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Critical values of hematocrit and mixed venous oxygen saturation as parameters for a safe cardiopulmonary bypass.

OBJECTIVE: Mixed venous oxygen saturation (SvO2) is high despite a low hematocrit implies that the relationship between oxygen demand and supply is in a safe state. This study was sought to determine the critical values for hematocrit and SvO2 for safe cardiopulmonary bypass. METHODS: Study 1: To evaluate the limit of hemodilution without cardiopulmonary bypass, normovolemic hemodilution with Dextran 40 (10%) was performed in 14 rabbits. SvO2 was monitored from the right atrium, and the hemodynamic parameters were recorded continuously. Study 2: To determine the critical values for hematocrit and SvO2 during cardiopulmonary bypass, normothermic and hypothermic cardiopulmonary bypass were performed in 13 rabbits and hemodynamic parameters were corrected. RESULTS: Study 1: The heart rate decreased to unsafe levels abruptly, when the SvO2 was < or = 43% or the hematocrit was < or = 10%. The lactate concentration increased when the SvO2 was < or = 46% or the hematocrit was < or = 12%. Study 2: When the hematocrit was < or = 12%, the SvO2 decreased gradually. Even when weaning was possible, the animals with a hematocrit < or = 12% collapsed hemodynamically within 40 minutes after cardiopulmonary bypass. Most of the animals could not be weaned from cardiopulmonary bypass during either normothermic or hypothermic cardiopulmonary bypass when the SvO2 was < or = 46%. CONCLUSIONS: Continuous monitoring of hematocrit and SvO2 provides evidence-based guidelines for safe cardiopulmonary bypass. The lower limits of critical range for a safer cardiopulmonary bypass are hematocrit of 12% and SvO2 of 46%.

Animals↗

Mechanism of hematocrit increase induced by the combined administration of morphine and adriamycin: role of histamine release.

The mechanism by which morphine interacts with Adriamycin to increase hematocrit has been investigated in mice. Treatment with Adriamycin (12.8 mg/kg, iv) or morphine (20 mg/kg, sc) resulted in slight increases in hematocrit 30 min postdose, while animals given sc morphine 30 min prior to iv Adriamycin exhibited significant increases in hematocrit as early as 1 min post-Adriamycin. The hematocrit increase reached maximal levels 12 min post-Adriamycin and returned to basal values 4 hr postdose. Splenectomizing animals prior to morphine and Adriamycin treatment had no effect on the drug-induced hematocrit increase. This indicates that red cell release from splenic contracture is not the mechanism for the hematocrit increase. Measurement of plasma histamine levels following drug treatment demonstrated a marked and rapid rise in plasma histamine levels reaching maximal values 1 min post-Adriamycin. Adriamycin alone triggered this release; however, morphine pretreatment resulted in a higher maximum and more prolonged elevation of plasma histamine levels. Treatment with pyrilamine (3.1-50 mg/kg, ip) prior to morphine and Adriamycin administration partially reversed drug-induced hematocrit increase and protected against resultant lethality. Cimetidine (50-200 mg/kg, ip) treatment was not effective. The temporal relationship between hematocrit and histamine increases suggests a cause/effect relationship between released histamine and hematocrit elevation. Protection by pyrilamine and not cimetidine further supports this cause/effect relationship and indicates the effects is mediated via histamine type 1 receptors.

Animals↗

Hematocrit values during pregnancy in a nurse-midwifery caseload.

This article reviews the normal hematologic changes in pregnancy and the kinetics of iron metabolism. The differences between iron depletion and anemia are described. The hematocrit levels of a nurse-midwifery caseload in a tertiary-care setting are described and compared with recently published population norms. Hematocrits of the sample compared favorably to the population hematocrits until 24 weeks' gestation, when the sample hematocrit mean became statistically lower and remained that way throughout pregnancy. Further analysis was done on the sample hematocrits, comparing differences in parity, age, pregnancy spacing, and AS versus AA hemoglobin. Parous women with a pregnancy interval > 12 months had a higher mean hematocrit than nulliparous women. Mean hematocrits of age groups varied significantly only at the 29-32-week interval, with women younger than 18 having lower mean hematocrits than those > or = 18. A trend of women with AS hemoglobin having higher hematocrits than women with AA hemoglobin was identified, reaching statistical significance at the 29-32-week interval.

