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PubMed2006

Blood pressure and hematocrit in diabetes and the role of endothelial responses in the variability of blood viscosity.

OBJECTIVE: To investigate the relationship between mean arterial blood pressure and hematocrit in a population of treated diabetic patients and a control population of healthy individuals. RESEARCH DESIGN AND METHODS: Data on hematocrit and blood pressure were obtained from 129 diabetic subjects (87 women and 42 men) and 103 healthy subjects (76 women and 27 men) enrolled in a cross-sectional study. Alcohol consumption, ischemic heart disease, stroke, neoplasia, renal, hepatic, and chronic inflammatory disease were exclusion criteria. RESULTS: The hematocrit of diabetic patients ranged from 0.35 to 0.52, and blood pressure had a bimodal distribution described by a second-order polynomial (P < 0.001), whereby elevated pressures correlated with low and high hematocrit, while the minimum average pressure was at hematocrit 0.43. Hematocrit of normal control subjects (range 0.28-0.55) was uncorrelated to blood pressure (averaged 99.7 +/- 9.7 mmHg). High blood pressure, low hematocrit diabetic subjects up to the minimum average hematocrit of 0.43 had a negative correlation (P < 0.0001) between these variables. CONCLUSIONS: Our findings are compatible with the hypothesis that diabetic patients present normal responses to hematocrit variation and therefore blood viscosity and shear stress in mediating the release of vasodilators and lack the ability to autoregulate blood pressure relative to differences in hematocrit by comparison to nondiabetic subjects. These findings also suggest that the treatment of diabetes should target maintaining an optimal hematocrit in order to lower cardiovascular risk.

Adult↗
PubMed2000

Effects of different hematocrit levels on glucose measurements with handheld meters for point-of-care testing.

OBJECTIVES: To determine the effects of low, normal, and high hematocrit levels on glucose meter measurements and to assess the clinical risks of hematocrit errors. DESIGN: Changes in glucose measurements between low and high hematocrit levels were calculated to determine hematocrit effects. The differences between glucose measured with meters and with a plasma glucose method (YSI 2300) also were compared. SETTING: Six hand-held glucose meters were assessed in vitro at low (19.1%), normal (38.5%), and high (58.3%) hematocrit levels, and at 6 glucose concentrations ranging from 2.06 mmol/L (37.1 mg/dL) to 30.24 mmol/L (544.7 mg/dL). RESULTS: Most systems, regardless of the reference to which they were calibrated, demonstrated positive bias at lower hematocrit levels and negative bias at higher hematocrit levels. Low, normal, and high hematocrit levels progressively lowered Precision G and Precision QID glucose measurements. Hematocrit effects on the other systems were more dependent on the glucose concentration. Overall, Accu-Chek Comfort Curve showed the least sensitivity to hematocrit changes, except at the lowest glucose concentration. CONCLUSIONS: We strongly recommend that clinical professionals choose glucose systems carefully and interpret glucose measurements with extreme caution when the patient's hematocrit value changes, particularly if there is a simultaneous change in glucose level.

Biosensing Techniques↗
PubMed2003

Noninvasive in vivo measurements of hematocrit.

OBJECTIVE: To develop a clinically applicable method for noninvasive acoustic determination of hematocrit values in vivo. METHODS: The value of hematocrit was determined initially in vitro from the pulseecho measurements of acoustic attenuation. The testing was carried out in a laboratory setup with an ultrasonic transducer operating at 20 MHz and with the use of human blood samples at 37 degrees C. The attenuation coefficient measurements in blood in vivo were implemented by multigated, 20-MHz pulsed Doppler insonation. The Doppler signal was recorded in the brachial and radial arteries. Both in vitro and in vivo hematocrit data were compared with those obtained by the centrifuge method. RESULTS: The attenuation coefficient in vitro was determined from the measurements of 168 samples with hematocrit values varying between 23.9% and 51.6%. The attenuation from 20-MHz data was equal to 3.66 + 0.089 hematocrit (decibels per centimeter). The uncertainty of in vivo measurements in the brachial artery was determined to be within +/- 5% hematocrit. However, the measurements in the radial artery resulted in a clinically unacceptable uncertainty of +/- 20% hematocrit. CONCLUSIONS: The method proposed appears to be promising for in vivo determination of hematocrit, because 5% hematocrit error is adequate for monitoring changes in patients in shock or during dialysis. It was found that the multigate system largely simplified placement of an ultrasonic probing beam in the center of the blood vessel. Current work focuses on enhancing the method's applicability to arbitrarily selected vessels and to reducing the hematocrit measurement error to much less than 5% hematocrit.

