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products is altered, what happens to the concentrations of the other reactants or products as a new equilibrium is achieved? In the equations that follows, the larger, bold arrow indicates the change that initiates a shift in acid-base balance. The resulting direction of change in the equilibrium reaction due to the perturbation is indicated by the arrow symbol (! or •).

Respiratory Acidosis

Rapid changes in plasma pH can occur because of alterations in pulmonary ventilation. For example, CO2 retention due to chronic lung disease, or drugs or diseases that affect the nervous system and depress respiration, will cause an increase in the arterial Pco2 and a decrease in the ratio of HCO- to CO2 concentrations, with concomitant acidosis. In pulmonary arrest, acidosis can be as threatening to life as hypoxia. In respiratory acidosis, the primary event is the increase in plasma PCO2 resulting in a shift in the equilibrium reactions by mass balance:

From the equilibrium reactions, we can see that the hallmark of primary respiratory acidosis is a rise in both H+ and HCO3- concentrations. In acute cases, we find that the HCO- concentration rises about 1 mmol/L per each 10 mm Hg rise in the PCO2. The renal response to hypercapnia (the high PCO2) is to increase the rate of H+ secretion in both the proximal and distal tubules. This results both in an increase in proximal HCO— reabsorption, despite the elevation in the plasma HCO— concentration (the bicarbonate excretion curve moves toward the right in Fig. 3), and in increased HCO3— generation in the distal tubule and collecting duct. Both mechanisms tend to counteract the acidosis by further increasing the plasma HCO3— concentration; however, this renal adaptation to hypercapnia begins slowly and requires at least 24-48 hr. Thus, the initial defense against hypercapnia falls on the plasma and tissue buffers.

As the kidney responds to the acidosis, it creates an increase in the plasma HCO3— concentration, which exceeds that due to the hypercapnia alone. This chronic renal compensation will raise the HCO3— concentration by about 3.5 mmol/L for each mm Hg that the Pco2 has risen above the normal level of 40 mm Hg. The increased plasma HCO— buffers the increase in H+, but this correction is never complete, so the acidosis persists even with the higher HCO3— concentration. Thus, both acute respiratory acidosis as well as chronic respiratory acidosis with metabolic compensation produce an increase in the concentration of both H+ and HCO— in the plasma. The latter state is sometimes referred to as a "compensated" respiratory acidosis.

Respiratory Alkalosis

Respiratory alkalosis is the converse of respiratory acidosis. It develops secondary to hyperventilation, which occurs in several settings in which ventilation exceeds the metabolic demands of the body. The light-headedness one feels after blowing up a few balloons is a manifestation of respiratory alkalosis. Perhaps the most common setting is in the patient on a respirator when the minute volume has been set too high. Respiratory alkalosis also occurs after hyperventilation in response to low ambient O2, as at high altitude. Mountain climbers are in a chronic state of respiratory alkalosis that is compensated only partially by the renal excretion of HCO—. Inappropriate hyperventilation may occur because of abnormal stimuli to the central nervous system respiratory centers by tumors, infections, or poisoning with drugs such as aspirin. The hyperventilation lowers PCO2 and increases the ratio of plasma HCO— to Pco2 as can be seen from the mass balance relationship:

Again, as in respiratory acidosis, the H+ and HCO3— concentrations move in the same direction, but in respiratory alkalosis, they fall rather than rise. The appropriate renal compensation for the acute hypocap-nia is to reduce the secretion of H+, thereby excreting HCO^ and reducing its plasma concentration. The primary mechanism involved is a decrease in proximal bicarbonate reabsorption that is reflected in a shift to the left of the HCO^ excretion curve in Fig. 3. This renal response is much more rapid than the increase in plasma HCO^ concentration seen in respiratory acidosis because the kidney can rapidly "dump" bicarbonate into the urine merely by failing to reabsorb the filtered load completely. Because of the rapid loss of HCO^ by the kidneys, even with the acute development of respiratory alkalosis the HCO^ concentration falls by about 2.5 mmol/L per each 10 mm Hg fall in the Pco2 below the normal 40 mm Hg. With chronic respiratory alkalosis, the plasma HCO^ concentration falls by about 5 mmol/L per each 10 mm Hg fall in the PCO2. Thus, the hallmark of respiratory alkalosis even with renal compensation is a fall in both H+ and HCO^.

Metabolic Acidosis

The primary event responsible for metabolic acidosis may fall into one of four broad categories: (1) increased acid intake, (2) increased metabolic production of acid, (3) decreased acid excretion by the kidneys, and (4) increased loss of alkali from the body. In the first three categories, the primary event is an increase in the total H+ concentration in the plasma, resulting in the following shift in the buffer equilibrium:

In other words, the excess H+ is buffered by plasma HCO3— which, by mass action, results in a fall in the plasma HCO3— concentration. The excess carbonic acid generated is in equilibrium with CO2, but the excess CO2 can be rapidly disposed of by pulmonary ventilation.

