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At least 109 records · Page 6Linked to original sources

PubMed1995

Effect of erythrocyte deformability on myocardial hematocrit gradient.

Myocardial hematocrit gradient was determined between epicardium and endocardium of the left ventricular wall in rat heart under the influence of erythrocyte deformability alterations. Hematocrit determinations were performed by measuring two different radionuclides labeling plasma (125I-labeled albumin) and erythrocytes (99mTc) in 100-microns-thick left ventricular myocardium slices. Myocardial hematocrit gradient calculated after exchange transfusions with partially hardened red blood cell suspensions was compared with the results of the control group, in which the exchange transfusions were done using normal, hematocrit-matched blood. In the control group, the hematocrit value in the myocardium adjacent to epicardium was 0.331 +/- 0.076 l/l and decreased to 0.232 +/- 0.054 l/l near the endocardium. Myocardial hematocrit between these two was represented by a linear gradient. In the group with impaired erythrocyte deformability, the hematocrit value was 0.359 +/- 0.074 l/l in the epicardial myocardium and remained at 0.341 +/- 0.082 l/l in the endocardial layer. These results indicate that tissue hematocrit gradient in the left ventricular myocardium may be disturbed if erythrocyte deformability is altered.

Animals↗

PubMed1989

Mechanisms underlying atriopeptin-induced increases in hematocrit and vascular permeation in rats.

Infusion of atriopeptin into humans and animals induces diuresis, natriuresis, hemodynamic changes, and an increase in arterial hematocrit. The objective of the present study was to elucidate the mechanism(s) responsible for the increase in hematocrit in rats given atriopeptin-24 (AP-24). Infusion of AP-24 for 30 minutes increased large vessel and total vascular hematocrits by 10-15% while decreasing microvascular hematocrits by 9-26% in numerous tissues. Regional vascular permeation by [131I] bovine serum albumin was markedly increased (2-5.6-fold) in many tissues, consistent with a 16% decrease in plasma volume. AP-24 infusion had no effect on extracellular fluid volume or the volume of circulating red cells. Vascular resistance was decreased and was associated with a significant increase in blood flow in many, but not all, tissues. In the atrium and in the small and large intestine the percentage decrease in microvascular hematocrit exceeded the increase in blood flow. These observations indicate that the increase in large vessel hematocrit induced by AP-24 infusion 1) is accompanied by a decrease in (microvascular) hematocrit in many tissues, 2) reflects an increase in overall (i.e., total vascular hematocrit), and 3) is the consequence of a decrease in plasma volume resulting from a marked increase in the rate of vascular permeation by plasma constituents in multiple tissues.

Animals↗

PubMed1986

Blood flow and oxygen delivery to the organs of the neonatal lamb as a function of hematocrit.

We chronically catheterized 15 newborn lambs (9.5 +/- 2.8 days) and measured the distribution of cardiac output by the radionuclide-microsphere technique at hematocrits ranging from 10 volumes % to 55 volumes %. Seven animals were made progressively anemic and eight polycythemic by means of exchange transfusions. Cardiac output and heart rate increased with decreasing hematocrit while whole body oxygen consumption showed a small decrease during severe anemia. Both cerebral and cardiac blood flow markedly increased during anemia which assured a relatively stable oxygen delivery to both organs. The changes seen for blood flow to the carcass (skin, bones, and muscle) were predictable from the effects of blood viscosity: small decreases in flow at the highest hematocrits and small increases in flow at the lowest hematocrits. Consequently, oxygen delivery was as low as 1 ml of oxygen/min/100 g at a hematocrit of 10 volumes %. Renal blood flow remained unchanged while oxygen delivery fell when hematocrit was decreased. Hepatic oxygenation was measured using a modification of the Fick principle. Hepatic blood flow showed only a small decrease as hematocrit increased and changed minimally during anemia resulting in a falling delivery of oxygen with anemia. A stable hepatic oxygen consumption was assured by a marked increase in oxygen extraction during anemia. Two differing organ responses to changes in hematocrit can be seen in the newborn: the brain and heart vary blood flow to assure an adequate delivery of oxygen while a number of other organs show less blood flow regulation and, most likely, vary oxygen removal from blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Anemia↗

PubMed1983

Relationship between hematocrit and CO2 contents in whole blood and true plasma.