Acoustics↗
PubMed1999

Influence of hematocrit on hemostasis in continuous venovenous hemofiltration during acute renal failure.

BACKGROUND: Hematocrit plays a major role in primary hemostasis by influencing blood viscosity and platelet adhesion. During continuous venovenous hemofiltration (CVVH), it is suspected that an increased hematocrit is accompanied by an activation of hemostasis and frequently leads to thromboses in the extracorporeal system. In order to examine this hypothesis, we studied the influence of hematocrit on hemostasis during CVVH. METHODS: Fourteen patients (8 men and 6 women, mean age 65+/-10 years) with acute renal failure undergoing CVVH were prospectively enrolled. Polysulfone hemofilters (AV 600; Fresenius, Oberursel, Germany) were used in all of the patients; blood flow rates were adjusted to 120 ml/min. No blood products and coagulation-related medication, except unfractionated heparin, were applied. Study exclusion criteria included a history of thromboembolism and artificial heart valves. Hemostasis activation markers (fibrinopeptide A, thrombin-antithrombin III complex, beta-thromboglobulin, platelet retention) and hematocrit values were determined before and at three-day intervals during the course of CVVH treatment. RESULTS: The mean hematocrit value (mean +/- SEM) was 29+/-1% (range, 22 to 35%). Patients with hematocrit values of less than 30% (N = 7) were compared with patients with higher hematocrit values (>30%, N = 7). The patients with a lower hematocrit (<30%) showed a stronger activation of hemostasis during CVVH when compared with those with a higher hematocrit (>30%), as indicated by a tendency toward higher values for fibrinopeptide A (25+/-8 vs. 14+/-5 ng/ml, P = 0.35), thrombin-antithrombin III complex (15+/-4 vs. 10+/-2 ng/ml, P = 0.66), and a higher beta-thromboglobulin/creatinine ratio (0.62+/-0.17 vs. 0.48+/-0.12, P = 0.8). CONCLUSION: Contrary to our hypothesis, hematocrit values of more than 30% are not accompanied by an increased hemostasis activation during CVVH. Concerning hemostasis activation, hematocrit values between 30 and 35% may be suitable for patients on CVVH.

Acute Kidney Injury↗
PubMed2003

Regional hematocrit changes related to blood flow conditions in the arterial bed.

Present study was aimed at specifying both the anatomical and physiological factors determining the regional hematocrit alterations. These latter were investigated in blood samples from specific vascular branches of rabbits, as well as from the skin and the jugular veins (reflecting the cerebral microcirculation) of humans. Principal findings were as follows: (1) Blood in the heart left ventricle has a higher hematocrit than blood flowing in the hind legs. (2) Blood flowing towards the cerebral vessels has a higher hematocrit than blood flowing to the hind legs. (3) Hematocrit in blood from the right brachial artery is higher than from the left one. (4) Analogous is the red cell/plasma relationship in the microcirculation from the humans' right and left hands' fingers. (5) Local hematocrit in the individual arterial branches of the rabbits' aortic arch is dependent on the blood flow velocity in them: the faster flow provides higher hematocrit in their lumen. (6) Microvascular hematocrit in rabbits was found significantly lowered during ischemia in the respective vascular beds. (7) Microvascular hematocrit in the human skin decreases during lowering of blood inflow, and vice versa, thus evidencing that the capillary hematocrit depends on the functional state of the feeding arterioles. We concluded, therefore, that the two basic factors determining the local hematocrit in arterial branches and in the respective microvascular networks are the anatomical outlines and the comparative velocities of blood flow in their lumina. However, in patients with strokes the hematocrit in blood flowing in the jugular veins was found lower than in blood from the carotid arteries. This might be related to the enhanced RBC aggregation and retention in the cerebral microvessels producing multiple blood stases in their lumina.

