Blood Volume Shifts Research Articles

Characterization of internal jugular vein region-specific distension and flow patterns during progressive volume shifting.

Blood volume shifts during postural adjustment leads to irregular distension of the internal jugular vein (IJV). In microgravity, distension may contribute to flow stasis and thromboembolism, though the regional implications and associated risk remain unexplored. We characterized regional differences in IJV volume distension and flow complexity during progressive head-down tilt (HDT) (0°, -6°, -15°, -30°) using conventional ultrasound and vector flow imaging. We also evaluated low-pressure thigh cuffs (40 mmHg) as a fluid shifting countermeasure during -6° HDT. Total IJV volume expanded 139±95% from supine (4.6±2.7 mL) to -30° HDT (10.3±5.0 mL). Blood flow profiles had greater vector uniformity at the cranial IJV region (P<0.01) and became more dispersed with increasing tilt (P<0.01). Qualitatively, flow was more uniform throughout the IJV during its early flow cycle phase, and more disorganized during late flow phase. This disorganized flow was accentuated closer to the vessel wall, near the caudal region, and during greater HDT. Low-pressure thigh cuffs during -6° HDT decreased IJV volume at the cranial region (-12±15%; P<0.01) but not the caudal region (P=0.20), although flow uniformity was unchanged (both regions,P>0.25). We describe a distensible IJV accommodating large volume shifts along its length. Prominent flow dispersion was primarily found at the caudal region, suggesting multi-directional blood flow. Thigh cuffs appear effective for decreasing IJV volume but effects on flow complexity are minor. Flow complexity along the vessel length is likely related to IJV distension during chronic volume shifting and may be a precipitating factor for flow stasis and future thromboembolism risk.

A game of chest: Where does blood volume shift?

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Esophageal Doppler-derived indices and arterial load variables provide useful hemodynamic information during assessment of fluid responsiveness in anesthetized dogs undergoing acute changes in blood volume.

To investigate the relationship between invasively measured stroke volume (SV) and (1) esophageal Doppler-derived indices such as stroke distance (StrokeD), flow time corrected (FTc), stroke distance variation (SDV), and peak velocity variation (PVV); and (2) arterial load (AL) variables during evaluation of fluid responsiveness (FR) in anesthetized dogs undergoing sudden hemodynamic shifts in blood volume. 6 healthy male dogs. Dogs were anesthetized with isoflurane, ventilated mechanically, and instrumented to undergo sequential, nonrandomized experimental stages. The dogs transitioned from normovolemia (NORMO-BL) to hypovolemia (30% blood loss; HYPO-30), followed by autologous blood transfusion, and then to hypervolemia (colloid bolus). During each stage, SV was quantified using pulmonary artery thermodilution and its relationship with StrokeD, FTc, SDV, and PVV; and AL variables such as effective arterial elastance (Ea), dynamic arterial elastance (Eadyn), and total arterial compliance (Ca) were established. As SV decreased significantly during HYPO-30 compared to NORMO-BL, there was a significant (P < .001) decrease in StrokeD, FTc, and Ca, with simultaneous increases in SDV, PVV, Ea, and Eadyn. Upon restoration of blood volume, these values stabilized closer to NORMO-BL. A significant (P < .001) correlation was observed between SV and StrokeD, FTc, Ea, Eadyn, and Ca. Minimally invasive StrokeD, FTc, SDV, and PVV act as SV surrogates and help assess FR during different blood volume stages in healthy dogs. During hypovolemia-induced hypotension, Ea, Eadyn, and Ca may be able to guide therapeutic decisions favoring improvement in blood pressure and SV.

Separating ventricular activity in thoracic EIT using 4D image-based FEM simulations

Abstract One challenge in central hemodynamic monitoring based on electrical impedance tomography (EIT) is to robustly detect ventricular signal components and the corresponding EIT image region without external monitoring information. Current stimulation and voltage measurement of EIT were simulated with finite element porcine torso models in presence of a multitude of thoracic blood volume shifts. The simulated measurement data was examined for linear dependence on changes in stroke volume. Based on the results the EIT measurement information regarding stroke volume changes is sparse

Effect of Exercise-Induced Reductions in Blood Volume on Cardiac Output and Oxygen Transport Capacity.

