Static Cerebral Autoregulation Research Articles

Abstract WP227: Magnetic Resonance Measurement Of Static Global And Regional Cerebral Autoregulation

Background: Reliable methods used to test static cerebral autoregulation are time-consuming and/or invasive. Objectives: To evaluate if noninvasive magnetic resonance measured oxygen extraction fraction (OEF), cerebral blood flow (CBF), and oxygen metabolic index (OMI=CBF×OEF) can consistently detect expected physiological changes in humans under normal and 10-15% lowered mean arterial pressure (MAP). Methods: Static cerebral autoregulation was determined by measuring changes in CBF using a pseudo continuous arterial spin labeling (pCASL) approach and Oxygen Extraction Fraction (OEF) using MRI T2‘-weighted asymmetric spin echo echo-planar imaging (EPI) sequences, in response to 10-15% reductions in MAP in stroke-free controls induced by using IV Nicardipine. Images were acquired in 3T MR scanner (Trio, Siemens Medical Systems Inc). Autoregulation was measured globally and regionally in the anterior (ACA), the middle (MCA) and the posterior cerebral artery (PCA) territories of the brain manually defined using autopsy based model. Autoregulatory Index (AI) was computed (AI = %CBF change/% MAP change) supplemented by CBF associated OEF changes. Baseline regional CBF and OEF, AI, CBF and OEF changes to 10-15% lowering of MAP Results: Nineteen normal volunteers (mean age 30, 95% male, 50% white, 40% black, 10% others) were consented to the protocol approved by the institutional review board. MAP lowering was successfully achieved in all subjects (Mean ± standard deviation of MAP lowering of 12.5 ± 5.6 mm Hg). At a global level this resulted in no significant change between pre-MAP lowering CBF (56.0 ± 8.5 ml/100g/min) and post-MAP lowering CBF (55.9± 8.8 ml/100g/min). This translated to a AI of 0 ± 1.2. The CBF results corroborated with no significant change in OEF and OMI. Baseline regional CBF was higher in the MCA territory (66.1 ± 7.6 ml/100g/min) compared with the ACA territory (52.8 ± 8.6ml/100g/min, p<0.001). The AIs were consistent (ANOVA p=0.15) at regional levels across ACA (-1.5 ± 3.1), MCA(-0.3± 2.1) and PCA (-0.1 ± 1.4) territories. Conclusions: Global and regional static cerebral autoregulation can be measured using MR measurement of CBF, OEF and OMI, before and after 10-15% reductions in MAP in healthy volunteers.

You say resistance, I say compliance; let's call the whole thing cerebral Windkessel control

You say resistance, I say compliance; let's call the whole thing cerebral Windkessel control

Different Cerebral Hemodynamic Responses Between Sexes and Various Vessels in Orthostatic Stress Tests

The argument about why the head-up tilt table test (HUT) does not include the posterior cerebral circulation, which is mainly responsible for syncope, as a monitor target has not been resolved. It is also unclear whether there is a sex difference in cerebral blood flow (CBF) changes. We hypothesized that orthostatic CBF changes more in the posterior circulation than in the anterior circulation and is different between sexes. Thirty healthy volunteers (13 female and 17 male) were recruited for the HUT. The blood pressure (BP), middle cerebral artery flow velocity (MCAFV), and posterior cerebral artery flow velocity (PCAFV) were monitored simultaneously. Static cerebral autoregulation (CA) was calculated. The female volunteers had a lower BP, but there was no difference in orthostatic BP changes (female versus male: 1.29% +/- 5.26% versus 4.22% +/- 12.65%; P = .65). The female volunteers had a significantly greater orthostatic drop in the PCAFV than in the MCAFV (23.8% +/- 9.1% versus 18.2% +/- 7.3%; P = .008). The static CA in the middle cerebral artery was better than in the posterior cerebral artery, although not significantly (13.6% +/- 34.8% versus - 2.8% +/- 12.2%; P = .15). Our study showed the different cerebral hemodynamic responses between anterior and posterior circulations and between sexes during the HUT. We conclude that HUT studies for syncope should include the posterior cerebral circulation, especially for female patients.

