Lung and heart water accumulation associated with hemodilution.
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Biomedical subjects
Publications and source records attributed to M B Laver.
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Selection criteria, clinical data, and physiological measurements obtained during five extracorporeal membrane lung perfusions for acute respiratory insufficiency are presented. Four patients died and 1 survived. A new technique of femoral artery cannulation to allow aortic arch perfusion is described. When properly monitored, this route provides improved oxygen delivery to the brain during venoarterial (VA) perfusion. The importance of monitoring the equivalent of carotid artery Po2 during VA perfusion is emphasized. Recognition of the effects of high cardiac output in limiting the quality of extracorporeal perfusion, plus the use of hypothermia to reduce output, are stressed. We have confirmed that perfusion can be accomplished with small quantities of heparin, so that bleeding is reduced, but thrombocytopenia and occasional hemorrhage continue to be persistent problems.
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Oxyhemoglobin dissociation (OHD) curves were performed on whole blood (WB) from 20 patients with anginal pain, normal hemodynamics, and normal coronary arteries, as demonstrated by selective coronary cinearteriography. OHD curves in 19 of 20 patients, from zero to full saturation, were nearly identical to those in normal control subjects with values for P(50) (Po(2) at 50% saturation and pH 7.4) of 26.7+/-1.5 (mean+/-SD of the mean) torr (mm Hg) and red blood cell (RBC) levels of 2,3-diphosphoglyceric acid (2, 3-DPG) of 0.72+/-0.10 (mean+/-SD of the mean) M/M hemoglobin (Hb). Normal values for nonsmoking adults were: P(50), 26.6+/-1.4 (mean+/-SD of the mean) torr: and RBC 2,3-DPG, 0.81+/-0.09 (mean+/-SD of the mean) M/M Hb. Mean levels of carbon monoxide were normal at 0.14+/-0.01 (mean+/-SEM) ml/100 ml WB in 10 patients who were nonsmokers and 0.45+/-0.15 (mean+/-SEM) ml/100 ml WB in 10 smokers. In one patient, a heavy smoker with markedly elevated blood carbon monoxide levels, an abnormal leftward shift of the OHD curve was observed. This was corrected after discontinuation of smoking. In utilizing these methods, we could not detect consistent abnormalities of Hb affinity for oxygen at rest in the patients studied, which suggests that a defect in oxygen transport at rest is an unlikely explanation for the symptoms of chest pain in patients with the anginal syndrome and normal coronary arteriograms.
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Studies have been performed on a 12-yr-old Chinese girl with compensatory erythrocytosis due to the presence of hemoglobin Bethesda comprising about 45% of the red cell hemoglobin. Her parents and three siblings were normal. The oxygen affinity of her blood was markedly increased: under physiological conditions (pH 7.40, 37 degrees C). P(50) was 12.8 mm Hg (normal = 26.5 mm Hg). The red cell 2,3-diphosphoglycerate (2.3-DPG) level was normal. The abnormal hemoglobin could not be separated from hemoglobin A by zone electrophoresis at pH 8.6 or isoelectric focusing on polyacrylamide gel. However, after the hemoglobin was split into free alpha and beta chains by treatment with p-hydroxymercuribenzoate (PMB) or 6 M urea, an abnormal beta chain was readily demonstrated having a higher isoelectric point (more positive net charge) than normal beta(A). Structural analysis of the variant beta chain demonstrated the substitution of histidine for tyrosine at position 145: hemoglobin Bethesda (alpha(2)beta(2) (145His)). From earlier chemical and crystallographic studies, it has been postulated that this residue is a critical determinant of hemoglobin function. Hemoglobin Bethesda was separated from hemoglobin A by column chromatography. Oxygen equilibria of purified hemoglobin Bethesda revealed an extremely high oxygen affinity (exceeding that of isolated alpha and beta chains), and markedly reduced cooperativity. The Bohr effect of hemoglobin Bethesda was 1/3 that of hemoglobin A. However, hemoglobin Bethesda showed a significant interaction with 2.3-DPG and inositol hexaphosphate.
In 10 patients with severe, acute respiratory failure we studied the effects of positive end-expiratory pressure when intermittent positive pressure ventilation (IPPV) with inspired oxygen (F(IO2)) up to 0.5 failed to maintain arterial oxygen tension (P(aO2)) above 70 torr.Positive end-expiratory pressures (PEEP) of 0, 5, 10, and 15 cm H(2)O were applied for 30-min periods each and in random order. Blood gas exchange, lung volumes, compliance, and hemodynamics were studied at each level of PEEP. P(aO2) (F(IO2) = 1.0) rose linearly with elevation of PEEP, the mean increase being from 152 to 347 torr, or 13 torr/cm H(2)O PEEP. Mean functional residual capacity (FRC) was 1.48+/-0.78 liters at zero PEEP (i.e., IPPV) and the increase was essentially linear, reaching 2.37 liters at 15 cm H(2)O PEEP. P(aO2) and FRC showed a close correlation. Total and lung static compliance were greater during ventilation with high than with low levels of PEEP. The increase in P(aO2) correlated with the specific lung compliance. Dynamic lung compliance decreased progressively with rising levels of PEEP except for an increase with 5 and 10 cm H(2)O PEEP in patients with initial values of 0.06 liter/cm H(2)O or higher. Cardiac index fell in some patients and rose in others and there was no correlation of mean cardiac index, systemic blood pressure, or peripheral vascular resistance with level of PEEP. The most probable explanation for the effect of PEEP on P(aO2) and compliance is recruitment of gas exchange airspaces and prevention of terminal airway closure.
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