from collapse to return of spontaneous circulation. PRO patients had less pneumonia (12.6% vs. 54.9%, p0.001) and less sepsis (1.2 vs. 5.7%, p0.001) compared to no-PRO patients. ICU length of stay (98 vs. 100 h, p = 0.2) and incidence of a good functional outcome (41.1 vs. 36.6%, p = 0.19) were similar between groups. Backwards stepwise logistic regression demonstrated PRO were independently associated with a lower incidence of pneumonia (OR 0.09, 95% 0.06-0.14, p0.001) and a similar incidence of good functional outcome.Prophylactic antibiotics were associated with a reduced incidence of pneumonia but a similar rate of good functional outcome.

Objective: In the last few years the genetic influence on health and disease outcome has become more apparent. The ACE genotype appears to play a significant role in the pathophysiology of several disease processes. This pilot study aims at showing the feasibility to examine the genetic influence of the ACE genotype on return of spontaneous circulation (ROSC) in out-of-hospital cardiac arrest (OHCA). Methods: We performed a prospective observational study of all OHCAs of presumed cardiac origin in a well-defined population. We collected prehospital blood samples for the determination of ACE genotype and used this information together with Utstein template parameters in a multivariable analysis to examine the relationship between ROSC and ACE genotype. Results: We collect blood samples in 156 of 361 patients with OHCA of presumed cardiac origin, 127 samples were analysed (mean age 67 years, 86% male, 79% witnessed OHCA, 80% bystander CPR, 62% had a shockable rhythm, ROSC 77%). Distribution of the ACE gene polymorphisms: insertion polymorphism (II) n=22, 17%, insertion/deletion polymorphism (ID) n=66, 52% and deletion polymorphism (DD) n=39, 31%. We found no significant association between ACE II vs ACE DD/DI and ROSC (OR 1.72; CI 0.52 to 5.73; p=0.38). Other ACE genotype groupings (II/ID vs DD or II vs DD) did not change the overall finding of lack of impact of ACE genotype on ROSC. Conclusions: This pilot study did not indicate a significant association between ACE gene polymorphism and ROSC. However, it has demonstrated that prehospital genetic studies including blood sampling are feasible and ethically acceptable. publishedVersion

Aim The reported incidence of injuries due to cardiopulmonary resuscitation using manual chest compressions (manual CPR) varies greatly. Our aim was to elucidate the incidence of CPR-related injuries by manual chest compressions compared to mechanical chest compressions with the LUCAS device (mechanical CPR) in non-survivors after out-of-hospital cardiac arrest. Methods In this prospective multicentre trial, including 222 patients (83 manual CPR/139 mechanical CPR), autopsies were conducted after unsuccessful CPR and the results were evaluated according to a specified protocol. Results Among the patients included, 75.9% in the manual CPR group and 91.4% in the mechanical CPR group (p = 0.002) displayed CPR-related injuries. Sternal fractures were present in 54.2% of the patients in the manual CPR group and in 58.3% in the mechanical CPR group (p = 0.56). Of the patients in the manual CPR group, there were 64.6% with at least one rib fracture versus 78.8% in the mechanical CPR group (p = 0.02). The median number of rib fractures among patients with rib fractures was 7 in the manual CPR group and 6 in the mechanical CPR group. No CPR-related injury was considered to be the cause of death. Conclusion In patients with unsuccessful CPR after out-of-hospital cardiac arrest, rib fractures were more frequent after mechanical CPR but there was no difference in the incidence of sternal fractures. No injury was deemed fatal by the pathologist.

Background Positive pressure mechanical ventilation causes rhythmic changes in thoracic pressure and central blood flow. If entrainment occurs, it could be easier for carbon dioxide to enter through a wounded vein during laparoscopic liver lobe resection (LLR). High-frequency jet ventilation (HFJV) is a ventilating method that does not cause pronounced pressure or blood flow changes. This study aimed to investigate whether HFJV could influence the frequency, severity, or duration of gas embolism (GE) during LLR. Methods Twenty-four anaesthetized piglets underwent lobe resection and were randomly assigned to either normal frequency ventilation (NFV) or HFJV (n=12 per group). During resection, a standardized injury to the left hepatic vein was created to increase the risk of GE. Haemodynamic and respiratory variables were monitored. Online blood gas monitoring and transoesophageal echocardiography were used. GE occurrence and severity were graded as 0 (none), 1 (minor), or 2 (major), depending on the echocardiography results. Results GE duration was shorter in the HFJV group (P=0.008). However, no differences were found between the two groups in the frequency or severity of embolism. Incidence of Grade 2 embolism was less than that found in previous studies and physiological responses to embolism were variable. Conclusion HFJV shortened the mean duration of GE during LLR and was a feasible ventilation method during the procedure. Individual physiological responses to GE were unpredictable.