The amount of CO2 liberated out of the red cell was measured by decreasing PCO2 in human blood with different fractional hematocrits of about 0.24, 0.45, and 0.75, respectively, in order to elucidate whether it depends on the hematocrit and the intracellular pH. From a venous PCO2 level the PCO2 of the sample blood was lowered to 12 Torr. PCO2, CO2 content, pH, Cl-, and Na+ were measured in whole blood and true plasma before and after the reduction of PCO2. Change in water concentration in plasma was calculated from change in plasma Na+ concentration. The bicarbonate shift well counterbalanced to the Cl- shift. As the hematocrit was decreased, the amount of CO2 released per mol of hemoglobin increased, while the change in intracellular bound CO2 concentration decreased. That is, the intracellular bound CO2 became higher in the lower hematocrit blood than in the higher hematocrit one. This fact suggested that the intracellular pH became higher as the hematocrit was lowered, and thus the amount of alkali bound with hemoglobin or the CO2 release was enhanced. The Donnan ratio of the bound CO2 at 12 Torr was independent of the hematocrit, though the pH was inversely related to the hematocrit.

Adult↗

PubMed2005

The effects of hematocrit and age on transcranial Doppler measurements in patients with recent ischemic stroke.

BACKGROUND: The effects of age and hematocrit on transcranial Doppler (TCD) velocities have not been evaluated in a large patient group with recent ischemic stroke. AIM: This study assessed the effects of age and hematocrit on TCD measurements in patients with recent ischemic stroke compared to patients with non-vascular diseases. SETTINGS AND DESIGN: University Hospital, retrospective study. MATERIALS AND METHODS: TCD records and data files of 862 consecutive patients (mean age, 57+/-16 years) with various neurological diagnoses were reviewed retrospectively. The peak systolic, end diastolic and mean flow velocities (FV), systolic/diastolic ratios and pulsatility indices (PI) in the middle cerebral arteries were averaged and the effect of age and hematocrit values on these TCD values was studied. Independent samples t test, Pearson's coefficients of correlation, and linear regression test were used for statistical analysis. RESULTS: Among 862 patients, 413 were women (mean age, 53+/-17 years) and 449 were men (mean age, 60+/-13 years). Peak systolic and mean FV were higher and hematocrit concentration was lower in women compared to men (P< 0.001). The relation of TCD velocities with age and hematocrit was more remarkable in the group of patients with non-vascular neurological disorders. PI values demonstrated a significant correlation to age (r=+0.47) (P< 0.001), but did not change significantly with hematocrit level. CONCLUSIONS: It should be remembered that blood FV measured by TCD may be significantly affected by age and hematocrit level. However, there seems to be no significant association between TCD velocities and hematocrit in patients with a recent ischemic stroke.

Adolescent↗

PubMed1999

[The association of hematocrit with blood pressure and left ventricular mass in subjects over 55].

