Changes 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.

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.

To identify normovolemia in humans: The stroke volume response to passive leg raising vs. head-down tilt.

Volume responsiveness can be evaluated by tilting maneuvers such as head‐down tilt (HDT) and passive leg raising (PLR), but the two procedures use different references (HDT the supine position; PLR the semi‐recumbent position). We tested whether the two procedures identify “normovolemia” by evaluating the stroke volume (SV) and cardiac output (CO) responses and whether the peripheral perfusion index (PPI) derived from pulse oximetry provides similar information. In randomized order, 10 healthy men were exposed to both HDT and PLR, and evaluations were made also when the subjects fasted. Central cardiovascular variables were derived by pulse contour analysis and changes in central blood volume assessed by thoracic electrical admittance (TEA). During HDT, SV remained stable (fasted 110 ± 16 vs. 109 ± 16 ml; control 113 ± 16 vs. 111 ± 16 ml, p > 0.05) with no change in CO, TEA, PPI, or SV variation (SVV). In contrast during PLR, SV increased (fasted 108 ± 17 vs. 117 ± 17 ml; control 108 ± 18 vs. 117 ± 18 ml, p < 0.05) followed by an increase in TEA (p < 0.05) and CO increased when subjects fasted (6.7 ± 1.5 vs. 7.1 ± 1.5, p = 0.007) with no change in PPI or SVV. In conclusion, SV has a maximal value for rest in supine men, while PLR restores SV as CBV is reduced in a semi‐recumbent position and the procedure thereby makes healthy volunteers seem fluid responsive.

The central blood volume as measured by thoracic electrical impedance and plasma proANP is not compromised by donation of 900 mL of blood in men.

To evaluate whether the donation of 900 mL of blood reduces the central blood volume (CBV) assessed by thoracic electrical impedance (TI) and plasma pro-atrial natriuretic peptide (proANP). Donation of 450 mL of blood carries a 1% risk of a vasovagal reaction. Withdrawal of 900 mL of blood decreases cardiac output; however, the effect on CBV remains unknown. A randomised, single-blinded, placebo-controlled, crossover design was used, where 21 healthy semi-recumbent men donated 2 × 450 mL blood or were sham-phlebotomised. Changes in CBV were estimated by proANP and TI at 1.5 (TI1.5 ) and 100 (TI100 ) kHz, reflecting extracellular volume and (regional) total body water, respectively, and the index value (IDX; 1/T1.5 -1/TI100 ) was used to estimate changes in intracellular (red cell) volume. Systolic, diastolic and mean arterial blood pressure; heart rate; stroke volume; cardiac output; and systemic vascular resistance were monitored. After completion of the study, 1000 mL of isotonic saline was infused. Changes (mean% ± SD) in TI1.5 , TI100 and IDX were similar after 450 mL (-0.2 ± 1.6%, 0.0 ± 1.1%, -0.4 ± 10.1%) and 900 mL (0.1 ± 1.6%, 0.2 ± 1.5% and -2.0 ± 15.8%) of blood donation compared to after a sham donation of 450 mL (-0.9 ± 1.2%, -0.5 ± 1.5% and -0.1 ± 6.1%) and 900 mL (-1.2 ± 1.5%, -0.6 ± 1.3% and 0.5 ± 9.9%). In addition, changes in plasma proANP were similar after 450 and 900 mL of blood donation (-0.8 ± 6.7% and -7.6 ± 7.9%) as after sham donations (1.3 ± 7.3% and -4.5 ± 5.6%). Monitoring haemodynamic variables revealed that stroke volume decreased after the donation of 900 mL of blood (-12 ± 12 mL) compared to sham donations. During a 900-mL blood loss in semi-recumbent men, CBV measured by TI and plasma proANP is not affected.

Effect of Blood Volume Shift Simulated via Head-up Tilt on Photoplethysmography Morphology.

PPG can provide information on cardiovascular responses to fluid shifts from upper to lower part of body under the condition of orthostatic stress. The current study investigated ability of PPG derived LVET and other PPG derived features to identify progressive central hypovolemia induced by head up tilt (HUT) and evaluated potential use of LVET as early noninvasive indicator of blood loss. Continuous finger PPG, blood pressure, and electrocardiography were recorded simultaneously during 5-minutes of baseline and HUT of 20°, 40°, and 60° from 15 participants (age: 26.5 ± 3 years; height: 177 ± 8 cm; weight: 72 ± 10 kg, mean ± SD). Beat-by-beat pulse rate (PR), systolic amplitude (SA), systolic time (ST), diastolic time (DT), and PP Interval (PPI) and Ratio of pulse rate over systolic amplitude (PR/SA) were derived for each stage. LVET was derived from each stage. Friedman test followed by post-hoc analysis using Tukey-HSD was conducted to highlight the significance of changes induced by HUT. Application of 60° HUT (i.e. moderate category simulated hypovolemia) resulted in a significant change in PR (80±3 bpm vs 68±3 bpm, p=0.0008), DT (264±7 ms vs 303±4 ms, p=0.0008), ST (110±6 ms vs 117±7 ms, p=0.02), PP interval (764±39 ms vs 869±25 ms, p=0.0045), PR/SA (112±16 vs 82±21, p=0.012) , SA (0.875± 0.2 vs 1.69±0.6, p=0.012) and LVET(292 vs 351ms,p=0.0008) compared to baseline. LVET has a strong association with the change in central blood volume and may be used as a sensitive early marker of progressive hypovolemia. The findings of the study support the hypothesis of differentiating simulated hypovolemia based on PPG alone. Keywords: Hypovolemia, HUT, LVET.

