Integration of Blood Volume, Blood Pressure, Heart Rate and Bioimpedance Monitoring for the Achievement of Optimal Dry Body Weight during Chronic Hemodialysis

2007 ◽  
Vol 30 (12) ◽  
pp. 1098-1108 ◽  
Author(s):  
M. Bonello ◽  
A.A. House ◽  
D. Cruz ◽  
Y. Asuman ◽  
E. Andrikos ◽  
...  
1997 ◽  
Vol 82 (4) ◽  
pp. 1229-1236 ◽  
Author(s):  
González-Alonso, José ◽  
Ricardo Mora-Rodríguez ◽  
Paul R. Below ◽  
Edward F. Coyle

González-Alonso, José, Ricardo Mora-Rodrı́guez, Paul R. Below, and Edward F. Coyle.Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise. J. Appl. Physiol. 82(4): 1229–1236, 1997.—We identified the cardiovascular stress encountered by superimposing dehydration on hyperthermia during exercise in the heat and the mechanisms contributing to the dehydration-mediated stroke volume (SV) reduction. Fifteen endurance-trained cyclists [maximal O2consumption (V˙o2 max) = 4.5 l/min] exercised in the heat for 100–120 min and either became dehydrated by 4% body weight or remained euhydrated by drinking fluids. Measurements were made after they continued exercise at 71%V˙o2 maxfor 30 min while 1) euhydrated with an esophageal temperature (Tes) of 38.1–38.3°C (control); 2) euhydrated and hyperthermic (39.3°C); 3) dehydrated and hyperthermic with skin temperature (Tsk) of 34°C; 4) dehydrated with Tesof 38.1°C and Tskof 21°C; and 5) condition 4 followed by restored blood volume. Compared with control, hyperthermia (1°C Tesincrease) and dehydration (4% body weight loss) each separately lowered SV 7–8% (11 ± 3 ml/beat; P < 0.05) and increased heart rate sufficiently to prevent significant declines in cardiac output. However, when dehydration was superimposed on hyperthermia, the reductions in SV were significantly ( P< 0.05) greater (26 ± 3 ml/beat), and cardiac output declined 13% (2.8 ± 0.3 l/min). Furthermore, mean arterial pressure declined 5 ± 2%, and systemic vascular resistance increased 10 ± 3% (both P < 0.05). When hyperthermia was prevented, all of the decline in SV with dehydration was due to reduced blood volume (∼200 ml). These results demonstrate that the superimposition of dehydration on hyperthermia during exercise in the heat causes an inability to maintain cardiac output and blood pressure that makes the dehydrated athlete less able to cope with hyperthermia.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Stacy T Sims ◽  
Sandra Tsai ◽  
Marcia L Stefanick

Background: Barriers to physical activity for obese women include overheating, sweating, fatigue, exhaustion, and rapid heart rate. Adipose tissue acts as a thermal insulator, promoting a greater heat load on the nonfat tissues, reducing heat tolerance; exercise causes a rise in body temperature with an inability to dissipate heat contributing to reduced exercise tolerance. With difficulties of thermoregulation in the sedentary obese population, the aspect of attenuating the discomfort thus associated may encourage continuation of exercise. A heat sink applied to palmar surfaces extracts heat and cools the venous blood, reducing thermal strain by enhancing the volume of cooled venous return. We hypothesized that palmar cooling using a rapid thermal exchange device (RTX) during exercise would attenuate the thermal discomfort of exercise of sedentary obese women, improving exercise tolerance. Methods: To examine whether palmar cooling would impact exercise tolerance in obese women, 24 healthy women aged 30–45 years, with no history of long term structured exercise, a body mass of 120–135% above ideal and/or BMI between 30 and 34.9 were recruited. Women were randomized into a cooling (RXT with 16°C water circulating) or a control (RTX with 37°C water circulating) group and attended 3 exercise sessions a week for 3-months (12 weeks). Each session was comprised of 10 min body weight exercises, 25–45 min treadmill walking at 70–85% HRR with the RTX device, and 10 min of core strengthening exercises. The performance marker was a 1.5 mi walk for time; conducted on the first and last days of the intervention. Mixed models were used to model each of the outcomes as a function of thermal strain, time and treatment with covariates of speed, heart rate, distance, and the interaction of the main effects included in the model. Results: Groups were matched at baseline for key variables (time for 1.5 mile walk test, resting and exercising heart rate [HR], blood pressure [BP], waist circumference [WC], body weight, body mass index [BMI]). Among the cooling group, time to complete the 1.5mile walk test was significantly faster (31.6 ± 2.3 vs. 24.6 ± 2.5 min, pre vs. post, P< 0.01). A greater average exercising HR was observed (136 vs. 154 bpm, pre vs. post, P <0.001), with a significant reduction in WC (41.8 ± 3.1 vs. 39.1 ± 2.2 inches, pre vs. post, P< 0.01) and resting BP (139/84 ± 124/70 mmHg, pre vs. post, P < 0.025). There were no significant differences observed in the control group. Conclusion: Results indicate that exercise tolerance in obese women improved with cooling during exercise, more so than those women who did not have cooling. An improvement in blood pressure, heart rate, waist circumference, and overall aerobic fitness was observed. These findings suggest that by reducing thermal discomfort during exercise, tolerance increases, thus improving cardiovascular parameters of obese women.