OBJECTIVE: To establish the association between hematocrit, blood pressure (BP), and left ventricular mass (LVM) in persons older than 55 years. PATIENTS AND METHODS: One hundred patients older than 55 years (46 males and 54 females) with a wide range in BP were studied on an ambulatory basis. The following parameters were determined: hematocrit, casual BP (CBP), 24-h ambulatory blood pressure monitoring (ABPM), left ventricular mass index (LVMI) determined by echocardiography (according to the Devereux's formula), cardiac output (CO) (determined by cardiac echocardiography), peripheral vascular resistances (PVR) (determined according to mean blood pressure and cardiac output), and levels of creatinine in plasma and sodium in 24-hour urine. RESULTS: Mean age of patients was 65 years (range 55 to 83 years). Twenty-two percent of patients were smokers (17 males and 5 females) with a mean of 13 +/- 6 cigarettes/day. Mean hematocrit value was 41.4 +/- 3.6% (43.3 +/- 3.5 for males and 39.7 +/- 2.7% for females) (p < 0.001). Thirty-five percent of males and 26% of females had mild-moderate hypertension with an hematocrit of 42.3 +/- 3.5% versus 40.8 +/- 3.6% (p < 0.05). The LVMI was 132 +/- 37 g/m2 (139 +/- 38 g/m2 for males and 127 +/- 36 g/m2 for females). A significant linear association was observed between hematocrit value and diastolic BP: casual (r = 0.25; p < 0.05, 24 h mean (r = 0.34; p < 0.001), mean from 7 to 23 hours (r = 0.32; p < 0.001), mean from 23 to 7 hours (r = 0.37; p < 0.001). For females, these relationships were: r = 0.41, 0.36; 0.34 and 0.41, respectively (p < 0.01). No significant association was observed between these parameters among males. Among hypertensive patients this association was observed 24-h mean diastolic BP and mean from 23 and 7 hours (r = 0.39; p < 0.05). Among normotensive patients the values for this association were: r = 0.25; p < 0.05 and r = 0.26; p < 0.05, respectively. No significant association was observed between hematocrit value and LVMI for the total group and for the established subgroups. CONCLUSIONS: Among patients older than 55 years a weak significant association was found between hematocrit value and diastolic BP (both casual and in that obtained with ambulatory monitoring), but not with the left ventricular mass. The mean hematocrit value was significantly higher for hypertensive than for normotensive patients.

Aged↗

PubMed2005

Clinical significance of hematocrit interference in the tacrolimus II microparticle enzyme immunoassay: a tentative approach.

Recently, the possible interference of hematocrit on the results of the Abbott Tacrolimus II microparticle enzyme immunoassay (MEIA) has been described, although its significance in clinical practice has not been established as yet. The aim of our study was the evaluation of the significance of this analytical interference in therapeutic tacrolimus monitoring. In 1121 cases selected at random over a 9-month period from kidney (n=379) and liver (n=742) transplant patients, an estimation was made of errors caused by the hematocrit in the results provided by the Tacrolimus II MEIA. In accordance with the available data, it was assumed that an error may be produced beyond the range of hematocrit values from 30% to 40%, either positive or negative respectively, of 3% per unit of hematocrit. The acceptance criterion for accuracy was no more than 15% of deviation (error) with respect to the experimental concentration of tacrolimus. In 160 cases (14.3%) the results of the Tacrolimus II MEIA would not be acceptable due to hematocrit-dependent errors, both with positive (hematocrit <25%) in 108 cases (9.7%) and negative values (hematocrit >45%) in 52 cases (4.6%). The obtained results demonstrate the practical interest of the subject, although additional studies are required in order to validate our approach to the clinical significance of this hematocrit-dependent interference in the Tacrolimus MEIA.

Artifacts↗

PubMed1988

The effect of temperature and hematocrit level of oxygenated cardioplegic solutions on myocardial preservation.

