Acid-Base Disorders

Published on 10/02/2015 by admin

Filed under Emergency Medicine

Last modified 22/04/2025

Print this page

This article have been viewed 1115 times

160 Acid-Base Disorders

Matthew T. Robinson, Alan C. Heffner

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

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).

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)

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:

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

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:

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.

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

The historical range for the AG was 12 ± 4 (8 to 16 mEq/L). With the adoption of ion-specific electrodes, chloride is measured at a higher concentration such that the currently accepted range of AG is 7 ± 3 (4 to 10 mEq/L). More importantly, the AG must be corrected for individual patients. Albumin accounts for 80% of the AG in health. Consequently, large and important deviations may occur if serum albumin is assumed to be normal. AG is thus commonly corrected for serum albumin to improve sensitivity of the AG as a screening tool.⁸ The correction factor is calculated as follows:

Delta-Delta Calculation

The AG is also useful for investigating the presence of mixed metabolic disturbances. In simple AG acidosis, bicarbonate is presumably titrated in a one-to-one fashion by organic acid such that the following relationship is noted:

The difference between the change in the AG and the change in serum bicarbonate is called the delta gap, or delta-delta calculation. Deviations from this stoichiometric relationship indicate a mixed metabolic disturbance. When the change (delta) in the AG is greater than the change in bicarbonate, a preexisting or concomitant metabolic alkalosis is present. Alternatively, a change in AG less than the change in bicarbonate identifies a coexisting non-AG acidosis. A delta gap higher than 6 is generally considered significant.⁹

Serum Osmolar Gap

Osmolarity is defined as the number of particles within a volume of fluid (mmol/L), and osmolality is defined as the number of particles in a mass of fluid (mmol/kg). The terms are used interchangeably because the density of water is 1 kg/L. The size of the particle contributing to serum osmolality (Sosm) is unimportant; that is, small ions contribute equally with large proteins.

Sosm is elevated in the presence of osmotically active particles such as alcohols, glycols, and sugars. The difference in measured and calculated Sosm is termed the osmolar gap. An elevated osmolar gap confirms the presence of unmeasured osmotically active particles, which may be helpful when investigating the cause of unexplained AG acidosis. Osmolar gaps greater than 10 mOsm/kg are considered abnormal and may reflect the presence of a toxic alcohol as the source of the acidosis. However, delayed evaluation after the ingestion of toxic alcohol will show little to no elevation in the osmolar gap as a result of metabolism of the offending alcohol. Likewise, normal osmolar gap values are imprecisely defined, with ranges of −13 to +14.0 mOsm/kg noted in healthy patients.^10,¹¹ This wide variation in the normal range may lead to a normal osmolar gap in the presence of a significant ingestion.

Evaluation of Mixed Acid-Base Disorders

By applying the formulas for AG, delta gap, and expected physiologic compensation, a stepwise approach to the evaluation of simple and mixed acid-base problems can be developed.¹² This process is summarized in Box 160.3.

Box 160.3

Five-Step Approach to Acid-Base Disorders

Rule 1: Determine the pH status (alkalemia or acidemia: >7.44 or <7.40)

Rule 2: Determine whether the primary process is respiratory, metabolic, or both

• Alkalemia

• Respiratory alkalosis: if PCO₂ substantially <40 mm Hg

• Metabolic alkalosis: if HCO₃⁻ >25 mEq/L

• Acidemia

• Respiratory acidosis: if PCO₂ >44 mm Hg

• Metabolic acidosis: if HCO₃⁻ <25 mEq/L

Rule 3: Calculate the anion gap*

• Anion gap = Na⁺ + (Cl⁻ + HCO₃⁻)

• Increased anion gap (>10 mEq/L) may indicate metabolic acidosis

• Increased anion gap (>20 mEq/L) always indicates metabolic acidosis

Rule 4: Check the degree of compensation

• Metabolic acidosis: PCO₂ = 1.5 [HCO₃⁻] + 8

• Metabolic alkalosis: increase in PCO₂ = 0.6 increase in bicarbonate

• 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

Rule 5: Determine whether there is a 1 : 1 relationship between the change in the anion gap and the change in serum bicarbonate

• Each 1-point increase in the anion gap should be accompanied by a 1-mEq/L decrease in bicarbonate

• If bicarbonate is higher than predicted, a metabolic alkalosis is also present

• If bicarbonate is lower than predicted, a non–anion gap metabolic acidosis is present

Modified from Whittier WL, Rutecki GW. Primer on clinical acid-base problem solving. Dis Mon 2004;50:122–62.

