Heel Blood Flow During Loading and Off-Loading in Bedridden Older Adults With Low and Normal Ankle–Brachial Pressure Index

2012 ◽  
Vol 15 (3) ◽  
pp. 285-291 ◽  
Author(s):  
Nami Masaki ◽  
Junko Sugama ◽  
Mayumi Okuwa ◽  
Misako Inagaki ◽  
Junko Matsuo ◽  
...  

The purpose of this study was to evaluate the differences in heel blood flow during loading and off-loading in bedridden adults older than 65 years. The patients were divided into three groups based on ankle–brachial pressure index (ABI) and transcutaneous oxygen tension (tcPO2): (1) patients with an ABI ≥ 0.8 (Group A); (2) patients with an ABI < 0.8 and heel tcPO2 ≥ 10 mmHg (Group B); and (3) patients with an ABI < 0.8 and heel tcPO2 < 10 mmHg (Group C). Heel blood flow was monitored using tcPO2 sensors. Data were collected with the heel (1) suspended above the bed surface (preload), (2) on the bed surface for 30 min (loading), and (3) again suspended above the bed surface for 60 min (off-loading). Heel blood flow during off-loading was assessed using three parameters: oxygen recovery index (ORI), total tcPO2 for the first 10 min, and change in tcPO2 after 60 min of off-loading. ORI in Group C ( n = 8) was significantly shorter than in Groups A ( n = 22) and B ( n = 15). Total tcPO2 for the first 10 min of off-loading in Group C was significantly less than that in Groups A and B. Change in tcPO2 after 60 min of off-loading in Group C was less than in Group A. Based on these findings, additional preventive care against heel blood flow decrease in older adults with an ABI < 0.8 and heel tcPO2 < 10 mmHg might be necessary after loading.

Perfusion ◽  
2018 ◽  
Vol 34 (1) ◽  
pp. 84-89 ◽  
Author(s):  
Omar Mutlak ◽  
Mohammed Aslam ◽  
Nigel J. Standfield

Objectives: The real mechanism for the development of the later stages of chronic venous insufficiency still remains unclear. Venous hypervolemia and microvascular ischemia have been reported to be the consequences of venous insufficiency. The aim of this study was to investigate the effects of induced venous hypovolemia by dorsiflexion exercise in patients with venous leg ulcers. Methods: Thirty-six participants, all of whom had an ankle brachial pressure index between 0.8 and 1.2 mmHg, were chosen for this study. The participants were divided into two groups: Group A, a non-exercise group and Group B which performed regular exercise in the form of dorsiflexion. The basic assessment, including the history and examination, ankle-brachial pressure index (ABPI), Duplex scan and tcPO2 measurements, was performed on two occasions at the beginning of the trial and after three months. Results: The tcPO2 level was low in the beginning in all the subjects, but the picture was different at the end of the trial. There was a significant increase in the tcPO2 level (p<0.001) in the patients who performed exercise while there was no difference in the measurements (p>0.05) in the non-exercise group. Conclusions: Induced venous hypovolemia through regular evacuation of the peripheral venous system improved tissue oxygenation at skin level. Venous hypervolemia may be the main contributing factor for the development of venous hypoxia and microvascular ischemia.


VASA ◽  
2015 ◽  
Vol 44 (3) ◽  
pp. 0220-0228 ◽  
Author(s):  
Marion Vircoulon ◽  
Carine Boulon ◽  
Ileana Desormais ◽  
Philippe Lacroix ◽  
Victor Aboyans ◽  
...  

