Bicarbonate/Carbon Dioxide Buffer
The pH of any buffer system is determined by the concentration ratio of the buffer pairs and the pKa of the system p. 378). The pH of a bicarbonate solution is the concentration ratio of bicarbonate and dissolved carbon dioxide ([HCO3-]/[CO2]), as defined in the Henderson-Hasselbalch equation (^ A1). Given [HCO3] = 24mmol/L and [CO2] = 1.2mmol/l, [HCO3-]/ [CO2] = 24/1.2 = 20. Given log20 = 1.3 and pKa = 6.1, a pH of 7.4 is derived when these values are set into the equation (^ A2). If [HCO 3 ] drops to 10 and [CO2] decreases to 0.5 mmol/L, the ratio of the two variables will not change, and the pH will remain constant.
When added to a buffered solution, H+ ions combine with the buffer base (HCO3- in this case), resulting in the formation of buffer acid (HCO3- + H+ ^ CO2 + H2O). In a closed system from which CO2 cannot escape (^ A3), the amount of buffer acid formed (CO2) equals the amount of buffer base consumed (HCO3 ). The inverse holds true for the addition of hydroxide ions (OH- + CO2 ^ HCO3 ). After addition of 2 mmol/L of H+, the aforementioned baseline ratio [HCO3-]/[CO2] of 24/1.2 (^ A2) changes to 22/3.2, making the pH fall to 6.93 (^ A3). Thus, the buffer capacity of the HCO3-/ CO2 buffer at pH 7.4 is very low in a closed system, for which the pKa of 6.1 is too far from the target pH of 7.4 (^ pp. 138,378 ff).
If, however, the additionally produced CO2 is eliminated from the system (open system; ^ A4), only the [HCO3 ] will change when the same amount of H+ is added (2 mmol/L). The corresponding decrease in the [HCO3-]/[CO2] ratio (22/1.2) and pH (7.36) is much less than in a closed system. In the body, bicarbonate buffering occurs in an open system in which the partial pressure (PCO2) and hence the concentration of carbon dioxide in plasma ([CO2] = a •PCO2; ^ p. 126) are regulated by respiration (^ B). The lungs normally eliminate as much CO2 as produced by metabolism (1500020 000 mmol/day), while the alveolar PCO2 remains constant (^ p. 120ff.). Since the plasma PCO2 adapts to the alveolar PCO2 during each respiratory cycle, the arterial Pco2 (Paco2) also remains constant. An increased supply of H+ in the periphery leads to an increase in the Pco2 of venous blood (H+ + HCO3- ^ CO2 + H2O) B1 ). The lungs eliminate the additional CO2 so quickly that the arterial PCO2 remains practically unchanged despite the addition of H+ (open system!).
The following example demonstrates the quantitatively small impact of increased pulmonary CO2 elimination. A two-fold increase in the amount of H+ ions produced within the body on a given day (normally 60 mmol/day) will result in the added production of 60 mmol more of CO2 per day (disregarding non-bicarbonate buffers). This corresponds to only about 0.3% of the normal daily CO2 elimination rate.
An increased supply of OH- ions in the periphery has basically similar effects. Since OH- + CO2 ^ HCO3-, [HCO3-] increases and the venous PCO2 becomes smaller than normal. Because the rate of CO2 elimination is also reduced, the arterial PCO2 also does not change in the illustrated example (^ B2).
At a pH of 7.4, the open HCO3/CO2 buffer system makes up about two-thirds of the buffer capacity of the blood when the PCO2 remains constant at 5.33 kPa (^ p. 138). Mainly intracellular non-bicarbonate buffers provide the remaining buffer capacity.
Since non-bicarbonate buffers (NBBs) function in closed systems, their total concentration ([NBB base] + [NBB acid]) remains constant, even after buffering. The total concentration changes in response to changes in the hemoglobin concentration, however, since hemoglobin is the main constituent of NBBs (^ pp. 138,146). NBBs supplement the HCO3-/ CO2 buffer in non-respiratory (metabolic) acid-base disturbances (^ p. 142), but are the only effective buffers in respiratory acid-base disturbances (^ p. 144).
I— A. Bicarbonate buffers in closed and open systems
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