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PubMed2001

Diaspirin crosslinked hemoglobin enables extreme hemodilution beyond the critical hematocrit.

BACKGROUND: Normovolemic hemodilution is an effective strategy to limit perioperative homologous blood transfusions. The reduction of hematocrit related to hemodilution results in reduced arterial oxygen content, which initially is compensated for by an increase in cardiac output and oxygen extraction ratio. To increase the efficacy of hemodilution, a low hematocrit should be aimed for; however, this implies the risk of myocardial ischemia and tissue hypoxia. OBJECTIVE: To assess whether hemodilution can be extended to lower hematocrit values by the use of a hemoglobin-based artificial oxygen carrier solution. DESIGN: Prospective, randomized, controlled. SETTING: Animal laboratory of a university hospital. SUBJECTS: Twelve anesthetized, mechanically ventilated pigs. INTERVENTIONS: Isovolemic hemodilution was performed with either 10% diaspirin crosslinked hemoglobin (DCLHb Baxter Healthcare, Boulder, CO; n = 6) or 8% human albumin solution (HSA, oncotically matched to DCLHb, Baxter Healthcare; n = 6) to a hematocrit of 15%, 8%, 4%, 2%, and 1%. MEASUREMENTS AND MAIN RESULTS: In both groups, measurements were performed at baseline at the previously mentioned preset hematocrit values and at the onset of myocardial ischemia characterized by critical hematocrit (significant ST-segment depression >0.1 mV and/or arrhythmia). To determine peripheral tissue oxygenation and myocardial perfusion and function, the following variables were evaluated: total body oxygen transport variables, tissue oxygen partial pressure (tPo2, MDO-Electrode, Eschweiler Kiel, Germany) on the surface of the skeletal muscle, coronary perfusion pressure, left ventricular (LV) end-diastolic pressure, global and regional myocardial contractility (maximal change in pressure over time, LV segmental shortening, microsonometry method), LV myocardial blood flow (fluorescent microsphere technique), LV oxygen delivery, and the ratio between LV subendocardial and subepicardial myocardial perfusion. In the HSA group, critical hematocrit was found at 6.1 (1.8)% (hemoglobin, 2 g x dL(-1)), whereas all DCLHb-treated animals survived hemodilution until hematocrit 1.2 (0.2)% (hemoglobin, 4.7 g x dL(-1)) was achieved without signs of hemodynamic instability. Although arterial oxygen content was higher in the DCLHb group at 1.2% hematocrit than in the HSA group at critical hematocrit (i.e., hematocrit, 6.1%; hemoglobin, 2 g.dL-1) neither oxygen delivery and oxygen uptake nor median tPo2 and hypoxic tPo2 values on the skeletal muscle were different between groups. In contrast, subendocardial ischemia was absent in DCLHb-diluted animals until 1.2% hematocrit was achieved. This was attributable to a higher coronary perfusion pressure (65 (22) mm Hg vs. 19 (8) mm Hg; p <.05), higher subendocardial perfusion (4.1 (2.6) mL.min-1.g-1 vs. 1.2 (0.4) mL x min(-1) x g(-1)), and subendocardial oxygen delivery (5.7 (2) mL x min(-1) x g(-1), p <.05) in DCLHb-diluted animals, resulting in superior myocardial contractility reflected by maximal change in pressure over time (3829 (1914) vs. 1678 (730); p <.05) and higher regional myocardial contractility (11 (8)% vs. 6 (2)%; p <.05). An increased LV end-diastolic pressure reflected LV myocardial pump failure in HSA-diluted animals but was unchanged in DCLHb-diluted animals. In the DCLHb group, systemic vascular resistance index remained at baseline values throughout the protocol, whereas coronary vascular resistance decreased. In contrast, both variables decreased in HSA-diluted animals. CONCLUSION: DCLHb as a diluent allowed for hemodilution beyond the hematocrit value, determined "critical" after hemodilution with HSA (6.1% (1.8)%). Even at 1.2% hematocrit (hemoglobin, 4.7 g x dL(-1)) myocardial perfusion and function were maintained, although at the expense of peripheral tissue oxygenation. This discrepancy in regional oxygenation might be caused by a redistribution of blood flow favoring the heart, which is related to a disproportionate decrease of coronary vascular resistance index during hemodilution with DCLHb.