Dynamic Cerebral Autoregulation and Monitoring Cerebral Perfusion

Cerebral autoregulation (CA) describes the capability of the brain to maintain its flow as relatively stable over a wide rage of mean arterial pressures (MAPs), for example, from 60 to 150 mm Hg. Because the brain is encompassed in the skull, CA is vital for preventing cerebral edema and hemorrhage, as illustrated in some patients experiencing acute liver failure.1 Also, CA counteracts the effect on cerebral blood flow (CBF) of a reduction in MAP in response to, for example, hemorrhage or a change in body position. Yet, when rising from a supine or seated position, one sometimes experiences symptoms indicative of a reduced CBF, like blurred vision.2 Thus, CA is of general clinical interest. For example, diabetic patients have increased risk of developing ischemic or hemorrhagic stroke, and in some diabetic patients CA is affected. Evidence for CA was provided in the 1930s when Fog,3 through a cranial window, observed the pial artery reaction to manipulation of MAP. For humans, CBF was measured with introduction of the method of Kety-Schmidt in 1948,4 and it was used in 1954 by Finnerty et al5 to determine cerebral hemodynamics of the ischemic brain after an acute reduction in MAP in attempt to define what now would be considered the lower limit of CA. However, it was the review by Lassen6 that introduced the concept of CA by plotting CBF against MAP to illustrate the relative stability of CBF over a wide range of blood pressure. Also, the lower and upper limits of CA were identified by a decrease in CBF at a low MAP and an increase …

Influence of Changes in Blood Pressure on Cerebral Perfusion and Oxygenation

Cerebral autoregulation (CA) is a critical process for the maintenance of cerebral blood flow and oxygenation. Assessment of CA is frequently used for experimental research and in the diagnosis, monitoring, or prognosis of cerebrovascular disease; however, despite the extensive use and reference to static CA, a valid quantification of "normal" CA has not been clearly identified. While controlling for the influence of arterial Pco(2), we provide the first clear examination of static CA in healthy humans over a wide range of blood pressure. In 11 healthy humans, beat-to-beat blood pressure (radial arterial), middle cerebral artery blood velocity (MCAv; transcranial Doppler ultrasound), end-tidal Pco(2), and cerebral oxygenation (near infrared spectroscopy) were recorded continuously during pharmacological-induced changes in mean blood pressure. In a randomized order, steady-state decreases and increases in mean blood pressure (8 to 14 levels; range: approximately 40 to approximately 125 mm Hg) were achieved using intravenous infusions of sodium nitroprusside or phenylephrine, respectively. MCAv(mean) was altered by 0.82+/-0.35% per millimeter of mercury change in mean blood pressure (R(2)=0.82). Changes in cortical oxygenation index were inversely related to changes in mean blood pressure (slope=-0.18%/mm Hg; R(2)=0.60) and MCAv(mean) (slope=-0.26%/cm . s(-1); R(2)=0.54). There was a progressive increase in MCAv pulsatility with hypotension. These findings indicate that cerebral blood flow closely follows pharmacological-induced changes in blood pressure in otherwise healthy humans. Thus, a finite slope of the plateau region does not necessarily imply a defective CA. Moreover, with progressive hypotension and hypertension there are differential changes in cerebral oxygenation and MCAv(mean).

Decreased upright cerebral blood flow and cerebral autoregulation in normocapnic postural tachycardia syndrome