Background: A combined thoraco-laparoscopic technique for esophageal resection is technically possible, but it requires special attention to ventilation. The positive insufflation pressure normally used in laparoscopy will, when communication between thorax and abdomen is established, create a pneumothorax. Methods: We performed an experimental study of differential lung ventilation with different levels of positive end-expiratory pressure (PEEP) settings during thoracolaparoscopy in anesthetized pigs. Results: Positive pressure insufflation of carbon dioxide (CO 2 ) resulted in elevated pulmonary capillary wedge pressure, hypercarbia, and respiratory acidosis. Hypoxemia, however, developed only at lower settings of PEEP. Heart rate, mean arterial pressure, and cardiac output remained relatively stable. Conclusion: Pneumopleuroperitoneum under positive CO 2 insufflation pressure had adverse effects on blood gases. Hypercarbia, respiratory acidosis, and hypoxemia were early manifestations that occurred even in the presence of hemodynamic stability. The application of PEEP equal to or above CO 2 insufflation pressure improved blood gases; in particular, the hypoxia could be avoided. No beneficial effects of differential lung ventilation were documented.

The apparent inability of epinephrine to improve outcome after cardiopulmonary resuscitation (CPR) could be caused by direct negative effects on the cerebral circulation. Constant aortic occlusion with a balloon catheter could be an alternative way to improve coronary and cerebral perfusion during CPR. The objective of the present study was to compare the effects of standard-dose epinephrine with balloon occlusion of the descending aorta on cortical cerebral blood flow augmentation during CPR. Ventricular fibrillation was induced in 24 anaesthetised piglets. A non-intervention interval of 9 min was followed by open-chest CPR. The animals were randomised to receive repeated intravenous bolus doses of epinephrine 20 microg/kg or balloon occlusion of the descending aorta. Focal cortical cerebral blood flow was measured continuously using laser-Doppler flowmetry. Balloon occlusion of the aorta resulted in a significantly higher mean cortical cerebral blood flow and a lower cerebral oxygen extraction ratio than epinephrine during CPR. After restoration of spontaneous circulation the cerebral perfusion appeared compromised to the same extent in both groups, with lower blood flow compared to baseline, high cerebral oxygen extraction and cerebral tissue acidosis. No difference in cerebral cortical vascular resistance between the two groups could be detected. It is concluded that aortic balloon occlusion was superior to epinephrine in cerebral blood flow augmentation during resuscitation and did not generate adverse effects on cerebral blood flow, oxygenation or tissue pH after restoration of spontaneous circulation. No evidence of cerebral vasoconstriction induced by standard-dose epinephrine was found.

Vasopressin has been investigated as a possible alternative to epinephrine during cardiopulmonary resuscitation (CPR). We tested the hypothesis that vasopressin, in comparison with epinephrine, would improve cerebral blood flow and metabolism during CPR as well as after restoration of spontaneous circulation (ROSC). A total of 22 anaesthetised piglets were subjected to 5 min of ventricular fibrillation followed by 8 min of closed-chest CPR. The piglets were randomly allocated to receive repeated boluses of either 45 microg/kg epinephrine or 0.4 U/kg vasopressin IV. Haemodynamic parameters, cerebral cortical blood flow and cerebral tissue pH and PCO(2) were continuously monitored during CPR and up to 4 h after ROSC. Cerebral oxygen extraction ratio was calculated. Cerebral cortical blood flow increased transiently after each bolus of epinephrine, while only the first bolus of vasopressin resulted in a sustained increase. The peak in cerebral cortical blood flow was reached approximately 30 s later with vasopressin. During the initial 5 min following ROSC, cerebral cortical blood flow was greater in the vasopressin group. In conclusion, there is a difference between epinephrine and vasopressin in the time from injection to maximal clinical response and the duration of their effect, but their overall effects on blood pressures and cerebral perfusion do not differ significantly during CPR. In contrast, vasopressin results in a greater cerebral cortical blood flow during a transient period after ROSC.

