Changes In Peripheral Resistance Research Articles

Incidence and associated factors for hypotension during continuous renal replacement therapy in critically ill patients.

This work aimed to analyse retrospective data on hypotension incidence and associated factors among patients requiring continuous renal replacement therapy. The incidence and risk factors of continuous renal replacement therapy-related hypotension have not been adequately explored. The study was designed as a retrospective analysis. Patients who required continuous renal replacement therapy in the ICU between January 2017 and June 2021 were reviewed. The multivariate logistic regression model was used to determine the associated factors of hypotension. Hypotension occurred in 242 out of 885 circuits (27.3%) among 140 patients. The logistic regression analysis identified seven factors associated with the occurrence of hypotension during CRRT: serum albumin (OR = 0.969, 95%CI: 0.934-0.999), serum calcium (OR = 0.514, 95%CI: 0.345-0.905), CO2CP (OR = 0.933, 95%CI: 0.897-0.971), use of vasopressors (OR = 5.731, 95%CI: 4.023-8.165), hypotension before CRRT initiation (OR = 2.779, 95%CI:1.238-6.242), age (OR = 1.016, 95%CI: 1.005-1.027), and fluid removal rate (OR = 1.002, 95%CI: 1.001-1.003). Hypotension frequently occurs in patients receiving continuous renal replacement therapy, especially in the early stages. Multiple factors can be associated with cardiac output or peripheral resistance changes, including excessive ultrafiltration, vasopressors, serum albumin and serum calcium levels, and carbon dioxide combining power.

Comparison of effects of peripheral vasculature on tonometric radial pulse and cuff-based brachial pulse waveform as used in estimation of central aortic pressures.

Aortic pressure estimation requires reliable peripheral pulse waveform acquisition. The peripheral waveform can change with local vascular effects that can be independent of aortic pressure. This study quantifies the effects of peripheral vasculature changes on radial and brachial waveforms. In 20 subjects (37± 15 years, 7 female), brachial volumetric displacement (cuff-based) and radial tonometry waveforms were simultaneously measured whilst a cuff around the hand on the same arm was inflated to induce transmural pressures of -60, -30, -15, 0, 15 and 30 mmHg, altering local peripheral resistance and compliance by graded arterial wall unloading. Aortic blood pressure (BP), augmentation index (AIx) and ejection duration were calculated from the measurements using a generalized transfer function. The parameters under unloaded conditions were compared to baseline measurements. Brachial systolic and diastolic BP did not change throughout the experiment. Altering peripheral resistance and compliance did not significantly change calculated aortic BP values, although changes were nominally greater for radial (maximum +8±1 mmHg) compared to brachial (maximum +2±1 mmHg) waveforms. AIx at 0 mmHg transmural pressure (maximum arterial wall unloading) was higher when derived from radial waveforms (+24±3%, p<0.001) but not when derived from brachial waveforms. Localized changes in peripheral resistance and compliance affect tonometer acquired radial waveforms but not volumetric displacement acquired brachial pressure waveforms, as judged by computed central aortic augmentation pressure parameters. This suggests aortic pressure estimation from the brachial cuff waveform is less sensitive to peripheral vasculature disturbances that alter the peripheral arterial pulse morphology.

Study on changes of cardiac function and peripheral vascular resistance in elderly patients with hypertension

ObjectiveTo investigate the changes of cardiac function and peripheral vascular resistance in elderly patiants with hypertention and their correlation with homocysteine (Hcy) and lipid levels.Methods126 hypertensive patients aged ≥60 years in the department of geriatrics, the first hospital of shanxi medical university from October 2017 to March 2019 were selected as the hypertension group, and 107 healthy patients aged ≥60 years in the same period were selected as the control group(The clinical study has passed ethical review). Serum Hcy and lipid levels in the two groups were measured, and parameters of cardiac function and peripheral vascular resistance were recorded by non‐invasive hemodynamic detector. The changes of Hcy, lipid profile, cardiac function and peripheral vascular resistance parameters in the two groups were compared, and the correlation between cardiac function and peripheral vascular resistance parameters and Hcy and lipid profile was analyzed.ResultsHcy, total cholesterol (TC), triglyceride (TG) and low‐density lipoprotein cholesterol (LDL‐C) in the hypertension group were higher than those in the control group (P&lt;0.05), while high‐density lipoprotein cholesterol (HDL‐C) was lower than those in the control group (P&lt;0.05). Peripheral vascular resistance (SSVR) and systemic resistance (SVR) in the hypertensive group were higher than those in the control group (P&lt;0.05), and cardiac function parameters (CO), SV, LSW and LVET were lower than those in the control group (P&lt;0.05). Pearson correlation analysis showed that hypertension group CO and Hcy in cardiac output, and negatively correlated with TC, LDL‐C, stroke volume SV and negatively correlated with Hcy, left ventricular stroke work LSW and negatively correlated with Hcy, LDL‐C, left ventricular ejection time (LVET)and negatively correlated with Hcy, peripheral vascular resistance index SSVR, SVR and Hcy, TC, TG, LDL‐C were positively correlated, and negatively correlated with the SVR and HDL‐C.ConclusionIn elderly patients with hypertension, cardiac function, including cardiac displacement and myocardial contractility, was significantly reduced, and peripheral vascular resistance was significantly increased. Moreover, such hemodynamic disorder was associated with Hcy and lipid levels.