Postural tachycardia syndrome (POTS), a chronic form of orthostatic intolerance, has signs and symptoms of lightheadedness, loss of vision, headache, fatigue, and neurocognitive deficits consistent with reductions in cerebrovascular perfusion. We hypothesized that young, normocapnic POTS patients exhibit abnormal cerebral autoregulation (CA) that results in decreased static and dynamic cerebral blood flow (CBF) autoregulation. All subjects had continuous recordings of mean arterial pressure (MAP) and CBF velocity (CBFV) using transcranial Doppler sonography in both the supine supine position and during a 70 degrees head-up tilt. During tilt, POTS patients (n = 9) demonstrated a higher heart rate than controls (n = 7) (109 +/- 6 vs. 80 +/- 2 beats/min, P < 0.05), whereas controls demonstrated a higher MAP than POTS (87 +/- 2 vs. 77 +/- 3 mmHg, P < 0.05). Also during tilt, mean CBFV decreased 19.5 +/- 2.6% in POTS patients versus 10.3 +/- 2.0% in controls (P < 0.05). We then used a transfer function analysis of MAP and CFBV in the frequency domain to quantify these changes. The low-frequency (LF; 0.04-0.15 Hz) component of CBFV variability increased during tilt in POTS patients (supine: 3 +/- 0.9 vs. tilt: 9 +/- 2, P < 0.02). In POTS patients, there was an increase in LF and high-frequency coherence between MAP and CBFV, an increase in LF gain, and a lack of significant change in phase. Static CA may be less effective in POTS patients compared with controls, since immediately after tilt CBFV decreased more in POTS patients and was highly oscillatory and autoregulation did not restore CBFV to baseline values until the subjects became supine. Dynamic CA may be less effective in POTS patients because MAP and CBFV during tilt became almost perfectly synchronous. We conclude that dynamic and static autoregulation of CBF are less effective in POTS patients compared with control subjects during orthostatic challenge.

Cerebral Autoregulation is affected in Postural Tachycardia Syndrome

Orthostatic intolerance (OI) is defined by symptoms and signs while upright, relieved by recumbency. Included are symptoms of CNS malperfusion. Chronic OI, also known as postural tachycardia syndrome (POTS), is associated with excessive upright tachycardia. We hypothesized that CNS symptoms are due to defects of dynamic and static cerebral autoregulation (CA). Nine normocapnic POTS patients and 6 control subjects, ages 15‐27, were continuously monitored for heart rate (HR), mean blood pressure (MAP), end‐tidal CO2, and cerebral blood flow velocity (CBFV) during a supine period and 70° head‐up tilt. Transfer function analysis, with low frequency (LF) between 0.04‐0.15 Hz and high frequency (HF) between 0.15‐0.40 Hz, compared MAP and CBFV. During tilt, POTS had a higher HR than controls (112 ± 14 vs. 83 ± 9 bpm) and lower systolic BP (110 ± 11 vs. 123 ± 4 mmHg). Supine CBFV decreased during tilt in POTS from 66 ± 21 to 54 ± 15.3 cm/s; whereas, in controls it dropped from 67 ± 16.5 to 61 ± 14.9 cm/s. Analysis during tilt showed that POTS exhibited a higher LF and HF coherence than controls (LF: 0.85 ± 0.11 vs. 0.30 ± 0.09; HF: 0.81 ± 0.16 vs. 0.24 ± 0.09). The greater decrease of CBFV during tilt in POTS compared to controls shows decreased static CA affecting CNS perfusion. The high coherence between MAP and CBFV in POTS implies decreased dynamic CA, which permits BP oscillations to further compromise phasic CBF.

Static Cerebral Pressure Autoregulation is Intact in Patients with Severe Traumatic Brain Injury

Static Cerebral Pressure Autoregulation is Intact in Patients with Severe Traumatic Brain Injury

One-Minute Dynamic Cerebral Autoregulation in Severe Head Injury Patients and its Comparison with Static Autoregulation. A Transcranial Doppler Study

To compare dynamic and static responses of cerebral blood flow to sudden or slow changes in arterial pressure in severe traumatic brain injury (TBI) patients. Prospective study. We studied 12 severe TBI patients, age 16-63 years, and median GCS 6. We determined the dynamic cerebral autoregulation: response of cerebral blood flow velocity to a step blood pressure drop, and the static cerebral autoregulation: change in cerebral blood flow velocity after a slow hypertensive challenge. During the dynamic response, the median drop in arterial pressure was 21 mm Hg. Dynamic response was graded between 9 (best) and 0 (worst). The median value was 5; four patients showed high values, (8-9), five patients showed intermediate values (4-6). In three patients (value = 0), the CBFV drop was greater than the cerebral perfusion pressure drop, and maintained through 60 s. The static cerebral autoregulation was preserved in 6/11 patients. The comparison between the two showed four different combinations. The five patients with impaired static cerebral autoregulation showed unfavorable outcome. A sharp dynamic vasodilator response could not be sustained, and a slow or absent reaction to a sudden hypotensive challenge could show an acceptable cerebral autoregulation in the steady state. We found that patients with impaired static cerebral autoregulation had a poor outcome, whereas those with preserved static cerebral autoregulation experience favorable outcomes.

