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Central Blood Volume (central + blood_volume)
Selected AbstractsMuscle metaboreflex control of the circulation during exerciseACTA PHYSIOLOGICA, Issue 4 2010R. Boushel Abstract This review covers the control of blood pressure, cardiac output and muscle blood flow by the muscle metaboreflex which involves chemically sensitive nerves located in muscle parenchyma activated by metabolites accumulating in the muscle during contraction. The efferent response to metaboreflex activation is an increase in sympathetic nerve activity that constricts the systemic vasculature and also evokes parallel inotropic and chronotropic effects on the heart to increase cardiac output. The metaboreflex elicits a significant blood pressure elevating response during exercise and functions to redistribute blood flow and blood volume. Regional specificity in the efferent response to the metaboreflex activated from either the leg or the arm is seen in the balance between signals for vasoconstriction to curtail blood flow and signals to increase cardiac output. The metaboreflex has dual functions. It can both elevate and decrease muscle blood flow depending on (1) the intensity and mode of contraction, (2) the limb in which the reflex is evoked, (3) the strength of the signal defined by the muscle mass, (4) the extent to which blood flow is redistributed from inactive vascular beds to increase central blood volume and (5) the extent to which cardiac output can be increased. [source] Forearm vascular and neuroendocrine responses to graded water immersion in humansACTA PHYSIOLOGICA, Issue 2 2000Gabrielsen The hypothesis that graded expansion of central blood volume by water immersion to the xiphoid process and neck would elicit a graded decrease in forearm vascular resistance was tested. Central venous pressure increased (P < 0.05) by 4.2 ± 0.4 mmHg (mean ± SEM) during xiphoid immersion and by 10.4 ± 0.5 mmHg during neck immersion. Plasma noradrenaline was gradually suppressed (P < 0.05) by 62 ± 8 and 104 ± 11 pg mL,1 during xiphoid and neck immersion, respectively, indicating a graded suppression of sympathetic nervous activity. Plasma concentrations of arginine vasopressin were suppressed by 1.5 ± 0.5 pg mL,1 (P < 0.05) during xiphoid immersion and by 2.0 ± 0.5 pg mL,1 during neck immersion (P < 0.05 vs. xiphoid immersion). Forearm subcutaneous vascular resistance decreased to the same extent by 26 ± 9 and 28 ± 4% (P < 0.05), respectively, during both immersion procedures, whereas forearm skeletal muscle vascular resistance declined only during neck immersion by 27 ± 6% (P < 0.05). In conclusion, graded central blood volume expansion initiated a graded decrease in sympathetic nervous activity and AVP-release. Changes in forearm subcutaneous vascular resistance, however, were not related to the gradual withdrawal of the sympathetic and neuroendocrine vasoconstrictor activity. Forearm skeletal muscle vasodilatation exhibited a more graded response with a detectable decrease only during immersion to the neck. Therefore, the forearm subcutaneous vasodilator response reaches saturation at a lower degree of central volume expansion than that of forearm skeletal muscle. [source] R-wave Amplitude in Lead II of an Electrocardiograph Correlates with Central Hypovolemia in Human BeingsACADEMIC EMERGENCY MEDICINE, Issue 10 2006John G. McManus MD Abstract Objectives Previous animal and human experiments have suggested that reduction in central blood volume either increases or decreases the amplitude of R waves in various electrocardiograph (ECG) leads depending on underlying pathophysiology. In this investigation, we used graded central hypovolemia in adult volunteer subjects to test the hypothesis that moderate reductions in central blood volume increases R-wave amplitude in lead II of an ECG. Methods A four-lead ECG tracing, heart rate (HR), estimated stroke volume (SV), systolic blood pressure, diastolic blood pressure, and mean arterial pressure were measured during baseline supine rest and during progressive reductions of central blood volume to an estimated volume loss of >1,000 mL with application of lower-body negative pressure (LBNP) in 13 healthy human volunteer subjects. Results Lower-body negative pressure resulted in a significant progressive reduction in central blood volume, as indicated by a maximal decrease of 65% in SV and maximal elevation of 56% in HR from baseline to ,60 mm Hg LBNP. R-wave amplitude increased (p < 0.0001) linearly with progressive LBNP. The amalgamated correlation (R2) between average stroke volume and average R-wave amplitude at each LBNP stage was ,0.989. Conclusions