Middle Cerebral Artery Blood Flow Velocity Research Articles

Middle cerebral artery blood flow velocity during a 4km cycling time trial.

This study sought to describe middle cerebral artery blood flow velocity (MCAv) during a 4km cycling time trial, and relate it to different pacing strategies adopted by participants. After familiarisation and a standardised exercise protocol, 15 male trained cyclists rode a 4km time trial on a cycling ergometer. MCAv was assessed via transcranial Doppler ultrasound in the right hemisphere at resting baseline, and throughout the time trial. Mean arterial pressure, end-tidal partial pressure of carbon dioxide (PetCO2) and heart rate were assessed alongside MCAv. Plasma lactate was assessed post time trial. Data were compared depending upon whether participants completed the time trial with a positive (first half faster than the last) or negative pacing profile although there was no difference in the time to completion with either pacing strategy (positive 344±23s, negative 334±14s; p=0.394). Lower mean MCAv (positive pacing -7.6±14.2%, negative pacing +21.2±15.0% compared to resting baseline measures; p=0.004) and lower PetCO2 (significant interaction p<0.001) towards the end of the time trial were observed with positive compared to negative pacing. Heart rate and lactate did not differ between pacing strategies. Changes in MCAv appear to depend on the pacing strategy adopted, with a positive pacing strategy likely to contribute to a hyperventilatory drop in PetCO2 and subsequent reduction in MCAv. Although lower cerebral blood flow cannot be directly linked to an inability to raise or maintain power output during the closing stages of the time trial, this potential contributor to fatigue is worth further investigation.

Biomarkers of Disease Severity Predict Neurocognitive Functioning in Pediatric SCD

Introduction: Research clearly documents the increased risk of silent and overt strokes in pediatric patients with sickle cell disease (SCD), as well as the associated neurocognitive deficits in domains such as working memory (WM) and attention regulation. However, less research has examined the effects of biomarkers of SCD severity, such as cerebral blood flow velocity (CBFV), hemoglobin, and blood pressure, on neurocognitive functioning. This investigation aimed to explore the utility of using biomarkers to predict caregiver-reported neurocognitive and behavioral functioning in pediatric SCD.Methods: Fifty-nine children with SCD ages 7-16 (M = 10.44, SD = 2.87, 42% male) enrolled in a larger study of the feasibility and efficacy of a computerized cognitive training program. As part of this study, a primary caregiver completed the Behavior Rating Inventory of Executive Function (BRIEF) and Conners-3, both caregiver-reported measures of behavioral, attentional, and emotional functioning in children and adolescents. Scores on the BRIEF and Conners-3 are both represented with T scores, where higher scores reflect greater problems. Complete blood count (CBC) and vital signs were extracted from patients' medical charts if results had been documented within 45 days of date caregivers completed the BRIEF and Conners-3. Transcranial Doppler (TCD) ultrasonography results were extracted if a TCD had been performed within 12 months of the testing date.Results: Mean hemoglobin was 9.05 (SD = 1.33), mean hematocrit was 25.84 (SD = 3.71), mean systolic blood pressure was 107.43 (SD = 8.89), and mean diastolic blood pressure was 63.69 (SD = 9.49). TCD results revealed a mean right middle cerebral artery (MCA) CBFV of 206.00 (SD = 21.30), left MCA CBFV of 127.84 (SD = 22.40), right distal cerebral artery (DiCA) CBFV of 86.44 (SD = 23.00), and left DiCA CBFV of100.45 (SD = 27.28). Bivariate Pearson correlations and linear regression analyses were conducted to examine the relationships between biomarkers (e.g., CBFV, blood pressure, CBC results) and caregiver-reported neurocognitive and behavioral functioning. Modest correlations were observed between CBC results (e.g., hemoglobin, hematocrit) and caregiver-rated cognitive and behavioral outcomes; though, these relationships were no longer significant after controlling for age and gender in subsequent regression analyses. However, higher left DiCA velocities significantly predicted more problems on the BRIEF Working Memory and Initiate subdomains (R2 = .569, b = 0.442, p < .001; R2 = .746, b = .466, p < .001, respectively). Additionally, higher left DiCA velocities significantly predicted more caregiver-rated problems on the BRIEF Organization of Materials and Plan/Organize scales (R2= .447, b = 0.191, p = .049; R2 = .377, b = 0.372, p = .00), respectively. TCD and blood pressure results also significantly predicted scores on the caregiver-reported Connors-3 Executive Functioning subscale, with higher left DiCA (R2 = .432, b = 0.446, p = .001) and systolic BP (R2 = .196, b = 0.859,p =.003) predicting more problems with executive functioning.Conclusion: Certain biomarkers of SCD severity appear to have a detectable and direct influence on neurocognitive and behavioral functioning in pediatric SCD. TCD results, specifically left DiCA CBFV, and systolic blood pressure significantly predicted scores on the BRIEF and Conners-3, two caregiver-reported measures of neurocognitive and behavioral functioning. More specifically, higher CBFV and systolic blood pressure were predictive of more caregiver-rated problems with working memory, executive functioning, and organizational skills. These cognitive and behavioral domains are of particular importance in children, who depend on such skills to learn and succeed academically. Progressive disease-related neurocognitive deficits may contribute to long-term difficulties in academic achievement, social functioning, and vocational attainment. Biomarkers of SCD severity, such as CBFV and blood pressure, may be useful indicators of worsening neurocognitive status and signal the need for preventative care to protect neurological integrity and preserve quality of life in pediatric patients with SCD. DisclosuresNo relevant conflicts of interest to declare.

