Acid-Base Disorders

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160 Acid-Base Disorders

Matthew T. Robinson, Alan C. Heffner

image      Key Points

• Normal pH or serum bicarbonate values can mask an important, underlying acidosis in the setting of a mixed disorder.

• An elevated anion gap is a sign of metabolic acidosis and should be calculated on each chemistry sample.

• Arterial and venous blood gas sampling is a useful emergency department test because of the strong association between arterial and venous HCO3− and pH.

• Correlation between venous PCO2 and arterial PCO2 is lacking, although venous PCO2 levels may be used as a screening tool for hypercapnia.

• Admission lactate level and standard base excess are markers of illness severity that correlate with patient morbidity and mortality in the hospital.

• The urine ketone dipstick test is highly sensitive for serum ketosis.

• Venous and arterial lactate samples are equivalent.

• Indiscriminate use of sodium bicarbonate for the treatment of undifferentiated metabolic acidosis should be avoided.

Pathophysiology

Regulation of Acid-Base Balance

The normal hydrogen ion (H+) concentration in serum is approximately 40 nanoequivalents per liter. This is approximately 1/1,000,000 the concentration of the other major serum ions, but the small size and high charge density of protons make them highly reactive and capable of inducing conformational and functional changes in body proteins. Rigid control of the free H+ concentration is therefore essential to life.

Daily metabolism produces an acid load of 150 mmol of nonvolatile (fixed) acid and 12,000 mmol of volatile acid (CO2). Physiologic, pathologic, and dysregulated endogenous production, as well as externally administered product, can all increase the systemic acid load.

Maintenance of systemic homeostasis in the setting of acid-base changes occurs via three main mechanisms:

1. Chemical buffering

2. Alterations in alveolar ventilation

3. Alterations in renal H+ excretion

Chemical Buffering

Extracellular buffers, including plasma proteins, phosphates, and bicarbonate, are the earliest defense against acidosis. The most prominent extracellular buffer is bicarbonate, which is highly abundant and acts as a dynamic buffer by independently regulating PCO2 through changes in alveolar ventilation. This feature increases buffering capacity by more than 10-fold. Buffering also occurs within the intracellular compartment but is delayed as H+ equilibrates over a period of hours. Intracellular buffers, including bone, inorganic phosphates, proteins, and hemoglobin, are eventually responsible for more than 50% of the overall chemical buffering capacity.

Alterations in Alveolar Ventilation

Alterations in alveolar ventilation provide compensation for acute acid-base disturbances. According to the Henderson-Hasselbalch equation, serum pH can be determined as follows:

image

Stimulation of peripheral chemoreceptors triggers changes in ventilation within minutes. By altering PCO2 through variations in minute ventilation, the HCO3−/PCO2 ratio remains relatively constant, and alterations in pH are thereby mitigated. The effectiveness of the ventilatory response is acutely limited by differences in the solubility of CO2 and H+ within the central nervous system (CNS). The hyperventilation induced by systemic acidosis is incomplete as a result of local alkalosis sensed by the central chemoreceptors as CO2 diffuses more rapidly across the blood-brain barrier.

Alterations in Renal Hydrogen Ion Excretion

Because of the inability of HCO3− to effectively buffer H2CO3 produced through acute CO2 retention as described, renal compensation is centrally important in the response to primary respiratory disorders. Renal compensatory mechanisms include enhanced proton excretion and increased HCO3− resorption. Renal compensation for acute acid-base disorders begins immediately; however, the full effect is not appreciated for 5 or 6 days.

Nomenclature

The normal range of serum pH is 7.38 to 7.42. Acidemia is defined by serum pH below 7.38. Likewise, alkalemia is defined by serum pH above 7.42. These terms describe the absolute directional change of measured pH but say nothing about the processes that alter pH from normal. The processes that alter pH are termed acidosis and alkalosis.

Acid-base disorders are often complex—pH may be normal in the setting of an obvious acid-base disorder because of the presence of a second or even a third coexisting acid-base process. For example, patients with a mixed disorder may have a normal or alkalemic pH during ketoacidosis if a concomitant alkalosis (metabolic or respiratory) is also present. It is therefore important to note that a normal pH does not exclude an important acid-base disorder.

Diagnostic Interpretation

Primary acid-base processes are divided into respiratory or metabolic disorders by examining PCO2 and serum bicarbonate. Primary elevations in PCO2 signify respiratory acidosis, whereas decreased serum bicarbonate identifies metabolic acidosis. Diagnostic assessment of acid-base disorders requires accurate measurement of these plasma variables, in addition to calculated values, to unmask mixed disorders. Coupling the clinical history and physical assessment with these values reveals important clues about the causative illness.

Serum testing includes direct evaluation of pH, PCO2, and HCO3− through arterial and venous blood sampling; calculation of the anion gap from serum chemistries; and additional measures (e.g., the standard base excess) in an attempt to quantify the metabolic component of acid-base disorders (see the “Facts and Formulas” box for basic formulas used in this chapter).

image Facts and Formulas

pH = 6.1 + Log[HCO3−]/0.03 × PCO2

Anion gap = Unmeasured anions − Unmeasured cations = Na+ − [Cl− + HCO3−]

Delta gap = Δ Anion gap − Δ HCO3 = [Calculated anion gap − 10] − [24 − Measured serum HCO3]

Calculated Sosm (mOsm/kg) = 2 (Na+) + BUN/2.8 + Glucose/18 + Ethanol/4.8

Osmolal gap = Measured Sosm − Calculated Sosm

Correction Formulas

Corrected anion gap = Anion gap + 2.5 (Normal albumin − Measured albumin)

Compensation Formulas

Metabolic acidosis: PCO2 = 1.5 (HCO3−) + 8

Metabolic alkalosis: Increase in PCO2 = 0.6 × Increase in HCO3−

Respiratory acidosis

• Acute: [HCO3−] increases by 1 mEq/L for each 10–mm Hg increase in PCO2
• Chronic: [HCO3−] increases by 4 mEq/L for each 10–mm Hg increase in PCO2

Respiratory alkalosis

• Acute: [HCO3−] decreases by 2 mEq/L for each 10–mm Hg decrease in PCO2
• Chronic: [HCO3−] decreases by 5 mEq/L for each 10–mm Hg decrease in PCO2

BUN, Blood urea nitrogen; Sosm, serum osmolarity.