Background: We compared one-year amputation and survival rates in patients fulfilling 1991 European consensus critical limb ischaemia (CLI) definition to those clas, sified as CLI by TASC II but not European consensus (EC) definition. Patients and methods: Patients were selected from the COPART cohort of hospitalized patients with peripheral occlusive arterial disease suffering from lower extremity rest pain or ulcer and who completed one-year follow-up. Ankle and toe systolic pressures and transcutaneous oxygen pressure were measured. The patients were classified into two groups: those who could benefit from revascularization and those who could not (medical group). Within these groups, patients were separated into those who had CLI according to the European consensus definition (EC + TASC II: group A if revascularization, group C if medical treatment) and those who had no CLI by the European definition but who had CLI according to the TASC II definition (TASC: group B if revascularization and D if medical treatment). Results: 471 patients were included in the study (236 in the surgical group, 235 in the medical group). There was no difference according to the CLI definition for survival or cardiovascular event-free survival. However, major amputations were more frequent in group A than in group B (25 vs 12 %, p = 0.046) and in group C than in group D (38 vs 20 %, p = 0.004). Conclusions: Major amputation is twice as frequent in patients with CLI according to the historical European consensus definition than in those classified to the TASC II definition but not the EC. Caution is required when comparing results of recent series to historical controls. The TASC II definition of CLI is too wide to compare patients from clinical trials so we suggest separating these patients into two different stages: permanent (TASC II but not EC definition) and critical ischaemia (TASC II and EC definition).


1989 ◽  
Vol 257 (3) ◽  
pp. H785-H790
Author(s):  
T. Sakamoto ◽  
W. W. Monafo

[14C]butanol tissue uptake was used to measure simultaneously regional blood flow in three regions of the brain (cerebral and cerebellar hemispheres and brain stem) and in five levels of the spinal cord in 10 normothermic rats (group A) and in 10 rats in which rectal temperature had been lowered to 27.7 +/- 0.3 degrees C by applying ice to the torso (group B). Pentobarbital sodium anesthesia was used. Mean arterial blood pressure varied minimally between groups as did arterial pH, PO2, and PCO2. In group A, regional spinal cord blood flow (rSCBF) varied from 49.7 +/- 1.6 to 62.6 +/- 2.1 ml.min-1.100 g-1; in brain, regional blood flow (rBBF) averaged 74.4 +/- 2.3 ml.min-1.100 g-1 in the whole brain and was highest in the brain stem. rSCBF in group B was elevated in all levels of the cord by 21-34% (P less than 0.05). rBBF, however, was lowered by 21% in the cerebral hemispheres (P less than 0.001) and by 14% in the brain as a whole (P less than 0.05). The changes in calculated vascular resistance tended to be inversely related to blood flow in all tissues. We conclude that rBBF is depressed in acutely hypothermic pentobarbital sodium-anesthetized rats, as has been noted before, but that rSCBF rises under these experimental conditions. The elevation of rSCBF in hypothermic rats confirms our previous observations.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Wasineenart Mongkolpun ◽  
Péter Bakos ◽  
Jean-Louis Vincent ◽  
Jacques Creteur

Abstract Background Continuous veno-venous hemofiltration (CVVH) can be used to reduce fluid overload and tissue edema, but excessive fluid removal may impair tissue perfusion. Skin blood flow (SBF) alters rapidly in shock, so its measurement may be useful to help monitor tissue perfusion. Methods In a prospective, observational study in a 35-bed department of intensive care, all patients with shock who required fluid removal with CVVH were considered for inclusion. SBF was measured on the index finger using skin laser Doppler (Periflux 5000, Perimed, Järfälla, Sweden) for 3 min at baseline (before starting fluid removal, T0), and 1, 3 and 6 h after starting fluid removal. The same fluid removal rate was maintained throughout the study period. Patients were grouped according to absence (Group A) or presence (Group B) of altered tissue perfusion, defined as a 10% increase in blood lactate from T0 to T6 with the T6 lactate ≥ 1.5 mmol/l. Receiver operating characteristic curves were constructed and areas under the curve (AUROC) calculated to identify variables predictive of altered tissue perfusion. Data are reported as medians [25th–75th percentiles]. Results We studied 42 patients (31 septic shock, 11 cardiogenic shock); median SOFA score at inclusion was 9 [8–12]. At T0, there were no significant differences in hemodynamic variables, norepinephrine dose, lactate concentration, ScvO2 or ultrafiltration rate between groups A and B. Cardiac index and MAP did not change over time, but SBF decreased in both groups (p < 0.05) throughout the study period. The baseline SBF was lower (58[35–118] vs 119[57–178] perfusion units [PU], p = 0.03) and the decrease in SBF from T0 to T1 (ΔSBF%) higher (53[39–63] vs 21[12–24]%, p = 0.01) in group B than in group A. Baseline SBF and ΔSBF% predicted altered tissue perfusion with AUROCs of 0.83 and 0.96, respectively, with cut-offs for SBF of ≤ 57 PU (sensitivity 78%, specificity 87%) and ∆SBF% of ≥ 45% (sensitivity 92%, specificity 99%). Conclusion Baseline SBF and its early reduction after initiation of fluid removal using CVVH can predict worsened tissue perfusion, reflected by an increase in blood lactate levels.