We wanted to demonstrate the relationship between blood volume, cardiac size, cardiac output and maximum oxygen uptake (O2max) and to quantify blood volume shifts during exercise and their impact on oxygen transport. Twenty-four healthy, non-smoking, heterogeneously trained male participants (27 ± 4.6 years) performed incremental cycle ergometer tests to determine O2max and changes in blood volume and cardiac output. Cardiac output was determined by an inert gas rebreathing procedure. Heart dimensions were determined by 3D echocardiography. Blood volume and hemoglobin mass were determined by using the optimized CO-rebreathing method. The O2max ranged between 47.5 and 74.1 mL⋅kg–1⋅min–1. Heart volume ranged between 7.7 and 17.9 mL⋅kg–1 and maximum cardiac output ranged between 252 and 434 mL⋅kg–1⋅min–1. The mean blood volume decreased by 8% (567 ± 187 mL, p = 0.001) until maximum exercise, leading to an increase in [Hb] by 1.3 ± 0.4 g⋅dL–1 while peripheral oxygen saturation decreased by 6.1 ± 2.4%. There were close correlations between resting blood volume and heart volume (r = 0.73, p = 0.002), maximum blood volume and maximum cardiac output (r = 0.68, p = 0.001), and maximum cardiac output and O2max (r = 0.76, p < 0.001). An increase in maximum blood volume by 1,000 mL was associated with an increase in maximum stroke volume by 25 mL and in maximum cardiac output by 3.5 L⋅min–1. In conclusion, blood volume markedly decreased until maximal exhaustion, potentially affecting the stroke volume response during exercise. Simultaneously, hemoconcentrations maintained the arterial oxygen content and compensated for the potential loss in maximum cardiac output. Therefore, a large blood volume at rest is an important factor for achieving a high cardiac output during exercise and blood volume shifts compensate for the decrease in peripheral oxygen saturation, thereby maintaining a high arteriovenous oxygen difference.

Mitral prolapsing volume is associated with increased cardiac dimensions in patients with mitral annular disjunction.

IntroductionIn patients with mitral annular disjunction (MAD), it can be difficult to assess the severity of mitral regurgitation (MR), as they present with a prolapsing volume (i.e. volume resulting from mitral valve prolapse, blood volume shift) rather than a regurgitant jet. The influence of the mitral prolapsing volume (MPV) on cardiac dimensions is unknown. We hypothesised that the severity of MR is underestimated in these patients. Our aim was to measure MPV and to investigate its influence on cardiac dimensions in patients with MAD.MethodsWe retrospectively included 131 consecutive patients with MAD from our institution’s echocardiographic database. Transthoracic echocardiography was used to assess MPV. Additionally, we established a control group of 617 consecutive patients with degenerative mitral valve disease and performed propensity score matching.ResultsMedian MPV in the MAD group was 12 ml. MPV was an independent predictor for left ventricular end-diastolic (LVEDD) and end-systolic diameter (LVESD) and left atrial volume (all p < 0.001). In patients with large prolapsing volumes (> 15 ml), LVEDD (56 ± 6 mm vs 51 ± 6 mm, p < 0.001), LVESD [38 mm (34–41) vs 34 mm (31–39), p < 0.01] and left atrial volume [105 ml (86–159) vs 101 ml (66–123), p = 0.04] were significantly increased compared to matched patients with degenerative mitral valve disease and similarly assessed severity of MR.ConclusionDue to a volume shift based on the MPV rather than an actual regurgitant jet, MR severity cannot be assessed adequately in MAD patients. Increased MPV induces ventricular and atrial enlargement. These findings warrant future studies to focus on MPV as an additional parameter for assessment of the severity of MR in MAD patients.Supplementary InformationThe online version of this article (10.1007/s12471-021-01575-6) contains supplementary material, which is available to authorized users.

