Abstract:Repetitive intravenous adrenaline doses increased ABP's and to some extent also CePP, but significantly decreased organ and brain perfusion. The institutional protocol number: Malmö/Lund Committee for Animal Experiment Ethics, approval reference number: M 192-10.
“…While epinephrine increases systemic arterial blood pressure, there are conflicting experimental results regarding its effect on cerebral blood flow (CBF) and cerebral tissue oxygenation. Specifically, animal studies have demonstrated both increases [13][14][15][16][17] and decreases [18][19][20][21] in various measurements of CBF following epinephrine administration during CPR. Maintaining CBF during CPR is an important physiologic target to minimize potentially devastating effects of cerebral hypoperfusion during this vulnerable period.…”
Background
Despite controversies, epinephrine remains a mainstay of cardiopulmonary resuscitation (CPR). Recent animal studies have suggested that epinephrine may decrease cerebral blood flow (CBF) and cerebral oxygenation, possibly potentiating neurological injury during CPR. We investigated the cerebrovascular effects of intravenous epinephrine in a swine model of pediatric in-hospital cardiac arrest. The primary objectives of this study were to determine if (1) epinephrine doses have a significant acute effect on CBF and cerebral tissue oxygenation during CPR and (2) if the effect of each subsequent dose of epinephrine differs significantly from that of the first.
Methods
One-month-old piglets (n = 20) underwent asphyxia for 7 min, ventricular fibrillation, and CPR for 10–20 min. Epinephrine (20 mcg/kg) was administered at 2, 6, 10, 14, and 18 min of CPR. Invasive (laser Doppler, brain tissue oxygen tension [PbtO2]) and noninvasive (diffuse correlation spectroscopy and diffuse optical spectroscopy) measurements of CBF and cerebral tissue oxygenation were simultaneously recorded. Effects of subsequent epinephrine doses were compared to the first.
Results
With the first epinephrine dose during CPR, CBF and cerebral tissue oxygenation increased by > 10%, as measured by each of the invasive and noninvasive measures (p < 0.001). The effects of epinephrine on CBF and cerebral tissue oxygenation decreased with subsequent doses. By the fifth dose of epinephrine, there were no demonstrable increases in CBF of cerebral tissue oxygenation. Invasive and noninvasive CBF measurements were highly correlated during asphyxia (slope effect 1.3, p < 0.001) and CPR (slope effect 0.20, p < 0.001).
Conclusions
This model suggests that epinephrine increases CBF and cerebral tissue oxygenation, but that effects wane following the third dose. Noninvasive measurements of neurological health parameters hold promise for developing and directing resuscitation strategies.
“…While epinephrine increases systemic arterial blood pressure, there are conflicting experimental results regarding its effect on cerebral blood flow (CBF) and cerebral tissue oxygenation. Specifically, animal studies have demonstrated both increases [13][14][15][16][17] and decreases [18][19][20][21] in various measurements of CBF following epinephrine administration during CPR. Maintaining CBF during CPR is an important physiologic target to minimize potentially devastating effects of cerebral hypoperfusion during this vulnerable period.…”
Background
Despite controversies, epinephrine remains a mainstay of cardiopulmonary resuscitation (CPR). Recent animal studies have suggested that epinephrine may decrease cerebral blood flow (CBF) and cerebral oxygenation, possibly potentiating neurological injury during CPR. We investigated the cerebrovascular effects of intravenous epinephrine in a swine model of pediatric in-hospital cardiac arrest. The primary objectives of this study were to determine if (1) epinephrine doses have a significant acute effect on CBF and cerebral tissue oxygenation during CPR and (2) if the effect of each subsequent dose of epinephrine differs significantly from that of the first.
Methods
One-month-old piglets (n = 20) underwent asphyxia for 7 min, ventricular fibrillation, and CPR for 10–20 min. Epinephrine (20 mcg/kg) was administered at 2, 6, 10, 14, and 18 min of CPR. Invasive (laser Doppler, brain tissue oxygen tension [PbtO2]) and noninvasive (diffuse correlation spectroscopy and diffuse optical spectroscopy) measurements of CBF and cerebral tissue oxygenation were simultaneously recorded. Effects of subsequent epinephrine doses were compared to the first.
Results
With the first epinephrine dose during CPR, CBF and cerebral tissue oxygenation increased by > 10%, as measured by each of the invasive and noninvasive measures (p < 0.001). The effects of epinephrine on CBF and cerebral tissue oxygenation decreased with subsequent doses. By the fifth dose of epinephrine, there were no demonstrable increases in CBF of cerebral tissue oxygenation. Invasive and noninvasive CBF measurements were highly correlated during asphyxia (slope effect 1.3, p < 0.001) and CPR (slope effect 0.20, p < 0.001).
