Intravenous Administration Of Epinephrine Research Articles

Sequence of Epinephrine and Advanced Airway Placement After Out-of-Hospital Cardiac Arrest

While epinephrine and advanced airway management (AAM) (supraglottic airway insertion and endotracheal intubation) are commonly used for out-of-hospital cardiac arrest (OHCA), the optimal sequence of these interventions remains unclear. To evaluate the association of the sequence of epinephrine administration and AAM with patient outcomes after OHCA. This cohort study analyzed the nationwide, population-based OHCA registry in Japan and included adults (aged ≥18 years) with OHCA for whom emergency medical services personnel administered epinephrine and/or placed an advanced airway between January 1, 2014, and December 31, 2019. The data analysis was performed between October 1, 2022, and May 12, 2023. The sequence of intravenous epinephrine administration and AAM. The primary outcome was 1-month survival. Secondary outcomes were 1-month survival with favorable functional status and prehospital return of spontaneous circulation. To control imbalances in measured patient demographics, cardiac arrest characteristics, and bystander and prehospital interventions, propensity scores and inverse probability of treatment weighting (IPTW) were performed for shockable and nonshockable initial rhythm subcohorts. Of 259 237 eligible patients (median [IQR] age, 79 [69-86] years), 152 289 (58.7%) were male. A total of 21 592 patients (8.3%) had an initial shockable rhythm, and 237 645 (91.7%) had an initial nonshockable rhythm. Using IPTW, all covariates between the epinephrine-first and AAM-first groups were well balanced, with all standardized mean differences less than 0.100. After IPTW, the epinephrine-first group had a higher likelihood of 1-month survival for both shockable (odds ratio [OR], 1.19; 95% CI, 1.09-1.30) and nonshockable (OR, 1.28; 95% CI, 1.19-1.37) rhythms compared with the AAM-first group. For the secondary outcomes, the epinephrine-first group experienced an increased likelihood of favorable functional status and prehospital return of spontaneous circulation for both shockable and nonshockable rhythms compared with the AAM-first group. These findings suggest that for patients with OHCA, administration of epinephrine before placement of an advanced airway may be the optimal treatment sequence for improved patient outcomes.

Changes in vital signs during adrenaline administration for hemostasis in intracordal injection: an observational study with a hypothetical design of endotracheal adrenaline administration in cardiopulmonary arrest

BackgroundThe background is that intravenous adrenaline administration is recommended for advanced cardiovascular life support in adults and endotracheal administration is given low priority. The reason is that the optimal dose of adrenaline in endotracheal administration is unknown, and it is ethically difficult to design studies of endotracheal adrenaline administration with non-cardiopulmonary arrest. We otolaryngologists think so because we administered adrenaline to the vocal folds for hemostasis after intracordal injection under local anesthesia, but have had few cases of vital changes. We hypothesized that examining vital signs before and after adrenaline administration for hemostasis would help determine the optimal dose of endotracheal adrenaline.MethodsWe retrospectively examined the medical records of 79 patients who visited our hospital from January 2018 to December 2020 and received adrenaline in the vocal folds and trachea for hemostasis by intracordal injection under local anesthesia to investigate changes in heart rate and systolic blood pressure before and after the injection.ResultsThe mean heart rates before and after injection were 83.96 ± 18.51 (standard deviation) beats per minute (bpm) and 81.50 ± 15.38 (standard deviation) bpm, respectively. The mean systolic blood pressure before and after the injection were 138.13 ± 25.33 (standard deviation) mmHg and 135.72 ± 22.19 (standard deviation) mmHg, respectively. Heart rate and systolic blood pressure had P-values of 0.136, and 0.450, respectively, indicating no significant differences.ConclusionsAlthough this study was an observational, changes in vital signs were investigated assuming endotracheal adrenaline administration. The current recommended dose of adrenaline in endotracheal administration with cardiopulmonary arrest may not be effective. In some cases of cardiopulmonary arrest, intravenous and intraosseous routes of adrenaline administration may be difficult and the opportunity for resuscitation may be missed. Therefore, it is desirable to have many options for adrenaline administration. Therefore, if the optimal dose and efficacy of endotracheal adrenaline administration can be clarified, early adrenaline administration will be possible, which will improve return of spontaneous circulation (ROSC) and survival discharge rates.