Sir George Johnson FRCP (1818-96), high blood pressure and the continuing altercation about its origins.

What is the topic of this review? The review takes a historical approach to examining where in the body it might be possible to identify the most common cause, or causes, of long-term hypertension. It gathers evidence from histology, human and animal physiology, and computational modelling. The burden of decades of controversy is noted. What advances does it highlight? The review highlights the distinctive pathology of the afferent renal circulation and what its consequences are for the widespread view that essential hypertension is caused by elevated peripheral vascular resistance. The widely promulgated notion that long-term elevation in mean arterial blood pressure (MAP) can be caused by raised peripheral vascular resistance remains a subject of vigorous debate. According to the 1967 mathematical model of Guyton and Coleman, such a causal relationship is impossible, kidney function being the determining factor. We explore this altercation starting with Sir George Johnson's 19th-century renal vascular histological observations in patients with Bright's disease. We note the striking physiological measurements in hypertensives by Gómez and Bolomey in the 1950s, moving on to the mathematical modelling of the circulation from the 1960s up to the ∼100-parameter computer models of the present day. Confusion has been generated by the fact that peripheral resistance is raised in hypertension in close proportion to MAP whilst cardiac output often stays normal, an apparent autoregulation, the mechanism of which is poorly understood. All models allowing for the circulation to be an open system show that isolated changes in peripheral resistance cannot lead to long-term hypertension, but models fail so frequently to account for results from experiments such as salt loading that their credibility with regard to this key finding is compromised. Laboratory animal models of adrenergic renal actions resonate with a contemporary emphasis on the sympathetic nerve supply to the kidney as contributing to the characteristically markedly elevated renal afferent resistance that appears to be the most common cause of hypertension. Remarkably, there remains no account of the way in which the fixed structural changes in vessels observed by Johnson relate to this sympathetic overactivity, which can itself be modified by drugs in the medium term. In this account, we seek to locate the crime scene and identify a smoking gun.

Aging and high-fat diet feeding lead to peripheral insulin resistance and sex-dependent changes in brain of mouse model of tau pathology THY-Tau22

BackgroundObesity leads to low-grade inflammation in the adipose tissue and liver and neuroinflammation in the brain. Obesity-induced insulin resistance (IR) and neuroinflammation seem to intensify neurodegeneration including Alzheimer’s disease. In this study, the impact of high-fat (HF) diet-induced obesity on potential neuroinflammation and peripheral IR was tested separately in males and females of THY-Tau22 mice, a model of tau pathology expressing mutated human tau protein.MethodsThree-, 7-, and 11-month-old THY-Tau22 and wild-type males and females were tested for mobility, anxiety-like behavior, and short-term spatial memory in open-field and Y-maze tests. Plasma insulin, free fatty acid, cholesterol, and leptin were evaluated with commercial assays. Liver was stained with hematoxylin and eosin for histology. Brain sections were 3′,3′-diaminobenzidine (DAB) and/or fluorescently detected for ionized calcium-binding adapter molecule 1 (Iba1), glial fibrillary acidic protein (GFAP), and tau phosphorylated at T231 (pTau (T231)), and analyzed. Insulin signaling cascade, pTau, extracellular signal-regulated kinase 1/2 (ERK1/2), and protein phosphatase 2A (PP2A) were quantified by western blotting of hippocampi of 11-month-old mice. Data are mean ± SEM and were subjected to Mann-Whitney t test within age and sex and mixed-effects analysis and Bonferroni’s post hoc test for age comparison.ResultsIncreased age most potently decreased mobility and increased anxiety in all mice. THY-Tau22 males showed impaired short-term spatial memory. HF diet increased body, fat, and liver weights and peripheral IR. HF diet-fed THY-Tau22 males showed massive Iba1+ microgliosis and GFAP+ astrocytosis in the hippocampus and amygdala. Activated astrocytes colocalized with pTau (T231) in THY-Tau22, although no significant difference in hippocampal tau phosphorylation was observed between 11-month-old HF and standard diet-fed THY-Tau22 mice. Eleven-month-old THY-Tau22 females, but not males, on both diets showed decreased synaptic and postsynaptic plasticity.ConclusionsSignificant sex differences in neurodegenerative signs were found in THY-Tau22. Impaired short-term spatial memory was observed in 11-month-old THY-tau22 males but not females, which corresponded to increased neuroinflammation colocalized with pTau(T231) in the hippocampi and amygdalae of THY-Tau22 males. A robust decrease in synaptic and postsynaptic plasticity was observed in 11-month-old females but not males. HF diet caused peripheral but not central IR in mice of both sexes.

