Increase In Central Blood Volume Research Articles

Selective elevation in external carotid artery flow during acute gravitational transition to microgravity during parabolic flight.

This study sought to determine to what extent acute exposure to microgravity (0 G) and related increases in central blood volume (CBV) during parabolic flight influence the regional redistribution of intra and extra cranial cerebral blood flow (CBF). Eleven healthy participants performed during two parabolic flights campaigns aboard the Airbus A310-ZERO G aircraft. The response of select variables for each of the 15 parabolas involving exposure to both 0 G and hypergravity (1.8 G) were assessed in the seated position. Mean arterial blood pressure (MAP) and heart rate (HR) were continuously monitored and used to calculate stroke volume (SV), cardiac output ([Formula: see text]), and systemic vascular resistance (SVR). Changes in CBV were measured using an impedance monitor. Extracranial flow through the internal carotid, external carotid, and vertebral artery ([Formula: see text]ICA, [Formula: see text]ECA, and [Formula: see text]VA), and intracranial blood velocity was measured by duplex ultrasound. When compared with 1-G baseline condition, 0 G increased CBV (+375 ± 98 mL, P = 0.004) and [Formula: see text] (+16 ± 14%, P = 0.024) and decreased SVR (-7.3 ± 5 mmHg·min·L-1, P = 0.002) and MAP (-13 ± 4 mmHg, P = 0.001). [Formula: see text]ECA increased by 43 ± 46% in 0 G (P = 0.030), whereas no change was observed for CBF, [Formula: see text]ICA, or [Formula: see text]VA (P = 0.102, P = 0.637, and P = 0.095, respectively).NEW & NOTEWORTHY Our findings demonstrate that in microgravity there is a selective increase in external carotid artery blood flow whereas global and regional cerebral blood flow remained preserved. To what extent this reflects an adaptive, neuroprotective response to counter overperfusion remains to be established.

PREGNANCY IN THE PERIOD OF THE DELTA VARIANT OF CORONAVIRUS DISEASE: SOMATIC AND PERINATAL ASPECTS

The purpose of this study is to investigate the clinical symptoms of the delta variant of the coronavirus disease in pregnant women, and to analyze the course of pregnancy in this period.
 Materials and methods. An assessment of the courses of the coronavirus disease and pregnancy in the period from September to November 2021 was carried out.
 The clinical manifestations of the disease are characterized by moderate severity due to respiratory disorders (86.2%), subfebrile body temperature and weakened breathing (20.6%), accompanied by wheezing (17.2%). A significant proportion of patients (20.6%) require oxygen support due to the respiratory complications. Common laboratory findings include anaemia and lymphopenia (11.5±1.1%), as well as elevated levels of ferritin (123.5±19.1 ng/mg), C-reactive protein (12.9±1.6 mg/l), prothrombin time (12.4±1.4 sec), and D-dimer (0.76±0.04 µg FEU/ml).
 The recommended treatment for this condition includes the administration of antipyretics, LMH (presumably low molecular weight heparin), antibiotics (in the case of bacterial complications), and corticosteroids.
 Pregnant women are particularly vulnerable during the second trimester (II trimester) of pregnancy. This vulnerability is attributed to the rapid growth of the uterus and the subsequent increase in central blood volume, which places additional strain on the cardiovascular system. As a result, the disease tends to have a more severe course during the second trimester compared to the first and third trimesters. Consequently, pregnant patients in the second trimester require hospitalization more frequently.
 Pregnant women with the delta variant of coronavirus disease can demonstrate various obstetric manifestations. These include oligohydramnios (6.8%) and polyhydramnios (3.4%), as well as placental thinning (10.3%) and placental thickening (3.4%). Additionally, moderate preeclampsia (6.8%) and gestational pyelonephritis (10.3%) have been reported. Changes in Doppler parameters such as a decrease in STV (systolic time interval) to 3.3±0.3 ms (in 29% of cases), an increase in PI (pulsatility index) to 0.8±0.05, and an increase in SDS (systolic-diastolic ratio) to 3.3±0.03, as well as an increase in IR (resistance index) to 0.8±0.05 in the umbilical cord artery have been observed. Preterm labour occurs in 6.9% of cases between 34 and 36+6 weeks, and in 3.4% of cases before 34 weeks. Other obstetric complications include primary uterine inertia (13.8%), secondary uterine inertia (10.3%), cephalopelvic disproportion (6.9%), fetal distress (3.4%), bleeding in the third stage of labour (3.4%), and caesarean section (17.2%) due to obstetric reasons.
 Neonates born to mothers with the delta variant of coronavirus disease may exhibit the following manifestations: the Apgar score at 1 minute is generally 7.8 ± 0.4 points, and at 5 minutes it is 8.2 ± 0.2 points; Respiratory functional impairment (10.3%) and low weight for gestational age (6.9%) have been observed, necessitating respiratory support in 6.9% of cases.
 Conclusion: The delta variant of coronavirus disease in pregnant women is characterized by respiratory disorders, tachycardia, hyperthermia, infiltrative lung changes, elevated inflammatory markers, hypercoagulability, and lymphopenia. The disease tends to have a more severe course during the second trimester due to increased cardiovascular and respiratory strain. Obstetric complications, such as changes in amniotic fluid volume and placental thickness, preeclampsia, gestational pyelonephritis, and compensated placental dysfunction, are thought to arise from inflammatory, hypercoagulable, and endothelial changes in the placenta. However, complications during childbirth and the condition of newborns do not appear to be directly related to the maternal disease.