Epinephrine-induced Effects on Cerebral Microcirculation and Oxygenation Dynamics Using Multimodal Monitoring and Functional Photoacoustic Microscopy.

The administration of epinephrine after severe refractory hypotension, shock, or cardiac arrest restores systemic blood flow and major vessel perfusion but may worsen cerebral microvascular perfusion and oxygen delivery through vasoconstriction. The authors hypothesized that epinephrine induces significant microvascular constriction in the brain, with increased severity after repetitive dosing and in the aged brain, eventually leading to tissue hypoxia. The authors investigated the effects of intravenous epinephrine administration in healthy young and aged C57Bl/6 mice on cerebral microvascular blood flow and oxygen delivery using multimodal in vivo imaging, including functional photoacoustic microscopy, brain tissue oxygen sensing, and follow-up histologic assessment. The authors report three main findings. First, after epinephrine administration, microvessels exhibited severe immediate vasoconstriction (57 ± 6% of baseline at 6 min, P < 0.0001, n = 6) that outlasted the concurrent increase in arterial blood pressure, while larger vessels demonstrated an initial increase in flow (108 ± 6% of baseline at 6 min, P = 0.02, n = 6). Second, oxyhemoglobin decreased significantly within cerebral vessels with a more pronounced effect in smaller vessels (microvessels to 69 ± 8% of baseline at 6 min, P < 0.0001, n = 6). Third, oxyhemoglobin desaturation did not indicate brain hypoxia; on the contrary, brain tissue oxygen increased after epinephrine application (from 31 ± 11 mmHg at baseline to 56 ± 12 mmHg, 80% increase, P = 0.01, n = 12). In the aged brains, microvascular constriction was less prominent yet slower to recover compared to young brains, but tissue oxygenation was increased, confirming relative hyperoxia. Intravenous application of epinephrine induced marked cerebral microvascular constriction, intravascular hemoglobin desaturation, and paradoxically, an increase in brain tissue oxygen levels, likely due to reduced transit time heterogeneity.

Endothelio- and cardioprotective effects of vitamin в6 and folic acid in modelling methionine-induced hyperhomocysteinemia

The endotelio- and cardioprotective effects of vitamin B6 (2 mg/kg) and folic acid (0.2 mg/kg) upon modeling of methionine-induced hyperhomocysteinemia via methionine intragastric administration at a dose of 3 g/kg were studied. It was shown that the combined use of vitamin B6 and folic acid allows on the background of a significant reduction in homocysteine concentrations normalizing the endothelial dysfunction coefficient and the parameters of maximum left ventricular pressure in response to intravenous administration of adrenaline. The research was partially supported by the grant of the President of the Russian Federation №MD-4711.2015.7.

Two cases of circulatory collapse due to suspected remimazolam anaphylaxis

BackgroundRemimazolam was approved in Japan in January 2020. We report two cases of circulatory collapse due to suspected remimazolam anaphylaxis during anesthetic induction.Case presentationCase 1: A 74-year-old male was scheduled for debridement and skin grafting for a severe burn injury. We induced anesthesia with 4 mg of remimazolam and 20 mg of ketamine. The patient subsequently developed treatment-resistant severe hypotension.Case 2: A 59-year-old male was scheduled for laparoscopic-assisted sigmoid colectomy. We induced anesthesia with 9 mg of remimazolam. Within a few minutes, the patient developed treatment-resistant severe hypotension.As serum tryptase was elevated in both cases and only intravenous administration of adrenaline was effective, we considered the circulatory collapse might be due to anaphylaxis.ConclusionWe experienced two cases of circulatory collapse due to suspected remimazolam anaphylaxis during anesthetic induction. The prevalence of remimazolam anaphylaxis is not yet known, and further research is needed.

Timing of Intravenous Epinephrine Administration During Out-of-Hospital Cardiac Arrest

Timing of Intravenous Epinephrine Administration During Out-of-Hospital Cardiac Arrest

Comparison of intraosseous and intravenous epinephrine administration during resuscitation of asphyxiated newborn lambs

ObjectiveIntraosseous access is recommended as a reasonable alternative for vascular access during newborn resuscitation if umbilical access is unavailable, but there are minimal reported data in newborns. We compared intraosseous...