^* For every 1 g/dL that albumin is less than normal (4.2 g/dL), add 2.5 to the calculated anion gap.

Additionally the clinical history is centrally important for proper interpretation of acid-base disorders (Box 160.4).

Box 160.4 Acid-Base Interpretation Based on Clinical History

Case 1

A 65-year-old man with a history of chronic obstructive pulmonary disease has a fever, increased shortness of breath, cough, and sputum production. The following arterial blood gas and serum HCO₃⁻ values are obtained:

Review shows decreased pH and elevated PCO₂, indicative of respiratory acidosis. The chronicity of the acidosis can be evaluated by calculating the expected metabolic compensation:

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

• Expected HCO₃⁻ = 24 + 2.5 = 26.5

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

• Expected HCO₃⁻ = 24 + 10 = 34

Comparing these values with the measured HCO₃⁻ reveals that HCO₃⁻ falls between the two calculated levels. Based on the history, the clinical diagnosis is acute on chronic respiratory acidosis.

Case 2

A 65-year-old man with a history of chronic obstructive pulmonary disease has had diarrhea for 1 week and his baseline PCO₂ is 65 mm Hg.

Based on his history, the patient’s HCO₃⁻ is lower than predicted, which represents acute metabolic acidosis in the presence of chronic respiratory acidosis.

Case 3

A 65-year-old man being treated long-term with diuretic therapy has an acute exacerbation of asthma.

His history indicates acute respiratory acidosis with an expected PCO₂ of 26.5 mm Hg. The elevated serum HCO₃⁻ indicates acute respiratory acidosis with concomitant metabolic alkalosis.

The renal compensatory response in chronic respiratory acidosis requires 3 to 5 days to develop and may be predicted by the following equation:

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

Specific Acid-Base Disorders

Respiratory Acidosis

Normal ventilatory control is regulated through central receptors that respond to elevated PCO₂ and through peripheral chemoreceptors in the carotid bodies that respond to hypoxia. Because the ventilatory response to hypercapnia is much stronger than that to hypoxemia, only minor elevations in PCO₂ are required to increase minute ventilation. As a result of this vigorous response and the ability to significantly increase minute ventilation, respiratory acidosis almost always develops as a consequence of impaired alveolar ventilation and not from increased production of CO₂.

Elevated PCO₂ causes a decrease in arterial pH and a variable, acute increase in plasma HCO₃⁻ as a result of shifts in equilibrium reactions and a similar, but chronic increase as a result of renal compensation through enhanced H⁺ excretion and HCO₃⁻ retention. CO₂ functions as a volatile acid:

Under normal conditions, this acid load is immediately buffered by intracellular and extracellular nonbicarbonate buffers. The acute rise in PCO₂ elicits a similar elevation in HCO₃⁻ through a highly predictable relationship:

In chronic respiratory acidosis, elevations in PCO₂ are partially protective, with larger amounts of CO₂ able to be excreted at lower minute ventilation. The system also adapts to chronically elevated CO₂ by enhancing renal H⁺ excretion and HCO₃⁻ retention, thereby attenuating the ventilatory response to hypercapnia. The result of chronic respiratory acidosis is that the ventilatory drive becomes dependent on a hypoxic stimulus.

The renal compensatory response in patients with chronic respiratory acidosis requires 3 to 5 days to develop and may be predicted by the following equation:

Respiratory Alkalosis

Respiratory alkalosis is produced through alveolar hyperventilation and results in a decrease in arterial PCO₂ and an increase in arterial pH. Plasma HCO₃⁻ is variably decreased, acutely because of shifts in equilibrium and later because of renal HCO₃⁻ wasting. The decreased PCO₂ causes a decreased volatile acid load with secondary release of H⁺ from nonbicarbonate buffers (Buf) as follows:

The expected [HCO₃⁻] can be calculated from the following equation:

In chronic respiratory alkalosis, renal adaptive mechanisms result in diminished H⁺ secretion and enhanced HCO₃⁻ excretion. This combined response begins within hours and is completed within 2 to 3 days. The expected response may be calculated as follows:

Ventilation is primarily controlled through peripheral, central, and pulmonary mechanical receptors. Peripheral chemoreceptors respond to changes in PCO₂ and O₂, so it is not surprising that many cases of hyperventilation stem from hypoxemia.