Stretching our understanding of baroreflex control in humans: evidence of a positive feedback pulmonary baroreflex.

Stretching our understanding of baroreflex control in humans: evidence of a positive feedback pulmonary baroreflex.

Interaction between graviception and carotid baroreflex function in humans during parabolic flight-induced microgravity.

The aim of the present study was to assess carotid baroreflex (CBR) function during acute changes in otolithic activity in humans. To address this question, we designed a set of experiments to identify the modulatory effects of microgravity on CBR function at a tilt angle of -2°, which was identified to minimize changes in central blood volume during parabolic flight. During parabolic flight at 0 and 1 g, CBR function curves were modeled from the heart rate (HR) and mean arterial pressure (MAP) responses to rapid pulse trains of neck pressure and neck suction ranging from +40 to -80 Torr; CBR control of HR (carotid-HR) and MAP (carotid-MAP) function curves, respectively. The maximal gain of both carotid-HR and carotid-MAP baroreflex function curves were augmented during microgravity compared with 1 g (carotid-HR, -0.53 to -0.80 beats·min-1·mmHg-1, P < 0.05; carotid-MAP, -0.24 to -0.30 mmHg/mmHg, P < 0.05). These findings suggest that parabolic flight-induced acute change of otolithic activity may modify CBR function and identifies that the vestibular system contributes to blood pressure regulation under fluctuations in gravitational forces. NEW & NOTEWORTHY The effect of acute changes in vestibular activity on arterial baroreflex function remains unclear. In the present study, we assessed carotid baroreflex function without changes in central blood volume during parabolic flight, which causes acute changes in otolithic activity. The sensitivity of both carotid heart rate and carotid mean arterial pressure baroreflex function was augmented in microgravity compared with 1 g, suggesting that the vestibular system contributes to blood pressure regulation in humans on Earth.

Internal dysregulation of the renin system in patients with stable liver cirrhosis

Sodium retention in cirrhosis is associated with changes in the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system (SNS), and the glomerular filtration rate (GFR). We hypothesized that in cirrhosis the acute reactions of RAAS and SNS to volume expansion are qualitatively intact, but occurring from elevated baseline levels. Acute cardiovascular, neurohumoral and renal responses to central blood volume changes were studied in cirrhotic patients and healthy controls. In patients, baseline plasma renin concentration (PRC) was elevated 5-fold compared to controls (p < .001); it increased during standing (+144%, p < .001) and remained elevated during subsequent sitting (+118%, p < .001). At baseline, plasma angiotensin II (pANGII) was not elevated significantly (14 ± 2 vs. 9 ± 2 pg/mL) in contrast to plasma aldosterone (pAldo, +160%, p < .001). During orthostatic RAAS activation, the rise in pAngII per unit increase in PRC was 0.04 pg AngII/mIU and 0.48 pg AngII/mIU in patients and controls, respectively (p < .001); similarly, the change in pAldo per unit change in pANGII was 3.6 in patients and 14.5 pg/pg in controls (p < .001). Plasma noradrenaline was elevated in the patients, but the dynamic changes were virtually identical to those of controls. During standing, abrupt decreases in renal blood flow (−63%, p < .001) and GFR (−42% p < .04) occurred only in patients. In conclusion, in stable cirrhosis, static and dynamic dysregulation exists within the RAAS; in the supine position pAngII levels are inappropriately low, and the AngII-mediated regulation of aldosterone secretion is severely impeded. In cirrhotic patients, profound reductions in renal blood flow and GFR occur during standing.

The Influence of Gender and Anthropometry on Haemodynamic Status at Rest and in Response to Graded Incremental Head-Up Tilt in Young, Healthy Adults.

