Clinical Assessment of Acid-Base and Oxygenation Status

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Clinical Assessment of Acid-Base and Oxygenation Status

Classification Versus Interpretation

Chapter 10 discusses the concept of respiratory and metabolic acid-base disturbances and the compensatory responses they elicit. This chapter introduces a systematic method for the classification, or categorization, of arterial blood gases in terms of acid-base balance and oxygenation status. Classification is the first essential step in the development of a rational therapeutic basis for correcting acid-base and oxygenation problems. The classification process focuses attention on the general problem areas and provides a starting point for interpretation, or the in-depth exploration and comprehension of the underlying disorder.

Arterial blood gas interpretation entails the evaluation of blood gases in the context of the patient’s total clinical picture. The patient’s medical history, physical examination findings, current therapy, and other clinical diagnostic information must be integrated with blood gas results to arrive at a sound interpretation. Respiratory therapists not only must comprehend the processes that led to the current blood gases but also must anticipate future blood gas changes. Only then can an informed, definitive arterial blood gas interpretation be made; only then can the respiratory therapist arrive at a rational basis for therapeutic intervention.

Classification of Acid-Base Disturbances

Acid-base disturbances and oxygenation problems should be evaluated separately as two distinct entities. Although these two problems are sometimes interrelated, evaluating them separately helps identify these relationships.

The relevant arterial blood gas components in evaluating acid-base status are pH, PCO2, and [HCO3]. Arterial pH reflects hydrogen ion activity of extracellular fluid (plasma), which generally correlates with intracellular fluid pH. Chapter 10 emphasizes the importance of regulating the pH from a cellular enzyme standpoint. Abnormal pH values also affect the central nervous system, causing the clinical manifestations shown in Figure 13-1. Generally, a low arterial pH (acidemia) depresses neuronal excitability, whereas a high pH (alkalemia) has the opposite effect (greatly increased excitability).1 An extremely low pH (pH <7.00) causes a coma, whereas an extremely high pH (pH >7.80) causes convulsions and tetany (a state of sustained muscle spasm). Low arterial pH values (pH <7.10) also predispose patients to ventricular arrhythmias and reduce heart muscle contractility.2

Systematic Classification

The most consistent, reliable results are achieved when an orderly, systematic, unvarying approach is used to analyze acid-base problems. If exactly the same step-by-step approach is used for each problem, confusion and premature conclusions can be avoided. A systematic approach also helps identify inconsistencies and errors in blood gas data. Box 13-1 outlines four steps in acid-base classification. The order of steps 1 through 3 is not as important as following the same sequence for each situation.

Step 2: Analyze Respiratory Involvement (PaCO2)

The PaCO2 is controlled by alveolar ventilation and is thus the indicator of respiratory involvement. The normal range for PaCO2 in humans is 35 to 45 mm Hg and is not affected by age or gender; high and low PaCO2 values are called hypercapnia and hypocapnia. The PaCO2 is analyzed, keeping the pH (step 1) in mind. A PaCO2 greater than 45 mm Hg means blood H+ levels (from dissociated carbonic acid) are abnormally high; this is compatible with acidemia and hypoventilation. A PaCO2 less than 35 mm Hg has the opposite meaning; it is compatible with alkalemia and hyperventilation. If the pH is abnormal, the following question should be asked: Could the observed PaCO2 help explain the pH abnormality? For example, if the pH is 7.50 (alkalemia) and the PaCO2 is 30 mm Hg (hyperventilation), the respiratory system must be at least partly, if not entirely, responsible for the alkalemia.

Step 3: Analyze Nonrespiratory (Metabolic) Involvement ([HCO3])

Because it is primarily determined by nonrespiratory, or so-called metabolic factors, plasma bicarbonate concentration is the logical indicator of nonrespiratory involvement in acid-base disturbances. The normal range for arterial plasma [HCO3] in humans is 22 to 26 mEq/L and is unaffected by age or gender. Bicarbonate is a chemical base; high plasma bicarbonate (>26 mEq/L) is compatible with alkalemia, and low plasma bicarbonate (<22 mEq/L) is compatible with acidemia.

