Intraosseous fluid resuscitation causes systemic fat emboli in a porcine hemorrhagic shock model

Background Intraosseous cannulation can be life-saving when intravenous access cannot be readily achieved. However, it has been shown that the procedure may cause fat emboli to the lungs and brain. Fat embolization may cause serious respiratory failure and fat embolism syndrome. We investigated whether intraosseous fluid resuscitation in pigs in hemorrhagic shock caused pulmonary or systemic embolization to the heart, brain, or kidneys and if this was enhanced by open chest conditions. Methods We induced hemorrhagic shock in anesthetized pigs followed by fluid-resuscitation through bilaterally placed tibial (hind leg) intraosseous cannulas. The fluid-resuscitation was limited to intraosseous or i.v. fluid therapy, and did not involve cardiopulmonary resuscitation or other interventions. A subgroup underwent median sternotomy with pericardiectomy and pleurotomy before hemorrhagic shock was induced. We used invasive hemodynamic and respiratory monitoring including Swan Ganz pulmonary artery catheter and transesophageal echocardiography and obtained biopsies from the lungs, heart, brain, and left kidney postmortem. Results All pigs exposed to intraosseous infusion had pulmonary fat emboli in postmortem biopsies. Additionally, seven of twenty-one pigs had coronary fat emboli. None of the pigs with open chest had fat emboli in postmortem lung, heart, or kidney biopsies. During intraosseous fluid-resuscitation, three pigs developed significant ST-elevations on ECG; all of these animals had coronary fat emboli on postmortem biopsies. Conclusions Systemic fat embolism occurred in the form of coronary fat emboli in a third of the animals who underwent intraosseous fluid resuscitation. Open chest conditions did not increase the incidence of systemic fat embolization.

The candidates for Class I methanol masers

The collisional excitation of methanol molecule in non-dissociative magnetohydro-dynamic shock waves is considered. All essential chemical processes that determine methanol abundance in the gas are taken into account in the shock model. The large velocity gradient approximation is used in the calculations of energy level populations of the molecule. We calculate the optical depth for inverted methanol transitions, and present the list of candidates for Class I methanol masers that have collisional pumping mechanism.

Intraosseous Fluid Resuscitation Causes Systemic Fat Emboli in a Porcine Hemorrhagic Shock Model

BackgroundIntraosseous cannulation can be life-saving when intravenous access cannot be readily achieved. However, it has been shown that the procedure may cause fat emboli to the lungs and brain. Fat embolization may cause serious respiratory failure and fat embolism syndrome. We investigated whether intraosseous fluid resuscitation in pigs in hemorrhagic shock caused pulmonary or systemic embolization to the heart, brain, or kidneys and if this was enhanced by open chest conditions.MethodsWe induced hemorrhagic shock in anesthetized pigs followed by fluid-resuscitation through bilaterally placed tibial intraosseous cannulas. A subgroup underwent median sternotomy with pericardiectomy and pleurotomy before hemorrhagic shock was induced. We used invasive hemodynamic and respiratory monitoring including Swan Ganz pulmonary artery catheter and transesophageal echocardiography and obtained biopsies from the lungs, heart, brain, and left kidney postmortem.ResultsAll pigs exposed to intraosseous infusion had pulmonary fat emboli in postmortem biopsies. Additionally, seven of twenty-one pigs had coronary fat emboli. None of the pigs with open chest had fat emboli in postmortem lung, heart, or kidney biopsies. During fluid-resuscitation, three pigs developed significant ST-elevations on ECG; all of these animals had coronary fat emboli on postmortem biopsies. ConclusionsSystemic fat embolism occurred in the form of coronary fat emboli in a third of the animals who underwent intraosseous fluid resuscitation. Open chest conditions did not increase the incidence of systemic fat embolization.