Background: Intravenous administration of vasopressin during cardiopulmonary resuscitation (CPR) has been shown to improve myocardial and cerebral blood flow. Aortic balloon occlusion during CPR may also augment myocardial and cerebral blood flow and can be used as a central route for the administration of resuscitative drugs. We hypothesized that, as compared with intravenously administered vasopressin, the administration of this drug above the site of an aortic balloon occlusion would result in a greater increase in cerebral perfusion and oxygenation during CPR and after restoration of spontaneous circulation (ROSC). Methods: Twenty piglets were subjected to 5 min of ventricular fibrillation followed by 8 min of closed-chest CPR and were treated with 0.4 U kg−1 boluses of vasopressin intravenously (the IV-vasopressin group with sham aortic balloon) or above the site for an aortic balloon occlusion (the balloon-vasopressin group). The aortic balloon catheter was inflated in the latter group 1 min after commencement of CPR and was deflated within 1 min after ROSC. Systemic blood pressures, cerebral cortical blood flow, cerebral tissue pH and PCO2 were monitored continuously and the cerebral oxygen extraction ratio was calculated. Results: During CPR, arterial blood pressure and cerebral perfusion pressure were greater in the balloon-vasopressin group, as compared with the IV-vasopressin group. These pressures did not differ between the groups after ROSC. Cerebral cortical blood flow was not significantly greater in the balloon-vasopressin group during CPR, whereas significantly higher cortical blood flow levels were recorded after ROSC. Cerebral tissue pH decreased in the IV-vasopressin group during the post-resuscitation hypoperfusion period. In contrast, decreasing pressures during the hypoperfusion period did not result in increasing tissue acidosis in the balloon-vasopressin group. Conclusions: During CPR, intra-aortic vasopressin combined with aortic balloon occlusion resulted in significantly greater perfusion pressures but not in greater cerebral cortical blood flow. After ROSC, however, a greater increase in cortical blood flow was recorded in the balloon-vasopressin group, even though the aortic balloon was deflated and perfusion pressures did not differ between the groups. This suggests that vasopressin predominantly gives vasoconstrictive effects on cerebral cortical vessels during CPR, but results in cerebral cortical vasodilatation after ROSC.

To study the effects of high-dose epinephrine, compared with standard-dose epinephrine, on the dynamics of superficial cortical cerebral blood flow as well as global cerebral oxygenation during experimental cardiopulmonary resuscitation. We hypothesized that high-dose epinephrine might be unable to improve cerebral blood flow during cardiopulmonary resuscitation as compared with standard-dose epinephrine.Randomized controlled study.University hospital research laboratory.A total of 20 male anesthetized piglets.Ventricular fibrillation was induced. A nonintervention interval of 8 mins was followed by open-chest cardiopulmonary resuscitation. The animals were randomized to receive repeated bolus injections of either 20 microg/kg (standard-dose group, n = 10) or 200 microg/kg (high-dose group, n = 10) of epinephrine.Focal cortical cerebral blood flow was measured continuously by using laser Doppler flowmetry. The duration of blood flow increase was significantly shorter in the high-dose group after the second dose of epinephrine. In the high-dose group there was also a consistent tendency for lower peak levels and shorter duration of flow increase in response to repeated bolus doses of epinephrine. Cerebral oxygen extraction ratio was significantly lower in the high-dose group after administration of epinephrine.Repeated bolus doses of epinephrine 200 microg/kg, as compared with 20 microg/kg, do not improve superficial cortical cerebral blood flow during experimental open-chest cardiopulmonary resuscitation. High-dose epinephrine appears to induce vasoconstriction of cortical cerebral blood vessels resulting in redistribution of blood flow from superficial cortex. This might be one explanation for the failure of high-dose epinephrine to improve overall outcome in clinical trials.

