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PubMed1994

In search of an optimal hematocrit level in dialysis patients: rehabilitation and quality-of-life implications.

Anemia is an inevitable and potentially serious complication of chronic renal failure and one of the most important limiting factors in patient rehabilitation. Although adequate dialysis can control many of the symptoms of uremia, dialysis does not reverse anemia-associated fatigue, and thus, many patients are not rehabilitated. Human recombinant erythropoietin (epoetin) therapy has proven to be effective in reversing anemia and increasing hematocrit levels in the majority of patients with chronic renal failure. Among this patient population, increases in hematocrit level have resulted in improvements in the symptomatology of organ hypoxia, neurobehavioral indices, anorexia, insomnia, depression, and sexual disinterest and dysfunction, as well as a reduction in cardiomegaly. However, despite the availability of epoetin and the dramatic improvements in the complications associated with the anemic state observed following therapy, it appears that patient rehabilitation remains a challenge. One aspect of the continuing problem of rehabilitation appears to be the reluctance of the medical community to increase hematocrit levels above 30%, despite the fact that higher hematocrit levels are associated with greater improvements and that potential adverse events related to hemodynamic adaptation are manageable. Indeed, a comparison of the results from two Epoetin alfa clinical trials, one in which hematocrit levels were maintained at 35% and a large phase IV study in which the target hematocrit level appears to have been approximately 30%, clearly demonstrate the benefits of optimizing hematocrit levels and thus improving the potential for rehabilitation.

Anemia, Hypochromic↗
PubMed1992

Flow-limited tracer oxygen distribution in the isolated perfused rat liver: effects of temperature and hematocrit.

We used the multiple-indicator dilution technique to examine the kinetics of tracer oxygen distribution and uptake in the rat liver perfused in a nonrecirculating fashion with blood. 51Cr-labeled 18O2-saturated erythrocytes, labeled albumin, sucrose and water (the tracers for oxygen and vascular, interstitial and cellular references) were injected simultaneously into the portal vein. Timed anaerobic samples were collected from the hepatic vein and analyzed by mass spectrometry for relative 18O2 enrichment and radioactivity. In a set of experiments performed at 32 degrees C, oxygen uptake was substantially diminished; tracer oxygen profiles approached those expected for a completely recovered, flow-limited substance. At 37 degrees C, much larger tracer oxygen sequestration occurred. Experiments were carried out at each temperature at higher and lower hematocrit, and oxygen consumption at each temperature was found to be independent of hematocrit. The tissue space of distribution for tracer oxygen relative to the total sinusoidal vascular content was influenced by the hematocrit: it was smaller at higher hematocrit and larger at lower hematocrit, as expected. The derived partition coefficient of oxygen for liver cells relative to plasma (expressed in terms of the liver and plasma water spaces) was, on average, 2.62 ml/ml; it was independent of the hematocrit. Analysis of the indicator dilution experiments indicates that the tracer oxygen is distributed into tissue in a flow-limited rather than a barrier-limited fashion, and that with this, an ongoing concomitant intracellular sequestration of tracer can be seen.

Animals↗
PubMedDate not supplied

Assessing microvascular volume change and filtration from venous hematocrit variation of canine liver and lung.

The volume increase of canine liver after 1 min of a 10 mmHg elevation in hepatic venous pressure has been reported as 251 ml/kg tissue. An analysis of the transient hematocrit variation in hepatic venous blood indicated that 16% of the volume change results from transcapillary filtration, 72% from microvascular expansion, and 12% from macrovascular expansion. In the analysis, we first used the temporal change of the liver volume to determine the time course of the filtration and microvascular and macrovascular volume change. We next deduced, for a permeable microcirculation with a microvascular hematocrit lower than the feed hematocrit (the Fahraeus effect), how the filtration and microvascular volume change (MVC) produce a hematocrit variation in the blood leaving microcirculation. By accounting for the dispersion of the blood flow, the analysis predicted a hematocrit variation in the hepatic venous blood that matched well with the measured variation over the 1-min course of experiment. A reasonable fit with the hematocrit variation of pulmonary blood also was obtained for experiment with an 8 mm/Hg increase in the arterial and venous pressure perfusing the canine left lower lung lobe. The tissue and vascular volume increase at 1 min was 149 ml/kg tissue with 4% as a result of filtration, 41% as a result of microvascular expansion, and 55% as a result of macrovascular expansion. The large MVCs from the hepatic and pulmonary circulation indicate their microcirculations function as a reservoir in controlling blood volume redistribution.