Adult↗

Reduction in hematocrit level after pioglitazone treatment is correlated with decreased plasma free testosterone level, not hemodilution, in women with polycystic ovary syndrome.

Thiazolidinediones have gained widespread use for the treatment of type 2 diabetes mellitus and other insulin resistance states, including polycystic ovary syndrome (PCOS). In thiazolidinedione-treated patients a small reduction in hemoglobin and hematocrit levels often is observed, and this generally has been attributed to fluid retention. Because testosterone is a hematopoietic hormone, we investigated whether a reduction in plasma free testosterone concentration was associated with the decrease in hemoglobin and hematocrit levels in 22 nondiabetic women (9 with normal glucose tolerance and 13 with impaired glucose tolerance; mean age, 29 +/- 5 years; mean body mass index, 35.6 +/- 5.8 kg/m2) with PCOS who were treated with pioglitazone, 45 mg/d. Before treatment and after 4 months, subjects underwent an oral glucose tolerance test and measurement of total body water content with bioimpedance. Plasma testosterone, androstenedione, dehydroepiandrosterone sulfate, hemoglobin, and hematocrit levels were evaluated at baseline and every month for 4 months. The fasting plasma glucose concentration (98 +/- 9 mg/dL) was unchanged after pioglitazone treatment, whereas the 2-hour plasma glucose concentration declined from 146 +/- 41 to 119 +/- 20 mg/dL (P = .002). Both the free androgen index and the free testosterone levels calculated according to Vermeulen et al decreased significantly (from 14.4 +/- 7.1 to 10.6 +/- 7.8 [P = .02] and from 59.4 +/- 23.4 to 46.6 +/- 23.3 [P = .03], respectively). The plasma androstenedione level declined from 259 +/- 134 to 190 +/- 109 ng/dL (P = .01), whereas the dehydroepiandrosterone sulfate level did not change significantly (from 139 +/- 90 to 127 +/- 84 mug/dL, P = .2 [not significant]). The levels of both hemoglobin (from 13.6 +/- 1.0 to 12.8 +/- 1.1 g/dL, P = .0002) and hematocrit (from 39.7% +/- 2.2% to 37.9% +/- 2.7%, P = .002) fell slightly after 4 months of pioglitazone administration. Collectively, before and after pioglitazone administration, the plasma free testosterone level according to Vermeulen et al correlated positively with the levels of hemoglobin (r = 0.49, P < .0001) and hematocrit (r = 0.40, P < .0001), as well as the free androgen index (r = 0.38 [P < .0003] with hemoglobin and r = 0.29 [P < .006] with hematocrit); the decrement in plasma free testosterone level and free androgen index also correlated with the decrements in the levels of both hemoglobin (r = 0.51 [P = .01] and r = 0.54 [P = .01], respectively) and hematocrit (r = 0.42 [P = .05] and r = 0.50 [P = .02], respectively). Body weight increased from 90.5 +/- 17.3 to 92.4 +/- 18.8 kg after pioglitazone administration (P = .05), as did body fat content (from 42.7 +/- 15.3 to 44.8 +/- 17.1 kg, P = .03), which could explain the increase in weight, because edema did not develop in any of the subjects. Total body water content did not change significantly after pioglitazone administration (from 37.7 +/- 5.0 to 37.8 +/- 4.9 L, P = .68 [not significant]). In summary, pioglitazone treatment is associated with a mild decline in hematocrit or hemoglobin level, which is correlated with the reduction in plasma testosterone level. These results suggest that increased body water content cannot explain the reduction in hematocrit or hemoglobin level in women with PCOS. Further studies are necessary to evaluate whether the same scenario is applicable to normoandrogenic women and individuals with type 2 diabetes mellitus.

