Cerebral hypoperfusion modifies the respiratory chemoreflex during orthostatic stress

2013 ◽  
Vol 125 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Hidehiro Nakahara ◽  
Kazunobu Okazaki ◽  
Damian M. Bailey ◽  
Tadayoshi Miyamoto
Keyword(s):  
Cerebral Hypoperfusion ◽  
Orthostatic Stress ◽  
Respiratory Chemoreflex

Cerebral hypoperfusion modifies the respiratory chemoreflex during orthostatic stress

2013 ◽  
Vol 125 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Hidehiro Nakahara ◽  
Kazunobu Okazaki ◽  
Damian M. Bailey ◽  
Tadayoshi Miyamoto
Keyword(s):  
Lower Body Negative Pressure ◽  
Minute Ventilation ◽  
Regression Line ◽  
Cerebral Hypoperfusion ◽  
Orthostatic Stress ◽  
Respiratory Chemoreflex ◽  
Underlying Mechanisms ◽  
End Tidal ◽  
Induced Changes ◽  
The Relationship

The respiratory chemoreflex is known to be modified during orthostatic stress although the underlying mechanisms remain to be established. To determine the potential role of cerebral hypoperfusion, we examined the relationship between changes in MCA Vmean (middle cerebral artery mean blood velocity) and V̇E (pulmonary minute ventilation) from supine control to LBNP (lower body negative pressure; −45mmHg) at different CO2 levels (0, 3.5 and 5% CO2). The regression line of the linear relationship between V̇E and PETCO2 (end-tidal CO2) shifted leftwards during orthostatic stress without any change in sensitivity (1.36±0.27 l/min per mmHg at supine to 1.06±0.21 l/min per mmHg during LBNP; P=0.087). In contrast, the relationship between MCA Vmean and PETCO2 was not shifted by LBNP-induced changes in PETCO2. However, changes in V̇E from rest to LBNP were more related to changes in MCA Vmean than changes in PETCO2. These findings demonstrate for the first time that postural reductions in CBF (cerebral blood flow) modified the central respiratory chemoreflex by moving its operating point. An orthostatically induced decrease in CBF probably attenuated the ‘washout’ of CO2 from the brain causing hyperpnoea following activation of the central chemoreflex.

Cerebral hemodynamics during orthostatic stress assessed by nonlinear modeling

2006 ◽  
Vol 101 (1) ◽  
pp. 354-366 ◽  
Author(s):  
Georgios D. Mitsis ◽  
Rong Zhang ◽  
Benjamin D. Levine ◽  
Vasilis Z. Marmarelis
Keyword(s):  
Cerebral Blood Flow Velocity ◽  
Lower Body Negative Pressure ◽  
Nonlinear Modeling ◽  
Cerebral Hemodynamics ◽  
Cerebral Hypoperfusion ◽  
Orthostatic Stress ◽  
Cerebrovascular Reserve ◽  
Vasomotor Reactivity ◽  
Arterial Blood ◽  
Cerebral Vasomotor Reactivity