Animals↗
PubMed1978

Optimal hematocrit value in critically ill postoperative patients.

Failling hematocrit values are traditionally used to observe the course of active bleeding, since hematocrit values usually reflect acute blood losses. However, evidence from the literature suggests that, after volume replacement, some degree of normovolemic hemodilution may be desirable and that return to normal hematocrit values is not necessarily the appropriate goal of transfusion therapy. The optimal hematocrit value was defined empirically by three methods in a series of 94 critically ill postoperative patients. First, the mortality rates of postoperative patients were lowest with hematocrit values between 27 and 33 per cent. Second, mortality rates were examined when both hematocrit values and the important cardiorespiratory variables were reduced; significantly increased mortalties occurred when hematocrit values were less than an average of 32 per cent. Finally, oxygen availability and oxygen consumption increased significantly after whole blood and packed red cell transfusions were given when hematocrit values were less than 32 per cent but not above 33 per cent. When accurate blood volume measurements are not available, hematocrit values of 32 per cent are optimal; when volume therapy is indicated, blood may be given with hematocrit values less than 32 per cent, crystalloids or colloids are preferred with hematocrit values greater than 32 per cent.

Adult↗
PubMed1991

Optimal hematocrit theory during activity in the bullfrog (Rana catesbeiana).

1. There is an exponential relationship between blood viscosity (cP) and hematocrit (%) for the bullfrog; eta = 1.81 e0.033Hct. The in vitro optimal hematocrit calculated for blood flow through tubes, from this relationship for bullfrog blood, is 30%. 2. Amphibian blood is a non-Newtonian fluid with viscosity dependent on shear rate. It has a finite yield shear stress of about 1.5 dynes cm-2. 3. Hematocrit of bullfrogs was increased from 27% (control) to 57% by isovolemic erythrocythemia (constant volume blood-doping). There was a slight increase in systolic, diastolic and venous blood pressure with elevated hematocrit. 4. Systemic arch blood flow rate was inversely related to blood viscosity for erythrocythemic bullfrogs. The decrease in systemic arch blood flow at high hematocrits was due primarily to reduced pulse volume rather than reduced heart rate. 5. Systemic arch blood flow, when standardised between individuals, was inversely related to blood viscosity; Qbl = 0.185 + 3.73 eta -1. This relationship was significantly different from that predicted by the Poiseuille-Hagen flow formula. The in vivo optimal hematocrit calculated from this relationship was 41%. 6. Optimal hematocrit theory appears to be generally applicable for Rana catesbeiana in vitro and in vivo. Most individuals had an in vivo optimal hematocrit, but the absence of a clear optimal hematocrit for some individuals could reflect methodological variability, or in vivo physiological compensation for the increased blood viscosity at high hematocrit.

Animals↗
PubMed2006

Influence of hematocrit and localisation of punch in dried blood spots on levels of amino acids and acylcarnitines measured by tandem mass spectrometry.

BACKGROUND: Detection of amino acids (AA), acylcarnitines (AC), and guanidinoacetate (GAA) in dried blood spots by tandem mass spectrometry has made it possible to detect different inborn errors of metabolism in neonatal screening programs. Despite its proven sensitivity many issues related to sample preparation remain unsolved. Hematocrit has a profound effect on blood viscosity, and may thereby influence flux and diffusion properties of the blood. As newborn infants show a considerable interindividual variability of hematocrit levels, we investigated its effect on levels of AA and AC in dried blood spots. METHODS: Blood samples with defined hematocrit levels (20%, 30%, 40%, 50%, 60%) were produced by diluting blood cells with plasma from a single donor. Forty dried blood spots were made for each hematocrit level and a central as well as a peripheral 3 mm disk was punched and analysed for AA, AC, and GAA, respectively. RESULTS: Levels of most AA and GAA increased significantly with increasing hematocrit (p<0.001), while the effect of hematocrit on some AA was less pronounced. Total AC, free carnitine, some long, medium and short chain AC correlated positively with hematocrit levels (p<0.001). In samples with low hematocrit, levels of most AA and free carnitine were higher in the peripheral than in the central disk (p<0.0001). CONCLUSIONS: Both hematocrit and position of the disk within the dried blood spot have a significant and sometimes additive effect on levels of AA, AC and GAA in dried blood spots. Theoretically, diagnoses may be missed depending on hematocrit and position of the disk.