Development and Evaluation of a Novel Mouse Model of Asphyxial Cardiac Arrest Revealed Severely Impaired Lymphopoiesis After Resuscitation.

BackgroundAnimal disease models represent the cornerstone in basic cardiac arrest (CA) research. However, current experimental models of CA and resuscitation in mice are limited. In this study, we aimed to develop a mouse model of asphyxial CA followed by cardiopulmonary resuscitation (CPR), and to characterize the immune response after asphyxial CA/CPR.Methods and ResultsCA was induced in mice by switching from an O2/N2 mixture to 100% N2 gas for mechanical ventilation under anesthesia. Real‐time measurements of blood pressure, brain tissue oxygen, cerebral blood flow, and ECG confirmed asphyxia and ensuing CA. After a defined CA period, mice were resuscitated with intravenous epinephrine administration and chest compression. We subjected young adult and aged mice to this model, and found that after CA/CPR, mice from both groups exhibited significant neurologic deficits compared with sham mice. Analysis of post‐CA brain confirmed neuroinflammation. Detailed characterization of the post‐CA immune response in the peripheral organs of both young adult and aged mice revealed that at the subacute phase following asphyxial CA/CPR, the immune system was markedly suppressed as manifested by drastic atrophy of the spleen and thymus, and profound lymphopenia. Finally, our data showed that post‐CA systemic lymphopenia was accompanied with impaired T and B lymphopoiesis in the thymus and bone marrow, respectively.ConclusionsIn this study, we established a novel validated asphyxial CA model in mice. Using this new model, we further demonstrated that asphyxial CA/CPR markedly affects both the nervous and immune systems, and notably impairs lymphopoiesis of T and B cells.

Timing of Intravenous Epinephrine Administration During Out-of-Hospital Cardiac Arrest.

Current guidelines for cardiopulmonary resuscitation recommend that standard dose of epinephrine be administered every 3 to 5 min during cardiac arrest. However, there is controversy about the association between timing of epinephrine administration and outcomes after out-of-hospital cardiac arrest (OHCA). This study aimed to determine whether the timing of intravenous epinephrine administration is associated with outcomes after OHCA. We analyzed Japanese government-led nationwide population-based registry data for OHCA. Adult OHCA patients who received intravenous epinephrine by emergency medical service personnel in the prehospital setting from 2011 to 2017 were included. Multivariable logistic regression models were used to assess the associations between time to first epinephrine administration and outcomes after OHCA. Subsequently, associations between early (≤20 min) versus delayed (>20 min) epinephrine administration and outcomes after OHCA were examined using propensity score-matched analyses. The primary outcome was 1-month neurologically favorable survival. A total of 119,946 patients (mean [SD] age, 75.2 [14.8] years; 61.4% male) were included. The median time to epinephrine was 23 min (interquartile range, 19-29). Longer time to epinephrine was significantly associated with a decreased chance of 1-month neurologically favorable survival (multivariable adjusted OR per minute delay, 0.91 [95% CI, 0.90-0.92]). In the propensity score-matched cohort, when compared with early (≤20 min) epinephrine, delayed (>20 min) epinephrine was associated with a decreased chance of 1-month neurologically favorable survival (959/42,804 [2.2%] vs. 330/42,804 [0.8%]; RR, 0.34; 95% CI, 0.30-0.39; NNT, 69). Delay in epinephrine administration was associated with a decreased chance of 1-month neurologically favorable survival among patients with OHCA.

Intraosseous versus intravenous administration of adrenaline in patients with out-of-hospital cardiac arrest: a secondary analysis of the PARAMEDIC2 placebo-controlled trial.

