The Efficacy of Epinephrine in Cardiac Arrest - Literature review Example

An Emergency Medical Intervention Analysis Name Institution Date An Emergency Medical Intervention Analysis Part A The Efficacy of Epinephrine in Cardiac Arrest Epinephrine produces beneficial effects during a cardiac arrest due to its α-adrenergic receptor-stimulating aspects which increase both coronary and cerebral perfusion pressure during Cardiopulmonary resuscitation (CPR). Accordingly, the efficacy of epinephrine in cardiac arrest results from the ability of this drug to increase aortic blood pressure and hence this increases coronary perfusion pressure when the chest compresses (Sunde, et al, 2012). In case CPR fails to produce coronary perfusion pressure higher than 15-20 mm Hg, the cardiac mechanical activity hardly ever returns or never takes place. The capacity of epinephrine to elevate coronary perfusion during CPR has been validated and therefore administration of epinephrine during CPR elevates the likelihood of cardiac activity pulses restoration, which is a fundamental transitional step towards lasting survival of the patients with cardiac arrest (Wik, 2006). However, restoration of pulses following a cardiac arrest is probably an instant step towards recovery but it does not warrant good patient results. Still, the importance as well as safety of β-adrenergic results of epinephrine is contentious since these effects can increase myocardial work and consequently decrease subendocardial perfusion. With this in mind, this narrative refutes the continued use of epinephrine in cardiac arrest. According to Dumas (2010), induced hypothermia along with integrated care plans have augmented the percentage of patients who hospitalized following CPR who stay alive and are discharged from the hospital. Such experiences have raised prospects that resuscitation treatments, such as epinephrine are supposed to improve not only short-term results like pulses return but should also enhance longer-term as well as patient-centered results, for instance functional status and also quality of life (Steen, et al, 2009). Additionally, according to a study done by Hagihara et.al (2012), pre-hospital administration of epinephrine, in spite of escalating the rates of pulse return (18% vs 5%), is linked to a more modest rise in the number of patients who survive after one month (5.4% vs 4.7%) and reduced rates of good functional status. When regulated for imperative covariates or when utilizing predisposition-matched cases, the probability of one-month survival along with improved functional status were noticeably lower within patients who had been treated using epinephrine (probability ratios, 0.21 to 0.71). These results were validated in a variety of sensitivity analyses that accounted for in-hospital epinephrine usage as well as CPR interval. Accordingly, the link of pre-hospital epinephrine with worse significant results seems to be existent and robust (Dumas, et al, 2010). Therefore, in case such observations are valid, pre-hospital epinephrine usage increases morbidity as well as mortality following pulses restoration to a level that more than counteracts its immediate benefits. This contradictory effect can be allied to epinephrine’s mechanism of action. Epinephrine elevates CPR-produced aortic pressures through vasoconstriction that is mediated by α-adrenergic receptor-stimulating aspects (Holmberg, et al, 2002). Consequently, epinephrine elevates coronary perfusion pressure through reducing flow of blood to other organs, and such an effect can continue after pulses are restored. Laboratory studies have shown that epinephrine impairs cerebral microcirculation during and also after CPR (Annet, 2008). In addition, the total epinephrine dose is linked to impaired tissue oxygen use in as well as impaired lactate clearance for hours following CPR in human beings. These studies show that epinephrine offers a short-term benefit during a cardiac arrest through incurring a metabolic debt from the body along with the brain and the debt might be too high for several patients (Martens, & Vandyycke, 2007). Furthermore, there are other post-CPR adverse effects of epinephrine use which consist of β-adrenergic stimulation, which prompts dysrhythmias and also raises myocardial oxygen demand. Additionally, epinephrine activates platelets as well as coagulation (Larsson, et al, 1989). Stimulating a pro-thrombotic state might worsen myocardial ischemia, which is the major cause of cardiac arrest. Earlier observational studies have discovered that elevating epinephrine