The body's ability to rapidly and appropriately regulate blood pressure in response to changing physiological demand is a key feature of a healthy cardiovascular system. Passively tilting the body, thereby changing central blood volume, is a well-recognized and controlled method of evaluating this ability. However, such studies usually involve single tilt angles, or intermittent tilting separated by supine, resting periods; valuable information concerning the adaptive capacity of the regulatory systems involved is therefore currently lacking. Furthermore, despite increasing recognition that men and women differ in the magnitude of their haemodynamic response to such stimuli, little is known about the degree to which gender differences in body composition and anthropometry influence these regulatory pathways, or indeed if these differences are apparent in response to graded, incremental tilting. In the present study we measured, in 23 young, healthy adults (13 men, 10 women), the continuous beat-to-beat haemodynamic response to graded, incremental tilting (0°, 20°, 40°, 60°, and back to 40°) with each tilt angle lasting 16 min. On average, we observed increases in heart rate (+41%), blood pressure (+10%), and total peripheral resistance (+16%) in response to tilting. However, whilst men showed an immediate decrease in cardiac output upon tilting (−8.9%) cardiac output in women did not change significantly from supine values. Interestingly, the decrease in stroke volume observed in women was significantly less than that observed in men (−22 vs. −36%, p < 0.05); although the present study could not determine if this difference was due to gender per se or due to differences in body size (in particular height) between the two gender groups. Such disparities in the magnitude of autonomic response may indicate (in the case of our gradual incremental tilt procedure) a better buffering capacity to progressive changes in central blood volume in women; which warrants further investigation, particularly in light of the well-recognized differences in cardiovascular disease risk between men and women.

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.

Do intravascular hypovolaemia and hypervolaemia result in changes in pulmonary blood volume?

Hypovolaemia is generally believed to induce centrali sation of blood volume. Therefore, we evaluated whether hypovolaemia and hypervolaemia result in a change in central blood volume (that is, pulmonary blood volume (PBV)) and we explored the effects on the distribution between PBV and circulating blood volume (Vd circ).

Whole-body cryostimulation increases parasympathetic outflow and decreases core body temperature

The cardiovascular, autonomic and thermal response to whole-body cryostimulation exposure are not completely known. Thus the aim of this study was to evaluate objectively and noninvasively autonomic and thermal reactions observed after short exposure to very low temperatures. We examined 25 healthy men with mean age 30.1±3.7 years and comparable anthropomorphical characteristic. Each subject was exposed to cryotherapeutic temperatures in a cryogenic chamber for 3min (approx. −120°C). The cardiovascular and autonomic parameters were measured noninvasively with Task Force® Monitor. The changes in core body temperature were determined with the Vital Sense® telemetric measurement system. Results show that 3min to cryotherapeutic temperatures causes significant changes in autonomic balance which are induced by peripheral and central blood volume changes. Cryostimulation also induced changes in core body temperature, maximum drop of core temperature was observed 50–60 min after the stimulation. Autonomic and thermal reactions to cryostimulation were observed up to 6h after the exposure and were not harmful for examined subjects.

Manipulation of central blood volume and implications for respiratory control function.

The respiratory operating point (ventilatory or arterial PCO2 response) is determined by the intersection point between the controller and plant subsystem elements within the respiratory control system. However, to what extent changes in central blood volume (CBV) influence these two elements and the corresponding implications for the respiratory operating point remain unclear. To examine this, 17 apparently healthy male participants were exposed to water immersion (WI) or lower body negative pressure (LBNP) challenges to manipulate CBV and determine the corresponding changes. The respiratory controller was characterized by determining the linear relationship between end-tidal PCO2 (PetCO2 ) and minute ventilation (Ve) [Ve = S × (PetCO2 - B)], whereas the plant was determined by the hyperbolic relationship between Ve and PetCO2 (PetCO2 = A/Ve + C). Changes in Ve at the operating point were not observed under either WI or LBNP conditions despite altered PetCO2 (P < 0.01), indicating a moving respiratory operating point. An increase (WI) and a decrease (LBNP) in CBV were shown to reset the controller element (PetCO2 intercept B) rightward and leftward, respectively (P < 0.05), without any change in S, whereas the plant curve remained unaltered at the operating point. Collectively, these findings indicate that modification of the controller element rather than the plant element is the major factor that contributes toward an alteration of the respiratory operating point during CBV shifts.

Are you bleeding? Validation of a machine-learning algorithm for determination of blood volume status: application to remote triage