Hemispheric Differences in Cerebral Autoregulation in Children with Moderate and Severe Traumatic Brain Injury

To examine hemispheric differences in cerebral autoregulation in children with traumatic brain injury (TBI). After IRB approval and consent, subjects underwent static cerebral autoregulation testing during the first 9 days after PICU admission. Cerebral autoregulation was quantified using the autoregulatory index (ARI). Forty-two (27 M:15 F) children (10 +/- 5 years) with TBI and admission Glasgow coma scale score (5 +/- 2) were enrolled. Seven (54%) of the 13 children with focal TBI and 8 (28%) of 29 children with diffuse TBI had impairment or absence of cerebral autoregulation of at least one hemisphere. In patients with isolated focal TBI, ARI was lower (0.40 +/- 0.40 vs. 0.67 +/- 0.40; P = 0.03) in the side of TBI than in the unaffected hemisphere, but cerebral autoregulation was often impaired on the side without TBI or shift (5/13) on head CT. There was no difference in ARI between hemispheres in children with diffuse TBI, with or without superimposed focal lesions (P = 0.17). Patients with bilateral intact cerebral autoregulation tended to have higher 6 month Glasgow Outcome Score (GOS) than patients with either unilateral or bilateral cerebral autoregulation impairment (GOS 4.0 +/- 0.60 vs. 3.6 +/- 0.80; P = 0.08). Hemispheric differences in cerebral autoregulation were common in children with isolated focal TBI. Absence of TBI on CT was not always associated with intact cerebral autoregulation. Patients with bilaterally intact cerebral autoregulation tended to have better outcomes.

Cerebral Autoregulation: From Models to Clinical Applications

Short-term regulation of cerebral blood flow (CBF) is controlled by myogenic, metabolic and neurogenic mechanisms, which maintain flow within narrow limits, despite large changes in arterial blood pressure (ABP). Static cerebral autoregulation (CA) represents the steady-state relationship between CBF and ABP, characterized by a plateau of nearly constant CBF for ABP changes in the interval 60-150 mmHg. The transient response of the CBF-ABP relationship is usually referred to as dynamic CA and can be observed during spontaneous fluctuations in ABP or from sudden changes in ABP induced by thigh cuff deflation, changes in posture and other manoeuvres. Modelling the dynamic ABP-CBFV relationship is an essential step to gain better insight into the physiology of CA and to obtain clinically relevant information from model parameters. This paper reviews the literature on the application of CA models to different clinical conditions. Although mathematical models have been proposed and should be pursued, most studies have adopted linear input-output ('black-box') models, despite the inherently non-linear nature of CA. The most common of these have been transfer function analysis (TFA) and a second-order differential equation model, which have been the main focus of the review. An index of CA (ARI), and frequency-domain parameters derived from TFA, have been shown to be sensitive to pathophysiological changes in patients with carotid artery disease, stroke, severe head injury, subarachnoid haemorrhage and other conditions. Non-linear dynamic models have also been proposed, but more work is required to establish their superiority and applicability in the clinical environment. Of particular importance is the development of multivariate models that can cope with time-varying parameters, and protocols to validate the reproducibility and ranges of normality of dynamic CA parameters extracted from these models.

Role of the altitude level on cerebral autoregulation in residents at high altitude