The increase in cardiac output induced by a decrease in positive end-expiratory pressure reliably detects volume responsiveness: the PEEP-test study

BackgroundIn patients on mechanical ventilation, positive end-expiratory pressure (PEEP) can decrease cardiac output through a decrease in cardiac preload and/or an increase in right ventricular afterload. Increase in central blood volume by fluid administration or passive leg raising (PLR) may reverse these phenomena through an increase in cardiac preload and/or a reopening of closed lung microvessels. We hypothesized that a transient decrease in PEEP (PEEP-test) may be used as a test to detect volume responsiveness.MethodsMechanically ventilated patients with PEEP ≥ 10 cmH2O (“high level”) and without spontaneous breathing were prospectively included. Volume responsiveness was assessed by a positive PLR-test, defined as an increase in pulse-contour-derived cardiac index (CI) during PLR ≥ 10%. The PEEP-test consisted in reducing PEEP from the high level to 5 cmH2O for one minute. Pulse-contour-derived CI (PiCCO2) was monitored during PLR and the PEEP-test.ResultsWe enrolled 64 patients among whom 31 were volume responsive. The median increase in CI during PLR was 14% (11–16%). The median PEEP at baseline was 12 (10–15) cmH2O and the PEEP-test resulted in a median decrease in PEEP of 7 (5–10) cmH2O, without difference between volume responsive and unresponsive patients. Among volume responsive patients, the PEEP-test induced a significant increase in CI of 16% (12–20%) (from 2.4 ± 0.7 to 2.9 ± 0.9 L/min/m2, p < 0.0001) in comparison with volume unresponsive patients. In volume unresponsive patients, PLR and the PEEP-test increased CI by 2% (1–5%) and 6% (3–8%), respectively. Volume responsiveness was predicted by an increase in CI > 8.6% during the PEEP-test with a sensitivity of 96.8% (95% confidence interval (95%CI): 83.3–99.9%) and a specificity of 84.9% (95%CI 68.1–94.9%). The area under the receiver operating characteristic curve of the PEEP-test for detecting volume responsiveness was 0.94 (95%CI 0.85–0.98) (p < 0.0001 vs. 0.5). Spearman’s correlation coefficient between the changes in CI induced by PLR and the PEEP-test was 0.76 (95%CI 0.63–0.85, p < 0.0001).ConclusionsA CI increase > 8.6% during a PEEP-test, which consists in reducing PEEP to 5 cmH2O, reliably detects volume responsiveness in mechanically ventilated patients with a PEEP ≥ 10 cmH2O.Trial registration ClinicalTrial.gov (NCT 04,023,786). Registered July 18, 2019. Ethics Committee approval CPP Est III (N° 2018-A01599-46).

Effect of adrenaline on serum mid-regional pro-atrial natriuretic peptide and central blood volume.

