STUDIES OF RESPIRATORY INSUFFICIENCY IN NEWBORN INFANTS

PEDIATRICS ◽  
1957 ◽  
Vol 19 (3) ◽  
pp. 387-398
Author(s):  
Herbert C. Miller ◽  
Franklin C. Behrle ◽  
Ned W. Smull ◽  
Richard D. Blim

Serial determinations of pH, carbon dioxide tension, carbon dioxide content and oxygen saturation of the blood were made on newborn infants and correlated with the trends of their respiratory rates. Some infants whose respiratory rates were normal from birth and some whose rates were initially high but subsequently returned to normal levels exhibited mild uncompensated respiratory acidosis for 3 or 4 hours after birth. Thereafter, acid-base balances were normal. All infants whose respiratory rates followed either of the above two trends oxygenated their blood 91% or better within a few minutes of birth. There was a marked tendency for infants whose respiratory rates increased significantly on the first day or two after birth to have a moderate to severe uncompensated respiratory acidosis which was worse at birth and sometimes persisted for several days, usually with improvement. Some of the infants whose respiratory rates increased significantly after birth had moderate to severe hypoxemia, which also was worse at birth and tended to improve with increasing age. The hypothesis was advanced that one of the basic difficulties in neonatal respiratory insufficiency was a reduction of resting tidal volume; the latter was universally associated with a significant increase in respiratory rates during the first day or two after birth and sometimes with an uncompensated respiratory acidosis and occasionally with hypoxemia.

1957 ◽  
Vol 191 (2) ◽  
pp. 384-387 ◽  
Author(s):  
Billy James Williamson ◽  
Smith Freeman

The effects of acute disturbances in acid-base balance on renal cation excretion were studied in dogs. Special attention was given to the excretory mechanism for calcium. Four different states were produced experimentally: respiratory acidosis, metabolic acidosis, metabolic alkalosis and compensated metabolic alkalosis. Additional experiments were carried out in normal and alkalotic animals subjected to calcium loading. Calcium reabsorption was found to vary directly with the filtered load of calcium. The increased excretion of calcium in acidosis appears to be due to an increase in filtered calcium. The percentage of reabsorption of filtered calcium was 98–99% in normal and acidotic dogs, but decreased to approximately 90% in animals made acutely alkalotic. However, the relative loss of water to calcium in the urine in acute alkalosis was decreased, resulting in an elevated renal threshold of retention of calcium in metabolic alkalosis. Data are included on the behavior of inorganic phosphate in the various states studied. Elevated carbon dioxide tension was associated with phosphate mobilization from the tissues regardless of whether or not the carbon dioxide excess was compensated for by extra alkali.


2020 ◽  
pp. 30-32
Author(s):  
D.V. Dobrianskyi ◽  
R.I. Ilnytskyi ◽  
G.L. Gumeniuk ◽  
А.І. Zavatska ◽  
О.О. Ilyk

Background. Community-acquired pneumonia is a frequent complication of chronic obstructive pulmonary disease (COPD), especially in patients with small weight. Respiratory acidosis is a natural manifestation of COPD, which clinically is characterized by dominated obstructive pulmonary ventilation. Respiratory acidosis is a form of acid-base deviation which associated with insufficient excretion of carbon dioxide by the lungs. But in patients with comorbid pathology (COPD and community-acquired pneumonia) in addition to respiratory acidosis also can be evolved a metabolic acidosis (MA) conditioned by tissue hypoxia, intense systemic inflammation with next disturbances in correlation between pro-inflammatory and anti-inflammatory mediators, accelerating catabolic processes. The severity of acid-base deviation in patients with the possibility of developing decompensated acidosis depends not only on the degree of obstructive ventilation disorders, but also increasingly to the gravity of community-acquired pneumonia which causes severe acidotic metabolic changes. Objective. To evaluate the expediency of application 4.2 % buffered sodium bicarbonate solution (Soda-buffer) in the case of mixed acidosis in patients with comorbid pathology: COPD which is compounded by community-acquired pneumonia. Materials and methods. To all patients with comorbid pathology aged from 18 to 75 were prescribed the drug Soda-buffer manufactured by “Yuria-Pharm” (Ukraine), which contains 42 mg of sodium bicarbonate intravenously at a rate of 1.5 mmol/kg per hour (4.2 % Soda-buffer – 3 ml/kg per hour) under control of blood pH, acid-base and water-electrolyte (water-salt) balance of the body. Results and discussion. Qualified treatment of patients with comorbid pathology (COPD and community-acquired pneumonia) should be comprehensive and directed towards the struggle against the manifestations of obstructive ventilation disorders and hypoxemia, lower respiratory tract infection, intense inflammatory process in the lung parenchyma and bronchial tree. The complex treatment includes not only modern antibacterial drugs in combination with systemic glucocorticoids, but also methods of correction of metabolic, hemodynamic and coagulation disorders. With the aim of acidosis correction the most effective way is using infusion solutions which contain sodium bicarbonate. Due to dissociation of sodium bicarbonate has released a bicarbonate anion that binds hydrogen ions to form of carbonic acid, which then decomposes into water and carbon dioxide. In case of severe respiratory insufficiency oxidation of sodium hydrocarbonate can contribute increasing of hypercapnia by the connection with the accumulated CO2. It was found that 4.2 % buffered sodium bicarbonate solution in the comprehensive therapy of patients with comorbid pathology of COPD and community-acquired pneumonia helps to restore acid-base balance, reduce metabolic disorders and improve the clinical condition of patients. In the matter of normalization of the function of external respiration and reduction of the manifestations of respiratory insufficiency, usually substantially reduces not only respiratory, but also MA. Therefore, during correction of concomitant MA by Soda-buffer we should compensate the deficiency of bases not more than half percentage. In situation with rapid balancing of acidosis, particularly in the case of impaired pulmonary ventilation, the rapid release of CO2 may exacerbate cerebral acidosis. It’s a well known fact that small uses of Soda-buffer together with other infusion solutions with an acidic pH are provided a neutralizing agent and prevent the appearance of post-infusion phlebitis after administration of widely used infusion solutions (glucose fluids of different concentrations, chloride solution, ciprofloxacin and some other fluoroquinolones). Conclusions. Soda-buffer (4.2 % sodium bicarbonate buffered solution) is an effective infusion agent for the correction of MA in patients with comorbid pathology (COPD and community-acquired pneumonia) in condition of provided effective gas exchange. This solution is a physiological bicarbonate buffer that maintains a constant pH level, prevents abrupt alkalization of the blood and provides a smooth correction of acidosis at the same time with increasing alkaline blood reserves. The drug also increases the excretion of sodium and chlorine ions, osmotic diuresis, alkalizes urine.