Animals↗
PubMed1997

Mapping genes controlling hematocrit in the spontaneously hypertensive rat.

The genes that determine the baseline hematocrit level in humans and experimental animals are unknown. The spontaneously hypertensive rat (SHR), the most widely used animal model of human essential hypertension, exhibits an increased hematocrit when compared with the normotensive Brown Norway (BN-Lx) strain (0.54 +/- 0.02 vs. 0.44 +/- 0.02, p < 0.01). Distribution of hematocrit values among recombinant inbred (RI) strains derived from SHR and BN-Lx progenitors was continuous, which suggests a polygenic mode of inheritance. The narrow heritability of the hematocrit was estimated to be 0.32. The Eno2 marker on Chromosome (Chr) 4 showed the strongest association (p < 0.0001) with the observed variability of hematocrit among RI strains. The erythropoietin (Epo) gene, originally reported to be syntenic with Eno2, has been mapped to Chr 12, thus excluding it as a potential candidate gene for the increased hematocrit in the SHR. The current linkage data extend homologies between rat, mouse, and human chromosomes.

Animals↗
PubMedDate not supplied

Effect of hematocrit on adenosine diphosphate-induced aggregation of human platelets in tube flow.

Both chemical and physical effects of red cells are known to play a role in the adenosine diphosphate (ADP)-induced aggregation of human platelets in sheared blood. Using a previously described double infusion technique (Bell et al., 1989a), we studied the effect of increasing hematocrit from 10 to 60% on the rate and extent of platelet aggregation with 0.2 microM ADP in citrated whole blood undergoing tube flow. Blood and agonist were rapidly mixed in a small chamber and the suspensions flowed through lengths of 1.19 mm-diameter polyethylene tubing at mean transit times from 0.2 to 42.8 s at a mean tube shear rate = 335 s-1. Effluent was collected into 0.5% glutaraldehyde, the red cells removed by centrifugation through Percoll, and all single platelets and aggregates in the volume range 1-10(5) microns3 counted and sized using an aperture impedance counter. Both the initial rate (over the first 8.6 s) and the extent of aggregation with time increased with increasing mean hematocrit up to 35.8%, being significantly greater than in citrated plasma (cPRP). However, at 61.5% hematocrit, the extent of aggregation decreased markedly to a level close to that in cPRP. We also studied the effect of washed red cells at 39% hematocrit on the aggregation of washed platelets in Tyrodes-albumin fibrinogen-free suspensions. It had previously been shown that, at > or = 335 s-1, washed platelets in platelet-rich Tyrodes (PRT) aggregated with 0.7 microM ADP. We found that red cells markedly increased the extent of aggregation from that in PRT, and promoted the formation of large aggregates, absent in PRT. Spontaneous aggregation in whole blood or washed cell suspensions in the absence of added ADP at = 42.8 s was < 10% of that in the presence of ADP. The results indicate that a physical effect of red cells, likely manifested as an increase in the efficiency of aggregate formation (Goldsmith et al., 1995), plays an important role at low and normal hematocrits; however, at high hematocrits, particle crowding impedes the formation of aggregates.

Adenosine Diphosphate↗
PubMed1985

A density method to quantify pulmonary microvascular hematocrit.

We perfused the left lower lobe of a dog with autologous blood having a hematocrit Ha. When the vascular pressure perfusing the lobe was elevated, we observed a transient increase in the density of venous blood. Converting the density increase to a rise in hematocrit, we could calculate a volume (Vr) of red blood cells (RBC) over their normal outflow that was released by the lobe as a result of the elevation. We measured the weight gain of the lobe to determine the increase in pulmonary vascular volume, V' - V. We found that the ratio, Vr/Ha/(V' - V), is 0.11 +/- 0.02. To determine the implication of this ratio, we divided the lobular vasculature into an arterial, microvascular, and venous compartment. Due to the Fahraeus effect, the tube hematocrit in the microvascular compartment (Hc) is lower than that of two macrovascular compartments, Ha. An analysis on the balance of RBC and plasma flows through the lobe identified the volume Vr as (Vc' - Vc) (Ha - Hc) with Vc' - Vc being the volumetric increase of the lobular microvascular compartment. Based on the reported volumetric fractional change of microvascular compartment, we estimated that the microvascular (tube) hematocrit in pulmonary capillaries is 80% (ranging from 78 to 82%) of the hematocrit perfusing the lobe. Since the additional RBC volume (Vr) being released from the lobe cannot be accounted for by transcapillary filtration or capillary recruitment, we conclude from this analysis that the measurement of the transient density change in pulmonary outflow can be used to quantify the microvascular hematocrit of the lung.