New Findings What is the central question in this study? Atrial natriuretic peptide (ANP) is secreted in response to atrial wall distension and thus allows for evaluation, albeit indirect, of the central blood volume. Adrenaline has chronotropic and inotropic effects. We evaluated whether the chronotropic and inotropic effects of adrenaline were reflected in mid‐regional proANP. What is the main finding and its importance? Central blood volume remained stable with infusion of adrenaline and yet mid‐regional proANP increased. Thus, the chronotropic and inotropic state of the heart or adrenaline directly induces release of ANP variants from the myocytes. Atrial natriuretic peptide (ANP) has vasodilatory, natriuretic and diuretic properties. It is secreted in response to atrial wall distension and thereby provides an indirect evaluation of central blood volume (CBV). Adrenaline has chronotropic and inotropic effects that increase cardiac output. In the present study, we evaluated whether these effects were influenced by an increase in CBV and reflected in mid‐regional proANP (MR‐proANP) concentrations in the circulation, a stable proxy marker of bioactive ANP. Changes in CBV were evaluated by thoracic electrical admittance and haemodynamic variables monitored by pulse‐contour analysis during two intervals with graded infusion of adrenaline. Adrenaline infusion increased heart rate (by 33 ± 18%) and stroke volume (by 6 ± 13%), hence cardiac output (by 42 ± 23%; all P < 0.05). The increase in cardiac output did not result from an increase in CBV, because thoracic electrical admittance remained stable (−3 ± 17%; P = 0.230). Serum MR‐proANP concentrations were increased (by 26 ± 25%; P < 0.001) by adrenaline infusion and remained elevated 60 min postinfusion. We conclude that MR‐proANP in the circulation is affected not only by CBV, but also by increased chronotropy/inotropy of the heart, or that adrenaline directly induces release of ANP variants from the myocytes.

Acute Elevations in Apnea‐Induced Spleen Contraction Provoked by Thermoneutral Head Out Water Immersion

INTRODUCTIONThe spleen serves as a repository of erythrocytes that can be jettisoned into circulation following sympathetic stimulation, such as hypoxia or apnea. Evidence supports that there may be a functional benefit to spleen contraction during breath‐hold diving, likely by increasing oxygen carrying and pH buffering capacities. However, the magnitude of apnea‐induced spleen contraction during immersion, and the corresponding hematological changes, have not been quantified. We have recently identified that spleen volume increases after 30 min of thermoneutral head out water immersion (HOWI), likely due to initial hydrostatic pressure‐induced increases in central blood volume, and remains elevated through 135 min, despite immersion‐induced diuresis. Whether these HOWI‐induced changes in spleen volume modify the magnitude of apnea‐induced spleen contraction is unknown. Cross‐sectional observations indicate that there is a positive relation between baseline spleen volume and the magnitude of apnea‐induced spleen contraction.PURPOSETest the hypothesis that the magnitude of apnea‐induced spleen contraction increases during thermoneutral HOWI.METHODSSpleen volume was measured pre‐ and post‐ a set of five apneas in eight healthy adults (3 women; 27 ± 4 y) before, during (at 30 and 135 min) and 20 min following thermoneutral (36 ± 1°C) HOWI. At each timepoint, spleen length, width, and thickness were measured via ultrasound and spleen volume was calculated using the Pilström equation (test‐retest CV: 2 ± 2%). Hemoglobin concentration ([Hb]) and hematocrit were measured pre‐ and post‐ each set of apneas via capillary blood samples. Urine was collected at 60 min and 120 min of HOWI. Data are presented as mean ± SD.RESULTSCompared to pre‐HOWI (97 ± 32 s), average apnea times were higher at 30 min (115 ± 36 s, p=0.02) and 135 min (120 ± 43 s, p&lt;0.01) of HOWI, but returned to pre‐ levels at post‐HOWI (103 ± 38 s, p=0.70). [Hb] increased from pre‐ to post‐ apneas (main effect: p&lt;0.01), but the magnitude of the increase did not differ between timepoints (pre‐HOWI: +0.4 ± 0.3, 30 min of HOWI: +0.3 ± 0.5, 135 min of HOWI: +0.3 ± 0.5, post‐HOWI: +0.2 ± 0.2 g/dL, p=0.68). Hematocrit did not change from pre‐ to post‐ apneas (main effect: p=0.72), and the magnitude of changes from pre‐ to post‐ apneas did not differ between timepoints (p=0.43). Spleen volume decreased from pre‐ to post‐apneas at each timepoint (p&lt;0.01). The reduction in spleen volume was greater than pre‐HOWI (‐41 ± 18 mL) at 30 min of HOWI (‐65 ± 26 mL, p=0.03), but did not differ from pre‐HOWI at 135 min of HOWI (‐50 ± 12 mL, p =0.44), despite marked diuresis (urine volume: 425 ± 193 mL), or at post‐HOWI (‐40 ± 13 mL, p=0.99).CONCLUSIONApnea‐induced spleen contraction was acutely increased at 30 mins of HOWI. However, following immersion‐induced diuresis the magnitude of spleen contraction at 130 min of HOWI returned to pre‐HOWI levels. Increases in [Hb], which were presumably caused by spleen contraction, were not modified by HOWI, suggesting the hematological response to apnea‐induced spleen contraction is not modified by immersion.

