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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 48 individuals (age 1 day to 13 years) with congenital heart disease, blood oxygen transport function was studied in order to evaluate adaptive changes in shunt hypoxemia and to investigate the in vivo regulation of erythrocyte 2, 3-diphosphoglycerate concentration (RBC 2, 3-DPG) in the presence of fetal hemoglobin (HbF). Arterial pO2 and oxygen content, oxygen capacity, acid base status, oxygen affinity, HbF fraction, plasma pH, red cell pH, and RBC 2, 3-DPG were determined. During the first 50 days of life values of standard P50 (stdP50) (37, pH 7.4), actual in vivo P50 (actP50), RBC 2, 3-DPG, O2 capacity, arterial plasma pH, and red cell pH were scattered around the normal range, although tending to low values for stdP50 and arterial plasma pH and to high values for O2 capacity. After the third month, stdP50 actP50, RBC 2, 3-DPG, O2 capacity, and red cell pH were found to be elevated. Plasma pH and actP50 were scattered around the normal range (Figs. 1 and 2). Intraerythrocytic pH in hypoxemic infants was increased compared with normal children when related to plasma pH (Fig. 3). A close to normal intraerythrocytic pH was therefore found in the hypoxemic infants with low plasma pH, and an increased intraerythrocytic pH in the hypoxemic children with normal plasma pH (Fig. 1). A significant negative correlation exists between erythrocyte H+ ion and 2, 3-DPG concentration (Fig. 5); regression constants derived from data at high (mean 47%) and low (mean 9%) fractions of HbF are not significantly different (Regression Equations 8 and 11 in Table 1). Thus, the known difference in 2, 3-DPG binding to fetal or adult deoxyhemoglobin does not measurably influence the erythrocyte 2, 3-DPG concentration, indicating that in vivo the 2, 3-DPG synthesis in hypoxia is virtually regulated by the erythrocyte pH, which in turn is determined by plasma pH and the oxygenation state of hemoglobin.
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PMID:Oxygen transport in congenital heart disease: influence of fetal hemoglobin, red cell pH, and 2,3-diphosphoglycerate. 0 99

The acute effects of an injection of contrast material (Renovist) on intraerythrocytic and extracellular pH was studied at cardiac catheterization in 72 patients with congenital heart disease. A decrease in mean extracellular (plasma) pH (7.444 plus or minus .006 to 7.419 plus or minus 0.009) and an increase in mean intraerythrocytic pH (7.204 plus or minus .005 to 7.232 plus or minus .006) were observed within minutes after injection (p smaller than .01). In 17/72 patients, simultaneous measurements of oxygen affinity for hemoglobin as characterized by P50 (oxygen tension at 50% O-2 saturation) corrected to in vivo arterial pH decreased from a mean of 26.4 to 25.2 mm Hg (p smaller than .01). It is postulated that the acute increase in intraerythrocyte pH and increased affinity of hemoglobin for oxygen are due to a decrease in intracellular hydrogen ion concentration induced by the increase in plasma osmolality with subsequent shift of hemoglobin oxygen equilibrium via the Bohr effect.
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PMID:The relationship between angiography, intraerythrocytic pH and hemoglobin oxygen equilibrium. 23 27

The results of treatment of iron deficiency anemia in 217 children and infants (aged 8 months to 12 years) with ferrosulfate serin complex are demonstrated: 208 children with simple iron deficiency anemia with hemoglobin 9.1 g/100 ml before treatment had in the first 4 weeks a daily increase of 0.082 g/10000 ml hemoglobin; in 3 children with severe anemia of chronic blood loss the daily increase was 0.21 mg/100 ml and in 6 children with hypoxic polycythemia with congenital heart disease and so called latent iron deficiency anemia the increse was 0.16 g/100 ml. Through the better absorption of this serin-ferrosulfate complex the required dosis is only 3 mg/kg/d. The benefit of this small dosis is the low rate of side effects.
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PMID:[Treatment of iron deficiency anemia with ferrosulfate serin komplex (author's transl)]. 62 90