Animals↗
PubMed1995

The relationship between peak velocity in the fetal descending aorta and hematocrit in rhesus isoimmunization.

OBJECTIVE: To correlate the peak velocity in the fetal descending aorta, as measured by pulsed Doppler ultrasound, with fetal hematocrit values assessed by funipuncture in pregnancies complicated by rhesus isoimmunization. METHODS: One hundred twelve consecutive funipunctures were performed on 33 rhesus-negative gravidas of 21-36 weeks' gestation (median 30). Doppler flow, corrected for angle, was measured on the fetal descending aorta with pulsed Doppler equipment immediately before funipuncture. Differences between observed peak velocities and the calculated gestational age-dependent upper confidence limits (delta peak velocities) were compared with corresponding differences between observed hematocrits and the calculated lower confidence limits (delta hematocrits), and a regression analysis on the above paired difference values was performed. In addition, the correlation coefficient between delta peak velocities and delta hematocrits was calculated for the first procedure per pregnancy only. RESULTS: The mean peak aortic velocity of anemic fetuses was higher than that of unaffected fetuses (P < .001); delta peak aortic velocities correlated negatively with delta hematocrits (r = -0.66, P < .001). The correlation coefficient between delta peak aortic velocities and delta hematocrits for the first procedure peer pregnancy only was r = -0.72 (P < .001). Prediction of fetal anemia by Doppler using gestational age-dependent 95% confidence limits was possible with positive and negative predictive values of 73 and 66%, respectively. CONCLUSION: Peak aortic velocity, a noninvasive assessment of fetal anemia, may be used as an additional test for monitoring pregnancies complicated by rhesus isoimmunization. However, the limited predictive capacity hampers its clinical usefulness.

Anemia↗
PubMed1995

Adapting the dialysis unit to increased hematocrit levels.

Recombinant human erythropoietin (epoetin) therapy had a significant impact on the practice of nephrology before its widespread use in the dialysis arena. Since then, a number of long-term studies have provided physicians with parameters for optimizing therapeutic response and patient outcomes with epoetin therapy. Fears of accelerated hypertension syndromes or increased fistula clotting are recognized as largely unfounded. There is a marked improvement in well-being, as measured by both subjective and objective parameters, as the level of anemia is reduced. Fortunately, epoetin was recognized early as essential therapy in patients on dialysis and thus was reimbursed by the Health Care Financing Administration (HCFA) and other payers, albeit through various methods of payment. Why is it, then, that hematocrit levels are still averaging approximately 30%? Perhaps the basic concern that all practitioners share is the potential for increased morbidity at "higher" hematocrit levels. Increased access clotting was not reported in the recently completed Epogen (Epoetin alfa; Amgen Inc, Thousand Oaks, CA) phase IV postmarketing study. Needle size, however, needs to be considered, because higher blood flow rates accompanied by higher hematocrit levels may lead to increased hemolysis. The venous needle size is especially important in patients who experience large weight gains. It is important to keep these issues in mind as one decides on an appropriate hematocrit level for a given patient. Hull and Eschbach reviewed postdialysis data from patients with naturally occurring high hematocrit levels and found no major changes in hematocrit level, thus alleviating the concern of significant postdialysis inspissation as a common cause for fistula clotting.

Adult↗
PubMed1991

Relation between blood viscosity and hematocrit in rabbits subjected to repeated treatment with endotoxin.