In the case of excessive alkali loss from the body, which may occur from the gastrointestinal tract or the kidney, the primary event is a fall in the plasma HCO— concentration with the following consequences to the equilibrium:

The HCO3— losses are partially replaced by dissociation of H2CO3 resulting in the acidemia. But, in the cases of both a primary H+ excess as well as a HCO3— loss, note that the hallmark of metabolic acidosis is acidemia with a fall in HCO—, exactly the opposite pattern from that observed in respiratory acidosis. To maintain electro-neutrality, this fall in HCO" concentration must be compensated by a corresponding rise in the plasma concentration of Cl" or of the anionic weak base form of the ingested or metabolically produced acid, for example, lactate. Examination of the relative changes in Cl" and HCO" concentrations provides a useful tool in establishing the cause of a metabolic acidosis (see next section on the anion gap).

The pulmonary system responds to a fall in plasma pH by an increase in minute ventilation, and the resulting drop in PCO2 normally compensates partially for the metabolic acidosis. Because of the rapidity with which an increase in minute ventilation can change the plasma PCO2, respiratory compensation is usually found to coexist with the metabolic acidosis, a state also referred to as compensated metabolic acidosis. There is a decrease of approximately 1.25 mm Hg in the Pco2 for each 1 mmol/L fall in the HCO" concentration (below the normal 24 mmol/L) produced by the metabolic acidosis. However, note what happens to the mass balance relations as the PCO2 falls with hyperventilation. As would be desired, the H+ concentration falls, although not completely back to normal, but the HCO3" concentration also falls. Therefore, with the respiratory compensation the plasma is less acid, but the HCO3" concentration falls even lower. Thus, in metabolic acidosis, whether compensated or not, acidemia coexists with a low plasma HCO3" concentration.

The eventual correction of a metabolic acidosis depends on the loss of the excess acid or a net gain of HCO". The kidney can return the lost HCO" by conserving all the filtered HCO3" (as it normally does), and by increasing the rate at which it generates new HCO3" by the excretion of titratable acidity and ammonium. These processes are usually adequate to reverse completely the tendency toward metabolic acidosis from normal metabolism, but in disease states the kidney may be incapable of keeping up with the demand for HCO3" production and chronic acidosis will persist until the original cause is corrected.

TABLE 5 Causes of Metabolic Acidosis

With an increase in unmeasured Without an increase in unmeasured anions (anion gap > ~16) anions (anion gap < ~16)

Diabetic ketoacidosis Renal failure Starvation Salicylate poisoning Alcoholic ketoacidosis Ethylene glycol poisoning Methyl alcohol poisoning Paraldehyde poisoning Lactic acidosis

Diarrhea

Renal tubular acidosis Hypoaldosteronism Hyperparathyroidism Carbonic anhydrase inhibitors Ammonium chloride ingestion Drainage of pancreatic juice Ureterosigmoidostomy routine blood chemistries. These anions normally include sulfate, phosphate, lactate, urate, oxalate, pyru-vate, and small concentrations of several other organic acids.

In analyzing the cause of a metabolic acidosis, calculation of the anion gap helps to focus on the possible etiology, as summarized in Table 5. The anion gap in patients with normal renal function and no acid-base disturbance will be 12 mmol/L or less. An anion gap greater than 12, signals the presence of increased concentrations of acid anions usually associated with the conditions in the left-hand column. In the presence of renal failure, a large anion gap indicates accumulation of anions such as HPO4" and SO4" because of the decrease in glomerular filtration. Metabolic acidosis not associated with an increase in immeasurable anions in a patient with normal renal function will immediately focus attention on the eight possibilities listed in the right-hand column of Table 5.

Metabolic Alkalosis

Metabolic alkalosis results when there is an excessive loss of H+ from the body or excessive HCO" retention. It may also occur, but more rarely, when there is an excessive production of HCO". When H+ is lost from the body, as in vomiting, the HCO" concentration rises:

Anion Gap

The anion gap is a means of approximating the total concentrations of anions other than Cl" and HCO3" in the plasma. It is calculated as the difference between the plasma Na+ concentration and the sum of the Cl" and HCO" concentrations: ([Na+] + [K+]) - ([Cl"] + [HCO"]). This difference is normally about 12 mmol/L (normal range 8-16 mmol/L). Because there must be equal concentrations of anions and cations in the plasma for electroneutrality, the anion gap indicates that about 12 mmol/L of anions are not measured in

On the other hand, if HCO3" intake or production is increased, mass action causes the H+ concentration to fall:

Note that in either case metabolic alkalosis is characterized by a rise in plasma HCO". Respiratory compensation occurs by hypoventilation to increase Pco2, which partially corrects the alkalemia but results in a further

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