1999 ◽  
Vol 87 (6) ◽  
pp. 2025-2031 ◽  
Author(s):  
Holger Kraiczi ◽  
Jarkko Magga ◽  
Xiang Ying Sun ◽  
Heikki Ruskoaho ◽  
Xiaohe Zhao ◽  
...  

We investigated whether the effect of long-term intermittent hypoxia (LTIH) on cardiovascular function may be modified by preexisting genetic traits. To induce LTIH experimentally, cycles of 90-s hypoxia (nadir 6%) followed by 90-s normoxia were applied to six Wistar-Kyoto and six spontaneously hypertensive rats during 8 h daily. Comparison with the same number of control animals after 70 days revealed no alteration of intra-arterial blood pressure or heart rate. Blood pressure responsiveness to a brief hypoxic stimulus was enhanced in the LTIH animals, regardless of strain, whereas the hypoxia-induced increase in heart rate was abolished. In the spontaneously hypertensive but not the Wistar-Kyoto rats, LTIH increased left ventricular weight-to-body weight ratio and content of atrial natriuretic peptide mRNA. Expression of B-type natriuretic peptide was unchanged (Northern blot). Slightly increased right ventricular weight-to-body weight ratios in the LTIH animals were associated with higher right ventricular atrial natriuretic peptide and B-type natriuretic peptide mRNA amounts. Consequently, the effects of LTIH on different components of cardiovascular function appear incompletely related to each other and differentially influenced by constitutional traits.


1960 ◽  
Vol 199 (5) ◽  
pp. 797-799 ◽  
Author(s):  
S. Deavers ◽  
E. L. Smith ◽  
R. A. Huggins

Mean control data on a series of 100 dogs are presented. Cell volume, measured with Cr51-tagged red cells and plasma volume determined simultaneously by T-1824 dye was 33.5 ± 0.74 cc/kg and 50.2 ± 1.11 cc/kg, respectively. The venous hematocrit was 45.2% and the circulatory/venous hematocrit ratio was 0.89 ± 0.01 for the group. The plasma protein concentration of these animals was 6.25 ± 0.07 gm/100 cc. No difference in blood volume per unit of body weight was found between large (12.6 kg) and small (5.8 kg) dogs. The femoral mean systolic pressure was 139.0 ± 2.53 mm Hg, the diastolic pressure 65.6 ± 1.46 mm Hg and the heart rate 85.9 ± 2.86/min.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Takuhiro Moromizato ◽  
Kunitoshi Iseki ◽  
OCTOPUS Study Group

Abstract Background and Aims Increase in resting heart rate might influence mortalities of dialysis patients, and the use of β-blocker might improve their survival probability. However, the influence of heart rate and benefits of β-blocker on their survival are difficult to quantify because of following obstacles: prone to measurement errors; inherent association of heart rate with blood pressures, comorbidities, and medication use; and a necessity of repeated measurements of vital signs and medication use. Therefore, at the design process of our previous randomized control trial on the Olmesartan Clinical Trial in Okinawan patients under OKIDS (OCTOPUS), we included the repeated measures design to quantify the influence of vital sign values on the survival retrospectively. We combined the repeated measurement data and additional the long-term prognosis information of the participants obtained after the OCTOPUS with aim of investigating the influence of time varying covariates: heart rates, blood pressures, and β-blocker use, on the long-term survival of hemodialysis patients. Method We investigated 461 adult OCTOPUS participants who received chronic hemodialysis and antihypertensive medications in Okinawa. The OCTOPUS trial, which was conducted between June 2006 and June 2011, did not detect the survival benefit of angiotensin receptor blocker (ARB)NDT 2013, but the study and the additional follow-up of participants’ prognosis provided us with information to investigate influence of predictors on long-term survival in the population. Throughout the OCTOPUS trial, study participants were measured pre-dialysis blood pressures, pre-dialysis resting heart rates, and their medication use for one week at their dialysis centers every six months after their participations. Following the trial, we collected the prognosis information of all participants until July 31st, 2018. Finally, we merged the multiple-measured data during the OCTOPUS with the prognosis data. Mean values of three measurements of blood pressures and heart rates and β-blocker use were introduced to the Cox-regression model as time-varying covariates with essential non-time varying covariates, which include age, gender, and diabetes. Results In this retrospective cohort study, 221 (47.9%) out of 461 participants deceased, and the median follow-up length was 10.21 years. Initial mean resting heart rate and pre-dialysis mean blood pressure were 78(±10) per minute and 159.5(±14) mmHg, respectively. 10% of participants were prescribed β-blocker initially. The resting heart rate of all participants significantly decreased by 1.75 and 2.45 per minutes after two and four years respectively. β-blocker could significantly decrease the mean heart rate by 3.54 and 2.90 per minutes after two and four years. With our Cox-regression with the time varying covariates, increase of heart rate was significantly associated with higher mortality (P=0.002), but the use of β-blocker was not associated with the mortality. (P=0.691) Additionally, we could not detect the interaction of heart rate and β-blocker use on the mortality. (P= 0.796) Although lower blood pressure was significantly associated with higher mortality in our initial Cox-regression analysis, an introduction of interaction term of heart rate and blood pressure remove the significance of influence of blood pressure on the survival. Conclusion In hypertensive chronic hemodialysis patients, higher heart rate is associated with higher mortality. However, use of beta-blocker was not associated with improvement of their mortality.