1990 ◽  
Vol 259 (6) ◽  
pp. G1010-G1018 ◽  
Author(s):  
T. Kawasaki ◽  
F. J. Carmichael ◽  
V. Saldivia ◽  
L. Roldan ◽  
H. Orrego

The relationship between portal tributary blood flow (PBF) and hepatic arterial blood flow (HAF) was studied in awake, unrestrained rats with the radiolabeled microsphere technique. Six distinct patterns of response emerged. In group A (PBF+, HAF 0), ethanol, acetate, glucagon, prostacyclin, and a mixed diet increased PBF without a change in HAF; in group B (PBF+, HAF+), adenosine and histamine increased both PBF and HAF; in group C (PBF 0, HAF+), isoflurane and triiodothyronine did not change PBF but increased HAF; and in group D (PBF-, HAF+), halothane and vasopressin decreased PBF and increased HAF. Acute partial portal vein ligation decreased PBF (56%) and increased HAF (436%). Hypoxia (7.5% O2) decreased PBF (28%) and increased HAF (110%). In group E (PBF+, HAF-), acute hepatic artery ligation increased PBF (35%) and reduced HAF (74%), while in group F (PBF-, HAF-), thyroidectomy reduced PBF and HAF (36 and 47%, respectively). All blood flow responses were accompanied by the expected changes in both portal tributary and hepatic arterial vascular resistances. The data suggest that the portal and hepatic arterial vascular territories have regulatory mechanisms that allow for independent changes.


1991 ◽  
Vol 75 (4) ◽  
pp. 619-624 ◽  
Author(s):  
Steven J. Barker ◽  
John Hyatt ◽  
Christopher Clarke ◽  
Kevin K. Tremper

2007 ◽  
Vol 28 (1) ◽  
pp. 126-134 ◽  
Author(s):  
Michael Pedersen ◽  
Christian T Brandt ◽  
Gitte M Knudsen ◽  
Christian Østergaard ◽  
Peter Skinhøj ◽  
...  

In the present study, we studied the effect of bacteremia on cerebral blood flow (CBF) autoregulation in a rat model of pneumococcal bacteremia and meningitis. Anesthetized rats were divided into five groups (A to E) and inoculated with pneumococci intravenously and normal saline intracisternally (group A, N = 10); saline intravenously and pneumococci intracisternally (group B, N = 10); pneumococci intravenously and pneumococci intracisternally (group C, N = 5); saline intravenously, antipneumococcal antibody intravenously (to prevent bacteremia), and pneumococci intracisternally (group D, N = 10); or saline intravenously and saline intracisternally (group E, N = 10), respectively. Positive cultures occurred in the blood for all rats in groups A, B, and C, and in the cerebrospinal fluid for all rats in groups D and E. Twenty-four hours after inoculation, CBF was measured with laser-Doppler ultrasound during incremental reductions in cerebral perfusion pressure (CPP) by controlled hemorrhage. Autoregulation was preserved in all rats without meningitis (groups A and E) and was lost in 24 of 25 meningitis rats (groups B, C, and D) ( P <0.01). In group A, the lower limit was higher than that of group E ( P <0.05). The slope of the CBF/CPP regression line differed between the meningitis groups ( P < 0.001), being steeper for group B than groups C and D, with no difference between these two groups. The results suggest that pneumococcal bacteremia in rats triggers cerebral vasodilation, which right shifts the lower limit of, but does not entirely abolish, CBF autoregulation in the absence of meningitis, and which may further aggravate the vasoparalysis induced by concomitant pneumococcal meningitis.


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