INTRODUCTION

Changes in hydrogen ion concentration in the body are associated with molecular changes that can have significant physiologic effects. Consequently, homeostasis aims to maintain a normal hydrogen ion concentration. Hydrogen ion concentration is measured as pH, the negative base-10 logarithm of the hydrogen ion concentration, [H⁺]. The normal extracellular pH is generally in the range of 7.4. Elevated blood hydrogen ion levels (pH <7.4) are described as an acidemia, and reduced hydrogen ion levels (pH >7.4) are described as an alkalemia.¹

There is a widely held misunderstanding that the body regulates hydrogen ion concentration within very narrow limits. This is a result of the observation that normal pH is approximately 7.41 in dogs and 7.39 in cats and that changes in pH become life threatening if pH falls below 7.1 or rises above 7.7. The misconception that this represents exquisite control of [H⁺] is a result of the logarithmic nature of the pH scale. In reality, the life-threatening alarm values for pH represent a [H⁺] that ranges from 80 nanoEq/L at a pH of 7.1 to 20 nanoEq/L at a pH of 7.7. This is a four-fold difference in [H⁺] between the low and high alarm values. This is equivalent to the statement that sodium concentration is well regulated because its concentration must fall below 75 mEq/L or rise above 300 mEq/L before we become alarmed. Clearly sodium is regulated much more closely, and as clinicians we are alarmed well before the concentration reaches these extremes.

Several approaches to acid-base analysis have been developed. They include the Henderson-Hasselbalch, or conventional, approach that uses pH, partial pressure of carbon dioxide (PCO₂), bicarbonate (, base excess (BE), and anion gap, and the Stewart approach, which uses pH, PCO₂, strong ion difference (SID), and the quantity of weak acids (A_TOT). As clinicians, we find ourselves naming acid-base disturbances while gaining little understanding of the etiology of the patient’s acid-base problems and little insight into effective therapy. The primary problem is that within each of these traditional approaches multiple etiologic factors are grouped together. The clinician needs a way to isolate cause and effect to assess the mechanisms behind the disturbance and to focus treatment.

Both approaches to acid-base analysis start with a measurement of pH, a parameter that represents the chemical summation of all acid-base disturbances. An abnormal pH is interpreted as acidemia or alkalemia. This is the net change in [H⁺] that results from all acidifying events (acidosis) and all alkalinizing events (alkalosis). Rarely is an acidemia or alkalemia so severe that the clinician’s objective is to treat the disturbance without regard to etiology. The real value in acid-base analysis is to discover the multiple compensating and counterbalancing causes that are common in critical care patients.

Acid-base disturbances are broadly categorized as respiratory or metabolic in nature. Conventional acid-base analysis is based on the Henderson-Hasselbalch equation (Box 59-1), which uses bicarbonate concentration, [], as the sole measure of the metabolic contribution to acid-base balance and the PCO₂ as the single causative agent for respiratory acid-base disturbances. Using this conventional approach the primary abnormality (metabolic or respiratory) is the system that is responsible for the initial change in pH. For example, an acidemia with a low and low PCO₂ would be considered a primary metabolic acidosis, because the acidemia must be a result of the low .^1,2 The conventional approach identifies four acid-base abnormalities; these are described in Table 59-1.

Table 59-1 Acid-Base Disturbances Identified With the Conventional Approach

The PCO₂ is universally considered the sole causative agent for respiratory acid-base disturbances. However, the parameter(s) used to assess metabolic disturbances varies with the analytic approach chosen. For clinical application, acid-base disturbances should be studied from the perspective of the individual etiologic agents that cause them (Table 59-2).

Table 59-2 Acid-Base Disturbances Based on Etiology

RESPIRATORY ACID-BASE DISTURBANCES

Carbon dioxide acts as an acid because of its ability to react with water to produce carbonic acid. In this way, the PCO₂ affects the buffer system and ultimately the hydrogen ion concentration.

Because carbon dioxide is a gas for which concentration in the blood is controlled by pulmonary ventilation, the lung plays a role in controlling acid-base status. This is a rapid process that can alter blood pH within minutes. Normal arterial PCO₂ in dogs is 37 mm Hg and in cats it is 31 mm Hg. The PCO₂ is maintained by normal pulmonary function, normal function of the diaphragm and respiratory muscles, normal pleural space dynamics, and normal respiratory drive controlled by the brain.

If the PCO₂ is abnormal, there is a respiratory component to the acid-base disturbance, but it is not necessarily pathologic. PCO₂ is determined directly by effective alveolar minute ventilation which, in turn, is controlled by the respiratory center of the brain. CO₂, oxygen, and pH can all alter alveolar minute ventilation via central and peripheral chemoreceptors. Chemoreceptors do not respond to changes in PCO₂ directly; rather they detect associated changes in [H⁺]. Hence abnormalities in PCO₂ can be subsequent to primary respiratory disorders or can occur in response to metabolic acid-base abnormalities and their associated changes in [H⁺]. When metabolic processes occur that increase [H⁺], the respiratory center will respond with hyperventilation to lower PCO₂. Conversely when [H⁺] is low, hypoventilation will occur to increase PCO₂ appropriately. This is the normal respiratory response to a metabolic alteration and serves to minimize the overall change in pH.^1,4

Conventional acid-base nomenclature states that a metabolic disturbance that is accompanied by an appropriate compensatory respiratory change is classified as a simple metabolic disturbance and the respiratory component is not named. A compensatory change is considered “appropriate” if it is of a magnitude similar to that predicted by the calculated compensatory response. These calculations are provided in Table 59-3 and are discussed further later in this chapter.^1,3

Table 59-3 Expected Compensatory Changes to Primary Acid-Base Disorders

Primary Disorder	Expected Compensation
Metabolic acidosis	↓ PCO2 of 0.7 mm Hg per 1 mEq/L decrease in [] ±3
Metabolic alkalosis	↑ PCO2 of 0.7 mm Hg per 1 mEq/L decrease in [] ±3
Respiratory acidosis—acute	↑ [] of 0.15 mEq/L per 1 mm Hg ↑ PCO2 ±2
Respiratory acidosis—chronic	↑ [] of 0.35 mEq/L per 1 mm Hg ↑ PCO2 ±2
Respiratory alkalosis—acute	↓ [] of 0.25 mEq/L per 1 mm Hg ↓ PCO2 ±2
Respiratory alkalosis—chronic	↓ [] of 0.55 mEq/L per 1 mm Hg ↓ PCO2 ±2

[], Bicarbonate concentration measured in mEq/L; PCO₂, partial pressure of carbon dioxide measured in mm Hg, ↑, increased; ↓, decreased.

In clinical practice it may be beneficial to identify the respiratory component, because this physiologic response may have more serious consequences for the patient than the initial metabolic disturbance. For example, a patient in shock with serious head trauma may present with a metabolic acidosis and appropriate respiratory compensation. Although the respiratory alkalosis in this case is compensatory and not considered an acid-base abnormality, it may be clinically significant because the low PCO₂ causes cerebral vasoconstriction, which may be dangerous in this patient. Further assessment, including clinical monitoring, will identify if the respiratory change is likely to be physiologic or if there are other, pathologic, respiratory disturbances that may amplify or attenuate the physiologic response.

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