The effects of orthostatic stress, induced by lower body negative pressure (LBNP), on cerebral hemodynamics were examined in a nonlinear context. Spontaneous fluctuations of beat-to-beat mean arterial blood pressure (MABP) in the finger, mean cerebral blood flow velocity (MCBFV) in the middle cerebral artery, as well as breath-by-breath end-tidal CO2 concentration (PetCO2) were measured continuously in 10 healthy subjects under resting conditions and during graded LBNP to presyncope. A two-input nonlinear Laguerre-Volterra network model was employed to study the dynamic effects of MABP and PetCO2 changes, as well as their nonlinear interactions, on MCBFV variations in the very low (VLF; below 0.04 Hz), low (LF; 0.04–0.15 Hz), and high frequency (HF; 0.15–0.30 Hz) ranges. Dynamic cerebral autoregulation was described by the model terms corresponding to MABP, whereas cerebral vasomotor reactivity was described by the model PetCO2 terms. The nonlinear model terms reduced the output prediction normalized mean square error substantially (by 15–20%) and had a prominent effect in the VLF range, both under resting conditions and during LBNP. Whereas MABP fluctuations dominated in the HF range and played a significant role in the VLF and LF ranges, changes in PetCO2 accounted for a considerable fraction of the VLF and LF MCBFV variations, especially at high LBNP levels. The magnitude of the linear and nonlinear MABP-MCBFV Volterra kernels increased substantially above −30 mmHg LBNP in the VLF range, implying impaired dynamic autoregulation. In contrast, the magnitude of the PetCO2-MCBFV kernels reduced during LBNP at all frequencies, suggesting attenuated cerebral vasomotor reactivity under dynamic conditions. We speculate that these changes may reflect a progressively reduced cerebrovascular reserve to compensate for the increasingly unstable systemic circulation during orthostatic stress that could ultimately lead to cerebral hypoperfusion and syncope.

scholarly journals Cerebral Vasomotor Reserve in Hypertension during Head-up Tilt

Stroke ◽  
2001 ◽  
Vol 32 (suppl_1) ◽  
pp. 347-347
Author(s):  
Vera Novak ◽  
Andrew Slivka ◽  
Roly Kanard ◽  
Peter Novak ◽  
Phillip Binkley
Keyword(s):  
Mild Hypertension ◽  
Cerebral Arteries ◽  
Cerebral Hypoperfusion ◽  
Orthostatic Stress ◽  
Hypertensive Patients ◽  
Middle Cerebral Arteries ◽  
Head Up Tilt ◽  
Blood Flow Velocities ◽  
Mild Hypertensive ◽  
Significant Increment

P44 Objective: To evaluate cerebral vasomotor reserve in hypertension during head-up tilt with hypo- and hypercapnia. Background: Cerebral vasoregulation determines degree of perfusion during increased metabolic demands such as orthostatic stress, hypo- and hypercapnia. With hypertension, silent hypoperfusion may develop if vasomotor reserve is compromised due to remodeling of the vessel wall and impaired vasodilation. Methods: We studied 15 mild hypertensive (BP 145/95 mm Hg) and 15 control men and women (aged 35–65 years) using Transcranial Doppler. Blood flow velocities (BFV) from both middle cerebral arteries (MCA), brachial artery (BRA), heart rate, blood pressure (BP), respiration and carbon dioxide (CO 2 ) were simultaneously recorded during: hyperventilation (3 min), apnea (1 min) and CO 2 rebreathing (3 min) in supine rest and head-up tilt at 80 O . Vasomotor reserve (VMR) was calculated from systolic (VMRS), diastolic (VMRD) and mean BFVs (VMRM) using regression analysis as percentual increment between hypo-, normo- and hypercapnia. Results: In controls, BFVs and VMR reserve were symmetric in both MCAs and there were no significant differences between rest and head-up tilt. In hypertensive patients, VMRM and were significantly reduced during supine rest (p<0.05) and head-up tilt (p<0.01) compared to the controls by about 50% (Table 1)in both MCAs. In controls, VMRD doubled during hypercapnia, while no significant increment was found in hypertensive patients. Systolic BFVs and VMR were similar in both groups. Conclusions: Vasomotor reserve was reduced even with mild hypertension due to impaired vasodilation. Impaired vasoregulation during orthostatic stress may be associated with silent cerebral hypoperfusion.