Animals↗
PubMed2003

[Hematocrit as an indicator for coronary intervention in patients with acute myocardial infarction].

OBJECTIVES: Primary coronary intervention in patients with acute myocardial infarction complicated by persistent massive intracoronary thrombus is frequently difficult. Higher incidence of thrombus formation is associated with high hematocrit score. This study investigated the relationship between high hematocrit score and primary coronary intervention in patients with acute myocardial infarction. METHODS: Forty-five patients with acute myocardial infarction were divided into two groups according to hematocrit score on admission, the high hematocrit group (hematocrit > or = 48%, n = 8) and the low hematocrit group (hematocrit < 48%, n = 37). Time period required for coronary intervention (intervention time), number of balloon inflations, presence of persistent massive intracoronary thrombus, need for adjunctive intracoronary thrombolysis, need for intraaortic balloon pumping and achieved rate of Thrombolysis in Myocardial Infarction (TIMI) 3 were compared between the two groups. The relationships between hematocrit and intervention time or number of balloon inflations were also investigated. RESULTS: Intervention time (2.7 +/- 1.4 vs 1.4 +/- 0.7 hr, p = 0.0003), number of balloon inflations (12 +/- 9 vs 3 +/- 2 times, p = 0.0001), presence of persistent massive intracoronary thrombus (100% vs 5%, p < 0.0001), intracoronary thrombolysis (63% vs 3%, p = 0.0003), and intraaortic balloon pumping (63% vs 14%, p = 0.0092) were significantly higher in the high hematocrit group. However, the rate of TIMI 3 (25% vs 95%, p < 0.0001) was significantly lower in the high hematocrit group. The relationships between hematocrit and intervention time (r2 = 0.16, p = 0.0033), and hematocrit and number of balloon inflations (r2 = 0.19, p = 0.0015) showed positive correlations. CONCLUSIONS: Primary coronary intervention for patients with acute myocardial infarction showing high hematocrit score on admission is likely to be difficult due to the presence of persistent massive intracoronary thrombus. Therefore, coronary interventional strategy for intracoronary thrombolysis in patients with acute myocardial infarction should include measurement of hematocrit score.

Aged↗
PubMed1997

Minimum hematocrit for normothermic cardiopulmonary bypass in dogs.

BACKGROUND: The purpose of this study was to determine the minimum hematocrit supporting cerebral oxygenation during normothermic cardiopulmonary bypass (CPB) in dogs. The effect of hemodilution on cerebral blood flow (CBF), cerebral metabolic rate (CMRO2), and cerebral oxygen delivery (CDO2) was determined over a range of hematocrits. METHODS AND RESULTS: Measurements were obtained during 37.5 degrees C CPB with progressive normovolemic hemodilution (hematocrit 0.39 to 0.9) in eight anesthetized animals. Dextran 70 (6%) was used as a diluent. CBF was measured using the sagittal sinus outflow technique. CMRO2 and CDO2 were calculated using standard formula. Hemodilution was associated with a reciprocal rise in CBF. CBF at a hematocrit of 0.09 was 240% of the CBF when the hematocrit was 0.39. Increases in CBF compensated for decreased arterial oxygen content and CDO2 was maintained to a mean hematocrit of 0.14+/-0.02. At a hematocrit of 0.09+/-0.02, CDO2 and CMRO2 declined. Intracranial pressure remained stable throughout. Thus, the critical hematocrit for brain (the hematocrit at which metabolism becomes delivery-dependent) was between 0.09 and 0.14 during normothermic CPB in dogs. CONCLUSIONS: This is the first systematic attempt to determine the critical hematocrit supporting cerebral oxygenation during warm CPB. The curve describing the relationship between hematocrit and cerebral oxygen balance has a broad plateau and a genu near a hematocrit value of 0.15. While we do not advocate hemodilution to a hematocrit of 15% during "warm" CPB, these data provide a physiological foundation for our hemodilution practice and offer an explanation why low hematocrits are tolerated in certain patient populations.

Animals↗
PubMedDate not supplied

Diagnostic value of arterial hematocrits in neonatal polycythemia.