Balloon occlusion of the descending aorta during cardiopulmonary resuscitation (CPR) improves coronary and cerebral blood flow. In comparison with an equivalent dose administered through a central venous catheter it has been suggested that epinephrine administration above the aortic occlusion might produce a more rapid increase in coronary perfusion pressure and a shorter time to restoration of spontaneous circulation (ROSC). In a recent study, however, outcome was not improved after intra-aortic epinephrine administration. We hypothesised that epinephrine administered above the aortic occlusion could impose adverse effects on cerebral blood flow and oxygenation, possibly because of an alpha-adrenergic mediated vasoconstriction in the cerebral vascular beds. Twenty-six piglets underwent 5 min of non intervention cardiac arrest followed by 8 min of closed-chest CPR. They were randomised to receive bolus doses of 45 microg/kg epinephrine either above the aortic occlusion or through a central venous catheter. Cerebral cortical blood flow was continuously measured using laser-Doppler technique. Cerebral tissue pH and PCO(2) were also measured using a multi-parameter fiberoptic device and cerebral oxygen extraction was calculated. Balloon inflation resulted in an immediate enhancement of cerebral cortical blood flow. Each of the epinephrine boluses through the central venous catheter resulted in a transient increase in cerebral cortical blood flow. When administered above the aortic balloon occlusion, epinephrine did not result in a further increase in cerebral cortical blood flow, though a significant increase in cerebral perfusion pressure was recorded throughout the CPR period. Cerebral tissue pH monitoring revealed severe acidosis during CPR and long after ROSC, which was refractory to buffering. No differences in the cerebral oxygen extraction ratio were observed between the groups. In conclusion, epinephrine administration above an aortic balloon occlusion was unable to improve cerebral blood flow and oxygenation. In fact, it may even attenuate the beneficial effects of aortic balloon occlusion on cerebral blood flow due to an alpha-adrenergic mediated cerebral vasoconstriction. Further studies, including dose-response and volumes of distribution, are needed to identify the effective beneficial dosage of epinephrine during aortic occlusion with the least possible adverse effects.

Intra-aortic balloon occlusion during experimental cardiopulmonary resuscitation (CPR) improves coronary perfusion pressure and resuscitability and provides unique access to the central circulation. It has been hypothesized that administration of epinephrine into the aortic arch in combination with aortic occlusion would further improve haemodynamics during CPR, resuscitability and 24 h survival. In 16 anaesthetised dogs intravascular catheters were placed for hemodynamic and blood gas monitoring. An aortic balloon catheter was placed by femoral artery insertion with its tip just distal to the left subclavian artery. Ventricular fibrillation for 7.5 min without CPR, 2.5 min of Basic Life Support with chest compressions and ventilation with 100% oxygen were followed by 30 min of Advanced Cardiac Life Support (ACLS) with systemic canine drug dosages. The intra-aortic balloon was inflated when ACLS started and gradually deflated shortly after restoration of spontaneous circulation (ROSC). Epinephrine, in 100 microg/kg boluses every 5 min until the heart was restarted or 30 min had elapsed was administered through the intra-aortic catheter in the experimental group (n = 8) and via a central venous catheter in the control group (n = 8). Coronary perfusion pressure increased during the ACLS period in both groups (P < 0.05) with no difference between the groups and there was no difference in the frequency of ROSC (experimental group 5/8, control group 4/8). Furthermore with respect to 24 h survival, there was no difference between the experimental group (2/8) and the control group (3/8). Severe macroscopic haemorrhagic necrosis of the myocardium in the dogs with ROSC was found in 4/5 in the experimental group compared to 1/4 in the control group. In conclusion, intra-aortic administration of 100 microg/kg epinephrine doses combined with aortic occlusion during experimental CPR did not alter outcome.