Previous investigations in our unit indicated that acute cardiogenic pulmonary edema is associated not only with an increase in left ventricular end-diastolic pressure and pulmonary arterial wedge pressure but also with a relative increase in colloid osmotic (oncotic) pressure and peripheral hemoglobin concentration. This combination of changes suggested that acute congestive heart failure with pulmonary edema, unlike chronic congestive heart failure, is associated with a contraction of intravascular blood volume. In this study, plasma volume changes were measured before and during the treatment of acute cardiogenic pulmonary edema in 14 patients with arteriosclerotic heart disease. The plasma volume measurement in all 14 patients before the initiation of treatment was either normal or decreased. After treatment with the alpha adrenergic blocking agent phentolamine, the plasma volume increased rather than decreased when measured 4 and 12 hours after the initiation of treatment. During this time colloid osmotic pressure and peripheral hemoglobin concentration progressively decreased. These findings suggest that acute cardiogenic pulmonary edema is associated with the extravasation of large quantities of plasma water from the intravascular compartment into the interstitial compartment and contraction of the intravascular plasma volume. The treatment of acute cardiogenic pulmonary edema is associated with the return of hypo-oncotic fluid from the interstitial compartment back into the intravascular compartment with expansion of plasma volume and reduction of colloid osmotic pressure and hemoglobin concentration.
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PMID:Effect of afterload reduction on plasma volume during acute heart failure. 70 95

Mechanical circulatory support was accomplished in 20 calves (mean, 140 days) and in 5 patients following operation for acquired heart disease (range, 1 hour to 8 days) employing a pneumatically actuated xenograft-valved assist pump interposed between the left ventricular apex and aorta. Following pump implantation in calves, hematocrit and platelets decreased transiently and returned to normal within 14 days. Plasma hemoglobin and erythrocyte mechanical fragility values were elevated for 48 hours. Platelet survival was slightly reduced, but erythrocyte survival values were similar to controls. In patients who received assist pumps, plasma hemoglobin and erythrocyte mechanical fragility were transiently elevated, but rapidly decreased to normal. Thrombocytopenia occurred only in the presence of bleeding and renal failure requiring hemodialysis. Pump flow of the left ventricular assist device was maintained above 2.0 L/min/m2 despite serious arrhythmias. Postmortem examination revealed no evidence of thromboemboli in the clinical patients although anticoagulant agents were not administered.
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PMID:An appraisal of blood trauma and blood-prosthetic interface during left ventricular bypass in the calf and humans. 75 57

Infants with bounding arterial pulses frequently show a visible or palpable arterial pulsation of the fontanel. This simple clinical sign is neither described in the textbooks nor mentioned in connection with congenital heart diseases (CHD). To investigate its significance 501 infants were examined 178(35,5%) showed an arterial pulse of the fontanel. Out of 421 with no sign of cardiovascular malformation or disease on physical examination, 111(26,4%) had a fontanal pulse (f.p.). Out of 80 infants with CHD, 67(83,8%) exhibited a fontanel pulse (f.p.), while only 13(16,2%) did not. All infants with CHD had an ECG and biplane chest x-rays taken. In some of them also cardiac catheterization and heart or vessel surgery were performed. 23(79,3%) of 29 infants with PDA and eight of twelve with a VSD had a f.p.. Since other cardiac diagnoses were encountered less frequently, their relation to the presence or absence of f.p. could not be evaluated. From the variety of diagnoses, however, it became obvious that not only lesions with "early aortic runoff" may be accompanied by a f.p. Other clinical features like blood pressure, hemoglobin content and body temperature were discussed as possible causes of f.p.. Only the first mentioned, a high systemic pressure, was frequently accompanied by f.p.. Since the percentage of infants with f.p. and CHD was relatively high (37,6%) this clinical sign is considered to be of some value in the early detection of heart disease in infancy.
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PMID:[Arterial fontanel pulsation]. 83 92