dosage results into worse survival or neurological result following cardiac arrest. Nonetheless, the studies have had restricted influence on practice since sicker patients who never responded to treatment methodically were administered with more epinephrine (Sunde, et al, 2007). Moreover, randomized clinical trial data does not support positive outcome of epinephrine on patient-oriented results. Epinephrine dose higher than 1 mg did not produce incremental rise in survival to hospital release, even in cases where higher doses of epinephrine increased the rate of pulses return (Hagihara, 2012). Two latest randomized trials established no survival increase when epinephrine was administered during out-of-hospital cardiac arrest in spite of an immediate increase in pulses’ return. The first trial evaluated survival when out-of-hospital cardiac arrest patients took intravenous drugs from paramedics while others did not take intravenous drugs. The other trial evaluated survival when patient were administered with standard 1-mg epinephrine boluses while the others were administered with placebo (Jacobs, et.al, 2011). Indicating the disinclination of abandoning convectional treatments, out-of-hospital emergency staffs within the two studies were hesitant of withholding drugs or epinephrine in a cardiac arrest during the trial and went back to using epinephrine after the trials as usual therapy even though during the trial the results indicated that epinephrine did not have benefits (Sunde, et al, 2007). The common argument to administer repetitive epinephrine doses is that pulses’ restoration is a fundamental step towards long-term survival of patient with cardiac arrest. In pulses’ restoration is successful, then probably better intensive care can repeal the damage or reinstate the deficits that result from elevated flow of blood to the heart at the expense of other body organs. Hagihara et.al (2012) was unable to evaluate in-hospital intensive case, but this study implies that intensive care was reasonably constant when the study was conducted. Additionally, the constant epinephrine usage has been supported since some patient recovered after epinephrine is administered. Therefore, it is necessary that future researches to establish of there are subsets of patient whom epinephrine usage in a cardiac arrest is actually beneficial. The best observational evidence that is available illustrates that epinephrine usage in cardiac arrest might be harmful to patients during and there are conceivable biological reasons supporting this observation (Tang, et al, 2009). In conclusion, basing on findings reported be several studies, epinephrine usage during a cardiac arrest should be refuted. Part B Annet, C. (2008). The Efficacy of Epinephrine or Vasopressin for Resuscitation during Epidural Anesthesia. Summa Health System. The source compared the efficacy of epinephrine or vasopressin for resuscitation during epidural anesthesia and the results indicated that epinephrine use in cardiac arrest normally results into adverse effects such as acidosis, increased cardiac oxygen use and do not improve survival of the patient and hence provided valuable information regarding efficacy of epinephrine in cardiac arrest Abstract During epidural anesthesia, CPR is regarded as complex due to reduced coronary pressure. The efficacy of epinephrine and vasopressin in such a setting is not known. During this study, 30 minutes prior to cardiac arrest initiation, sixteen pigs were administered with epidural anesthesia with bupivacaine whereas the other twelve pigs were administered with saline epidurally (Annet, 2008). Throughout basic life-support CPR, coronary perfusion pressure was considerably lesser following epidural bupivacaine administration as compared to epidural saline administration. Following impulsive circulation return, bradycardia necessitated treatment within animals that had been administered with vasopressin, in particular with epidural anesthesia. Systemic acidosis was elevated within animals that had been administered with epinephrine as compared to those administered with vasopressin, irrespective of whether epidural anesthesia was present or not (Annet, 2008). Introduction/Background/Literature Review Long epidural anesthesia along with sympathetic blockage results to vasodilation of the arteries and hence reduced arterial pressure. Additionally, sympathetic blockage hinders efficient baroreceptor-driven cardio-circulatory compensation and this leads to low arterial pressure without fast heart pulses. Venodilation, in particular of the