Blood rheology was studied in rabbits repeatedly treated with endotoxin at a dose of 0.1 mg administered 3 times, at intervals of 3 days. On the 7th day after the last endotoxin injection, blood was sampled 3 times from the femoral artery under anesthesia using pentobarbital sodium. Blood viscosity was determined at a shear rate of 150 s-1 at 37 degrees C using a cone-plate viscometer. Plasma fluidity was determined using the filtration method. Hematocrit and whole blood viscosity showed no significant differences between the untreated rabbits (Group A) and rabbits treated with endotoxin (Group B). Plasma fluidity was significantly lowered in Group B. Whole blood viscosity correlated well with hematocrit in Group A, but there was no correlation in Group B. The ratio of hematocrit to whole blood viscosity, which is considered to be the index of oxygen delivery from the blood rheological point of view, indicated no significant difference between the two groups. The optimal hematocrit to oxygen delivery, however, was higher in Group B than in Group A. These data suggest that the high hematocrit rather becomes an advantage to oxygen delivery in endotoxicosis because the hematocrit-viscosity relation is disturbed.

Animals↗
PubMed2004

Catheter-based impedance measurements in the right atrium for continuously monitoring hematocrit and estimating blood viscosity changes; an in vivo feasibility study in swine.

Hematocrit is the most important determinant of whole blood viscosity and it affects thrombosis. As hematocrit can be measured accurately in vitro by using an electrical impedance technique, aim of the present study is to investigate the diagnostic potential of using this technique in vivo to continuously monitor hematocrit. Characteristics of a special catheter for in vivo measurement of electrical resistivity in blood in the right atrium are described. In five anesthetized swine hematocrit is monitored continuously with this catheter while different levels of hemoconcentration are induced. In addition, blood viscosity is increased by inducing 'acute phase' reaction the day before surgery, resulting in variable degree of elevated fibrinogen levels in the five swine. Good reproducibility of the resistivity measurements (S.D < 0.01) and excellent correlation between resistivity data in vivo and hematocrit levels in each swine are found (r2 = 0.95-0.99). Furthermore, stepwise regression analysis of data from all swine shows a highly significant contribution also of other important parameters of blood viscosity, such as fibrinogen, total protein and temperature (cumulative r2 = 0.97). Determining hematocrit continuously in vivo by electrical resistivity measurements with a catheter in the right atrium is feasible and these measurements correlate significantly also with other important parameters of blood viscosity.

Animals↗
PubMed2004

Interaction of temperature with hematocrit level and pH determines safe duration of hypothermic circulatory arrest.

OBJECTIVE: Previous studies have demonstrated that both hematocrit level and pH influence the protection afforded by deep hypothermic circulatory arrest. The current study examines how temperature modulates the effect of hematocrit level and pH in determining a safe duration of circulatory arrest. The study also builds on previous work investigating the utility of near-infrared spectroscopy as a real-time monitor of cerebral protection during circulatory arrest. METHODS: Seventy-six piglets (9.3 +/- 1.2 kg) underwent circulatory arrest under varying conditions with continuous monitoring by means of near-infrared spectroscopy (hematocrit level of 20% or 30%; pH-stat or alpha-stat strategy; temperature of 15 degrees C or 25 degrees C; arrest time of 60, 80, or 100 minutes). Neurologic recovery was evaluated daily by a veterinarian, and the brain was fixed in situ on postoperative day 4 to be examined on the basis of histologic score in a blinded fashion. RESULTS: Multivariable analysis of total histologic score revealed that higher temperature, lower hematocrit level, more alkaline pH, and longer hypothermic circulatory arrest duration were predictive of more severe damage to the brain (P <.01). Regression modeling revealed that higher temperature exacerbated the disadvantage of a lower hematocrit level and longer arrest times but not pH strategy. Normalized oxyhemoglobin nadir time, derived from near-infrared spectroscopy, was positively correlated with neurologic recovery on the fourth postoperative day and with total histologic injury score (P <.0001). CONCLUSION: Hematocrit level and pH, as well as temperature, determine the safe duration of hypothermic circulatory arrest. Near-infrared spectroscopy is a useful real-time monitor of safe duration of circulatory arrest.