The ideal temperature and hematocrit level of blood cardioplegia has not been clearly established. This study was undertaken (a) to determine the optimal temperature of blood cardioplegia and (b) to study the effect of hematocrit levels in blood cardioplegia. A comparison of myocardial preservation was done among seven groups of animals on the basis of variations in hematocrit levels and temperature of oxygenated cardioplegic solution. The experimental protocol consisted of a 2-hour hypothermic cardioplegic arrest followed by 1 hour of normothermic reperfusion. Group 1 received oxygenated crystalloid cardioplegic solution at 10 degrees C. Groups 2 through 7 received oxygenated blood cardioplegic solution with the following hematocrit values and temperatures: (2) 10%, 10 degrees C; (3) 10%, 20 degrees C; (4) 10%, 30 degrees C; (5) 20%, 10 degrees C; (6) 20%, 20 degrees C; and (7) 20%, 30 degrees C. Parameters studied include coronary blood flow, myocardial oxygen extraction, myocardial oxygen consumption, and myocardial high-energy phosphate levels of adenosine triphosphate and creatine phosphate during control (prearrest), arrest, and reperfusion. Myocardial oxygen consumption at 30 degrees C during arrest was significantly higher than at 10 degrees C and 20 degrees C, which indicates continued aerobic metabolic activity at higher temperature. Myocardial oxygen consumption and the levels of adenosine triphosphate and creatine phosphate during reperfusion were similar in all seven groups. Myocardial oxygen extraction (a measure of metabolic function after ischemia) during initial reperfusion was significantly lower in the 30 degrees C blood group than in the 10 degrees C blood group at either hematocrit level and in the oxygenated crystalloid group, which suggests inferior preservation. The hematocrit level of blood cardioplegia did not affect adenosine triphosphate or myocardial oxygen consumption or extraction. It appears from this study that blood cardioplegia at 10 degrees C and oxygenated crystalloid cardioplegia at 10 degrees C are equally effective. Elevating blood cardioplegia temperature to 30 degrees C, however, reduces the ability of the solution to preserve metabolic function regardless of hematocrit level. Therefore, the level of hypothermia is important in blood cardioplegia, whereas hematocrit level has no detectable impact, and cold oxygenated crystalloid cardioplegia is as effective as hypothermic blood cardioplegia.

Adenosine Triphosphate↗

PubMed1994

Effect of hematocrit on dialyzer urea and creatinine clearance indices in a hemodialysis patient with erythrocytosis.

The association between azotemic index dialyzer clearances and hematocrit was investigated in a 63-year-old dialysis-dependent man with acquired renal cysts. During 43 months of hemodialysis, hematocrit rose from 27.3 to 65.0 vol%, as a consequence of high serum erythropoietin levels. Concomitantly, dry weight also increased from 116.8 to 140.8 kg. Both hematocrit and dry weight correlated with: (a) urea reduction ratio, (b) creatinine reduction ratio (CRR), and (c) KT/V urea. All correlations were negative. Stepwise regression showed that only hematocrit was an independent correlate of the CRR (CRR = 0.662 - 007* Hct, R2 = 0.770); whereas, both hematocrit (Hct) and weight (W) were independent correlates of KT/V urea (KT/V = 2.070 - 0.005*Hct - 0.009*W,R2 = 0.721). In addition to creatinine clearance, urea clearance through the dialyzer is reduced by a rising hematocrit. The effect of hematocrit on urea clearance is relatively small. Therefore, it requires large changes in hematocrit in order to be detected.

Creatinine↗

PubMed1996

Measurement of regional cerebral plasma pool and hematocrit with copper-62-labeled HSA-DTS.

UNLABELLED: We developed copper-62-labeled human serum albumin-dithiosemicarbazone (62Cu-HSA-DTS) as a blood-pool imaging agent for PET. To evaluate 62Cu-HSA-DTS for plasma-pool imaging and to measure the regional cerebral hematocrit, 12 normal volunteers and 7 patients with cerebrovascular disease underwent PET studies with 62Cu-HSA-DTS and 15O-labeled carbon monoxide (C15O). METHODS: The normal subjects were studied with both C15O and 62Cu-HSA-DTS. All patients were examined by 15O-gas studies to measure cerebral perfusion and oxygen metabolism, followed by measurement of plasma volume with 62Cu-HSA-DTS for analysis of regional cerebral hematocrit. Regional cerebral hematocrit was calculated from regional cerebral red cell volume (rCRCV) measured by C15O and regional plasma volume (rCPV) measured by 62Cu-HSA-DTS in each subject, and the regional cerebral/large-vessel hematocrit ratio was obtained for both cerebral hemispheres in each subject. RESULTS: Mean regional cerebral hematocrit and mean cerebral/large-vessel hematocrit ratio in the 12 normal volunteers were 38.3 +/- 3.45% and 0.88 +/- 0.06, respectively. In the seven patients with cerebrovascular disease, regional cerebral hematocrit was significantly lower on the hypoperfused side than the normal hemisphere. The images of rCPV and rCRCV from these patients demonstrated a greater increase in rCPV than rCRCV in the hypoperfused area. CONCLUSION: These results suggest that 62Cu-HSA-DTS can be used for measurement of plasma volume and that regional cerebral hematocrit may provide valuable information regarding the microcirculation in the brain.

