Automated emergency ventilation devices in a simulated unprotected airway.

BACKGROUND: Automated ventilation devices are becoming more popular for emergency ventilation, but there is still not much experience concerning the optimal ventilation mode. METHODS: In a bench model representing a non-intubated patient in respiratory and cardiac arrest, we compared a pressure-cycled with a time- and volume-cycled automated ventilation device in their completely automated modes. The main study endpoints were inspiratory time, respiratory rate, stomach inflation, and lung tidal volumes. RESULTS: The pressure-cycled device inspired for 6.7 s in the respiratory arrest setting (respiratory rate 5.6/min), and never reached its closing pressure in the cardiac arrest setting (respiratory rate 1 breath/min). The time- and volume-cycled device inspired in both settings for 1.7 s (respiratory rate 13 breaths/min). In the respiratory arrest setting, mask leakage was 620 ± 20 mL for the pressure-cycled device vs. 290 ± 10 mL for the time- and volume-cycled device (p < 0.0001); lung tidal volume was 1080 ± 50 mL vs. 490 ± 20 mL, respectively (p < 0.0001); and there was no stomach inflation for either device. In the cardiac arrest setting, pressure-cycled device mask leakage was 5460 ± 60 mL vs. 240 ± 20 mL (p < 0.0001) for the time- and volume-cycled device (p < 0.0001); stomach inflation was 13,100 ± 100 mL vs. 90 ± 10 mL, respectively (p < 0.0001); and lung tidal volume 740 ± 60 mL vs. 420 ± 20 mL, respectively (p < 0.0001). CONCLUSION: In a simulated respiratory arrest setting, ventilation with an automated pressure-cycled ventilation device resulted in lower respiratory frequency and larger tidal volumes compared to a time- and volume-cycled device. In a simulated cardiac arrest setting, ventilation with an automated pressure-cycled ventilation device, but not a time- and volume-cycled device, resulted in continuous gastric insufflation.

Effects of stomach inflation on haemodynamic and pulmonary function during cardiopulmonary resuscitation in pigs.

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

Effects of stomach inflation on haemodynamic and pulmonary function during spontaneous circulation in pigs.

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

Comparison of mechanical characteristics of the human and porcine chest during cardiopulmonary resuscitation.

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

The effects of multiple infusion line extensions on occlusion alarm function of an infusion pump.

BACKGROUND: For anesthesia or conscious sedation of patients undergoing diagnostic or therapeutic procedures in computed tomography or magnetic resonance imaging scans, an extension of infusion lines for continuous drug delivery of anesthetics or vasopressors is often necessary. In this study, we tried to determine if the length of the infusion line influenced the time until an alarm sounded after occlusion at the end of the infusion line. METHODS: We connected 2 infusion pump systems of the same model with 1, 2 or 3 infusion lines in series or with a spiral nonkinking low compliance infusion line, and started the infusion for 60 s. The end of the infusion line was then occluded by turning a stopcock to occlude the fluid flow. A pressure sensor was connected to the infusion line to record the actual pressure change in the line. The time until the pressure occlusion alarm sounded was measured 5 consecutive times at flow rates of 5, 20, and 50 mL/h. RESULTS: When using a single infusion line, pressure occlusion alarms were triggered after 2.4 +/- 0.1 min for infusion pump 1 and 2.6 +/- 0.2 min for infusion pump 2 at 50 mL/h, after 6.6 +/- 0.4 min and 5.6 +/- 0.5 min at 20 mL/h, and after 23.0 +/- 2.8 min and 20.9 +/- 3.6 min at 5 mL/h, respectively. When adding a second infusion line, a pressure occlusion alarm was triggered after 27.1 +/- 1.8 min for infusion pump 1 (P = 0.1) and after 29.2 +/- 1.4 min for infusion pump 2 (P = 0.07) at 5 mL/h. With 3 infusion lines, the pressure occlusion alarm of infusion pumps 1 and 2 were significantly prolonged when compared with 1 infusion line and were released at 31.6 +/- 3.0 min (P = 0.01) and 35.1 +/- 1.1 min (P = 0.001) at 5 mL/h, respectively. The pressure level triggering an alarm ranged in both infusion pumps between about 900 and 1100 Mbar. CONCLUSIONS: When simulating low flow rate infusions (5 mL/h) as for vasopressor support, occlusion alarm time was critically prolonged, especially with an increased length of infusion lines.

A prediction model for out-of-hospital cardiopulmonary resuscitation.

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.

Preventing cardiac arrest during hemorrhagic shock with vasopressin.

The optimal strategy of stabilizing hemodynamic function in uncontrolled traumatic hemorrhagic shock states is unclear. Although fluid replacement is established in controlled hemorrhagic shock, its use in uncontrolled hemorrhagic shock is controversial, because it may worsen bleeding. In the refractory phase of severe hemorrhagic shock, arginine vasopressin has been shown to be beneficial in selected cases due to an increase in arterial blood pressure, shift of blood away from a subdiaphragmatic bleeding site toward the heart and brain, and decrease in fluid-resuscitation requirements. Especially in patients with severe traumatic brain injury, rapid stabilization of cardiocirculatory function is essential to ensure adequate brain perfusion, thus, to prevent neurologic damage and to improve outcome. In addition, despite wide distribution of highly developed and professional emergency medical systems in western industrialized countries, survival chances of patients with uncontrolled traumatic hemorrhagic shock in the preclinical setting are still poor.