Metabolic Acidosis

Metabolic acidosis is induced by the addition of H⁺ ions or by the loss of HCO₃⁻. Addition of H⁺ may occur as a result of exogenous administration or endogenous production of acids associated with pathologic states. Loss of bicarbonate occurs primarily through gastrointestinal or renal wasting, with acidosis being produced by driving the equilibrium reaction to the left:

As discussed previously, the initial response to acidosis is extracellular and intracellular buffering, combined with respiratory compensation via increased alveolar ventilation. These protective mechanisms attempt to minimize free H⁺ within the system until a full renal response excretes the excess acid load.

It is important to remember that compensatory responses do not fully normalize pH. If a normal pH is seen in a patient with metabolic acidosis, a second acid-base disorder must be present. The typical laboratory pattern of metabolic acidosis is decreased pH and bicarbonate with a compensatory decrease in PCO₂ (Box 160.5).

Box 160.5 Diabetic Patient with Mixed Acid-Base Disorder

A 26-year-old woman with a history of diabetes mellitus is vomiting and has had generalized malaise for the past 3 days.

Laboratory evaluation shows the following:

• Na⁺ = 134; K⁺ = 4.6; Cl⁻ = 94; HCO₃⁻ = 20 mEq/L; pH = 7.38; PCO₂ = 35 mm Hg

Step 1: Arterial blood gas analysis shows that the patient is minimally acidemic

Step 2: Serum bicarbonate is less than 25 mEq/L, indicative of metabolic acidosis

Step 3: The anion gap is elevated: 134 − 94 − 20 = 20

Step 4: Respiratory compensation is appropriate: 1.5 [HCO₃⁻] + 8 = [1.5 × 20] + 8 = 38 mm Hg

Step 5: Calculation of the delta gap reveals that the change in HCO₃⁻ (24 − 20 = 4 units) is significantly less than the change in anion gap (20 − 10 = 10 units). This indicates the presence of a concomitant metabolic alkalosis that is masking the significant anion gap acidosis. These findings are explained by vomiting-induced alkalosis in a patient with diabetic ketoacidosis

Enhanced alveolar ventilation is triggered through pH-mediated stimulation of peripheral chemoreceptors. Minute ventilation is augmented via increased tidal volume (hyperpnea) and later followed by an increased respiratory rate (tachypnea), depending on the degree of acidosis. The expected PCO₂ is calculated by the following equation:

This equation assesses the adequacy of respiratory compensation. A PCO₂ that is significantly higher or lower than this calculated value signals the presence of a secondary respiratory acidosis or alkalosis, which may have a profound impact on treatment decisions (Box 160.6).

This protective effect lasts only a few days, however, because the chronically diminished PCO₂ paradoxically signals renal bicarbonate wasting. The final effect is that arterial pH in chronic metabolic acidosis is the same, with or without respiratory compensation.

Causes of metabolic acidosis are classified according to the presence or absence of an elevated AG. However, even in the absence of an AG, there may be accumulation of unmeasured anions.

Non-AG acidoses are those that add HCl to the system. The acid anion in these cases is chloride; because of its inclusion in the AG equation, no change in the gap is noted. The most common causes of non-AG acidosis include renal and gastrointestinal bicarbonate wasting (Box 160.7).

Box 160.7 Four-Year-Old Boy with Diarrhea for 5 Days

Physical examination reveals dry mucous membranes.

Vital Signs:

Blood pressure, 80/50; heart rate, 170 beats/min; temperature, 99.1° F; respiratory rate, 44 breaths/min

Laboratory Data:

Na⁺ = 134; K⁺ = 4.8; Cl⁻ = 114; HCO₃⁻ = 3; pH = 6.98; PCO₂ = 13 mm Hg; PO₂ = 110 mm Hg

Step 1: The patient is found to be acidemic on examination of arterial blood gases

Step 2: Serum bicarbonate is less than 25 mEq, indicative of the presence of metabolic acidosis

Step 3: The anion gap is elevated: 134 − 116 − 3 = 15

Step 4: Respiratory compensation is appropriate: 1.5 × [HCO₃⁻] + 8 = [1.5 × 3] + 8 = 12.5

Step 5: Calculation of the delta gap reveals that the change in HCO₃⁻ (24 − 3 = 21 units) is significantly greater than that the change in anion gap (15 − 10 = 5 units). This indicates the presence of a concomitant non–anion gap acidosis that is overshadowing the anion gap acidosis. The mixed acidosis can be clinically explained by the presence of diarrhea (non–anion gap acidosis) with dehydration (anion gap acidosis)

Metabolic Alkalosis

Metabolic alkalosis is characterized by the net gain of base equivalent, as reflected by elevated plasma bicarbonate. Direct proton loss from extracellular fluid produces an elevation in serum bicarbonate by shifting the following equilibrium reaction to the right:

The elevated plasma pH produces compensatory hypoventilation to increase PCO₂. Because serum pH is determined by the ratio of HCO₃⁻ to PCO₂ and not by the absolute HCO₃⁻ level, this compensatory response acts to minimize the change in serum pH.