2-Chloroprocaine and Bupivacaine for lower abdomen and lower limb surgeries under spinal anesthesia: Effects on Haemodynamics

Systemic absorption of local anesthetics produces effects on the cardiovascular and central nervous systems. At blood concentrations achieved with normal therapeutic doses, changes in cardiac conduction, excitability, refractoriness, contractility, and peripheral vascular resistance are minimal. However, toxic blood concentrations depress cardiac conduction and excitability, which may lead to atrioventricular block and ultimately to cardiac arrest. In addition, with toxic blood concentrations myocardial contractility may be depressed and peripheral vasodilation may occur, leading to decreased cardiac output and arterial blood pressure. Patients aged between 18 to 60 years of either gender, belonging to ASA Grade I and II, for elective lower limb and lower abdominal surgeries under spinal anaesthesia. In this present study, diastolic blood pressure recordings were not statistically significant between the two groups observed at different time intervals.

The effects of extracellular volume and intradialytic peripheral resistance changes on ambulatory blood pressure in hemodialysis patients with and without recurrent intradialytic hypertension.

BackgroundHypertension and extracellular volume (ECV) overload are interrelated mortality risk factors in hemodialysis (HD) patients, but confounding related to changes in ECV and vasoconstriction during and between treatments obfuscate their relationship. We sought to clarify independent contributions of post-HD ECV and intradialytic changes in vasoconstriction on ambulatory blood pressure (BP) in patients with and without recurrent intradialytic hypertension (IH).MethodsIn this prospective observational study, we obtained measurements of pre- and post-HD ECV with bioimpedance spectroscopy (BIS), pre- and post-HD total peripheral resistance index and 44-h ambulatory BP. Linear regression determined associations between post-HD ECV/weight and intradialytic change in total peripheral resistance index (TPRI) with interdialytic BP and slope.ResultsIn fully-adjusted models for participants with complete data, post-HD ECV/weight associated with mean ambulatory BP (β = 133, P = 0.01; n = 52) and ambulatory BP slope (β = −4.28, P = 0.03; n = 42). ECV/weight was associated with mean ambulatory BP in those with recurrent IH (β = 314, P = 0.0005; n = 16) and with ambulatory BP slope in those without recurrent IH (β = −4.56, P = 0.04; n = 28). Interdialytic weight gain percentage and intradialytic TPRI change were not associated with ambulatory BP or slope in any analyses.ConclusionAmbulatory BP in HD patients is more strongly associated with post-HD ECV assessed with BIS than with intradialytic TPRI changes or interdialytic ECV increases. These findings highlight the essential role of recognizing and managing chronic ECV overload to improve ambulatory BP in HD patients, particularly so for those with IH.

