Epinephrine in Resuscitation: Curse or Cure?

Attaran, Robert R.; Ewy, Gordon A.

doi:10.2217/fca.10.24

Cited by 24 publications

(14 citation statements)

References 102 publications

(26 reference statements)

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“…In our study, mean and diastolic CAP and CBF increased only after adrenaline was administered. Adrenaline restores cardiac function by increasing cardiac contractility (via β-adrenergic receptors) and peripheral vasoconstriction (via α-adrenergic receptors), consequently increasing venous return (20). It is unknown whether increased cardiac contractility or peripheral vasoconstriction has the greatest influence, although the peripheral vascular bed should be maximally vasoconstricted in response to the asphyxia.…”

Section: Discussionmentioning

confidence: 99%

Effects of chest compressions on cardiovascular and cerebral hemodynamics in asphyxiated near-term lambs

et al. 2015

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Background: Chest compressions (CC) and adrenaline administration are recommended in asphyxiated newborns with persistent bradycardia despite effective ventilation. The effects of CC on cerebral blood flow in newborns at birth are unknown. Our aim was to determine the effects of CC, with or without adrenaline administration, on the return of spontaneous circulation, carotid blood flow (CBF), and carotid arterial pressure (CAP) in asphyxiated near-term lambs. Methods: Asphyxia was induced in near-term lambs by clamping the umbilical cord and delaying ventilation onset until spontaneous circulation ceased. Lambs were then resuscitated by positive pressure ventilation along with CC followed by adrenaline administration. CAP and CBF were continuously recorded. results: Mean CAP did not increase significantly during CC and only increased following adrenaline administration. CC did not increase mean CBF but increased CBF amplitude due to increased peak flow and the onset of retrograde flow during diastole. Adrenaline increased mean CBF from 1 ± 2 to 15 ± 5 ml/kg/min and abolished retrograde diastolic CBF, leading to the return in spontaneous circulation. conclusion: We conclude that CC with adrenaline administration was required to increase CBF and restore spontaneous circulation in asphyxiated lambs. Low CBF and retrograde diastolic CBF during CC indicate hypoperfusion to the brain. a pproximately 5% of all newborns worldwide will require some form of assisted ventilation at birth and about 0.03% of newborns will require more advanced resuscitation such as intubation, chest compressions (CCs), and drug administration (1,2). Severely asphyxiated newborn infants are born bradycardic and apneic and require resuscitation to establish pulmonary gas exchange and restore cardiac function after birth. As the initiation of ventilation and the establishment of a functional capacity also trigger the increase in pulmonary blood flow at birth, it plays a dual role in severely asphyxiated newborn infants (3). That is, it is responsible for both increasing oxygenation and for facilitating the increase in cardiac output by providing preload for the left ventricle (3,4). If low cardiac output persists despite effective positive pressure ventilation, the newborn is likely to suffer increasingly severe hypoxia and acidemia, leading to hypoxic/ischemic injury. Continued asphyxia further depresses myocardial function, leading to low systolic and diastolic blood pressures despite a chemoreceptor-mediated peripheral vasoconstriction (5,6). Current international neonatal resuscitation guidelines recommend that if heart rate is less than 60 BPM despite effective positive pressure ventilation, CCs should be applied (7,8). CC will assist to mechanically pump blood until the myocardium is sufficiently oxygenated to recover spontaneous function (9). If heart rate remains below 60 BPM despite effective CC, then adrenaline should be administered (7,8).Given the infrequent use of CC and adrenaline, rigorous clinical studies to optimize CC and adren...

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Section: Discussionmentioning

confidence: 99%

Effects of chest compressions on cardiovascular and cerebral hemodynamics in asphyxiated near-term lambs

et al. 2015

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“…[13] It is a non-selective alpha and beta adrenergic agonist, and its value in resuscitation is due largely to the alpha-1 receptor mediated vasoconstrictive activity. [14] Alpha-1 activity increases diastolic blood pressure, which leads to increased coronary perfusion, as the coronary arteries receive blood during diastole. Yet, despite its long time use and incorporation into guidelines, epinephrine suffers from a paucity of evidence regarding its influence on survival.…”