Adult↗

PubMed1988

Heart and lung hypertrophy, changes in blood volume, hematocrit and plasma renin activity in rats chronically exposed to increasing carbon monoxide concentrations.

Changes in blood volume, heart and lung mass and composition and plasma renin activity were examined in two strains of male albino rats inhaling incrementally-increasing concentrations of CO: 250 ppm for 17 days, 500 ppm for 13-14 days, 750 ppm for 10 days, and 1300 ppm for 10 days. Blood volume increased 86% and erythrocyte mass increased 212% at 1300 ppm, while plasma volume was unchanged or decreased slightly. 'Real' hematocrit (hematocrit corrected for plasma trapping) increased from 50% in controls to a peak of 75% at 1300 ppm CO. Wet weight of right ventricle (RV) and combined right and left atria (2A) increased linearly with CO concentration, paralleling changes in blood volume; while real hematocrit increased non-linearly. Left ventricle + interventricular septum (LV + S) wet weight increased less than RV, but more in Sprague-Dawley than in Wistar rats. Plots of RV, LV + S and 2A weight vs real hematocrit showed sharp upward inflections at real hematocrit 65%, suggesting a possible role of increased viscosity in CO cardiomegaly at the higher hematocrit. Assymetric septal hypertrophy was not present. Lung weight increased with CO concentration, but was not due to increased lung blood volume or edema. Hydroxyproline measurements on heart and lung failed to show increased collagen content. Plasma renin activity measured by radioimmunoassay was depressed at 500 ppm, but was normal at 750 and 1300 ppm CO. Neither heart, lung, liver nor plasma renin measurements suggest congestive heart failure, supporting previous studies in the rat with chronic carboxyhemoglobinemia, in spite of enormously increased blood volume, hematocrit and heart weight.

Animals↗

PubMed2002

Reference value of presenile human hematocrit and geographical factors.

The aim of this study was to provide a scientific basis for a unified standard of the reference value of healthy presenile human hematocrit in China. We studied the relationship between the reference values of healthy presenile human hematocrit, tested according to Wintrobe's laws, and five geographical factors. It was found that altitude is the most important factor affecting the reference value of the hematocrit. As the altitude gradually increases, the reference value of the hematocrit also increases. The relationship is quite significant. By using the method of stepwise regression analysis, two multivariate regression equations were deduced: Y1 = 39.7 + 0.00328X1 + 0.00169X2 + 0.00117X5 +/- 2.3, Y2 = 38.8 + 0.00275X1 + 0.000578X2 -0.00298X4 +/- 2.2 In these equations, Y1 is the reference value of presenile men's hematocrit (%); Y2 is the reference value of presenile women's hematocrit (%); X1 is altitude (m); X2 is the average annual hours of sunshine (h); X4 is the average annual temperature (degrees C), and X5 is the average annual precipitation (mm). If the geographical index values in a particular area in China are known, the reference value of presenile human hematocrit in this area can be calculated approximately by means of the regression equations.

China↗

PubMed2003

Why is erythropoietin made in the kidney? The kidney functions as a 'critmeter' to regulate the hematocrit.

