Background: If invasive measurement of arterial blood pressure is not warranted, finger cuff technology can provide continuous and noninvasive monitoring. Finger and radial artery pressures differ; Nexfin (BMEYE, Amsterdam, The Netherlands) measures finger arterial pressure and uses physiologic reconstruction methodologies to obtain values comparable to invasive pressures. Methods: Intra-arterial pressure (IAP) and noninvasive Nexfin arterial pressure (NAP) were measured in cardiothoracic surgery patients, because invasive pressures are avail-

Background and Purpose-We addressed whether dynamic cerebral autoregulation (dCA) is affected in middle cerebral artery (MCA) territory (MCAS) and lacunar ischemic stroke (LS). Methods-Blood pressure (MAP) and MCA velocity (V) were measured in 10 patients with large MCAS (National Institutes of Health Stroke score, 17Ϯ2; meanϮSEM), in 10 with LS (score, 9Ϯ1), and in 10 reference subjects. dCA was evaluated in time (delay of the MCA V mean counter-regulation during changes in MAP) and frequency domains (cross-spectral MCA V mean -to-MAP phase lead). Results-In reference subjects, latencies for MAP increments (5.3Ϯ0.5 seconds) and decrements (5.6Ϯ0.5 seconds) were comparable, and low frequency MCA V mean -to-MAP phase lead was 56Ϯ5 and 59Ϯ5°(left and right hemisphere). In MCAS, these latencies were 4.6Ϯ0.7 and 5.6Ϯ0.5 seconds in the nonischemic hemisphere and not detectable in the ischemic hemisphere. In the unaffected hemisphere, phase lead was 61Ϯ6°versus 26Ϯ6°on the ischemic side (PϽ0.05). In LS, no latency and smaller phase lead bilaterally (32Ϯ6 and 33Ϯ5°) conformed to globally impaired dCA. Conclusions-In large MCAS infarcts, dynamic cerebral autoregulation was impaired in the affected hemisphere. In LS, dynamic cerebral autoregulation was impaired bilaterally, a finding consistent with the hypothesis of bilateral small vessel disease in patients with lacunar infarcts. (Stroke. 2005;36:2595-2600.)

Background-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. Methods and Results-In 8 patients with mean arterial pressure (MAP) Ͼ140 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 (30Ϯ8°versus 58Ϯ5°, meanϮSEM; PϽ0.05), 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 22Ϯ4%, along with a 27Ϯ3% reduction in MAP (from 166Ϯ4 to 121Ϯ6 mm Hg; PϽ0.05) in a linear fashion (averaged slope, 0.82Ϯ0.15% cm · s Ϫ1 · % mm Hg

Background Up to two-thirds of patients are either dependent or dead 3 months after thrombectomy for acute ischemic stroke (AIS). Loss of cerebral autoregulation may render patients with AIS vulnerable to decreases in mean arterial pressure (MAP). Objective To determine whether a fall in MAP during intervention under general anesthesia (GA) affects functional outcome. Methods This subgroup analysis included patients from the MR CLEAN trial treated with thrombectomy under GA. The investigated variables were the difference between MAP at baseline and average MAP during GA (ΔMAP) as well as the difference between baseline MAP and the lowest MAP during GA (ΔLMAP). Their association with a shift towards better outcome on the modified Rankin Scale (mRS) after 90 days was determined using ordinal logistic regression with adjustment for prognostic baseline variables. Results Sixty of the 85 patients treated under GA in MR CLEAN had sufficient anesthetic information available for the analysis. A greater ΔMAP was associated with worse outcome (adjusted common OR (acOR) 0.95 per point mm Hg, 95% CI 0.92 to 0.99). An average MAP during GA 10 mm Hg lower than baseline MAP constituted a 1.67 times lower odds of a shift towards good outcome on the mRS. For ΔLMAP this association was not significant (acOR 0.97 per mm Hg, 95% CI 0.94 to 1.00, p=0.09). Conclusions A decrease in MAP during intervention under GA compared with baseline is associated with worse outcome. Trial registration number NTR1804; ISRCTN10888758; post-results. BACKGROUND

In the normocapnic range, middle cerebral artery mean velocity (MCA Vmean) changes approximately 3.5% per mmHg carbon-dioxide tension in arterial blood (PaCO2) and a decrease in PaCO2 will reduce the cerebral blood flow by vasoconstriction (the CO2 reactivity of the brain). When standing up MCA Vmean and the end-tidal carbon-dioxide tension (PETCO2) decrease, suggesting that PaCO2 contributes to the reduction in MCA Vmean. In a fixed body position, PETCO2 tracks changes in the PaCO2 but when assuming the upright position, cardiac output (Q) decreases and its distribution over the lung changes, while ventilation (VE) increases suggesting that PETCO2 decreases more than PaCO2. This study evaluated whether the postural reduction in PaCO2 accounts for the postural decline in MCA Vmean). From the supine to the upright position, VE, Q, PETCO2, PaCO2, MCA Vmean, and the near-infrared spectrophotometry determined cerebral tissue oxygenation (CO2Hb) were followed in seven subjects. When standing up, MCA Vmean (from 65.3+/-3.8 to 54.6+/-3.3 cm s(-1) ; mean +/- SEM; P<0.05) and cO2Hb (-7.2+/-2.2 micromol l(-1) ; P<0.05) decreased. At the same time, the VE/Q ratio increased 49+/-14% (P<0.05) with the postural reduction in PETCO2 overestimating the decline in PaCO2 (-4.8+/-0.9 mmHg vs. -3.0+/-1.1 mmHg; P<0.05). When assuming the upright position, the postural decrease in MCA Vmean seems to be explained by the reduction in PETCO2 but the small decrease in PaCO2 makes it unlikely that the postural decrease in MCA Vmean can be accounted for by the cerebral CO2 reactivity alone.