Adult↗

Blood flow and oxygen delivery to fetal organs as functions of fetal hematocrit.

The purpose of our experiments was to relate blood flow and oxygen delivery (blood flow x arterial blood oxygen concentration) to fetal organs as functions of fetal hematocrit. In 12 chronically catheterized fetal lambs, we observed two patterns of responses of fetal organs and tissues to isovolemic alterations in fetal hematocrit from 12% to 55%. In group 1 organs (brain, heart, adrenal glands), blood flows increased as hematocrit was either raised or lowered from normal such that oxygen delivery to these organs was stable over the entire range of hematocrits studied. In group 2 organs (gastrointestinal tract organs, spleen, kidneys, placenta, and carcass), blood flows varied little over the range of hematocrits from 12% to 40% or 45% but decreased at hematocrits greater than or equal to 40% to 45%. Because of these flow responses, oxygen delivery to these organs and tissues was maximal at hematocrits ranging from 32% to 38%. Our data indicate that the various organs of the unanesthetized fetal lamb respond in different ways to alterations in hematocrit. It is of particular interest that, in the great majority of the organs of the fetus, oxygen delivery is maximal at hematocrits considered normal for the fetal lamb in utero.

Adrenal Glands↗

Relationship between hematocrit and renal function in men and women.

BACKGROUND: Anemia is a known complication of renal insufficiency, but the relationship between level of renal function and magnitude of reduction in hematocrit is not well defined. Men have higher hematocrit and absolute glomerular filtration rate (GFR) than women; however, it is unknown whether the level of clearance associated with decreased hematocrit is the same in men and women. METHODS: We conducted a cross-sectional study of 12,055 adult ambulatory patients. General linear models were used to analyze the relationship between hematocrit and Cockcroft-Gault equation estimated creatinine clearance (C(Cr); mL/min) and Modification of Diet in Renal Disease (MDRD) formula estimated the GFR indexed to body surface area (mL/min/1.73 m(2)). RESULTS: The hematocrit decreased progressively below estimated C(Cr) 60 mL/min in men and 40 mL/min in women. Compared with subjects with C(Cr)> 80 mL/min, men with C(Cr) 60 to 50 mL/min, 50 to 40 mL/min, 40 to 30 mL/min, 30 to 20 mL/min, and < or =20 mL/min had mean hematocrits that were lower by 1.0, 2.4, 3.7, 3.5, and 10.0%, respectively; the corresponding reductions in women with C(Cr) 40 to 30 mL/min, 30 to 20 mL/min, and < or =20 mL/min were 1.7, 2.9, and 6.3% (all P < 0.05). This between-sex difference diminished when renal function measurement was indexed to body size. Compared with subjects with GFR> 80 mL/min/1.73 m(2), men with GFR 50 to 40 mL/min/1.73 m(2), 40 to 30 mL/min/1.73 m(2), 30 to 20 mL/min/1.73 m(2), and < or =20 mL/min/1.73 m(2) had mean hematocrits that were lower by 2.0, 4.4, 5.3, and 9.4%; the corresponding reductions in women with GFR 50 to 40 mL/min/1.73 m(2), 40 to 30 mL/min/1.73 m(2), 30 to 20 mL/min/1.73 m(2) and < or =20 mL/min/1.73 m(2) were 0.6, 1.6, 3.8, and 5.3% (all P < 0.05). CONCLUSIONS: A decrease in hematocrit is apparent even among patients with mild to moderate renal insufficiency. At any given level of renal function below estimated C(Cr) 60 mL/min, men have a larger decrease in hematocrit than women.

Adult↗

Hematocrit levels and associated Medicare expenditures.