Retrospective analysis of the hemodynamic consequences of prehospital supplemental oxygen in acute stroke

ObjectiveHyperoxia, the delivery of high levels of supplemental oxygen (sO2) despite normoxia, may increase cerebral oxygenation to penumbral tissue and improve stroke outcomes. However, it may also alter peripheral hemodynamic profiles with potential negative effects on cerebral blood flow (CBF). This study examines the hemodynamic consequences of prehospital sO2 in stroke. MethodsA retrospective analysis of adult acute stroke patients (aged ≥18 years) presenting via EMS to an academic Comprehensive Stroke Center between January 1, 2013 and December 31, 2017 was conducted using demographic and clinical characteristics obtained from Get with the Guidelines-Stroke registry and subjects' medical records. Outcomes were compared across three groups based on prehospital oxygen saturation and sO2 administration. Chi-square, ANOVA, and multivariable linear regression were used to determine if sO2 was associated with differences in peripheral hemodynamic profiles. ResultsAll subjects had similar initial EMS vitals except for oxygen saturation. However, both univariate and multivariable analysis revealed that hyperoxia subjects had slightly lower average ED mean arterial pressures (MAP) compared to normoxia (Cohen's d = 0.313). ConclusionsPrehospital-initiated hyperoxia for acute stroke is associated with a small, but significant decrease in average ED MAP, without changes in heart rate, compared to normoxia. While limited by the inability to link changes in peripheral hemodynamical profiles directly to changes in CBF, this study suggests that hyperoxia may result in a relative hypotension. Further studies are needed to determine if this small change in peripheral vascular resistance translates into a clinically significant reduced CBF.

Developmental programming: Prenatal testosterone-induced changes in epigenetic modulators and gene expression in metabolic tissues of female sheep

Prenatal testosterone (T)-treated female sheep manifest peripheral insulin resistance and tissue-specific changes in insulin sensitivity with liver and muscle manifesting insulin resistance accompanied by inflammatory, oxidative and lipotoxic state. In contrast, visceral (VAT) and subcutaneous (SAT) adipose tissues are insulin sensitive in spite of VAT manifesting changes in inflammatory and oxidative state. We hypothesized that prenatal T-induced changes in tissue-specific insulin resistance arise from disrupted lipid storage and metabolism gene expression driven by changes in DNA and histone modifying enzymes. Changes in gene expression were assessed in liver, muscle and 4 adipose (VAT, SAT, epicardiac [ECAT] and perirenal [PRAT]) depots collected from control and prenatal T-treated female sheep. Prenatal T-treatment increased lipid droplet and metabolism genes PPARA and PLIN1 in liver, SREBF and PLIN1 in muscle and showed a trend for decrease in PLIN2 in PRAT. Among epigenetic modifying enzymes, prenatal T-treatment increased expression of 1) DNMT1 in liver and DNMT3A in VAT, PRAT, muscle and liver; 2) HDAC1 in ECAT, HDAC2 in muscle with decrease in HDAC3 in VAT; 3) EP300 in VAT and ECAT; and 4) KDM1A in VAT with increases in liver histone acetylation. Increased lipid storage and metabolism genes in liver and muscle are consistent with lipotoxicity in these tissues with increased histone acetylation likely contributing to increased liver PPARA. These findings are suggestive that metabolic defects in prenatal T-treated sheep may arise from changes in key genes mediated, in part, by tissue-specific changes in epigenetic-modifying enzymes.

Arterial Hypertension and Unusual Ascending Aortic Dilatation in a Neonate With Acute Kidney Injury: Mechanistic Computer Modeling.

BackgroundNeonatal asphyxia caused kidney injury and severe hypertension in a newborn. An unusually dilatated ascending aorta developed. Dialysis and pharmacological treatment led to partial recovery of the ascending aortic diameters. It was hypothesized that the aortic dilatation may be associated with aortic stiffening, peripheral resistance, and cardiovascular changes. Mathematical modeling was used to better understand the potential causes of the hypertension, and to confirm our clinical treatment within the confines of the model’s capabilities.MethodsThe patient’s systolic arterial blood pressure showed hypertension. Echocardiographic exams showed ascending aorta dilatation during hypertension, which partially normalized upon antihypertensive treatment. To explore the underlying mechanisms of the aortic dilatation and hypertension, an existing lumped parameter hemodynamics model was deployed. Hypertension was simulated using realistic literature informed parameter values. It was also simulated using large parameter perturbations to demonstrate effects. Simulations were designed to permit examination of causal mechanisms. The hypertension inducing effects of aortic stiffnesses, vascular resistances, and cardiac hypertrophy on blood flow and pressure were simulated. Sensitivity analysis was used to stratify causes.ResultsIn agreement with our clinical diagnosis, the model showed that an increase of aortic stiffness followed by augmentation of peripheral resistance are the prime causes of realistic hypertension. Increased left ventricular elastance may also cause hypertension. Ascending aortic pressure and flow increased in the simultaneous presence of left ventricle hypertrophy and augmented small vessel resistance, which indicate a plausible condition for ascending aorta dilatation. In case of realistic hypertension, sensitivity analysis showed that the treatment of both the large vessel stiffness and small vessel resistance are more important in comparison to cardiac hypertrophy.Conclusion and DiscussionLarge vessel stiffness was found to be the prime factor in arterial hypertension, which confirmed the clinical treatment. Treatment of cardiac hypertrophy appears to provide significant benefit but may be secondary to treatment of large vessel stiffness. The quantitative grading of pathophysiological mechanisms provided by the modeling may contribute to treatment recommendations. The model was limited due to a lack of data suitable to permit model identification.