Plasma [HCO3] is not as specific and accurate in indicating metabolic acid-base disturbances as PaCO2 is in indicating respiratory disturbances. The reason is that plasma bicarbonate responds slightly to pure respiratory (i.e., PCO2) changes. The carbon dioxide hydration reaction explains this phenomenon. As explained in Chapter 10, an acute increase in PaCO2 of 10 mm Hg increases [HCO3] by about 1 mEq/L. Thus, the plasma [HCO3] must be evaluated with caution; if it falls outside of the normal range but the abnormality can be explained by the effect of the carbon dioxide hydration reaction, the [HCO3] level is not responsible for any existing acid-base disorder.

Keeping the foregoing limitation in mind, the [HCO3] is inspected and compared with the pH. If the pH is abnormal, one must ask: Can the observed [HCO3] explain the pH abnormality? For example, if the arterial pH is 7.25 (acidemia) and [HCO3] is low (18 mEq/L), this is compatible with acidemia. Therefore, metabolic (nonrespiratory) factors are at least partly, if not entirely, responsible for the acidosis.

Step 4: Assess for Compensation

When the acid-base abnormality has been identified as either respiratory or metabolic, the degree of compensation present, if any, must be determined. In other words, if a respiratory acidosis exists (increased PaCO2), have the kidneys compensated by elevating the plasma [HCO3]? Conversely, if a metabolic acidosis exists (decreased HCO3), have the lungs compensated by hyperventilating and lowering the PaCO2?

If the pH has been restored to the normal range (7.35 to 7.45), full compensation has occurred even though pH remains on the acid or alkaline side of the range. Compensation is partial if the pH is still outside of the normal range but the noncausative component (either PaCO2 or HCO3) is also abnormal in a way that brings the pH back toward the normal range. A compensated acid-base disturbance is sometimes referred to as a chronic acidemia or chronic alkalemia because a certain amount of time is required to bring about compensation. Partial compensation means compensatory activity has begun but has not had enough time to restore the pH to normal. The term uncompensated means the acid-base disturbance is of such recent origin that compensatory activity has not yet started. Therefore, an uncompensated condition is sometimes called an acute acidemia or acute alkalemia.

It is assumed that compensation for a primary acid-base disorder is never truly complete in the sense of restoring arterial pH all the way to 7.40.3 In a compensated disorder, the pH is on the acid or alkaline side of the normal range, depending on whether the primary causative disorder created an acidosis or an alkalosis. That is, if the pH is on the acid side of normal (<7.40 but at least ≥7.35), the main cause of the original acid-base imbalance is the component (PaCO2 or HCO3) that, by itself, would cause an acidosis. For example, if the pH is 7.36, PaCO2 is 80 mm Hg, and HCO3 is 44 mEq/L, compensation is present because the pH is in the normal range, although it is on the acid side of normal. The primary cause of the original acid-base disturbance (before compensatory activity started) must be the factor that would produce acidemia (i.e., the increased PaCO2 of 80 mm Hg). Thus, this set of blood gases would be classified as compensated (chronic) respiratory acidosis. The primary disturbance is of respiratory origin, and the increased [HCO3] is a secondary metabolic compensatory response. The reason the pH is on the acid side of the normal range is that the body generally does not overcompensate; it does not increase the [HCO3] so much that it converts the previously acidotic environment to one with a pH on the alkaline side of normal. Conversely, if the pH is 7.15, PaCO2 is 80 mm Hg, and HCO3 is 26 mEq/L, no compensation has occurred; that is, HCO3 is still normal, not elevated as would be expected if compensatory action were underway.

Compensatory activity does not correct the primary acid-base disturbance; the primary defect is still present. Compensatory activity merely works to restore the pH to the normal range. Table 13-1 summarizes acid-base and ventilatory classification. Table 13-2 classifies the degree of compensation for acid-base disturbances.