In order to study the correlation among arterial, capillary and venous hematocrits, sixty newborn babies delivered in our hospital were chosen after receiving their parents' consents for hematocrits study within their first eight hours of life. The venous hematocrits of them (59.77 +/- 14.15%) correlate with arterial hematocrits (57.84 +/- 14.36%) very well (r = 0.95, p less than 0.001). Whereas, the venous and arterial hematocrits correlate with capillary hematocrits (66.63 +/- 15.56%) also significantly (r = 0.72, p less than 0.001 for both). Arterial hematocrits of more than 62% is proportionate to venous hematocrits of 64% and above. The relationship between arterial and venous hematocrits does not change even after we divide the subjects into those venous hematocrits above 64% and those below 64%. Furthermore, the capillary hematocrits of above 70% can be used as the criteria of polycythemia in the neonatal screening. If the capillary hematocrit is above 70%, then venous hematocrit should be checked for the confirmation of polycythemia.

Arteries↗
PubMed1988

Association of maternal hematocrit with premature labor.

An examination of the association of maternal hematocrit with the occurrence of premature birth revealed a continuous relationship between these two factors with an increasing rate of prematurity occurring with decreasing maternal hematocrit. The lowest risk of premature birth was found when maternal hematocrit was between 41% and 44%. Statistically increases in prematurity were noted at all hematocrit levels of less than or equal to 38%. A woman with a hematocrit of 37% had twice the risk of having a premature birth as a woman whose hematocrit was between 41% and 44% (p less than 0.01). In a logistic regression analysis with premature birth as the dependent variable and hematocrit as the only predictor variable, it was noted that decreasing the hematocrit by a single point was associated with a 24% increase in the risk of prematurity (odds ratio = 1.24) while a five-point decrease in hematocrit was associated with a tripling in the risk of prematurity (odds ratio = 2.98). In a multivariable logistic regression analysis hematocrit was noted to explain more of the variation in prematurity than any of the other risk factors included in the model. An investigation of this association in specific groups at high risk of having premature births revealed that 46% of the increased risk of prematurity in black women and 49% of the increased risk of prematurity in women receiving welfare was related to hematocrit or some factor associated with hematocrit.

Adult↗
PubMed1995

Use of hematocrit changes as an indicator of blood loss in adult trauma patients who receive intravenous fluids.

OBJECTIVES: To validate the use of changes in hematocrit as an indicator of blood loss in adult trauma patients receiving IV fluids and to identify parameters of hematocrit changes that may differentiate between patients with and without hemorrhage. DESIGN: A descriptive, retrospective chart review. SAMPLE/SETTING: A convenience sample of 90 adult trauma patients at an urban level I trauma center emergency department who received IV fluids for whom hematocrit measurements were available. METHODS: Records were reviewed for patients with documented hematocrit readings before and after receiving 2 L of IV fluid, noting the time between hematocrit measurements. Patients were divided into groups: Group 1 consisted of 74 subjects with no hemorrhaging (< 500 ml blood loss); group 2 consisted of 16 subjects in whom hemorrhage occurred (> 500 ml of blood loss). RESULTS: In group 1 (nonhemorrhage group), the mean hematocrit change was -5.3%; in group 2 (hemorrhage group) the hematocrit change was -8.3%. The findings showed a statistically significant difference (p < 0.05) between the groups for both the repeat hematocrit scores and the change in hematocrit scores. On the basis of a hematocrit decrease of 5% or less, 97% of the patients would have been correctly assigned to the nonhemorrhage group. CONCLUSION: Hematocrit determinations are a valid indicator of blood loss in trauma patients receiving IV therapy. The use of repeat hematocrit readings for clinicians trying to differentiate those with significant blood loss and the effects of IV fluid administration remains limited.

Adult↗
PubMed1998

Optimal hematocrit in patients on dialysis therapy.