NOTA SUI LIMITI FISIOLOGICI DELLE IMMERSIONI PROFONDE IN APNEA

This article discusses the limits of deep breath-hold diving in humans. After a short historical introduction and a discussion of the evolution of depth records, the classical theories of breath-hold diving limits are presented and discussed, namely that of the ratio between total lung capacity and residual volume and that of blood shift, implying an increase in central blood volume. Then the current vision is introduced, based on the principles of the energetics of muscular exercise. The new vision has turned the classical vision upside down, moving the discussion to a different level. A direct consequence of the new theory is the importance of having large lung volumes at the start of a dive, in order to increase body oxygen stores. I finally discuss the role of anaerobic lactic metabolism as a possible mechanism of oxygen preservation, thus prolonging breath-hold duration.

Characterization of the inflammatory-metabolic phenotype of heart failure with a preserved ejection fraction: a hypothesis to explain influence of sex on the evolution and potential treatment of the disease.

Accumulating evidence points to the existence of an inflammatory‐metabolic phenotype of heart failure with a preserved ejection fraction (HFpEF), which is characterized by biomarkers of inflammation, an expanded epicardial adipose tissue mass, microvascular endothelial dysfunction, normal‐to‐mildly increased left ventricular volumes and systolic blood pressures, and possibly, altered activity of adipocyte‐associated inflammatory mediators. A broad range of adipogenic metabolic and systemic inflammatory disorders – e.g. obesity, diabetes and metabolic syndrome as well as rheumatoid arthritis and psoriasis – can cause this phenotype, independent of the presence of large vessel coronary artery disease. Interestingly, when compared with men, women are both at greater risk of and may suffer greater cardiac consequences from these systemic inflammatory and metabolic disorders. Women show disproportionate increases in left ventricular filling pressures following increases in central blood volume and have greater arterial stiffness than men. Additionally, they are particularly predisposed to epicardial and intramyocardial fat expansion and imbalances in adipocyte‐associated proinflammatory mediators. The hormonal interrelationships seen in inflammatory‐metabolic phenotype may explain why mineralocorticoid receptor antagonists and neprilysin inhibitors may be more effective in women than in men with HFpEF. Recognition of the inflammatory‐metabolic phenotype may improve an understanding of the pathogenesis of HFpEF and enhance the ability to design clinical trials of interventions in this heterogeneous syndrome.

Causal analyses to study autonomic regulation during acute head-out water immersion, head-down tilt and supine position.

What is the central question of this study? Can Granger causality analysis of R-R intervals, systolic blood pressure and respiration provide evidence for the different physiological mechanisms induced during thermoneutral water immersion, 6deg head-down tilt and supine position tests that are not accessible using traditional heart rate variability and baroreflex methods? What is the main finding and its importance? The Granger analysis demonstrated a significant difference in the causal link from R-R intervals to respiration between water immersion and head-down tilt. The underlying physiological mechanism explaining this difference could be the variation in peripheral resistances. Thermoneutral head-out water immersion (WI) and 6deg head-down tilt (HDT) are used to simulate SCUBA diving, swimming and microgravity, because these models induce an increase in central blood volume. Standard methods to analyse autonomic regulation have demonstrated an increase in parasympathetic activity and baroreflex sensitivity during these experimental conditions. However, such methods are not adapted to quantify all closed-loop interactions involved in respiratory and cardiovascular regulation. To overcome this limitation, we used Granger causality analysis between R-R intervals (RR), systolic blood pressure (SBP) and respiration (RE) in eight young, healthy subjects, recorded during 30min periods in the supine position, WI and HDT. For all experimental conditions, we found a bidirectional causal relationship between RE and RR and between RR and SBP, with a dominant direction from RR to SBP, and a unidirectional causality from RE to SBP. These causal relationships remained unchanged for the three experimental tests. Interestingly, there was a lower causal relationship from RR to RE during WI compared with HDT. This causal link from RR to RE could be modulated by peripheral resistances. These results highlight differences in cardiovascular regulation during WI and HDT and confirm that Granger causality might reveal physiological mechanisms not accessible with standard methods.

Is hepatojugular reflux a good predictor of heart failure with preserved ejection fraction?

Hypertension may occur with left ventricular (LV) diastolic dysfunction, and the consequence may be symptoms and signs of heart failure (HF). Hepatojugular reflux (HJR), described as a sign of regurgitation of the tricuspid valve, may reflect structural and functional changes of the LV in the hypertensive patient. The signal may be present in the presence of HF. Case: male, 49 years old with uncontrolled blood pressure. Physical examination showed jugular turgescence, HJR, and elevated blood pressure. Complementary exams showed signs of atrial and left ventricular overload in the electrocardiogram and, the echocardiogram showed left atrium volume increase, concentric LV hypertrophy and signs of grade I diastolic dysfunction. DISCUSSIO: The HJR present correlates with pulmonary artery pressure and probably reflect the increase in central blood volume.