Influence of ventilation strategies on survival in severe controlled hemorrhagic shock.

OBJECTIVE: To investigate the effect of different ventilation settings on hemodynamic stability in severe controlled hemorrhagic shock. DESIGN: Prospective, randomized, controlled animal study. SETTING: Research laboratory in a university hospital. SUBJECTS: Approximately 35-45 kg domestic pigs. INTERVENTIONS: Twenty-four domestic pigs were bled 45 mL/kg (estimated 65% of their calculated blood volume) and then ventilated with either 0 cm H2O positive end-expiratory pressure and a respiratory rate of 14 ventilations/min (positive end-expiratory pressure 0 respiratory rate 14), or with 5 cm H2O positive end-expiratory pressure, a respiratory rate of 28 ventilations/min, and a tidal volume reduced by half (positive end-expiratory pressure 5 respiratory rate 28), or with 5 cm H2O positive end-expiratory pressure and a respiratory rate of 14 ventilations/min (positive end-expiratory pressure 5 respiratory rate 14). After 1 hr study phase surviving animals, received fluid resuscitation and were monitored for further 1 hr. MEASUREMENTS AND MAIN RESULTS: Pulmonary variables, hemodynamic variables, and short-term survival. There were no significant differences in mean arterial blood pressure and cardiac index after hemorrhage. After 20 mins of different ventilation strategies mean arterial blood pressure was 40 +/- 3 mm Hg in the positive end-expiratory pressure 0 respiratory rate 14 group, vs. 24 +/- 6 mm Hg the positive end-expiratory pressure 5 respiratory rate 28 group (p < 0.05) vs. 19 +/- 3 mm Hg in the positive end-expiratory pressure 5 respiratory rate 14 group (p < 0.01). Cardiac index was 65 +/- 5 mL/min/kg in the positive end-expiratory pressure 0 respiratory rate 14 group vs. 37 +/- 5 mL/min/kg in the positive end-expiratory pressure 5 respiratory rate 28 group(p < 0.01) and 20 +/- 3 mL/min/kg in the positive end-expiratory pressure 5 respiratory rate 14 group (p < 0.01). Mean airway pressure and positive end-expiratory pressure correlated strongly with mean arterial blood pressure and cardiac index. None of the positive end-expiratory pressure 0 respiratory rate 14 animals died in the study phase, whereas six of seven positive end-expiratory pressure 5 respiratory rate 28 animals, and all seven positive end-expiratory pressure 5 respiratory rate 14 animals died. CONCLUSIONS: In this porcine model of severe hemorrhagic shock, reduction of positive end-expiratory pressure was the most important ventilation strategy component influencing hemodynamic stability. Reducing mean airway pressure by decreasing tidal volumes and increasing respiratory rates seemed to have less influence on cardiopulmonary function and survival than 0 cm H2O positive end-expiratory pressure.

Developing alternative strategies for the treatment of traumatic haemorrhagic shock.

PURPOSE OF REVIEW: The optimal strategy of stabilizing haemodynamic function in uncontrolled traumatic haemorrhagic shock states is unclear. Although fluid replacement is established in controlled haemorrhagic shock, its use in uncontrolled haemorrhagic shock is controversial, because it may worsen bleeding. RECENT FINDINGS: In the refractory phase of severe haemorrhagic shock, arginine vasopressin has been shown to be beneficial in selected cases due to an increase in arterial blood pressure, shift of blood away from a subdiaphragmatic bleeding site towards the heart and brain, and decrease in fluid resuscitation requirements. Especially in patients with severe traumatic brain injury, rapid stabilization of cardiocirculatory function is essential to ensure adequate brain perfusion and thus to prevent neurological damage and to improve outcome. In addition, despite wide distribution of highly developed and professional emergency medical systems in western industrialized countries, survival chances of patients with uncontrolled traumatic haemorrhagic shock in the prehospital setting are still poor. SUMMARY: A multicenter, randomized, controlled, international clinical trial is being initiated to assess the effects of arginine vasopressin (10 IU) vs. saline placebo in prehospital traumatic haemorrhagic shock patients, not responding to standard shock treatment, being managed by helicopter emergency medical services [vasopressin in traumatic haemorrhagic shock (VITRIS.at) study].

Improving countershock success prediction during cardiopulmonary resuscitation using ventricular fibrillation features from higher ECG frequency bands.

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

Effects of a suction laryngoscope in a model with simulated severe airway hemorrhage.