1999 ◽  
Vol 277 (2) ◽  
pp. H576-H583 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle

We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (V˙o 2 max) 4.7 ± 0.4 l/min (mean ± SE)] cycled for 30 min in the heat (35°C) in the upright and in the supine positions (V˙o 2 2.93 ± 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (Tes) was 37.8–38.0°C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (Tes = 38.7–38.8°C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 ± 6 ml, 3.0 ± 0.7 l/min, 6 ± 2 mmHg, 22 ± 8%, 14 ± 2 beats/min, and 50–96%, respectively; all P < 0.05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 ± 2 vs. 9 ± 1%) and the reductions in SV (13 ± 4 vs. 21 ± 3%) and cardiac output (8 ± 3 vs. 14 ± 3%) (all P< 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure.


2000 ◽  
Vol 278 (2) ◽  
pp. H321-H330 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle

Euhydrated and dehydrated subjects exercised in a hot and a cold environment with our aim to identify factors that relate to reductions in stroke volume (SV). We hypothesized that reductions in SV with heat stress are related to the interaction of several factors rather than the effect of elevated skin blood flow. Eight male endurance-trained cyclists [maximal O2 consumption (V˙o 2 max) 4.5 ± 0.1 l/min; means ± SE] cycled for 30 min (72%V˙o 2 max) in the heat (H; 35°C) or the cold (C; 8°C) when euhydrated or dehydrated by 1.5, 3.0, or 4.2% of their body weight. When euhydrated, SV and esophageal temperature (Tes 38.2–38.3°C) were similar in H and C, whereas skin blood flow was much higher in H vs. C (365 ± 64% higher; P < 0.05). With each 1% body weight loss, SV declined 6.4 ± 1.3 ml (4.8%) in H and 3.4 ± 0.4 ml (2.5%) in C, whereas Tes increased 0.21 ± 0.02 and 0.10 ± 0.02°C in H and C, respectively ( P < 0.05). However, reductions in SV were not associated with increases in skin blood flow. The reduced SV was highly associated with increased heart rate and reduced blood volume in both H ( R = 0.96; P < 0.01) and C ( R = 0.85; P < 0.01). In conclusion, these results suggest that SV is maintained in trained subjects during exercise in euhydrated conditions despite large differences in skin blood flow. Furthermore, the lowering of SV with dehydration appears largely related to increases in heart rate and reductions in blood volume.


2005 ◽  
Vol 83 (2) ◽  
pp. 191-197 ◽  
Author(s):  
A Roger Hohimer ◽  
Lowell E Davis ◽  
Daniel C Hatton

We found in mice that repeated single daily subcutaneous (s.c.) isoproterenol (ISO) injections, like constant infusions using osmotic minipumps, caused increased biventricular mass or weight relative to body weight (VW/BW). We found that 5 (1/d) s.c. injections of 2, 10, or 20 µg/g body weight caused equivalent VW/BW increases as compared with 5-d infusions at 20 µg/(g·d)). While it is often presumed that ISO elicits hypertrophy by a direct effect on the myocytes, growth may also be secondary to systemic hemodynamic effects. The 2 modes of ISO administration had different effects on mean arterial blood pressure (MABP) and heart rate. Using telemetry we observed that single injections of ISO (0, 0.5, 2, and 10 µg/g) were associated with hypotension and tachycardia with a duration but not a magnitude that was dose dependent. MABP dropped rapidly to 60 mm Hg for more than 2 h at the highest dose. Constant s.c. infusion of ISO at 20 µg/(g·d) initially lowered MABP to about 70 mm Hg for 24 h. At 48 h MABP was normal, but rose 10 mm Hg higher than baseline by day 5. Thus, different routes of administration of ISO that cause comparable increases in VW/BW had different effects on MABP. Thus when evaluating mouse models of ISO-induced cardiac hypertrophy, both repeated daily injections or infusions can cause similar increases in VW/BW, but the daily doses that are required are not the same. Furthermore, these different routes of administration have different hemodynamic sequelae and could potentially evoke different cardiac phenotypes.Key words: C57BL6 mouse, hypotension, heart rate, cardiac hypertrophy, β-adrenergic.


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