Clinical studies and the National Kidney Foundation-Dialysis Outcomes Quality Initiative guidelines suggest that a target hematocrit of 33% to less than 36% is appropriate for patient benefit. Previous studies have shown an association of lower risks for death and hospitalization when hematocrits were 33% to less than 36%. In this study, we assessed the relationship between hematocrit value and associated Medicare expenditures, analyzing incident Medicare hemodialysis patients from January 1, 1991, through June 30, 1995. All patients survived at least 90 days to normalize eligibility and an additional 6-month entry period to assess comorbidity and hematocrit values. All patients were followed up from July 1, 1991, through December 31, 1996. We assessed the association between hematocrit values in the 6-month entry period and the Medicare-allowable Part A and Part B per-member-per-month (PMPM) expenditures in the follow-up period, controlling for other variables, including patient demographic characteristics, comorbid conditions, and severity of disease. We found that hematocrits of 33% to less than 36% and 36% and higher were associated with lower Medicare-allowable payments in the follow-up period. Compared with reference patients with hematocrits of 30% to less than 33%, the Medicare-allowable PMPM expenditures were significantly greater for patients with hematocrits less than 27% and 27% to less than 30% (12. 7% and 5.3%, respectively), and the Medicare-allowable PMPMs were significantly less for patients with hematocrits of 33% to less than 36% and 36% and higher (6.0% and 8.2%, respectively). Although these findings suggest that the treatment of anemia may be associated with significant savings in total patient Medicare expenditures, caution should be considered because these findings are associations and should not be deemed as showing causality.

Adult↗

Normalization of hematocrit in hemodialysis patients with cardiac disease does not increase blood pressure.

UNLABELLED: Since the earliest reports of the use of Epoetin alfa in hemodialysis patients, it has been described that Epoetin alfa may exacerbate preexisting hypertension or induce hypertension in End Stage Renal Disease (ESRD) patients not previously hypertensive. We undertook this study to determine if the correction of anemia in ESRD patients with cardiac disease from a hematocrit of 30+/-3% to 42+/-3% with the use of Epoetin alfa would result in increased blood pressure. This study was a substudy of the "Normal hematocrit Study". METHODS: Thirty-one patients were randomized into one of two arms. Patients in Group A had their hematocrit increased with the use of slowly escalating doses of Epoetin alfa to 42+/-3% and patients in Group B were maintained with a hematocrit of 30+/-3% throughout the course of the study. All patients had their blood pressure recorded with a 24 hour ambulatory BP device at study entry and at 28 weeks following randomization when they had achieved their target hematocrit. Pre-dialysis systolic and diastolic BP was also recorded. RESULTS: The mean hematocrit increased in Group A from 29.1+/-2.4% to 40.8+/-5.2% after 30 weeks. The hematocrit in Group B remained stable at 30+/-3% throughout the course of the study. There was no difference in mean daytime, mean nighttime or 24 hour systolic or diastolic blood pressure between Groups A and B at either baseline or follow-up. Neither was there a difference in mean pre-dialysis systolic or diastolic BP between Groups A or B at baseline or Follow-up. Four patients in Group A and 4 patients in Group B required an increase in their antihypertensive medication during the course of the study. CONCLUSION: It is possible to increase hematocrit to normal levels in hemodialysis with the administration of Epoetin alfa. The increase in hematocrit from 30+/-3% to 42+/-3% is not associated with increased blood pressure.

Adult↗

Distribution of hematocrit values after aneurysmal subarachnoid hemorrhage.

Low hematocrit values are common after subarachnoid hemorrhage and may be associated with elevated cerebral blood flow and transcranial Doppler ultrasound (TCD) velocities, which may confound the interpretation of velocity as an indicator of vasospasm. The exact distribution of hematocrit among a neurosurgical population would be useful in assessing the magnitude of this difficulty but has not been previously reported. A database containing hematocrit values recorded at TCD examinations over a period of 7 years was reviewed. Two thousand four hundred thirteen hematocrit values were recorded for 575 patients. The distribution of hematocrit values was recorded among patients and among TCD studies. Eighteen percent of the patient population achieved a hematocrit of 26% or less at some point in their hospital stay, whereas 57% of patients achieved a hematocrit of 30% or less. Six percent of the TCD studies were associated with a hematocrit of 26% or less, while 33% of the studies were associated with a hematocrit of 30% or less.