The normal hematocrit is not a random number, but one that maximizes oxygen delivery. While the feedback loop wherein tissue oxygen pressure determines the production of erythropoietin, which further drives the production of red blood cells in the bone marrow, explains how the hematocrit is generated, it does not speak to how the hematocrit is regulated. The regulation of the hematocrit requires the coordination of the plasma volume and the red cell mass. By controlling red cell mass via erythropoietin and plasma volume through excretion of salt and water, the kidney is able to generate the hematocrit. It is hypothesized that the kidney functions as a critmeter by sensing the relative volumes of each component of the blood through the common signal of tissue oxygen tension. The kidney's unique ability to sense ECF volume through tissue oxygen signal allows it to coordinate these two volumes to produce the normal hematocrit. Hence, it may be the kidneys ability to report a measure of ECF volume as a tissue oxygen signal and thus to regulate the hematocrit that establishes it as the logical site of erythropoietin production. The critmeter is proposed to be a functional unit located at the tip of the cortical labyrinth at the juxta-medullary region of the kidney where erythropoietin is made physiologically. Renal vasculature and nephron segment heterogeneity in sodium reabsorption likely provides the anatomical construct to generate the marginal tissue oxygen pressure required to trigger the production of erythropoietin. The balance of oxygen consumption for sodium reabsorption and oxygen delivery is reflected by the tissue oxygen pressure. This balance hence determines RBC mass adjusted to plasma volume. Factors that affect blood supply and sodium reabsorption in a discordant manner may modulate the critmeter, e.g. angiotensin II. The objective of this work is to describe the hypothesis of the kidney's function as a critmeter, including the anatomical and physiological components, and the role of the renin-angiotensin system in modulating erythropoietin. Clinical examples of the dysregulation of the critmeter may be found in the anemia of renal failure and in sports anemia.

Anemia↗

PubMed1979

Optimal hematocrit for canine skeletal muscle during rhythmic isotonic exercise.

Contractile power, blood flow, O2-uptake, and O2-extraction during isotonic, rhythmic exercise were determined in the isolated canine gastrocnemius muscle during perfusion with blood with hematocrits between 0.21 and 0.81. The results obtained in 36 measurements on nine muscles showed that maximal O2-delivery to the muscle if found at hematocrits between 0.5 and 0.6. Both in the range of hemodilution, and in the range of extreme hemoconcentration, O2-delivery decreases significantly. O2-consumption and contractile power of the muscles are almost unaffected in the hematocrit range between 0.4 and 0.7; beyond and below this hematocrit range both parameters decrease. O2-extraction is virtually constant in the hematocrit range between 0.3 and 0.6, but increase both below and above these hematocrit levels. It is concluded that due to reduced vasodilatory reserve in working skeletal muscle compared to resting muscle the optimal hematocrit is shifted to higher values.

Animals↗

PubMed2006

Does obstructive sleep apnea increase hematocrit?

This study assessed the relationship between hematocrit levels and severity of obstructive sleep apnea (OSA) and examined how this relationship was affected by the degree of hypoxia as well as by possible confounding factors. Two-hundred sixty three subjects (189 men and 74 women) underwent nocturnal polysomnography with oximetry and had measurements of hematocrit, hemoglobin, white blood cell count, body mass index (BMI), blood pressure (BP), and 24-h urine norepinephrine (NE). Patients with severe OSA [respiratory disturbance index (RDI) >30] had significantly higher hematocrit values than patients with mild to moderate OSA or nonapneic controls (p < 0.01). However, only one patient had a hematocrit in the range of clinical polycythemia. Hematocrit levels were significantly correlated with BMI, BP, urinary NE, RDI, percent of time spent at oxygen saturation <90%, and with mean oxygen saturation. Multiple linear regression analysis revealed that mean oxygen saturation, RDI, and percent of time spent at oxygen saturation <90% were significant predictors of hematocrit level, even after controlling for gender, ethnicity, 24-h urine NE, BMI, and BP (p < 0.05). The severity of OSA is significantly associated with increased hematocrit, even after controlling for possible confounding variables. However, nocturnal hypoxemia in OSA does not usually lead to clinical polycythemia.

Adult↗

PubMed1985

Relationship of fetal oxygen consumption and acid-base balance to fetal hematocrit.