Importance A strategy using mechanical chest compressions might improve the poor outcome in out-of-hospital cardiac arrest, but such a strategy has not been tested in large clinical trials. Objective To determine whether administering mechanical chest compressions with defibrillation during ongoing compressions (mechanical CPR), compared with manual cardiopulmonary resuscitation (manual CPR), according to guidelines, would improve 4-hour survival. Design, setting, and participants Multicenter randomized clinical trial of 2589 patients with out-of-hospital cardiac arrest conducted between January 2008 and February 2013 in 4 Swedish, 1 British, and 1 Dutch ambulance services and their referring hospitals. Duration of follow-up was 6 months. Interventions Patients were randomized to receive either mechanical chest compressions (LUCAS Chest Compression System, Physio-Control/Jolife AB) combined with defibrillation during ongoing compressions (n = 1300) or to manual CPR according to guidelines (n = 1289). Main outcomes and measures Four-hour survival, with secondary end points of survival up to 6 months with good neurological outcome using the Cerebral Performance Category (CPC) score. A CPC score of 1 or 2 was classified as a good outcome. Results Four-hour survival was achieved in 307 patients (23.6%) with mechanical CPR and 305 (23.7%) with manual CPR (risk difference, -0.05%; 95% CI, -3.3% to 3.2%; P > .99). Survival with a CPC score of 1 or 2 occurred in 98 (7.5%) vs 82 (6.4%) (risk difference, 1.18%; 95% CI, -0.78% to 3.1%) at intensive care unit discharge, in 108 (8.3%) vs 100 (7.8%) (risk difference, 0.55%; 95% CI, -1.5% to 2.6%) at hospital discharge, in 105 (8.1%) vs 94 (7.3%) (risk difference, 0.78%; 95% CI, -1.3% to 2.8%) at 1 month, and in 110 (8.5%) vs 98 (7.6%) (risk difference, 0.86%; 95% CI, -1.2% to 3.0%) at 6 months with mechanical CPR and manual CPR, respectively. Among patients surviving at 6 months, 99% in the mechanical CPR group and 94% in the manual CPR group had CPC scores of 1 or 2. Conclusions and relevance Among adults with out-of-hospital cardiac arrest, there was no significant difference in 4-hour survival between patients treated with the mechanical CPR algorithm or those treated with guideline-adherent manual CPR. The vast majority of survivors in both groups had good neurological outcomes by 6 months. In clinical practice, mechanical CPR using the presented algorithm did not result in improved effectiveness compared with manual CPR. Trial registration clinicaltrials.gov Identifier: NCT00609778.

To investigate whether there were any changes in and correlations between anxiety, depression and health-related quality of life (HRQoL) over time, between hospital discharge and one and six months after cardiac arrest (CA), in patients treated with therapeutic hypothermia (TH).During a 4-year period at three hospitals in Sweden, 26 patients were prospectively included after CA treated with TH. All patients completed the questionnaires Hospital Anxiety and Depression Scale (HADS), Euroqol (EQ5D), Euroqol visual analogue scale (EQ-VAS) and Short Form 12 (SF12) at three occasions, at hospital discharge, and at one and 6 months after CA.There was improvement over time in HRQoL, the EQ5D index (p=0.002) and the SF12 physical component score (PCS) (p=0.005). Changes over time in anxiety and depression were not found. Seventy-three percent of patients had an EQ-VAS score below 70 (scale 0-100) on overall health status at discharge from hospital; at 6 months the corresponding figure was 41%. Physical problems were the most common complaint affecting HRQoL. A correlation was found between depression and HRQoL, and this was strongest at six months (rs=-0.44 to -0.71, p≤0.001).HRQoL improves over the first 6 months after a CA. Patients reported lower levels of HRQoL on the physical as compared to mental component. The results indicate that the less anxiety and depression patients perceive, the better HRQoL they have and that time can be an important factor in recovery after CA.

To describe differences over time in outcome, physical and cognitive function among survivors of cardiac arrest treated with hypothermia and to examine survivors' life satisfaction 6 months after cardiac arrest as well as gender differences.The study was prospective and included 45 cardiac arrest survivors admitted to three Swedish hospitals between 2008 and 2012. Participants were followed from intensive care unit discharge to one and six months after cardiac arrest. In addition to cerebral performance category (CPC), participants were asked to complete questionnaires regarding activities in daily life (Barthel index), cognitive function (mini mental state examination), and life satisfaction (LiSat-11).Outcome measured using CPC scores improved over time. At 6 months, all participants were classified as having a good outcome. At one month, participants were impaired but improved over time in their activities in daily life and cognitive function. At 6 months satisfaction with "life as a whole" was seen in 70%.Cardiac arrest survivors are satisfied with life as a whole despite a severe illness that has impaired their physical and cognitive function, which seemed to improve over time. Predicting patients' functional outcome in early stages is difficult, and the CPC score alone is not sufficient to assess patients' function. It is a need to reach a consensus to which instruments best reflect physical and cognitive function as well as to specify a rehabilitation plan.