Gunshot model of junctional femoral artery hemorrhage in swine under ultrasonic guidance

Background In a combat setting, uncontrolled junctional hemorrhage constitutes a major source of potentially preventable deaths. It is very important to establish a model of massive hemorrhage of gunshot wound at junction area which can simulate field rescue conditions. Methods Picco monitoring was instrumented for the anesthetized Landrace pigs, and the right femoral artery was located by portable ultrasound. The pistol bullet hit the right femoral artery, resulting in an artery rupture. After 30 seconds of uncontrolled hemorrhage, the ballistic wound was filled with combat gauze (QuikClot) to stop bleeding in the BT group (n = 10). Combat gauze was used to stop bleeding when the mean arterial pressure (MAP) decreased by 30% in the MD group (n = 10). The sham-operated pigs (n = 10) underwent the same anesthetic and surgical procedures, but neither shooting nor gauze filling therapy was performed. Blood samples were taken 15 min before injury, and then 10 min, 30 min, and 60 min after the injury. Results Histologic anatomy indicated that the right femoral artery and vein were completely ruptured in all 20 swine of MD and BT groups. The blood loss of pre-tamponade (4.97 ± 2.47 mL/kg vs 18.26 ± 3.47 mL/kg, P < 0.001), pro-tamponade (4.58 ± 1.49 mL/kg vs 7.20 ± 1.99 mL/kg, P = 0.004) and the total amount of bleeding (9.54 ± 3.80 mL/kg vs 25.46 ± 3.68 mL/kg, P < 0.001) in MD group were more than those in BT group. There were differences in body temperature, PH, PT, LAC of MD group compared with BT and SHAM groups 60 minutes after injury (all P < 0.0167). The survival time of MD group was shorter than that of BT group (P = 0.029). Conclusion We established a reliable gunshot model of junctional hemorrhage in swine, which had high accuracy for femoral arterial rupture under ultrasonic guidance and provided consistent and reproducible field-simulation conditions. In this junctional hemorrhage model, blood loss of 30-second free bleeding did not meet the criteria for shock. The MAP decrease of 30% emerged as a better predictor of a successful shock model.

Reliability evaluation of m-consecutive- k, l-out-of-n: F system subjected to shocks

In this paper, we propose a shock model for an m-consecutive- k, l-out-of- n: F system. This paper presents a reliability analysis of an m-consecutive- k, l-out-of- n: F system subjected to shocks that destroy a random number of components. One of the main random variables is the number of components affected by successive shocks. Phase-type distributions have been used to model the intervals between successive shocks. The main objective of this study is to show how phase-type distributions can be used to determine the reliability of m-consecutive- k, l-out-of- n: F systems subjected to shocks, which destroy a random number of components. Consideration is given to the optimal replacement time problem, which addresses the minimization of the total long-run average cost per unit time.

Changes of Operative Performance of Pulse Pressure Variation As A Predictor of Fluid Responsiveness in a Swine Model of Endotoxin Shock

Background Several limitations regarding pulse pressure variation (PPV) use have been reported. Our aim was to describe changes in the PPV operative performance as a predictor of fluid responsiveness during the development of a swine endotoxin shock model and to assess hemodynamic variables associated with PPV changes. Methods A swine porcine endotoxin shock model was established (E. Coli 055:B5 endotoxin) in 7 pigs, and 3 pigs were included in the control group. The endotoxin was infused until the mean arterial pressure (MAP) dropped below 50 mmHg (TH0); then, the model animal was reanimated with fluids and vasopressors. We performed fluid challenges every hour for 6 hours. ROC curve analysis was conducted. Additionally, a linear mixed model was performed. Results The area under the curve (AUC) of PPV decreased from 0.95 (0.81–1.00) to 0.60 (0.17–1.00) at TH0. Its cutoff increased from 10.5–22.00% at TH0. PPV showed an inverse relationship with stroke volume, mean systemic filling pressure (MSFP), MAP, and systemic vascular resistance (SVR) (p < 0,001, AIC = 111.85). Conclusions The PPV operative performance as a predictor of fluid responsiveness decreased with the progression of endotoxic shock. This result could be due to the inverse association with MAP and SVR.