Effect of Hyperoxia on Cerebral Blood Flow Velocity and Regional Oxygen Saturation in Patients Operated on for Severe Traumatic Brain Injury–The Influence of Cerebral Blood Flow Autoregulation

The effect of normobaric hyperoxia on brain oxygenation in the presence or absence of intact autoregulation has not been studied previously in acute traumatic brain injury (TBI). In this prospective clinical investigation of 50 patients operated on for severe TBI, cerebral blood flow (CBF) velocity in the middle cerebral artery was measured using transcranial Doppler. Regional cerebral oxygen saturation using near-infrared spectroscopy at 3 different fractions of inspired oxygen (Fio2) (0.4, 0.6, and 1) was measured in the last 25 of these patients. There was no difference in the hemodynamic and respiratory variables except for Pao2, which increased with increasing Fio2. The CBF velocities and pulsatility indices did not vary at different levels of Fio2 (0.4, 0.6, and 1) both on the operated and on the nonoperated side. The regional cerebral oxygen saturation as evaluated by bifrontal near-infrared spectroscopy sensors increased with increasing Fio2 on the operated (pathologic) side with impaired cerebral autoregulation and not with intact autoregulation. In severe TBI, middle cerebral artery CBF velocity is not affected by hyperoxia in both the pathologic and the normal side. The cerebral oxygen saturation increased with increasing arterial hyperoxia in the operated cerebral hemisphere and remained within baseline range in the nonoperated hemisphere. Impairment in the cerebral autoregulation in the pathologic hemisphere contributes to this luxury oxygenation.

OP.3C.05] CHARACTERISTICS OF CEREBRAL HEMODYNAMICS AND CAROTID STIFFNESS IN PATIENTS WITH ISCHEMIC LEUKOARAIOSIS AND NEW ULTRASOUND INDICES OF ISCHEMIC LEUKOARAIOSIS

Objective: Leukoaraiosis (ILA) is believed to be ischaemic in origin due its association with cerebrovascular risk factors and similar location as lacunar infarctions. Its pathophysiology is not well understood and its diagnosis is still based on magnetic resonance imaging (MRI) as well as exclusion of other causes of white matter hyperintensities (WMH). So far there are no known confirming or screening diagnostic tests of ILA. Ultrasound studies have recently shown increased large artery stiffness, increased cerebrovascular resistance and lower cerebral blood flow in ILA patients. Increased arterial stiffness and decreased blood flow could have a synergistic effect and their ratio could be a useful diagnostic index of ILA. Design and method: We used Trans Cerebral Doppler sonography (TCD) and carotid duplex ultrasound to compeare cerebral blood flow and carotid stiffness in 53 ILA patients to 40 risk factor matched controls. The ILA diagnosis was based on head MRI and exclusion of other causes of WMH. Middle cerebral artery (MCA) systolic, diastolic and mean blood flow velocities (v-MCAs, v-MCAd, v-MCAm) and resistance indices (RI, PI) were determined. Carotid stiffness was accessed by pulse wave velocityβ (PWVβ, m/s), pressure–strain elasticity modulus (Ep, kPa) and β index. In addition we introduced new ILA indices (ILAi) that are rations of carotid stiffness parameters and MCA mean blood flow velocity. The diagnostic significance of ILAi for the prediction of ILA was analysed. Results: We found significantly lower diastolic, systolic and mean MCA blood flow velocities and increased carotid stiffness in the ILA group (p < 0,05). Higher pulsatility and resistivity indices of MCA were found in the ILA group, but they did not reached statistical significance. All the ILAi were significantly higher in the ILA group, the most significant was PWVβ/v-ACMm (p = 0.003). All ILAi were allso significantly associated with ILA and were sensitive and specific for predicting ILA (p < 0.05). Conclusions: MCA blood flow velocities are lower and carotid stiffness increased in ILA patients compared to risk factors matched controls. The combination of lower velocities and increased carotid stiffness represented as ILA indices could have a potential diagnostic value for ILA.