Artifact removal from neurophysiological signals: impact on intracranial and arterial pressure monitoring in traumatic brain injury

2020 ◽  
Vol 132 (6) ◽  
pp. 1952-1960 ◽  
Author(s):  
Seung-Bo Lee ◽  
Hakseung Kim ◽  
Young-Tak Kim ◽  
Frederick A. Zeiler ◽  
Peter Smielewski ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurological Status ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Clinical Parameters ◽  
Artifact Removal ◽  
Clinical Events ◽  
Arterial Blood ◽  
Before And After

OBJECTIVEMonitoring intracranial and arterial blood pressure (ICP and ABP, respectively) provides crucial information regarding the neurological status of patients with traumatic brain injury (TBI). However, these signals are often heavily affected by artifacts, which may significantly reduce the reliability of the clinical determinations derived from the signals. The goal of this work was to eliminate signal artifacts from continuous ICP and ABP monitoring via deep learning techniques and to assess the changes in the prognostic capacities of clinical parameters after artifact elimination.METHODSThe first 24 hours of monitoring ICP and ABP in a total of 309 patients with TBI was retrospectively analyzed. An artifact elimination model for ICP and ABP was constructed via a stacked convolutional autoencoder (SCAE) and convolutional neural network (CNN) with 10-fold cross-validation tests. The prevalence and prognostic capacity of ICP- and ABP-related clinical events were compared before and after artifact elimination.RESULTSThe proposed SCAE-CNN model exhibited reliable accuracy in eliminating ABP and ICP artifacts (net prediction rates of 97% and 94%, respectively). The prevalence of ICP- and ABP-related clinical events (i.e., systemic hypotension, intracranial hypertension, cerebral hypoperfusion, and poor cerebrovascular reactivity) all decreased significantly after artifact removal.CONCLUSIONSThe SCAE-CNN model can be reliably used to eliminate artifacts, which significantly improves the reliability and efficacy of ICP- and ABP-derived clinical parameters for prognostic determinations after TBI.

scholarly journals Intradialytic Cerebral Hypoperfusion as Mechanism for Cognitive Impairment in Patients on Hemodialysis

2019 ◽  
Vol 30 (11) ◽  
pp. 2052-2058 ◽  
Author(s):  
Dawn F. Wolfgram
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Perfusion ◽  
Ischemic Injury ◽  
Hemodialysis Patients ◽  
Cognitive Outcomes ◽  
Cerebral Injury ◽  
Cerebral Hypoperfusion ◽  
Increased Risk ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic

The high frequency of cognitive impairment in individuals on hemodialysis is well characterized. In-center hemodialysis patients are disproportionately affected by cognitive impairment compared with other dialysis populations, identifying hemodialysis itself as a possible factor. The pathophysiology of cognitive impairment has multiple components, but vascular-mediated cerebral injury appears to contribute based on studies demonstrating increased cerebral ischemic lesions and atrophy in brain imaging of patients on hemodialysis. Patients on hemodialysis may be at increased risk for cerebral ischemic injury disease due to vasculopathy associated with ESKD and from their comorbid diseases, such as hypertension and diabetes. This review focuses on the intradialytic cerebral hypoperfusion that can occur during routine hemodialysis due to the circulatory stress of hemodialysis. This includes a review of current methods used to monitor intradialytic cerebral perfusion and the structural and functional cognitive outcomes that have been associated with changes in intradialytic cerebral perfusion. Monitoring of intradialytic cerebral perfusion may become clinically relevant as nephrologists try to avoid the cognitive complications seen with hemodialysis. Identifying the appropriate methods to assess risk for cerebral ischemic injury and the relationship of intradialytic cerebral hypoperfusion to cognitive outcomes will help inform the decision to use intradialytic cerebral perfusion monitoring in the clinical setting as part of a strategy to prevent cognitive decline.

Experimental rat model of chronic cerebral hypoperfusion–reperfusion mimicking normal perfusion pressure breakthrough phenomenon

Neurocirugía ◽  
2020 ◽  
Vol 31 (5) ◽  
pp. 209-215
Author(s):  
Juan Manuel Revuelta ◽  
Álvaro Zamarrón ◽  
José Fortes ◽  
Gregorio Rodríguez-Boto ◽  
Jesús Vaquero ◽  
...  
Keyword(s):  
Rat Model ◽  
Perfusion Pressure ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Experimental Rat Model ◽  
Normal Perfusion Pressure Breakthrough
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