To evaluate the blood flow and perfusion pressure differences observed during open- vs. closed-chest cardiopulmonary resuscitation (CPR), including the effects of epinephrine and sodium bicarbonate administration.Prospective, randomized, controlled trial.Experimental animal laboratory in a university hospital.A total of 35 anesthetized piglets.After tracheostomy and insertion of arterial, right atrial, and pulmonary arterial catheters, thoracotomy was performed with placement of a pulmonary arterial flow probe and left atrial catheter. Ventricular fibrillation was induced and followed by 15 mins of either open-chest (n = 14) or closed-chest (n = 21) CPR. A 4-min infusion of 50 mmol of sodium bicarbonate or saline was added at the start of CPR. After 8 mins of CPR, 0.5 mg of epinephrine was given intravenously, and after 15 mins, direct current (DC) shocks were used to revert the heart to sinus rhythm.Blood flow was studied using transit-time ultrasound flowmetry. In an extended group, intrathoracic pressure was measured for calculation of transmural pressure. Before epinephrine administration, mean pulmonary arterial flow (cardiac output) was reduced: a) during closed-chest CPR relatively more than pulmonary perfusion pressure but in proportion to systemic perfusion pressure; b) during open-chest CPR relatively less than pulmonary perfusion pressure but still in proportion to systemic perfusion pressure. Epinephrine administration temporarily increased systemic perfusion pressure during both closed- and open-chest CPR but temporarily decreased pulmonary perfusion pressure only during closed-chest CPR. After epinephrine administration, cardiac output temporarily decreased during both closed-and open-chest CPR.Open-chest CPR resulted in better cardiac output and systemic perfusion pressure than closed-chest CPR. However, cardiac output values obtained with both methods were much lower than previously reported. After epinephrine administration, cardiac output became extremely low with both methods.

Background The combination of cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC) is a curative treatment option for peritoneal carcinomatosis (PC). There have been few studies on the pulmonary adverse events (AEs) affecting patient recovery after this treatment, thus this study investigated these factors. Methods Between January 2005 and December 2006, clinical data on all pulmonary AEs and the recovery progress were reviewed for 76 patients with after CRS and HIPEC. Patients with pulmonary interventions (thoracocenthesis and chest tubes) were compared with the non-intervention patients. Two senior radiologists, blinded to the post-operative clinical course, separately graded the occurrence of pulmonary AEs. Results Of the 76 patients, 6 had needed thoracocentesis and another 6 needed chest tubes. There were no differences in post-operative recovery between the intervention and non-intervention groups. The total number of days on mechanical ventilation, the length of stay in the intensive care unit, total length of hospital stay, tumor burden, and an American Society of Anesthesiologists (ASA) grade of greater than 2 were correlated with the occurrence of atelectasis and pleural effusion. Extensive atelectasis (grade 3 or higher) was seen in six patients, major pleural effusion (grade 3) in seven patients, and signs of heart failure (grade 1–2) in nine patients. Conclusions Clinical and radiological post-operative pulmonary AEs are common after CRS and HIPEC. However, most of the pulmonary AEs did not affect post-operative recovery.

Only approximately 10% of patients encountering a cardiac arrest (CA) and subsequent cardiopulmonary resuscitation survive to a meaningful life. One of the most important causes for this low survival rate is the ischemia-reperfusion injury that hits the brain. This review summarizes some of the more important mechanisms causing cerebral injury. Thus, we describe some of our findings when performing genome-wide transcriptional profiling as well as histological and immunohistological staining of cerebral cortical areas. In order to shed some light on therapeutic opportunities, our findings relating to the use of induced mild hypothermia and methylene blue as neuroprotective agents are reviewed. Furthermore, we would like to share some interesting data on gender differences and effects of estrogen on the ensuing cerebral injury occurring after hypovolemic CA.