Analysis of the causes of age-related decline in the velocity of cerebral blood flow

Goal. Determining the causes of age-related decrease of blood flow velocity (BFV) in the middle cerebral artery (MCA) in healthy subjects and in patients during surgical lengthening of stunted limbs. Methods. BFV in MCA was determined by transcranial Doppler. The analysis of the indicator in functional muscle sample of 30 healthy people 18-60 years old and 30 patients 3-62 years of lagging in the growth of one of the lower limbs in the course of its operational extension. As an indicator of cerebral autoregulation used swing changes BFV indicators during the second holding muscle functional test. Results. The age-related reduction in flow rate in the middle cerebral artery was more pronounced in patients with disorders of the musculoskeletal system. At the same time, the average value of the magnitude of blood flow velocity index changes during the functional test in healthy individuals older than 10 years, as well as in patients before treatment and during the fixation is stable (17-25 %). Conclusion. Age-related decline in the BFV at MCA is a prerequisite for the preservation of cerebral autoregulation. Disorders of cerebral autoregulation in patients undergoing distraction of limbs greatly reduces their tolerance to physical exercise.

The Effect of Breaking up Prolonged Sitting on Cerebral Blood Flow

Prolonged sitting has a detrimental effect on peripheral conduit artery endothelial function, whilst breaking up prolonged sitting time can prevent such impairments. The effect of prolonged sitting and breaking up sitting time on cerebral blood flow (CBF) is currently unknown. Importantly, decreased CBF is related to lower cognitive functioning and increased risk of cognitive impairment and dementia. PURPOSE:To determine the effect of uninterrupted sitting and breaking up sitting time with light intensity walking on CBF in healthy subjects. METHODS: Thirteen healthy participants (8 male, 37.3±10.1 years old, BMI: 25.6±3.4 kg/m2) completed, on separate days, three 4 hr conditions in a counterbalanced order: a) uninterrupted sitting, b) sitting with 2-min light intensity walking breaks every 30 mins, or c) sitting with 8-min light intensity walking breaks every 2 hrs. Middle cerebral artery blood flow velocity (MCAv) was measured using transcranial Doppler in a supine position at BASELINE, 2HRS and 4HRS. Beat-to-beat blood pressure was assessed (Finometer), enabling the calculation of cerebrovascular conductance (CVC). Between each measurement participants remained seated and were permitted to complete desk-based tasks. RESULTS:There was no change over time in MCAv (BASELINE: 57.3±2.4 cm/s, 2HRS: 56.5±2.3 cm/s, 4HRS: 56.3±2.1 cm/s; p=0.77) or CVC (BASELINE: 0.71±0.04 cm/s/mmHg, 2HRS: 0.70±0.04 cm/s/mmHg, 4HRS: 0.67±0.03 cm/s/mmHg; p=0.18), or between the conditions (MCAv: p=0.18; CVC: p=0.11). Moreover, there was no interaction between condition and time for MCAv (p=0.56) or CVC (p=0.64). CONCLUSIONS:Contrary to previous findings which indicate that prolonged sitting can reduce peripheral endothelial function, our data suggest that neither CBF velocity nor CVC are altered following prolonged sitting for 4 hrs. Additionally, breaking up this sitting time with walking breaks did not further affect CBF velocity or CVC. Whilst our data indicate unaltered CBF following uninterrupted sitting, changes in cerebrovascular function may occur independent of changes in blood flow. Further research is therefore needed to determine whether measures of cerebrovascular function, including autoregulation and reactivity, are influenced by prolonged sitting. Supported by BBSRC Grant BB/L017237/1