Conclusions
This model suggests that epinephrine increases CBF and cerebral tissue oxygenation, but that effects wane following the third dose. Noninvasive measurements of neurological health parameters hold promise for developing and directing resuscitation strategies.
“…They found that administration of 0.04 mg/kg of epinephrine during CPR significantly decreased carotid blood flow and EtCO 2 and discussed potential increase in macrocirculation and ventilation-perfusion mismatch when epinephrine was given as the most likely explanation of their findings. Similarly, Martin et al 31 and Hardig et al 32 examined the effects of epinephrine dosing on EtCO 2 in dog and swine models of cardiac arrest. Martin et al found that using 0.045 mg/kg IV of epinephrine resulted in significant decrease of EtCO 2 , while Hardig et al found that using 0.02 to 0.03 mg/kg of epinephrine resulted in a significant reduction in EtCO 2 when compared with normal saline.…”
The aim of this study was to examine the use of volumetric capnography monitoring to assess cardiopulmonary resuscitation (CPR) effectiveness by correlating it with cardiac output (CO), and to evaluate the effect of epinephrine boluses on both end-tidal carbon dioxide (EtCO2) and the volume of CO2 elimination (VCO2) in a swine ventricular fibrillation cardiac arrest model. Planned secondary analysis of data collected to investigate the use of noninvasive monitors in a pediatric swine ventricular fibrillation cardiac arrest model was performed. Twenty-eight ventricular fibrillatory arrests with open cardiac massage were conducted. During CPR, EtCO2 and VCO2 had strong correlation with CO, measured as a percentage of baseline pulmonary blood flow, with correlation coefficients of 0.83 (p < 0.001) and 0.53 (p = 0.018), respectively. However, both EtCO2 and VCO2 had weak and nonsignificant correlation with diastolic blood pressure during CPR 0.30 (p = 0.484) (95% confidence interval [CI], –0.51–0.83) and 0.25 (p = 0.566) (95% CI, –0.55–0.81), respectively. EtCO2 and VCO2 increased significantly after the first epinephrine bolus without significant change in CO. The correlations between EtCO2 and VCO2 and CO were weak 0.20 (p = 0.646) (95% CI, −0.59–0.79), and 0.27 (p = 0.543) (95% CI, −0.54–0.82) following epinephrine boluses. Continuous EtCO2 and VCO2 monitoring are potentially useful metrics to ensure effective CPR. However, transient epinephrine administration by boluses might confound the use of EtCO2 and VCO2 to guide chest compression.
“…However, other authors suggest that patients who require the administration of adrenaline during CPR have a higher chance of achieving a return of spontaneous circulation, which does not necessarily influence long-term neurological functioning (e.g., according to the CPC scale) or the risk of long-term mortality [18, 19]. Repeating adrenaline doses after the cessation of circulation impairs microcirculatory perfusion in the central nervous system and exacerbates already existing metabolic disturbances [20]. This has been reflected in the current guidelines for resuscitation: their authors advise caution when considering the administration of adrenaline [1].…”
IntroductionThe prognosis in out-of-hospital sudden cardiac arrest (OHCA) remains unfavorable and depends on a number of demographic and clinical variables, the reversibility of its causes and its mechanisms.AimTo investigate the risk factors of prehospital death in patients with OHCA in Bielsko County.Material and methodsThe study analyzed all dispatch cards of the National Emergency Medical Services (EMS) teams in Bielsko-Biala for the year 2013 (n = 23 400). Only the cards related to sudden cardiac arrest in adults were ultimately included in the study (n = 272; 190 men, 82 women; median age: 71 years).ResultsSixty-seven victims (45 men, 22 women) were pronounced dead upon the arrival of the EMS team, and cardiopulmonary resuscitation (CPR) was not undertaken. In the remaining group of 205 subjects, CPR was commenced but was ineffective in 141 patients (97 male, 44 female). Although univariate analysis indicated 6 predictors of prehospital death, including OHCA without the presence of witnesses (odds ratio (OR) = 4.2), OHCA occurring in a public place (OR = 3.1), no bystander CPR (OR = 9.7), no bystander cardiac massage (OR = 13.1), initial diagnosis of non-shockable cardiac rhythm (OR = 7.0), and the amount of drugs used for CPR (OR = 0.4), logistic regression confirmed that only the lack of bystander cardiac massage (OR = 6.5) and non-shockable rhythm (OR = 4.6) were independent determinants of prehospital death (area under ROC curve = 0.801).ConclusionsNon-shockable rhythm of cardiac arrest and lack of bystander cardiac massage are independent determinants of prehospital death in Bielsko-Biala inhabitants suffering from OHCA.
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