To conduct a pilot study to evaluate the prognostic potential of serum tau protein measurements to predict neurological outcome 6 months following resuscitation from cardiac arrest.In this retrospective observational study, we employed a new ultra sensitive digital immunoassay technology to examine serial serum samples from 25 cardiac arrest patients to examine tau release into serum as a result of brain hypoxia, and probe for its significance predicting six-month neurological outcome. Serial blood samples were obtained from resuscitated cardiac arrest survivors during their first five days in an intensive care unit, and serum total tau was measured. Cerebral function assessments were made using Cerebral Performance Categorization (CPC) at discharge from the ICU and six months later. Tau data were analyzed in the context of 6-month CPC scores.Tau elevations ranged from modest (10 pg/mL) to very high (hundreds of pg/mL), and exhibited unexpected bi-modal kinetics in some patients. Early tau elevations appeared within 24h of cardiac arrest, and delayed elevations appeared after 24-48 h. In patients with delayed elevations, areas under the curves of tau concentration vs. hours since cardiac arrest were highly predictive of 6-month outcome (P0.0005).High-sensitivity serum tau measurements combined with an understanding of tau release kinetics could have utility for hypoxic brain injury assessment and prediction of cerebral function outcome.

Objectives: We aimed to examine organizational, structural and routine infection control measures provided by European ICUs and staff practices in ventilator-associated pneumonia prevention in relation with current recommendations. Methods: European ICU staffs were invited to complete a web-based 20 closed-item questionnaire. Results: 675 nurses and 886 physicians from 13 countries answered the questionnaire. Median number of respondents per country was 118.0 (64.5-155.5). Availability and organizational aspects of infection control revealed wide variations between countries. Among them, single-patient rooms was the aspect with the lowest availability (median availability 38%), but the largest variation ranging from 15 to 84%. Self-reported median adherence rate to recommendations was 72% (34.5-83.0) with a strong correlation between nurses and physicians responses (r(2) = 0.96; p

Only approximately 10% of patients encountering a cardiac arrest (CA) and subsequent cardiopulmonary resuscitation survive to a meaningful life. One of the most important causes for this low survival rate is the ischemia-reperfusion injury that hits the brain. This review summarizes some of the more important mechanisms causing cerebral injury. Thus, we describe some of our findings when performing genome-wide transcriptional profiling as well as histological and immunohistological staining of cerebral cortical areas. In order to shed some light on therapeutic opportunities, our findings relating to the use of induced mild hypothermia and methylene blue as neuroprotective agents are reviewed. Furthermore, we would like to share some interesting data on gender differences and effects of estrogen on the ensuing cerebral injury occurring after hypovolemic CA.

Carbon dioxide (CO(2)) embolism is a potential complication in laparoscopic liver surgery. Gas embolism (GE) is thought to occur when central venous pressure (CVP) is lower than the intra-abdominal pressure (IAP). This study aimed to investigate whether an increased CVP due to induction of PEEP could influence the frequency and severity of GE during laparoscopic liver resection.Twenty anaesthetized piglets underwent laparoscopic left liver lobe resection and were randomly assigned to either 5 or 15 cm H(2)O PEEP (n=10 per group). During resection, a standardized injury to the left hepatic vein [venous cut (VC)] was created to increase the risk of GE. Haemodynamic and respiratory variables were monitored, and online arterial blood gas monitoring and transoesophageal echocardiography (TOE) were used. The occurrence and severity of embolism was graded as 0 (none), 1 (minor), or 2 (major), depending on the TOE results.No differences were found between the two groups regarding the frequency or severity of GE, during either the VC (P=0.65) or the rest of the surgery (P=0.24). GE occurred irrespective of the CVP-IAP gradient.Mechanisms other than the CVP-IAP gradient seemed during laparoscopic liver surgery to contribute to the formation of CO(2) embolism. This is of clinical importance to the anaesthetists.