Blood pressure waveform contour analysis for assessing peripheral resistance changes in sepsis

BackgroundThis paper proposes a methodology for helping bridge the gap between the complex waveform information frequently available in an intensive care unit and the simple, lumped values favoured for rapid clinical diagnosis and management. This methodology employs a simple waveform contour analysis approach to compare aortic, femoral and central venous pressure waveforms on a beat-by-beat basis and extract lumped metrics pertaining to the pressure drop and pressure-pulse amplitude attenuation as blood passes through the various sections of systemic circulation.ResultsValidation encompasses a comparison between novel metrics and well-known, analogous clinical metrics such as mean arterial and venous pressures, across an animal model of induced sepsis. The novel metric Ofe → vc, the direct pressure offset between the femoral artery and vena cava, and the clinical metric, ΔMP, the difference between mean arterial and venous pressure, performed well. However, Ofe → vc reduced the optimal average time to sepsis detection after endotoxin infusion from 46.2 min for ΔMP to 11.6 min, for a slight increase in false positive rate from 1.8 to 6.2%. Thus, the novel Ofe → vc provided the best combination of specificity and sensitivity, assuming an equal weighting to both, of the metrics assessed.ConclusionsOverall, the potential of these novel metrics in the detection of diagnostic shifts in physiological behaviour, here driven by sepsis, is demonstrated.

Evaluation of Peak Wall Stress in an Ascending Thoracic Aortic Aneurysm Using FSI Simulations: Effects of Aortic Stiffness and Peripheral Resistance.

It has been reported clinically that rupture or dissections in thoracic aortic aneurysms (TAA) often occur due to hypertension which may be modelled with sudden increase of peripheral resistance, inducing acute changes of blood volumes in the aorta. There is clinical evidence that more compliant aneurysms are less prone to rupture as they can sustain such changes of volume. The aim of the current paper is to verify this paradigm by evaluating computationally the role played by the variation of peripheral resistance and the impact of aortic stiffness onto peak wall stress in ascending TAA. Fluid-structure interaction (FSI) analyses were performed using patient-specific geometries and boundary conditions derived from 4D MRI datasets acquired on a patient. Blood was assumed incompressible and was treated as a non-Newtonian fluid using the Carreau model while the wall mechanical properties were obtained from the bulge inflation tests carried out in vitro after surgical repair. The Navier-Stokes equations were solved in ANSYS Fluent. The Arbitrary Lagrangian-Eulerian formulation was used to account for the wall deformations. At the interface between the solid domain and the fluid domain, the fluid pressure was transferred to the wall and the displacement of the wall was transferred to the fluid. The two systems were connected by the System Coupling component which controls the solver execution of fluid and solid simulations in ANSYS. Fluid and solid domains were solved sequentially starting from the fluid simulations. Distributions of blood flow, wall shear stress and wall stress were evaluated in the ascending thoracic aorta using the FSI analyses. We always observed a significant flow eccentricity in the simulations, in very good agreement with velocity profiles measured using 4D MRI. The results also showed significant increase of peak wall stress due to the increase of peripheral resistance and aortic stiffness. In the worst case scenario, the largest peripheral resistance (1010kgsm-4) and stiffness (10MPa) resulted in a maximal principal stress equal to 702kPa, whereas it was only 77kPa in normal conditions. This is the first time that the risk of rupture of an aTAA is quantified in case of the combined effects of hypertension and aortic stiffness increase. Our findings suggest that a stiffer TAA may have the most altered distribution of wall stress and an acute change of peripheral vascular resistance could significantly increase the risk of rupture for a stiffer aneurysm.