Amino Acids↗
PubMed2002

Factors that predict low hematocrit levels in the postpartum patient after vaginal delivery.

OBJECTIVE: The purpose of this study was to provide a viable alternative to routine postpartum hematocrit measurement, by a determination of the clinical risk factors that identify patients with anemia and an examination of the resulting cost savings. STUDY DESIGN: In this retrospective review, cases (postpartum hematocrit level, <26%; subgroup hematocrit level, <23%) and control subjects were culled from the records of all vaginal deliveries from February 1997 to July 1998. Charts were reviewed for demographic characteristics, medical history, nursing assessments, and postpartum hematocrit measurements. Logistic regression modeling determined the best set of risk factors for the identification of low postpartum hematocrit levels. RESULTS: From 1484 vaginal deliveries, 117 of the women (8%) had postpartum hematocrit levels of <26%. Estimated blood loss of >500 mL, Hispanic ethnicity, dizziness, or third- or fourth-degree laceration were the factors that identified 82.9% of the women with hematocrit levels of <26% and identified 97.4% of the women with hematocrit levels of <23%. Only 39.3% of the women would have required postpartum hematocrit measurement to obtain these detection rates. CONCLUSION: Four risk factors (estimated blood loss of >500 mL, Hispanic ethnicity, dizziness, and third- or fourth-degree laceration) can safely determine the necessity of a postpartum hematocrit measurement.

Adult↗
PubMed1979

Microvascular hematocrit and red cell flow in resting and contracting striated muscle.

Microvascular hematocrit and its possible relation to oxygen supply were systematically examined. We studied the red cell volume fraction (hematocrit) in arterial blood and in capillaries under a variety of circumstances. Control capillary hematocrit averaged 10.4 +/- 2.0% (SE) and arteriolar (14.2 micrometer ID) hematocrit averaged 13.9 +/- 1.2% in cremaster muscles of pentobarbital-anesthetized hamsters. Carotid artery hematocrit was 53.2 +/- 0.6%. The low microvessel hematocrit could not be entirely explained by a high red cell flux through arteriovenous channels other than capillaries (shunting). Hematocrit was not only low at rest, but varied with physiological stimuli. A 1-Hz muscle contraction increased capillary hematocrit to 18.5 +/- 2.4%, and maximal vasodilation induced a rise to 39.3 +/- 9.5%. The quantitative relations between capillary red cell flux, arterial hematocrit, and total blood flow could be explained by a two-element model of microvascular blood flow that incorporated a relatively slow-moving plasma layer (1.2 micrometer). Such a model would generate a low microvessel hematocrit and might reduce the diffusion capacity of individual capillaries, but would not reduce time-averaged red cell flux or alter steady-state vascular oxygen supply.

Animals↗
PubMed1998

Cerebral hematocrit decreases with hemodynamic compromise in carotid artery occlusion: a PET study.

BACKGROUND AND PURPOSE: This study investigated whether in patients with internal carotid artery occlusion the regional cerebral hematocrit correlates with cerebral hemodynamics or metabolic state and, if so, how the regional cerebral hematocrit changes in the hemodynamically compromised region. METHODS: We used positron emission tomography to study seven patients with unilateral internal carotid artery occlusion and no cortical infarction in the chronic stage. The distributions of red blood cell and plasma volumes were assessed using oxygen-15-labeled carbon monoxide and copper-62-labeled human serum albumin-dithiosemicarbazone tracers, respectively. The calculated hematocrit value was compared with the hemodynamic and metabolic parameters measured with the oxygen-15 steady-state technique. RESULTS: In the cerebral cortex, the value of the cerebral hematocrit varied but was correlated with the hemodynamic and metabolic status. Stepwise regression analysis revealed that the large vessel hematocrit, the cerebral metabolic rate of oxygen, and the cerebral blood flow or the oxygen extraction fraction accounted for a significant proportion of variance of the cerebral hematocrit. The oxygen extraction fraction and the cerebral metabolic rate of oxygen negatively correlated with the cerebral hematocrit, whereas the cerebral blood flow correlated positively: patients with reduced blood supply relative to metabolic demand (decreased blood flow with increased oxygen extraction fraction) showed low hematocrit values. CONCLUSIONS: In carotid artery occlusion in the chronic stage, regional cerebral hematocrit may vary according to cerebral hemodynamics and metabolic status. Regional cerebral hematocrit may decrease with hemodynamic compromise unless oxygen metabolism concomitantly decreases.