Various techniques are used to transect the liver. With increase in laparoscopic liver resections (LLR), it is of even more interest to develop surgical techniques to minimize bleeding and the risk for gas embolism during transection. Instrument like argon enhanced coagulator provides good hemostasis but increases the danger of gas embolism. The CO2 pneumoperitoneum that is routinely used in most types of laparoscopic surgery can be modified by the use of different gas pressure. It can be assumed that different pressure influences bleeding but also the risk for gas embolism.In presented porcine studies, three instrumental combinations have been studied. In study I sixteen piglets were randomized to LLR with either the cavitron ultrasonic aspirator (CUSA™) in combination with vessels sealing system (Ligasure™) or with CUSA™ and ultrascision scissors (Autosonix™), with the endpoints of intra-operative bleeding and gas embolism. In study IV sixteen piglets were randomized to LLR either with staple device (Endo-GIA™) or the Ligasure™ - CUSA™ combination with same primary endpoints and additionally secondary endpoints of effect on gas-exchange, systemic- and pulmonary hemodynamic.Focusing on intra-abdominal pressure (IAP) in study II, sixteen piglets were randomized to LLR with an IAP of either 8 or 16 mmHg. Primary endpoints were bleeding and gas embolism and secondary endpoints, effect on gas-exchange, systemic- and pulmonary hemodynamic.In study III effect of argon gas was tested during LLR. Sixteen piglets were randomized to either argon pneumoperitoneum or CO2 pneumoperitoneum. Primary endpoints were effect on gas-exchange, systemic- and pulmonary hemodynamic.In presented studies, we tested efficacy and safety of different techniques for LLR. CUSA™ can be used in combination with either Ligasure™ or Autosonix™. However, Ligasure™ reduces the amount of bleeding. The recent introduction of staplers seems promising with a further reduction in bleeding, gas embolism, and operating time. The IAP influences both the amount of bleeding as well as gas embolism. It seems reasonable to use a higher IAP to decrease bleeding with caution and with close monitoring for gas embolism. Argon gas embolism gives more extensive effect on gas-exchange and hemodynamic and should probably be avoided in this type of surgery.

Intranasal cooling can be used to initiate therapeutic hypothermia. However, direct measurement of brain temperature is difficult and the intra-cerebral distribution of temperature changes with cooling is unknown. The purpose of this study was to measure the brain temperature of human volunteers subjected to intranasal cooling using non-invasive magnetic resonance (MR) methods. Intranasal balloons catheters circulated with saline at 20A degrees C were applied for 60 min in ten awake volunteers. No sedation was used. Brain temperature changes were measured and mapped using MR spectroscopic imaging (MRSI) and phase-mapping techniques. Heart rate and blood pressure were monitored throughout the experiment. Rectal temperature was measured before and after the cooling. Mini Mental State Examination (MMSE) test and nasal inspection were done before and after the cooling. Questionnaires about the subjects' personal experience were completed after the experiment. Brain temperature decrease measured by MRSI was -1.7 +/- A 0.8A degrees C and by phase-mapping -1.8 +/- A 0.9A degrees C (n = 9) at the end of cooling. Spatial distribution of temperature changes was relatively uniform. Rectal temperature decreased by -0.5 +/- A 0.3A degrees C (n = 5). The physiological parameters were stable and no shivering was reported. The volunteers remained alert during cooling and no cognitive dysfunctions were apparent in the MMSE test. Postcooling nasal examination detected increased nasal secretion in nine of the ten volunteers. Volunteers' acceptance of the method was good. Both MR techniques revealed brain temperature reductions after 60 min of intranasal cooling with balloons circulated with saline at 20A degrees C in awake, unsedated volunteers.

To investigate the association between adverse events recorded during critical care and mortality in out-of-hospital cardiac arrest patients treated with therapeutic hypothermia.Prospective, observational, registry-based study.Twenty-two hospitals in Europe and the United States.Between October 2004 and October 2008, 765 patients were included.None.Arrhythmias (7%-14%), pneumonia (48%), metabolic and electrolyte disorders (5%-37%), and seizures (24%) were common adverse events in the critical care period in cardiac arrest patients treated with therapeutic hypothermia, whereas sepsis (4%) and bleeding (6%) were less frequent. Sustained hyperglycemia (blood glucose8 mmol/L for4 hrs; odds ratio 2.3, 95% confidence interval 1.6-3.6, p.001) and seizures treated with anticonvulsants (odds ratio 4.8, 95% confidence interval 2.9-8.1, p.001) were associated with increased mortality in a multivariate model. An increased frequency of bleeding and sepsis occurred after invasive procedures (coronary angiography, intravascular devices for cooling, intra-aortic balloon pump), but bleeding and sepsis were not associated with increased mortality (odds ratio 1.0, 95% confidence interval 0.46-2.2, p = .91, and odds ratio 0.30, 95% confidence interval 0.12-0.79, p = .01, respectively).Adverse events were common after out-of-hospital cardiac arrest. Sustained hyperglycemia and seizures treated with anticonvulsants were associated with increased mortality. Bleeding and infection were more common after invasive procedures, but these adverse events were not associated with increased mortality in our study.