splanchnic circulation, reduces cardiac filling, and might prompt additional sympathetic withdrawal as well as vagal hyperactivity (Annet, 2008). These mechanisms can cause abrupt cardiovascular fail during epidural blockage indicating a disastrous problem of local anesthesia. Additionally, the efficacy of epinephrine during CPR is contentious. Within experimental CPR studies, epinephrine is linked to increased myocardial oxygen use, ventricular arrhythmia, ventilation-perfusion defect, in addition to worse postresuscitation myocardial dysfunction (Annet, 2008). Aims and Objectives To examine the effects of epinephrine as compared to that of vasopressin on coronary perfusion pressure with and with no epidural anesthesia and ensuing cardiac arrest (Annet, 2008). Methodology Dilutions of both vasopressin and epinephrine was done to 10 mL with normal saline and afterward injected into the right atrium. Researchers collecting data and carrying out CPR were blinded to the vasopressor’s identity. Measurement of hemodynamic variable was done after cardiac arrest was induced, following 3 minute of CPR, and 90 seconds and 5 minutes following every drug administration. Following 19 minute of cardiac arrest up to five counter-shocks were administered. Within the post-resuscitation duration, measurement of hemodynamic variables was done at 5th, 15th, 30th, and 60th minute following spontaneous circulation return. When the experimental protocol ended, the animals were killed and necropsied (Annet, 2008). ECG signal recording and analysis was done. One-way analysis of variance was utilized in determining statistical significance between groups. Variance analysis was utilized in identifying statistically significant variations between epinephrine groups and vasopressin groups (Annet, 2008). Sample 28 healthy, 12–16 wk-old Tyrolean domestic pigs of either gender weighing 35–45 kg (Annet, 2008). Ethics Approval was granted the Austrian Federal Animal Investigational Committee and the study was carried out in accordance with Utstein-style guiding principles (Annet, 2008). Data Analysis/Results/Findings Prior to administering epidural block, there were no weight, hemodynamic variables as well as blood gases variations between groups. 30 minutes after bupivacaine or saline was administered epidurally, mean arterial pressure, coronary perfusion pressure in addition to systemic vascular resistance reduced with about 20-30 percent within animals that received epidural bupivacaine and the value were considerably lesser when compared to animals that received epidural saline (Annet, 2008). Within control animals, the first vasopressin dosage generated a considerably higher increase within coronary perfusion when compared with epinephrine. Additionally, coronary pressure was notably higher within animals that received vasopressin five minutes after the 1st, 2nd, and 3rd vasopressin administration in comparison to epinephrine during those times. After eighteen minutes of CPR, six of six animals that had been administered with vasopressin and two of the six animals that had been treated with epinephrine had return of impulsive cardiac blood circulation and also survived the sixty minute post resuscitation phase (Annet, 2008). This indicates that survival rate when epinephrine is used is much lower when compared to vasopressin and so is return of spontaneous cardiac blood circulation (Geocadin, et al, 2011). Qualitative Studies This is a qualitative study. Discussion The results of the study show that closed-chest CPR is modestly successful following epidural anesthesia administration. However, epinephrine and also vasopressin generate preliminary elevations within coronary perfusion pressure. Nonetheless, treatment using epinephrine causes severe metabolic acidosis as compared to vasopressin (Geocadin, et al, 2011). Coronary perfusion response to epinephrine disappeared in epidural and control animals, in five minutes while vasopressin response continued. Accordingly, vasopressin appears to be a better vasopressin during CPR. The results also indicated that there animals that received vasopressin had better survival trend, irrespective of the condition of epidural block (McGeorge, et al, 1994). Within a laboratory study, administering vasopressin led to increased systemic blood pressure but a momentarily lesser cardiac index throughout early post-resuscitation in comparison to epinephrine. In this study, myocardial function following administration of vasopressin was similar to pre-arrest values, while animals administrated with epinephrine suffered