ALTHOUGH hyaline-membrane disease, the respiratory-distress syndrome of the newborn infant, has been the object of increased clinical and research interest in the past ten years, little attention has been paid to its possible sequelae.1 , 2 It is stated that most of these infants who survive the first three days of life will recover completely, and by seven to ten days of life will have normal lungs radiographically.3 , 4 Recent experience with critically ill infants at the Stanford Premature Infant Research Center demonstrates that intensive therapy may modify the acute syndrome so as to permit the development of a previously unrecorded abnormality of . . .

Pulmonary disease following respirator therapy of hyaline-membrane disease. Bronchopulmonary dysplasia.

Reference values play an important role in establishing whether, in an individual, measured volumes fall within a range to be expected for a healthy person of the same sex, similar stature, age, and other characteristics. Hence, reference values should be chosen that are appropriate to the person being investigated. Ideally, the reference values should be consistent; in the context of this paper, it implies that predictions for the various lung volumes have been derived from the same reference population, with the same techniques. Comparing measured with reference values is fraught with difficulties, as it may lead to disease going undetected. This is because the scatter in predicted values is sufficiently large to allow a sick person to lose, e.g. much of his total lung capacity (TLC), whilst still remaining in the range observed in comparable healthy persons. In addition, measurements in an "abnormal range" are not diagnostic of a specific disease, as many diagnostic entities may cause static lung volumes to be abnormal. Hence, in the follow-up of a patient, reliance should be placed much more on the effects of drugs or challenges with pharmacological, chemical or physical stimuli or allergens, and on the rate of change of lung volumes, than on the relationship of an isolated result to published "normative data". In fact, the best reference value is the value observed in a period when the disease is stable and minimal for that person. In studies such as the effects of drugs in patients with lung disease, or of adverse effects of environmental factors on the lungs, observed values should not be compared with reference values; instead, a comparison should be made with values obtained in an appropriately chosen control group.

https://erj.ersjournals.com/content/erj/8/3/492.full.pdf

Reference values for residual volume, functional residual capacity and total lung capacity. ATS Workshop on Lung Volume Measurements. Official Statement of The European Respiratory Society.

Neonatal respiratory morbidity and mode of delivery at term: influence of timing of elective caesarean section

Considerable controversy regarding the effects of hypoxia on the pulmonary vasculature has arisen over the past few decades. The literature has been extensively reviewed by Fishman (1), and it is now generally accepted that hypoxia is a pulmonary vasoconstrictor. Much of the controversy has centered around the interpretation of a small elevation of pulmonary arterial pressure in the face of an increase in cardiac output related to the hypoxic stimulus. Some investigators calculated a small increase of pulmonary vascular resistance, whereas others could not confirm this observation. Most studies were performed in adult animals, or in adult humans, but more recently attention has been directed to hypoxic responses in the newborn animal, in view of the greater responsiveness of the pulmonary vasculature at this age. The relationship between the degree of pulmonary vascular response and the level of hypoxia has received only little attention, and usually a constrictor response to a single low oxygen gas inhalation has been reported. Recently Thilenius, Hoffer, Fitzgerald, and Perkins (2) attempted to relate pulmonary vascular resistance change to the level of inspired gas oxygen tension, but no obvious relationship could be demonstrated. Liljestrand (3) in 1958 suggested that the pulmonary vascular response to hypoxia may be related to the production of local Ho ion concentration changes in the lung. More recently Enson and as-

/pdf/response-of-the-pulmonary-vasculature-to-hypoxia-and-h-ion-38lzrl853q.pdf

Response of the pulmonary vasculature to hypoxia and H+ ion concentration changes.

The biological effects of carbon monoxide on the pregnant woman, fetus, and newborn infant☆

The endogenous production of carbon monoxide ( V(CO)) in newborn infants was measured by serial determinations of blood carboxyhemoglobin during rebreathing in a closed system Mean V(CO) in nine full-term infants was 137 +/-36 mul CO/kg per hr (SD), and in four erythroblastotic infants V(CO) ranged from 37 to 154 mul CO/kg per hr preceding exchange transfusion Mean red cell life-span (MLS) and total bilirubin production were calculated from V(CO) MLS in normal newborns was 88 +/-15 days (SD), and bilirubin production was 85 +/-23 mg/kg per 24 hr This is more than twice the amount of bilirubin normally produced in the adult per kilogram of body weight Normal infants achieved a net excretion of bilirubin of at least 56 +/-23 mg/kg per 24 hr (SD) as calculated from the bilirubin production and the measured rise in serum bilirubin concentrationThe measurement of V(CO) should prove valuable in the study of red blood cell survival and bilirubin metabolism in the newborn infant

/pdf/endogenous-production-of-carbon-monoxide-in-normal-and-36m152gx49.pdf

Endogenous production of carbon monoxide in normal and erythroblastotic newborn infants

The venous admixture component of the total alveolar-arterial gradient for oxygen (AaD-O2) has been measured in 26 normal infants less than 4 days of age and in 12 others with the respiratory distr...

Pulmonary function in the newborn infant: the alveolar-arterial oxygen gradient

The arterial-alveolar tension gradient for CO2 has been investigated in 17 normal new born infants and in 15 with some degree of respiratory distress. Whereas the normal infants had virtually no Pco2 gradient from pulmonary capillary to alveolus, an average difference of 13.9 mm Hg was detected in sick infants. This gradient for Pco2 is caused by increased alveolar (and total physiological dead space, the relative amount of which closely parallels the clinical course of the disease. The data obtained indicate the increase in alveolar dead space to be largely due to poor perfusion of ventilated alveoli. In severely ill infants more than 60% of ventilated alveoli appear to be under-perfused.

PULMONARY FUNCTION IN THE NEWBORN INFANT II. Perfusion—Estimation by Analysis of the Arterial-Alveolar Carbon Dioxide Difference

https://dm5migu4zj3pb.cloudfront.net/manuscripts/104000/104869/JCI63104869.pdf

Nicholas M. Nelson

Papers

Endogenous production of carbon monoxide in normal and erythroblastotic newborn infants

Pulmonary function in the newborn infant: the alveolar-arterial oxygen gradient

PULMONARY FUNCTION IN THE NEWBORN INFANT II. Perfusion—Estimation by Analysis of the Arterial-Alveolar Carbon Dioxide Difference

Pulmonary function in the newborn infant. v. trapped gas in the normal infant's lung

NIH consensus development statement on cesarean childbirth