Cardiovascular deconditioning during long-term spaceflight through multiscale modeling

Human spaceflight has been fascinating man for centuries, representing the intangible need to explore the unknown, challenge new frontiers, advance technology, and push scientific boundaries further. A key area of importance is cardiovascular deconditioning, that is, the collection of hemodynamic changes—from blood volume shift and reduction to altered cardiac function—induced by sustained presence in microgravity. A thorough grasp of the 0G adjustment point per se is important from a physiological viewpoint and fundamental for astronauts’ safety and physical capability on long spaceflights. However, hemodynamic details of cardiovascular deconditioning are incomplete, inconsistent, and poorly measured to date; thus a computational approach can be quite valuable. We present a validated 1D–0D multiscale model to study the cardiovascular response to long-term 0G spaceflight in comparison to the 1G supine reference condition. Cardiac work, oxygen consumption, and contractility indexes, as well as central mean and pulse pressures were reduced, augmenting the cardiac deconditioning scenario. Exercise tolerance of a spaceflight traveler was found to be comparable to an untrained person with a sedentary lifestyle. At the capillary–venous level significant waveform alterations were observed which can modify the regular perfusion and average nutrient supply at the cellular level. The present study suggests special attention should be paid to future long spaceflights which demand prompt physical capacity at the time of restoration of partial gravity (e.g., Moon/Mars landing). Since spaceflight deconditioning has features similar to accelerated aging understanding deconditioning mechanisms in microgravity are also relevant to the understanding of aging physiology on the Earth.

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.

Pulling back on the push-pull effect: use of lower body negative pressure to protect against drops in cerebral perfusion during airflight manoeuvres.

Pulling back on the push-pull effect: use of lower body negative pressure to protect against drops in cerebral perfusion during airflight manoeuvres.

Benefits of the Subdural Evacuating Port System (SEPS) Procedure Over Traditional Craniotomy for Subdural Hematoma Evacuation.

There remains no consensus on the optimal primary intervention for subdural hematoma (SDH). Although historically favored, craniotomy carries substantial morbidity and incurs significant costs. Contrastingly, the subdural evacuating port system (SEPS) is a minimally invasive bedside procedure. We assessed the benefits of SEPS over traditional craniotomy for SDH evacuation. A single-center retrospective cohort study of SDH patients receiving craniotomy or SEPS between 2012 and 2017 was performed. Information regarding demographics, medical history, presentation, surgical outcomes, cost, and complications was collected. Pre- and postoperative hematoma volumes were calculated using 3D image segmentation using Vitrea software. Multivariate regression models were employed to assess the influence of intervention choice. Of 107 patients, 68 underwent craniotomy and 39 underwent SEPS. There were no differences in age, sex, blood thinner use, platelet count, INR, hematoma lateralization, age, volume, or midline shift at presentation between intervention groups. Although there was no difference in percent residual hematoma volume 24-hour postintervention (44.1% vs 45.1%, P = .894), SEPS was associated with lower hospitalization costs ($108 391 vs $166 318, *P = .002), shorter length of stay (4.0 vs 5.8 days, *P = .0002), and fewer postoperative seizures (2.6% vs 17.7%, *P = .048). Reoperation rate was higher after SEPS overall (33.3% vs 13.2%, *P = .048) but comparable to craniotomy in chronic SDH (12.50% vs 7.69%, P = 1.000). In this retrospective cohort, SEPS was noninferior to craniotomy at reducing SDH hematoma volume. The SEPS procedure was also associated with decreased length of stay hospitalization costs, and postoperative seizures and demonstrated a comparable recurrence rate to craniotomy for chronic SDH in particular.

Tachycardia Induced Cardiomyopathy (TIC) in Patients with Postural Orthostatic Tachycardia Syndrome (POTS) and Ehlers-Danlos Syndromes (EDS)

