10 hours ago · In conclusion, we have described a case of cardiovascular crisis which took place after a small amount of epinephrine was injected in a healthy patient without any heart disease. The complex cardiovascular interactions of treatment with β-blockers and, possibly, lidocaine, must be appreciated in order to prevent severe complications such as pulmonary edema and … >> Go To The Portal
After local application of 0.01% epinephrine-soaked nasal pledgets and infiltration of 3 mL 0.001% epinephrine, the patient developed a severe hypertension of 205/126 mmHg, followed by ventricular tachycardia. Cardiac arrest ensued after intravenous injection of lidocaine and esmolol in an attempt to control ventricular arrhythmia.
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In conclusion, we have described a case of cardiovascular crisis which took place after a small amount of epinephrine was injected in a healthy patient without any heart disease.
Epinephrine still has a role in the treatment of cardiac arrest; the best way to use epinephrine remains uncertain. Epinephrine still has a role in the treatment of cardiac arrest; the best way to use epinephrine remains uncertain. Epinephrine for cardiac arrest: knowns, unknowns and controversies Curr Opin Crit Care.
Ristagno G, Tang W, Huang L, Fymat A, Chang YT, Sun S, et al. Epinephrine reduces cerebral perfusion during cardiopulmonary resuscitation. Crit Care Med. 2009;37:1408–1415. [ PubMed] [ Google Scholar] 18.
Yet, despite its long time use and incorporation into guidelines, epinephrine suffers from a paucity of evidence regarding its influence on survival.
A further risk to the cardiac patient is the ability of epinephrine to irritate cardiac pacemaker cells and cause dysrhythmias. Thus, the injudicious use of epinephrine can be harmful to a patient with cardiac disease.
Purpose of review: Epinephrine is the primary drug administered during cardiopulmonary resuscitation (CPR) to reverse cardiac arrest. Epinephrine increases arterial blood pressure and coronary perfusion during CPR via alpha-1-adrenoceptor agonist effects.
The maximum dose of epinephrine in local anaesthesia for a healthy subject is 0.2 mg, though this can be lowered to 0.04 mg if patient has severe cardiovascular disease (ASA III and IV) [11].
Hence, epinephrine causes constriction in many networks of minute blood vessels but dilates the blood vessels in the skeletal muscles and the liver. In the heart, it increases the rate and force of contraction, thus increasing the output of blood and raising blood pressure.
There are no absolute contraindications against using epinephrine. Some relative contraindications include hypersensitivity to sympathomimetic drugs, closed-angle glaucoma, anesthesia with halothane. Another unique contraindication to be aware of is catecholaminergic polymorphic ventricular tachycardia.
Administer first dose of epinephrine after the second defibrillation.
According to the literature reviewed, the use of 1 to 2 cartridges of local anesthetics with 1:80,000, 1:100,000 or 1:200,000 epinephrine in patients with controlled Hypertension and/ or Coronary disease is safe.
Addition of adrenaline to local anaesthetic solution is contraindicated for the following diseases like heart diseases, untreated or uncontrolled severe hypertension, uncontrolled hyperthyroidism, uncontrolled diabetes etc.
The added risks attributed to the use of epinephrine in hypertensive patients include: Through the direct action of epinephrine-greater probability of acute hypertensive crisis (dangerously high blood pressure), angina pectoris and myocardial infarction, as well as cardiac arrthymias.
Adrenaline (epinephrine) reacts with both α- and β-adrenoceptors, causing vasoconstriction and vasodilation, respectively.
Clinical studies suggest that epinephrine facilitates ventricular fibrillation (VF) although mechanisms remain unclear. We tested the hypothesis that epinephrine increases the probability of inducing VF and stabilizes VF in association with shortening of fibrillation action potential duration.
Epinephrine injection is indicated in the emergency treatment of type I allergic reactions, including anaphylaxis. It is also used to increase mean arterial blood pressure in adult patients with hypotension associated with septic shock.
Epinephrine has been the cornerstone of cardiac resuscitation and advanced cardiac life support (ACLS) from the birth of modern cardiopulmonary resuscitation (CPR) in the early 1960s.[4] The provision of epinephrine is currently suggested by both the American Heart Association (AHA) and the European Resuscitation Council in both shockable and nonshockable rhythms.[5] Epinephrine is vital to improving the return of spontaneous circulation (ROSC). However, standard-dose epinephrine does not increase and may actually reduce long-term survival and neurological recovery after CPR.
Epinephrine is the primary drug administered during cardiopulmonary resuscitation (CPR) to reverse cardiac arrest. The evidence for the use of adrenaline in out-of-hospital cardiac arrest (OHCA) and in-hospital resuscitation is inconclusive. We conducted a systematic review on the clinical efficacy of adrenaline in adult OHCA patients to evaluate whether epinephrine provides any overall benefit for patients.