Arterial and Venous Blood Gases

The ability to substitute venous blood gas samples for arterial samples is appealing because of the pain, difficulty, and complications associated with arterial sampling. Arterial pH and venous pH vary by less 0.04 in most situations.1–3 Patients in clinical shock are an important exception, however, because arteriovenous PCO2 (and therefore pH) can vary significantly.

Despite incomplete correlation between venous and arterial PCO2, venous PCO2 may be used to screen for arterial hypercapnia. In hemodynamically normal patients, PCO2 higher than 45 mm Hg is sensitive (but less than 50% specific) for the detection of arterial hypercapnia, which is defined as PCO2 higher than 50 mm Hg. Venous blood gas screening led to a 29% reduction in arterial sampling in one study.4 Finally, arterial blood gas analysis enables precise interpretation of respiratory compensation when needed.

Standard Base Excess

Although the serum bicarbonate level may describe an acid-base disorder, the amount of acid or base added to the system cannot be calculated unless PCO2 is held constant. The concept of the standard base excess (SBE) was introduced to address this problem and is defined as the quantity of strong acid or base required to restore plasma pH to 7.40 when PCO2 is held constant at 40 mm Hg. A negative value indicates excess acid, whereas a positive value indicates excess base.

SBE has been studied extensively as a resuscitation end point in trauma and as a marker of tissue acidosis. Preresuscitation base excess values are reliably linked to the degree of tissue acidosis and serve as independent predictors of mortality in critically ill patients. Base excess has been shown to correlate with hypovolemia, length of hospital stay, and transfusion requirements, whereas the rate of normalization correlates with patient survival.5,6

Lactate

Lactic acid is generated through the reduction of pyruvate with the reduced form of nicotinamide adenine dinucleotide (NADH) as follows:

image

Lactate is produced by skeletal muscle, brain, intestines, and kidneys, with normal blood lactate levels maintained below 2 mmol/L and the threshold for lactic acidosis defined by a serum level higher than 4 mmol/L.

Arterial lactate sampling is considered the most reliable measure for detecting hyperlactatemia; however, venous and capillary sampling is also used. Central venous sampling is highly correlated with arterial lactate measurements. Peripheral venous samples are sufficient to screen for hyperlactatemia but retain poor specificity (57%) when compared with arterial samples.7 Elevations in venous lactate should be confirmed with arterial sampling.

Anion Gap

Within serum, the requirement for electroneutrality dictates that the net serum cation charge equal the net total anion charge. The calculated difference in commonly measured serum ions is termed the anion gap (AG). It is important to note that the AG represents anions that are present but unmeasured (at least historically) and that an AG is present during health. Fortunately, the difference between unmeasured anions and unmeasured cations may change (increased or decreased AG) and therefore provide a clue to disease states (Box 160.1).

Box 160.1 Causes of Measured Changes in the Anion Gap

Increased Anion Gap

Increased unmeasured anions

• Organic acids: lactate, ketones, phosphate, sulfate
• Toxins and metabolites: formate (methanol), oxalate (ethylene glycol), salicylates
• Severe volume depletion (hyperalbuminemia)
• IgA paraproteinemia

Decreased unmeasured cations

• Calcium, magnesium, potassium
• Laboratory error
• Metabolic alkalosis
• Respiratory alkalosis

Decreased Anion Gap

Laboratory error

• Overestimation of chloride or bicarbonate
• Underestimation of sodium
• Bromide intoxication (overestimation of chloride)
• Iodine intoxication (overestimation of chloride)

Decreased unmeasured anions

• Hypoalbuminemia

Increased unmeasured cations

• Lithium
• Paraproteins (myeloma)
• Bromide intoxication
• Hypermagnesemia
• Hypercalcemia
• Hyperlipidemia
• IgG gammopathy
• Polymyxin B

The greatest utility of the AG is identification and discrimination of metabolic acidosis. The potential for a mixed acid-base disturbance to mask acidosis by normalizing pH and serum bicarbonate highlights the importance of calculating the AG on every chemistry sample. An increased AG almost always signifies a process causing a “wide-gap” metabolic acidosis. Furthermore, calculation of the AG assists in discriminating the cause of undifferentiated metabolic acidosis (e.g., AG versus non-AG processes carry different differential diagnoses).

When acids are added to the system, bicarbonate is replaced by the acid anion (X) as follows:

image

Titration and replacement of bicarbonate by unmeasured organic acid produce a relative equimolar elevation in the AG.

In contrast, bicarbonate loss (or addition of protons) can occur in the absence of an endogenous or exogenous anion contribution.

image

Hyperchloremia maintains electroneutrality without altering the AG. Gastrointestinal and renal losses are the most common causes of non-AG metabolic acidosis (Box 160.2).

Box 160.2 Causes of Non–Anion Gap Metabolic Acidosis

Gastrointestinal HCO3− Loss

Diarrhea

Renal HCO3− Loss

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