tachycardia and had hypertension throughout post-resuscitation period. This can be allied to too much β-stimulation when epinephrine was administered (Geocadin, et al, 2011). Limitations The pathophysiologic cause of epidural cardiac arrest within the clinical setting might vary from the study’s laboratory model (Sterz, et al, 1998). Additionally, limitations of the study design consist of lack of evaluation of levels of bupivacaine in addition to that, the study lacked dose-response data. Conclusion Therefore, the conclusion of this study is that vasopressin is a better vasopressin during a cardiac arrest since the response to a sole dose lasts longer, and also acidosis in epinephrine is extremely severe following multiple doses while in vasopressin acidosis is less severe. Overall Judgment Epinephrine and vasopressin increases coronary perfusion pressure. However, vasopressin is better during epidural block since the response to one dosage lasts longer and also because epinephrine causes severe acidosis following multiple dosages while acidosis is less severe when vasopressin is used (Geocadin, et al, 2011). Jacobs, I, et.al. (2011). Effect of epinephrine on survival in out-hospital cardiac arrest: A randomized double-blind placebo controlled trial. Resuscitation. Vol. 82/1138-1143. This source was selected because it is a thoroughly conducted and effectively powered clinical trial that compares epinephrine with placebo during a cardiac arrest. The results of the study indicate epinephrine does not make any difference in survival and thus supports the stand that its continued use in cardiac arrest should be refuted. Abstract/Summary There is inadequate evidence from clinical trials that using epinephrine in treatment of cardiac arrest enhances survival in spite of epinephrine being regarded as standard of care for a long time. The study was performed to establish the effect of epinephrine on patient survival to hospital discharge in out of hospital cardiac arrest. A double blind randomized placebo controlled trial of epinephrine in out-of-hospital cardiac arrest was performed. Preparation of matching study vials with either epinephrine 1:1000 or placebo was done and patients were randomly allotted to get 1 ml aliquots of the trial drug (epinephrine). Results examined encompassed survival to hospital discharge, pre-hospital return of spontaneous circulation in addition to neurological result. Screening of 4103 cardiac arrests was done during the study where 601 went randomization (Jacobs, et.al, 2011). Introduction/Background/Literature Review Cardiac arrest happening out of hospital is a considerable public health subject. The routine utilization of epinephrine in cardiac arrest treatment has been supported for a long time. Laboratory studies have demonstrated that epinephrine enhances both coronary and cerebral perfusion (Paradis, et al, 1990). A meta-analysis of higher dosage of epinephrine indicated improved return of spontaneous circulation but there was no effect in survival to hospital release. Epinephrine has been associated with adverse outcomes on post cardiac arrest myocardial function as well as cerebral microcirculation and hence this study was conducted to address this issue (Jacobs, et.al, 2011). Aims and Objectives To examine the effect of epinephrine on patient survival to hospital discharge in out of hospital cardiac arrest (Jacobs, et.al, 2011). Methodology A double blind randomized placebo controlled trial of epinephrine in out-of-hospital cardiac arrest was performed. Preparation of equivalent research vials with either epinephrine 1:1000 or placebo (sodium chloride 0.9%) was done. Random allocation of patient was done for them to get 1 ml aliquots of the epinephrine in accordance with advanced life support instructions. Results that were evaluated encompassed survival to hospital discharge, pre-hospital return of spontaneous circulation in addition to neurological result (Jacobs, et.al, 2011). Sample The study sample size for each group was 2213 patient where the total number of patients that were enrolled in this study was 5000 (Jacobs, et.al, 2011). Data Collection Demographic and clinical data for each and every cardiac arrest patient was recorded manually and after review it was entered into the SPSS statistical package. All records were then linked to information obtained through the ambulance service computer aided dispatch system (Jacobs, et.al, 2011). Ethics Before carrying out this study, approval was sought from the Human Research Ethics Committee of the University of Western Australia