Cerebral autoregulation is impaired in Himalayan high-altitude residents who live above 4,200 m. This study was undertaken to determine the altitude at which this impairment of autoregulation occurs. A second aim of the study was to test the hypothesis that administration of oxygen can reverse this impairment in autoregulation at high altitudes. In four groups of 10 Himalayan high-altitude dwellers residing at 1,330, 2,650, 3,440, and 4,243 m, arterial oxygen saturation (Sa(O(2))), blood pressure, and middle cerebral artery blood velocity were monitored during infusion of phenylephrine to determine static cerebral autoregulation. On the basis of these measurements, the cerebral autoregulation index (AI) was calculated. Normally, AI is between zero and 1. AI of 0 implies absent autoregulation, and AI of 1 implies intact autoregulation. At 1,330 m (Sa(O(2)) = 97%), 2,650 m (Sa(O(2)) = 96%), and 3,440 m (Sa(O(2)) = 93%), AI values (mean +/- SD) were, respectively, 0.63 +/- 0.27, 0.57 +/- 0.22, and 0.57 +/- 0.15. At 4,243 m (Sa(O(2)) = 88%), AI was 0.22 +/- 0.18 (P < 0.0005, compared with AI at the lower altitudes) and increased to 0.49 +/- 0.23 (P = 0.008, paired t-test) when oxygen was administered (Sa(O(2)) = 98%). In conclusion, high-altitude residents living at 4,243 m have almost total loss of cerebral autoregulation, which improved during oxygen administration. Those people living at 3,440 m and lower have still functioning cerebral autoregulation. This study showed that the altitude region between 3,440 and 4,243 m, marked by Sa(O(2)) in the high-altitude dwellers of 93% and 88%, is a transitional zone, above which cerebral autoregulation becomes critically impaired.

Brain activity affects dynamic but not static autoregulation

A close correlation between neuronal activity and cerebral blood flow was documented (activation-flow coupling). The matter of an activity-related effect on autoregulation remains elusive. We modulated cortical activity by GABAergic inhibition in 10 pre-anestesized rats and compared effects on activation-flow coupling and autoregulation. Contralateral forepaw stimulation was used to assess activation-flow coupling. Somatosensory potentials as well as local flow velocity responses were recorded with surface electrodes and laser-Doppler flowmetry. Performing intermittent carotid compression we calculated from the laser-Doppler data the transient hyperemic response ratio as a parameter of dynamic cerebral autoregulation. Recovery of cerebral perfusion at the end of the compression phase served as an index of static autoregulation. Tests were performed at baseline and after four successive doses of midazolam (0.5 mg/kg), applied at 30 min intervals. Reversibility of the changes was evaluated by application of flumazenil (0.2 mg/kg). Resting flow velocity levels (162 ± 52 vs. 110 ± 62 U; p < 0.001), evoked potentials (N2-P1-amplitude; 13 ± 4 vs.6 ± 3 μV; p < 0.005), and resultant flow velocity responses (28 ± 12 vs. 4 ± 3%; p < 0.0001) decreased after the first dose of midazolam and then remained stable. A dose-dependent decrease was found for the transient hyperemic response ratio (28 ± 13 to 22 ± 14 to 15 ± 10 ( p < 0.05) to 9 ± 5% ( p < 0.025)) but not static autoregulation. After antagonism, all changes were reversible. Dynamic but not static cerebral autoregulation depends from neuronal activity and thus metabolic demand of neurons.

Assessment of dynamic changes in cerebral autoregulation

Cerebral autoregulation (CA) is a control mechanism that adjusts cerebral vasomotor tone in response to changes in arterial blood pressure (ABP) to ensure a nearly constant cerebral blood flow. Patient treatment could be optimized if CA monitoring were possible. Whereas the concept of static CA assessment is simply based on comparison of mean values obtained from two stationary states (e.g., before and after a pressure change), the evaluation of dynamic CA is more complex. Among other methods, moving cross-correlation analysis of slow waves in ABP and cerebral blood flow velocity (CBFV) seems to be appropriate to monitor CA quasi-continuously. The calculation of an "instantaneous transfer function" between ABP and CBFV oscillations in the low-frequency band using the Wigner-Ville distribution may represent an acceptable compromise in time-frequency resolution for continuous CA monitoring.

Indomethacin and cerebral autoregulation in severe head injured patients: a transcranial Doppler study