49. Adaptation of cardiac output and systemic vascular resistance during pregnancy: Systematic review and meta-analysis

Introduction Insights in the adaptation of cardiac output (CO) and peripheral systemic vascular resistance in normal pregnancy may aid in identifying women with deviant adaptation. These women are thought to be at risk for hypertensive related complications during pregnancy. Objectives First, to describe the pattern of CO and peripheral resistance changes in normotensive singleton pregnancies. Second, to explore the adaptation of these variables in pregnancies complicated by hypertension, pre-eclampsia and/or foetal growth restriction. Methods We performed a meta-analysis of systematically reviewed literature on CO and peripheral resistance throughout normotensive and complicated pregnancies, using PubMed (NCBI) and Embase (Ovid) databases. Only studies reporting measurements during pregnancy and non-pregnant reference values were included. Pooled mean differences between pregnant and non-pregnant women were calculated for predefined intervals of gestational age using a random-effects model. Results In total, 92 studies were included in this meta-analysis. In uncomplicated pregnancies, CO progressively increased from the first weeks on. After peaking in the early third trimester (+1.47 L/min, over 30% increase as compared to the non-pregnant reference group), CO declined slightly until term. Next to that, peripheral resistance decreased progressively until early third trimester (−316 dyn · s · cm−5, −24% as compared to the non-pregnant group), after which it increased a little. In the first trimester of complicated pregnancies, an augmented increase in CO was observed (+1.36 L/min versus +0.73 L/min in the uncomplicated pregnancies, p Discussion During normal pregnancy, CO increases and peripheral resistance decreases by 30% and 24% respectively, reaching their maximum measure in the second half of pregnancy. Deviant hemodynamic adaptations showing an initial augmented increase with a cross-over to a low cardiac output might identify pregnancies that will be complicated by hypertension and/or growth restriction.

Thoracoabdominal asynchrony correlates with peripheral vascular resistance changes in a cohort of obese children.

Objective:&nbsp;The purpose of this study was to assess the relationship between the thoracoabdominal asynchrony (phase angle), as an index of inspiratory airflow resistance, pulse transit time arousal index (PTT Ar/I), as changes in peripheral vascular resistance and intrathoracic pressure, and obstructive apnea index (OA), Oxygen Desaturation Index (ODI), snoring (% estimated Total Sleep Time - eTST) and apnea-hypopnea index (AHI) in a cohort of exogenous obese children. Material and Methods:&nbsp;Body mass index (BMI) and BMI z-scores were calculated according to age and sex in 36 consecutive obese children. Nasal patency, tonsil size, Friedman palate position scoring were also recorded. An overnight sleep respiratory recording was performed using an polygraphic ambulatory device. Results:&nbsp;&nbsp;Subjects studies had normal to mild sleep respiratory involvement (assessed by respiratory polysomnographic scoring). Phase angle correlated significantly with PTT Ar/I, but not with AHI (n/hr), OA (n/hr), ODI (n/hr) and snoring (% eTST), even adjusting for nasal patency, tonsil hypertrophy, palate position and BMI (z-score). Conclusion:&nbsp;Thoracoabdominal asynchrony (phase angle) is correlated with peripheral vascular resistance changes (PTT Ar/I), suggesting a subclinical upper respiratory airflow anomaly with autonomic activation in obese subjects

Head-up tilt test provokes dynamic alterations in total peripheral resistance and cardiac output in children with vasovagal syncope.

This study examined the total peripheral vascular resistance (TPVR) and cardiac output changes due to the head-up tilt test (HUTT) in children with vasovagal syncope (VVS). From December 2013 to January 2016, we recruited 77 children diagnosed with VVS group at Peking University First Hospital, China, and 28 children without VVS provided the control group. Heart rate, blood pressure, TPVR, cardiac output and baroreflex sensitivity were monitored during the HUTT. In the supine position, TPVR and baroreflex sensitivity were higher in the patients with VVS than the controls, but cardiac output did not differ between the two groups. There were obvious increases in the VVS patients from TPVR in the supine position to the prepositive response period (p<0.05), then the positive response period (p<0.01). However, we noted the opposite trend in cardiac output, from the supine position to the prepositive response period (p<0.01) then the positive response period (p<0.01). During HUTT, children with VVS demonstrated increases in TPVR but decreases in cardiac output, during the transition from the supine position to the positive response. This response might be involved in the pathogenesis of VVS.