Sudden cardiac arrest causes 544,000 deaths in China each year, with survival occurring in <1% of cases (compared with 12% in the United States). The American Heart Association recommends the use of epinephrine in patients with cardiac arrest, as part of advanced cardiac life support. There is a clear evidence of an association between epinephrine and increased return of spontaneous circulation (ROSC). However, there are conflicting results regarding long-term survival and functional recovery, particularly neurological outcome, after CPR. There is currently insufficient evidence to support or reject epinephrine administration during resuscitation. We believe that epinephrine may have a role in resuscitation, as administration of epinephrine during CPR increases the probability of restoring cardiac activity with pulses, which is an essential intermediate step toward long-term survival.
A higher rate of prehospital ROSC in the epinephrine group while no difference in survival to discharge
Epinephrine increases coronary perfusion pressure by decreasing blood flow to all other organs, an effect that may persist after the restoration of pulses.[12] On the basis of observational data and limited clinical trials, standard-dose epinephrine does not increase and may actually reduce long-term survival and neurological recovery after CPR.[11] Potentially harmful effects are α- and β-receptor mediated and include reduced cerebral microvascular blood flow and exacerbation of neurological outcome. Cardiovascular instability, such as increased myocardial work and increased risk of tachydysrhythmia, promotes thrombogenesis and platelet activation after ROSC and adverse immunomodulatory and metabolic effects.[10,12,20] Experimental studies have shown that β-blocker treatment may mitigate some of these deleterious effects.[21] An animal study indicated that epinephrine reduced capillary blood flow in swine brain.[22] Epinephrine-induced cerebral hypoperfusion persisted during CPR was attributable to the α-1 agonist effects of reduced cerebral microcirculatory blood flow and increased cerebral ischemia, determined by decreased brain tissue pO2and increased pCO2.[4] Epinephrine also has adverse effects on myocardium mediated by β-receptor stimulation.[4] Epinephrine impairs myocardial function despite increasing coronary perfusion pressure.[4] Epinephrine is known to increase the frequency of transitions from PEA to ROSC and extend the time window for the development of ROSC at a cost of greater cardiovascular instability after ROSC, with a higher rate of rearresting.[23] Similarly, the total dose of epinephrine is associated with impaired lactate clearance for hours and gastric mucosal perfusion after CPR in humans.[11,12]
Overall and neurologically intact survival at 1 month or at discharge
Survival to hospital discharge, to 30 days, and to 90 days; neurological performance
Dumas notes that this study underscores the need for caution when using epinephrine. Administering epinephrine to patients in cardiac arrest has been shown to improve ROSC, but the new study adds to mounting evidence suggesting the drug harms patients’ chances of surviving past the post-resuscitation period with brain function intact.
For patients in cardiac arrest, administering epinephrine helps to restart the heart but may increase the overall likelihood of death or debilitating brain damage, according to a study published Dec. 1 the Journal of the American College of Cardiology.
Timing also appears to be an important factor. Patients receiving epinephrine in the later stages of resuscitation were more likely to die than those who got their first epinephrine dose shortly after collapsing. The adverse effects of epinephrine appeared to be unaffected by the use of post-resuscitation medical treatments, such as techniques to cool the body to reduce tissue damage or interventions to restore the flow of blood through blocked arteries.
The American Heart Association recommends the use of epinephrine in patients with cardiac arrest, as part of advanced cardiac life support. There is a clear evidence of an association between epinephrine and increased return of spontaneous circulation (ROSC). However, there are conflicting results regarding long-term survival ...
We believe that epinephrine may have a role in resuscitation, as administration of epinephrine during CPR increases the probability of restoring cardiac activity with pulses, which is an essential intermediate step toward long-term survival.
However, it appears that the use of adrenaline is associated with no benefit on survival to hospital discharge or survival with favorable neurological outcome after OHCA, and it may have a harmful effect. Larger placebo-controlled, double-blind, randomized control trials are required to definitively establish the effect of epinephrine.
The administration of adrenaline was associated with improved short-term survival (ROSC). However, it appears that the use of adrenaline is associated with no benefit on survival to hospital discharge or survival with favorable neurological outcome after OHCA, and it may have a harmful effect.
However, it appears that the use of adrenaline is associated with no benefit on survival to hospital discharge or survival with favorable neurological outcome after OHCA, and it may have a harmful effect. Large …. The administration of adrenaline was associated with improved short-term survival (ROSC). However, it appears that the use of adrenaline ...