To assess the effect of indomethacin on cerebral autoregulation, systemic and cerebral haemodynamics, in severe head trauma patients. Prospective, controlled clinical trial, with repeated measurements. A 12-bed adult general intensive care unit in a third level referral university hospital. 16 severely head injured patients, 14 males, age range 17-60. Indomethacin was administrated as a load plus continuous infusion. Indomethacin reactivity was assessed as the estimated cerebral blood flow change elicited by the load. Dynamic and static cerebral autoregulation tests were performed before indomethacin administration, and during its infusion. Systemic and cerebral haemodynamic changes were assessed through continuous monitoring of mean arterial pressure, transcranial Doppler cerebral blood flow velocity, intracranial pressure, cerebral perfusion pressure, and jugular venous oxygen saturation. Indomethacin loading dose was immediately followed by a cerebral blood flow median decrease of 36 or 29% (p = ns) evaluated by two different methods, by an ICP decrease and by an AVDO(2) increase from 3.52 to 6.15 mL/dL (p = 0.002). Dynamic autoregulation increased from a median of 28 to 57% (p<0.05) during indomethacin infusion; static autoregulation also increased, from a median of 72 to 89% (p = ns). Indomethacin decreased intracranial pressure and cerebral blood flow, and increased cerebral perfusion pressure, while maintaining tissue properties of further extracting O(2). The increase in both autoregulatory values reveals an enhancement of cerebral microvasculature reactivity under indomethacin, during hypertensive and--especially--during hypotensive situations.

Preservation of static and dynamic cerebral autoregulation after mild hypothermic cardiopulmonary bypass

Dysfunction of cerebral autoregulation might contribute to neurological morbidity after cardiac surgery. In this study, our aim was to assess the preservation of cerebral autoregulation after cardiac surgery involving cardiopulmonary bypass (CPB). Dynamic and static components of cerebral autoregulation were evaluated in 12 patients undergoing coronary artery bypass graft surgery, anaesthetized with midazolam, fentanyl, and propofol, and using mild hypothermic CPB (31-33 degrees C). Arterial pressure (ABP), central venous pressure (CVP), and blood flow velocity in the middle cerebral artery (CBFV) were recorded. The cerebral perfusion pressure (CPP) was calculated as a difference between mean ABP and CVP. Rapid decrease of CPP was caused by a sudden change of patients' position from Trendelenburg to reverse Trendelenburg. Cerebral vascular resistance (CVR) was calculated by dividing CPP by CBFV. Index of static cerebral autoregulation (CAstat) was calculated as the change of CVR related to change of CPP during the manoeuvre. Dynamic rate of autoregulation (RoRdyn) was determined as the change in CVR per second during the first 4 s immediately after a decrease in CPP, related to the change of CPP. Measurements were obtained after induction of anaesthesia, and 15, 30, and 45 min after termination of CPB. No significant changes were found in CAstat or RoRdyn after CPB. Significant changes in CVR could be explained by concomitant changes in body temperature and haematocrit. Autoregulation of cerebral blood flow remains preserved after mild hypothermic CPB.

Cerebral autoregulation is preserved in postural tachycardia syndrome

To test whether cerebral autoregulation is impaired in patients with postural tachycardia syndrome (POTS), we evaluated 17 healthy control subjects and 27 patients with POTS. Blood pressure, heart rate, and cerebral blood velocity (transcranial Doppler) were recorded at rest and during 80 degree head-up tilt (HUT). Static cerebral autoregulation, as assessed from the change in cerebrovascular resistance during HUT, was the same in POTS and in controls. The properties of dynamic cerebral autoregulation were inferred from transfer gain, coherence, and phase of the relationship between blood pressure and cerebral blood velocity estimated from filtered data segments (0.02-0.8 Hz). Dynamic cerebral autoregulation of patients with POTS did not differ from that of controls. The patients' dynamic cerebral autoregulation did not change over the course of HUT, despite increased tachycardia suggestive of worsening orthostatic stress. Inflation of military anti-shock trouser pants substantially reduced the tachycardia of patients with POTS without affecting cerebral autoregulation. Symptoms of orthostatic intolerance were reduced in one-half of the patients following military anti-shock trouser pants inflation. We conclude that cerebral perfusion and autoregulation in many patients with POTS do not differ from that of normal control subjects.

Impaired cerebral autoregulation in patients with malignant hypertension.