To compare the effectiveness of the intravenous (IV) and intraosseous (IO) routes for drug administration in adults with a cardiac arrest enrolled in the Pre-Hospital Assessment of the Role of Adrenaline: Measuring the Effectiveness of Drug Administration in Cardiac Arrest (PARAMEDIC2) randomised, controlled trial. Patients were recruited from five National Health Service Ambulance Services in England and Wales from December 2014 through October 2017. Patients with an out-of-hospital cardiac arrest who were unresponsive to initial resuscitation attempts were randomly assigned to 1mg adrenaline or matching placebo. Intravascular access was established as soon as possible, and IO access was considered if IV access was not possible after two attempts. Among patients with out-of-hospital cardiac arrest, 3631 received adrenaline and 3686 received placebo. Amongst these, 1116 (30.1%) and 1121 (30.4%) received the study drug via the IO route. The odds ratios were similar in the IV and IO groups for return of spontaneous circulation (ROSC) at hospital handover [adjusted odds ratio (aOR) 4.07 (95% CI 3.42-4.85) and (aOR 3.98 (95% CI 2.86-5.53), P value for interaction 0.90]; survival to 30days [aOR 1.67 (1.18-2.35) versus 0.9 (0.4-2.05), P = 0.18]; and favourable neurological outcome [aOR 1.39 (0.93-2.06) versus 0.62 (0.23-1.67), P = 0.14]. There was no significant difference in treatment effect (adrenaline versus placebo) on ROSC at hospital handover between drugs administered by the intraosseous route or by the intravenous route. We could not detect any difference in the treatment effect between the IV and IO routes on the longer term outcomes of 30-day survival or favourable neurological outcome at discharge (ISRCTN73485024).

P251 Right ventricular free wall dissection clearly detected and recorded by echocardiography: a fatal complication after inferior myocardial infarction

Abstract An 81-year-old man was transferred to our institution by ambulance because of poor feeding, general fatigue and slight disorientation lasting for a week. On arrival, he was awake and able to speak, however, his blood pressure was low at 61/43 mmHg in spite of his medical history of hypertension. His ECG showed abnormal Q waves and ST elevation in II, III, aVF leads. The echo exam detected severe hypokinesis in the left ventricular inferior wall and reduced ejection fraction at 30%. Pericardial effusion was not observed in the first echo exam. The patient was diagnosed as cardiogenic shock due to recent inferior myocardial infarction. Coronary angiography was performed, which detected total occlusion of mid right coronary artery, followed by a successful percutaneous coronary intervention (PCI) with a drug-eluting stent under the support of intra-aortic balloon pumping. Nevertheless, his blood pressure remained low and intravenous adrenaline administration was necessary during and even after PCI. To detect the cause of prolonged low blood pressure, echo was performed again immediately after PCI. The echo exam detected new findings: right ventricular posterior free wall was dissected and abnormal shunt flows were obviously observed from left ventricle to right atrium through the dissection cavity during systole. An urgent surgical repair was considered as the only option for his survival, however, his family did not accept it because the operation itself was too risky. On the next day of his admission, he passed away. Right ventricular free wall dissection is a very rare but fatal complication after inferior myocardial infarction, nevertheless, we could detect it by echocardiography with clearly recorded images. Abstract P251 Figure.

Anaphylaxis after rocuronium administration during induction of anesthesia

Anaphylaxis during anesthesia is rare, but often fatal. Rocuronium is a neuromuscular relaxant used for induction of anesthesia. We experienced a case of anaphylaxis after rocuronium administration during induction of anesthesia. A 64-year-old female patient was scheduled for bilateral radius fracture fixation. The history of patient showed no specific findings other than hypersensitivity to mackerel. She had no previous experience of anesthesia. Anesthesia was induced by intravenous injection of propofol 100 mg and continuous infusion was begun with remifentanil 0.25 μg/kg/min, followed by rocuronium 40 mg. Immediately after intravenous administration of rocuronium, the manual ventilation became difficult, and the patient developed erythema and severe hypoten sion. The patient was diagnosed with anaphylaxis based on clinical features and started treatment. First, we performed endotra cheal intubation promptly. Then, immediate intravenous administration of epinephrine and fluid followed. Despite adequate treat ment, hypotension was not corrected and intravenous epinephrine was administered. However, ventricular tachycardia occurred which was successfully treated with a defibrillator. Later, the patient uneventfully recovered in the intensive care unit. The patient was not tested for skin prick test, but rocuronium was the most likely cause of anaphylaxis at that time. The authors unexpectedly experienced drug-induced anaphylaxis, which is life-threatening to the patient. Clinicians should be aware of the diagnosis, treat ment, and prevention as anaphylaxis can be hazardous to the patient. (Allergy Asthma Respir Dis 2018;6:225-228)

