Acid-Base Disorders (Case 14)

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Chapter 21
Acid-Base Disorders (Case 14)

Kavita Ahuja DO and Ilene Miller MD

Case: A 46-year-old man is found unconscious on the bathroom floor by his family. The family states the patient has a medical history significant only for depression and gastroesophageal reflux disease (GERD). His medications include escitalopram and omeprazole. Upon arrival to the emergency department the patient is more responsive but still confused and drowsy. A few episodes of vomiting are noted. On exam, the patient is afebrile with a blood pressure (BP) of 90/50 mm Hg, respiratory rate (RR) of 24 breaths per minute, and heart rate (HR) of 120 beats per minute (bpm). His pupils are reactive to light with a nonfocal neurologic exam. He has dry mucous membranes and mild diffuse abdominal tenderness to palpation. No alcoholic fetor is noted. Laboratory studies are as follows: Na 132 mEq/L, K 3.4 mEq/L, Cl 90 mEq/L, serum bicarbonate (HCO3) 10 mEq/L, BUN 60 mg/dL, Cr 1.6 mg/dL, and glucose 80 mg/dL. Arterial blood gas (ABG) reveals a pH of 7.2 and PCO2 of 25 mm Hg. Serum ethanol, acetone, and serum β-hydroxybutyrate are negative. The measured serum lactate is 1.6 mmol/L. Urinalysis reveals 4+ calcium oxalate crystals.

Differential Diagnosis

Increased Anion Gap Metabolic Acidosis

Normal Anion Gap Metabolic Acidosis

Metabolic Alkalosis

Methanol and ethylene glycol poisoning

Gastrointestinal (GI) bicarbonate loss

Contraction alkalosis



Milk alkali syndrome

Lactic acidosis


Salicylate intoxication


Speaking Intelligently

When encountering a patient whose workup reveals a significant acid-base disorder, a thorough history and physical exam, along with appropriate lab data, will help identify the underlying diagnosis. These patients may require immediate attention (i.e., hemodynamic stabilization, volume resuscitation, and optimization of oxygenation). An ABG is the best test to assess the presence of an acid-base disorder. If a toxic ingestion is suspected, a toxicology screen should be performed to aid in identifying the agent, and a poison control center should be contacted for additional guidance.


Clinical Thinking

• An acid is a substance that donates H+ ions, while a base is a substance that accepts H+ ions. pH is inversely related to [H+]. In other words, an increase in [H+] reduces the pH, while a decrease in [H+] increases the pH. The normal pH of extracellular blood is 7.40, correlating to an extracellular [H+] of 40 nmol/L. A pH of less than 7.35 is considered to be acidemic, while a pH of above 7.45 is alkalemic.

Metabolic acidosis is associated with a low pH and low HCO3 concentration.

Respiratory acidosis is associated with a low pH and a high PCO2 concentration, indicating retention of CO2.

Metabolic alkalosis consists of a high pH with an increased HCO3 concentration.

Respiratory alkalosis is associated with a high pH and a low PCO2.

• The approach to identifying and managing acid-base disturbances should be a stepwise approach, as follows (also see Table 21-1):

1. First, identify the primary disturbance based on the pH of arterial blood to determine if it is acidemic or alkalemic. In this case, the pH of 7.2 indicates an acidemia.

2. Next, determine whether the acidemia is secondary to a metabolic or respiratory cause by interpreting the PCO2 and HCO3. If the PCO2 is elevated, the disturbance is primarily a respiratory acidosis. If the HCO3 is low, the disturbance is primarily a metabolic acidosis. In this case the low serum HCO3 (10 mEq/L) indicates a primary metabolic acidosis.

3. To determine if the disorder is a simple disorder or a mixed acid-base disorder, you must next determine compensation. In metabolic acidosis, the expected compensation or expected PCO2 can be calculated using Winter’s formula in which expected PCO2 = 1.5 [serum HCO3] + 8 ± 2. The expected PCO2 for this patient is 23 mm Hg.

