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-

Monitoring of continuous blood pressure and cardiac output is important to prevent hypoperfusion and to guide fluid administration, but only few patients receive such monitoring due to the invasive nature of most of the methods presently available. Noninvasive blood pressure can be determined continuously using finger cuff technology and cardiac output is easily obtained using a pulse contour method. In this way completely noninvasive continuous blood pressure and cardiac output are available for clinical use in all patients that would otherwise not be monitored. Developments and state of art in hemodynamic monitoring are reviewed here, with a focus on noninvasive continuous hemodynamic monitoring form the finger.

Sickle cell disease (SCD) is associated with a high incidence of ischemic stroke. SCD is characterized by hemolytic anemia, resulting in reduced nitric oxidebioavailability, and by impaired cerebrovascular hemodynamics. Cerebrovascular CO 2 responsiveness is nitric oxide dependent and has been related to an increased stroke risk in microvascular diseases. We questioned whether cerebrovascular CO 2 responsiveness is impaired in SCD and related to hemolytic anemia. Transcranial Doppler-determined mean cerebral blood flow velocity (V mean ), near-infrared spectroscopy-determined cerebral oxygenation, and end-tidal CO 2 tension were monitored during normocapnia and hypercapnia in 23 patients and 16 control subjects. Cerebrovascular CO 2 responsiveness was quantified as ⌬% V mean and ⌬mol/L cerebral oxyhemoglobin, deoxyhemoglobin, and total hemoglobin per mm Hg change in end-tidal CO 2 tension. Both ways of measurements revealed lower cerebrovascular CO 2 responsiveness in SCD patients versus controls (V mean , 3.7, 3.1-4.7 vs 5.9, 4.6-6.7 ⌬% V mean per mm Hg, P < .001; oxyhemoglobin, 0.36, 0.14-0.82 vs 0.78, 0.61-1.22 ⌬mol/L per mm Hg, P ‫؍‬ .025; deoxyhemoglobin, 0.35, 0.14-0.67 vs 0.58, 0.41-0.86 ⌬mol/L per mm Hg, P ‫؍‬ .033; total-hemoglobin, 0.13, 0.02-0.18 vs 0.23, 0.13-0.38 ⌬mol/L per mm Hg, P ‫؍‬ .038). Cerebrovascular CO 2 responsiveness was not related to markers of hemolytic anemia. In SCD patients, impaired cerebrovascular CO 2 responsiveness reflects reduced cerebrovascular reserve capacity, which may play a role in pathophysiology of stroke. (Blood. 2009;114:3473-3478) IntroductionCerebral infarction is one of the most devastating complications of sickle cell disease (SCD), occurring in approximately 10% of patients in the first 2 decades of life. 1-3 Furthermore, silent cerebral infarctions occur in approximately 17% of pediatric patients 4,5 and are associated with poor educational and cognitive functioning. 6 SCD is characterized by chronic hemolytic anemia and ongoing vaso-occlusion with exacerbations often requiring medical care. [7][8][9] The vaso-occlusive process in SCD is of a complex nature mediated by red cell and leukocyte adhesion, inflammation, oxidative stress, and a hypercoagulable state, all resulting in endothelial injury and dysfunction. 8 In addition, by reducing the nitric oxide (NO) bioavailability and by damaging the endothelium through the catalyzation of oxidative reactions in endothelial cells, chronic hemolysis leads to vascular complications. [10][11][12] Elevated cerebral blood flow (CBF) velocity (Ն 200 cm/s), measured by transcranial Doppler (TCD), has been identified as a risk factor for stroke in SCD. 13 However, little is known about the mechanism of (ischemic) stroke in SCD patients, and it has not been elucidated whether the increased CBF velocity plays a causative role in stroke or whether it is a result of SCD-related hemodynamic disturbances.CBF is tightly regulated to maintain constancy of cerebral perfusion in the face of various systemic blood pressures by both ...

Standing up shifts blood to dependent parts of the body, and blood vessels in the leg become filled. The orthostatic blood volume accumulation in the small vessels is relatively unknown, although these may contribute significantly. We hypothesized that in healthy humans exposed to the upright posture, volume accumulation in small blood vessels contributes significantly to the total fluid volume accumulated in the legs. Considering that near-infrared spectroscopy (

