Co2

Any one of the above three concentrations (or pH) can be derived from the other two using either the Henderson-Hasselbalch equation (Eq. [7]) or the equivalent Henderson equation (Eq. [8]).

Table 1 gives the equivalent hydrogen ion concentration in nM for various pH values in the physiologic

TABLE 1 Relation between pH and H+ Concentration

7.00 100 ffi79 x 1.25

7.40 40 (normal reference values)

range. One can easily convert one to the other from one remembered value in this table. For an increase in pH of 0.1 unit, the H+ concentration falls to 0.8 times the previous H+ concentration. For a decrease in pH of 0.1 unit, the H+ concentration is 1.25 times the previous value. For example, remembering that a pH of 7.4 is 40 nmol/L H+, one can compute the H+ concentration corresponding to a pH of 7.3 as (1.25 • 40) 50 nmol/L, or for pH 7.5 as (0.8 • 40) 32 nmol/L H+. Use of the Henderson equation and this scheme has the distinct advantage of eliminating the use of logarithms in the solution of clinical problems, and it enables one to focus more directly on the important parameter of interest: the hydrogen ion concentration.

Both the Henderson-Hasselbalch and Henderson equations show that the HCO"/CO2 buffer system can be manipulated to change the plasma pH by altering the ratio of the plasma HCO" concentration to Pco2. Changes in the plasma HCO" concentration are produced by alterations in the renal retention or excretion of HCO", and changes in Pco2 are brought about by changes in the rate of respiration. The physiologic regulation of plasma pH by these mechanisms is considered in the next sections.

PULMONARY REGULATION OF Pco2

As shown earlier, when a strong acid is buffered in the plasma, the concentration of bicarbonate falls, whereas buffering of a base has the opposite effect. In both situations, changes in the pulmonary excretion of CO2 will serve to return the pH toward normal. As noted earlier, the pulmonary regulation of CO2 is the major biologic advantage of the HCO^/CO2 buffer system.

In metabolic acidosis (discussed later), the HCO^ concentration falls because it buffers the excess hydrogen ions. In response to the acidosis, hyperventilation lowers Pco2 and maintains plasma pH nearer to normal. This is referred to as respiratory compensation for the metabolic acidosis. Clinically, the increased ventilation in the severely acidotic patient is discernible to the physician as a deep, unhastened breathing referred to as Kussmaul breathing. In this respiration pattern, the acidotic patient increases his or her tidal volume to dilute the concentration of CO2 in alveolar air and, thus, in the arterial plasma. This slow, deep breathing, which is characteristic of acidosis, can be easily distinguished from the shallow, rapid breathing that occurs in pulmonary congestion because of pulmonary edema, infarction, or infection.

In contrast to the respiratory response to metabolic acidosis, in metabolic alkalosis hypoventilation occurs. This increases the concentration of alveolar CO2 and, hence, its partial pressure in body fluids. The increase in the concentration of H2CO3 in the body fluids results in increased formation of both H+ and HCO", which counteract the alkalosis. However, the hypoventilatory effect in alkalosis is not as effective as that of hyperventilation in acidosis. In metabolic alkalosis, respiratory compensation requires a decreased minute volume of ventilation, which also decreases arterial Po2, and which would be opposed by normal regulatory feedback mechanisms that counteract hypoxia.

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