Arterial Blood Carbonic Acid Inversely
Determines Lactic and Organic Acids
2514-2517
Correspondence
Dr. Christopher Geoffrey Alexander Aiken,
729 Frankley Road, New Plymouth 4371, New Zealand.
Phone: +64 6 753 2950, E-mail: geoffaiken@xtra.co.nz
Objective: To establish that arterial blood carbonic acid varies inversely with lactic acid in accordance with bicarbonate exchanging for lactate across cell membranes through the anion exchange mechanism to maintain the Gibbs-Donnan equilibrium.
Study Design: Over 5 years, lactate was measured on all blood gases taken from neonatal admissions, as well as organic acid whenever electrolytes were required.
Results: Arterial blood gases from 63 infants given high calcium TPN were analyzed. Twenty two needed continuous positive airways pressure (CPAP) only and 31 intermittent positive pressure ventilation (IPPV) and surfactant followed by CPAP to treat respiratory distress syndrome in 51 and meconium aspiration syndrome in 2. All survived and were free of infection. Excluded gases were those with high and falling lactate soon after delivery representing perinatal asphyxia, and those on dexamethasone. Strong inverse relations between carbonic and lactic acids were found at all gestational ages and, independent of glomerular filtration, between carbonic and organic acids. Lactate (mmol/L) = 62.53 X PCO2 -0.96(mmHg) r2 0.315, n 1232, p <0.001. Sixty divided by PCO2 is a convenient measure of physiological lactate at any given PCO2. In the first week, 9.13 ± 2.57% of arterial gases from infants on IPPV had lactates above 120/PCO2, significantly more than 4.74 ± 2.73% on CPAP (p<0.05) and 2.47 ± 2.39% on no support.
Conclusion: Changes in arterial blood carbonic acid cause immediate inverse changes in lactic acid, because their anions interchange across cell membranes according to the Gibbs –Donnan equilibrium. Increasing PCO2 from 40 to 120 mmHg decreased lactate from 1.5 mmol/L to 0.5 mmol/L, so that the sum of carbonic and lactic acids increased from 2.72 mmol/L to only 4.17 mmol/L. This helps explain the neuroprotective effect of hypercapnoea and highlights the importance of avoiding any degree of hypocapnoea in infants on IPPV.