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pH-bicarbonate diagram (Fig. 6B), as described later. The reader is referred to Chapter 31 for more details about renal mechanisms.

Respiratory Acidosis

A respiratory acidosis occurs when Pco2 increases. Increased Pco2 decreases the [HCO^]/ Pco2 ratio and decreases pH along the blood buffer line, between points A and B in Fig. 6B. Hypercapnia, or an increase in arterial Pco2, occurs when ventilation is not sufficient for the existing level of CO2 production. Ventilation may be depressed at rest, for example, with a drug overdose that depresses respiratory centers (see Chapter 22), or ventilation may not increase sufficiently for increased metabolism during exercise (see Chapter 21).

If an acute respiratory acidosis is not corrected, then it is said to be a chronic respiratory acidosis, and renal mechanisms will increase HCO^, as described in Chapter 31, to return pH toward normal. The movement from point B to D on Fig. 6B is termed a metabolic compensation (or renal compensation) for a chronic respiratory acidosis, and it represents an increase in base excess. The final acid-base status at point D (Fig. 6B) is called a compensated respiratory acidosis. Metabolic compensation takes 1-2 days, and pH is not restored to a completely normal value of 7.4 in reality. A hallmark of an acute or compensated respiratory acidosis is an increase in [HCO^] and [H+].

Respiratory Alkalosis

A respiratory alkalosis occurs when Pco2 decreases. This increases the [HCO^]/Pco2 ratio and increases pH along the blood-buffer line, between points A and C in Fig. 6B. A respiratory alkalosis increases pH, but [HCO^] is decreased because less total acid is present. Hypocapnia, or a decrease in arterial Pco2, occurs when ventilation is in excess of that necessary for CO2 production, for example, when ventilation is stimulated by low O2 levels at high altitude (Chapter 22).

If the respiratory alkalosis is chronic, then renal mechanisms will decrease [HCO^], as described in Chapter 31, to return pH toward normal. The movement from point C to F on Fig. 6B is termed a metabolic or renal compensation for a chronic respiratory alkalosis, and base excess is decreased. The final acid-base status at point F (Fig. 6B) is called a compensated respiratory alkalosis. Renal compensation for a respiratory alkalosis can occur more quickly than compensation for a respiratory acidosis, but it still takes a day or more and does not return pH completely to normal. Both [HCO^] and [H+] are decreased in a compensated respiratory alkalosis.

Metabolic Acidosis

A metabolic acidosis occurs when the kidneys do not excrete sufficient fixed acid, or retain sufficient bicarbonate, to maintain the normal [HCO^]/Pco2 ratio when Pco2 = 40 mm Hg. Metabolic acidosis increases [H+] but decreases [HCO^], and causes a parallel shift of the blood-buffer line from points A to G in Fig. 6B. Base excess is decreased (or base deficit is increased) in a metabolic acidosis. Physiologic mechanisms causing a metabolic acidosis are detailed in Chapter 31.

With a chronic metabolic acidosis, the respiratory control system senses decreased pHa and causes a reflex increase in ventilation (see Chapter 22). Increased ventilation causes Pco2 to decrease, increases the base excess, and returns pHa toward normal (point G to F in Fig. 6B). In such a compensated metabolic acidosis, pH may not return completely to normal because decreased Paco2 may limit the increase in ventilation necessary for complete compensation (see Chapter 22). With an acute, or compensated, metabolic acidosis, [H+] is increased but [HCO^] is decreased.

Metabolic Alkalosis

A metabolic alkalosis occurs when the kidneys excrete excess fixed acid, or retain too much bicarbonate, for the normal [HCO^]/Pco2 ratio when Pco2 = 40 mm Hg. Metabolic alkalosis increases pH and [HCO^], and causes a parallel shift of the blood-buffer line from points A to E in Fig. 6B as base excess increases. Physiologic mechanisms causing a metabolic alkalosis are detailed in Chapter 31.

Respiratory compensation for a chronic metabolic alkalosis involves decreased ventilation, which increases Pco2 (points E to D in Fig. 6B). However, increased Paco2 and possible decreases in arterial O2 levels (see Chapter 22), prevent a complete return to normal pH with a compensated metabolic alkalosis. With an acute, or compensated, metabolic alkalosis, [H+] is decreased, but [HCO^] is increased.

Diagnosing Acid-Base Disturbances

The primary cause of a chronic acid-base disturbance cannot be determined from a bicarbonate-pH diagram, or Pco2, pH, and [HCO^] data alone. Notice that the data are similar for a compensated respiratory acidosis and a compensated metabolic alkalosis (point D, Fig. 6B), or a compensated respiratory alkalosis and compensated metabolic acidosis (point F, Fig. 6B). Therefore, other details of the patient's history, pulmonary function, or blood chemistry (see Chapter 31) must be obtained for a proper diagnoses.

Suggested Readings

Bauer C. Structural biology of hemoglobin. In Crystal RG, West JB, Weibel ER, Barnes PJ, eds. The lung: Scientific foundations, Vol 1, 2nd ed. Philadelphia: Lippincott-Raven, 1997, pp 1615-1624. Davenport HW. The ABC of acid base chemistry, 6th ed. Chicago: University of Chicago Press, 1974.

Jian L, et al. S-nitrosohaemoglobin: A dynamic activity of blood involved in vascular control. Nature 1996;380:221.

Roughton FJw. Transport of oxygen and carbon dioxide. In Perm wO, Rahn H, eds. Handbook of physiology, Section 3, Respiration. Bethesda, MD: American Physiological Society, 1964, pp 767-826.

Stewart PA. Independent and dependent variables of acid-base control. Respir Physiol 1978;33:9.

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