and waiver approval was given. Registration of the research was done with the Australian and New Zealand Clinical Trials Register (Jacobs, et.al, 2011). Data Analysis/Results/Findings The study results indicated epinephrine resulted in a statistically significant improvement in regard to survival to hospital release even though there was a considerably enhanced probability of accomplishing pre-hospital return of spontaneous circulation. Nonetheless, just two survivors who showed a poor neurological result had been administered with epinephrine. These findings match other observational researches as well as non-randomized trials in that epinephrine does not improve survival to hospital discharge (Jacobs, et.al, 2011). Quantitative Studies This is a quantitative study. Discussion, Conclusion and Limitations Usage of epinephrine in cardiac arrest considerably enhances the percentage of patients attaining pre-hospital return of spontaneous circulation but does not improve survival to hospital release. The limitation of this study was inadequate sample size (Zaritsky, et al, 2005). Overall Judgment The results of this study are relatively valid because other previous studies support the study findings (Tang, et al, 2009). References Annet, C. (2008). The Efficacy of Epinephrine or Vasopressin for Resuscitation during Epidural Anesthesia. Summa Health System. Cifu, A, & Ioannidis, J. (2012). Reversals of established medical practices: evidence to abandon ship.  JAMA. Vol. 307(1):37-38. Dumas, F, et al.  (2010). Immediate percutaneous coronary intervention is associated with better survival after out-of-hospital cardiac arrest: insights from the PROCAT (Parisian Region Out of Hospital Cardiac Arrest) registry.  Circ Cardiovasc Interv. Vol. 3(3):200-207. Geocadin, G, et al. (2011). American Heart Association Emergency Cardiovascular Care Committee; Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation.  Primary outcomes for resuscitation science studies: a consensus statement from the American Heart Association.  Circulation. Vol. 124(19):2158-2177.Prasad, V, Hagihara, A, et.al. (2012). Prehospital epinephrine use and survival among patients with out-of- hospital cardiac arrest.  JAMA. Vol. 307(11):1161-1168. Holmberg, M, et al. (2002). Low chance of survival among patients requiring adrenaline (epinephrine) or intubation after out-of-hospital cardiac arrest in Sweden.  Resuscitation. Vol. 54 (1):37-45. Jacobs, I, et.al. (2011). Effect of epinephrine on survival in out-hospital cardiac arrest: A randomized double-blind placebo controlled trial. Resuscitation. Vol. 82/1138-1143. Larsson, P, et al. (1989). Altered platelet function during mental stress and adrenaline infusion in humans: evidence for an increased aggregability in vivo as measured by filtragometry.  Clin Sci (Lond). Vol. 76 (4):369-376. Martens, P, & Vandyycke, C. (2007). Effects of epinephrine and vasopressin on cerebral microcirculatory flows during and after cardiopulmonary resuscitation. Crit Care Med. Vol. 35:2145-2149. McGeorge, T, et al. (1994). The effect of the total cumulative epinephrine dose administered during human CPR on hemodynamic, oxygen transport, and utilization variables in the postresuscitation period.  Chest. Vol. 106(5):1499-1507. Paradis, N, et al.  (1990). Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation.  JAMA. Vol. 263(8):1106-1113. Redding, S, & Pearson W. (1968). Resuscitation from ventricular fibrillation: drug therapy.  JAMA. Vol. 203(4):255-260. Steen, A, et al. (2009). Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.  JAMA. Vol. 302(20):2222-2229. Sterz, F, et al. (1998). Cumulative epinephrine dose during cardiopulmonary resuscitation and neurologic outcome.  Ann Intern Med. Vol. 129(6):450-456 Sunde, K, et al (2012). Outcome when adrenaline (epinephrine) was actually given vs. not given—post hoc analysis of a randomized clinical trial.  Resuscitation. Vol. 83(3):327- 332. Sunde, K, et al. (2007).  Implementation of a standardized treatment protocol for post resuscitation care after out-of-hospital cardiac arrest.  Resuscitation. Vol. 73(1):29-39. Tang, W, et al. (2009). Epinephrine reduces cerebral perfusion during cardiopulmonary resuscitation.  Crit Care Med. Vol. 37(4):1408-1415. Wik, L. (2006). Haemodynamic effects of adrenaline (epinephrine) depend on chest compression quality during cardiopulmonary resuscitation in pigs. Resuscitation. Vol. 2006; 71:369- 378. Zaritsky, et al. (2005). The evidence evaluation process for the 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation. Vol. 67:167-170. Read More