Muscle metaboreflex-induced central blood volume mobilization in heart failure.

Underperfusion of active skeletal muscle causes metabolites to accumulate and stimulate group III and IV skeletal muscle afferents, which triggers a powerful pressor response termed the muscle metaboreflex. Muscle metaboreflex activation (MMA) during submaximal dynamic exercise in healthy individuals increases arterial pressure mainly via substantial increases in cardiac output (CO). The increases in CO occur via the combination of tachycardia and increased ventricular contractility. Importantly, MMA also elicits substantial central blood volume mobilization, which allows the ventricular responses to sustain the increases in CO. Otherwise preload would fall and the increases in CO could not be maintained. In subjects with systolic heart failure (HF), the ability to increase CO during exercise and MMA is markedly reduced, which has been attributed to impaired ventricular contractility. Whether the ability to maintain preload during MMA in HF is preserved is unknown. Using a conscious chronically instrumented canine model, we observed that MMA in HF is able to raise central blood volume similarly as in normal subjects. Therefore, the loss of the ability to raise CO during MMA in HF is not because of the loss of the ability to mobilize blood volume centrally. NEW & NOTEWORTHY In normal subjects during dynamic exercise muscle metaboreflex activation elicits large increases in cardiac output that occur via increases in heart rate, ventricular contractility, and, importantly, marked central blood volume mobilization that acts to maintain ventricular preload, thereby allowing the changes in cardiac function to maintain the increases in cardiac output. In subjects with heart failure, the ability to raise cardiac output during muscle metaboreflex activation is impaired. We investigated whether this is because of the inability to maintain ventricular preload. We found that this reflex is still able to elicit large increases in central blood volume, and therefore the limited ability to raise cardiac output likely stems from ventricular dysfunction and not the ability to maintain preload.

Transjugular intrahepatic portosystemic shunt: impact on systemic hemodynamics and renal and cardiac function in patients with cirrhosis.

Transjugular intrahepatic portosystemic shunt (TIPS) alleviates portal hypertension and possibly increases central blood volume (CBV). Moreover, renal function often improves; however, its effects on cardiac function are unclear. The aims of our study were to examine the effects of TIPS on hemodynamics and renal and cardiac function in patients with cirrhosis. In 25 cirrhotic patients, we analyzed systemic, cardiac, and splanchnic hemodynamics by catheterization of the liver veins and right heart chambers before and 1 wk after TIPS. Additionally, we measured renal and cardiac markers and performed advanced echocardiography before, 1 wk after, and 4 mo after TIPS. CBV increased significantly after TIPS (+4.6%, P < 0.05). Cardiac output (CO) increased (+15.3%, P < 0.005) due to an increase in stroke volume (SV) (+11.1%, P < 0.005), whereas heart rate (HR) was initially unchanged. Cardiopulmonary pressures increased after TIPS, whereas copeptin, a marker of vasopressin, decreased (-18%, P < 0.005) and proatrial natriuretic peptide increased (+52%, P < 0.0005) 1 wk after TIPS and returned to baseline 4 mo after TIPS. Plasma neutrophil gelatinase-associated lipocalin, renin, aldosterone, and serum creatinine decreased after TIPS (-36%, P < 0.005; -65%, P < 0.05; -90%, P < 0.005; and -13%, P < 0.005, respectively). Echocardiography revealed subtle changes in cardiac function after TIPS, although these were within the normal range. TIPS increases CBV by increasing CO and SV, whereas HR is initially unaltered. These results indicate an inability to increase the heart rate in response to a hemodynamic challenge that only partially increases CBV after TIPS. These changes, however, are sufficient for improving renal function. NEW & NOTEWORTHY For the first time, we have combined advanced techniques to study the integrated effects of transjugular intrahepatic portosystemic shunt (TIPS) in cirrhosis. We showed that TIPS increases central blood volume (CBV) through improved cardiac inotropy. Advanced echocardiography demonstrated that myocardial function was unaffected by the dramatic increase in preload after TIPS. Finally, renal function improved due to the increase in CBV. Recognition of these physiological changes significantly contributes to our clinical understanding of TIPS.