Effects of short-term mechanical hyperventilation on cerebral blood flow and dynamic cerebral autoregulation in critically ill patients with sepsis

In sepsis, higher PaCO2 levels are associated with impaired dynamic cerebral autoregulation (dCA), which may expose the brain to hypo- and hyperperfusion during acute fluctuations in blood pressure. We hypothesised that short-term mechanical hyperventilation would dCA in critically ill patients with sepsis. Seven mechanically ventilated septic patients were included. We assessed dCA before and after 30 min of mechanical hyperventilation. Transfer function analysis of spontaneous oscillations in transcranial Doppler-based middle cerebral artery blood flow velocity (MCAv) and invasive mean arterial blood pressure was used to assess dCA. Mechanical enhance hyperventilation reduced the median PaCO2 from 5.3 (IQR, 5.0–6.5) to 4.7 (IQR, 4.2–5.1) kPa (p < 0.05). This was associated with a reduction in the median MCAv from 57 (IQR, 33–68) to 32 (IQR, 21–40) cm sec−1 (p < 0.05). Apart from a small increase in gain in the low frequency range (2.32 [IQR 1.80–2.41] vs. 2.59 (2.40–4.64) cm mmHg−1 sec−1; p < 0.05), this was not associated with any enhancement in dCA. In conclusion, cerebral CO2 vasoreactivity was found to be preserved in septic patients; nevertheless, and in contrast to our working hypothesis, short-term mechanical hyperventilation did not enhance dCA.

Characteristics of Cerebral Hemodynamics in Patients with Ischemic Leukoaraiosis and New Ultrasound Indices of Ischemic Leukoaraiosis

The diagnosis of ischemic leukoaraiosis (ILA) is based on head magnetic resonance imaging (MRI) and exclusion of other causes of white matter hyperintensities (WMHs). Recent studies have shown increased arterial stiffness and diminished carotid flow in ILA patients. So far, there are very little data on intracerebral hemodynamic parameters in ILA. Due to the specific structure of the intracranial arteries, our aim was to investigate intracerebral hemodynamic parameters in ILA patients and, possibly, to find a reliable ultrasound index of combined intra- and extracranial cerebral arteries. We compared different hemodynamic parameters in the middle cerebral artery (MCA) and local carotid stiffness parameters in 53 ILA patients to 40 gender and risk factor-matched controls with normal head MRI. The ILA diagnosis was based on head MRI and exclusion of other causes of WMH. In addition, we introduced new ischemic leukoariosis indices (ILAi) that are ratios of carotid stiffness parameters and MCA mean blood flow velocity. The diagnostic significance of ILAi for the prediction of ILA was analyzed. We found significantly lower diastolic, systolic, and mean MCA blood flow velocities and increased carotid stiffness in the ILA group (P ≤ .05). All ILAi significantly differed between the groups (P < .05), were significantly associated with ILA (P < .01), and were sensitive and specific for predicting ILA (P < .05). MCA blood flow velocities in ILA patients are lower compared to risk factor-matched controls. A combination of lower velocities and increased carotid stiffness represented as ILAi could have a potential diagnostic value for ILA.

Cerebrovascular, cardiovascular and strength responses to acute ammonia inhalation.

Ammonia is used as a stimulant in strength based sports to increase arousal and offset fatigue however little is known about its physiological and performance effects. The purpose of this study was twofold (1) establish the physiological response to acute ammonia inhalation (2) determine whether the timing of the physiological response corresponds with a performance enhancement, if any. Fifteen healthy males completed two trials. Trial one investigated the beat-to-beat middle cerebral artery blood flow velocity (MCAv), heart rate (HR) and mean arterial pressure (MAP) response to ammonia inhalation. During trial two, participants performed a maximal single mid-thigh pull (MTP) at various time points following ammonia inhalation in a randomised order: MTPs were conducted immediately, 15, 30 and 60s following ammonia inhalation. A MTP with no ammonia inhalation served as the control. During this trial maximal MTP force, rate of force development (RFD) and electromyography (EMG) activity were recorded. MCAvmean increased and peaked on average by 6cms(-1) (P<0.001), 9.4±5.5s following ammonia inhalation. Similarly, HR was increased by 6±11 beats per minute 15s following ammonia inhalation (P<0.001). MAP remained unchanged following inhalation (P=0.51). The use and timing of ammonia inhalation had no effect on maximal force, RFD or EMG (all P>0.2) compared to control. MCAv was elevated despite no increase in MAP occurring; this is indicative of a cerebrovascular vasodilation. Despite the marked cerebrovascular and cardiovascular response to ammonia inhalation no ergogenic effect was observed during the MTP, irrespective of the timing of administration.

