The effect of fluid bolus administration on cerebral tissue oxygenation in post-cardiac arrest patients

Resuscitation ◽  
2021 ◽  
Vol 168 ◽  
pp. 1-5
Author(s):  
E. Bogaerts ◽  
B. Ferdinande ◽  
P.J. Palmers ◽  
M.L.N.G. Malbrain ◽  
N. Van Regenmortel ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Tissue Oxygenation ◽  
Bolus Administration ◽  
Cerebral Tissue ◽  
Fluid Bolus ◽  
Cerebral Tissue Oxygenation

Low Cerebral Oxygenation Levels during Resuscitation in Out-of-hospital Cardiac Arrest Are Associated with Hyperfibrinolysis

2015 ◽  
Vol 123 (4) ◽  
pp. 820-829 ◽  
Author(s):  
Anne Duvekot ◽  
Victor A. Viersen ◽  
Simone E. Dekker ◽  
Leo M. G. Geeraedts ◽  
Lothar A. Schwarte ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Plasminogen Activator ◽  
Protein C ◽  
Tissue Oxygenation ◽  
Cerebral Oxygenation ◽  
Fibrinolytic System ◽  
Cerebral Tissue ◽  
Cerebral Tissue Oxygenation ◽  
Hospital Cardiac Arrest

Abstract Background: The authors investigated whether patients with out-of-hospital cardiac arrest with an initial low cerebral oxygen level during cardiopulmonary resuscitation are more prone to develop hyperfibrinolysis than patients with normal cerebral oxygenation levels and which part of the fibrinolytic system is involved in this response. Methods: In 46 patients, hyperfibrinolysis was diagnosed immediately upon emergency department admission using rotational thromboelastometry and defined as a lysis more than 15%. Simultaneously, initial cerebral tissue oxygenation was measured using near-infrared spectroscopy, and oxygen desaturation was defined as a tissue oxygenation index (TOI) of 50% or less. Blood sample analysis included markers for hypoperfusion and fibrinolysis. Results: There was no difference in prehospital cardiopulmonary resuscitation duration between patients with or without hyperfibrinolysis. An initial TOI of 50% or less was associated with more clot lysis (91% [17 to 100%; n = 16]) compared with patients with a normal TOI (6% [4 to 11%]; n = 30; P < 0.001), with lower levels of plasminogen (151.6 ± 61.0 vs. 225.3 ± 47.0 μg/ml; P < 0.001) and higher levels of tissue plasminogen activator (t-PA; 18.3 ± 7.4 vs. 7.9 ± 4.7 ng/ml; P < 0.001) and plasminogen activator inhibitor-1 (19.3 ± 8.9 vs. 12.1 ± 6.1 ng/ml; P = 0.013). There were no differences in (activated) protein C levels among groups. The initial TOI was negatively correlated with t-PA (r = −0.69; P < 0001). Mortality rates were highest in patients with hyperfibrinolysis. Conclusion: Activation of the fibrinolytic system is more common in out-of-hospital cardiac arrest patients with an initial cerebral tissue oxygenation value of 50% or less during resuscitation and is linked to increased levels of t-PA rather than involvement of protein C.

Abstract 159: Epinephrine Increases Cerebral Perfusion and Oxygenation in a Pre-Clinical Model of Pediatric In-Hospital Cardiac Arrest

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Constantine D Mavroudis ◽  
Tiffany S Ko ◽  
Ryan W Morgan ◽  
Marco M Hefti ◽  
William P Landis ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Tissue Oxygenation ◽  
Cerebral Oxygenation ◽  
Neurological Injury ◽  
Tissue Oxygen Saturation ◽  
Swine Model ◽  
Cerebral Tissue ◽  
Clinical Model ◽  
Cerebral Tissue Oxygenation ◽  
Hospital Cardiac Arrest

