Epinephrine is widely used for treatment of life-threatening hypotension, although new vasopressor drugs may merit evaluation. The purpose of this study was to determine the effects of vasopressin vs. epinephrine vs. saline placebo on hemodynamic variables, regional blood flow, and short-term survival in an animal model of uncontrolled hemorrhagic shock and delayed fluid resuscitation. Prospective, randomized, laboratory investigation that used a porcine model for measurement of hemodynamic variables and regional abdominal organ blood flow. University hospital laboratory. A total of 21 pigs weighing 32 +/- 3 kg. The anesthetized pigs were subjected to a penetrating liver injury, which resulted in a mean +/- sem loss of 40% +/- 5% of estimated whole blood volume within 30 mins and mean arterial pressures of <20 mm Hg. When heart rate declined progressively, pigs randomly received a bolus dose and continuous infusion of either vasopressin (0.4 units/kg and 0.04 units.kg-1.min-1, n = 7), or epinephrine (45 microg/kg and 5 microg.kg(-1).min(-1), n = 7), or an equal volume of saline placebo (n = 7), respectively. At 30 mins after drug administration, all surviving animals were fluid resuscitated while bleeding was surgically controlled. Mean +/- sem arterial blood pressure at 2.5 and 10 mins was significantly (p <.001) higher after vasopressin vs. epinephrine vs. saline placebo (82 +/- 14 vs. 23 +/- 4 vs. 11 +/- 3 mm Hg, and 42 +/- 4 vs. 10 +/- 5 vs. 6 +/- 3 mm Hg, respectively). Although portal vein blood flow was temporarily impaired by vasopressin, it was subsequently restored and significantly (p <.01) higher when compared with epinephrine or saline placebo (9 +/- 5 vs. 121 +/- 3 vs. 54 +/- 22 mL/min and 150 +/- 20 vs. 31 +/- 17 vs. 0 +/- 0 mL/min, respectively). Hepatic and renal artery blood flow was significantly higher throughout the study in the vasopressin group; however, no further bleeding was observed. Despite a second bolus dose, all epinephrine- and saline placebo-treated animals died within 15 mins after drug administration. By contrast, seven of seven vasopressin-treated animals survived until fluid replacement, and 60 mins thereafter, without further vasopressor therapy (p <.01). Moreover, blood flow to liver, gut, and kidney returned to normal values in the postshock phase. Vasopressin, but not epinephrine or saline placebo, improved short-term survival in a porcine model of uncontrolled hemorrhagic shock after liver injury when surgical intervention and fluid replacement was delayed.

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

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

Removing cardiopulmonary resuscitation (CPR)-related artifacts from human ventricular fibrillation (VF) electrocardiogram (ECG) signals provides the possibility to continuously detect rhythm changes and estimate the probability of defibrillation success. This could reduce ldquohands-offrdquo analysis times which diminish the cardiac perfusion and deteriorate the chance for successful defibrillations. Our approach consists in estimating the CPR part of a corrupted signal by adaptive regression on lagged copies of a reference signal which correlate with the CPR artifact signal. The algorithm is based on a state-space model and the corresponding Kalman recursions. It allows for stochastically changing regression coefficients. The residuals of the Kalman estimation can be identified with the CPR-filtered ECG signal. In comparison with ordinary least-squares regression, the proposed algorithm shows, for low signal-to-noise ratio (SNR) corrupted signals, better SNR improvements and yields better estimates of the mean frequency and mean amplitude of the true VF ECG signal. The preliminary results from a small pool of human VF and animal asystole CPR data are slightly better than the results of comparable previous studies which, however, not only used different algorithms but also different data pools. The algorithm carries the possibility of further optimization.

Traditional power grids are mainly based on centralized power generation and subsequent distribution. The increasing penetration of distributed renewable energy sources and the growing number of electrical loads is creating difficulties in balancing supply and demand and threatens the secure and efficient operation of power grids. At the same time, households hold an increasing amount of flexibility, which can be exploited by demand-side management to decrease customer cost and support grid operation. Compared to the collection of individual flexibilities, aggregation reduces optimization complexity, protects households’ privacy, and lowers the communication effort. In mathematical terms, each flexibility is modeled by a set of power profiles, and the aggregated flexibility is modeled by the Minkowski sum of individual flexibilities. As the exact Minkowski sum calculation is generally computationally prohibitive, various approximations can be found in the literature. The main contribution of this paper is a comparative evaluation of several approximation algorithms in terms of novel quality criteria, computational complexity, and communication effort using realistic data. Furthermore, we investigate the dependence of selected comparison criteria on the time horizon length and on the number of households. Our results indicate that none of the algorithms perform satisfactorily in all categories. Hence, we provide guidelines on the application-dependent algorithm choice. Moreover, we demonstrate a major drawback of some inner approximations, namely that they may lead to situations in which not using the flexibility is impossible, which may be suboptimal in certain situations.