Intro POTS is said to be a type of dysautonomia characterized by Tachycardia brought about by postural shifts in blood volume and circulation. This results in various Symptoms (Sx) including dizziness, lightheadedness, syncope, palpitations and tremulousness. POTS is often associated with EDS, a rare inherited connective tissue disorder pertaining to the production and processing of collagen. POTS causes abnormal increases in HR. If left untreated, pts can suffer from TIC indicated by an increasing Left Ventricle End Diastolic Diameter (LVEDD). Methods Electronic health records of 1300 POTS pts were reviewed retrospectively. Female pts with EDS between the ages of 20-40 who had imaging records of 3 or more echocardiograms in the past 5 yrs, with no more than 1 yr between consecutive echocardiograms were randomly selected. Our records identified 94 pts fulfilling this criteria. An assessment of the relation between associated Sx and corresponding Echocardiogram LVEDD values was made by observing pts reported Sx such as shortness of breath, chest pain, dizziness/lightheadedness, palpitations, and their overall feeling of well-being. Corresponding Functional Capacity (FC) values of each pt analyzed by reviewing Cardiopulmonary Exercise Stress Tests were also noted. Lastly, treatment modalities including drugs, exercise and I/V fluids were also monitored. A timeline with regards to changes in LVEDD was established to determine the effectiveness of various treatments. Results Of the 94 pts fulfilling the inclusion criteria: Mean age was 30 +/- 6.3 yrs. Mean LVEDD of pts reporting min Sx was 4.02 +/- 0.43. Mean LVEDD of pts reporting max Sx was 4.28 +/- 0.45. T-Test (p-value The average FC of pts experiencing min Sx was 69% while it was 63% for pts experiencing max Sx. T-Test (p-value = 0.006665) indicates that the mean of FC with least Sx is significantly higher than FC with maximum Sx. The average Decrease in FC per 0.1 cm Increase in LVEDD was 2.55% Pts with LVEDD of 4.04 +/- 0.48 were seen to have the highest FC >70%. Overall, 40 pts were seen to have >70% FC at LVEDD with the Lowest Sx. At >70% FC, 44 pts showed improvement with medication (Midodrine 20, Florinef 12, Beta Blockers 12), 25 pts with exercise and 11 on IV Fluids (including saline and/or albumin infusions). Conclusion Pts with POTS and EDS, tend to develop a worsening of Sx as LVEDD progressively increases resulting in a Tachycardia Induced Cardiomyopathy. However, aggressive management of Sx with medication and a dedicated exercise regimen can improve Sx, decrease LVEDD and cause reversal of the disease process. From the evidence collected, it can be recommended that POTS pts’ LVEDD values be maintained between 3.8 - 4.2 cm, as this range was seen to produce the least amount of Sx as well as a higher FC (>70%).

Non‐Invasive Pulmonary Gas Exchange Measurements Following Deep Breath‐Hold Diving

Breath‐hold diving is a ubiquitous activity, with recreational, fishing, military and competitive divers. During a dive, immersion and the increasing hydrostatic pressure of descent facilitate cardiovascular adjustments that promote a blood volume shift into the heart and chest vasculature, further augmenting autonomic responses (i.e. diving bradycardia, peripheral vasoconstriction, and splenic contraction) to conserve O2. Exceeding the compliant capacity of the lung and associated tissues can result in pulmonary injury called squeeze, which is characterized by post‐dive coughing, wheezing and hemoptysis. To provide insight into the consequences of such lung squeeze, our objective was to evaluate the time‐course of a maximal deep dive on pulmonary gas exchange, pulmonary artery systolic pressures (PASP), and ultrasound lung comets (ULCs). Ten healthy trained breath‐hold divers (33±9 yr; 80±15 kg; 185±9 cm) performed a maximal effort dive (55±12 m; range 40–76 m). Pulmonary gas exchange and PASP were performed at baseline, and repeated at 10 and 60 min post dive. Pulmonary gas exchange was non‐invasively measured by collecting end‐tidal PO2 and PCO2 during steady‐state breathing, and derived arterial PO2 via pulse oximetry. O2 deficit was defined as the difference between end‐tidal and calculated arterial PO2; consistent with the Bohr effect by utilizing end‐tidal PCO2. The ULCs were collected bilaterally, parasternal to mid‐axillary, at baseline and again 2.5 h post dive. Following the dive, although there was an impairment of pulmonary gas exchange, evident by an increase in O2 deficit from 10.9±4.5 mmHg at baseline to 22.9±5.1 mmHg 10‐min post dive (p=0.02), this deficit had normalized by 60‐min post. There was persistent hyperventilation up to 60 min post dive, reflected by reductions in end‐tidal PCO2 (p=0.02). PASP was unaltered post‐dive. Although ULCs trended to increase from baseline to 2.5 h post dive (3.7±3 to 10.4±13.2 comets; p=0.09), the delta change in ULC from baseline to post‐dive was positively correlated with depth (r=0.67, p=0.04) and, to a lesser extent, with both change in SpO2 (r=−0.62, p=0.06) and O2 deficit (r=0.58, p=0.08). The findings of this novel study suggest impairment in pulmonary gas exchange is present following diving to depth, even up to 10 min after surfacing. The mechanism(s) driving the slight hyperventilation are unclear, but potentially could be mediated via mild pulmonary edema and/or stimulation of juxtapulmonary capillary receptors. Together, there is transient impairment in gas exchange and associations with ULC during ‘modest’ dives. The development of pathological pulmonary edema, and severe and sustained impairment in pulmonary gas exchange, would seem likely at the forefront of breath‐hold diving performances (e.g, &gt;100 m). There remains little data regarding safe return‐to‐dive practices following a squeeze, and non‐invasive pulmonary gas exchange monitoring could provide valuable utility.Support or Funding InformationCanada Research Chair, NSERCThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Intradialytic hypotension and splanchnic shifting: Integrating an overlooked mechanism with the detection of ischemia-related signals during hemodialysis.