Although recombinant erythropoietin (rHuEPO) has been available for use in dialysis patients since 1989, there is little information available on the optimal hematocrit to target in this patient population. The optimal hematocrit is the value that supplies the amount of oxygen to specific tissues and organs that maximizes the efficiency and effectiveness of organ function. Very few prospective studies have been published on this issue, and the retrospective review of clinical practice data is inadequate because of the small number of patients maintained with a hematocrit greater than 36%. Several recent abstracts shed light on this issue, however, and additional publications are likely soon. The available data indicate that brain and cognitive function are better at a normal hematocrit compared with the currently achieved values (31% to 32%). In addition, quality of life and exercise capacity improve as hematocrit is normalized. The AMGEN Normal Hematocrit Cardiac Trial (NHCT), studying the effects of normalizing the hematocrit in dialysis patients with heart disease, does not clearly show the benefit or harm of a normal hematocrit in this patient setting, although within both study groups (hematocrit of 30% v 42%), survival was better in patients with higher hematocrits. The challenge for clinicians is to determine the optimal hematocrit for a specific patient that maximizes organ function but does not cause adverse effects. Over the next few years, several studies should be published based on current abstracts, and if the results remain as reported, the evidence will be accumulating that normal hematocrits are beneficial in end-stage renal disease (ESRD) patients.

Cardiovascular System↗
PubMed1992

The effect of acute and chronic hematocrit changes on cardiovascular hemodynamics in spontaneously hypertensive rats.

Heparin given over a long term by a subcutaneous route consistently lowers blood pressure in the hypertensive rat models. The decrease in blood pressure is accompanied by a parallel decrease in hematocrit suggesting a causal relationship between hematocrit and blood pressure. The aim of this study was to define the relationships between acute and chronic hematocrit changes and blood pressure in the normotensive and hypertensive states. Normotensive Wistar (NWR) and spontaneously hypertensive (SHR) rats were used. Hematocrit was decreased acutely by blood-letting, and chronically by treatment with either heparin (H) or phenylhydrazine (P) for 4 weeks. Acute and chronic hematocrit increase was accomplished by packed cells transfusion. Systolic blood pressure was measured weekly; and at the end of the experimental period, plasma volume, cardiac output, and mean arterial pressure were obtained. Acute hematocrit decrease or increase (hematocrit ranging from 25 to 65%) did not affect blood pressure in either strain of rats; whereas chronic hematocrit changes (hematocrit ranging from 35 to 61%) significantly affected blood pressure only in SHR. Thus, chronic hematocrit decrease induced by H or P resulted in a significant fall in blood pressure compared to control (201 +/- 3 v 175 +/- 4, 167 +/- 4 mm Hg, respectively; P < .05). Conversely, a chronic hematocrit increase resulted in a significant rise in blood pressure (201 +/- 3 v 219 +/- 4 mm Hg; P < .05). Similar hematocrit changes produced in NWR, as in SHR, did not affect blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Microvessel hematocrit: measurement and implications for capillary oxygen transport.

Microvascular preparations of the hamster cheek pouch and cremaster muscle were used to establish the relationship among three measures of red cell distribution: 1) the systemic hematocrit defined as the volume percentage of red cells sampled from a toe clip; 2) the tube hematocrit defined as the instantaneous volume fraction of red cells in a microvessel segment of measured length and diameter; and 3) the discharge hematocrit defined as the volume percentage of red cells that flowed into micropipettes inserted into microvessels. The results show the tube hematocrit is low and highly variable in the presence of a nearly constant systemic hematocrit. The discharge hematocrit, in contrast, consistently approximated systemic values in blood taken from arterioles or venules with diameters of 6-98 micron. Indeed, the mean ratio of the discharge to the systemic hematocrit did not differ from unity (P greater than 0.25). The observed similarity between the discharge and systemic hematocrit indicates that red cells are distributed uniformly across capillary networks. Differences between the absolute value and variance of the tube hematocrit compared with the discharge hematocrit imply that the anatomical volume of a microvessel can differ from the volume available to cells and plasma within a microvessel. Thus moment-to-moment variation in the tube hematocrit or capillary red cell spacing may be indicative of a change in the effective capillary flow cross section and not solely on the inflow hematocrit.

Animals↗
PubMed1982

Optimal hematocrit for oxygenation of canine intestine.