The Frank–Starling mechanism describes the relationship between stroke volume and preload to the heart, or the volume of blood that is available to the heart—the central blood volume. Understanding the role of the central blood volume for cardiovascular control has been complicated by the fact that a given central blood volume may be associated with markedly different central vascular pressures. The central blood volume varies with posture and, consequently, stroke volume and cardiac output () are affected, but with the increased central blood volume during head-down tilt, stroke volume and do not increase further indicating that in the supine resting position the heart operates on the plateau of the Frank–Starling curve which, therefore, may be taken as a functional definition of normovolaemia. Since the capacity of the vascular system surpasses the blood volume, orthostatic and environmental stress including bed rest/microgravity, exercise and training, thermal loading, illness, and trauma/haemorrhage is likely to restrict venous return and . Consequently the cardiovascular responses are determined primarily by their effect on the central blood volume. Thus during environmental stress, flow redistribution becomes dependent on sympathetic activation affecting not only skin and splanchnic blood flow, but also flow to skeletal muscles and the brain. This review addresses the hypothesis that deviations from normovolaemia significantly influence these cardiovascular responses.

Abstract-Type 2 diabetes mellitus is associated with microvascular complications, hypertension, and impaired dynamic cerebral autoregulation. Intensive blood pressure (BP) control in hypertensive type 2 diabetic patients reduces their risk of stroke but may affect cerebral perfusion. Systemic hemodynamic variables and transcranial Doppler-determined cerebral blood flow velocity (CBFV), cerebral CO 2 responsiveness, and cognitive function were determined after 3 and 6 months of intensive BP control in 17 type 2 diabetic patients with microvascular complications (T2DMϩ), in 18 diabetic patients without (T2DMϪ) microvascular complications, and in 16 nondiabetic hypertensive patients. Cerebrovascular reserve capacity was lower in T2DMϩ versus T2DMϪ and nondiabetic hypertensive patients (4.6Ϯ1.1 versus 6.0Ϯ1.6 [PϽ0.05] and 6.6Ϯ1.7 [PϽ0.01], ⌬% mean CBFV/mm Hg). After 6 months, the attained BP was comparable among the 3 groups. However, in contrast to nondiabetic hypertensive patients, intensive BP control reduced CBFV in T2DMϪ (58Ϯ9 to 54Ϯ12 cm ⅐ s Ϫ1 ) and T2DMϩ (57Ϯ13 to 52Ϯ11 cm ⅐ s Ϫ1 ) at 3 months, but CBFV returned to baseline at 6 months only in T2DMϪ, whereas the reduction in CBFV progressed in T2DMϩ (to 48Ϯ8 cm ⅐ s Ϫ1 ). Cognitive function did not change during the 6 months. Static cerebrovascular autoregulation appears to be impaired in type 2 diabetes mellitus, with a transient reduction in CBFV in uncomplicated diabetic patients on tight BP control, but with a progressive reduction in CBFV in diabetic patients with microvascular complications, indicating that maintenance of cerebral perfusion during BP treatment depends on the progression of microvascular disease. We suggest that BP treatment should be individualized, aiming at a balance between BP reduction and maintenance of CBFV. (Hypertension. 2011;57:738-745.) • Online Data Supplement

In the upright position, cerebral blood flow is reduced, maybe because arterial carbon dioxide partial pressure (Pa(CO(2))) decreases. We evaluated the time-dependent influence of a reduction in Pa(CO(2)), as indicated by the end-tidal Pco(2) tension (Pet(CO(2))), on cerebral perfusion during head-up tilt. Mean arterial pressure, cardiac output, middle cerebral artery mean flow velocity (MCA V(mean)), and dynamic cerebral autoregulation at supine rest and 70 degrees head-up tilt were determined during free breathing and with Pet(CO(2)) clamped to the supine level. The postural changes in central hemodynamic variables were equivalent, and the cerebrovascular autoregulatory capacity was not significantly affected by tilt or by clamping Pet(CO(2)). In the first minute of tilt, the decline in MCA V(mean) (10 +/- 4 vs. 3 +/- 4 cm/s; mean +/- SE; P < 0.05) and Pet(CO(2)) (6.8 +/- 4.3 vs. 1.7 +/- 1.6 Torr; P < 0.05) was larger during spontaneous breathing than during isocapnic tilt. However, after 2 min in the head-up position, the reduction in MCA V(mean) was similar (7 +/- 5 vs. 6 +/- 3 cm/s), although the spontaneous decline in Pet(CO(2)) was maintained (P < 0.05 vs. isocapnic tilt). These results suggest that the potential contribution of Pa(CO(2)) to the postural reduction in MCA V(mean) is transient, leaving the mechanisms for the sustained restrain in MCA V(mean) to be identified.

With standing, haemodynamic variables change similarly in older and younger individuals. The opposite changes in reflection magnitude and peripheral resistance suggest that reflection and pressure augmentation are not solely dependent on peripheral resistance.