In the most simple analysis, a patient's hematocrit during hemodialysis will rise when the rate of ultrafiltration exceeds the rate at which the fluid is mobilized from extravascular spaces; the greater the rise in hematocrit, the lower blood volume is and the more likely intradialytic hypotension (IDH) is to occur. A secondary mechanism of IDH may be due to sudden shift of blood volume away from the heart under conditions of borderline cardiac filling. A substantial portion of blood volume resides in the splanchnic venous system. During the early part of dialysis, a centripetal shift of red cells from this anatomical region to the central circulation has been documented to occur. The magnitude of this shift is unpredictable, and it may depend on the level of splanchnic vasoconstriction predialysis. The amount of splanchnic shift may also be reduced in patients with autonomic dysfunction. Once this central shift in blood volume has occurred, it can be reversed during further ultrafiltration due to ischemia-induced release of vasodilatory molecules that cause dilation of upstream splanchnic arterioles; this causes increased transmission of arterial pressure to the splanchnic veins, acutely increasing their capacity. The increased splanchnic venous capacity may cause a sudden shift of blood away from the central circulation to fill these veins under conditions where cardiac filling has already been reduced. The result can be severe IDH due to insufficient cardiac filling and cardiac output. One fruitful preventive approach might be to continuously monitor the blood or dialysate for the sudden appearance of such ischemia-related molecules or other signals which may herald not only dialysis hypotension but tissue stunning, warning that the fluid removal rate should be immediately reduced.

Quantitative Susceptibility Mapping to Assess Cerebral Vascular Compliance.

This study explored whether autoregulatory shifts in cerebral blood volume induce susceptibility changes large enough to be depicted by quantitative susceptibility mapping. Eight healthy subjects underwent fast quantitative susceptibility mapping at 3T while lying down to slowly decrease mean arterial pressure. A linear relationship between mean arterial pressure and susceptibility was observed in cortical and subcortical structures, likely representing vessels involved in autoregulation. The slope of this relationship is assumed to indicate the extent of cerebral vascular compliance.

The Effect of Microgravity on Central Aortic Blood Pressure.

Background Blood pressure has been traditionally measured at peripheral arteries. In the past decade, evidence has grown that central aortic blood pressure may be a more powerful predictor for cardiovascular events, but data on its regulation are rare. The present work examines the impact of microgravity on central blood pressure for the first time. Methods We performed 7 parabolic flights with 22 seconds of weightlessness in each parabola. Hemodynamic parameters including central systolic blood pressure were measured noninvasively in a free-floating position in 20 healthy subjects (19-43 years of age). Results Arterial elasticity at rest was normal in all participants (augmentation index 14% (interquartile range (IQR) 10-22), pulse wave velocity 5.2 m/s (IQR 5.0-5.4)). Transition of 1g to 0g led to a significant increase of central systolic blood pressure from 124 (IQR 118-133) to 127 (IQR 119-133) mm Hg (P = 0.017). Cardiac index augmented significantly from 2.5 (IQR 2.2-2.8) to 2.7 (IQR 2.3-3.0) l/min/m2 (P 0.05). Conclusion Whereas there is a multitude of studies on the effects of microgravity on peripheral blood pressure, this study provides first data on central aortic blood pressure. An acute loss of gravity leads to a central blood volume shift with an augmentation of cardiac output. In healthy subjects with normal arterial stiffness, the compensatory decrease of peripheral resistance does not outweigh this effect resulting in an increase of central blood pressure.