Aged↗
PubMed1970

Effects of hematocrit on renal hemodynamics and sodium excretion in hydropenic and volume-expanded dogs.

The effects of hematocrit on renal hemodynamics and sodium excretion were studied in anesthetized dogs during both hydropenia and volume expansion. The hematocrit was decreased by isovolemic exchange with the animal's own previously harvested plasma and increased by isovolemic exchange with fresh, washed red blood cells. Renal perfusion pressure was maintained constant throughout the experiments by the adjustment of a suprarenal aortic clamp. During hydropenia, a decrease in hematocrit was associated with an increase in sodium and potassium excretion and solutefree water reabsorption. These changes were accompained by an increase in renal plasma flow and renal blood flow and a decrease in renal vascular resistance. Glomerular filtration rate was unchanged and filtration fraction was significantly decreased as hematocrit was lowered. Increasing hematocrit during hydropenia had the opposite effects on electrolyte excretion, solute-free water reabsorption, and renal hemodynamics. In another group of animals, hematocrit was lowered during volume expansion with either saline or plasma, then returned to the control level by isovolemic exchange with washed red blood cells. This increase in hematocrit during volume expansion had a similar effect on electrolyte excretion, solute-free water reabsorption, and renal hemodynamics as during hydropenia. These results therefore suggest that acute changes in hematocrit may significantly affect sodium excretion and renal hemodynamics during both hydropenia and volume expansion. The changes in solute-free water reabsorption and potassium excretion suggest that the alterations in hematocrit may affect primarily the reabsorption of sodium in the proximal tubule. The concommitant effects of hematocrit on renal vascular resistance and filtration fraction may mediate this change in sodium reabsorption by altering hydrostatic and oncotic pressures in the peritubular circulation.

Animals↗
PubMed2005

Prognostic value of the hematocrit in patients with severe COPD receiving long-term oxygen therapy.

BACKGROUND: Although traditionally associated with polycythemia, COPD has a systemic inflammatory component that could interfere with erythropoiesis. This study describes the distribution and prognostic value of the hematocrit in patients with severe COPD receiving long-term oxygen therapy (LTOT). METHODS: A total of 2,524 patients with COPD, FEV1/vital capacity (VC) < 70%, FEV1 < 80% of predicted, and Pa(O2) < 7.3 kPa in whom a hematocrit was available at entry was identified between 1980 and 1999 in the French Association Nationale pour le Traitement à Domicile de l'Insuffisance Respiratoire chronic respiratory insufficiency and home-care database (male/female ratio, 5/1; mean +/- SD age, 68 +/- 10 years for men, and 70 +/- 10 years for women). Correlations between hematocrit, demographic data, and pulmonary function data were examined. A multivariate Cox proportional hazard regression was performed to identify prognostic factors. RESULTS: Mean hematocrit was 45.9 +/- 7.0% in men and 43.9 +/- 6.0% in women (< 39% in 12.6% of men, and < 36% in 8.2% of women) according to the World Health Organization definition of anemia. Hematocrit was negatively correlated with age (r = - 0.245) and FEV1/VC (r = - 0.068) and was positively correlated with Pa(CO2) (r = 0.161) and body mass index (r = 0.127). Multivariate analysis found hematocrit to be an independent predictor of survival, hospital admission rate, and cumulative duration of hospitalization. The 3-year survival was 24% (95% confidence interval, 16 to 33%) when the hematocrit was < 35%, and 70% (63 to 76%) when the hematocrit was > or = 55%. CONCLUSIONS: A low hematocrit is not uncommon in LTOT/COPD patients. Hematocrit is negatively associated with mortality and morbidity. Whether the association is causative or not and whether or not corrective measures are warranted remain to be determined.

