Chapter 7, cont…(Page 2)

Acid­base balance

ACID­BASE NOMOGRAM

Since the Henderson­Hasselbalch equation deals with the log of two variables in a ratio (Equation2), knowing the pH and the PaCO₂ does not lend itself to easy mental calculation of the HCO₃^-. Several nomograms have been developed that graphically solve the Henderson­Hasselbalch equation; they provide a solution to the equation as well as an introduction to diagnosing clinical acid­base problems.

The nomogram in Fig. 7­2 plots the PcO₂ on the abscissa against the pH on one ordinate and hydrogen ion concentration ([H⁺]) on the other. The HCO₃^- isopleths (lines of equal HCO₃^-) radiate out from the left lower corner of the graph. (There are other ways of graphing the Henderson­Hasselbalch equation; for example, some nomograms plot PaCO₂ against HCO₃^-, with pH lines radiating out in a fan­shape. All are equally valid, but I prefer the nomogram in Fig. 7­2 because it emphasizes what is actually measured: pH and PaCO₂.)

The following are two examples using the Henderson­Hasselbalch nomogram:

1. Given a pH of 7.1 and a PaCO₂ of 70 mm Hg, what is the HCO₃^-? Drawing a line horizontally from a pH of 7.1 to where it intersects a vertical line up from a PaCO₂ of 70 mmHg, the HCO₃^- is 21 mEq/L.

2. Given a pH of 7.4 and a PaCO₂ of 10 mm Hg, what is the HCO₃^-? Doing the same procedure shown in the first example, the lines intersect the HCO₃^- isopleth at 6 mEq/L.

The same HC03 values may be obtained by solving the Henderson­Hasselbalch equation; this nomogram merely does the calculation for you.

Fig. 7­2. Graphic solution of the Henderson­Hasselbalch equation.

ACIDEMIA AND ALKALEMIA

In the past there was much confusion over the terminology of acid­base disorders. This confusion arose mainly because some workers looked at acid­base disorders in terms of blood changes only, whereas others viewed the same disorders as in vivo, physiologic processes. Both the "laboratory" and "clinical" proponents were often saying the same thing but were using different terms. Agreement was reached in the 1960's, and there is now an internationally accepted terminology, one that adopts a clinical approach.

In terms of pH, the blood can reflect either acidemia or alkalemia. Acidemia indicates an acid pH (less than 7.36), and alkalemia indicates an alkaline pH (greater than 7.44). The terms acidemia and alkalemia provide no specific information about acidosis vs. alkalosis, metabolic disorder vs. respiratory disorder, or the underlying clinical causes. To characterize a patient's blood as having acidemia or alkalemia, only one value is needed: pH.

ACIDOSIS AND ALKALOSIS

Since pH is determined by a ratio of HCO₃^- to PaCO₂, the Henderson­Hasselbalch equation may be conveniently reduced for clinical use to

The kidneys are responsible for maintaining HCO₃^-, and the lungs are responsible for maintaining PaCO₂ (see Chapter 4). Thus

Since the kidneys affect HCO₃^- changes slowly (from hours to days) and since the lungs may affect changes in PaCO₂ quickly (within minutes), the ratio determining pH is viewed as slow over fast; this concept is important when considering the compensatory changes for acid­base disturbances. For example, a compensation that involves altering the HCO₃^- occurs relatively slowly. Understanding acid­base disorders depends on knowing how the kidneys and the lungs act and react to the acid­base disorder. This knowledge leads to the concept of acidosis and alkalosis.

In contrast to acidemia and alkalemia, which refer to the in vitro determination of blood pH, acidosis and alkalosis refer to the physiologic processes occurring in the patient. Acidosis and alkalosis cannot be fully characterized without reference to the patient's history, physical examination, serum electrolyte values, and other relevant laboratory data. Acidosis and alkalosis cannot be defined by reference to blood changes only.

The numerator of the Henderson­Hasselbalch equation, HCO₃^-, is called the metabolic component, and the denominator, PaCO₂, is called the nonmetabolic or respiratory component (the term respiratory is used henceforth instead of nonmetabolic). There may be both metabolic and respiratory causes of acid­base disorders. The primary change determines the type of disorder; these disorders are defined in the box on p. 135.

Compensatory processes are secondary changes; as such, they occur after the primary process has begun and occur solely as an attempt to correct the pH change brought about by the primary disorder. Compensatory changes are not termed acidosis or alkalosis.