The Effect of Microgravity on Central Aortic Blood Pressure.

Blood pressure has been traditionally measured at peripheral arteries. In the past decade, evidence has grown that central aortic blood pressure may be a more powerful predictor for cardiovascular events, but data on its regulation are rare. The present work examines the impact of microgravity on central blood pressure for the first time. We performed 7 parabolic flights with 22 seconds of weightlessness in each parabola. Hemodynamic parameters including central systolic blood pressure were measured noninvasively in a free-floating position in 20 healthy subjects (19-43 years of age). Arterial elasticity at rest was normal in all participants (augmentation index 14% (interquartile range (IQR) 10-22), pulse wave velocity 5.2 m/s (IQR 5.0-5.4)). Transition of 1g to 0g led to a significant increase of central systolic blood pressure from 124 (IQR 118-133) to 127 (IQR 119-133) mm Hg (P = 0.017). Cardiac index augmented significantly from 2.5 (IQR 2.2-2.8) to 2.7 (IQR 2.3-3.0) l/min/m2 (P < 0.001), while peripheral vascular resistance showed a decrease from 1.30 (IQR 1.14-1.48) to 1.25 (IQR 1.15-1.40) s × mm Hg/ml (P = 0.037). Peripheral systolic blood pressure did not change significantly (P > 0.05). Whereas there is a multitude of studies on the effects of microgravity on peripheral blood pressure, this study provides first data on central aortic blood pressure. An acute loss of gravity leads to a central blood volume shift with an augmentation of cardiac output. In healthy subjects with normal arterial stiffness, the compensatory decrease of peripheral resistance does not outweigh this effect resulting in an increase of central blood pressure.

THE EFFECT OF MICROGRAVITY ON CENTRAL AORTIC BLOOD PRESSURE

Objective: BACKGROUND: Blood pressure has been traditionally measured at peripheral arteries. In the past decade evidence has grown, that central aortic blood pressure may be a more powerful predictor for cardiovascular events, but data on its regulation are rare. The present works examines the impact of microgravity on central blood pressure for the first time. Methods: We performed seven parabolic flights with 22 seconds of weightlessness in each parabola. Hemodynamic parameters including central systolic blood pressure were measured non-invasively in a free-floating position in 20 healthy subjects (19–43 years of age). Results: Arterial elasticity at rest was normal in all participants (augmentation index 14% [interquartile range IQR 10–22], pulse wave velocity 5.2 m/s [IQR 5.0–5.4]). Transition of 1 g to 0 g led to a significant increase of central systolic blood pressure from 124 (IQR 118–133) to 127 (IQR 119–133) mmHg (p = 0.017). Cardiac index propelled significantly from 2.5 (IQR 2.2–2.8) to 2.7 (IQR 2.3–3.0) l/min/m2 (p < 0.001), whilst peripheral vascular resistance showed a decrease from 1.30 (IQR 1.14–1.48) to 1.25 (IQR 1.15–1.40) s*mmHg/ml (p = 0.037). Peripheral systolic blood pressure did not change significantly (p > 0.05). Conclusion: Whereas there is a multitude of studies on the effects of microgravity on peripheral blood pressure, this study provides first data on central aortic blood pressure. An acute loss of gravity leads to a central blood volume shift with an augmentation of cardiac output. In healthy subjects with normal arterial stiffness the compensatory decrease of peripheral resistance does not outweigh this effect resulting in an increase of central blood pressure.

