Arterial PO2 Values Research Articles

Interpretation of the Arterial Oxygen and Carbon Dioxide Partial Pressures: A Simplified Approach for Bedside Use

Arterial Po2 and Pco2 values give valuable information regarding gas exchange function of the lungs and oxygen transport by the blood. Alveolar ventilation varies inversely as arterial Pco2 the latter measurement, therefore, is an indication of the adequacy of CO2 elimination by the lungs. The alveolar Po2 can be readily calculated using the arterial Pco2 as a measure of alveolar Pco2 and either a simplified version of the alveolar air equation or an O2-CO2 diagram. An abnormally widened alveolar-arterial Po2 difference indicates impaired oxygen exchange function of the lungs, although whether the abnormality is due to anatomic right-to-left shunting, ventilation/perfusion imbalance or diffusion abnormality is not revealed. A normal alveolar-arterial Po2 difference in the presence of hypoxemia indicates alveolar hypoventilation or a decreased inspired Po2. Saturation of hemoglobin with O2 can be calculated from the arterial Po2 and the O2 hemoglobin dissociation curve. Oxygen content can be calculated from the product of O2 saturation and hemoglobin O2 capacity; the latter is directly related to hemoglobin concentration. Cardiac output and regional circulatory factors are also of great importance in O2 delivery to tissues.

The effect of arterial hypoxemia upon acid-base parameters in arterial blood and cisternal cerebrospinal fluid of the rat.

AbstractThe effects of hypoxemia on the acid‐base parameters of the arterial blood and CSF were studied in anesthetized constant ventilated rats. The results showed that there was a one to one relationship between the increase in the CSF lactate and the decrease in the CSF bicarbonate concentration over a wide range of arterial Po2 values. However, the decrease in the CSF pH at constant ventilation was much less than could be expected from the decrease in bicarbonate. This was due to a concomitant fall in the CSF CO2 tension, partly caused by a fall in the arterial CO2 tension and partly by a decrease in the Po2 difference between CSF and arterial blood.

Early treatment of neonatal acidosis in low birgh weight infants in relation to respiratory distress syndrome

The effects of early vs late correction of acidosis on the clinical course of the respiratory distress syndrome (RDS) was evaluated in 82 pre-term infants weighing less than 2,250 grams. Criterion for inclusion into the study was a pH of less than 7.25 either from fetal scalp, cord or umbilical arterial blood samples within 20 min of age. The infants were randomly grouped into: A, birth weight <1500 gm, early treatment (intravascular NaHCO3 infusion within 30 min of age); B, <1500 gm, late Rx (2–3 hrs of age); C, 1501–2250 gms, early Rx, and D, 1501–2250 gm, late Rx, Infants were otherwise similarly managed. AT designated intervals predetermined clinical parameters were used to make the diagnosis and to grade the severity of RDS. No significant differences were observed in arterial blood pH and PO2 values between groups during the first 30 min of life prior to Rd. In the early Rx groups, the arterial blood pH was significantly higher during the first 12 hrs. Base deficits were significantly smaller for the first 3 hrs in the Group A and for the first 24 hrs for group C. The PaO2 and PaCO2 values were not significantly different between early and late Rx groups. The incidence of RDS between groups was similar. The degree of severity of RDS was significantly greater in the late treatment groups from 12–96 hrs of age. A higher mortality rate was observed in infants weighing between 1001–2250 gms with late Rx. This study suggests that early correction of neonatal acidemia favorably influences the course of RDS, and that it may reduce the mortality of infants between 1001 and 2250 gms.

Rational use of oxygen administration by nasal catheter

4 different methods of nasal oxygen insufflation were studied in healthy adults and patients with broncho-pulmonary diseases: (1) O2-delivery by short double nasal catheter; (2) O2-delivery by short single nasal catheter; (3) O2-delivery by long nasopharyngeal catheter; (4) O2-delivery by short nasal catheter with compress (method of Poulsen). Results. In healthy adults and in hypoxemic patients the methods 3 and 4 yielded significantly higher values of arterial pO2 (application of 2 and 41 O2/min than the methods 1 and 2. Method 4, however, showed optimal oxygen delivery in combination with optimal humidification and warming of gas and should be prefe-red. A paradoxical fall of arterial pO2 during nasal oxygen administration is caused by augmented tidal and minute volume. This phenomena is demonstrated and discussed.