To determine the direct effects of hematocrit on intestinal oxygen consumption and to determine whether an optimal hematocrit exists for intestinal oxygenation, we perfused isolated canine gut loops at a constant pressure (120 mm Hg) and varied hematocrit from 80% to 10%. As hematocrit fell, blood flow rose while arterial oxygen content fell. The regression of blood flow on hematocrit was linear, whereas the relationship between oxygen uptake and hematocrit was parabolic, showing a maximal oxygen uptake at an hematocrit of 48.7%. To determine whether the optimal hematocrit for intestinal oxygenation could be altered by changes in vasomotor tone, we performed two other series of experiments. Raising perfusion pressure to 180 mm Hg did not significantly alter the optimal hematocrit for oxygen uptake. However, when we increased the oxygen demands of the gut by placing transportable solutes within the intestinal lumen, the optimal hematocrit for oxygen uptake increased markedly. We conclude that the optimal hematocrit for intestinal oxygenation is slightly higher than the normal range, a finding that could possibly be explained by the plasma skimming known to occur in the intestinal mucosa. Our experimental design and method of data analysis could be used to determine the optimal hematocrit in other organs.

Animals↗
PubMed1991

The effect of hematocrit alterations on cerebral vascular CO2 reactivity in newborn baboons.

To evaluate whether baseline hematocrit affects cerebral vascular reactivity to CO2, we studied the cerebral blood flow velocity in the internal carotid artery of newborn baboons, using a pulsed Doppler technique with direct imaging. Velocity responses to varying arterial CO2 tension (PaCO2) levels were first tested under baseline hematocrit (mean +/- SD, 35.9 +/- 4.7%), after hemodilution (hematocrit 20.3 +/- 2.7%), and after hemoconcentration (hematocrit 52.7 +/- 5.2%). The data were analyzed using multiple regression models, in which blood flow velocity values were the dependent variables, and PaCO2, hematocrit, and their interaction terms (product) were the independent variables. Models for the maximum systolic velocity, time-averaged mean velocity, and the end-diastolic velocity revealed a highly significant PaCO2 effect; with each mm Hg PaCO2 increase, the velocities increased between 2.9 and 3.6% (21.8-27% per 1 kPa). PaCO2 and hematocrit interaction terms were also highly significant and inversely related to velocity (negative slopes) in the maximum systolic velocity and time-averaged mean velocity models, suggesting that when the hematocrit is high, the PaCO2-induced increase in flow velocity would be attenuated, and when the hematocrit is low, such a response would be accentuated. The hematocrit effect on PaCO2 reactivity was maximal on maximum systolic velocity and least on end-diastolic velocity. Systolic velocity acceleration slope was significantly reduced when the hematocrit was high, and increased when the hematocrit was low. Based on these findings, we conclude that hematocrit is an important variable affecting the rate of kinetic energy change in the large vessels, thereby influencing cerebral vascular PaCO2 reactivity as assessed in Doppler studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Blood viscosity and optimal hematocrit in preterm and full-term neonates in 50- to 500-micrometer tubes.

Blood viscosity is an important determinant of blood flow resistance. Because a substantial part of flow resistance arises in small arteries and arterioles with diameters of 100 microns and less, rheologic properties of blood from preterm infants (24 to 36 wk of gestation), full-term neonates, and adults were measured in glass tubes with diameters of 50, 100, and 500 microns for a wide range of adjusted feed hematocrits (0.15-0.70). At each of the feed hematocrits, blood viscosity decreased when going from a 500-microns tube to a 50-microns tube. The viscosity reduction increased with increasing hematocrit. Moreover, the viscosity reduction was more pronounced in the neonates than in the adults. At a hematocrit of 0.70, the viscosity reduction averaged 56% in preterm infants, 50% in full-term neonates, and 39% in adults (p less than 0.005). However, the viscosity reductions at a hematocrit of 0.30 were only 35, 29, and 19%, respectively (p less than 0.05). In all four groups, blood viscosity increased exponentially with increasing hematocrit. The steepness of the hematocrit-viscosity curves decreased with decreasing tube diameter and with decreasing maturity of the infants. Erythrocyte transport efficiency (hematocrit/blood viscosity) was calculated to estimate the optimal hematocrit (i.e. hematocrit with maximum erythrocyte transport). In 500-microns tubes, the optimal hematocrit was about 0.40 in all of the groups. In 100-microns tubes, the optimal hematocrit was 0.44 +/- 0.05 in the adults and 0.52 +/- 0.04 in the neonates (p less than 0.05). In 50-microns tubes, the optimal hematocrit was 0.51 +/- 0.04 in adults and 0.60 +/- 0.05 in the neonates.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

The paradox of hematocrit in exercise physiology: which is the "normal" range from an hemorheologist's viewpoint?