Introduction: Despite controversies, epinephrine remains a mainstay of 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. Hypothesis: Epinephrine will increase CBF and cerebral oxygenation during CPR. Methods: One-month old piglets (n=20, 8-10kg) underwent asphyxia for 7 minutes, VF, and CPR according to AHA guidelines for 10-20 minutes. Epinephrine boluses (20 mcg/kg) were administered at minutes 2, 6, 10, and 14 of CPR. Invasive (laser Doppler) and noninvasive (diffuse optical) continuous measurements of CBF and oxygenation were recorded. Wilcoxon Rank-Sum test was used to compare measurements 15 seconds prior to epinephrine doses to sequential measurements at 1-minute intervals following epinephrine; data are described as median [IQR]. Results: Compared to pre-epinephrine values, CBF was most significantly increased one minute after the first dose of epinephrine (noninvasive: +37.7% [6.1, 79]; invasive: +24% [-0.3, 118], p<0.004 for both) and returned to baseline by 3 minutes post-epinephrine. Cerebral tissue oxygenation was also most significantly increased one-minute after the first dose of epinephrine (noninvasive: +25.2% [9.0, 45]; invasive: +160% [30.3, 428], p<0.001 for both) and remained elevated 4 minutes post-epinephrine. Effects were also significant one minute following the second dose on CBF (noninvasive: +11.5% [4.5, 29]; invasive: +9.5% [0.6, 19, p<0.03 for both) and on cerebral tissue oxygenation (noninvasive: +12.3% [1.6, 19]; invasive: +17.8% [-2.3,34, p<0.037 for both). There was no significant effect on any parameter following the third and fourth doses. Conclusions: In a swine model of pediatric in-hospital cardiac arrest, bolus-dosed epinephrine increases CBF and cerebral tissue oxygen saturation. These effects are only significant following the first two doses. Our findings are underscore the importance of further research to elucidate the transient pharmacodynamics of epinephrine to optimize both survival and neurological outcomes.

scholarly journals Epinephrine’s effects on cerebrovascular and systemic hemodynamics during cardiopulmonary resuscitation

Critical Care ◽  
2020 ◽  
Vol 24 (1) ◽  
Author(s):  
Constantine D. Mavroudis ◽  
Tiffany S. Ko ◽  
Ryan W. Morgan ◽  
Lindsay E. Volk ◽  
William P. Landis ◽  
...  
Keyword(s):  
Cardiopulmonary Resuscitation ◽  
Animal Studies ◽  
Tissue Oxygenation ◽  
Cerebral Oxygenation ◽  
Acute Effect ◽  
Correlation Spectroscopy ◽  
Neurological Injury ◽  
Swine Model ◽  
Cerebral Tissue ◽  
Cerebral Tissue Oxygenation

Abstract 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.

scholarly journals Physiologically based cord clamping improves cardiopulmonary haemodynamics in lambs with a diaphragmatic hernia

2019 ◽  
Vol 105 (1) ◽  
pp. 18-25 ◽  
Author(s):  
Aidan J Kashyap ◽  
Ryan J Hodges ◽  
Marta Thio ◽  
Karyn A Rodgers ◽  
Ben J Amberg ◽  
...  
Keyword(s):  
Diaphragmatic Hernia ◽  
Tissue Oxygenation ◽  
Lung Hypoplasia ◽  
Physiological Changes ◽  
Cerebral Tissue ◽  
Maximum Delay ◽  
Cord Clamping ◽  
Physiologically Based ◽  
Cerebral Tissue Oxygenation ◽  
Surgically Induced

ObjectiveLung hypoplasia associated with congenital diaphragmatic hernia (CDH) results in respiratory insufficiency and pulmonary hypertension after birth. We have investigated whether aerating the lung before removing placental support (physiologically based cord clamping (PBCC)), improves the cardiopulmonary transition in lambs with a CDH.MethodsAt ≈138 days of gestational age, 17 lambs with surgically induced left-sided diaphragmatic hernia (≈d80) were delivered via caesarean section. The umbilical cord was clamped either immediately prior to ventilation onset (immediate cord clamping (ICC); n=6) or after achieving a target tidal volume of 4 mL/kg, with a maximum delay of 10 min (PBCC; n=11). Lambs were ventilated for 120 min and physiological changes recorded.ResultsPulmonary blood flow (PBF) increased following ventilation onset in both groups, but was 19-fold greater in PBCC compared with ICC lambs at cord clamping (19±6.3 vs 1.0±0.5 mL/min/kg, p<0.001). Cerebral tissue oxygenation was higher in PBCC than ICC lambs during the first 10 min after cord clamping (59%±4% vs 30%±5%, p<0.001). PBF was threefold higher (23±4 vs 8±2 mL/min/kg, p=0.01) and pulmonary vascular resistance (PVR) was threefold lower (0.6±0.1 vs 2.2±0.6 mm Hg/(mL/min), p<0.001) in PBCC lambs compared with ICC lambs at 120 min after ventilation onset.ConclusionsCompared with ICC, PBCC prevented the severe asphyxia immediately after birth and resulted in a higher PBF due to a lower PVR, which persisted for at least 120 min after birth in CDH lambs.

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