“Float first and kick for your life”: Psychophysiological basis for safety behaviour on accidental short-term cold water immersion

IntroductionAccidental cold-water immersion (CWI) evokes the life threatening cold shock response (CSR) which increases the risk of drowning. Consequently, the safety behaviour selected is critical in determining survival; the present advice is to ‘float first’ and remain stationary (i.e. rest). We examined whether leg only exercise (i.e., treading water; ‘CWI-Kick’) immediately on CWI could reduce the symptoms of the CSR, offset the reduction in cerebral blood flow that is known to occur and reduce the CSR's symptoms of breathlessness. We also examined whether perceptual responses instinctive to accidental CWI were exacerbated by this alternative behaviour. We contrasted CWI-Kick to a ‘CWI-Rest’ condition and a thermoneutral control (35°C); ‘TN-Rest’. MethodSeventeen participants were tested (9 males, 8 females). All immersions were standardised; water temperature in cold conditions (i.e., 12°C) was matched ±/0.5°C within participant. Middle cerebral artery blood flow velocity (MCAv) and cardiorespiratory responses were measured along with thermal perception (sensation and comfort) and dyspnoea. Data were analysed using repeated measures ANOVA (alpha level of 0.05). ResultsMCAv was significantly reduced in CWI-Rest (−6 (9)%; 1st minute of immersion) but was offset by leg only exercise immediately on cold water entry; CWI-Kick MCAv was never different to TN-Rest (−3 (16)% cf. 5 (4)%). All CWI cardiorespiratory and perceptual responses were different to TN-Rest but were not exacerbated by leg only exercise. DiscussionTreading water may aid survival by offsetting the reduction in brain blood flow velocity without changing the instinctive behavioural response (i.e. perceptions). “Float first — and kick for your life” would be a suitable amendment to the water safety advice.

Non-Linear Characterisation of Cerebral Pressure-Flow Dynamics in Humans.

Cerebral metabolism is critically dependent on the regulation of cerebral blood flow (CBF), so it would be expected that vascular mechanisms that play a critical role in CBF regulation would be tightly conserved across individuals. However, the relationships between blood pressure (BP) and cerebral blood velocity fluctuations exhibit inter-individual variations consistent with heterogeneity in the integrity of CBF regulating systems. Here we sought to determine the nature and consistency of dynamic cerebral autoregulation (dCA) during the application of oscillatory lower body negative pressure (OLBNP). In 18 volunteers we recorded BP and middle cerebral artery blood flow velocity (MCAv) and examined the relationships between BP and MCAv fluctuations during 0.03, 0.05 and 0.07Hz OLBNP. dCA was characterised using project pursuit regression (PPR) and locally weighted scatterplot smoother (LOWESS) plots. Additionally, we proposed a piecewise regression method to statistically determine the presence of a dCA curve, which was defined as the presence of a restricted autoregulatory plateau shouldered by pressure-passive regions. Results show that LOWESS has similar explanatory power to that of PPR. However, we observed heterogeneous patterns of dynamic BP-MCAv relations with few individuals demonstrating clear evidence of a dCA central plateau. Thus, although BP explains a significant proportion of variance, dCA does not manifest as any single characteristic BP-MCAv function.

Postexercise orthostatic intolerance: influence of exercise intensity.