The paradox of hematocrit in exercise physiology is that artificially increasing it by autotransfusion or erythropoietin doping improves VO2 max and performance, while in normal conditions there is a strong negative correlation between hematocrit and fitness, due to a training-induced "autohemodilution". We aimed at investigating: (a) which is the physiological range of hematocrit in highly trained professional footballers; (b) what are the characteristics of athletes with high vs low hematocrit? We determined in 77 healthy male footballers the physiological range (mean +/- sd) of hematocrit: 42.3+/-2.74, (range -2sigma/+2sigma = 36.8-47.8%) thus defining boundaries of quintiles of distribution for this parameter: 40, 41.6, 42.9, 44.6. In another sample of 42 male footballers we compared three groups: lowest quintile (n = 8), highest quintile (n = 5) and the three middle quintiles considered together (n = 29). Athletes in the lowest quintile compared to those in the four other quintiles had a lower value of blood viscosity (-8%, p < 0.01) but this difference disappeared after correction for hematocrit. These subjects with low hematocrit had also higher values of the following parameters: aerobic working capacity (p < 0.01); isometric adductor strength (p = 0.02); crossover point of carbohydrate oxidation (70% carbohydrates/30% lipids) (p < 0.05); insulin like growth factor binding protein 1 (p < 0.0001). Athletes in the highest quintile had higher red cell aggregability (Myrenne index "M1" 8.45+/-0.38 vs 6.82+/-0.62, p < 0.04) and a higher disaggregability threshold gammaD (72.6+/-22.63 vs 44.49+/-1.37, p < 0.01) and a lower percentage of water in fat-free mass (p < 0.02). On the whole sample hematocrit was negatively correlated with aerobic working capacity (W170 r = -0.329, p = 0.007; Wmax (% of expected value) r = -0.552, p = 0.008; VO2 max (% of expected value) r = -0.543, p = 0.009) and with ferritin (r = -0.33, p = 0.031), and positively correlated with the overtraining score (r = 0.352, p = 0.019) which was in turn negatively correlated with ferritin r = -0.312, p = 0.02). Besides, hematocrit behaves as a major determinant of blood viscosity (correlation with blood viscosity r = 0.997, p < 10(-7)) and erythrocyte disaggregability gammaD (r = 0.384, p = 0.03), but the hematocrit/viscosity ratio (h/eta index of O2 delivery) remains maintained almost constant over the range of values studied. These results show that (a) physiological values of hematocrit in these athletes are comprised between 36 and 48%; (b) "low" hematocrit (<40%) was associated with a higher aerobic capacity; (c) subjects with the higher hematocrits (>44.6%) were frequently overtrained and/or iron-deficient, and their blood viscosity (and red cell disaggregability) tended to be increased.

Adaptation, Physiological↗
PubMedDate not supplied

Admission hematocrit: a simple, useful and early predictor of severe pancreatitis.

Existing predictor systems of severe pancreatitis are cumbersome and can require up to 48 hr to complete. This study aimed to determine whether useful likelihood ratios exist for the prediction of severe pancreatitis, corresponding to various ranges of admission hematocrit. A retrospective cohort of 200 patients admitted with acute pancreatitis was identified. Likelihood ratios were calculated for a priori defined hematocrit ranges. Using multivariate logistic regression, initial hematocrit was evaluated as a predictor of severe pancreatitis as defined a priori by local and/or systemic complications (Atlanta criteria, 1992). Planned subgroup analysis was performed on those with a hematocrit >50%, stratified by 24-hr hematocrit. Fourteen patients (7%) developed severe pancreatitis. Likelihood ratios were 0.45, 0.70, and 7.5 for hematocrit ranges of < or =45, 45.1-49.9, and > or =50%, respectively. Hematocrit (as increases by 5%) was a significant predictor of severe pancreatitis (odds ratio [OR] = 2.8; P = 0.001), length of stay (P < 0.0001), necrosis (OR = 3.9; P = 0.001), and need for intensive care (OR 4.5; P = 0.002). The negative predictive value of the lowest range and positive predictive value of the highest range were 97% (95% CI: 92-99%) and 37% (16-62%), respectively. Lack of normalization of hematocrit by 24 hr did not predict severe pancreatitis. Initial hematocrit appears to be an early, simple, and useful predictor of severe pancreatitis. A normal 24-hr hematocrit does not appear to alter the prediction made by the initial hematocrit.