Hypoxia Attenuates Cardiopulmonary Reflex Control Of The Sympathetic Nerve Activity During Dynamic Leg Exercise

PURPOSE: The purpose of the present study was to test the hypothesis that cardiopulmonary baroreflex control of sympathetic vasomotor outflow is modulated by a powerful sympatho-excitatory drive from exercise pressor reflex, central command, and/or arterial chemoreflex. To test this hypothesis, under hypoxic conditions, muscle sympathetic nerve activity (MSNA) was recorded during leg cycling with an increase in central blood volume by increasing pedal frequency to increase the activity of cardiopulmonary baroreceptors. METHODS: Subjects performed mild leg cycle exercise at different pedal frequencies of 60 and 80 rpm (60EX and 80EX trials) while breathing a hypoxic gas mixture (inspired oxygen fraction = 0.12). The exercise workload of the 80EX trial was adjusted to get the same oxygen uptake as the 60EX trial. Stroke volume (SV) and cardiac output (CO) were measured non-invasively using impedance cardiology. MSNA was recorded via microneurography of the right median nerve at the elbow. RESULTS: Changes in thoracic impedance, SV, and CO in the 80EX trial were greater than those in the 60EX trial. MSNA burst frequency during hypoxic exercise in the 80EX trial (39±4 bursts/min) did not differ from that in the 60EX trial (39±3 bursts/min). CONCLUSIONS: These results suggest that a cardiopulmonary baroreflex of sympathetic vasomotor outflow during dynamic exercise is modulated by hypoxia-induced heightened sympathetic nerve activity.

Effect of an acute increase in central blood volume on cerebral hemodynamics.

Systemic blood distribution is an important factor involved in regulating cerebral blood flow (CBF). However, the effect of an acute change in central blood volume (CBV) on CBF regulation remains unclear. To address our question, we sought to examine the CBF and systemic hemodynamic responses to microgravity during parabolic flight. Twelve healthy subjects were seated upright and exposed to microgravity during parabolic flight. During the brief periods of microgravity, mean arterial pressure was decreased (-26 ± 1%, P < 0.001), despite an increase in cardiac output (+21 ± 6%, P < 0.001). During microgravity, central arterial pulse pressure and estimated carotid sinus pressure increased rapidly. In addition, this increase in central arterial pulse pressure was associated with an arterial baroreflex-mediated decrease in heart rate (r = -0.888, P < 0.0001) and an increase in total vascular conductance (r = 0.711, P < 0.001). The middle cerebral artery mean blood velocity (MCA Vmean) remained unchanged throughout parabolic flight (P = 0.30). During microgravity the contribution of cardiac output to MCA Vmean was gradually reduced (P < 0.05), and its contribution was negatively correlated with an increase in total vascular conductance (r = -0.683, P < 0.0001). These findings suggest that the acute loading of the arterial and cardiopulmonary baroreceptors by increases in CBV during microgravity results in acute and marked systemic vasodilation. Furthermore, we conclude that this marked systemic vasodilation decreases the contribution of cardiac output to CBF. These findings suggest that the arterial and cardiopulmonary baroreflex-mediated peripheral vasodilation along with dynamic cerebral autoregulation counteracts a cerebral overperfusion, which otherwise would occur during acute increases in CBV.

The effect of an acute increase in central blood volume on the response of cerebral blood flow to acute hypotension.

The purpose of the present study was to examine whether the response of cerebral blood flow to an acute change in perfusion pressure is modified by an acute increase in central blood volume. Nine young, healthy subjects voluntarily participated in this study. To measure dynamic cerebral autoregulation during normocapnic and hypercapnic (5%) conditions, the change in middle cerebral artery mean blood flow velocity was analyzed during acute hypotension caused by two methods: 1) thigh-cuff occlusion release (without change in central blood volume); and 2) during the recovery phase immediately following release of lower body negative pressure (LBNP; -50 mmHg) that initiated an acute increase in central blood volume. In the thigh-cuff occlusion release protocol, as expected, hypercapnia decreased the rate of regulation, as an index of dynamic cerebral autoregulation (0.236 ± 0.018 and 0.167 ± 0.025 s(-1), P = 0.024). Compared with the cuff-occlusion release, the acute increase in central blood volume (relative to the LBNP condition) with LBNP release attenuated dynamic cerebral autoregulation (P = 0.009). Therefore, the hypercapnia-induced attenuation of dynamic cerebral autoregulation was not observed in the LBNP release protocol (P = 0.574). These findings suggest that an acute change in systemic blood distribution modifies dynamic cerebral autoregulation during acute hypotension.