Metabolic alkalosis is the second most common acid-base disorder and is found in approximately one third of hospitalized patients. It can be caused by several processes: increased H⁺ loss, typically through renal or gastrointestinal wasting; increased bicarbonate resorption; infusion or ingestion of bicarbonate; intracellular shifts in H⁺; or contraction of extracellular fluid around a stable HCO₃⁻ pool (Box 160.8).

Because of the kidneys’ ability to excrete excess HCO₃⁻, maintenance of metabolic alkalosis requires impairment of this process. The majority of the filtered bicarbonate is reclaimed in the proximal tubule, with approximately 10% of HCO₃⁻ being reabsorbed in the distal segments. Type B cells in the cortical collecting tubule may also actively secrete excess bicarbonate. Maintenance of metabolic alkalosis requires failure of these mechanisms. This generally results from contraction of extracellular volume, which stimulates Na⁺ retention and enhanced activity of the Na⁺-H⁺ antiporter in the proximal tubule.

Hyperaldosteronism induced by extracellular fluid depletion also plays a role in maintaining alkalosis by increasing H⁺ secretion in the distal nephron through activation of H⁺-transporting adenosine triphosphatase (H⁺-ATPase). Hypokalemia and hyperaldosteronism maintain the alkalosis through stimulation of proximal and distal bicarbonate resorption, transcellular exchange of K⁺ and H⁺, and increased ammoniagenesis.

The most frequent causes of metabolic alkalosis are loss of gastric secretion and use of diuretics. Loss of gastric secretion generates an equimolar gain in HCO₃⁻ for the lost H⁺. Likewise, loss of gastric secretion is associated with a contracted volume of extracellular fluid, which maintains alkalosis through volume depletion and hyperaldosteronism. Diuretics also induce an alkalosis through secondary hyperaldosteronism associated with hypovolemia, hypokalemia, and enhanced distal H⁺ secretion.

The respiratory compensation for metabolic alkalosis is variable. On average, PCO₂ can be predicted as follows:

Compensation rarely results in a PCO₂ greater than 55 mm Hg. Significant deviations from this compensatory response indicate a superimposed respiratory acidosis or alkalosis.

The signs and symptoms of alkalosis are commonly related to the associated volume contraction. Weakness, fatigue, coma, seizure, carpopedal spasm, respiratory depression, and neuromuscular irritability are observed, probably related to decreased ionized calcium as a result of alkalemia. Neuromuscular signs and symptoms are uncommon in patients with metabolic alkalosis because of the slow movement of charged HCO₃⁻ into the CNS.

Urine chloride helps determine the cause and treatment of the metabolic alkalosis. Urine chloride levels less than 20 mEq/L indicate appropriate renal chloride avidity and imply that the source of the metabolic alkalosis is extrarenal. Accordingly, fluid and chloride repletion is the mainstay of therapy in these saline- or chloride-responsive conditions. In contrast, urine chloride levels higher than 40 mEq/L indicate renal chloride wasting and implicate altered renal function at a source of the metabolic alkalosis.

Treatment

Metabolic Acidosis

Initial treatment of metabolic acidosis includes reversing the source of the metabolic acidosis and treating with exogenous bicarbonate when indicated. A second priority is assessing the adequacy of respiratory compensation and providing ventilatory support as needed. Respiratory exhaustion with concomitant respiratory acidosis compounds the patient’s dilemma.

Alkali therapy is aimed at reversing the acid-induced organ dysfunction. However, the effects of bicarbonate therapy are complex. Indiscriminate use may be more deleterious than helpful. Sodium bicarbonate infusions introduce an additional volatile acid load because bicarbonate produces CO₂ on reaction with water (serum):

This additional CO₂ load must be excreted by the lungs to have an impact on pH. Additionally, CO₂ diffuses freely across cell membranes and paradoxically exacerbates intracellular and CNS acidemia. Sodium bicarbonate is associated with complications that include hypertonicity, hypernatremia, hypervolemia, increased organic acid (lactate) production, and impaired oxygen unloading.

