PubMed Health⌕ Search

Biomedical subjects

B J SPROULE

Publications and source records attributed to B J SPROULE.

At least 19 recordsLinked to original sources
PubMed1965

THE CLINICAL SIGNIFICANCE OF ELEVATED BLOOD LACTATE.

Three patients with elevated blood lactate values are described. The first, despite moderate hyperlactatemia of 5.3 mEq./1. and severe acidosis with an arterial blood pH of 6.98, had no "excess lactate". In a second patient, moderate acidosis with a pH of 7.27 and blood lactate of 7.5 mEq./1., of which 33% was excess lactate, was found to be secondary to tissue hypoxia on an ischemic basis and preceded the onset of clinical shock by four hours. A third patient, diabetic and under treatment with phenformin hydrochloride, presented with many features suggestive of pulmonary embolism, including marked pulmonary hypertension. A diagnosis of idiopathic lactic acidosis was established when the arterial blood pH was found to be 6.77 and a blood lactate value of 14.2 mEq./1., 60% as excess lactate, was discovered in the absence of a demonstrable cause of tissue hypoxia. Exploration of the pulmonary vascular bed showed no sign of mechanical blockage. The diagnostic, therapeutic and prognostic value of measuring blood lactic acid, and of quantitating the proportion circulating as "excess lactate", is emphasized.

Acidosis↗
PubMed1964

EFFECTS OF ETHAMIVAN IN PATIENTS WITH CHRONIC RESPIRATORY DISEASE.

Nineteen patients suffering from chronic respiratory disease were evaluated before, during and after ethamivan administration by serial measurement of arterial pH, pCO(2), plasma ethamivan levels and alveolar ventilation. Ethamivan was administered intravenously as a single injection of 50 mg. in five patients; as an injection of 25 mg./kg. in five patients; as an intravenous injection of (a) 50 mg. over 15 minutes and (b) 150 mg. over 15 minutes in five patients; and finally as an oral dose of 300 to 500 mg. in five patients.Plasma levels of ethamivan became unmeasurable within 15 minutes of receiving the largest dose. Alveolar ventilation increased only in patients receiving the highest intravenous dose, and no significant changes in blood gases were elicited in any patient.

Acidosis↗
PubMed1964

STUDIES ON THE SYNDROME OF FAT EMBOLIZATION.

Three patients, all of whom were well-muscled young adult males who had suffered fractures of long bones, were studied by means of measurement of ventilatory function and arterial blood gases. They had degrees of mental change varying from mild confusion to stupor. Anemia, hypocalcemia, skin petechiae and radiologic pulmonary infiltrates were demonstrated in all three.In the absence of any clinical cyanosis, profound arterial O(2) desaturation was demonstrated in all. Physiologic studies indicated that the desaturation was the result of a diffusion defect early in the course of the syndrome and later from venous admixture. The lungs were stiff and the work of breathing was increased. The anemia appeared to be hemolytic in type.It is suggested that anemia, hypocalcemia and arterial O(2) desaturation may contribute significantly to the cerebral symptomatology associated with the syndrome of fat embolization.

Adult↗
PubMed1963

HYPOVENTILATION, CYANOSIS AND POLYCYTHEMIA IN A THIN MAN.

A lack of respiratory centrogenic drive of undetermined origin is a rare cause of cyanosis. In this condition, voluntary hyperventilation restores arterial oxygen saturation to normal. Secondary changes consist of polycythemia, somnolence, headache and right heart failure. The present report of a 43-year-old thin man with idiopathic alveolar hypoventilation is combined with a review of 12 similar patients reported by others. His resting oxygen saturation increased from 60% to 98% with hyperventilation. The pulmonary artery pressure was 68/26 mm. Hg and cardiac output 12.3 l./min. Death resulted from pulmonary infarction, and no specific abnormalities were found in the brain.

Cyanosis↗