Articles on Medical Diseases and Conditions

Tag: alkalosis

  • Interpretation of Acid-Base Data

    Acid-base data interpretation has always been one of the more difficult areas of laboratory medicine. In most uncomplicated untreated cases the diagnosis can be achieved with reasonable ease. There are several ways of approaching an acid-base problem. One way is to examine first the arterial PCO2 value. Since primary respiratory disorders result from hypoventilation or hyperventilation, which, in turn, are reflected by a change in arterial PCO2, normal PCO2 with abnormal pH is strong evidence against a primary respiratory disorder and should be an uncompensated metabolic disorder.

    If PCO2 is decreased, there are two major possibilities:

    1. The primary disorder could be respiratory alkalosis (hyperventilation). If so, pH should be increased in acute (uncompensated) cases or partially compensated cases. In fully compensated cases pH is within reference range, but frequently it is more than 7.40 even within the reference range.

    2. The primary disorder could be metabolic acidosis. If so, pH should be decreased in partially compensated cases. In fully compensated cases pH is within its reference range (similar to fully compensated respiratory alkalosis), but frequently it is less than 7.40 even within the reference range.

    If PCO2 is increased, there are also two major possibilities:

    1. The primary disorder could be respiratory acidosis (hypoventilation). If so, pH should be decreased in acute (uncompensated) cases or partially compensated cases. In fully compensated cases pH is within reference range, but frequently it is less than 7.40 even within reference range.

    2. The primary disorder could be metabolic alkalosis. If so, pH should be increased in partially compensated cases. In fully compensated cases pH is within its reference range (similar to fully compensated respiratory acidosis), but pH frequently is more than 7.40 even within the reference range.

    There is another way to interpret the data. If one first inspects pH, decreased pH means acidosis and increased pH means alkalosis. One then inspects the PCO2 value. If the PCO2 has changed in the same direction as the pH, the primary disorder is metabolic. If the PCO2 has changed in the opposite direction from that of the pH, the primary disorder is respiratory.

    Base excess analysis is not a vital part of this type of algorithm. However, base excess can sometimes be helpful, both as additional evidence for certain types of acid-base disorders or to help detect the presence of active acid-base disorder in fully compensated cases. A negative base excess is found in metabolic acidosis and, to a lesser extent, in respiratory alkalosis. A positive base excess is found in metabolic alkalosis and, to a lesser extent, in respiratory acidosis.

  • Summary of Acid-Base Changes

    To summarize plasma pH problems, in metabolic acidosis there is eventual HCO–3 deficit, leading to decreased plasma pH and decreased CO2 content (or CO2 combining power). In respiratory acidosis there is primary H2CO3 excess, which causes decreased plasma pH, but the CO2 content is increased due to renal attempts at compensation. In metabolic alkalosis there is eventual bicarbonate excess leading to increased plasma pH and increased CO2 content. In respiratory alkalosis there is primary carbonic acid deficit, which causes increased plasma pH, but the CO2 content is decreased due to renal attempts at compensation. The urine pH usually reflects the status of the plasma pH except in hypokalemic alkalosis, where there is acid urine pH despite plasma alkalosis.

    As noted, CO2 content or combining capacity essentially constitutes the numerator of the Henderson-Hasselbalch equation. PCO2 is essentially a measurement of the equation denominator and can be used in conjunction with pH to indicate acid-base changes. This is the system popularized by Astrup and Siggaard-Anderson. PCO2 follows the same direction as the CO2 content in classic acid-base syndromes. In metabolic acidosis, PCO2 is decreased, because acids other than H2CO3 accumulate, and CO2 is blown off by the lungs in attempts to decrease body fluid acidity. In metabolic alkalosis, PCO2 is increased if the lungs compensate by hypoventilation; in mild or acute cases, PCO2 may remain normal. In respiratory alkalosis, PCO2 is decreased because increased ventilation blows off more CO2. In respiratory acidosis, PCO2 is increased because of CO2 retention due to decreased ventilation.

  • Metabolic Alkalosis

    Alkalosis may also be divided into metabolic and respiratory types. In metabolic alkalosis, three relatively common situations should be discussed.

    Alkali administration. Alkali administration most commonly occurs when sodium bicarbonate is taken in large quantities for the treatment of peptic ulcer symptoms. If this happens, excess HCO–3 is absorbed above the amount needed to neutralize stomach hydrochloric acid (HCl). The numerator of the Henderson-Hasselbalch equation is increased, the normal 20:1 ratio is increased, and the pH therefore rises. The CO2 content also rises because of the additional HCO–3. Lactate, citrate, or acetate in sufficient quantities may also produce alkalosis, since they are metabolized to HCO–3.

    Acid-losing alkalosis. Acid-losing alkalosis most frequently results from severe or protracted vomiting, as may occur with pyloric stenosis. Gastric HCl is lost in vomiting. Gastric HCl was originally produced by conversion of H2CO3 to HCO–3 and H+, mediated by carbonic anhydrase of the gastric mucosa. The HCO–3 is kept in the bloodstream, but the H+ is secreted into the gastric lumen as HCl. When HCl is lost through vomiting, the H+ component of HCl is also continually being lost. The CO2 content becomes increased, because the HCO–3 that is released when HCl is produced remains in the bloodstream and increases when additional HCl is formed to replace that which is being lost. Therefore, the 20:1 ratio is increased and the pH is increased. Since H2CO3 is decreased, as it is being continually used to produce more HCl, the lungs tend to retain CO2 to compensate. Therefore, PCO2 may actually increase, although not enough to prevent increase of the 20:1 ratio.

    Hypokalemic alkalosis. Hypokalemic alkalosis is most commonly due to excess potassium ion (K+) loss by the kidney, as might happen with overuse of certain diuretics that cause K+ as well as sodium ion (Na+) loss. Normally, most body K+ is intracellular, whereas most Na+ and H+ is extra-cellular. When excess K+ is lost in the urine, intracellular K+ diffuses out of the cells to replace some of that being lost from plasma; Na+ and H+ move into the cells to replace the K+ that has moved out. Thus, H+ is lost from extracellular fluid and plasma. A second mechanism depends on the fact that sodium is reabsorbed from the urine into the renal distal tubule cells by an active transport mechanism. This transport mechanism involves excretion of H+ and K+ into the urine to replace the reabsorbed Na+. In this exchange (or transport) system, H+ and K+ compete with each other. Therefore, if an intracellular deficit of K+ exists (in the tubule cells), more H+ is excreted into the urine to allow the reabsorption of the same quantity of sodium without losing as much K+. The result of renal H+ loss and extracellular H+ loss is an acid-losing type of alkalosis. Therefore, more H+ is manufactured by the kidney from H 2CO3 to replace lost extracellular fluid H+: more HCO–3 ions are thereby formed, and the numerator of the Henderson-Hasselbalch equation is increased. The denominator is eventually increased if the lungs attempt to compensate by increasing CO2 retention by slower breathing. However, respiratory compensation is frequently minimal or insignificant in hypokalemic alkalosis, so that the PCO2 frequently remains normal. Also, the urine pH is decreased because of the excess H+ being excreted in the urine. This is the opposite of what one would ordinarily expect, because in acidosis, the kidney usually attempts to compensate by excreting more H+(acid urine), whereas in alkalosis it normally tries to conserve H+ and thus produces a urine of higher pH (alkaline urine).