Cerebrovascular Reactivity in Hypertensive and Healthy Adolescents: TCD With Vasodilatory Challenge

Settakis, Georgios; Páll, Dénes; Molnár, Csilla; Bereczki, Dániel; Csiba, László; Fülesdi, Béla

doi:10.1111/j.1552-6569.2003.tb00166.x

Cited by 49 publications

(23 citation statements)

References 49 publications

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“…The most common method used to assess CVR though, is transcranial Doppler ultrasonography (TCD) (Dahl et al 1994;Markwalder et al 1984;Ringelstein et al 1988;Settakis et al 2003). TCD provides a low-cost, non-invasive means to measure blood flow velocities in the larger cerebral blood vessels in real-time.…”

Section: Introductionmentioning

confidence: 99%

Tissue Pulsatility Imaging of Cerebral Vasoreactivity During Hyperventilation

Kucewicz

Dunmire

Giardino

et al. 2008

Ultrasound in Medicine & Biology

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Tissue Pulsatility Imaging (TPI) is an ultrasonic technique that is being developed at the University of Washington to measure tissue displacement or strain due to blood flow over the cardiac and respiratory cycles. This technique is based in principle on plethysmography, an older non-ultrasound technology for measuring expansion of a whole limb or body part due to perfusion. TPI adapts tissue Doppler signal processing methods to measure the "plethysmographic" signal from hundreds or thousands of sample volumes in an ultrasound image plane. This paper presents a feasibility study to determine if TPI can be used to assess cerebral vasoreactivity. Ultrasound data were collected transcranially through the temporal acoustic window from four subjects before, during, and after voluntary hyperventilation. In each subject, decreases in tissue pulsatility during hyperventilation were observed that were statistically correlated with the subject's end-tidal CO 2 measurements.

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Section: Introductionmentioning

confidence: 99%

Tissue Pulsatility Imaging of Cerebral Vasoreactivity During Hyperventilation

Kucewicz

Dunmire

Giardino

et al. 2008

Ultrasound in Medicine & Biology

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“…Meanwhile, changing partial pressure of carbon dioxide in arterial blood (PaCO 2 ) is the strongest modulator of CBF because a linear relationship exists between PaCO 2 and CBF within a normal physiological range of PaCO 2 (20-75 mmHg) [12]. However, when considering cerebrovascular reactivity to PaCO 2 , other factors such as MAP, use of anaesthetic agents and disease states should be taken into account [12][13][14][15][16][17][18][19].In practice, cerebrovascular reactivity to PaCO 2 can be assessed by measuring cerebral oxygen saturation (rSO 2 ) with a near-infrared spectroscopy device [20], which has been used as a non-invasive and continuous monitoring method for detecting cerebral ischaemia in various clinical situations [8]. It measures the ratio of oxygenated haemoglobin and deoxygenated haemoglobin, and rSO 2 values are calculated based on the assumption of a fixed reference ratio of 25% arterial and 75% venous contribution [21].…”

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confidence: 99%

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confidence: 99%

Modelling of the Effect of End‐Tidal Carbon Dioxide on Cerebral Oxygen Saturation in Beach Chair Position under General Anaesthesia

Kim¹,

Chae

Chun

et al. 2016

Basic Clin Pharma Tox

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Patients undergoing shoulder surgery in the beach chair position (BCP) under general anaesthesia may be at risk of cerebral desaturation. Increasing end-tidal carbon dioxide (EtCO 2 ) is the most convenient and powerful method for the management of cerebral desaturation. The purpose of this study was to investigate the quantitative relationship between EtCO 2 and cerebral oxygen saturation (rSO 2 ) and to identify the associated influencing factors. Fifty-one patients undergoing arthroscopic shoulder surgery in the BCP under general anaesthesia completed this study. Desflurane and remifentanil were used, and EtCO 2 was steadily increased and then decreased by adjusting the ventilator settings every 3 min. so that time lag of rSO 2 response to EtCO 2 changes could be delineated. Near-infrared spectroscopy was used to monitor rSO 2 response. An indirect response model was used to examine the relationship between EtCO 2 and rSO 2 . To determine the relevant covariates, a stepwise approach was used. There was a linear relationship between rSO 2 and EtCO 2 with a slight delay in the peak of rSO 2 relative to EtCO 2 . Increase in end-tidal desflurane concentration led to a slower response of rSO 2 to the changes of EtCO 2 (p = 0.0002). The presence of diabetes mellitus reduced the reactivity of rSO 2 to EtCO 2 changes (p < 0.0001). This model-based approach revealed that diabetes mellitus attenuates the response of rSO 2 to changes in EtCO 2 . The management of cerebral desaturation by hypercapnia in patients with diabetes may be less effective than in non-diabetic patients under general anaesthesia with BCP.The beach chair position (BCP) under general anaesthesia with induced hypotension is commonly used in arthroscopic shoulder surgery [1]. Unlike the BCP in an awake state in which the compensatory mechanism to increase blood pressure occurs, the BCP under general anaesthesia is associated with significant hypotension and cerebral desaturation [2][3][4]. Further hypotension induced for better visualization of the surgical field might aggravate cerebral desaturation [4,5]. As cerebral desaturation during surgery is associated with postoperative cognitive dysfunction and stroke [6,7], prevention and treatment of cerebral desaturation is necessary.As cerebral oxygenation is dependent on cerebral perfusion and oxygen transport, interventions for the prevention and treatment of cerebral desaturation during shoulder surgery include increasing systemic arterial pressure with vasopressors, increasing end-tidal carbon dioxide (EtCO 2 ) with ventilation adjustment and increasing fraction of inspired oxygen (FiO 2 ) [3,4,8,9]. Although increases in systemic arterial pressure may cause rapid increases in cerebral blood flow (CBF), CBF returns to its baseline value within a few seconds by the mechanism of cerebral autoregulation, which aims to maintain a stable CBF over a wide range of mean arterial pressures (MAP) of 70-150 mmHg [10][11][12]. Moreover, increases in arterial pressure may worsen visualization of the sur...