TABLE 13-1

Acid-Base and Ventilatory Classification

Component Classification Ranges
pH (arterial) Normal status 7.35-7.45
  Acidemia <7.35
  Alkalemia >7.45
PaCO2 (mm Hg) Normal ventilatory statusRespiratory acidosis (hypoventilation)Respiratory alkalosis (hyperventilation) 35-45>45<35
[HCO3] (mEq/L) Normal metabolic statusMetabolic acidosisMetabolic alkalosis 22-26<22>26

image

TABLE 13-2

Degrees of Acid-Base Compensation

Compensating (Noncausative) Component pH Classification
Within normal range Abnormal Noncompensated (acute)
Out of normal range in the expected direction Abnormal Partially compensated
Out of normal range in the expected direction Normal Compensated (chronic)

Respiratory Acidosis (Inadequate Ventilation)

Any physiological process causing an increased PaCO2 (>45 mm Hg) produces respiratory acidosis. The increased PaCO2 (hypercapnia) decreases the arterial pH because dissolved carbon dioxide produces carbonic acid and hydrogen ions, as the following reaction shows:

< ?xml:namespace prefix = "mml" />CO2+H2OH2CO3HCO3+H+

image

Therefore, hypercapnia is synonymous with respiratory acidosis.

Causes

Hypoventilation causes hypercapnia, which implies inadequate ventilation. Any process that hinders alveolar ventilation can

cause respiratory acidosis. Chronic obstructive pulmonary disease (COPD) is the most frequent cause of respiratory acidosis, mostly because the airways resistance of a patient with severe COPD is so high that the patient cannot sustain the ventilatory work required to maintain a normal PaCO2.3 Central nervous system depression (drug-induced), extreme obesity (impaired diaphragmatic movement), and neuromuscular disorders (spinal cord lesions, paralytic neuromuscular diseases) are other causes of hypoventilation and respiratory acidosis. Hypercapnia may occur in different ways. A person may have an absolute decrease in ventilation because of drug-induced central nervous system depression, or a patient with COPD and a limited ventilatory reserve may sustain a normal PaCO2 at rest but may not accommodate the increased carbon dioxide production associated with increased physical activity.

Uncompensated hypercapnia implies the presence of acute ventilatory failure; the resulting respiratory acidosis is manifested by a low arterial pH, increased PaCO2, and normal or slightly high [HCO3]. In this situation, a slightly increased [HCO3] is not a sign that the kidneys have started compensatory activity; it merely reflects the effect of the carbon dioxide hydration reaction on [HCO3] (see Chapter 10).

Compensation

Renal (kidney) compensation for respiratory acidosis begins as soon as PaCO2 increases. The kidney reclaims HCO3 from the renal tubular filtrate, returning it to the blood. The arterial pH is brought into the normal range because the [HCO3]-dissolved carbon dioxide ratio is restored near its normal 20:1 range (see Chapter 10). However, this process cannot keep pace with an acutely increasing PaCO2. Full compensation may take several days.

Over the course of developing COPD, a person’s PaCO2 increases gradually, allowing the compensatory process enough time to keep pace with the rising PaCO2. The arterial pH is thus maintained in the normal range. Partly compensated respiratory acidosis is characterized by increased PaCO2, increased [HCO3], and an acid pH still not quite in the normal range. A compensated respiratory acidosis is characterized by a pH on the acid side of the normal range (<7.40 but at least ≥7.35), increased PaCO2, and increased [HCO3]. The high [HCO3] in the presence of a high PaCO2 is a sign that the PaCO2 has been elevated for a considerable time (i.e., the kidneys have had sufficient time to compensate). Thus, compensated respiratory acidosis is synonymous with chronic ventilatory inadequacy. Although the pH is in the normal range, the underlying pathological process that produces hypercapnia is still present; the kidneys simply mask the problem by maintaining a normal pH range. Because hypercapnia persists, the term acidosis is retained in classifying this condition (compensated respiratory acidosis). This term emphasizes that lung function is still abnormal and has the potential to produce an acidosis.

Clinical Manifestations

Patients with neuromuscular weakness or mechanical breathing difficulties usually breathe shallowly and rapidly and are short of breath; they are often anxious and in obvious distress. Drug-induced central nervous system depression produces slow, shallow breathing and possibly apnea. Acute respiratory acidosis produces more serious physiological consequences than chronic respiratory acidosis. Rapidly increasing PaCO2 causes cerebral vasodilation and increased intracranial pressure (ICP), possibly leading to retinal venous distention and retinal hemorrhages; in addition, the patient may develop myoclonus (spasmodic muscle jerks), asterixis (a hand-flapping tremor in which the patient cannot keep the wrists flexed with the arms extended), and mental confusion.3 An abrupt onset of hypercapnia in which PaCO2 rises beyond 70 mm Hg can lead to coma, although patients with chronic hypercapnia can tolerate much higher PaCO2 values.3 Hypercapnia increases the cardiac output and dilates peripheral vessels, often resulting in a bounding pulse and warm, flushed skin.