Animals↗
PubMed2005

Valsartan-induced hematocrit changes in renal transplant patients.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor type 1 blockers (ARB) are frequently prescribed for renal transplant patients. The main reasons for their use are that their antihypertensive and antifibrogenic effects may prevent chronic renal allograft dysfunction, potentially improving transplant survival. Furthermore, ACE and ARB have been used to reduce the hematocrit in patients with posttransplant erythrocytosis. We evaluated the effects of the ARB valsartan on the evolution of hematocrit in stable renal transplant patients treated with cyclosporine (CsA), azathioprine (Aza), and prednisone. PATIENTS AND METHODS: Twenty-six stable renal transplant patients treated with valsartan 80 mg/d orally were followed for 6 months. Evaluations were performed prior to as well as at 3 and 6 months following the initiation of valsartan. RESULTS: The hematocrit levels decreased significantly at 3 months (46.1 +/- 7.3 vs 39.9 +/- 5.8 ; P < .0001) in patients with a normal hematocrit, namely a level over 38%, with no further reduction at 6 months. In recipients with an hematocrit less than 38%, there was no significant reduction, either at 3 or 6 months follow-up. Valsartan was well tolerated without significant side effects. CONCLUSION: We postulate that inhibition of the proerythropoietic effects of angiotensin II and/or the reduction in hypoxia within the renal tubulointerstitium as well as the vasodilator effects on the efferent arterioles, represent possible mechanisms for the reduction and stabilization of the hematocrit in stable renal transplant patients.

Adult↗
PubMed2004

Neurocognitive function and quality of life in relation to hematocrit levels in chronic hemodialysis patients.

OBJECTIVE: We examined the putative association between the levels of hematocrit and improvement of cognitive function as well as quality of life in patients with end-stage renal disease (ESRD). METHODS: Fifty-six ESRD patients were divided into two groups according to their hematocrit levels: Group A consisted of 28 patients with hematocrit levels lower than the median (27.2 g%), while Group B, the remaining 28 patients, with higher than the median level. Neurocognitive function and the quality of life in these two groups were compared. RESULTS: Although patients with higher hematocrit levels scored better in the neurocognitive function tests such as the forward digit-span (P=.034) and digit-symbol (P=.023), their quality of life evaluated by three scales (Karnofsky Scale, Index of Well-Being, and SF-36) was not any better than those with lower hematocrit group. CONCLUSIONS: The present study indicated that in chronic hemodialysis patients, the higher hematocrit levels improve neurocognitive function but not the quality of life.

Adult↗
PubMed1988

Microcirculatory hematocrit and blood flow.

Direct measurements from many laboratories indicate that the oxygen tension in skeletal muscle is significantly less than in the large veins draining these tissues. Harris (1986) has proposed that because of the parallel anatomic arrangement of large arterioles and venules in skeletal muscle, a counter-current exchange between these vessels can occur. He theorized that diffusion of O2 between arteriole and venule would lower the PO2 in the blood as it enters capillaries and result in a decreased tissue PO2 and an increase in large vein PO2. Calculations (Appendix) show that the amount of O2 transferred between arteriole and venule is inadequate to account for this difference in PO2 between tissue and veins due to the small surface area that is involved. It is well documented that the microcirculatory hematocrit ranges between 20 and 50% of that in the supply vessels. The reduced hematocrit lowers the oxygen content in these vessels and results in a low oxygen tension in the surrounding tissue. True arteriovenous shunts are not present in most skeletal muscles, but 15-20% of the microvessels represent thoroughfare or preferential flow channels. It is suggested that these vessels contain a greater than normal hematocrit to account for a conservation of red cell mass across the microcirculation. Furthermore, it is shown that the hematocrit in the preferential flow channels is an inverse function of the flow rate for any level of the microcirculatory hematocrit. The increased hematocrit raises the flow resistance in these vessels which reduces flow further and represents a positive feedback condition which may contribute to the intermittent and uneven flow patterns which are present within the microcirculation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Subcutaneous erythropoietin results in lower dose and equivalent hematocrit levels among adult hemodialysis patients: Results from the 1998 End-Stage Renal Disease Core Indicators Project.

