scholarly journals Targeted high mean arterial pressure aggravates cerebral hemodynamics after extracorporeal resuscitation in swine

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Yael Levy ◽  
Alice Hutin ◽  
Fanny Lidouren ◽  
Nicolas Polge ◽  
Rocio Fernandez ◽  
...  
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Hemodynamics ◽  
Reactivity Index ◽  
Extracorporeal Cardiopulmonary Resuscitation ◽  
Standard Map ◽  
Carotid Blood Flow ◽  
Arterial Blood

Abstract Background Extracorporeal cardiopulmonary resuscitation (E-CPR) is used for the treatment of refractory cardiac arrest. However, the optimal target to reach for mean arterial pressure (MAP) remains to be determined. We hypothesized that MAP levels critically modify cerebral hemodynamics during E-CPR and tested two distinct targets (65–75 vs 80–90 mmHg) in a porcine model. Methods Pigs were submitted to 15 min of untreated ventricular fibrillation followed by 30 min of E-CPR. Defibrillations were then delivered until return of spontaneous circulation (ROSC). Extracorporeal circulation was initially set to an average flow of 40 ml/kg/min. The dose of epinephrine was set to reach a standard or a high MAP target level (65–75 vs 80–90 mmHg, respectively). Animals were followed during 120-min after ROSC. Results Six animals were included in both groups. During E-CPR, high MAP improved carotid blood flow as compared to standard MAP. After ROSC, this was conversely decreased in high versus standard MAP, while intra-cranial pressure was superior. The pressure reactivity index (PRx), which is the correlation coefficient between arterial blood pressure and intracranial pressure, also demonstrated inverted patterns of alteration according to MAP levels during E-CPR and after ROSC. In standard-MAP, PRx was transiently positive during E-CPR before returning to negative values after ROSC, demonstrating a reversible alteration of cerebral autoregulation during E-CPR. In high-MAP, PRx was negative during E-CPR but became sustainably positive after ROSC, demonstrating a prolonged alteration in cerebral autoregulation after ROSC. It was associated with a significant decrease in cerebral oxygen consumption in high- versus standard-MAP after ROSC. Conclusions During early E-CPR, MAP target above 80 mmHg is associated with higher carotid blood flow and improved cerebral autoregulation. This pattern is inverted after ROSC with a better hemodynamic status with standard versus high-MAP.

Abstract 9934: High Mean Arterial Pressure Aggravates Cerebral Hemodynamics After Extracorporeal Resuscitation in Swine

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Yael Levy ◽  
Alice Hutin ◽  
Nicolas Polge ◽  
fanny lidouren ◽  
Matthias Kohlhauer ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cerebral Hemodynamics ◽  
Reactivity Index ◽  
Extracorporeal Cardiopulmonary Resuscitation ◽  
Standard Map ◽  
Arterial Blood

Introduction: Extracorporeal cardiopulmonary resuscitation (E-CPR) is used for the treatment of refractory cardiac arrest but the optimal target to reach for mean arterial pressure (MAP) remains to be determined. Hypothesis: We hypothesized that MAP levels modify cerebral hemodynamics during E-CPR. Accordingly, we tested two MAP targets (65-75 vs 80-90 mmHg) in a porcine model of E-CPR. Methods: Pigs were anesthetized and instrumented for the evaluation of cerebral and systemic hemodynamics. They were submitted to 15 min of untreated ventricular fibrillation followed by 30 min of E-CPR. Electric attempts of defibrillation were then delivered until resumption of spontaneous circulation (ROSC). Extracorporeal circulation was initially set to an average flow of 40 ml/kg/min with a standardized volume expansion in both groups. The dose of epinephrine was set to reach either a standard or a high MAP target level (65-75 vs 80-90 mmHg, respectively). Animals were followed during 120 min after ROSC. Results: Six animals were included in both groups. After cardiac arrest, MAP was maintained at the expected level (Figure). During E-CPR, high MAP transiently improved carotid blood flow as compared to standard MAP. This blood flow progressively decreased after ROSC in high vs standard MAP, while intra-cranial pressure increased. Interestingly, this was associated with a significant decrease in cerebral oxygen consumption (26±8 vs 54±6 L O 2 /min/kg at 120 min after ROSC, respectively; p<0.01) (Figure). The pressure reactivity index (PRx), which is the correlation coefficient between arterial blood pressure and intracranial pressure, became positive in high MAP (0.47±0.02) vs standard MAP group (-0.16±0.10), demonstrating altered cerebral autoregulation with high MAP. Conclusion: Increasing MAP above 80 mmHg with epinephrine aggravates cerebral hemodynamics after E-CPR. Figure: Mean arterial pressure (MAP), cerebral blood flow and oxygen consumption (*, p<0.05)

Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training

2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.