Correction

The corrective action in acute respiratory acidosis is to restore alveolar ventilation. Various respiratory therapy modalities ranging from secretion mobilization and bronchodilator drugs to endotracheal intubation and mechanical ventilation may be

needed to restore ventilation. However, if hypoventilation is chronic and compensation has restored arterial pH to the normal range, corrective action aimed at reducing the PaCO2 is inappropriate and possibly harmful. In this situation, a rapidly decreasing PaCO2 induces a sudden alkalosis because of renal compensation and elevated blood HCO3 levels.

CLINICAL FOCUS 13-3   Fully Compensated Respiratory Acidosis

You are asked to assess a stable 60-year-old man with a long-standing history of cigarette smoking; he was diagnosed with severe COPD. Arterial blood gas values are as follows:

Respiratory Alkalosis (Alveolar Hyperventilation)

Any physiological process causing a decreased PaCO2 (<35 mm Hg) produces respiratory alkalosis. The decreased PaCO2 (hypocapnia) forces the hydration reaction to the left, decreasing H+ concentration and increasing the pH, as the following reaction shows:

CO2+H2OH2CO3HCO3+H+

image

Therefore, hypocapnia is synonymous with respiratory alkalosis.

Causes

Hyperventilation causes hypocapnia. Any process in which ventilatory elimination of carbon dioxide exceeds its production causes respiratory alkalosis. Causes can be divided into three categories: (1) hypoxia, (2) pulmonary diseases, and (3) central nervous system diseases. Probably the most common cause of hyperventilation in patients with pulmonary disease is arterial hypoxemia, mediated through the peripheral chemoreceptors.3 Hypoxia-induced respiratory alkalosis can be caused by high altitude or pulmonary diseases characterized by intrapulmonary shunting (e.g., pneumonia, pulmonary edema). Other pulmonary diseases associated with hyperventilation and respiratory alkalosis include interstitial fibrosis, pulmonary embolism, and acute asthma. J-receptor stimulation in the lung parenchyma may be involved in interstitial diseases, pneumonia, and pulmonary edema. The feeling of dyspnea from high airways resistance and resulting anxiety is a probable mechanism for respiratory alkalosis in acute asthma. General anxiety, fever, stimulating drugs, pain, and injuries of the central nervous system are other possible causes of hyperventilation.

Hyperventilation and respiratory alkalosis also may be iatrogenically induced (i.e., induced by health care personnel). Iatrogenic hyperventilation is most commonly associated with overly aggressive mechanical ventilation; it may also be associated with aggressive deep breathing and lung-expanding respiratory therapy procedures. Acute respiratory alkalosis is characterized by decreased PaCO2, a high pH, and normal-range [HCO3]. An extremely slight decrease in [HCO3] is expected to be present as a result of the hydration reaction’s effect.

Clinical Manifestations

An early sign of acute respiratory alkalosis (hypocapnia) is paresthesia, a numb or tingling sensation in the extremities; light-headedness may also occur. Severe hyperventilation and alkalosis is associated with hyperactive reflexes, muscle

cramping of the hands or feet (carpopedal spasm), and possibly tetanic convulsions (a fusion of many muscle spasms producing a sustained contraction without relaxation). The low PaCO2 level may constrict cerebral vessels enough to impair cerebral circulation, causing light-headedness, dizziness, and syncope (fainting). If respiratory alkalosis is anxiety-induced, the patient may show signs of panic and express feelings of impending doom. Vision may become impaired (tunnel vision), and speaking may become difficult.3

Compensation

The kidneys compensate for respiratory alkalosis by excreting HCO3 in the urine (bicarbonate diuresis). This activity brings the arterial pH down toward the normal range because the [HCO3]-dissolved carbon dioxide ratio is restored near its normal 20:1 range. However, renal compensation rarely causes [HCO3] to fall below 18 mEq/L.3 Renal compensation is a relatively slow process; it may take days until the compensation process is finally completed.