1963 ◽  
Vol 18 (4) ◽  
pp. 739-741
Author(s):  
Peter Salmon ◽  
Richard Stish ◽  
Maurice B. Visscher

Quantitative studies have been made of the changes in optical density of whole blood at two wavelengths at full oxygen saturation with changes in carbon dioxide tension and content. At both λ 630 mμ and λ 805 mμ there are lower densities with increasing pCO2 at full oxygen saturation. From pCO2 1.5 to 243 mm Hg the decrease is 0.133 OD units and is equal at the two wavelengths. The OD is linearly related to the pH change. The effect is ascribed to the differences in light scattering by erythrocytes with changing shape and/or volume of the cells. This effect results in a systematic error in measurements of oxygen content of blood when the carbon dioxide content varies, as it does between arterial and venous blood. Submitted on October 22, 1962


1960 ◽  
Vol 15 (3) ◽  
pp. 393-396 ◽  
Author(s):  
Leonard B. Berman ◽  
Thomas F. O'Connor ◽  
Peter C. Luchsinger

The administration of tris-(hydroxymethyl)aminomethane (THAM) to six normal adults was followed by a series of changes in ventilation, arterial blood and urine. Alveolar ventilation and oxygen saturation fell significantly, as did alveolar CO2 excretion and tidal volume. Alveolar and blood CO2 tension rose slightly. Blood bicarbonate rose while other electrolytes were essentially unchanged. Urinary pH and electrolyte excretion increased strikingly without any change in endogenous creatinine clearances. No toxic effects were observed. The findings suggest that THAM cannot presently be recommended for clinical use in the treatment of respiratory acidosis, unless some means of stimulating respiration are also provided. Submitted on November 19, 1959


1977 ◽  
Vol 43 (6) ◽  
pp. 931-935 ◽  
Author(s):  
D. R. Strome ◽  
R. L. Clancy ◽  
N. C. Gonzalez

Experiments were performed to determine the relative effects of a net extracellular-to-intracellular HCO3- flux and of elevated carbon dioxide tension (PCO2) on cellular acid-base regulation. Isolated rabbit hearts were perfused by recirculating a small volume of Ringer solution in which the PCO2 and the HCO3- concentration could be independently altered. Net HCO3- flux was assessed by the disappearance of HCO3- from perfusate. Between 40 and 100 Torr PCO2, a HCO3- flux into the cell occurs only when perfusate HCO3- concentration is increased. Therefore, by selective manipulation of perfusate HCO3- and PCO2 it is possible to induce hypercapnia with or without an accompanying HCO3- flux. When perfusate HCO3- concentration was increased from 20 to 36 mM, cellular HCO3- concentration increased from 22.5 +/- 0.8 to 26.1 +/- 1.0 mM at 40 Torr PCO2 and from 27.8 +/- 0.7 to 34.1 +/- 1.4 mM at 98 Torr PCO2. These increases can be accounted for by the amount of HCO3- that disappeared from the perfusate. The results suggest that most of the initial cell CO2 buffering is provided by the net HCO3- flux in addition to the passive physicochemical buffering.


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