These results support our hypothesis that reduction of central blood volume in human beings is associated with increased R-wave amplitude in lead II of an ECG. [source] Hemodynamic and Volume Changes during HemodialysisHEMODIALYSIS INTERNATIONAL, Issue 3 2003Robert M. Lindsay Background:,Volume overload is a factor in the hypertension of hemodialysis (HD) patients. Fluid removal is therefore integral to the hemodialysis treatment. Fluid removal by hemodialysis ultrafiltration (UF) may cause intradialytic hypotension and leg cramps. Understanding blood pressure (BP) and volume changes during UF may eliminate intradialytic hypotension and cramps. Studies (S1, S2, and S3) were carried out to determine the amount and direction of changes in body fluid compartments following UF and to determine the relationships between BP, changes in blood volume (,BV), central blood volume (CBV), cardiac output (CO), peripheral vascular resistance (PVR) plus total body water (TBW), and intra- and extracellular fluid volumes (ICF, ECF) in both the whole body and body segments (arms, legs, trunk). Methods:,Indicator dilution technology (Transonic) was used for CBV, CO, and PVR; hematocrit monitoring (Crit-Line) was used for ,BV segmental bioimpedance (Xitron) for TBW, ICF, and ECF. Results:,S1 (n = 21) showed UF sufficient to cause ,BV of ,7% and lead to minor changes (same direction) in CBV and CO, and with cessation of UF, vascular refilling was preferential to CBV. S2 (n = 20) showed that predialysis HD patients are ECF-expanded (ECF/ICF ratio = 0.96, controls = 0.74 [P < 0.0001]) and BP correlates with ECF (r = 0.47, P = 0.35). UF to cause ,BV of ,7% was associated with a decrease in ECF (P < 0.0001) and BP directly (r = 0.46, P = 0.04) plus ,BV indirectly (r = ,0.5, P = 0.024) correlated with PVR, while CBV and CO were maintained. S3 (n = 11) showed that following UF, total-body ECF changes were correlated with leg ECF (r = 0.94) and arm ECF (r = 0.72) but not trunk ECF. Absolute ECF reduction was greatest from the legs. Conclusions:,Predialysis ECF influences BP and UF reduces ,BV and ECF, but CBV and BP are conserved by increasing PVR. ECF reduction is mainly from the legs, hence may cause cramps. Intradialytic hypotension is caused by failure of PVR response. [source] Humoral and cardiac effects of TIPS in cirrhotic patients with different "effective" blood volumeHEPATOLOGY, Issue 6 2003Francesco Salerno M.D. The aim of this study was to evaluate the cardiac effects of transjugular intrahepatic portosystemic shunts (TIPS) in cirrhotic patients with different effective blood volume. Two-dimensional echocardiography was performed before and 7 and 28 days after TIPS insertion in 7 cirrhotic patients with PRA <4 ng/mL/h (group A, normal effective blood volume) and 15 with PRA >4 ng/mL/h (group B, reduced effective blood volume). Before TIPS, most cirrhotic patients showed diastolic dysfunction as indicated by reduced early maximal ventricular filling velocity (E)/late filling velocity (A) ratio. Patients of group B differed from patients of group A because of smaller left ventricular volumes and stroke volume, indicating central underfilling. After TIPS insertion, portal decompression was associated with a significant increase of cardiac output (CO) and a decrease of peripheral resistances. The most important changes were recorded in patients of group B, who showed a significant increase of both the end-diastolic left ventricular volumes and the E/A ratio and a significant decrease of PRA. In conclusion, these results show that the hemodynamic effects of TIPS differ according to the pre-TIPS effective blood volume. Furthermore, TIPS improves the diastolic cardiac function of cirrhotic patients with effective hypovolemia. This result is likely due to a TIPS-related improvement of the fullness of central blood volume. [source] Relationship between stroke volume, cardiac output and filling of the heart during tiltACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2009M. BUNDGAARD-NIELSEN Background: Cardiac function curves are widely accepted to apply to humans but are not established for the entire range of filling of the heart that can be elicited during head-up (HUT) and head-down tilt (HDT), taken to represent minimal and maximal physiological filling of the heart, respectively. With the supine resting position as a reference, we assessed stroke volume (SV), cardiac output (CO) and filling of the heart during graded tilt to evaluate whether SV and CO are maintained during an assumed maximal physiological filling of the heart elicited by 90° HDT in healthy resting humans. Methods: In 26 subjects, central blood