Interaction of vasopressin and opioids during rapid hemorrhage in conscious rabbits

1991 ◽  
Vol 260 (2) ◽  
pp. R373-R381 ◽  
Author(s):  
J. C. Schadt ◽  
E. M. Hasser
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Endogenous Opioids ◽  
Adrenergic Blockade ◽  
Arterial Blood ◽  
Conscious Rabbits

We investigated possible interactions between arginine vasopressin (AVP) and endogenous opioid peptides during rapid hypotensive hemorrhage and subsequent opioid receptor blockade in conscious rabbits. Plasma AVP concentration did not change after normotensive hemorrhage but increased after hypotensive hemorrhage. Blockade of V1-AVP receptors (AVPX) did not affect prehemorrhage arterial pressure, heart rate, or hindquarter blood flow and vascular resistance. AVPX did not alter the hemodynamic response to hemorrhage or the blood loss required to reduce mean arterial pressure to less than 40 mmHg. However, hindquarter blood flow was higher and mean arterial pressure and hindquarter resistance lower after hypotensive hemorrhage in AVPX-treated animals. These differences were maintained after naloxone or saline injection. Naloxone increased mean arterial pressure and hindquarter resistance and decreased heart rate with or without AVPX. At 2 min postinjection, plasma AVP values were greater after saline than after naloxone. When naloxone's pressor response was reduced by alpha-adrenergic blockade, plasma AVP values were higher after naloxone than after saline. Thus AVP was not vital to maintenance of blood pressure during rapid normotensive hemorrhage or to the abrupt decrease in arterial blood pressure and resistance after rapid hypotensive hemorrhage. AVP release was important to spontaneous recovery from acute hypotensive hemorrhage but only of minor importance to naloxone's pressor response. Finally, AVP release appeared to be inhibited by endogenous opioids during acute hemorrhagic hypotension.

scholarly journals Mathematical Modelling of Cerebral Blood Circulation and Cerebral Autoregulation: Towards Preventing Intracranial Hemorrhages in Preterm Newborns

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Renée Lampe ◽  
Nikolai Botkin ◽  
Varvara Turova ◽  
Tobias Blumenstein ◽  
Ana Alves-Pinto
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Cerebral Autoregulation ◽  
Coupled Model ◽  
Equation Model ◽  
Polynomial Coefficients ◽  
Arterial Blood ◽  
Cerebral Blood Circulation ◽  
Preterm Newborns

Impaired cerebral autoregulation leads to fluctuations in cerebral blood flow, which can be especially dangerous for immature brain of preterm newborns. In this paper, two mathematical models of cerebral autoregulation are discussed. The first one is an enhancement of a vascular model proposed by Piechnik et al. We extend this model by adding a polynomial dependence of the vascular radius on the arterial blood pressure and adjusting the polynomial coefficients to experimental data to gain the autoregulation behavior. Moreover, the inclusion of a Preisach hysteresis operator, simulating a hysteretic dependence of the cerebral blood flow on the arterial pressure, is tested. The second model couples the blood vessel system model by Piechnik et al. with an ordinary differential equation model of cerebral autoregulation by Ursino and Lodi. An optimal control setting is proposed for a simplified variant of this coupled model. The objective of the control is the maintenance of the autoregulatory function for a wider range of the arterial pressure. The control can be interpreted as the effect of a medicament changing the cerebral blood flow by, for example, dilation of blood vessels. Advanced numerical methods developed by the authors are applied for the numerical treatment of the control problem.

scholarly journals Cerebral hemodynamics: a mathematical model including autoregulation, baroreflex and extracranial peripheral circulation

2021 ◽  
Author(s):  
Francisco Ambrosio Garcia ◽  
Deusdedit Lineu Spavieri Junior ◽  
Andreas Linninger
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cerebral Autoregulation ◽  
Peripheral Circulation ◽  
Flow Regulation ◽  
Pressure Waves ◽  
Vascular Bed ◽  
Blood Flow Regulation

Increasing evidence supports that cerebral autoregulation and mean arterial pressure regulation via baroreflex contribute to cerebral blood flow regulation. It is unclear whether the extracranial vascular bed of the head and neck helps reestablishing cerebral blood flow during changes in mean arterial pressure. Current computational models of cerebral blood flow regulation do not address the relationships between the intracranial and extracranial blood flow dynamics. We present a model of cerebral autoregulation, extracranial peripheral circulation and baroreflex control of heart rate and of peripheral vasculature that was included to the model of intracranial dynamics proposed by Linninger et al. (2009), which incorporates the fully coupled blood, cerebrospinal fluid and brain parenchyma systems. Autoregulation was modelled as being pressure-mediated at the arteries and arterioles and flow-mediated at the microcirculation. During simulations of a bout of acute hypotension, cerebral blood flow returns rapidly to baseline levels with a very small overshoot, whereas the blood flow to the peripheral circulation of the head and neck suffers a prolonged suppression in accordance with experimental evidence. The inclusion of baroreflex regulation at the extracranial vascular bed had a negligible effect on cerebral blood flow regulation during dynamic changes in mean arterial pressure. Moreover, the results suggest that the extracranial blood flow carries only modest information about cerebral blood flow in dynamic situations in which cerebral autoregulation is preserved and mean arterial pressure suffers alterations. This information is likely higher when the autoregulation is impaired. Steady-state cerebral blood flow in the model is kept within normal ranges despite variations in mean arterial pressure from 50 to 175 mmHg. By inputting aortic pressure waves from individuals with increasing arterial rigidity, increasing arterial systolic and pulse pressures, the model predicts the generation of intracranial pressure waves with accordingly increasing peaks and amplitudes.