The Effect Of An Acute Increase In Central Blood Volume On Dynamic Cerebral Autoregulation

Previous investigations demonstrated that cerebral blood flow was influenced by changes in central blood volume and arterial blood pressure even within the range of cerebral autoregulation (60-150 mmHg). Recently, we found that during acute microgravity (parabolic flight condition), the acute increase in central blood volume decreased gradually arterial blood pressure via the arterial and cardiopulmonary baroreflexes. Despite the acute hypotension and central hypervolemia, steady-state cerebral blood flow was well maintained during this condition. However, the dynamic relationship between central blood volume and cerebrovascular control remains unclear. PURPOSE: The purpose of the present study was to examine dynamic cerebral autoregulation during an acute hypotension with central hypervolemia. METHODS: Nine young healthy subjects voluntarily participated in this study. In order to measure dynamic cerebral autoregulation, change in middle cerebral artery mean blood flow velocity (MCA Vmean) was analyzed during acute hypotension caused by two methods: 1) thigh-cuff occlusion release (without change in central blood volume) and 2) lower body negative pressure (-50 mmHg, LBNP) release (with acute increase in central blood volume). RESULTS: As expected, the thigh-cuff occlusion release caused acute hypotension and decrease in MCA Vmean accordingly, but MCA Vmean returned to the baseline value quickly. LBNP release increased and then decreased arterial blood pressure acutely. During the phase of decreased arterial blood pressure, however, the rate of regulation, as an index of dynamic cerebral autoregulation during LBNP release, was significantly lower than that during cuff release (0.112 ± 0.116 and 0.236 ± 0.053 sec-1, respectively, P=0.030). CONCLUSIONS: These findings suggest that an acute change in central blood volume modifies dynamic cerebral autoregulation.

The effect of an acute increase in central blood volume on hypercapnia‐induced attenuation in dynamic cerebral autoregulation

It is well established that hypercapnia attenuates dynamic cerebral autoregulation. The impact of central blood volume on cerebral blood flow is controversial. The purpose of the present study was to examine whether hypercapnia‐induced attenuation in dynamic cerebral autoregulation is modified by acute central hypervolemia. Nine young healthy subjects voluntarily participated in this study. In order to measure dynamic cerebral autoregulation during normocapnic and hypercapnic (5%) conditions, the change in middle cerebral artery mean blood flow velocity (MCA Vmean) was analyzed during acute hypotension caused by two methods: 1) thigh‐cuff occlusion release (without change in central blood volume) and 2) lower body negative pressure (‐50 mmHg, LBNP) release (with acute increase in central blood volume). As expected, hypercapnia decreased the rate of regulation, as an index of dynamic cerebral autoregulation (0.236±0.053 and 0.167±0.074 sec‐1, respectively, P=0.025). In contrast, this attenuation was disappeared during central hypervolemia (P=0.574). This phenomenon may be associated with hypervolemia‐induced attenuation of dynamic cerebral autoregulation (P=0.009). These findings suggest that an acute change in central blood volume modifies carbon dioxide‐induced changes in dynamic cerebral autoregulation.

Enhanced muscle pump during mild dynamic leg exercise inhibits sympathetic vasomotor outflow.

Muscle sympathetic nerve activity (MSNA) is not increased during leg cycling at light and mild intensities, despite activation of central command and the exercise pressor reflex. We determined whether increasing central blood volume and loading the cardiopulmonary baroreceptors modulate sympathetic vasomotor outflow during leg cycling. To this end, we changed the pedaling frequency to enhance skeletal muscle pump. Subjects performed two leg cycle exercises at differential pedal rates of 60 and 80 rpm (60EX and 80EX trials) for two conditions (with and without MSNA measurement). In each trial, subjects completed leg cycling with a differential workload to maintain constant oxygen consumption (VO2). MSNA was recorded via microneurography at the right median nerve of the elbow. Without MSNA measurement, thoracic impedance, stroke volume (SV), and cardiac output (CO) were measured non‐invasively using impedance cardiography. Heart rate and VO2 during exercise did not differ between the 60EX and 80EX trials. Changes in thoracic impedance, SV, and CO during the 80EX trial were greater than during the 60EX trial. MSNA during the 60EX trial was unchanged compared with that at rest (25.8 ± 3.1 [rest] to 28.3 ± 3.4 [exercise] bursts/min), whereas a significant decrease in MSNA was observed during the 80EX trial (25.8 ± 2.8 [rest] to 19.7 ± 2.0 [exercise] bursts/min). These results suggest that a muscle pump‐induced increase in central blood volume, and thereby loading of cardiopulmonary baroreceptors, could inhibit sympathetic vasomotor outflow during mild dynamic leg exercise, despite activation of central command and the exercise pressor reflex.