Electrolyte Disturbances in Patients with Diabetes Mellitus

Diabetic patients frequently develop a constellation of electrolyte disorders. These derangement results from insulin deficiency, hyperglycemia and hyperketonemia. Hyperglycemia sets the internal environment for osmotic diuresis while causing a dilutional effect on electrolyte concentrations.The osmotic effect of glucose results in decreased circulating blood volume and fluid shift from the intracellular spaces causing cellular dehydration. These disturbances are particularly common in decompensated diabetes, especially in the context of diabetic ketoacidosis or non ketotic hyperglycemic hyperosmolar syndrome.These patients are markedly sodium, magnesium and phosphate depleted. Diabetes mellitus is linked to both hypo and hyperkalemia and also hypo and hypercalcemia reflecting coexistence of hyperglycemia related mechanisms, which tend to change serum potassium and calcium to opposite directions. This article provides an overview of the electrolyte disturbances occurring in Diabetes and mechanisms underlying those disturbances.Bangladesh J Med Biochem 2017; 10(1): 27-35

Computer simulation of syringomyelia in dogs

BackgroundSyringomyelia is a pathological condition in which fluid-filled cavities (syringes) form and expand in the spinal cord. Syringomyelia is often linked with obstruction of the craniocervical junction and a Chiari malformation, which is similar in both humans and animals. Some brachycephalic toy breed dogs such as Cavalier King Charles Spaniels (CKCS) are particularly predisposed. The exact mechanism of the formation of syringomyelia is undetermined and consequently with the lack of clinical explanation, engineers and mathematicians have resorted to computer models to identify possible physical mechanisms that can lead to syringes. We developed a computer model of the spinal cavity of a CKCS suffering from a large syrinx. The model was excited at the cranial end to simulate the movement of the cerebrospinal fluid (CSF) and the spinal cord due to the shift of blood volume in the cranium related to the cardiac cycle. To simulate the normal condition, the movement was prescribed to the CSF. To simulate the pathological condition, the movement of CSF was blocked.ResultsFor normal conditions the pressure in the SAS was approximately 400 Pa and the same applied to all stress components in the spinal cord. The stress was uniformly distributed along the length of the spinal cord. When the blockage between the cranial and spinal CSF spaces forced the cord to move with the cardiac cycle, shear and axial normal stresses in the cord increased significantly. The sites where the elevated stress was most pronounced coincided with the axial locations where the syringes typically form, but they were at the perimeter rather than in the central portion of the cord. This elevated stress originated from the bending of the cord at the locations where its curvature was high.ConclusionsThe results suggest that it is possible that repetitive stressing of the spinal cord caused by its exaggerated movement could be a cause for the formation of initial syringes. Further consideration of factors such as cord tethering and the difference in mechanical properties of white and grey matter is needed to fully explore this possibility.

Jackson-Pratt drainage in pediatric craniofacial reconstructive surgery: is it helping or hurting?

OBJECTIVE Jackson-Pratt drains (JPDs) are commonly employed in pediatric craniofacial reconstructive surgery (CRFS) to reduce postoperative wound complications, but their risk profile remains unknown. Perioperative blood loss and volume shifts are major risks of CFRS. The goal of this study was to evaluate the risks of JPD usage in CFRS, particularly with regard to perioperative blood loss, hyponatremia, intensive care unit (ICU) length of stay, and postoperative wound complications. METHODS The authors performed a retrospective review of data obtained in pediatric patients who underwent CFRS at a single institution, as performed by multiple surgeons between January 2010 and December 2014. Data were gathered from patients who did and did not receive JPDs at the time of surgery. Outcome measures were compared between the JPD and no-JPD groups. RESULTS The overall population 179 pediatric patients: 128 who received JPDs and 51 who did not. In their analysis, the authors found no significant differences in baseline patient characteristics between the two groups. The average JPD output over the first 48 hours was 222 ± 142 ml. When examining the immediate preoperative to immediate postoperative time period, no significant differences were noted between the groups with regard to the need for blood transfusion or changes in hemoglobin, hematocrit, or serum sodium levels. These differences were also not significant when examining the 48-hour postoperative period. Finally, no significant differences in hospital length of stay, ICU length of stay, or emergency department visits at 60 days were noted between the two groups. CONCLUSIONS In this retrospective study, the use of JPDs in pediatric CFRS was not associated with an increased risk of serious perioperative complications, although the benefits of this practice remain unclear.