The National Kidney Foundation's Dialysis Outcome Quality Initiative (NKF-DOQI) guidelines recommend that epoetin alfa should be administered by the subcutaneous route in hemodialysis patients. We determined whether hematocrit levels in hemodialysis patients differed by route of epoetin alfa administration after controlling for demographic factors and iron status. Data were available for 7,092 of the 7,658 patients randomly chosen for inclusion in the 1997 Health Care Financing Administration Core Indicators sample. Epoetin alfa was administered to 96% of the study cohort and was administered subcutaneously in 10% of patients. After controlling for hematocrit, patient characteristics, adequacy of dialysis, iron status, serum albumin, postdialysis weight, and duration of dialysis, the epoetin alfa dose by the intravenous route was 193.6 units/kg/wk (95% confidence interval, 189.5 to 197.8 units/kg/wk) compared with 167.4 units/kg/wk (95% confidence interval, 153.9 to 180.8 units/kg/wk) for the subcutaneous route (P < 0.001). The mean hematocrit for the subcutaneous route was 32.7% +/- 3.4% and for the intravenous route was 33.0% +/- 3.2% (P < 0.05). Factors independently associated with increased hematocrit included male gender, white race, older patient age, greater number of years on dialysis, higher serum albumin concentration, higher urea reduction ratio, and percent transferrin saturation (all P < 0.001). After controlling for patient factors and weekly epoetin alfa dose, there was no association between route of epoetin alfa administration and hematocrit level (P = 0.144). Patients receiving epoetin alfa by the subcutaneous route had comparable hematocrit values using a lower epoetin alfa dose than patients receiving epoetin alfa intravenously. These data support the NKF-DOQI recommendation that epoetin alfa be administered subcutaneously in long-term hemodialysis patients.

Age Factors↗
PubMedDate not supplied

Intravascular ultrasound imaging of blood: the effect of hematocrit and flow on backscatter.

This study evaluates two key parameters influencing the ultrasonic backscatter from blood--hematocrit and flow rate--at 30 MHz in an in vitro flow system. A range of hematocrits from 0 to 50% was studied at a constant flow rate; various flow rates between stagnation and physiologic levels were studied at a constant hematocrit. The relation between backscatter intensity and hematocrit was a convex function with a maximum between a hematocrit of 10% and 20%. In the flow rate studies, the blood backscatter intensity was a maximum at a flow rate of 0 and rapidly decreased at higher flow rates. These in vitro results suggest that blood backscatter intensity is minimally dependent on hematocrit in the physiologic range. However, a dramatic increase in backscatter intensity occurs with stagnant flow, presumably the result of red blood cell aggregation. Clinically, blood backscatter intensity may provide an index for risk of thrombus formation.

Animals↗
PubMed1999

Measurement of blood hematocrit inside the magnetically suspended centrifugal pump using an optical technique: application to assessment of pump flow.

To measure blood hematocrit inside the magnetically suspended centrifugal pump, we have performed both forward and backward light scattering measurements using a specially designed optical cell. In the forward scattering measurement, an optical fiber was used to guide the near infrared light at 780 nm into a 250 microns gap region, and the light that forward scattered toward a detector fiber was measured using a phototransistor. The light intensity decreased exponentially with an increase in the hematocrit to around 20%. The forward scattering method suffered from sensitivity at the hematocrit levels around 25-45% due to the diffusion effect. By making the optical path length larger than several millimeters, the sensitivity of the forward scattering method in terms of hematocrit change can be improved. In the back scattering method, however, better sensitivity in terms of hematocrit change from 0-50% was obtained. By making the optical fiber separation distance less than 1 mm, the system will measure the first order back scattering from the shallow layer while, by making the fiber separation distance larger than several millimeters, the system will primarily measure the diffuse reflectance from the deeper layer. Both approaches will yield sensitive optical intensity change in terms of the physiological hematocrit range.

Algorithms↗
PubMedDate not supplied

Rejection of prospective blood donors due to systematic errors in hematocrit measurement.

Following a change from earstick to fingerstick hemoglobin estimations, donor deferrals increased from 8.8% to 13.6%. Coincident with the change to fingersticks, hematocrit measurement with miniature centrifuges was begun as the reference method to verify donor rejection by the copper sulfate test. A study of 525 donors deferred for fingerstick hematocrits showed that 46.7% were deferred inappropriately as determined by venous hematocrit measurements. The difference between fingerstick and venous hematocrits persisted even after an intensive staff inservice on technique. In further studies, no significant difference was found between venous and fingerstick hematocrits measured on the same centrifuge, but there was a significant difference between measurements on the miniature centrifuges versus a standard laboratory microhematocrit centrifuge. This small error resulted in the loss of 3.8% of presenting donors during the study period. Hematocrit measurements have now been replaced by a fingerstick cyanmethemoglobin method.

Blood Donors↗