Hemodynamic response to fluid removal during hemodialysis: categorization of causes of intradialytic hypotension.

Intradialytic hypotension is a clinically significant problem, however, the hemodynamics that underlie ultrafiltration and consequent hypotensive episodes has not been studied comprehensively. Intradialytic cardiac output, cardiac power and peripheral resistance changes from pretreatment measurements were evaluated using a novel regional impedance cardiographic device (NICaS, NI Medical, Peta Tikva, Israel) in 263 hemodialysis sessions in 54 patients in dialysis units in the USA and Brazil with the goal of determining the various hemodynamic trends as blood pressure decreases. Hypotensive episodes occurred in 99 (13.5%) of 736 intra- and postdialytic evaluations. The hemodynamic profiles of the episodes were categorized: (i) The cardiac power index significantly decreased in 35% of episodes by 36%, from 0.66 [95% confidence interval (CI) 0.60-0.72] to 0.43 (95% CI 0.37-0.48) [w/m2] with a small reduction in the total peripheral resistance index. (ii) The total peripheral resistance index significantly decreased in 37.4% of episodes by 33%, from 3342 (95% CI 2824-3859) to 2251 (95% CI 1900-2602) [dyn × s/cm5 × m2] with a small reduction in the cardiac power index. (iii) Both the cardiac power index and total peripheral resistance index significantly decreased in 27.3% of episodes, the cardiac power index by 25% from 0.63 (95% CI 0.57-0.70) to 0.48 (95% CI 0.42-0.53) [w/m2] and the total peripheral resistance index by 23% from 2964 (95% CI 2428-3501) to 2266 (95% CI 1891-2642). The hemodynamic profiles clearly define specific hemodynamic mechanisms of cardiac power reduction and/or vasodilatation as underlying intradialytic hypotensive episodes. A reduction in cardiac power (reduction of both blood pressure and cardiac output) could be the result of preload reduction due to a high ultrafiltration rate with not enough refilling or low target weight. A reduction in peripheral resistance (reduction in blood pressure and increase in cardiac output) could be the result of relative vasodilatation as arteries do not contract to compensate for volume reduction due to autonomous dysfunction. As both phenomena are independent, they may appear at the same time. Based on these results, a reduction of ultrafiltration rate and an increase in target weight to improve preload or immediate therapeutic actions to increase peripheral resistance are rational measures that could be taken to maintain blood pressure and prevent hypotensive ischemic complications in dialysis patients.

Cardiovascular responses to isometric handgrip exercise in young patients with recurrent vasovagal syncope.

Arterial blood pressure (BP) increased in healthy humans in response to isometric handgrip (IHG), but the pattern of the relative contribution of cardiac output (CO) and total peripheral resistance (TPR) changes to the pressor response is different among individuals. We investigated weather patients with recurrent vasovagal syncope (VVS) have a similar pattern of individual CO, TPR and pressor responses to IHG, as healthy subjects. 32 patients (27.5 ± 2.6 years), and 30 age-matched controls. Autonomic function was evaluated using finger-photoplethysmography to measure BP and heart rate (HR) response to gravitational stress (ΔBP, ΔHR), Valsalva maneuver (VM) and baroreflex sensitivity (BRS), and BP HR and CO changes during IHG. ΔBP, ΔHR, VM and IHG tests did not show significant difference between VVS patients and controls, although BRS was lower in VVS group (p < 0.05). Pattern of individual pressor, CO and TPR responses to IHG was significantly different between VVS patients and healthy subjects (Chi square, p = 0.0246). In 100% of the healthy subjects BP increased during IHG, but in a 19% of the patients BP (CO and TPR) did not increased during IHG. In VVS patients, the autonomic tests (ΔBP, ΔHR, VM and BRS) showed no significant differences between the group with BP increase and the group without pressor response. In VVS patients, the pattern of individual CO and TPR changes to IGH is different from healthy subjects. VVS patients may present an abnormal regulation of cardiovascular responses to IHG, with preserved cardiovagal and cardiac sympathetic function.