We evaluated the effects of alterations in fetal hematocrit on fetal oxygenation in 10 chronically catheterized fetal lambs. Hematocrit was varied from 10% to 55% by slow isovolemic exchange transfusions with plasma or packed red blood cells obtained freshly from donor fetuses. At each hematocrit studied, we measured umbilical blood flow (Qumb) and the oxygen concentrations in umbilical venous blood (CUVO2) and arterial blood (CAO2) and calculated fetal oxygen delivery (Qumb X CUVO2), oxygen extraction [(CUVO2 - CAO2)/CUVO2], and oxygen consumption [Qumb (CUVO2 - CAO2)]. Fetal oxygen delivery was maximal at a fetal hematocrit of 33% (mean oxygen delivery = 23 ml of oxygen per minute per kilogram of fetus) and decreased as hematocrit was raised or lowered from that value. Despite these reductions in oxygen delivery, fetal oxygen consumption was relatively stable (at about 7 ml of oxygen per minute per kilogram) at hematocrits ranging from about 16% to 48% because of compensatory increases in fetal oxygen extraction. Regardless of whether oxygen delivery decreased because of anemia or polycythemia, fetal oxygen consumption was maintained as long as oxygen delivery was greater than about 14 ml of oxygen per minute per kilogram of fetus. When oxygen delivery was less than 14 ml of oxygen per minute per kilogram, fetal oxygen consumption fell while arterial blood base deficit increased, indicating that oxygen supply was inadequate for fetal oxygen demands. These results indicate that fetal aerobic metabolism can be sustained over a wide range of fetal hematocrits. Furthermore, our data support the concept that the level of fetal oxygen delivery is an important determinant of the adequacy of fetal oxygenation.

Acid-Base Equilibrium↗

PubMed2003

Relationship of initial hematocrit level to discharge destination and resource utilization after ischemic stroke: a pilot study.

OBJECTIVE: To examine the association between initial hematocrit level at the time of ischemic stroke, discharge destination, and resource utilization. DESIGN: Case series. SETTING: University hospital. PARTICIPANTS: A total of 1012 consecutive patients with ischemic stroke admitted to a university health system between August 3, 1995, and June 24, 1999. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Length of stay, hospital cost, and discharge disposition. RESULTS: Of 1012 patients presenting with ischemic stroke, 58% were discharged home, 10% were discharged home with home care services, 15% were discharged to a rehabilitation hospital, 11% were discharged to a skilled or intermediate care facility, and 6% died. After adjusting for age, sex, race, and comorbidities, a significant association (P=.009) existed between discharge outcome and initial hematocrit level. The probability of achieving an equivalent or less favorable outcome increased at both high and low hematocrit levels, with a minimum probability at a hematocrit level of approximately 45%. CONCLUSIONS: An association exists between hematocrit level at the time of ischemic stroke and discharge outcome. Midrange hematocrit levels appear to be associated with discharge to home rather than to an inpatient rehabilitation unit or to a nursing facility. Further study is indicated to examine the relationship among hematocrit level, stroke severity, and outcome.

Aged↗

PubMed1997

A comparative study of hematocrits drawn from a standard venipuncture and those drawn from a saline lock device.

BACKGROUND: Most trauma patients in the emergency department have multiple hematocrits drawn to monitor hypovolemia. These venipunctures are painful to the patient and frustrating for hospital staff when venipuncture sites are difficult to locate. PURPOSE: The purpose of this study was to determine whether the hematocrit values of blood samples obtained with saline lock devices agree or are different from those blood specimens obtained by standard venipuncture. If they agree, can the traditional venipuncture route of blood collection be replaced by collection from a saline lock device? METHODS: The study used a quasiexperimental, repeated measures design. The research was conducted at a teaching, regional level I trauma center with annual ED visits of 65,000. Each subject had hematocrit samples obtained by venipuncture (control) according to standard trauma protocols. Within 5 minutes of obtaining each control specimen, a hematocrit sample was obtained with a saline lock device (experimental) after a 5 ml discard volume was obtained. RESULTS: Results were analyzed by measures of central tendency and paired t test. There were no differences in mean hematocrit values in blood obtained by saline locks (41.1 +/- 4.4) and those drawn from direct venipunctures (41.0 +/- 3.9). CONCLUSIONS: Obtaining samples for determination of hematocrit values from a saline look device is an accurate method of obtaining serial hematocrit values.

Adolescent↗