What is the central question of this study? Following exercise, hypotension is often reported and syncope is more likely. It is unresolved whether the postexercise hypotension associated with different exercise intensities contributes to the rate at which syncope develops. What is the main finding and its importance? The physiological events that induce presyncope are the same both before and after exercise; however, more intense exercise accelerated the development of hypocapnia, hypotension and, ultimately, syncope. These data indicate that higher intensity exercise induces a postexercise hypotension that reduces cardiovascular reserve, an earlier development of hypocapnia and, ultimately, cerebral hypoperfusion. After exercise, a reduction in mean arterial pressure is often experienced and is referred to as postexercise hypotension. Whilst syncope is more likely following exercise, it is unknown whether orthostatic tolerance is impacted by any exercise intensity-mediated effect on postexercise hypotension. We examined the effect of exercise intensity on time to presyncope, induced via combined head-up tilt and lower body negative pressure following 1h of cycling at 30 and 70% of heart rate range. Healthy participants (n = 8; mean±SD, 28±5 years old) completed orthostatic testing to presyncope before and after exercise. Beat-to-beat middle cerebral artery blood flow velocity (MCAv), mean arterial pressure and cerebral oxygenation (measured by near-infrared spectroscopy) were recorded continuously throughout orthostatic testing. During exercise, heart rates were 95±6 and 147±5beatsmin(-1) for 30 and 70% heart rate range, respectively, with average power outputs of 103±22 and 221±45W, respectively. Time to presyncope occurred 32% sooner after the 70% heart rate range trial (952±484 versus 1418±435s; P = 0.004). Both before and after exercise, presyncope occurred at the same reduction in MCAv (grouped mean, -30±11cms(-1) ), mean arterial pressure (-18±13mmHg), total oxygenation index (-6±2%) and partial pressure of end-tidal CO2 (-16±8mmHg; all P >0.1). At presyncope following exercise, the MCAv response was related more to the change in partial pressure of end-tidal CO2 from the baseline preceding orthostatic testing (r(2) =0.50, P=0.01) than to the hypotension (r(2) =0.12, P=0.17). Presyncope both before and after exercise occurred as a result of the same physiological perturbations, albeit greatly accelerated following more intense exercise.

Effects of preeclampsia on the amplitude integrated electroencephalography activity in preterm infants.

Preeclampsia leads to chronic intrauterine hypoxia by interfering with placental blood supply. The aim of this study was to investigate whether preeclampsia exposure has an influence on the central nervous system of infants, as monitored by amplitude integrated electroencephalography (aEEG). We recruited 52 infants with gestational age between 30 and 34 weeks. Twenty-seven infants were born to preeclamptic mothers, and 25 gestational age-matched infants whose mothers were healthy were enrolled as a control group. aEEG recordings were performed between 24 and 48 h of life using a cerebral function monitor (CFM) (Olympic Brainz monitor). Along with aEEG, middle cerebral artery (MCA) blood flow velocities (BFV) were measured using Doppler ultrasound. The duration of quiet sleep was significantly shorter (P=0.001), and Burdjalov score was lower (P=0.04) in the preeclampsia group. However, there was no change in MCA BFV in this group. Preeclampsia altered cerebral electrical activity of premature infants born to preeclamptic mothers.

Voluntary suppression of hyperthermia-induced hyperventilation mitigates the reduction in cerebral blood flow velocity during exercise in the heat.

Hyperthermia during prolonged exercise leads to hyperventilation, which can reduce arterial CO2 pressure (PaCO2 ) and, in turn, cerebral blood flow (CBF) and thermoregulatory response. We investigated 1) whether humans can voluntarily suppress hyperthermic hyperventilation during prolonged exercise and 2) the effects of voluntary breathing control on PaCO2 , CBF, sweating, and skin blood flow. Twelve male subjects performed two exercise trials at 50% of peak oxygen uptake in the heat (37°C, 50% relative humidity) for up to 60 min. Throughout the exercise, subjects breathed normally (normal-breathing trial) or they tried to control their minute ventilation (respiratory frequency was timed with a metronome, and target tidal volumes were displayed on a monitor) to the level reached after 5 min of exercise (controlled-breathing trial). Plotting ventilatory and cerebrovascular responses against esophageal temperature (Tes) showed that minute ventilation increased linearly with rising Tes during normal breathing, whereas controlled breathing attenuated the increased ventilation (increase in minute ventilation from the onset of controlled breathing: 7.4 vs. 1.6 l/min at +1.1°C Tes; P < 0.001). Normal breathing led to decreases in estimated PaCO2 and middle cerebral artery blood flow velocity (MCAV) with rising Tes, but controlled breathing attenuated those reductions (estimated PaCO2 -3.4 vs. -0.8 mmHg; MCAV -10.4 vs. -3.9 cm/s at +1.1°C Tes; P = 0.002 and 0.011, respectively). Controlled breathing had no significant effect on chest sweating or forearm vascular conductance (P = 0.67 and 0.91, respectively). Our results indicate that humans can voluntarily suppress hyperthermic hyperventilation during prolonged exercise, and this suppression mitigates changes in PaCO2 and CBF.