Aged↗
PubMed1996

Elevation of serum cholesterol at high altitude and its relationship to hematocrit.

The positive relationship between hematocrit and serum cholesterol may be due to dilution. Accordingly, high hematocrits would yield reduced serum pools for dilution of cholesterol, thus producing higher levels. To test this effect, the relationships between hematocrit and cholesterol were evaluated at low-altitude and high-altitude clinics. Retrospective chart reviews were conducted at Madison, WI (264 m) and Leadville, CO (3105 m) to identify family practice patients who underwent hematocrit and serum cholesterol determinations on the same day. We excluded patients with medical conditions or on medications that affect cholesterol, patients with high glucose and triglyceride levels, and patients with extreme cholesterol levels. Remaining patients (153 in each altitude group) were matched by age and sex. The mean hematocrits and cholesterol levels were compared using analysis of variance. The linear relationships between hematocrit and cholesterol were compared using analysis of covariance. The mean hematocrit was significantly higher at high altitude (47.5% versus 41.3%; p < 0.0005) as were the mean serum cholesterol (190 mg/dL versus 177 mg/dL; p < 0.002) and the low-density lipoprotein:high-density lipoprotein ratio (2.80 versus 2.27; p < 0.05). Whereas a significant, positive relationship existed between hematocrit and cholesterol at low altitude (2.15 mg/dL per %; p < 0.002), no such relationship was found at high altitude. Hematocrit and serum cholesterol were elevated for family practice patients living at high altitudes. Differences exist between altitudes in the relationship between hematocrit and cholesterol. Acclimatization to high altitude and its resultant erythropoiesis may increase serum cholesterol levels. Consequently, relocation to a high altitude may increase the risk of arteriosclerotic cardiovascular disease.

Acclimatization↗
PubMed1999

Hematocrit level and associated mortality in hemodialysis patients.

Although a number of clinical studies have shown that increased hematocrits are associated with improved outcomes in terms of cognitive function, reduced left ventricular hypertrophy, increased exercise tolerance, and improved quality of life, the optimal hematocrit level associated with survival has yet to be determined. The association between hematocrit levels and patient mortality was retrospectively studied in a prevalent Medicare hemodialysis cohort on a national scale. All patients survived a 6-mo entry period during which their hematocrit levels were assessed, from July 1 through December 31, 1993, with follow-up from January 1 through December 31, 1994. Patient comorbid conditions relative to clinical events and severity of disease were determined from Medicare claims data and correlated with the entry period hematocrit level. After adjusting for medical diseases, our results showed that patients with hematocrit levels less than 30% had significantly higher risk of all-cause (12 to 33%) and cause-specific death, compared to patients with hematocrits in the 30% to less than 33% range. Without severity of disease adjustment, patients with hematocrit levels of 33% to less than 36% appear to have the lowest risk for all-cause and cardiac mortality. After adjusting for severity of disease, the impact of hematocrit levels of 33% to less than 36% is vulnerable to the patient sample size but also demonstrates a further 4% reduced risk of death. Overall, these findings suggest that sustained increases in hematocrit levels are associated with improved patient survival.

Adult↗
PubMed1996

Hematocrit and risk of NIDDM.