scholarly journals Regulation of Optic Nerve Head Blood Flow during Combined Changes in Intraocular Pressure and Arterial Blood Pressure

2013 ◽  
Vol 33 (12) ◽  
pp. 1850-1856 ◽  
Author(s):  
Agnes Boltz ◽  
Doreen Schmidl ◽  
René M Werkmeister ◽  
Michael Lasta ◽  
Semira Kaya ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intraocular Pressure ◽  
Mean Arterial Pressure ◽  
Optic Nerve ◽  
Arterial Pressure ◽  
Optic Nerve Head ◽  
Isometric Exercise ◽  
Doppler Flowmetry ◽  
Ocular Perfusion ◽  
Arterial Blood

In the choroid, there is evidence that blood flow does not only depend on ocular perfusion pressure (OPP), but also on absolute mean arterial pressure (MAP) and intraocular pressure (IOP). The present study included 40 healthy subjects to investigate whether such behavior is also found in the optic nerve head (ONH). The ONH blood flow (ONHBF) was studied using laser Doppler flowmetry during a separate increase in IOP and MAP as well as during a combined elevation. Mean arterial pressure was increased by isometric exercise and IOP by the suction method. During both, the change in ONHBF was less pronounced than the change in OPP indicating autoregulation. Correlation analysis was performed for the combined experiments after pooling all data according to IOP and MAP values. A correlation between ONHBF and MAP was found at IOPs 25 mm Hg ( P<0.001), but not at IOPs>25 mm Hg ( P=0.79). Optic nerve head blood flow and IOP were significantly correlated ( P<0.001), and ONHBF was only slightly dependent on MAP. The data of the present study indicate a complex regulation of ONHBF during combined changes in MAP and IOP. Our results may be compatible with myogenic mechanisms underlying autoregulation, and indicate better ONHBF regulation during an increase in MAP than during an increase in IOP.

scholarly journals Cerebral Blood Flow–Guided Manipulation of Arterial Blood Pressure Attenuates Hippocampal Apoptosis After Asphyxia‐Induced Cardiac Arrest in Rats

2020 ◽  
Vol 9 (13) ◽  
Author(s):  
Chih‐Hung Wang ◽  
Wei‐Tien Chang ◽  
Chien‐Hua Huang ◽  
Min‐Shan Tsai ◽  
Shing‐Hwa Liu ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Neuronal Damage ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Arterial Blood ◽  
Induced Cardiac Arrest

Background In most post–cardiac arrest patients, the autoregulation mechanism of cerebral blood flow ( CBF ) is dysregulated. We examined whether recovery of CBF by adjusting mean arterial pressure mitigates post–cardiac arrest neuronal damage. Methods and Results Wistar rats that underwent 8‐minute asphyxia‐induced cardiac arrest and resuscitation were computer‐randomized to norepinephrine or control groups. The CBF was measured at the dorsal hippocampal CA 1 region of the left hemisphere. In the norepinephrine group, the mean arterial pressure was adjusted to recover CBF to 80% to 100% of baseline. Twenty‐four hours following resuscitation, neurological outcomes were assessed, and brain tissues and blood samples were harvested for neuronal apoptosis and injury assessment. Thirty resuscitated rats were randomized into 2 groups, each containing 12 rats that completed the experiments. Norepinephrine infusion effectively prevented posthyperemia hypoperfusion and recovered CBF to pre‐arrest baseline levels; a moderate positive linear correlation between mean arterial pressure and CBF during this period was also observed ( P <0.001). There were no significant between‐group differences in neurological recovery. In the norepinephrine group compared with the control group, upregulated cleaved caspase‐3 protein expression in brain tissue determined by Western blot was reduced ( P =0.02) and the densities of apoptotic cells in hippocampal CA 1 and CA 3 regions determined by terminal deoxynucleotidyl transferase‐mediated dUTP biotin nick‐end labeling were decreased ( P <0.001). No significant differences in serum neuron‐specific enolase or S100β levels were detected between the 2 groups. Conclusions CBF recovery demonstrated neuroprotective effects by reducing activation of cerebral apoptosis and number of apoptotic neurons. However, these effects did not significantly improve clinical neurological function, necessitating further investigation.

scholarly journals Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons

2015 ◽  
Vol 309 (10) ◽  
pp. R1273-R1284 ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Partial Loss ◽  
Rat Pups ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
Long Term Facilitation

The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.

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