This event rate is, however, higher than the reported adverse event rate with using ketamine as a single agent.This discrepancy may be due to the fact that children in this study may have had more than one adverse event documented during a single sedation, such as apnea, oxygen desaturation, and BMV. Previous studies have shown that ketamine has a low side-effect profile with the most common adverse events being those related to respiratory compromise and emesis.In fact, the odds of respiratory adverse events associated with ketamine use increases when it is administered intramuscularly instead of intravenously.In addition, ketamine-associated emesis can be reduced by administering ondansetron prior to the start of PSA.However, neither of the two patients who had emesis during PSA in this study received ondansetron as a premedication. Moreover, while the authors did not evaluate NPO status and how this relates to emesis, previous studies have shown that the NPO time does not affect the rate of major adverse events during PSA.Despite advances in the field of resuscitation science and modest improvement in outcomes, mortality from in-hospital cardiopulmonary arrest remains relatively high.However, a common denominator in recent reports of modest outcome improvements in CPA resuscitation has been the link to quality of cardiopulmonary resuscitation.In particular, high-quality chest compressions have been described as the foundation that all additional, “downstream” resuscitative efforts are built upon and highly associated with improved survival and favorable neurological outcomes.Most recently, high-quality chest compressions have been defined by the updated 2015 American Heart Association adult guidelines as a depth of 2-2.4 in, full chest recoil, a rate between 100-120 beats per minute, and a chest compression fraction of at least 60%.Even when delivered according to guidelines,cannabis grow supplier external manual chest compressions are inherently inefficient, providing only 30% to 40% of normal blood flow to the brain and less than one third of normal blood flow to the heart.
This inefficiency highlights the need for rescuers to deliver the highest-quality chest compressions in a timely and consistent manner.Although the relationship between high-quality chest compressions and improved survival has been well described, concern remains with the reports of trained rescuers performing suboptimal compression depth, rate, and hands-off fraction time.Rescuer overestimation of depth and underestimation of rate, as well as increased performance fatigue in prolonged situations, may be primary forces in the relatively poor adherence to current guidelines.Real-time, CPR performer feedback via defibrillator has been a relatively recent approach in maintaining chest compression performance and associated with continuous high-quality chest compression.Currently, there are no studies investigating the ability to maintain high-quality chest compressions within the current 2015 AHA guidelines with and without the influence of real-time audiovisual feedback , which may assist in maintaining high-quality chest compression. The goal of this study was to assess the ability to maintain high-quality chest compressions by 2015 updated guidelines both with and without AVF in a simulated arrest scenario.This was a randomized, prospective, observational study conducted within a community hospital with over 22,000 annual inpatient admissions. All participants were voluntary emergency department and medical-surgery nursing staff with both Basic and Advanced Cardiac Life Support certification. We obtained institutional review board approval, and written consent was required prior to participation. We defined CPR providers as a two-person team consisting of one participant performing chest compressions while the second administered ventilations via bag-valve mask. Chest compressions and ventilations were performed on a Little Anne CPR Training Manikin. AVF on chest compression rate and depth was provided to participants through ZOLL See-Thru CPR® on R Series® defibrillators. In a “mock code” scenario, 98 teams were randomly assigned to perform CPR +/- AVF chest compression feedback.
Participants were further randomly assigned to perform either standard chest compressions with a compression-to-ventilation ratio of 30:2 to simulate CPR without an advanced airway or continuous chest compressions to simulate CPR with an advanced airway for a total of four distinct groups.Chest compressions were performed for two minutes, representing a standard cycle interposed between rhythm/pulse checks and/or compressor switch. Defibrillator data for analysis included chest compression rate, depth, and compression fraction over the entire two minutes. The primary outcome measured was ability to maintain high-quality chest compressions as defined by current 2015 AHA guidelines.Secondary outcomes included group differences in chest compression depth, rate, and fraction time. Based on recent findings per Wutzler et al. on the ability to maintain effective chest compressions we estimated a sample size of at least 68 teams to maintain a two-sided alpha of 0.05, and a power of 80%.27 Data are presented as means and standard deviations. We compared CPR variables between respective groups by Mann-Whitney U test or continuous variables and by chi squared test for categorical variables. Only participants with technically adequate data available were used in this comparison. We considered p values < 0.05 statistically significant. No participants were excluded.Previous iterations of the AHA’s CPR and Emergency Cardiovascular Care guidelines have recommended chest compression rate ≥ 100 compression/min; however, the 2015 updates have called for a chest compression-rate upper limit of 120/min. The recommendation appears to be based on both animal studies as well as recent clinical observations from large out-of-hospital cardiac arrest registries describing an association between chest compression rates, return of spontaneous circulation , and survival to hospital discharge.This makes sense as observations in animal studies have described anterograde coronary blood flow as positively correlated with diastolic aortic pressures and subsequently compression rate. However, at rates greater than 120 compressions/min, this relationship weakens as diastolic coronary perfusion time decreases.Regarding human data,cannabis drainage system recent observations from the Resuscitation Outcomes Consortium registry suggest an optimum target of between 100 and 120 compressions per minute.In this randomized, controlled study we report that overall, AVF is associated with a greater ability to provide simultaneously guideline-recommended rate and depth.