Sympathetic Outflow during Leg Cycling is Suppressed by Muscle Pump-Induced Increase in Central Blood Volume

Sympathetic Outflow during Leg Cycling is Suppressed by Muscle Pump-Induced Increase in Central Blood Volume

A Randomized Trial Comparing Colloid Preload to Coload During Spinal Anesthesia for Elective Cesarean Delivery

Hypotension after spinal anesthesia for cesarean delivery is common. Previous studies have demonstrated that a crystalloid fluid "coload" (rapid administration of a fluid bolus starting at the time of intrathecal injection) is superior to the conventional crystalloid preload (fluid administered before the intrathecal injection) for preventing hypotension. Colloid preload provides a sustained increase in central blood volume. We hypothesized that, in contrast to crystalloid, a colloid preload may be more effective than colloid coload for reducing the incidence of spinal anesthesia-induced hypotension. In this double-blind study, 178 patients were randomly assigned to receive a preload of 500 mL of hydroxyethyl starch over a period of 15-20 min before initiation of spinal anesthesia (n = 90) or an identical fluid bolus of hydroxyethyl starch starting at the time of identification of cerebrospinal fluid (n = 88). Vasopressors (ephedrine or phenylephrine) were administered if systolic arterial blood pressure decreased less than 80% of the baseline pressure and <100 mm Hg, or with smaller decreases in blood pressure if accompanied by nausea, vomiting, or dizziness. The primary outcome was the incidence of hypotension (defined as the administration of at least one dose of vasopressor). There was no significant difference between the groups in the incidence of hypotension (68% in preload group and 75% in coload group, 95% confidence interval of difference -6%-20%; P = 0.28), doses of ephedrine and phenylephrine, and number of vasopressor unit doses. The incidence of severe hypotension (systolic blood pressure <80 mm Hg) was 16% in the preload group and 22% in the coload group (P = 0.30). There were no differences in the incidence of nausea and/or vomiting, or neonatal outcome between the groups. There was no difference in the incidence of hypotension in women who received colloid administration before the initiation of spinal anesthesia compared with at the time of initiation of anesthesia. Both modalities are inefficient as single interventions to prevent hypotension.

Haemodynamic effects of plasma-expansion with hyperoncotic albumin in cirrhotic patients with renal failure: a prospective interventional study

BackgroundPatients with advanced cirrhosis of the liver typically display circulatory disturbance. Haemodynamic management may be critical for avoiding and treating functional renal failure in such patients. This study investigated the effects of plasma expansion with hyperoncotic albumin solution and the role of static haemodynamic parameters in predicting volume responsiveness in patients with advanced cirrhosis.MethodsPatients with advanced cirrhosis (Child B and C) of the liver receiving albumin substitution because of renal compromise were studied using trans-pulmonary thermodilution. Paired measurements before and after two infusions of 200 ml of 20% albumin per patient were recorded and standard haemodynamic parameters such as central venous pressure (CVP), mean arterial pressure (MAP), systemic vascular resistance index (SVRI), cardiac index (CI) and derived variables were assessed, including global end-diastolic blood volume index (GEDVI), a parameter that reflects central blood volumeResults100 measurements in 50 patients (33 m/17 w; age 56 years (± 8); Child-Pugh-score 12 (± 2), serum creatinine 256 μmol (± 150) were analyzed. Baseline values suggested decreased central blood volumes GEDVI = 675 ml/m2 (± 138) despite CVP within the normal range (11 mmHg (± 5). After infusion, GEDVI, CI and CVP increased (682 ml/m2 (± 128) vs. 744 ml/m2 (± 171), p < 0.001; 4.3 L/min/m2 (± 1.1) vs. 4.7 L/min/m2 (± 1.1), p < 0.001; 12 mmHg (± 6) vs. 14 mmHg (± 6), p < 0.001 respectively) and systemic vascular resistance decreased (1760 dyn s/cm5/m2 (± 1144) vs. 1490 dyn s/cm5/m2 (± 837); p < 0.001). Changes in GEDVI, but not CVP, correlated with changes in CI (r2 = 0.51; p < 0.001). To assess the value of static haemodynamic parameters at baseline in predicting an increase in CI of 10%, receiver-operating-characteristic curves were constructed. The areas under the curve were 0.766 (p < 0.001) for SVRI, 0.723 (p < 0.001) for CI, 0.652 (p = 0.010) for CVP and 0.616 (p = 0.050) for GEDVI.ConclusionIn a substantial proportion of patients with advanced cirrhosis, plasma expansion results in an increase in central blood volume. GEDVI but not CVP behaves as an indicator of cardiac preload, whereas high baseline SVRI is predictive of fluid responsiveness.