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“…Although many reports substantiate the link between risks for atherosclerosis and blood flow at a global cerebral or lobar level (Claus et al, 1996;Novak et al, 2006;Selim et al, 2008;Groschel et al, 2007;Settakis et al, 2003), there is only a limited information about the influence of these factors on CBF in structures directly related to memory function. Hippocampus is a major anatomical substrate of memory (Eichenbaum, 2004;Shapiro, 2001), and its structural and functional abnormalities predict Alzheimer's disease (AD) (Glodzik-Sobanska et al, 2005;Mosconi, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Similarly, atherosclerosis risk factors impair vascular response to hypercapnia (Groschel et al, 2007;Settakis et al, 2003), as evidenced by Doppler studies.…”

Section: Introductionmentioning

confidence: 99%

Framingham Cardiovascular Risk Profile Correlates with Impaired Hippocampal and Cortical Vasoreactivity to Hypercapnia

Glodzik

Rusinek

Bryś

et al. 2010

J Cereb Blood Flow Metab

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Vascular risk factors affect cerebral blood flow (CBF) and cerebral vascular reactivity, contributing to cognitive decline. Hippocampus is vulnerable to both Alzheimer's disease (AD) pathology and ischemia; nonetheless, the information about the impact of vascular risk on hippocampal perfusion is minimal. Cognitively, healthy elderly (NL = 18, 69.9 ± 6.7 years) and subjects with mild cognitive impairment (MCI = 15, 74.9 ± 8.1 years) were evaluated for the Framingham cardiovascular risk profile (FCRP). All underwent structural imaging and resting CBF assessment with arterial spin labeling (ASL) at 3T magnetic resonance imaging (MRI). In 24 subjects (NL = 17, MCI = 7), CBF was measured after a carbon dioxide rebreathing challenge. Across all subjects, FCRP negatively correlated with hippocampal (q = À0.41, P = 0.049) and global cortical (q = À0.46, P = 0.02) vasoreactivity to hypercapnia (VR h ). The FCRP-VR h relationships were most pronounced in the MCI group: hippocampus (q = À0.77, P = 0.04); global cortex (q = À0.83, P = 0.02). The FCRP did not correlate with either volume or resting CBF. The hippocampal VR h was lower in MCI than in NL subjects (Z = À2.0, P = 0.047). This difference persisted after age and FCRP correction (F [3,20] = 4.6, P = 0.05). An elevated risk for vascular pathology is associated with a reduced response to hypercapnia in both hippocampal and cortical tissue. The VR h is more sensitive to vascular burden than either resting CBF or brain volume.

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Cerebrovascular Reactivity in Hypertensive and Healthy Adolescents: TCD With Vasodilatory Challenge

Abstract: Cerebral vasoreactivity is decreased among hypertensive individuals as compared to healthy controls.

Cited by 49 publications

References 49 publications

Tissue Pulsatility Imaging of Cerebral Vasoreactivity During Hyperventilation

Tissue Pulsatility Imaging of Cerebral Vasoreactivity During Hyperventilation

Modelling of the Effect of End‐Tidal Carbon Dioxide on Cerebral Oxygen Saturation in Beach Chair Position under General Anaesthesia

Framingham Cardiovascular Risk Profile Correlates with Impaired Hippocampal and Cortical Vasoreactivity to Hypercapnia

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