Acute Disease↗
PubMed2003

Adverse effects of low hematocrit during cardiopulmonary bypass in the adult: should current practice be changed?

BACKGROUND: Hemodilutional anemia during cardiopulmonary bypass can lead to inadequate oxygen delivery and, consequently, to ischemic organ injury. In adult bypass, the nadir hematocrit can vary widely with body size and prebypass hematocrit variations, yet its effects on perioperative organ dysfunction and patient outcomes remain largely unknown. METHODS: To elucidate these effects, we retrospectively analyzed operative results and resource utilization data from 5000 consecutive cardiac operations with cardiopulmonary bypass performed on adults (1994 to 2000). Rolling decile groups (500 patients each; 75% overlapping) of increasing lowest hematocrit values were used to characterize hemodilution-outcome relationships. Intermediate-term (0 to 6 years) survival was assessed for coronary artery bypass patients (n = 3800) via Kaplan-Meier analysis in quintile subgroups based on lowest hematocrit. Multivariate logistic regression (operative mortality and morbidity) and Cox proportional hazard model (0- to 6-year mortality) analyses were used to determine independent predictors of poor outcomes. RESULTS: Stroke, myocardial infarction, low cardiac output, cardiac arrest, renal failure, prolonged ventilation, pulmonary edema, reoperation due to bleeding, sepsis, and multiorgan failure were all significantly and systematically increased as lowest hematocrit value decreased below 22%. Consequently, intensive care requirements, hospital stays, operative costs, and operative deaths were also significantly greater as a function of hemodilution severity. Longer-term survival was improved systematically for increasing lowest hematocrit coronary artery bypass grafting quintiles; for example, 6-year survival was 80.5% and 92.3% for quintiles I (lowest hematocrit = 16.1%) and V (lowest hematocrit = 27.5%). The continuous variable lowest hematocrit was an independent predictor of (1) operative mortality, (2) prolonged cardiovascular intensive case (>2 days) and postoperative hospital (>8 days) stays, and (3) worse 0- to 6-year survival. CONCLUSIONS: Increased hemodilution severity during cardiopulmonary bypass was associated with worse perioperative vital organ dysfunction/morbidity and increased resource use, as well as greater short- and intermediate-term mortality. We speculate that these results derive from inadequate oxygen delivery causing ischemic and/or inflammatory vital organ injury, as recently demonstrated intravitally in cerebral tissues. Although this analysis of a large observational study offers evidence linking low on-pump hematocrit values to these adverse outcomes, prospective randomized trials are needed (1) to establish whether a causal effect of hemodilution on poor outcomes actually exists and (2) to test the potential efficacy of maintaining on-pump hematocrit above 22% for improving outcomes of cardiopulmonary bypass.

Aged↗
PubMed1998

The effects of normal as compared with low hematocrit values in patients with cardiac disease who are receiving hemodialysis and epoetin.