A whole-grain diet reduces peripheral insulin resistance and improves glucose kinetics in obese adults: A randomized-controlled trial

BackgroundWhole-grain intake is associated with lower risk of type 2 diabetes but the mechanisms are unclear. PurposeWe tested the hypothesis that a WG diet reduces insulin resistance and improves glucose use in individuals at risk for type 2 diabetes compared with an isocaloric-matched refined-grain diet. MethodsA double-blind, randomized, controlled, crossover trial of 14 moderately obese adults (Age, 38 ± 2 y; BMI, 34.0 ± 1.1 kg/m2). Insulin resistance and glucose metabolism was assessed using an oral glucose tolerance test combined with isotopic tracers of [6,6-2H2]-glucose and [U-13C]-glucose, and indirect calorimetry. Peripheral and hepatic insulin resistance was assessed as 1/(rate of disposal/insulin), and endogenous glucose rates of appearance (Ra) iAUC60–240 × insulin iAUC60–240, respectively. Both diets met ADA nutritional guidelines and contained either whole-grain (50 g per 1000 kcal) or equivalent refined-grain. All food was provided for 8 wk. with an 8–10 wk. washout period between diets. ResultsPost-prandial glucose tolerance, peripheral insulin sensitivity, and metabolic flexibility (insulin-stimulated – fasting carbohydrate oxidation) improvements were greater after whole-grain compared to the refined-grain diet (P < 0.05). Compared to baseline, body fat (~2 kg) and hepatic Ra insulin resistance was reduced by both diets, while fasting glucose and exogenous glucose-meal were unchanged after both interventions. Changes in peripheral insulin resistance and metabolic flexibility correlated with improved glucose tolerance (P < 0.05). ConclusionWhole-grains reduced diabetes risk and the mechanisms appear to work through reduced post-prandial blood glucose and peripheral insulin resistance that were statistically linked to enhanced metabolic flexibility.

Stroke Volume Recruitability during the Third Trimester of Pregnancy.

It is unknown whether the heart operates in the ascending or flat portion of the Starling curve during normal pregnancy. Pregnant women do not respond to the passive leg-raising maneuver secondary to mechanical obstruction of the inferior vena cava by the gravid uterus. Our objective was to evaluate if administration of a fluid bolus increases baseline stroke volume (SV) among healthy pregnant patients during the third trimester. Healthy pregnant women who underwent elective term cesarean sections were included. A noninvasive cardiac output monitor was used to measure hemodynamic variables at baseline and after administration of a 500-mL crystalloid bolus. Forty-five women were included in the study. Fluid administration was associated with a statistically significant increase in SV from a baseline value of 71 ± 11 to 90 ± 19 mL (95% confidence interval [CI]: 13.67-21.49; p < 0.01) and a significant decrease in maternal heart rate from a baseline of 87 ± 9 beats per minute to 83 ± 8 after the fluid bolus (95% CI: -6.81 to -2.78; p = 0.03). No changes in peripheral vascular resistances or any other measured hemodynamic parameters were noted with volume expansion. In healthy term pregnancy, the heart operates in the ascending portion of the Starling's curve, rendering it fluid responsive.

Evolution of aortic pressure during normal ageing: A model-based study.

BackgroundThe age-related increase in pulse pressure (PP) and systolic blood pressure (SBP) is often attributed to alterations in the wave reflection profile and augmented contributions of the reflected waves. However, clinical evidence shows that the stiffening of the proximal aorta with age and the consequent augmentation of the forward pressure wave plays an equally important role. The relative importance of the forward and reflected wave components in essential hypertension has not yet been fully elucidated.ObjectiveThe aim of the current investigation was to simulate the major ageing mechanisms in the arterial system and the heart using a mathematical one-dimensional model of the arterial tree and to assess the evolution of systolic and pulse pressure during normal (non-pathological) ageing.Methods and resultsOur state-of-the-art 1-D model was extended to include turbulence and inertial effects of the flow exiting the left ventricle. Literature data on the age-associated changes in arterial stiffness, peripheral resistance and cardiac contractility were gathered and used as an input for the simulations. The predicted evolution of pressure and augmentation index with age followed accurately the curves obtained in a number of large-scale clinical studies. Analysis of the relative contribution of the forward and backward wave components showed that the forward wave becomes the major determinant of the increase in central and peripheral SBP and PP with advancing age.ConclusionsThe 1-D model of the ageing tree and heart captures faithfully and with great accuracy the central pressure evolution with ageing. The stiffening of the proximal aorta and the resulting augmentation of the forward pressure wave is the major contributor of the systolic pressure augmentation with age.