Impact of rapid response car system on ECMO in out-of-hospital cardiac arrest: A retrospective cohort study

IntroductionExtracorporeal life support (ECLS) has been reported to be more effective than conventional cardiopulmonary resuscitation (CPR). In ECLS, a shorter time from arrival to implantation of extracorporeal membrane oxygenation (ECMO; door-to-ECMO) time was predicted to be associated with better survival rates. This study aimed to examine the impact of the physician-based emergency medical services (P-EMS) using a rapid response car (RRC) on door-to-ECMO time in patients with out-of-hospital cardiac arrest (OHCA). MethodsIn this retrospective cohort study, adult patients with OHCA who were admitted to a Japanese tertiary care hospital from April 2012 to December 2016 and underwent venoarterial ECMO were included. Patients were either transferred by emergency medical service (EMS only group) or RRC (RRC group). Primary outcome was door-to-ECMO time. Wilcoxon rank-sum test was used to compare the outcome between the two groups. ResultsA total of 34 patients were included in this study, and outcome data were available for all patients. The door-to-ECMO time was significantly shorter in the RRC group than in the EMS only group (median, 23min vs. 36min; P=0.006). Additionally, the RRC was also associated with earlier successful intubation and intravenous adrenaline administration. ConclusionThe physician-based RRC system was associated with a shorter door-to-ECMO time and successful advanced procedures in prehospital settings. Combination of the RRC system with ECLS may lead to better outcomes in patients with OHCA.

Temporal trends in the utilization of vasopressors in intensive care units: an epidemiologic study

BackgroundThe choice of vasopressor use in the intensive care unit (ICU) depends primarily on provider preference. This study aims to describe the rate of vasopressor utilization and the trends of each vasoactive agent usage in the ICU over the span of 7 years in a tertiary referral center.MethodsAll adult ICU admissions, including medical, cardiac, and surgical ICUs from January 1st, 2007 through December 31st, 2013 were included in this study. Vasopressor use was defined as the continuous intravenous administration of epinephrine, norepinephrine, phenylephrine, dopamine, or vasopressin within a given ICU day. The vasopressor utilization index (VUI) was defined as the proportion of ICU days on each vasoactive agent divided by the total ICU days with vasopressor usage.ResultsDuring the study period, 72,005 ICU admissions and 272,271 ICU days were screened. Vasopressors were used in 19,575 ICU admissions (27 %) and 59,811 ICU days (22 %). Vasopressin was used in 24,496 (41 %), epinephrine in 23,229 (39 %), norepinephrine in 20,648 (34 %), dopamine in 9449 (16 %), and phenylephrine in 7508 (13 %) ICU days. The VUInorepinephrine increased from 0.24 in 2007 to 0.46 in 2013 and VUIphenylephrine decreased from 0.20 in 2007 to 0.08 in 2013 (p < 0.001 both). For epinephrine, dopamine, and vasopressin VUI did not change over the course of study.ConclusionVasopressors were used in about one fourth of ICU admissions and about one-fifth of ICU days. Although vasopressin is the most commonly used vasopressor, the use of norepinephrine found to have an increasing trajectory.Electronic supplementary materialThe online version of this article (doi:10.1186/s40360-016-0063-z) contains supplementary material, which is available to authorized users.

Adrenaline aggravates lung injury caused by liver ischemia-reperfusion and high-tidal-volume ventilation in rats.