Partially compensated respiratory alkalosis is characterized by decreased PaCO2, decreased [HCO3], and an alkaline pH that is still not quite down in the normal range. Compensated respiratory alkalosis is characterized by decreased PaCO2, decreased [HCO3], and pH on the alkaline side of normal (pH >7.40 but ≤7.45). Compensated respiratory alkalosis is sometimes called chronic respiratory alkalosis or chronic alveolar hyperventilation. The underlying hyperventilation and hypocapnia are still present. Thus, the term alkalosis is used in classifying this condition, although the pH is in the normal range.

Alveolar Hyperventilation Superimposed on Compensated Respiratory Acidosis

A patient with advanced but stable COPD and compensated respiratory acidosis may exhibit the following arterial blood gas values:

The HCO3 level is high because of renal compensatory activity. If the person now experiences an acute exacerbation of disease and becomes severely hypoxic, this may stimulate the peripheral chemoreceptors enough to increase alveolar ventilation and acutely decrease PaCO2 despite the patient’s deranged lung mechanics.

In this case, let us assume that the patient was incapable of hyperventilating enough to decrease PaCO2 all the way down into the normal range. Although PaCO2 is still above normal, the acute lowering of the PaCO2 coupled with the preexisting high compensatory level of HCO3 causes the pH to swing from the acidic to the alkalotic side of normal, as the following values illustrate:

If one pays attention to only the blood gas data and applies the strict criteria for interpretation as outlined earlier in this chapter, one would arrive at the completely incorrect interpretation of compensated metabolic alkalosis. This interpretation would lead the novice to conclude that the patient is hypoventilating to compensate for a preexisting primary metabolic alkalosis; in light of this patient’s medical history, this would be an absurd conclusion. This example illustrates the fact that blood gas data alone are an insufficient basis for rational acid-base assessment. The patient’s medical history, the physical examination, and the nature of the current problem are vital in accurately evaluating blood gas abnormalities. The above-listed blood gases are correctly described as acute

CLINICAL FOCUS 13-5   Partially Compensated Respiratory Alkalosis Progressing to Completely Compensated (Chronic) Alkalosis

hyperventilation superimposed on compensated respiratory acidosis.

Metabolic (Nonrespiratory) Acidosis

Any process that lowers plasma [HCO3] is called metabolic acidosis. A reduction in the [HCO3] decreases the blood pH because the amount of base relative to the amount of acid (dissolved CO2) in the blood is reduced. The [HCO3]-dissolved carbon dioxide ratio becomes less than 20:1 (e.g., 15:1 or 10:1). According to the Henderson-Hasselbalch equation, this produces an acid pH.

Causes

Metabolic acidosis can occur in two general ways: (1) the accumulation of fixed (nonvolatile) acid in the blood or (2) an excessive loss of HCO3 from the body. For example, a lack of blood flow leads to tissue hypoxia, anaerobic metabolism, and production of lactic acid (a fixed acid). The resulting accumulation of hydrogen ions reacts with bicarbonate ions, lowering the blood [HCO3], producing nonrespiratory or metabolic acidosis. Another example is severe diarrhea, in which large stores of HCO3 are lost from the bowel, again producing nonrespiratory acidosis.

Because of their different causative mechanisms, these two types of metabolic acidosis are treated differently; the identification of the underlying mechanism is necessary to treat metabolic acidosis effectively. The analysis of plasma electrolytes—specifically, the so-called anion gap—is helpful in determining whether metabolic acidosis was caused by a gain of fixed acids or by a loss of base.

Anion Gap

The law of electroneutrality states that the total number of positive charges in the body fluids must equal the total number of negative charges. Plasma cations (positively charged ions) are exactly balanced by anions (negatively charged ions); that is, the plasma has no net electrical charge. The routinely measured plasma electrolytes (cations and anions) in clinical medicine include only Na+, K+, Cl, and HCO3, although body fluids contain many other cations and anions. The normal plasma concentrations of these routinely measured electrolytes are such that the cations (Na+ and K+) outnumber the anions (Cl and HCO3), causing what seems to be an anion gap. Generally, K+ is ignored in calculating the anion gap because of its very low concentration:

Aniongap(mEq/L)=[Na+]([Cl]+[HCO3])

image

The “anion gap” can be thought of as a measure of the concentrations of other anions in the plasma besides Cl and HCO3. Figure 13-2, A

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