Chapter 7, cont…(Page 3)

Acid­base balance

ACID­BASE MAP

To know how much compensation to expect for each acid­base disorder, the arrows in Table 7­3 must be replaced with real numbers. Studies of some primary acid­base disorders have defined the actual human compensation when the disorder is uncomplicated by another primary acid­base disturbance.

A summary of this work appears in Fig. 7­3. This figure is the same nomogram as in Fig. 7­2, with the addition of superimposed radiating confidence bands for the primary acid­base disorders. When confidence bands are placed on the nomogram, the entire arrangement is called an acid­base map.

The confidence bands are areas in which 95% of the studied population fell when their blood gas results were plotted. For example, to generate the band for metabolic acidosis, blood gas results from patients with uncomplicated diabetic ketoacidosis were obtained before they received treatment. The blood gas data were analyzed statistically, and a narrow band was drawn that included 95% of the values for pH and PaCO₂.

Fig. 7­3. Acid­base map. (From Goldberg, M., Green, S.B., Moss, M.L., et al.: JAMA 223:269­275, 1973, Copyright 1973, American Medical Association.)

IN VIVO TITRATION CURVE FOR CARBON DIOXIDE

The long, diagonal band in Fig. 7­3 defines the in vivo titration curve for carbon dioxide (including its confidence limits). This curve was developed from two separate studies. To determine the band for respiratory alkalosis, patients undergoing elective surgery (e.g., routine hysterectomy) were acutely hyperventilated while under the effects of general anesthesia, and arterial samples were collected. A steady state was reached in 10 minutes, and blood gas results from this group defined the band for acute respiratory alkalosis.

To generate the band for acute carbon dioxide retention, healthy human volunteers breathed 5% and 7% carbon dioxide in an environmental chamber, and blood gas samples were collected from an indwelling arterial line. A steady state was also reached in 10 minutes, and blood gas results from these subjects defined the band for acute respiratory acidosis. These two bands, when connected, represent the in vivo titration curve for carbon dioxide and show how the healthy person titrates acute changes in carbon dioxide. Note that a sudden change in the PaCO₂ of 20 mm Hg alters the HCO₃^- approximately 2 to 3 mEq/L. Since this change occurs within 10 minutes, it reflects a biochemical reaction only and has nothing to do with renal compensation, which occurs much later. The direction of change is predicted by the hydration equation for carbon dioxide (Equation 7). As carbon dioxide is acutely retained, it combines with water and the equation is driven to the right, forming more HC03. As carbon dioxide is acutely excreted, the equation is driven to the left and HCO₃^- falls.

(Eqn 7-7)

The amount of change in HCO₃^-, and hence the resulting pH, cannot be predicted from the mere addition of carbon dioxide to blood. Carbon dioxide is buffered in the interstitium and intracellular compartments, and only in vivo human studies can show the actual result of buffering an acute change in carbon dioxide.

From the in vivo band, it can be noted that for every 10 mm Hg acute increase in the PaCO₂, the pH decreases approximately 0.07 units; every 10 mmHg decrease in the PaCO₂ raises the pH approximately 0.08 units. This is a shorthand way of memorizing the carbon dioxide titration curve. Knowing the expected changes in both pH and HCO₃^- sharpens diagnostic ability.

BASE EXCESS

Base excess is an in vitro measurement that was introduced to characterize the metabolic component of acid­base disorders. Base excess was widely used before studies showed the human response to primary acid­base disorders (the in vivo confidence bands). Although the confidence bands are more accurate than base excess in diagnosing the metabolic component, base excess is still calculated and reported in many blood gas laboratories. However, for the novice base excess is a confusing concept and probably impedes understanding of acid­base problems.

To calculate base excess, the blood sample is equilibrated at two CO₂ tensions different from the patient's PaCO₂, the pH is measured at both CO₂ levels, and the interpolated pH at PaCO₂ of 40 mmHg is used to calculate a standard bicarbonate (normal 24 mEq/L). Any change from this standard bicarbonate represents the metabolic component of the acid­base problem. The actual base excess (reported in mEq/L) is a derived value; the deviation from the standard bicarbonate is multiplied by a factor that takes into account hemoglobin content. If the patient's bicarbonate (calculated from blood gas measurements) is above the derived value, a positive base excess is present (i.e., a component of metabolic alkalosis); if the patient's bicarbonate is below the derived value, a negative base excess is present (i.e., a metabolic acidosis component).

A scientific critique of the base excess concept is provided in the article by Schwartz and Relman (1963).

ACUTE VS. CHRONIC RESPIRATORY DISORDERS

The acid­base map introduces the terms acute and chronic. In acid­base terminology these terms are synonymous with compensated and uncompensated; on the acid­base map, these terms apply only to respiratory acidosis and respiratory alkalosis.

· Acute respiratory acidosis occurs when carbon dioxide is retained acutely; it is the state of affairs before the kidneys have had a chance to compensate by retaining any HCO₃^-.

· Chronic respiratory acidosis occurs when the retained carbon dioxide has been, to some degree, buffered by the kidney's retention of HCO₃^-. The pH is higher than in acute respiratory acidosis, but it is still below 7.4. The HCO₃^- retention does not begin for at least a few hours and may take up to 3 days for maximal compensation.

· Acute respiratory alkalosis occurs when carbon dioxide is blown off acutely, before the kidneys have had a chance to compensate by excreting HCO₃^-. As with acute CO₂ retention, this change can occur quickly (within minutes) and may last for hours before there is any compensation.