Blood Flow Velocity↗

A two-fluid model for hematocrit distribution in microvascular networks.

A new theoretical network model for evaluating discharge hematocrits, explicitly based on plasma skimming at branches, is introduced. The particular network geometry chosen simulates bat wing microvasculature. Blood in vessels is approximated to be a two fluid with red cell suspension as the core and a plasma layer surrounding it. The plasma layer width depends on hematocrit, which leads to nonlinear hydrodynamic equations solved by iteration. Discharge hematocrit distributions are calculated by a computer for five generations of vessels. Dispersion of hematocrit values was found to be correlated to plasma skimming at branches. Contrary to previous suggestions, plasma skimming did not result in lowered mean hematocrit towards the capillaries. Network structure was found to be an important factor affecting the hematocrits. Mean discharge hematocrit remained steady against changes in vessel dimensions, capillary resistances, red cell concentration in plasma layer, and shape of the separation surface defining the streamlines entering the side branch. This high stable mean hematocrit is based on symmetry of the model network. Enhanced asymmetry tended to lower the hematocrit.

Animals↗

Effect of anemia on cardiac function, microvascular structure, and capillary hematocrit in rat hearts.

The effect of anemia on the coronary microcirculation was studied in young male rats. Chronic anemia resulted in increased left ventricular end-diastolic pressure and decreased functional reserve. Cardiac mass in anemic animals increased by 25%. Capillary and arteriolar densities in these hearts remained unchanged, indicating angiogenesis in this experimental situation (estimated aggregate capillary length in the left ventricle of anemic hearts was 3.06 km compared with 2.35 km in control hearts). Capillary hematocrit was decreased in chronic anemia less than systemic hematocrit: from 25 to 18% in anemia versus 45 to 28% in controls. Capillary hematocrit and red blood cell spacing were also studied after acute blood withdrawal. Here, capillary hematocrit was preserved even more: 22 versus 24% in systemic hematocrit. Finally, the same was studied in isolated hearts perfused with solutions of various hematocrits. After perfusion with low-hematocrit solution (14%), the capillary hematocrit (24%) was even higher than the perfusate hematocrit! In conclusion, we found evidence of angiogenesis in cardiomegaly induced by chronic anemia. Microvascular growth was accompanied by advantageous regulation of red blood cell spacing within these vessels. This was even more pronounced during acute hemodilution and in isolated perfused hearts.

Anemia↗

Hematocrit, blood pressure, and hypertension. The Gubbio Population Study.

Baseline data from the Gubbio Population Study in north central Italy were used to investigate the relation of hematocrit to blood pressure and hypertension among 2,809 men and women aged 25-74 years. Independent of gender, age, and other confounders, the hypertensive group had a higher hematocrit than the nonhypertensive group (p less than 0.001). In comparison with the untreated hypertensive group, the hypertensive group being treated with diuretics or with other drugs only had similar mean hematocrit levels despite significantly lower blood pressures. Hematocrit was positively correlated with systolic pressure (r = 0.085, p less than 0.01 and r = 0.264, p less than 0.001 for men and women, respectively) and diastolic pressure (r = 0.214, p less than 0.001 and r = 0.266, p less than 0.001). In both sexes, whether or not the treated hypertensive group was included, age-adjusted prevalence of hypertension and average blood pressure were higher for persons in higher quintiles of hematocrit (p less than 0.001). The association of hematocrit with blood pressure and hypertension was significant and independent of several confounders. The regression coefficient of blood pressure on hematocrit ranged between 0.410 and 0.620 mm Hg per unit of hematocrit for systolic pressure and between 0.371 and 0.581 for diastolic pressure, depending on gender and whether the treated hypertensive group was included in multiple regression analysis. Based on exponentiation of the multiple logistic coefficient, prevalence of hypertension was at least two times greater for persons whose hematocrit levels were higher by 10 units.