USE OF CAPILLARY BLOOD IN MEASUREMENT OF ARTERIAL PO2

In this study we investigated the possibility of obtaining accurate values of arterial Po2 from specimens of capillary blood stored in glass capillary tubes and measured in an oxygen microelectrode. It has been shown that Po2 measurements made on the Radiometer oxygen microelectrode are as accurate as those made on the macroelectrode and that the storage of blood is as satisfactory in glass capillary tubes as in glass syringes. The important feature in obtaining accurate values for arterial Po2 is the choice of the capillary bed and its method of preparation for sampling. If the ear lobe is massaged with thurfyl nicotinate (Trafuril) it is possible to obtain values of Po2 from the capillary blood which are in close agreement with arterial Po2 in normal, hyperoxic, and shocked vasoconstricted patients.

The Influence of Guaiacol Glycerol Ether on Cardiovascular and Respiratory Function in the Horse

SUMMARY The intravenous administration of 160 mg./kg. guaiacol glycerol ether was required to produce recumbency in conscious horses. This dose rate produced only minor changes in heart and respiratory rates and a slight fall in mean arterial blood pressure and in arterial blood pO2 values. Recumbency could be produced by the intravenous administration of 80 mg./kg. guaiacol glycerol ether in combination with 3·5 mg./kg. thiopentone sodium to conscious horses. The administration of these agents in combination produced a small fall in mean arterial blood pressure and increases in heart and respiratory rates along with a moderate fall in arterial blood pO2, values.

The effects of oxygen breathing in patients with acute myocardial infarction.

Haemodynamic and biochemical studies while breathing four different concentrations of oxygen showed increases in peripheral resistance and arterial pressure without an appreciable change in cardiac output. The patients with low cardiac outputs had lower arterial pO2 values. Lactate and pyruvate levels declined with time rather than the concentration of oxygen.

BLOOD-GAS TENSIONS IN BRONCHIAL ASTHMA

Arterial oxygen (Po 2) and carbon-dioxide (Pco 2) tensions were measured in 12 patients with clinically severe asthma (status asthmaticus) and 64 patients with clinically less severe asthma. Hypoxæmia, hypercapnia, and acidosis were common in patients in status asthmaticus. The greatest deviations from normal recorded were: Po 2 39 mm. Hg, Pco 2 200 mm. Hg, pH 6·81. Patients with clinically less severe asthma commonly showed disturbances of blood-gas tensions. Of 64 patients, arterial Po 2 was less than 60 mm. Hg in 14, and arterial Pco2 greater than 45 mm. Hg in 9. Arterial Po2 values were as low as 50 mm. Hg without elevation of arterial Pco 2. The demonstration of such disturbances of blood-gas tensions in patients whose asthma does not appear to be clinically severe provides a basis for sudden " unexpected " deterioration and death when airways obstruction increases further.

Blood P-CO2 and brain oxygenation at reduced ambient pressure.

Hyperventilation during breathing of 100% oxygen elevates the Po2 of alveolar gas by the same amount that it lowers its Pco2. Since the development of arterial hypocapnia causes cerebral vasoconstriction, brain oxygenation is drastically decreased even while arterial oxygenation is improved by hyperventilation. Administration of 30% CO2 with oxygen at an ambient pressure equivalent to that at 39,000-ft altitude prevented alkalemia and, in spite of hyperventilation, restored cerebral venous oxygenation to a level at least equivalent to that found when pure oxygen was breathed at rest at the same altitude. The respiratory minute volume during administration of CO2 with O2 was greater than when O2 alone was breathed at reduced ambient pressure. Since neither arterial Po2 nor cerebral venous Pco2 values differed in these two experimental situations, the respiratory stimulation may represent the quantitative demonstration in man of a respiratory effect of CO2 mediated by arterial chemoreceptor activation and unrelated to change in the level of central chemical stimulus. Submitted on March 16, 1962