BACKGROUND: In patients with end-stage renal disease, anemia develops as a result of erythropoietin deficiency, and recombinant human erythropoietin (epoetin) is prescribed to correct the anemia partially. We examined the risks and benefits of normalizing the hematocrit in patients with cardiac disease who were undergoing hemodialysis. METHODS: We studied 1233 patients with clinical evidence of congestive heart failure or ischemic heart disease who were undergoing hemodialysis: 618 patients were assigned to receive increasing doses of epoetin to achieve and maintain a hematocrit of 42 percent, and 615 were assigned to receive doses of epoetin sufficient to maintain a hematocrit of 30 percent throughout the study. The median duration of treatment was 14 months. The primary end point was the length of time to death or a first nonfatal myocardial infarction. RESULTS: After 29 months, there were 183 deaths and 19 first nonfatal myocardial infarctions among the patients in the normal-hematocrit group and 150 deaths and 14 nonfatal myocardial infarctions among those in the low-hematocrit group (risk ratio for the normal-hematocrit group as compared with the low-hematocrit group, 1.3; 95 percent confidence interval, 0.9 to 1.9). Although the difference in event-free survival between the two groups did not reach the prespecified statistical stopping boundary, the study was halted. The causes of death in the two groups were similar. The mortality rates decreased with increasing hematocrit values in both groups. The patients in the normal-hematocrit group had a decline in the adequacy of dialysis and received intravenous iron dextran more often than those in the low-hematocrit group. CONCLUSIONS: In patients with clinically evident congestive heart failure or ischemic heart disease who are receiving hemodialysis, administration of epoetin to raise their hematocrit to 42 percent is not recommended.

Aged↗
PubMed1989

Optimal hematocrit for canine gastric oxygenation.

To determine whether an optimal hematocrit exists at which gastric tissue is maximally oxygenated, chambered segments of resting canine stomach were perfused at a constant pressure while hematocrit was decreased in steps from 60 to 10%. The two groups of animals used were a control group and a second group given pentagastrin to elevate metabolic activity. Total blood flow was inversely related to hematocrit in both the control and pentagastrin-treated animals, and arteriovenous oxygen difference was directly related to hematocrit. Consequently, the relationship between gastric oxygen consumption and hematocrit was parabolic in both groups. Therefore, the oxygen uptake vs. hematocrit data from each experiment were fit to a quadratic equation that was used to calculate the maximal oxygen uptake and the optimal hematocrit for each preparation. Both the maximum oxygen uptake and the optimal hematocrit in the pentagastrin-treated group (2.1 +/- 0.4 ml.min-1.100 g-1 and 45.7 +/- 1.4%, respectively) were significantly greater than in the control group (1.5 +/- 0.4 ml.min-1.100 g-1 and 38.2 +/- 0.7%, respectively). We conclude that an optimal hematocrit exists for the oxygenation of gastric tissue and that it is within the normal hematocrit range under resting conditions. However, the optimal hematocrit is slightly higher than normal during periods of increased metabolic activity.

Animals↗
PubMed2001

Death, hospitalization, and economic associations among incident hemodialysis patients with hematocrit values of 36 to 39%.

Anemia treatment with epoetin has led to dramatic increases in hematocrit levels since 1989. Studies have demonstrated that morbidity and mortality rates are lower when hematocrit values are within the Disease Outcomes Quality Initiative (DOQI) target range (33 to 36%). Recently, clinical studies demonstrated that patients without cardiovascular disease exhibited lower morbidity rates and improved cognitive function with hematocrit values of >36%. One prospective trial, in contrast, demonstrated that normal hematocrit values among patients with cardiac disease were associated with higher mortality rates. These conflicting results have led to concerns regarding the risks and benefits associated with hematocrit values between 36 and 42%. To address these concerns, a recent cohort of 1996 to 1998 incident hemodialysis patients was studied, with assessments of the risks of death and hospitalization and the medical costs associated with hematocrit values of >36%. Patients survived at least 9 mo after dialysis initiation, and comorbidity, disease severity, and hematocrit levels were determined for months 4 to 9. Patients were grouped on the basis of hematocrit values, i.e., <30, 30 to <33, 33 to <36, 36 to <39, or > or =39%, with 1 yr of follow-up monitoring. A Cox regression model was used to evaluate all-cause and cause-specific mortality and hospitalization rates. The economic evaluations included analyses with Medicare Parts A and B allowable expenditures as the dependent variable and the same clinical characteristics as independent variables. For patients with hematocrit values of > or =36%, mortality rates were not different, hospitalization rates were 16 to 22% lower, and expenditures were 8.3 to 8.5% less, compared with patients with hematocrit values of 33 to <36%. These observations do not demonstrate causality. Additional long-term studies are needed to assess the risks of higher hematocrit values among all patients and patients with cardiovascular disease.

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