BackgroundWe often administer adrenaline to improve hypotension of patients undergoing systemic inflammation that is not treated with volume resuscitation. The effects of adrenaline on injured lungs during shock status have not been elucidated. We previously demonstrated that hepatic ischemia–reperfusion followed by high-tidal-volume ventilation-induced systemic inflammation, hypotension, and lung injury in rats. Using this animal model, we investigated the effects of adrenaline on lung injury and hemodynamics.MethodsAnesthetized rats were ventilated and underwent hepatic inflow interruption for 15 min twice. After the second liver ischemia–reperfusion, the tidal volume was increased to 24 ml · kg−1 body weight from 6 ml · kg−1, and 12 rats in each group were observed for 360 min after reperfusion with or without continuous intravenous adrenaline administration. Extra fluid was administered according to the decline in the arterial blood pressure.ResultsAdrenaline administration significantly reduced the volume of intravenous resuscitation fluid. The wet-to-dry weight ratio of the lungs was higher (7.53 ± 0.37 vs. 4.63 ± 0.35, P < 0.001), the partial oxygen pressure in arterial blood was lower (213 ± 48 vs. 411 ± 33, P = 0.004), and the tumor necrosis factor-α concentration in bronchoalveolar lavage (BAL) fluid was higher (102.64 ± 100.22 vs. 101.91 ± 100.27, P = 0.015), with adrenaline. Histopathological examinations revealed marked exudation in the alveolar spaces in rats receiving adrenaline.ConclusionsContinuous administration of adrenaline partially prevented a rapid decline in blood pressure but deteriorated lung injury in a rat model of liver ischemia–reperfusion with high-tidal-volume ventilation. A possibility that adrenaline administration aggravate ventilator-induced lung injury during systemic inflammation should be considered.

Abstract 154: Continuous Intravenous Administration of Adrenaline May Prevent the Biphasic Reaction of Anaphylaxis

Objective: Anaphylaxis is a multi-system syndrome resulting from the release of chemical mediators upon exposure to an allergen. Biphasic anaphylactic reactions may occur due to secondary elevation of the chemical mediators following the initial reaction. The initial treatment of anaphylaxis generally includes adrenaline injection, which results in decreased chemical mediator release. We hypothesize that continuous intravenous administration, rather than intramuscular injection of adrenaline, may inhibit the release of chemical mediators following the initial reaction, and thereby prevent biphasic reactions. Accordingly, in this study, we aimed to investigate the occurrence of biphasic reactions according to the type of administration of adrenaline. Methods: We included patients with anaphylaxis admitted to our hospital, who were treated with adrenaline between April 2005 and March 2014. We retrospectively investigated the occurrences of biphasic reactions after admission in patients treated with continuous intravenous adrenaline or intramuscular adrenaline injections. Patients were excluded if they had received intravenous bolus or complex methods of administration. The risk of biphasic reactions according to the method of administration was analyzed by logistic regression. Results: A total of 104 patients were included in the study (continuous intravenous administration: 56, intramuscular injection: 48). Eight patients (7.69%) experienced biphasic reactions, out of which one had received continuous intravenous administration, and seven had received intramuscular injection (p = 0.02). No patient had received adrenaline during the biphasic reaction in the continuous intravenous administration group compared to the three patients in the intramuscular injection group (p = 0.10). Logistic regression analysis revealed that the odds ratio of biphasic reactions for continuous intravenous administration vs. intramuscular injection of adrenaline was 0.11 (p = 0.04, 95% confidence interval: 0.01-0.90). Conclusions: Continuous intravenous administration of adrenaline may prevent the biphasic reaction of anaphylaxis.

Impact of catecholamines in cardiac arrest due to acute asphyxia--a study in piglets.

Early intravenous epinephrine administration may help to achieve return of spontaneous circulation in cardiac arrest (CA). However, venous access can be challenging in small children. This study investigates the effect of intravenous and intramuscular epinephrine in treatment of asphyxial CA. Twenty-eight, 2-5-weeks-old, anesthetized piglets were asphyxiated by ventilation withdrawal. CA was untreated for 8min, followed by 2min of basic life support. Following this, epinephrine iv (10μg·kg(-1) , group IV), epinephrine im (100μg·kg(-1) , group IM), or normal saline (group NS) were administered. Further doses of epinephrine were given in group IV every 4min, in group IM after 10min if required. After twenty-two minutes of CA, iv epinephrine was given to all animals still in CA. Outcome measures were survival and epinephrine plasma concentrations. Ten animals regained spontaneous circulation after 2min of basic life support. Therefore, no drug treatment was administered (drop out). Resuscitation was effective in 2 pigs of group IM (n=6), in 6 of group NS (n=8) and in all of group IV (n=4). Nonsurvivors had higher epinephrine (P<0.01) and norepinephrine (P<0.01) plasma concentrations prior to start of resuscitation. Median increase in epinephrine plasma concentration from T0 to T5 was 138, 134, and 29nm in group IV, IM, and NS, respectively. Intravenous and intramuscular administered epinephrine led to similar increase in plasma concentrations during resuscitation of asphyxial CA without hemodynamic or survival benefit. High endogenous epinephrine and norepinephrine plasma concentrations were negative predictors for survival.