There is limited evidence that raised hematocrit levels may be associated with insulin resistance, which links cardiovascular disease with NIDDM. The association between hematocrit level at screening and the subsequent development of physician-diagnosed NIDDM during 12.8 years of follow-up was examined in a prospective study of 7,735 middle-aged men drawn at random from general practice in 24 British towns. With the exclusion of men with missing hematocrit data and men with diabetes at screening, data were available for 7,193 men, in whom there were 187 new cases of NIDDM during follow-up. The risk of NIDDM increased significantly with increasing hematocrit levels. There was more than a fourfold increase in relative risk (RR) of diabetes among men with a hematocrit of > or = 48% relative to those with a hematocrit <42%, adjusted for age and BMI (RR 4.5; 95% CI 2.5-6.3). On further adjustment for predictors of NIDDM with which hematocrit is correlated, there remained a strong linear association with the risk of diabetes. There was a nearly fourfold increased risk of NIDDM in the highest relative to the lowest hematocrit group in the fully adjusted proportional hazard model (RR 3.6; 95% CI 1.7-7.6). The strong positive association between hematocrit level and risk of diabetes was seen even after exclusion of men with preexisting ischemic heart disease. The findings suggest that a raised hematocrit level, which is a major determinant of whole blood viscosity, should be added to the cluster of risk factors that link NIDDM with atheromatous, vascular disease.

Adult↗
PubMedDate not supplied

Hemodynamic effects of chronic alteration in hematocrit in spontaneously hypertensive rats.

This study describes the effect of a chronic decrease in hematocrit on blood pressure, cardiac output (CO), total peripheral resistance (TPR), and plasma volume in spontaneously hypertensive rats (SHR), and all but plasma volume in normotensive Wistar rats (NWR). Hematocrit was decreased by treatment with either heparin, vitamin K inhibitor ( pelentan ), or by repeated blood letting (BL). The results show that in SHR, a decrease in hematocrit, regardless of how produced, was associated with a significant decrease (p less than 0.01) in blood pressure. Prevention of heparin-induced decrease in hematocrit by repeated transfusions of red blood cells abolished the blood-pressure-lowering effect of heparin. By using combined data on hematocrit and systolic blood pressure in all five SHR groups, a significantly positive correlation and linear regression between hematocrit and blood pressure were obtained. When compared to control untreated SHR, heparin- or pelentan -treated SHR showed a significant (p less than 0.001) decrease in TPR and a significant increase in CO, while in SHR BL, no difference in TPR or CO was found. Plasma or blood volume did not differ among the groups. In NWR, heparin treatment resulted in significantly decreased hematocrit, decreased TPR, and increased CO compared to control normotensive rats. However, blood pressure did not change. Results confirming the authors' previous study and those of other investigators indicate a direct association between hematocrit and systemic hypertension. Lowering the hematocrit can effectively lower an elevated blood pressure. Moreover, the data suggest that heparin or pelentan induces a vasodilator effect that cannot be attributed to a decrease in hematocrit alone.

Animals↗
PubMed1997

Impact of minimum hematocrit during cardiopulmonary bypass on mortality in patients undergoing coronary artery surgery.

BACKGROUND: The hematocrit on cardiopulmonary bypass (CPB) frequently falls to a low level during many cardiac surgical procedures. This study was designed to explore the impact on mortality of minimum hematocrit level achieved during the CPB after coronary artery surgery. METHODS AND RESULTS: Two thousand seven hundred thirty-eight sequential isolated coronary artery surgery patients during a 42-month period at a tertiary academic center were included in this study. Thirty-one standardized preoperative risk factors used in a multiple logistic regression revealed eight statistically significant independent predictors for postoperative mortality. Minimum hematocrit level during CPB was then added to the regression model and was found to be an independent risk factor for mortality. The entire patient population was divided into dichotomous groups using different minimum hematocrit levels on CPB for the determination of cutoff points by multiple logistic regression. After adjusting for other risk factors, the minimum hematocrit level of 14% was found to be a statistically significant cutoff point. Patients with minimum hematocrit levels < or =14% were found to have an increased probability of risk-adjusted mortality (odds ratio, 2.70; P=.002). A subgroup analysis revealed that high-risk patients with minimum hematocrit levels < or =17% were found to have a significantly increased probability of postoperative mortality (odds ratio, 2.20; P=.017). CONCLUSIONS: Minimum hematocrit level during CPB is an independent risk factor for mortality after coronary artery surgery. There is a significantly increased risk of mortality for hematocrit levels < or =14%. For high-risk patients, there is a significantly increased risk of mortality for hematocrit levels < or =17%.

Adult↗