Jp Zock

CALCULATED CHANGES IN PH AND PCO2 IN ARTERIAL BLOOD-PLASMA ASSUMING ABSENCE OF ION AND WATER EXCHANGE BETWEEN PLASMA AND ERYTHROCYTES DURING THEIR EQUILIBRATION WITH ALVEOLAR GAS

As a contribution to solving the problem of pH disequilibrium in arterial blood, the results of two modes of gas exchange in the lung have been calculated using an equilibrium state model of the blood. In both cases the HCO3−/Cl− exchange was assumed to occur after the gas exchange in the pulmonary capillaries. When the gas exchange was assumed to be dependent on intra-erythrocytic carbonic anhydrase. the plasma pH in the arterial blood increased. Whe plasma and erythrocytes were assumed to equilibrate separately with the alveolar gas due to presence of extra-erythrocytic carbonic anhydrase, plasma pH in the arterial blood decreased. In each case there was a slight increase inpCO2 after the blood had left the pulmonary capillaries.

Influence of changes in cardiac output on the acid-base status of arterial and mixed venous blood

While maintaining the arterial CO2 tension constant near the normal level of the dog (4.3 kPa), we studied the influence of decreasing cardiac output on both the arterial and mixed-venous blood acid-base status in anaesthetized, artificially ventilated dogs. Cardiac output was manipulated by applying positive end-expiratory pressure (PEEP), and by β-adrenergic blockade to suppress a compensatory heart rate response. The systemic vascular response was attenuated by α-adrenergic blockade. Metabolic rate remained virtually unchanged when cardiac output decreased. Under these conditions a fall in cardiac output led to a shift of the arterial acid-base status in the direction of a metabolic acidosis. The changes occurring in the mixed-venous blood resembled those of an in-vivo CO2 bufferline, with the shift being such as if a respiratory acidosis was developing.

RELIABILITY OF NON-INVASIVE MEASUREMENT OF TOTAL-BODY WATER (TBW)

Up to now TBW is generally determined on the basis of measurements of D2O concentration in blood after an i.v. dose of D2O. We wondered if TBW could be determined on the basis of D2O concentrations in urine after giving D2O orally. Eight experiments were carried out in 6 preterm neonates (gest. age: 31.5 wk±3.5, birthweight: 1855 g±516, mean±SD). The D2O concentrations were measured in every portion of urine voided within 24 h (on the average 16 portions) after giving D2O (2 ml/kg) orally. In 5 experiments D2O concentrations were also determined in blood. TBW was calculated after extrapolating the regression line after the equilibration period (on the average 5 h) to time 0. After equilibration, the D2O concentration in urine decreased linearly (r= -0.99±0.01). Using D2O concentration in urine TBW was on the average 1.5% lower than calculated with D2O concentrations in blood.Conclusion: TBW can be measured on the basis of D2O in urine after giving D2O orally. Considering the high correlation coefficient, we suggest that TBW can be calculated using only 3 portions of urine collected between 6 to 24 h after giving D2O orally.