· Chronic respiratory alkalosis occurs when the reduction of carbon dioxide is compensated for by the renal excretion of HCO₃^- . The pH is lower than in acute respiratory alkalosis, but it is still above 7.4. The HCO₃^- excretion does not begin for at least a few hours and takes up to 3 days for maximal compensation.

The terms chronic and compensation do not imply "normal pH" (Fig. 7­3). Maximal compensation simply means that the body has done everything it can to return the pH toward normal. Rarely does compensation return pH to normal. A normal pH in the face of an acid­base disorder strongly suggests a mixed picture, with two or more primary disorders balancing each other. Occasionally patients can have a pH in the normal range when they have chronic respiratory acidosis or metabolic alkalosis, but the pH still does not return to the patient's true normal pH. For example, if a patient's normal pH is 7.40, compensation for respiratory acidosis might return it to 7.37 or 7.38 but not to 7.40.

ACUTE VS. CHRONIC METABOLIC DISORDERS

Why are there no acute bands for metabolic acidosis and metabolic alkalosis? The confidence bands shown for the metabolic disorders are in fact chronic. Patients whose blood gas values defined these bands had their condition long enough to reach their maximal physiologic compensation.

The compensation for metabolic acidosis occurs much more quickly than the compensation for respiratory disorders; in response to an acute reduction of HC0₃^-, the maximal reduction of PaCO₂ occurs within 12 to 24 hours.

Not much is known about how long it takes for the maximal compensation of metabolic alkalosis. Except when massive amounts of HC0₃^- are given to a patient, acute metabolic alkalosis is practically unknown in clinical practice. Also, not all patients seem to compensate for metabolic alkalosis with hypoventilation, making the band for metabolic alkalosis the least well characterized. Otherwise healthy people do not usually retain carbon dioxide to compensate for metabolic alkalosis, whereas patients suffering from severe lung disease or dehydration commonly retain carbon dioxide to compensate for this disorder.

Although acute and chronic changes are fairly well­defined for metabolic acidosis, acid­base maps generally omit the acute change. Fig. 7­4 shows the time course for acute metabolic acidosis based on the results from one human study (Pierce, Fedson, Brigham, et al., 1970); in this study patients who had cholera developed severe metabolic acidosis and took 11 to 24 hours to achieve maximal compensation. Their blood gas values moved along the pathway shown. Thus it should be kept in mind that a patient with early, uncomplicated metabolic acidosis may manifest blood gas values that do not fall into the commonly presented band for this disorder.

If the patient has had metabolic acidosis for at least 12 hours, his blood gas values can reasonably be expected to fall into the chronic metabolic acidosis confidence band (Fig. 7­3). After this period, gas values that fall above the band suggest a problem with compensation, e.g., a concomitant respiratory acidosis; gas values that fall below the band suggest a concomitant respiratory alkalosis.

The pitfall in diagnosing metabolic acidosis discussed above is one of several caveats regarding the acid­base map. Acid­base maps have probably been more abused than properly used. Although this map is used in figuring out acid­base problems, especially mixed disorders, it is important to point out pitfalls from the beginning. Most pitfalls can be avoided by practicing the author's First Law of Acid­Base Maps: The acid­base map does not diagnose any acid­base disorder. Reliable diagnosis can only be made clinically, in conjunction with the blood gas values and the other laboratory data.

Fig. 7­4. Time course for compensation of metabolic acidosis. (Based on data from Pierce, N.F., Fedson, D.S., Brigham, K.L., et al.: Ann. Intern. Med. 72:633. 1970.)

With this caveat firmly emblazoned, the following are realistic uses of the acid­base map:

1. To help confirm the presence of a primary acid­base disorder

2. To help rule out a primary disorder as the sole cause of a patient's acid­base disturbance

3. To help follow a patient's hour­to­hour or day­to­day course

MIXED ACID­BASE DISORDERS

So far simple or uncomplicated acid­base disorders have been emphasized. Patients with pulmonary disease often have two or more acid­base disorders occurring at the same time (see the box below); they are called mixed, or complicated, acid­base disorders. As a general rule, the more severe an acid­base disorder, the more likely it will be accompanied by another primary acid­base disturbance. For example, patients with severe respiratory acidosis (e.g., a PaCO₂ of 80 mm Hg) are more likely to manifest accompanying metabolic acidosis than when the respiratory acidosis is mild to moderate (e.g., a PaCO₂ of 50 mm Hg). This is simply because they are more likely to be severely hypoxemic or have cardiovascular impairment. The acid­base map is especially useful in sorting out these mixed disorders.

Theoretically, since the physiologic processes and not the blood pH define acid­base disorders, any possible combination of disorders, even three or more, may occur in one patient. Unusual but explainable combinations are listed in the box on this page.

Mixed acid­base problems are illustrated by the remaining cases. Detailed treatment of acid­base disorders, although outside the scope of this book, is discussed to some extent in these cases. The real key to treatment is understanding acid­base physiology in the clinical setting. This understanding, more than anything, assures rational management, whatever the underlying disturbance.

Two hours later she seems more tired, and her peak flow is less than 60 L/min. Blood gas values while breathing 40% inspired oxygen show pH, 7.20; PaCO₂, 52 mm Hg; PaO₂, 65 mm Hg. At this point intubation and assisted ventilation are considered. What is her acid­base status?
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