Adult↗

Hematocrit and risk for hypertension in middle-aged Japanese male office workers.

The association of hematocrit with development of hypertension over 9 years was studied in 784 hypertension-free Japanese men aged 40 to 59 years. The age-adjusted relative risk for hypertension above the borderline level and definite hypertension increased in a dose-dependent manner as hematocrit level increased (P for trend: 0.007 and 0.001, respectively). After controls for other potential factors of hypertension, the test for trend across increasing categories of hematocrit level remained as statistical significance for definite hypertension (P=0.015). The multivariate-adjusted relative risk for definite hypertension compared with less than 43.8% of hematocrit level was 1.29 [95% confidence interval (CI): 0.62-2.67] for 43.8 to 45.2% hematocrit level, 1.35 (95% CI: 0.62-2.95) for 45.3 to 46.3% hematocrit level, 1.96 (95% CI: 0.97-3.97) for 46.4 to 48.1% hematocrit level, and 2.06 (95% CI: 1.02-4.15) for 48.2% or more hematocrit level. These results suggest that hematocrit is closely associated with development of hypertension in middle-aged Japanese men.

Adult↗

Hemorheological parameters as determinants of myocardial tissue hematocrit values.

It is well known that the hematocrit in microvessels with diameters smaller than 1000 microm is lower than either venous or arterial hematocrit, thereby resulting in significantly lower mean hematocrit values for vessels perfusing a given tissue (i.e., lower tissue hematocrit). The mechanisms that underlie this reduction of microvascular hematocrit include axial migration, plasma skimming and the Fahraeus Effect. It has been previously demonstrated in rats that a linear hematocrit gradient normally exists through the thickness of the left ventricular myocardium, and that this gradient is sensitive to alterations of the rheological properties of the circulating blood. The gradient is abolished if the RBC in the perfusate are rigid; fibrinogen infusions, and thus increases of both plasma viscosity and RBC aggregation, also affect this gradient. In a new series of studies, it has been observed that enhanced RBC aggregation affects the myocardial hematocrit gradient regardless of alterations of plasma viscosity. Although the exact mechanisms responsible for the myocardial hematocrit gradient, as well as its physiological significance, are not yet clearly known, it is possible to speculate that alterations in local hematocrit could adversely affect myocardial perfusion and function.

Animals↗

Analysis of the hematocrit distribution in the mesenteric microcirculation.

The hematocrit in the microcirculation of the rat's mesentery was determined either by using measurements of optical density (in 56 arterioles and 52 venules) or by counting the number of red cells per unit vessel length (in 63 capillaries) from photographs. The systemic hematocrit (Hsys) averaged 0.42 +/- 0.025. The mean microvessel hematocrit (Hmicro) decreased and its standard deviation increased with decreasing vessel diameter; in capillaries, Hmicro/Hsys ranged between almost zero and 0.86 with an average of 0.36 +/- 0.23. In order to correct Hmicro for the Fahraeus effect, additional experiments were carried out in vitro, in which the tube hematocrit was obtained by centrifugation of glass tubes (I.D. 13-95 micron) perfused with rat's blood of different feed hematocrit. Even after correction for the Fahraeus effect the in vivo data seem to suggest a 'loss of red cells' in the microcirculation. To reconcile the observed hematocrit distribution with the law of mass conservation, model calculations were performed, in which the presence of shunt vessels was assumed on the one hand, and a proportionality between single vessel hematocrit and flow rate on the other. The experimental data are best described by a model which combines the flow dependence of hematocrit and a small shunt component. The positive correlation between single vessel flow rate and Hmicro which is contained in this model also explains an increase of average capillary hematocrit resulting from a more homogeneous flow distribution associated with vasodilatation.