Section: Introductionmentioning

confidence: 99%

Epinephrine in out-of-hospital cardiac arrest:A critical review

Reardon¹,

Magee²

2013

World Journal of Emergency Medicine

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BACKGROUND:Epinephrine is recommended in advanced cardiac life support guidelines for use in adult cardiac arrest, and has been used in cardiopulmonary resuscitation since 1896. Yet, despite its long time use and incorporation into guidelines, epinephrine suffers from a paucity of evidence regarding its influence on survival. This critical review was conducted to address the knowledge deficit regarding epinephrine in out-of-hospital cardiac arrest and its effect on return of spontaneous circulation, survival to hospital discharge, and neurological performance.METHODS:The EMBASE and MEDLINE (through the Pubmed interface) databases, and the Cochrane library were searched with the key words “epinephrine”, “cardiac arrest” and variations of these terms. Original research studies concerning epinephrine use in adult, out-of-hospital cardiac arrest were selected for further review.RESULTS:The search yielded nine eligible studies based on inclusion criteria. This includes five prospective cohort studies, one retrospective cohort study, one survival analysis, one case control study, and one RCT. The evidence clearly establishes an association between epinephrine and increased return of spontaneous circulation, the data were conflicting concerning survival to hospital discharge and neurological outcome.CONCLUSIONS:The results of this review exhibit the paucity of evidence regarding the use of epinephrine in out of hospital cardiac arrest. There is currently insufficient evidence to support or reject its administration during resuscitation. Larger sample, placebo controlled, double blind, randomized control trials need to be performed to definitively establish the effect of epinephrine on both survival to hospital discharge and the neurological outcomes of treated patients.

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“…22 Sustained or excessive activation of b 1 -adrenoceptors has been shown to cause apoptosis in cardiomyocytes. 23 Activation of b 1 -adrenoceptors also increases myocardial oxygen demand and promotes arrhythmia, 24,25 whereas activation of a 1 -adrenoceptors has been shown to induce prolonged vasoconstriction and ischaemia. 5,26 In the present study, the responses to adrenaline injections within the first 30 min were sympathetic vasoconstriction and increased HR, which caused transient hypertension.…”

Section: Discussionmentioning

confidence: 99%

“…Gasometry was performed using an ABL555 blood gas analyser (Radiometer America, Westlake, OH, USA). Lung compliance and airway pressure were measured continuously and recorded from anesthesia workstation (Primus Dr€ ager) at baseline and at 5,10,15,20,25,30,40,50, 60, 90, 120, 150, 180, 210, 240, 300, 330 and 360 min. The pulmonary shunt and AaDO 2 were calculated using standard formulae 50 (Fig.…”

Section: Measurement and Sampling Time Pointsmentioning

confidence: 99%

Myocardial protection induced by fentanyl in pigs exposed to high‐dose adrenaline

Luz¹,

Otsuki

Gonzalez³

et al. 2015

Clin Exp Pharma Physio

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The use of high doses of adrenaline is common in critical patients, especially during cardiac arrest. During these situations, myocardial dysfunction can be a result of multiple factors, including adrenaline use. In addition, opioids have been shown to have anti-arrhythmic and anti-ischemic mechanisms that may confer cardiac protection. This study aimed to evaluate the effects of fentanyl on myocardial function in pigs exposed to high-dose adrenaline. After institutional ethics committee approval, 26 pigs were randomly allocated to receive either 20 μg/kg fentanyl (n = 10; fentanyl group) administered 5 min before five doses of adrenaline (20 μg/kg), equivalent-volume saline (n = 10; saline group) using the same adrenaline dosing protocol, or neither fentanyl nor adrenaline (n = 6; sham group). The fentanyl group showed lower levels of troponin at the end of the sixth hour compared with the saline group (1.91 ± 1.47 vs 5.44 ± 5.35 ng/mL, P = 0.019). Transmission electron microscopy and immunohistochemistry also showed less myocardial injury in the fentanyl group. The conclusion was reached that fentanyl attenuates myocardial injury caused by high-dose adrenaline without blunting the hemodynamic effect of adrenaline.

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Epinephrine in Resuscitation: Curse or Cure?

Cited by 24 publications

References 102 publications

Effects of chest compressions on cardiovascular and cerebral hemodynamics in asphyxiated near-term lambs

Effects of chest compressions on cardiovascular and cerebral hemodynamics in asphyxiated near-term lambs

Epinephrine in out-of-hospital cardiac arrest:A critical review

Myocardial protection induced by fentanyl in pigs exposed to high‐dose adrenaline

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