Simultaneous red blood cell (RBC) and plasma volume determinations were obtained in 16 patients with cystic fibrosis (CF) and moderately severe pulmonary involvement. Hypervolemia with an increase in both RBC and plasma volumes was observed. Changes in blood volume were marked when values were indexed by weight but less significant when indexed by height. Decreasing systemic arterial oxygen saturation was associated with a progressive increase in RBC mass, hematocrit value, and hemoglobin level and a decrease in mean corpuscular hemoglobin concentration. RBC and total blood volumes were highest in patients with cor pulmonale and congestive heart failure. However, the compensatory polycythemic response in patients with CF was inadequate when compared with the response to hypoxemia in patients with cyanotic congenital heart disease. The insufficient oxygen-carrying capacity may compromise tissue oxygen delivery and necessitate treatment.
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PMID:Blood volume changes in patients with cystic fibrosis. 85 May 98

A search was made for predictors of sudden cardiac death (SCD) among 197 men, age 40 to 79, who had multiphasic health checkups and experienced SCD 2 days to 5 1/2 years later (mean 18.1 months). Two age-sex-race-matched control groups, one matched and one unmatched for standard coronary risk factors, have been compared to the cases. In this ambulatory population, SCD occurred largely in persons with prior diagnosed heart disease. Standard coronary risk factors were confirmed as predictors of SCD. Predictors among other laboratory and quantitative tests include chylous serum, uric acid, hemoglobin, leukocyte count, pulse rate, diminished lung volumes, and hearing loss. Some of these had predictive value independent of standard risk factors. Pain tolerance was not related to SCD or to death in, versus out of hospital. Most of these predictors were not related to terminal symptom duration; this suggests a relationship more to the underlying atherosclerotic process than to the terminal fatal mechanism.
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PMID:Predictors of sudden cardiac death. 118 69

The optimum and critical hemoglobin concentrations are determined by the oxygen demand of the tissues and several oxygen transport parameters (i.e., blood flow, arterial oxygen saturation, oxygen affinity of hemoglobin, and the critical venous oxygen pressure). Most of the oxygen transport parameters change markedly during the first weeks after birth. Oxygen consumption and cardiac output in neonates are three times those of adults on a body weight basis. Due to the high oxygen affinity of fetal hemoglobin, the oxygen unloading capacity of hemoglobin in neonates is about 50% less than in adults. From oxygen transport parameters and oxygen consumption we have calculated the optimum and the critical hemoglobin concentrations for preterm and full-term neonates during the first weeks after birth. A hemoglobin concentration of 15 g/dl appears optimal for preterm and full-term infants at birth as well as for adults. The calculated minimum acceptable hemoglobin concentration is 6 g/dl for children and adults, 12 g/dl for preterm infants and 11 g/dl for full-term neonates at birth. Due to the postnatal decrease in oxygen affinity, the minimum acceptable hemoglobin concentration decreases by approximately 1 g/dl/week for the first 5-6 weeks until the minimum value of 6 g/dl for children and adults is reached. The minimum hemoglobin concentration should be 2 g/dl higher in patients who require increased oxygen or suffer from other serious disorders. A minimum hemoglobin concentration of 10 g/dl is recommended in children with leukemia or other oncological disease. In infants and children with chronic hypoxemia (cyanotic congenital heart disease) the minimum hemoglobin concentration should be increased by the percentage of arterial oxygen desaturation.
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PMID:[The critical hemoglobin value in newborn infants, infants and children]. 128 12

Brain abscess is a serious complication of congenital cyanotic heart disease. We retrospectively evaluated the risk factors for brain abscess in 21 such patients treated between 1975 and 1990 in comparison with a control group. The mean arterial oxygen saturation, arterial partial pressure of O2, arterial blood oxygen content, and base excess in patients with brain abscess were significantly lower than in the control patients. The mean arterial partial pressure of CO2, pH, hematocrit, hemoglobin, and red blood cell content in patients with brain abscess were not significantly different. Patients with congenital cyanotic heart disease may develop minute encephalomalacia due to severe hypoxemia and increased blood viscosity resulting from compensatory polycythemia. The increased blood viscosity and reduced blood flow in the microcirculation may induce cerebral thrombosis or exaggerate minute encephalomalacia during dehydration or cardiac dysfunction, and shunted blood containing infectious organisms at such sites may be followed by focal cerebritis.
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PMID:Risk factors for brain abscess in patients with congenital cyanotic heart disease. 138 54


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