Animals↗

Hematocrit levels and physiologic factors in relationship to cardiovascular risk in Tecumseh, Michigan.

OBJECTIVE: To investigate the relationship between hematocrit, blood pressure and other known cardiovascular risk factors. DESIGN: The Tecumseh Blood Pressure Study includes a cohort of subjects of average age 29.5 years (346 male, 277 female) who reside in Tecumseh, Michigan, USA. METHODS: The body weight; home, work and clinic blood pressures; hematocrit level, plasma renin activity, baseline and mentally stimulated plasma catecholamines level; and fasting glucose, insulin and lipids levels were obtained. Since menstruation and childbearing affect the hematocrit, results are presented only for males. The males in Tecumseh were divided into tertiles of hematocrit (group I < or = 43.25, group II 43.26-45.2 and group III > 45.2%). RESULTS: Higher hematocrit levels were significantly related to higher blood pressures at home, at work and in the clinic, although all of the values measured were within the normotensive range (128/79 mmHg clinic blood pressure in group III). The metabolic factors weight, cholesterol, triglycerides, insulin and glucose levels were significantly elevated in group III. The weight affected only the relationship of hematocrit to plasma insulin levels and not the other variables including the blood pressure. Groups II and III showed signs of sympathetic overactivity; their plasma renin levels, heart rates and norepinephrine levels after mental stimulation were elevated. CONCLUSIONS: Although the relationship of blood pressure to the hematocrit level was previously known, in Tecumseh hematocrit is also found to be associated with several other cardiovascular risk factors and with signs of a hypersympathetic state. We intend to evaluate prospectively the relative prognostic significance of a higher hematocrit level versus the other associated risk factors.

Adult↗

The relationship between maternal hematocrit and pregnancy outcome: black-white differences.

Racial differences in hematocrit levels and the relationship between low and high hematocrit, intrauterine growth retardation, and preterm delivery were studied in a population of 17,149 low-income, iron- and folate-supplemented pregnant women. Hematocrit levels drawn during four gestational periods were considered. Evaluating pregnancy outcome in regard to hematocrit values at specific gestational ages eliminated the bias resulting in the previously reported association between a low hematocrit and preterm delivery in blacks. In contrast, in this study, in blacks, hematocrits of 27% to 30% were associated with lower but not significant reductions in the rates of intrauterine growth retardation and preterm delivery. Our major finding was that at 31 to 34 weeks, hematocrits > or = 40% were associated with significantly higher odds ratios for intrauterine growth retardation for both blacks and whites. These findings should prompt more attention to women who have high hematocrits in pregnancy while reducing concern for women of either race with low hematocrits.

Adult↗

Correlation of transfusion volume to change in hematocrit.

While it has generally been accepted that a 3% change in hematocrit is equivalent to a 1-"unit" loss of blood, few studies have been published to actually document this. A more complete understanding of this correlation would be helpful in estimating blood loss from changes in hematocrit in patients sustaining hemorrhage as well as in those receiving transfusions. In this retrospective study, we analyzed the post-transfusion alterations in hematocrit from 61 independent transfusions in 48 different pelvic fracture patients (age range, 16-62 years). Transfusion volumes were correlated with changes in hematocrit over 24-hr periods between the 5th and 12th hospital days, a time when there was no ongoing hemorrhage in these patients. The average increase in hematocrit per liter of packed red blood cells transfused was 6.4% +/- 4.1%. If 1 "unit" of packed red blood cells is approximately 300 mL, this becomes a change of hematocrit of 1.9% +/- 1.2% per "unit" of blood. The accepted correlation of about 1 "unit" of blood loss per 3% change in hematocrit would be valid for a 500-cc unit, but a typical unit of packed red blood cells is typically 300 cc. In addition, the variability is substantial as indicated by our standard deviation. Limitations of this study include hematocrit changes due to fluid resuscitation, dehydration, age, persistent hemorrhage, and the retrospective nature of the evaluation.

Adolescent↗