4. Next, calculate the anion gap to aid in your differential diagnosis. It is helpful to classify the metabolic acidosis into increased anion gap versus normal anion gap. The anion gap is the difference between measured serum cations and anions and can be calculated as Na+ − (Cl + HCO3). A normal anion gap is 12 ± 4. An increase in anion gap is most often caused by an increase in unmeasured anions, such as lactate or ketones. The anion gap in this patient is 32. Therefore, this patient has a high–anion gap metabolic acidosis with appropriate respiratory compensation.

5. Finally, determine the etiology of the acid-base disorder by formulating a differential diagnosis, which will guide further management. Management should focus on identifying and correcting the underlying disorder and restoring normal extracellular pH.

Table 21-1 Expected Changes in Primary Acid-Base Disorders



• History will provide key information and should be obtained from the patient, relatives, friends, and/or co-workers.

• Collect information regarding a history of alcoholism or drug abuse, depression, and/or previous suicide attempts, which would prompt an evaluation for possible ingestion or intoxication.

• Determine whether the patient has a history of diabetes mellitus, renal disease, recent infection, diarrhea, or vomiting, as all of these conditions can predispose to acid-base imbalances.

• Review the patient’s medications, as various medications are known to cause acid-base disturbances (e.g., salicylates).

Physical Examination

• Vital signs, including BP and HR, along with assessment of skin turgor, will help to determine the volume status of the patient.

• Determine if the patient is altering his or her respiratory rate in an attempt to compensate for alterations in serum HCO3.

• A complete neurologic exam, including assessment of mental status and pupil reactivity, should be performed. Methanol intoxication can cause an afferent papillary defect. Ethylene glycol intoxication can cause cranial nerve palsies.

• Look for signs of inebriation.

• Look for signs of malnutrition, as they may raise suspicion of alcoholic ketoacidosis.

Tests for Consideration

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ABG: The ABG is the best test to assess acid-base balance.
The respiratory component of acid-base balance is PCO2, and it changes through alterations in ventilation. Hypoventilation will cause retention of CO2 and result in respiratory acidosis.
Hyperventilation will cause loss of CO2 and result in respiratory alkalosis. The metabolic component of acid-base balance is HCO3 and is regulated by the kidney.


Serum chemistry and calcium: The serum chemistry will allow for calculation of the anion gap and detection of abnormalities in electrolyte concentrations and renal function.


Urine electrolytes: The measurement of urine Na+, K+, and Cl allows for calculation of the urine anion gap (UAG).
The UAG is calculated as UAG = [Na+] + [K+] − [Cl]. It is useful in normal anion gap, hyperchloremic metabolic acidosis to determine if acidosis is secondary to GI HCO3 loss or renal HCO3 loss. A negative UAG suggests that the HCO3 loss is via the bowel, while a positive UAG suggests that the acidosis is of renal etiology (RTA).
The urine electrolytes are also helpful when evaluating metabolic alkalosis.


Serum and urine ketones: Ketones should be measured in patients with an elevated anion gap. Ketones are produced when the body metabolizes adipose tissue for energy and the liberated fatty acids are metabolized to ketoacids (β-hydroxybutyric and acetoacetic acid), which can be detected in serum and urine.


Toxicology screen: A toxicology screen will allow for detection of acetaminophen, salicylate, alcohol, and/or opioid ingestion. It is necessary to measure in patients who present with altered mental status or an increased osmolar gap.


Serum osmolality: Measurement of the serum osmolality and calculation of serum osmolality allow for the detection of an osmolar gap. The osmolar gap is defined as the difference between the measured serum osmolality and the calculated osmolality. Serum osmolality is calculated as 2[Na+] + [glucose]/18 + [BUN]/2.8. If the osmolar gap is greater than 15 mOsm/kg, ingestion of a toxic substance should be suspected.


Urinalysis and examination for crystalluria: Urine sediment, when viewed under polarized light, can allow for detection of crystalluria. Ethylene glycol toxicity can lead to formation of needle- or dumbbell-shaped calcium oxalate monohydrate crystals or envelope-shaped calcium oxalate dihydrate crystals.