volume was manipulated with graded tilt from 60° HUT to 90° HDT. We measured SV, CO (Finometer®) and cardiac filling by echocardiography of the left ventricular end-diastolic volume (LVEDV; n=12). Results: From supine rest to 60° HUT, SV and CO decreased 23 ml [confidence intervals (CI): 16,30; P<0.001; 23%] and 0.9 l/min (0.4,1.4; P<0.0001; 14%), respectively, but neither SV nor CO changed during HDT up to 70°. However, during 90° HDT, SV decreased 12 ml (CI: 6,19; P<0.0001; 12%), with an increase of 21 ml (9,33; P=0.002; 16%) in LVEDV because HR increased 3 bpm and CO decreased 0.5 l/min (ns). Conclusion: This study confirmed that SV and CO are maximal in resting, supine, healthy humans and decrease during HUT. However, 90° HDT was associated with increased LVEDV and induced a reduction in SV. [source] Cardiovascular reflex responses after intrathecal ,-conotoxins or dexmedetomidine in the rabbitCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2003Duncan W Blake Summary 1.,The effects of thoracic intrathecal doses (1 µg/kg) of the ,2 -adrenoceptor agonist dexmedetomidine and ,-conotoxins MVIIA and CVID on vasoconstrictor and heart rate responses to acute central hypovolaemia were studied in seven chronically instrumented rabbits. 2.,Gradual inflation of an inferior vena cava cuff to reduce cardiac index (CI) by 8% per minute induced progressive vasoconstriction and an increase in heart rate (phase I). At approximately 40% of resting CI, there was sudden decompensation with failure of vasoconstriction and decrease in mean arterial pressure (MAP; phase II). 3.,Both intrathecal MVIIA and CVID decreased resting CI (by 20% at 3 h), but only MVIIA significantly reduced resting MAP (P = 0.003). Dexmedetomidine resulted in transient bradycardia, but no other significant change in the resting circulation. With simulated haemorrhage, the relationship between CI and vascular conductance was shifted after MVIIA (1,3 h after injection) so that there was less vasoconstriction and a reduced increase in heart rate by the end of phase I compared with other treatments (P = 0.002 and P = 0.009, respectively). One hour after injection, dexmedetomidine reduced the slope of the phase I vasoconstrictor response (P = 0.03), but did not significantly alter the end-point of the response. With failure of vasoconstriction and the onset of phase II, vascular conductance was higher after MVIIA compared with controls. Both conotoxins caused progressive failure of vasoconstriction rather than recovery during phase II (P < 0.001). 4.,Intrathecal injections of these drugs to control chronic pain may compromise cardiovascular responses to changes in central blood volume. At the single doses studied, there were significant differences between the responses to simulated haemorrhage after MVIIA or dexmedetomidine compared with CVID, with the prolonged effect after MVIIA most likely to be of clinical significance. [source] Normovolemia defined according to cardiac stroke volume in healthy supine humansCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 5 2010Morten Bundgaard-Nielsen Summary Background:, Both hypovolemia and a fluid overload are detrimental for outcome in surgical patients but the effort to establish normovolemia is hampered by the lack of an operational clinical definition. Manipulating the central blood volume on a tilt table demonstrates that the flat part of the Frank-Starling curve is reached when subjects are supine and that finding may be applicable for a clinical definition of normovolemia. However, it is unknown whether stroke volume (SV) responds to an increase in preload induced by fluid administration. Methods:, In 20 healthy subjects (23 ± 2 years, mean ± SD), SV was measured by esophageal Doppler before and after fluid administration to evaluate whether SV increases in healthy, non-fasting, supine subjects. Two hundred millilitres of a synthetic colloid (hydroxyethyl starch, HES 130/0·4) was provided and repeated if a ,10% increment in SV was obtained. Results:, None of the subjects increased SV ,10% following fluid administration but there was a minor increase in mean arterial pressure (92 ± 15 to 93 ± 12 mmHg, P = 0·01), while heart rate (HR) (66 ± 12 beats min,1; P = 0·32), cardiac output (4·8 ± 1·1 l min,1; P = 0·25) and the length of the systole corrected to a HR of 60 beats/min (corrected flow time; 344 ± 24 ms; P = 0·31) did not change. Conclusion:, Supporting the proposed definition of normovolemia, non-fasting, supine, healthy subjects are provided with a preload to the heart that does not limit SV suggesting that the upper flat part of the Frank-Starling relationship is reached. [source] | ||||||||||