Factors affecting the determination of cerebrovascular reactivity

Background and PurposeCerebrovascular reactivity (CVR), measures the ability of the cerebrovasculature to respond to vasoactive stimuli such as CO2. CVR is often expressed as the ratio of cerebral blood flow change to CO2 change. We examine several factors affecting this measurement: blood pressure, stimulus pattern, response analysis and subject position.MethodsStep and ramp increases in CO2 were implemented in nine subjects, seated and supine. Middle cerebral artery blood flow velocity (MCAv), and mean arterial pressure (MAP) were determined breath-by-breath. Cerebrovascular conductance (MCAc) was estimated as MCAv/MAP. CVR was calculated from both the relative and absolute measures of MCAc and MCAv responses.ResultsMAP increased with CO2 in some subjects so that relative CVR calculated from conductance responses were less than those calculated from CVR calculated from velocity responses. CVR measured from step responses were affected by the response dynamics, and were less than those calculated from CVR measured from ramp responses. Subject position did not affect CVR.Conclusions(1) MAP increases with CO2 and acts as a confounding factor for CVR measurement; (2) CVR depends on the stimulus pattern used; (3) CVR did not differ from the sitting versus supine in these experiments; (4) CVR calculated from absolute changes of MCAv was less than that calculated from relative changes.

Impaired cerebrovascular reactivity in the early phase of subarachnoid hemorrhage in good clinical grade patients does not predict vasospasm.

Subarachnoid hemorrhage (SAH) alters cerebrovascular reactivity (CVR) to carbon dioxide (CO2), which may be related to an increased risk of delayed ischemic neurological deficits (DINDs). We report the results of bedside CVR testing in the acute phase of SAH in good clinical grade patients without established vasospasm or signs of DIND. Eighteen patients with SAH and 26 healthy subjects underwent CVR testing using transcranial Doppler with standardized changes in CO₂. None of the patients had clinical or radiological evidence of vasospasm or DIND at time of testing. A CVR index was calculated as the change in the middle cerebral artery blood flow velocity (MCAv) divided by the change in the end-tidal CO₂partial pressure (PCO₂), ∆ MCAv/Δ PCO₂, and values were compared with controls. SAH patients had lower CVR when compared with normal controls (p = 0.0001 and p = 0.0094, respectively). Impaired CVR was not correlated with future vasospasm (p = 0.2). Patients with SAH had significantly lower CVR indexes compared with healthy controls. Although impaired CVR was present in 50 % of the patients early after SAH, no correlation with later occurrence of DINDs was found.

Hemodynamic monitoring of middle cerebral arteries during cognitive tasks performance.

The aim of this study was to obtain temporal pattern and hemispheric dominance of blood flow velocity (BFV) changes and to assess suitability of different cognitive tasks for monitoring of BFV changes in the middle cerebral arteries (MCA). BFV were recorded simultaneously in MCA during performance of phonemic verbal fluency test (pVFT), Trail Making Tests A and B (TMTA and TMTB) and Stroop tests in 14 healthy, right-handed volunteers aged 20-26 years. A significant increase of BFV in both MCA was obtained during performance of all cognitive tasks. Statistically significant lateralization was found during performance of Stroop test with incongruent stimuli, while TMTB was found to have the best activation potential for MCA. Our findings specify TMTB as the most suitable cognitive test for monitoring of BFV in MCA.

