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Biomedical subjects

W H Tooley

Publications and source records attributed to W H Tooley.

At least 55 records · Page 3Linked to original sources

Pneumothorax in the respiratory distress syndrome: incidence and effect on vital signs, blood gases, and pH.

We determined the incidence of pneumothorax in 295 infants (mean birthweight, 1,917 gm) with the respiratory distress syndrome (RDS) treated according to the same protocol. Fifty-five infants (mean birthweight, 1,594 gm) developed pneumothorax (incidence, 19%); incidence varied with severity of RDS and intensity of respiratory assistance. Pneumothorax occurred in 3.5% (2 of 58) of infants who received no assisted ventilation and in 11% (14 of 124) of infants who received continuous positive airway pressure (CPAP) as the only form of assisted ventilation; the difference between these two groups is not significant. Forty-nine infants initially treated with CPAP later required mechanical ventilation with positive end-expiratory pressure (PEEP). Pneumothorax occurred in 12 of the 49 (24%) and in 21 of 64 (33%) of those infants initially treated with PEEP; the incidence of pneumothorax for both these groups was significantly higher than for those treated with no assisted ventilation or CPAP only. To assess the value of frequent measurement of vital signs, blood gas tensions, and pH in the recognition of pneumothorax, we analyzed these variables by the cumulative sum statistical technique. We noted the following significant changes associated with pneumothorax: arterial blood pressure, heart rate, and respiratory rate decreased in 77% of cases; pulse pressure narrowed in 51% of cases; Po2 decreased in 17 of 20 cases in which ventilatory settings were constant for at least three hours prior to pneumothorax. However, pH and Pco2 showed consistent changes. Frequent measurements of vital signs and Po2 aid in the early diagnosis of pneumothorax.

Blood Pressure↗

Cardiorespiratory status of erythroblastotic newborn infants: III. Intravascular pressures during the first hours of life.

We measured aortic and central venous pressures beginning soon after birth in 40 prematurely born infants with moderate or severe erythroblastosis fetalis, including 13 with severe and 10 with mild hydrops fetalis. All but four were asphyxiated at birth and this affected intravascular pressures. Before resuscitation, aortic or central venous pressure or both were elevated in more than one third. All but two of the remaining infants had normal initial pressures. Following resuscitation which relieved acidosis, hypoxia, and anemia, but did not reduce blood acidosis, hypoxia, and anemia, but did not reduce blood volume, the high pressures usually fell to normal and occasionally to subnormal levels, normal pressures fell to subnormal in almost one half, and those with initial subnormal pressures remained hypotensive. In all, 40% were hypotensive after resuscitation; treatment with blood volume expanders consistently returned these pressures to normal. Only two of the 13 severely hydropic infants and none of the mildly hydropic had findings indicative of hypervolemia and myocardial failure which persisted after treatment of asphyxia.

Animals↗

Continuous positive airway pressure and pulmonary and circulatory function after cardiac surgery in infants less than three months of age.

Continuous positive airway pressure (CPAP) was used to support the ventilation of infants less than 3 months of age who had undergone thoractomy for cardiovascular surgery. The functional residual capacity, which was approximately 30 per cent of predicted at zero CPAP, increased 35 per cent in cyanotic and 33 per cent in acyanotic infants with the application of 5 mm Hg pressure. Increasing airway pressure from zero to 5 mm Hg increased PaO2 4 per cent in cyanotic and 13 per cent in acyanotic infants. There was no change in heart rate, respiratory rate, mean arterial pressure, pH or PaC02 under similar circumstances, but central venous pressure increased 1.5 mm Hg in cyanotic and 0.8 mm Hg in acyanotic infants.

Blood Circulation↗

Ontogeny of tracheal fluid, pulmonary surfactant, and plasma corticoids in the fetal lamb.

We examined fetal plasma corticoids and flow rate, electrolyte composition, and surfactant content of tracheal fluid in chronic experiments with eight fetal lambs. From 120 to 148 days of gestation the rate of fluid production was 4.5 ml/kg per h, and there was no change in mean fluid sodium (147.8 meq/1), chloride (153.1 meq/1), calcium (2.2 mg/100 ml), and pH (6.23). Tracheal fluid potassium increased from 4.3 meq/1 at 120-130 days to 8.9 meq/1 at term, while plasma sodium, chloride, calcium, pH, and potassium were constant at 146.1 meq/1, 110.0 meq/1, 12.1 mg/100 ml, 7.39, and 4.0 meq/1, respectively. Plasma corticoids were less than 1.5 mug/100 ml total (0.3 mug/100 ml free) until 130 days, when they increased rapidly to 10.5 total (3.2 free) at 148 days. Surfactant was first detected in tracheal fluid between 124 and 133 days and its secretion increased rapidly after 135 days to a value of 125 mug/kg per h at 148 days. A sudden increase in fetal plasma corticoids does not seem to be the stimulus for appearance of surfactant in the lamb, although these hormones may induce the rapid accumulation of surfactant prior to delivery.

Adrenal Cortex↗

Surfactant in the lung and tracheal fluid of the fetal lamb and acceleration of its appearance by dexamethasone.

We measured tracheal fluid production rate and pulmonary surfactant flux in 12 sets of twin fetal lambs of 102 to 135 days' gestation. In nine of these sets we also measured surfactant flux and the concentration of saturated lecithin in the lungs before and during dexamethasone infusion into one of the twins. The average tracheal fluid flow rate was 3.25 ml/kg/hr (SD 1.6) and, relative to body weight, did not change between 103 and 135 days' gestation or during the infusion of dexamethasone. In untreated fetuses, surfactant was detected between 108 and 130 days and its flux gradually increased but remained less than 150mug/kg/hr at 135 days' gestation; the amount of disaturated lecithin in the lung relative to body weight increased 13-fold from 108 to 134 days. From these data we calculated that the minimal rate of synthesis of disaturated lecithin was increased about 4-fold by dexamethasone from 108 to 120 days; this enhancement fell to about 1.8-fold by 135 days. The rate of secretion of disaturated lecithin, as estimated by surfactant flux in tracheal fluid, was increased by dexamethasone throughout the interval of the study.

Animals↗