Takotsubo-like left ventricular dysfuction following intravenous epinephrine administration

A 50-year old woman presented at her general practitioner following facial swelling due to an insect bite. She was treated with 100 mg Solucortef and 1 mg epinephrine of a 1: 10 000 solution intravenously. Minutes later she developed chest pain with concomitant non-specific changes in the electrocardiogram (ECG), and later significant Troponin I concentrations were demonstrated. She was treated with anticoagulants, and later a bedside echocardiography revealed reduced left ventricular ejection fraction and apical ballooning pattern as seen in Takotsubo Cardiomyopathy. During hospitalization the patient had an episode of Torsade’s de pointes ventricular tachycardia and several unexplained cerebral absences. Coronary angiography revealed normal coronary arteries, and the patient exhibited normal ejection fraction one month after hospital discharge. Physicians should avoid giving high doses of epinephrine by the intravenous route and only in cases of severe anaphylaxis

Coronary Perfusion Pressure Response to High-Dose Intraosseous versus Standard-Dose Intravenous Epinephrine Administration after Prolonged Cardiac Arrest

Background: This study was done to compare coronary perfusion pressure (CPP) prior to the first rescue shock (RS) among a group of animals that received intraosseous (IO) epinephrine 0.1 mg/ kg (high-dose epinephrine [HDE]) with a group that received intravenous (IV) epinephrine 0.01 mg/kg (standard-dose epinephrine [SDE]) during cardiac arrest resuscitation using a swine model of prolonged out-of-hospital ventricular fibrillation (VF) cardiac arrest. Methods: This was a secondary analysis of prospectively collected data from two IACUC approved protocols. Seventy-nine Yorkshire swine (25 - 35 kg) were surgically instrumented under anesthesia and VF was electrically induced. After 10 minutes of untreated VF in the IO study (n = 26) and 12 minutes of untreated VF in the IV study (n = 53), resuscitation commenced with closed chest compressions (CCC). A single dose of epinephrine (HDE IO or SDE IV, respectively) was given and flushed with saline. The CCC and RS attempts were standardized for all animals. The CPP was defined as aortic diastolic pressure minus right atrial diastolic pressure measured 2.5 minutes after medication delivery. Descriptive statistics were used to analyze the data. Results: Baseline group characteristics were mathematically the same. Just prior to the first RS, HDE IO resulted in a mean CPP of 33.2 mmHg (95%CI: 26.6, 39.9), while SDE IV resulted in a mean CPP of 25.0 mmHg (95%CI: 20.5, 29.4). Conclusion: This observation study reaffirms the assertion that HDE IO may be required to generate CPP values similar to SDE IV during resuscitation of prolonged VF.

Stress-induced phosphorylation of SNAP-25

Synaptosomal-associated protein of 25kDa (SNAP-25), a t-SNARE protein, plays a crucial role in neurotransmitter release by exocytosis. Protein kinase C phosphorylates SNAP-25 at Ser187, however the physiological significance of this phosphorylation event in brain function remains unclear. In the present study, we found that SNAP-25 phosphorylation increased rapidly in the mouse brain following cold-water restraint stress. Both basal and stress-induced phosphorylation of SNAP-25 were high in stress-related brain regions, including the cerebral cortex, hippocampus, and amygdala, and the extent of phosphorylation increased with increasing amounts of stress. Intravenous administration of adrenaline increased SNAP-25 phosphorylation, although stress-induced phosphorylation was still observed in adrenalectomized mice. These results indicate that SNAP-25 phosphorylation is regulated in a stress-dependent manner through both central and peripheral mechanisms.