Acidosis and alkalosis refer to what is happening in the patient, not necessarily to what is manifested in the blood. For example, a low pH may reflect an acidosis alone or may indicate an acidosis plus an alkalosis. If the physiologic process causing the disorder is uncomplicated by other acid­base disorders, then the blood is appropriately acidemic (low pH) from an acidosis or alkalemic (high pH) from an alkalosis. However, if another acid­base disorder is present, the resulting pH may be high or low. So­called mixed acid­base disorders are common in patients with respiratory disease and are discussed in a later section.

The box below lists some clinical conditions responsible for the primary acid­base disorders. Keep in mind that acidosis and alkalosis are physiologic processes caused by a clinical disturbance that result in a tendency to reduce or elevate HC03 or PaCO₂. The list is not exhaustive, but it does include many clinical causes of acid­base disorders.

ANION GAP

A useful aid in diagnosing both simple and mixed acid­base disorders is the anion gap (AG). The AG is the difference between the principal measured cations and anions. The measured cations are sodium (Na⁺) and potassium (K⁺), and the measured anions are chloride (Cl^­) and bicarbonate (HCO₃^-). Since potassium is of relatively low concentration, it is usually ignored when calculating the AG.

(Eqn 7-6)

The normal AG is 12 + 4 mEq/L and is a result of the presence of anion proteins, sulfates, and other molecules that are not routinely measured with the serum electrolytes. An elevated AG is almost always caused hy metabolic i~sis. However, not all cases of metabolic acidosis manifest an elevated AG. The AG is elevated when the metabolic acid added to the blood contains an "unmeasured" anion, such as lactate or ketones. States of metabolic acidosis that add no unmeasured anion to the blood do not elevate the AG and are called hyperchloremic metabolic acidosis. In hyperchloremic metabolic acidosis the reduced HCO₃^- is replaced by chloride, which is measured as part of the serum electrolytes.

PRIMARY VS. COMPENSATORY PROCESSES

A metabolic acidosis or metabolic alkalosis is a physiologic acid­base disorder in which the primary change is in the HC0₃-. A respiratory acidosis or respiratory alkalosis is one in which the primary change is in the PaCO₂. The key word is primary, meaning first change. If HCO₃^- changes first and then PaCO₂ changes as a compensatory event, the basic process is metabolic, not respiratory, and the patient has a metabolic acidosis or metabolic alkalosis with respiratory compensation. Similarly, if the primary event is a change in PaCO₂ and HCO₃^- changes as compensation, the basic process is either respiratory acidosis or respiratory alkalosis with metabolic compensation.

From the basic relationship expressed by the Henderson­Hasselbalch equation, what is the primary change and the compensatory response for metabolic acidosis? The body wants to keep pH in the normal range so that, given a primary event, the compensatory response should be predictable.

In metabolic acidosis, the primary event leads to reduction of HCO₃^-. This reduction may arise from an actual loss of HCO₃^- (renal or gastrointestinal) or from the buffering of fixed acid (e.g., lactic acid). Initially,

Primary event

As HCO₃^- decreases, pH falls. The body responds by decreasing the denominator (i.e., by hyperventilating) as much as possible. (The amount of hyperventilation is discussed in the section on confidence bands.) This decrease in the denominator alters pH back toward normal:

Primary event plus compensatory response

A smaller arrow than that shown for HCO₃^- is shown for the decrease in PaCO₂ because the compensatory PaCO₂ change is not of the same magnitude as the primary HCO₃^- change. As a result pH does not return completely to normal but remains somewhat decreased.

Table 7­3. Primary event and compensatory response for acid­base disorders
Acid­base disorder	Primary event	Compensatory response
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis

A common clinical cause of metabolic acidosis is lactic acidosis. For example, suppose a patient in shock produces enough lactic acid to lower his HCO₃^- to 12 mEq/L or half of normal. Before any compensatory response occurs, i.e., when the PaCO₂ is still normal, the pH will be 7.10.

Primary event

The compensatory response of hyperventilation, e.g., lowering the PaCO₂ to 30 mm Hg results in a ratio of HCO₃^- to PaCO₂ that elevates pH to 7.30.

Primary event plus compensatory response

A pH of 7.30 is not normal, but it is a lot safer than 7.10. The compensatory response in this example is hyperventilation and the response should not be termed respiratory alkalosis. Alkalosis implies a primary physiologic process; hyperventilation is only a secondary or compensatory phenomenon. This differentiation is not just an exercise in semantics; the terminology helps to distinguish between single acid­base disorders and mixed acid­base disorders, an area that is often confusing.

Table 7­3 shows the basic relationship of the Henderson­Hasselbalch equation for each of the primary acid­base disorders and their compensatory responses. The arrows represent relative changes in the components of the bicarbonate buffer system.

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