Blood flow velocity in the middle cerebral artery during transnasal endoscopic skull base surgery performed in controlled hypotension

Background and purposeTo assess blood flow velocity in the middle cerebral artery (MCA) during transnasal endoscopic procedures performed with decreased hemodynamic parameters. Materials and methodsIn 40 patients who underwent endoscopic skull base surgery in controlled hypotension (studied group) and in 13 patients operated without reduction of hemodynamic parameters (control group), blood flow velocity in MCA was assessed with transcranial color Doppler sonography. ResultsBlood flow velocity in MCA remained within the range of age-specific reference values in all patients before operation. It decreased significantly in both groups after induction of anesthesia and then dropped even further in studied group of patients when hemodynamic parameters were reduced; the systolic velocity fell below the normal reference values in 25% of patients, the mean velocity in 50% and the diastolic velocity in 57% of patients. The diastolic velocity was much more heavily influenced by diminished hemodynamic parameters than systolic velocity in the studied group as opposed to the control group where reduction of blood flow velocity pertained equally systolic and diastolic velocity. ConclusionDuring transnasal endoscopic procedures performed in moderate hypotension, in addition to significant drop of blood flow velocity to values well below the normal reference range, a divergent reduction of systolic and diastolic velocity was detected. Since divergent systolic and diastolic velocity may indicate an early phase of cerebral autoregulation compromise, and the decrease of mean blood flow velocity in MCA corresponds with a decrease of cerebral blood flow, further investigations in this field seem warranted.

Methodological considerations for cerebrovascular reactivity testing and analysis (1184.3)

The cerebral microvasculature is exquisitely sensitive to carbon dioxide (CO2) and this cerebrovascular reactivity (CVR) is often used as a measure of cerebrovascular function. However, a review of the current literature reveals that the details of CVR protocols and analyses vary considerably between research groups. The objective of this study is to determine the sensitivity of CVR to these methodologies.We used dynamic end‐tidal forcing to measure CVR to CO2 under conditions of controlled normoxia, hypoxia and hyperoxia. Low levels of end‐tidal CO2 were obtained by hyperventilation; high levels by hypoventilation with added inspired CO2. Supine blood pressure and middle cerebral artery blood flow velocity (MCAv) were continuously recorded, as were inspired and expired oxygen (O2) and CO2.Here we discuss the physiological implications of different analysis techniques and also consider the effects on quantitative outcomes. We include the rationale and results of: different types of curve fitting; methods of normalizing MCAv; accounting for blood pressure changes; controlling O2; and introducing a phase lag between end‐tidal CO2 and MCAv.It is difficult to know whether CVR results are widely generalizable, or reflect unique protocols or analyses. This work is intended to stimulate discussion and encourage the publication of transparent methods in an effort to improve research reproducibility.Grant Funding Source: Supported by the Heart and Stroke Foundation of B.C. and Yukon (V.E.C.)

Hemodynamic Response to Upright Resistance Exercise

Upright resistance exercise causes large transient fluctuations in blood pressure during and immediately after the performance. We examined the effect of resistance load and the number of repetitions on the middle cerebral artery blood flow velocity (MCAv) response during and after upright squatting exercise. Healthy males (n = 12; mean ± SD: 26 ± 5 yr) completed 30%, 60%, and 90% of their six-repetition maximum load, completing two and six repetitions of these loads during two visits (order randomized). Beat-to-beat MCAv, blood pressure, and continuous end-tidal PCO2 during exercise, at nadir, and during recovery are reported as the change from preexercise standing baseline. During exercise, MCAvmean increased 31% ± 16% (P < 0.001) across all loads (P = 0.74) and repetitions (P = 0.89), whereas mean arterial pressure (MAP) increased (all P < 0.05) as load and repetitions increased (e.g., 122 ± 9 (two repetitions) vs 135 ± 11 mm Hg (six repetitions) and 128 ± 13 vs 143 ± 14 mm Hg, at 30% and 60%, respectively). Within the six-repetition sets, peak MCAvmean remained unchanged across the set (P = 0.61), whereas MAP increased (P = 0.003). The 90% load produced the lowest MCAvmean nadir (pooled means, -18 ± 6 vs -10 ± 7 cm·s, P < 0.001 vs 30%) and MAP nadir (-34 ± 7 and -43 ± 5 mm Hg, for two and six repetitions, respectively; P < 0.001) after exercise. Postexercise MCAvmean reductions occurred via a selective, load-dependent (P < 0.001) decrease in diastolic MCAv. MCAvmean remained below baseline for the longest period after the 90% six-repetition set (10 s postexercise, P < 0.01) and took the longest to recover (14.8 ± 6.9 s, P = 0.002). These data indicate that higher relative loads produce a greater postexercise hypotension and result in a proportionate reduction in MCAvmean.