Due to limited remote triage monitoring capabilities, combat medics cannot currently distinguish bleeding soldiers from those engaged in combat unless they have physical access to them. The purpose of this study was to test the hypothesis that low-level physiological signals can be used to develop a machine-learning algorithm for tracking changes in central blood volume that will subsequently distinguish central hypovolemia from physical activity. Twenty-four subjects underwent central hypovolemia via lower body negative pressure (LBNP), and a supine-cycle exercise protocol. Exercise workloads were determined by matching heart rate responses from each LBNP level. Heart rate and stroke volume (SV) were measured via Finometer. ECG, heat flux, skin temperature, galvanic skin response, and two-axis acceleration were obtained from an armband (SenseWear Pro2) and used to develop a machine-learning algorithm to predict changes in SV as an index of central blood volume under both conditions. The algorithm SV was retrospectively compared against Finometer SV. A model was developed to determine whether unknown data points could be correctly classified into these two conditions using leave-one-out cross-validation. Algorithm vs. Finometer SV values were strongly correlated for LBNP in individual subjects (mean r = 0.92; range 0.75-0.98), but only moderately correlated for exercise (mean r = 0.50; range -0.23-0.87). From the first level of LBNP/exercise, the machine-learning algorithm was able to distinguish between LBNP and exercise with high accuracy, sensitivity, and specificity (all ≥90%). In conclusion, a machine-learning algorithm developed from low-level physiological signals could reliably distinguish central hypovolemia from exercise, indicating that this device could provide battlefield remote triage capabilities.

Changes in Left Ventricular Diastolic Function During Hemodialysis Sessions

Left ventricular diastolic dysfunction is common in hemodialysis patients and is associated with worse outcome. Previous studies have shown that diastolic function worsens from pre- to post-dialysis session, but this has not been studied during hemodialysis. We studied the evolution of diastolic function parameters early and late during hemodialysis. Observational study. 109 hemodialysis patients on a thrice-weekly dialysis schedule with a mean age of 62.5 ± 15.6 (SD) years were studied between March 2009 and March 2010. Hemodialysis with constant ultrafiltration rate and dialysate conductivity. Changes in diastolic function parameters. Mitral early inflow (E) and tissue Doppler early diastolic velocity (mean e') were evaluated by echocardiography predialysis, at 60 and 180 minutes intradialysis, and postdialysis. Relative blood volume changes were calculated from changes in hematocrit. Predialysis E and mean e' were 0.93 ± 0.24 m/s and 6.6 ± 2.1 cm/s, respectively. E and mean e' values decreased significantly during hemodialysis (P < 0.001). The steepest change occurred at 60 minutes intradialysis (E, -21.4% ± 17.6% and -30.5% ± 19.2% at 60 and 180 minutes, respectively; mean e', -16.0% ± 18.6% and -19.5% ± 21.8% at 60 and 180 minutes, respectively). At 60 minutes intradialysis, changes in relative blood volume and brain natriuretic peptide level were associated significantly with the change in E but not with the change in mean e'. Changes in relative blood volume may not fully reflect central blood volume changes and do not capture the effect of blood loss to the extracorporal circuit. Left atrial volume was not measured. Left ventricular diastolic function worsens early during a hemodialysis session. The decrease in mean e' at 60 minutes intradialysis was unrelated to changes in relative blood volume. Although this finding does not exclude a role of hypovolemia because of the limitations of the measurement of relative blood volume, it raises the possibility that non-volume-related mechanisms are involved in the early decrease in mean e' during hemodialysis.

Pneumatic compression devices during hemodialysis: a randomized crossover trial

Maintenance of central blood volume (CBV) is essential for hemodynamic stability during hemodialysis (HD), though preservation of CBV is poorly understood. Pneumatic compression devices (PCDs) during HD may help maintain CBV. We performed a randomized, crossover trial to determine the effect of PCDs on CBV during HD. Patients underwent two consecutive mid-week HD sessions, randomized to begin the first session either with or without PCDs [stratified by intradialytic hypotension (IDH)-prone status]. The primary outcome was change in CBV during HD. The secondary outcomes were change in other hemodynamic and volume status parameters. Fifty-one patients (median age 65 years, 75% male, 22% IDH-prone) were randomized; forty-six completed the study. During HD, the median change in CBV for PCD and control sessions was -0.08 versus -0.05 L (P = 0.62). There was no difference in the change in cardiac output (CO) (-0.63 versus -0.49 L/min, P = 0.78) or systemic vascular resistance (SVR) (+1.30 versus +1.55 mmHg/L/min, P = 0.67) for PCDs versus control. Based on the bioimpedance measurements, patients were not volume overloaded pre-dialysis. There was a greater reduction in total body water (TBW) (-2.6 versus -2.3 L, P = 0.05) and intracellular fluid (ICF) volume (-1.3 versus -1.1 L, P = 0.03), and no difference in change in the extracellular fluid (ECF) volume (1.3 versus 1.2 L, P = 0.09) with PCDs versus control. Similar results were observed in IDH-prone patients. Compared with standard of care, PCDs have no effect on intradialytic hemodynamic parameters, including CBV, although they may allow greater capacity for fluid removal. Further studies are required to better understand physiological and hemodynamic changes in patients during HD.

When filling the glass only leaves it half empty!– Insight into the cardiovascular physiology of haemorrhage under heat stress

When filling the glass only leaves it half empty!– Insight into the cardiovascular physiology of haemorrhage under heat stress