This is important as previous studies have focused on the proportion of correct chest compression rate and depth; however, it has been shown that despite adequate individual mean values, the actual proportion of chest compressions that fell within guideline criteria simultaneously for rate and depth was low.Overall comparisons between SC and CCC cohorts were without significant differences in compression dynamics. AVF appeared to have an effect regardless of chest compression strategy, with isolated analysis of both compression strategy groups notable for differences. Within the SC group, significant differences were noted in both average rate and proportion of compressions within current guideline recommendations. Analysis of the CCC cohort was notable for the association with AVF, a greater proportion of compression depth within current guidelines and proportion of time with ideal compressions. One potential explanation for the association between AVF and ability to perform “high quality” chest compressions on a more consistent basis is the ability to possibly avoid early fatigue by “pacing” an individual through the early periods of a highly stressful cardiac arrest situation where one could understandably want to push as fast and hard as possible, which in turn may lead to early fatigue and subsequently “poor quality.”Finally, similar to overall analysis, comparisons between compression strategies without AVF did not result in any significant compression differences. The isolated effect of AVF on compression dynamic overall appears to be related to compression strategy. Within the CCC cohort, the effect appears to be on ability to maintain ideal depth, while in the SC cohort, the effect appears to be related to rate control. We do note that within this cohort, although a statistically significant difference is noted in average rate of compressions, both are within current guidelines. However, it should be noted that the non-AVF cohort demonstrated an average rate at the most upper level of current recommendations, and more importantly was associated with a lower rate of proportion of compressions with rate within guideline recommendations over the testing period. This is important as recent studies have reported an inverse association between compression rates and depth, with rates above 120/min having the greatest impact on reducing compression depth.Recent reports have called this upper rate limit into question and suggest that faster rate limits may be actually associated with a higher likelihood of ROSC in in-hospital cardiac arrest.Unfortunately, in that study compression depth was not reported, leaving optimal rates in in-hospital arrest up to continued debate.Interestingly, within the AVF cohort, chest compression depth appeared to be both deeper on the average and out of guideline recommended depth for the SC cohort. Yet again, these differences did not translate to overall differences in the proportion of time within recommended depth between compression groups. Chest compression strategy and relationship with AVF may be related to the nature of the strategy. That is, with continuous compressions fatigue may become an issue and feedback on depth may be of greater importance over time while bursts of activity after brief pauses with standard compressions may require greater mindfulness in rate of compressions.Finally, we note that although the presence of AVF appears to have improved the quality of chest compressions, proportions of high-quality compressions were surprisingly low between all groups with a high of 25% and nadir of 3.3% 1, 2.
However, our findings are consistent with reported “effective compressions,” i.e., trial period with mean compression rate and depth within guidelines and CCF ≥80% per Wutzler et al. In their simulation-based study, there was an “effective compression” rate of 25.4% with feedback vs. 12.7% without.These findings warrant further investigation into possible influencing factors and sources of variation including fatigue, critical care experience, and time since last training update. The translation of preclinical theories of alcoholism etiology to clinical samples is fundamental to understanding alcohol use disorders and developing efficacious treatments. Human subjects research is fundamentally limited in neurobiological precision and experimental control, whereas preclinical models permit fine grained measurement of biological function. However, the concordance between preclinical models and human psycho pathology is often evidenced by face validity alone. The aim of this study, therefore, is to test the degree to which one prominent preclinical model of alcoholism etiology, the Allostatic Model, predicts the behavior and affective responses of human subjects in an experimental pharmacology design. The Allostatic Model was selected for translational investigation due to its focus on reward and reinforcement mechanisms in early vs. late stages of addiction. In this study, we advance a novel translational human laboratory approach to assessing the relationship between alcohol-induced reward and motivated alcohol consumption. A key prediction of the Allostatic Model is that chronic alcohol consumptions results in a cascade of neuroadaptations, which ultimately blunt drinking-relate hedonic reward and positive reinforcement, while simultaneously leading to the emergence of persistent elevations in negative affect, termed allostasis. Consequently, the model predicts that drinking in late-stage dependence should be motivated by the relief of withdrawal related negative affect, and hence, by negative reinforcement mechanisms. In other words, the Allostatic Model suggests a transition from reward to relief craving in drug dependence. The Allostatic Model is supported by studies utilizing ethanol vapor paradigms in rodents that can lead to severe withdrawal symptoms, escalated ethanol self-administration, high motivation to consume the drug as revealed by progressive ratio breakpoints, enhanced reinstatement, and reduced sensitivity to punishment. Diminished positive reinforcement in this model is inferred through examination of reward thresholds in an intracranial self-stimulation protocol. Critically, these allostatic neuroadaptations are hypothesized to persist beyond acute withdrawal, producing state changes in negative emotion ality in protracted abstinence. Supporting this hypothesis, exposure to chronic ethanol vapor produces substantial increases in ethanol consumption during both acute and protracted abstinence periods.. Despite strong preclinical support, the Allostatic Model has not been validated in human populations with AUD.Decades of human alcohol challenge research has demon strated that individuals differences in subjective responses to alcohol predict alcoholism risk. The Low Level of Response Model suggests that globally decreased sensitivity to alcohol predicts AUD. Critically however, research has demonstrated that SR is multi-dimensional. The Differ entiator Model as refined by King et al suggests that stimulatory and sedative dimensions of SR differentially predict alcoholism risk and binge drinking behavior. Specifically, an enhanced stimulatory and rewarding SR, particularly at peak BrAC is associated with heavier drinking and more severe AUD prospectively.