Type 2 diabetes is associated with an increased risk of endothelial dysfunction and microvascular complications with impaired autoregulation of tissue perfusion. Both microvascular disease and cardiovascular autonomic neuropathy may affect cerebral autoregulation. In the present study, we tested the hypothesis that, in the absence of cardiovascular autonomic neuropathy, cerebral autoregulation is impaired in subjects with DM+ (Type 2 diabetes with microvascular complications) but intact in subjects with DM- (Type 2 diabetes without microvascular complications). Dynamic cerebral autoregulation and the steady-state cerebrovascular response to postural change were studied in subjects with DM+ and DM-, in the absence of cardiovascular autonomic neuropathy, and in CTRL (healthy control) subjects. The relationship between spontaneous changes in MCA V(mean) (middle cerebral artery mean blood velocity) and MAP (mean arterial pressure) was evaluated using frequency domain analysis. In the low-frequency region (0.07-0.15 Hz), the phase lead of the MAP-to-MCA V(mean) transfer function was 52+/-10 degrees in CTRL subjects, reduced in subjects with DM- (40+/-6 degrees ; P<0.01 compared with CTRL subjects) and impaired in subjects with DM+ (30+/-5 degrees ; P<0.01 compared with subjects with DM-), indicating less dampening of blood pressure oscillations by affected dynamic cerebral autoregulation. The steady-state response of MCA V(mean) to postural change was comparable for all groups (-12+/-6% in CTRL subjects, -15+/-6% in subjects with DM- and -15+/-7% in subjects with DM+). HbA(1c) (glycated haemoglobin) and the duration of diabetes, but not blood pressure, were determinants of transfer function phase. In conclusion, dysfunction of dynamic cerebral autoregulation in subjects with Type 2 diabetes appears to be an early manifestation of microvascular disease prior to the clinical expression of diabetic nephropathy, retinopathy or cardiovascular autonomic neuropathy.

In man assuming the upright position, end-tidal P CO 2 (P ETCO 2 ) decreases. With the rising interest in cerebral autoregulation during posture change, which is known to be affected by P ETCO 2 , we sought to determine the factors leading to hypocapnia during standing up from the supine position. To study the contribution of an increase in tidal volume (V T ) and breathing frequency, a decrease in stroke volume (SV), a ventilation-perfusion (V/Q) gradient and an increase in functional residual capacity (FRC) to hypocapnia in the standing position, we developed a mathematical model of the lung to follow breath-to-breath variations in P ETCO 2 . A gravityinduced apical-to-basal V/Q gradient in the lung was modelled using nine lung segments. We tested the model using an eight-subject data set with measurements of V T , pulmonary O 2 uptake and breath-to-breath lumped SV. On average, the P ETCO 2 decreased from 40 mmHg to 36 mmHg after 150 s standing. Results show that the model is able to track breath-to-breath P ETCO 2 variations (r 2 = 0.74, P < 0.05). Model parameter sensitivity analysis demonstrates that the decrease in P ETCO 2 during standing is due primarily to increased V T , and transiently to decreased SV and increased FRC; a slight gravity-induced V/Q mismatch also contributes to the hypocapnia. The influence of cardiac output on hypocapnia in the standing position was verified in experiments on human subjects, where first breathing alone, and then breathing, FRC and V/Q were controlled.

Vasovagal syncope is the most common cause of transient loss of consciousness, and recurrent vasovagal fainting has a profound impact on quality of life. Physical countermaneuvers are applied as a means of tertiary prevention but have so far only proven useful at the onset of a faint. This placebo-controlled crossover study tested the hypothesis that leg crossing increases orthostatic tolerance. Nine naïve healthy subjects [6 females, median age 25 yr (range 20-41 yr), mean body mass index 23 (SD 2)] were subjected to passive head-up tilt combined with a graded lower body negative pressure challenge (20, 40, and 60 mmHg) determining orthostatic tolerance thrice, in randomized order: 1) control, 2) with leg crossing, and 3) with oral placebo. Blood pressure (Finometer), heart rate, and changes in thoracic blood volume (impedance), stroke volume, and cardiac output (Modelflow) were followed during orthostatic stress. Primary outcome was time to presyncope (systolic blood pressure /=140 beats/min). With leg crossing, orthostatic tolerance increased from 26 +/- 2 to 34 +/- 2 min (placebo 23 +/- 3 min, P < 0.001). During leg crossing, mean arterial pressure (81 vs. 81 mmHg) and cardiac output (95 vs. 94% supine) remained unchanged; heart rate increase was lower (13 vs. 18 beats/min, P < 0.05); stroke volume was higher (79 vs. 74% supine, P < 0.05); and there was a trend toward lower thoracic impedance. Leg crossing increases orthostatic tolerance in healthy human subjects. As a measure of prevention, it is a worthwhile addition to the management of vasovagal syncope.