In patients with a malignant hypertension, immediate parenteral treatment with blood pressure-lowering agents such as intravenous sodium nitroprusside (SNP) is indicated. In this study, we evaluated static and dynamic cerebral autoregulation (CA) during acute blood pressure lowering with SNP in these patients. In 8 patients with mean arterial pressure (MAP) >140 mm Hg and grade III or IV hypertensive retinopathy at hospital admission, middle cerebral artery blood velocity (MCA V) and blood pressure were monitored. Dynamic CA was expressed as the 0.1-Hz MCA V(mean) to MAP phase lead and static CA as the MCA V(mean) to MAP relationship during SNP treatment. Eight normotensive subjects served as a reference group. In the patients, the MCA V(mean) to MAP phase lead was lower (30+/-8 degrees versus 58+/-5 degrees , mean+/-SEM; P<0.05), whereas the transfer gain tended to be higher. During SNP treatment, target MAP was reached within 90 minutes in all patients. The MCA V(mean) decrease was 22+/-4%, along with a 27+/-3% reduction in MAP (from 166+/-4 to 121+/-6 mm Hg; P<0.05) in a linear fashion (averaged slope, 0.82+/-0.15% cm x s(-1) . % mm Hg(-1); r=0.70+/-0.07). In patients with malignant hypertension, dynamic CA is impaired. An MCA V(mean) plateau was not detected during the whole SNP treatment, indicating loss of static CA as well. This study showed that during the whole rapid reduction in blood pressure with SNP, MCA V(mean) decreases almost one on one with MAP.

The lower limit of cerebral autoregulation in children during sevoflurane anesthesia.

In adults, the lower limit of cerebral autoregulation (LLA) is generally considered to be a mean arterial pressure (MAP) of 60 mmHg. The LLA in healthy children has not been identified. The aim of this report is to describe the LLA in anesthetized children and relate it to age. Static cerebral autoregulation testing was performed in children 6 months to 14 years of age during <1 MAC sevoflurane anesthesia. Mean middle cerebral artery flow velocities (Vmca) were continuously measured using transcranial Doppler ultrasonography. MAP was increased with infusion of intravenous phenylephrine incrementally titrated to the greater of either: 1) 20% above baseline MAP or 2) 80 mmHg (<9 years), 90 mmHg (9-14 years). The LLA was defined by the point where the two linear regression lines fitting the Vmca/MAP crossed. The lower limit reserve (LLR) and autoregulatory reserve (ARR%) were defined as follows: LLR=Baseline MAP-LLA; ARR (%)=(LLR/Baseline MAP)x100. There were 13 subjects <2 years of age (group 1), 13 subjects 2 to 5 years of age (group 2), 14 subjects 6 to 9 years of age (group 3), and 13 subjects 10 to 14 years of age (group 4). Older children (groups 3 and 4) had a higher baseline MAP compared with younger children (groups 1 and 2) (82 +/- 10 mmHg vs. 70 +/- 10 mmHg, respectively; P=0.0001). However, there was no difference in LLA (59 +/- 17 mmHg vs. 60 +/- 8 mmHg; P=0.6) between older and younger children. Consequently, the LLR was greater in older children compared with younger children (25 +/- 12 mmHg vs. 12 +/- 10 mmHg, respectively; P=0.0007). Similarly, the ARR was significantly higher in older children compared with younger children (30% +/- 16% vs. 16% +/- 12%; P=0.002). In this study, we found no age-related differences in the LLA. Older children had a greater LLR and ARR compared with young children. The baseline MAP in young children may rest close to the LLA. These findings may have implications for managing hemodynamics in anesthetized children at risk for secondary brain injury.

Cerebral autoregulation indicesare unimpaired by hypertensionin middle aged and older people

Background Hypertension is known to increase the limits of static cerebral autoregulation (CA) but its effects on other aspects of CA such as efficiency and latency are unknown. In this study we test the hypothesis that dynamic cerebral autoregulation and the efficiency of static cerebral autoregulation are impaired by untreated hypertension. Methods Cerebral blood flow velocity was recorded using transcranial Doppler ultrasound, along with noninvasive beat-to-beat blood pressure (BP), electrocardiogram, and transcutaneous carbon dioxide levels, with subjects at rest and during isometric hand grip, thigh cuff, and the Valsalva maneuver. Static and dynamic CA indices were calculated. Results No significant difference was seen in static or dynamic CA indices between normotensive and hypertensive groups for any pressor or depressor stimulus. Spearman's rank correlation showed no relation between static or dynamic CA indices and systemic BP levels for all maneuvers, but a significant relationship between age and static CA index, determined using isometric handgrip ( P = .002), was found. Conclusions In middle-aged and older people, sustained untreated hypertension does not alter dynamic CA or the efficiency of static CA within the BP limits studied.