In severe airway hemorrhage, simultaneous suction and laryngoscopy may render intubation difficult. We built a suction laryngoscope that consists of an adjustable stainless steel-guide tube fixed at the lingual surface of a standard Macintosh laryngoscope blade. Via this steel-guide tube, a large suction catheter can be inserted and positioned exactly to suction pharyngeal blood or vomitus, rendering simultaneous suctioning and laryngoscopy possible. In contrast to previous suction laryngoscopes, our suction catheter has a large lumen, which enables fast suctioning and exact placement by adjusting the steel-guide tube. To assess whether our suction laryngoscope could provide better intubation conditions in comparison to a standard Macintosh laryngoscope in a bleeding airway scenario, 44 medical students intubated a manikin with severe simulated airway hemorrhage using our suction laryngoscope and a standard Macintosh laryngoscope in random order. There was no significant difference in time needed for intubation when using the suction versus the Macintosh laryngoscope (mean +/- SD: 43 +/- 13 vs 52 +/- 31 s; P = 0.07), but the number of esophageal intubations was significantly lower when using the suction laryngoscope [6 of 44 (13.6%) vs 19 of 44 (43.2%); P = 0.004]. In conclusion, when compared with a standard Macintosh laryngoscope, using a suction laryngoscope did not result in more rapid intubation, but significantly decreased the likelihood of esophageal intubations.

A comparison of the combination of epinephrine and vasopressin with lipid emulsion in a porcine model of asphyxial cardiac arrest after intravenous injection of bupivacaine.

BACKGROUND: In a porcine model, we compared the effect of the combination of vasopressin/epinephrine with that of a lipid emulsion on survival after bupivacaine-induced cardiac arrest. METHODS: After administration of 5 mg/kg of a 0.5% bupivacaine solution i.v., ventilation was interrupted for 2 +/- 0.5 (mean +/- SD) min until asystole occurred. Cardiopulmonary resuscitation (CPR) was initiated after 1 min of untreated cardiac arrest. After 2 min of CPR, 10 animals received, every 5 min, either vasopressin combined with epinephrine or 4 mL/kg of a 20% lipid emulsion. Three minutes after each drug administration, up to three countershocks (4, 4, and 6 J/kg) were administered; all subsequent shocks with 6 J/kg. Blood for determination of the plasma bupivacaine concentration was drawn throughout the experiment. RESULTS: In the vasopressor group, all five pigs survived, whereas none of five pigs in the lipid group had restoration of spontaneous circulation (P < 0.01). There was no significant difference between groups in the plasma concentration of total bupivacaine. CONCLUSION: In this model of a bupivacaine-induced cardiac arrest, the vasopressor combination of vasopressin and epinephrine compared with lipid emulsion resulted in higher coronary perfusion pressure during CPR and survival rates.

A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation.

BACKGROUND: Vasopressin is an alternative to epinephrine for vasopressor therapy during cardiopulmonary resuscitation, but clinical experience with this treatment has been limited. METHODS: We randomly assigned adults who had had an out-of-hospital cardiac arrest to receive two injections of either 40 IU of vasopressin or 1 mg of epinephrine, followed by additional treatment with epinephrine if needed. The primary end point was survival to hospital admission, and the secondary end point was survival to hospital discharge. RESULTS: A total of 1219 patients underwent randomization; 33 were excluded because of missing study-drug codes. Among the remaining 1186 patients, 589 were assigned to receive vasopressin and 597 to receive epinephrine. The two treatment groups had similar clinical profiles. There were no significant differences in the rates of hospital admission between the vasopressin group and the epinephrine group either among patients with ventricular fibrillation (46.2 percent vs. 43.0 percent, P=0.48) or among those with pulseless electrical activity (33.7 percent vs. 30.5 percent, P=0.65). Among patients with asystole, however, vasopressin use was associated with significantly higher rates of hospital admission (29.0 percent, vs. 20.3 percent in the epinephrine group; P=0.02) and hospital discharge (4.7 percent vs. 1.5 percent, P=0.04). Among 732 patients in whom spontaneous circulation was not restored with the two injections of the study drug, additional treatment with epinephrine resulted in significant improvement in the rates of survival to hospital admission and hospital discharge in the vasopressin group, but not in the epinephrine group (hospital admission rate, 25.7 percent vs. 16.4 percent; P=0.002; hospital discharge rate, 6.2 percent vs. 1.7 percent; P=0.002). Cerebral performance was similar in the two groups. CONCLUSIONS: The effects of vasopressin were similar to those of epinephrine in the management of ventricular fibrillation and pulseless electrical activity, but vasopressin was superior to epinephrine in patients with asystole. Vasopressin followed by epinephrine may be more effective than epinephrine alone in the treatment of refractory cardiac arrest.

Use of an inspiratory impedance threshold valve during chest compressions without assisted ventilation may result in hypoxaemia.

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

Prediction of countershock success using single features from multiple ventricular fibrillation frequency bands and feature combinations using neural networks.

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

An observational study of vasopressin infusion during uncontrolled haemorrhagic shock in a porcine trauma model: Effects on bowel function.

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.

Estimation of the duration of ventricular fibrillation using ECG single feature analysis.

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

Arginine vasopressin during sinus rhythm: effects on haemodynamic variables, left anterior descending coronary artery cross sectional area and cardiac index, before and after inhibition of NO-synthase, in pigs.

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.

Vasopressin improves survival in a porcine model of abdominal vascular injury.

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.