Abstract
BackgroundThe effects of adrenaline on cerebral blood vessels during cardiopulmonary resuscitation (CPR) are not well understood. We developed an extracorporeal CPR model that maintains constant low systemic blood flow while allowing adrenaline-associated effects on cerebral vasculature to be assessed at different mean arterial pressure (MAP) levels independently of the effects on systemic blood flow. MethodsAfter eight minutes of cardiac arrest, low-flow extracorporeal life support (ECLS) (30 ml/kg/min) was started in fourteen pigs. After ten minutes, continuous adrenaline administration was started to achieve MAP values of 40 (n = 7) or 60 mmHg (n = 7). Measurements included intracranial pressure (ICP), cerebral perfusion pressure (CePP), laser-Doppler-derived regional cerebral blood flow (CBF), cerebral regional oxygen saturation (rSO2), brain tissue oxygen tension (PbtO2) and extracellular cerebral metabolites assessed by cerebral microdialysis. ResultsDuring ECLS without adrenaline, regional CBF increased by only 5% (25th to 75th percentile: −3 to 14; p = 0.2642) and PbtO2 by 6% (0–15; p = 0.0073) despite a significant increase in MAP to 28 mmHg (25–30; p < 0.0001) and CePP to 10 mmHg (8–13; p < 0.0001). Accordingly, cerebral microdialysis parameters showed a profound hypoxic-ischemic pattern. Adrenaline administration significantly improved regional CBF to 29 ± 14% (p = 0.0098) and 61 ± 25% (p < 0.001) and PbtO2 to 15 ± 11% and 130 ± 82% (both p < 0.001) of baseline in the MAP 40 mmHg and MAP 60 mmHg groups, respectively. Importantly, MAP of 60 mmHg was associated with metabolic improvement. ConclusionThis study shows that adrenaline administration during constant low systemic blood flow increases CePP, regional CBF, cerebral oxygenation and cerebral metabolism.
Highlights
Administration of adrenaline during cardiopulmonary resuscitation (CPR) is primarily intended to increase coronary perfusion pressure and thereby coronary blood flow, which is closely associated with the return of spontaneous circulation (ROSC).[1]
Intracranial and cerebral perfusion pressure With induction of cardiac arrest (CA), mean arterial pressure (MAP) decreased to hydrostatic pressure (p < 0.0001), while intracranial pressure (ICP) initially increased (p < 0.0001) returning to baseline values until the end of CA
With commencement of low-flow extracorporeal life support (ECLS), MAP increased to 28 mmHg (25th to 75th percentile: 25–30 mmHg; p < 0.0001) and cerebral perfusion pressure (CePP) to 10 mmHg (8–13 mmHg; p < 0.0001), while ICP did not change (p = 0.1647)
Summary
Administration of adrenaline during cardiopulmonary resuscitation (CPR) is primarily intended to increase coronary perfusion pressure and thereby coronary blood flow, which is closely associated with the return of spontaneous circulation (ROSC).[1]. While CePP consistently increases following adrenaline administration, cerebral blood flow (CBF) improves in some studies and deteriorates in others due to disproportionate vasoconstriction.[5,6,12,13] Undoubtedly, a certain degree of systemic vasoconstriction to increase perfusion pressure is necessary to allow organ blood flow; too much concomitant cerebral vasoconstriction, may have negative effects on brain perfusion. Conclusion: This study shows that adrenaline administration during constant low systemic blood flow increases CePP, regional CBF, cerebral oxygenation and cerebral metabolism.
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