Use of bicarbonate infusions is appropriate for bicarbonate-wasting acidoses or toxic acidosis because systemic alkalinization facilitates removal of toxin through ion trapping. However, supplemental bicarbonate in patients with organic acidoses (lactic acidosis and ketoacidosis) has not been shown to affect outcome. In these states, therapy should be aimed at addressing the underlying cause of the acidosis and promoting regeneration of bicarbonate through metabolism of the accumulated anions. In hyperchloremic acidosis, no anions exist for the regeneration of bicarbonate, and therefore infusions can promptly reverse the acidemia and restore serum bicarbonate.

When used, the goal of bicarbonate infusion is to increase pH to 7.1 to 7.2 and restore buffering capacity (>12 mEq/L HCO₃⁻). Overzealous administration risks paradoxic alkalemia on metabolism of organ acids. The bicarbonate deficit may be calculated with the Henderson-Hasselbalch equation or by estimating the deficit at 1 mEq/kg and infusing one half the amount over a period of 20 to 30 minutes, with the remainder being infused over the next 2 to 4 hours. Bicarbonate also makes an excellent resuscitation or maintenance fluid. Isotonic bicarbonate is prepared by combining three ampules of sodium bicarbonate (50 mEq) with 1 L of sterile water, which creates an isotonic solution of 130 to 150 mEq/L NaHCO₃ (depending on removal of water before instillation). During this time, acid-base and volume status must be carefully monitored to avoid overshooting the pH correction.

Metabolic Alkalosis

Metabolic alkalosis is best treated by correcting the underlying cause of the alkalosis. Examination of urine chloride allows causes to be classified as saline responsive or saline resistant.

The majority of cases of metabolic alkalosis are saline responsive. Volume depletion is reversed with 0.9% normal saline. Concomitant hypokalemia is an important maintenance factor that should be reversed with potassium chloride. The total body potassium deficit may be profound and is often underappreciated.

Saline-resistant alkaloses display excessive mineralocorticoid activity, such as hyperaldosteronism, Cushing syndrome, and renal artery stenosis. Treatment of saline-resistant causes (urine chloride >20 mEq/L) is directed at the other causes of the metabolic alkalosis. Potassium deficits should be corrected by supplementation or direct antagonism of aldosterone with agents such as spironolactone. In patients with metabolic alkalosis and concomitant edematous states (e.g., congestive heart failure, cirrhosis, nephrotic syndrome), acetazolamide enables bicarbonate and volume excretion.

References

1 Kelly AM, McAlpine R, Kyle E. Venous pH can safely replace arterial pH in the initial evaluation of patients in the emergency department. Emerg Med J. 2001;18:340–342.

2 Eizadi-Mood N, Moein N, Saghaei M. Evaluation of relationship between arterial and venous blood gas values in the patients with tricyclic antidepressant poisoning. Clin Toxicol. 2005;43:357–360.

3 Gokel Y, Paydas S, Koseoglu Z, et al. Comparison of blood gas and acid-base measurements in arterial and venous blood samples in patients with uremic acidosis and diabetic ketoacidosis in the emergency room. Am J Nephrol. 2000;20:319–323.

4 Kelly AM, Kerr D, Middleton P. Validation of venous PCO₂ to screen for arterial hypercarbia in patients with chronic obstructive pulmonary disease. J Emerg Med. 2005;28:377–379.

5 Rutherford E, Morris JA, Jr., Reed GW, et al. Base deficit stratifies mortality and determines therapy. J Trauma. 1992;33:417–423.

6 Davis JW, Kaups KL, Parks SN. Base deficit is superior to pH in evaluating clearance of acidosis after traumatic shock. J Trauma. 1998;44:114–118.

7 Middleton P, Kelly AM, Brown J, et al. Agreement between arterial and venous values for pH, bicarbonate, base excess and lactate. Acad Emerg Med. 2005;12(5 Suppl 1):174.

8 Hatherill M, Waggie Z, Purves L, et al. Correction of the anion gap for albumin in order to detect occult tissue anions in shock. Arch Dis Child. 2002;87:526–529.

9 Wrenn K. The delta (delta) gap: an approach to mixed acid-base disorders. Ann Emerg Med. 1990;19:1310–1313.

10 Hoffman RS, Smilkstein MJ, Howland MA, et al. Osmol gaps revisited: normal values and limitations. Clin Toxicol. 1993;31:81–93.

11 McQuillen KK, Anderson AC. Osmol gaps in the pediatric population. Acad Emerg Med. 1999;6:27–30.

12 Whittier WL, Rutecki GW. Primer on clinical acid-base problem solving. Dis Mon. 2004;50:122–162.

Recent Posts

Meta

Categories

Search Engine

Acid-Base Disorders

Share this:

Related

Related posts: