# Blood Gases pH and Electrolytes

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1. Which of the following represents the Henderson–Hasselbalch equation as applied to blood pH?
A. pH = 6.1 + log HCO3–/PCO2
B. pH = 6.1 + log HCO3–/(0.03 ×PCO2)
C. pH = 6.1 + log dCO2/HCO3–
D. pH = 6.1 + log (0.03 ×PCO2)/HCO3–
• B. pH = 6.1 + log HCO3–/(0.03 ×PCO2)
•  The Henderson–Hasselbalch equation describes the pH of a buﬀer comprised of a weak acid and its salt. pH = pKa+ log salt/acid, where pKa is the negative logarithm of the dissociation constant of the acid. In this case, the salt is sodium bicarbonate and the acid is the dissolved CO2,which is equal to 0.03 (mmol/L per mm Hg) x PCO2. The pKa includes both the hydration and dissociation constant for dissolved CO2 in blood, 6.1 and is termed pK´.
2. What is the PO2 of calibration gas containing 20.0% O2, when the barometric pressure is 30 in.?
A. 60 mm Hg
B. 86 mm Hg
C.143 mm Hg
D. 152 mm Hg
• C.143 mm Hg
•  Convert barometric pressure in inches to mm Hg by multiplying by 25.4 (mm/in.). Next, subtract the vapor pressure of H2O at 37°C, 47 mm Hg, to give dry gas pressure. Multiply dry gas pressure by the %O2: 25.4 mm/in. × 30 in. = 762 mm Hg 762 mm Hg – 47 mm Hg (vapor pressure) = 715 mm Hg (dry gas pressure) 0.20 × 715 mm Hg = 143 mm Hg PO2
3. What is the blood pH when the partial pressure of carbon dioxide (PCO2) is 60 mm Hg and the bicarbonate concentration is 18 mmol/L?
A. 6.89
B. 7.00
C. 7.10
D. 7.30
• C. 7.10
• Solve using the Henderson–Hasselbalch equation. pH = pK´+ log HCO3–/(0.03 × PCO2), where pK´,the negative logarithm of the combined hydration and dissociation constants for dissolved CO2 and carbonic acid, is 6.1 and 0.03 is the solubility coeﬃcient for CO2 gas. pH = 6.1 + log 18/(0.03 × 60) = 6.1 + log 18/1.8 pH = 6.1 + log 10. Because log 10 = 1, pH = 7.10
4. Which of the following best represents the reference (normal) range for arterial pH?
A. 7.35–7.45
B. 7.42–7.52
C. 7.38–7.68
D. 6.85–7.56
• A. 7.35–7.45
•  The reference range for arterial blood pH is 7.35–7.45 and is only 0.03 pH units lower for venous blood owing to the buﬀering eﬀects of hemoglobin (Hgb) known as the chloride isohydric shift. Most laboratories consider less than 7.20 and greater than 7.60 the critical values for pH.
5. What is the normal ratio of bicarbonate to dissolved carbon dioxide (HCO3–:dCO2) in arterial blood?
A. 1:10
B. 10:1
C. 20:1
D. 30:1
• C. 20:1
• When the ratio of HCO3–:dCO2 is 20:1, the log of salt/acid becomes 1.3. Substituting this in the Henderson–Hasselbalch equation and solving for pH gives pH = 6.1 + log 20; pH = 6.1 + 1.3 = 7.4. Acidosis results when this ratio is decreased, and alkalosis when it is increased.
6. What is the PCO2 if the dCO2 is 1.8 mmol/L?
A. 24 mm Hg
B. 35 mm Hg
C. 60 mm Hg
D. 72 mm Hg
• C. 60 mm Hg
• Dissolved CO2 is calculated from the measured PCO2 × 0.0306, the solubility coeﬃcient for CO2 gas in blood at 37°C. dCO2= PCO2× 0.03 Therefore, PCO2= dCO2/0.03 PCO2= 1.8 mmol/L ÷ 0.03 mmol/ L per mm Hg = 60 mm Hg
7. In the Henderson–Hasselbalch expression pH = 6.1 + log HCO3–/dCO2, the 6.1 represents: A. The combined hydration and dissociation constants for CO2 in blood at 37°C
B. The solubility constant for CO2 gas
C. The dissociation constant of H2O
D. The ionization constant of sodium bicarbonate (NaHCO3)
• A. The combined hydration and dissociation constants for CO2 in blood at 37°C
• The equilibrium constant, Kh, for the hydration of CO2 (dCO2 + H2O →H2CO3) is only about 2.3 × 10–3M, making dCO2 far more prevalent than carbonic acid. The dissociation constant, Kd,for the reaction H2CO3 →H+ + HCO3– is about 2 × 10–4 M.The product of these constants is the combined equilibrium constant, K´. The negative logarithm of K´is thepK´, which is 6.103 in blood at 37°C.
8. Which of the following contributes the most to the serum total CO2?
A. PCO2
B. dCO2
C. HCO3–
D. Carbonium ion
• C. HCO3–
•  The total CO2 is the sum of the dCO2, H2CO3 (carbonic acid or hydrated CO2), and bicarbonate (as mainly NaHCO3). When serum is used to measure total CO2, the dCO2 is insigniﬁcant because all the CO2 gas has escaped into the air. Therefore, serum total CO2 is equivalent to the bicarbonate concentration. Total CO2 is commonly measured by potentiometry. An organic acid is used to release CO2 gas from bicarbonate and pCO2 is measured with a Severinghaus electrode. Alternately, bicarbonate can be measured by an enzymatic reaction using phosphoenol pyruvate carboxylase. The enzyme forms oxaloacetate and phosphate from phosphoenol pyruvate and bicarbonate. The oxaloacetate is reduced to malate by malate dehydrogenase and NADH is oxidized to NAD+. The negative reaction rate is proportional to plasma bicarbonate concentration.
9. In addition to sodium bicarbonate, what other substance contributes most to the amount of base in the blood?
A. Hemoglobin concentration
B. Dissolved O2 concentration
C. Inorganic phosphorus
D. Organic phosphate
• A. Hemoglobin concentration
•  The primary blood buﬀer bases preventing acidosis in order of concentration are bicarbonate, deoxyhemoglobin, albumin, and monohydrogen phosphate. At physiological pH, there is signiﬁcantly more H2PO4–1 than HPO4–2, and phosphate is a more eﬃcient buﬀer system at preventing alkalosis than acidosis. Since all of the blood buﬀer systems are in equilibrium, the pH can be calculated accurately from the concentration of bicarbonate and dissolved CO2 using theHenderson–Hasselbalch equation.
10. Which of the following eﬀects results from exposure of a normal arterial blood sample to room air?
A. PO2 increased PCO2 decreased pH increased
B. PO2 decreased PCO2 increased pH decreased
C. PO2 increased PCO2 decreased pH decreased
D. PO2 decreased PCO2 decreased pH decreased
• A. PO2 increased PCO2 decreased pH increased
• The PO2 of air at sea level (21% O2) is about 150 mm Hg. The PCO2 of air is only about 0.3 mm Hg. Consequently, blood releases CO2 gas and gains O2 when exposed to air. Loss of CO2 shifts the equilibrium of the bicarbonate buﬀer system to the right, decreasing hydrogen ion concentration and blood becomes more alkaline.
11. Which of the following formulas for O2 content is correct?
A. O2 content = %O2 saturation/100 ×Hgb g/dL × 1.39 mL/g + (0.0031 ×PO2)
B. O2 content = PO2 ×0.0306 mmol/L/mm
C. O2 content = O2 saturation ×Hgb g/dL ×0.003 mL/g
D. O2 content = O2 capacity ×0.003 mL/g
• A. O2 content = %O2 saturation/100 ×Hgb
• Oxygen content is the sum of O2 bound to Hgb and O2 dissolved in the plasma. It is dependent upon the Hgb concentration and the percentage of Hgb bound to O2 (O2 saturation). Each gram of Hgb binds 1.39 mL of O2. The dissolved O2 is determined from the solubility coeﬃcient of O2 (0.0031 mL per dL/mm Hg) and the PO2. O2 content = % Sat/100 × Hgb in g/dL × 1.39 mL/g + (0.0031 × PO2).
12. The normal diﬀerence between alveolar and arterial PO2 (PAO2–PaO2 diﬀerence) is:
A. 3 mm Hg
B. 10 mm Hg
C. 40 mm Hg
D. 50 mm Hg
• B. 10 mm Hg
• The PAO2–PaO2 diﬀerence results from the low ratio of ventilation to perfusion in the base of the lungs. The hemoglobin in the blood coming from the base of the lung has a lower O2 saturation. This blood will take up O2 from the plasma of blood leaving well-ventilated areas of the lung, thus lowering the mixed arterial PO2.
13. A decreased PAO2–PaO2 diﬀerence is found in: A. A/V (arteriovenous) shunting
B. V/Q (ventilation/perfusion) inequality
C. Ventilation defects
D. All of these options
• C. Ventilation defects
• Patients with A/V shunts, V/Q inequalities, and cardiac failure will have an increased PAO2–PaO2 diﬀerence. However, patients with ventilation problems have low alveolar PO2 owing to retention of CO2 in the airway. This reduces the PAO2–PaO2 diﬀerence.
14. The determination of the oxygen saturation of hemoglobin is best accomplished by:
A. Polychromatic absorbance measurements of a whole-blood hemolysate
B. Near infrared transcutaneous absorbance measurement
C. Treatment of whole blood with alkaline dithionite prior to measuring absorbance
D. Calculation using PO2 and total hemoglobin by direct spectrophotometry
• A. Polychromatic absorbance measurements of a whole-blood hemolysate
•  Measurement of oxyhemoglobin, deoxyhemoglobin (reduced hemoglobin), carboxyhemoglobin, methemoglobin, and sulfhemoglobin can be accomplished by direct spectrophotometry at multiple wavelengths and analysis of the absorptivity coeﬃcients of each pigment at various wavelengths. The O2 saturation is determined by dividing the fraction of oxyhemoglobin by the sum of all pigments. This eliminates much of the error that occurs in the other methods when the quantity of an abnormal hemoglobin pigment is increased.
15. Correction of pH for a patient with a body temperature of 38°C would require:
A. Subtraction of 0.015
B. Subtraction of 0.01%
D. Subtraction of 0.020
• A. Subtraction of 0.015
• The pH decreases by 0.015 for each degree Celsius above the 37°C. Because the blood gas analyzer measures pH at 37°C, the in vivo pH would be 0.015 pH units below the measured pH.
16. Select the anticoagulant of choice for blood gas studies.
A. Sodium citrate 3.2%
B. Lithium heparin 100 U/mL blood
C. Sodium citrate 3.8%
D. Ammonium oxalate 5.0%
• B. Lithium heparin 100 U/mL blood
• Heparin is the only anticoagulant that does not alter the pH of blood; heparin salts must be used for pH and blood gases. Solutions of heparin are air equilibrated and must be used sparingly to prevent contamination of the sample by gas in the solution.
17. What is the maximum recommended storage time and temperature for an arterial blood gas sample drawn in a plastic syringe?
A. 10 min 2°C–8°C
B. 20 min 2°C–8°C
C. 30 min 2°C–8°C
D. 30 min 22°C
• D. 30 min 22°C
• Arterial blood gas samples collected in plastic syringes should be stored at room temperature because cooling the sample allows oxygen to enter the syringe. Storage time should be no more than 30 minutes because longer storage results in a signiﬁcant drop in pH and PO2 and increased PCO2.
18. A patient’s blood gas results are as follows: pH = 7.26 dCO2 = 2.0 mmol/L HCO3– = 29 mmol/L These results would be classiﬁed as:
A. Metabolic acidosis
B. Metabolic alkalosis
C. Respiratory acidosis
D. Respiratory alkalosis
• C. Respiratory acidosis
•  Imbalances are classiﬁed as respiratory when the primary disturbance is with PCO2 because PCO2 is regulated by ventilation. PCO2 = dCO2/0.03 or 60 mm Hg (normal 35–45 mm Hg). Increased dCO2 will increase hydrogen ion concentration, causing acidosis. Bicarbonate is moderately increased, but a primary increase in NaHCO3 causes alkalosis. Thus, the cause of this acidosis is CO2 retention (respiratory acidosis), and it is partially compensated by renal retention of bicarbonate.
19. A patient’s blood gas results are: pH = 7.50 PCO2 = 55 mm Hg HCO3– = 40 mmol/L These results indicate:
A. Respiratory acidosis
B. Metabolic alkalosis
C. Respiratory alkalosis
D. Metabolic acidosis
• B. Metabolic alkalosis
• A pH above 7.45 corresponds with alkalosis. Both bicarbonate and PCO2 are elevated. Bicarbonate is the conjugate base and is under metabolic (renal) control, while PCO2 is an acid and is under respiratory control. Increased bicarbonate (but not increased CO2) results in alkalosis; therefore, the classiﬁcation is metabolic alkalosis, partially compensated by increased PCO2.
20. Which set of results is consistent with uncompensated respiratory alkalosis?
A. pH 7.70 HCO3 30 mmol/L PCO2 25 mm Hg B. pH 7.66 HCO3 22 mmol/L PCO2 20 mm Hg C. pH 7.46 HCO3 38 mmol/L PCO2 55 mm Hg D. pH 7.36 HCO3 22 mmol/L PCO2 38 mm Hg
• B. pH 7.66 HCO3 22 mmol/L PCO2 20 mm Hg
• Respiratory alkalosis is caused by hyperventilation, inducing low PCO2. Very often, in the early phase of an acute respiratory disturbance, the kidneys have not had time to compensate, and the bicarbonate is within normal limits. In answer A, the bicarbonate is high and PCO2 low; thus, both are contributing to alkalosis and this would be classiﬁed as a combined acid–base disturbance. In answer C, the pH is almost normal, and both bicarbonate and PCO2 are increased. This can occur in the early stage of a metabolic acid– base disturbance when full respiratory compensation occurs or in a combined acid–base disorder. In answer D, both bicarbonate and PCO2 are within normal limits (22–26 mmol/L, 35–45 mm Hg, respectively) as is the pH.
21. Which of the following will shift the O2 dissociation curve to the left?
A. Anemia
B. Hyperthermia
C. Hypercapnia
D. Alkalosis
• D. Alkalosis
• A left shift in the oxyhemoglobin dissociation curve signiﬁes an increase in the aﬃnity of Hgb for O2. This occurs in alkalosis, hypothermia, and in those hemoglobinopathies such as Hgb Chesapeake that increase the binding of O2 to heme. A right shift in the oxyhemoglobin dissociation curve lowers the aﬃnity of Hgb for O2. This occurs in anemia due to increased 2,3-diphosphoglycerate (2,3-DPG), with increased body temperature, increased hydrogen ion concentration, hypercapnia (increased PCO2), and in some hemoglobinopathies, such as Hgb Kansas.
22. In which circumstance will the reporting of calculated oxygen saturation of hemoglobin based on PO2, PCO2, pH, temperature, and hemoglobin be in error?
A. Carbon monoxide poisoning
B. Diabetic ketoacidosis
C. Patient receiving oxygen therapy
D. Assisted ventilation for respiratory failure
• A. Carbon monoxide poisoning
•  CO has about 200 times the aﬃnity as O2 for hemoglobin and will displace O2 from hemoglobin at concentrations that have no signiﬁcant eﬀect on the PAO2. Consequently, calculated oxygen saturation will be erroneously high. Other cases in which the calculated O2Sat should not be used include any hemoglobinopathy that aﬀects oxygen aﬃnity and methemoglobinemia. The other situations above aﬀect the O2 saturation of hemoglobin in a manner that can be predicted by the eﬀect of pH, PO2, and PCO2 on the oxyhemoglobin dissociation curve.
23. Which would be consistent with partially compensated respiratory acidosis?
A. pH PCO2 Bicarbonate increased increased increased
B. pH PCO2 Bicarbonate increased decreased decreased
C. pH PCO2 Bicarbonate decreased decreased decreased
D. pH PCO2 Bicarbonate decreased increased increased
• D. pH PCO2 Bicarbonate decreased increased increased
• Acidosis = low pH; respiratory = disturbance of PCO2; a low pH is caused by increased PCO2. In partially compensated respiratory acidosis, the metabolic component of the buﬀer system, bicarbonate, is retained. This helps to compensate for retention of PCO2 by titrating hydrogen ions. The compensatory component always moves in the same direction as the cause of the acid–base disturbance.
24. Which condition results in metabolic acidosis with severe hypokalemia and chronic alkaline urine?
A. Diabetic ketoacidosis
B. Phenformin-induced acidosis
C. Renal tubular acidosis
D. Acidosis caused by starvation
• D. Acidosis caused by starvation
• Metabolic acidosis can be caused by any condition that lowers bicarbonate. In nonrenal causes, the kidneys will attempt to compensate by increased acid excretion. However, in renal tubular acidosis (RTA), an intrinsic defect in the tubules prevents bicarbonate reabsorption. This causes alkaline instead of acidic urine. Excretion of bicarbonate as potassium bicarbonate (KHCO3) results in severe hypokalemia.
25. Which of the following mechanisms is responsible for metabolic acidosis?
A. Bicarbonate deﬁciency
B. Excessive retention of dissolved CO2
C. Accumulation of volatile acids
D. Hyperaldosteronism
• A. Bicarbonate deﬁciency
•  Metabolic acidosis is caused by bicarbonate deﬁciency and metabolic alkalosis by bicarbonate excess. Respiratory acidosis is caused by PCO2 retention (defective ventilation), and respiratory alkalosis is caused by PCO2 loss (hyperventilation). Important causes of metabolic acidosis include renal failure, diabetic ketoacidosis, lactate acidosis, and diarrhea.
26. Which of the following disorders is associated with lactate acidosis?
A. Diarrhea
B. Renal tubular acidosis
C. Hypoaldosteronism
D. Alcoholism
• D. Alcoholism
• Lactate acidosis often results from hypoxia, which causes a deﬁcit of nicotinamide adenine dinucleotide, the oxidized form (NAD+). This promotes the reduction of pyruvate to lactate, regenerating NAD+ needed for glycolysis. In alcoholic acidosis, oxidation of ethanol to acetaldehyde consumes the NAD+. In diabetes, lactate acidosis can result from depletion of Krebs cycle intermediates. Diarrhea and renal tubular acidosis result in metabolic acidosis via bicarbonate loss. Hypoaldosteronism causes metabolic acidosis via hydrogen and potassium ion retention.
27. Which of the following is the primary mechanism of compensation for metabolic acidosis?
A. Hyperventilation
B. Release of epinephrine
C. Aldosterone release
D. Bicarbonate excretion
• A. Hyperventilation
• In metabolic acidosis, the respiratory center is stimulated by chemoreceptors in the carotid sinus, causing hyperventilation. This results in increased release of CO2. Respiratory compensation begins almost immediately unless blocked by pulmonary disease or respiratory therapy. Hyperventilation can bring the PCO2 down to approximately 10–15 mm Hg.
28. The following conditions are all causes of alkalosis. Which condition is associated with respiratory (rather than metabolic) alkalosis?
A. Anxiety
B. Hypovolemia
C. Hyperaldosteronism
D. Hypoparathyroidism
• A. Anxiety
• Respiratory alkalosis is caused by hyperventilation, which leads to decreased PCO2. Anxiety and drugs such as epinephrine that stimulate the respiratory center are common causes of respiratory alkalosis. Excess aldosterone increases net acid excretion by the kidneys. Low parathyroid hormone causes increased bicarbonate reabsorption, resulting in alkalosis. Hypovolemia increases the relative concentration of bicarbonate. This is common and is called dehydrational alkalosis, chloride responsive alkalosis, or alkalosis of sodium deﬁcit.
29. Which of the following conditions is associated with both metabolic and respiratory alkalosis? A. Hyperchloremia
B. Hypernatremia
C. Hyperphosphatemia
D. Hypokalemia
• D. Hypokalemia
• Which of the following conditions is associated with both metabolic and respiratory alkalosis? A. Hyperchloremia B. Hypernatremia C. Hyperphosphatemia D. Hypokalemia
30. Which PCO2 value would be seen in maximally compensated metabolic acidosis? A. 15 mm Hg B. 30 mm Hg C. 40 mm Hg D. 60 mm Hg
• A. 15 mm Hg
• In metabolic acidosis, hyperventilation increases the ratio of bicarbonate to dissolved CO2. The extent of compensation is limited by the rate of both gas diﬀusion and diaphragm contraction. The lower limit is between 10 and 15 mm Hg PCO2, which is the maximum compensatory eﬀect.
31. In uncompensated metabolic acidosis, which of the following will be normal?
A. Plasma bicarbonate
B. PCO2
C. p50
D. Total CO2
• B. PCO2
• The normal compensatory mechanism for metabolic acidosis is respiratory hyperventilation. In uncompensated cases, the PCO2 is not reduced, indicating a concomitant problem in respiratory control.
32. Which of the following conditions is classiﬁed as normochloremic acidosis?
A. Diabetic ketoacidosis
B. Chronic pulmonary obstruction
C. Uremic acidosis
D. Diarrhea
• A. Diabetic ketoacidosis
• Bicarbonate deﬁcit will lead to hyperchloremia unless the bicarbonate is replaced by an unmeasured anion. In diabetic ketoacidosis, acetoacetate and other ketoacids replace bicarbonate. The chloride remains normal or low and there is an increased anion gap.
33. A patient has the following arterial blood gas results: pH = 7.56 PCO2 = 25 mm Hg PO2 = 100 mm Hg HCO3– = 22 mmol/L These results are most likely the result of which condition?
A. Improper specimen collection
B. Prolonged storage
C. Hyperventilation
D. Hypokalemia
• C. Hyperventilation
• The pH is alkaline (reference range 7.35–7.45) and this can be caused by either low PCO2 or increased bicarbonate. This patient has a normal bicarbonate (reference range 22–26 mmol/L) and a low PCO2 (reference range 35–45 mm Hg). Low PCO2 is always caused by hyperventilation, and therefore, this is a case of uncompensated respiratory alkalosis. The acute stages of respiratory disorders are often uncompensated. Prolonged storage would cause the pH and PO2 to fall, and the PCO2 to rise. Hypokalemia causes alkalosis, but usually is associated with the retention of CO2 as compensation
34. Why are three levels used for quality control of pH and blood gases?
A. Systematic errors can be detected earlier than with two controls
B. Analytical accuracy needs to be greater than for other analytes
C. High, normal, and low ranges must always be evaluated
D. A diﬀerent level is needed for pH, PCO2, and PO2
• A. Systematic errors can be detected earlier than with two controls
• Error detection occurs sooner when more controls are used. Some errors, such as those resulting from temperature error and protein coating of electrodes, are not as pronounced near the calibration point, as in the acidosis and alkalosis range. The minimum requirement for blood gas QC is one sample every 8 hours and three levels (acidosis, normal, alkalosis) every 24 hours. Three levels of control are also used commonly for therapeutic drug monitoring and hormone assays because precision diﬀers signiﬁcantly in the high and low ranges.
35. A single-point calibration is performed between each blood gas sample in order to: A. Correct the electrode slope
B. Correct electrode and instrument drift
C. Compensate for temperature variance
D. Prevent contamination by the previous sample
• B. Correct electrode and instrument drift
• Calibration using a single standard corrects the instrument for error at the labeled value of the calibrator but does not correct for analytic errors away from the set point. A two-point calibration adjusts the slope response of the electrode, eliminating proportional error caused by poor electrode performance.
36. In which condition would hypochloremia be expected?
A. Respiratory alkalosis
B. Metabolic acidosis
C. Metabolic alkalosis
D. All of these options
• C. Metabolic alkalosis
• Chloride is the major extracellular anion and is retained or lost to preserve electroneutrality. Low chloride will occur in metabolic alkalosis because excess bicarbonate is present. Low chloride also will occur in partially compensated respiratory acidosis because the kidneys compensate by increased retention of bicarbonate.
37. Given the following serum electrolyte data, determine the anion gap. Na = 132 mmol/L Cl = 90 mmol/L HCO3– = 22 mmol/L
A. 12 mmol/L
B. 20 mmol/L
C. 64 mmol/L
D. Cannot be determined from the information provided
• B. 20 mmol/L
• The anion gap is deﬁned as unmeasured anions minus unmeasured cations. It is calculated by subtracting the measured anions (bicarbonate and chloride) from the serum sodium (or sodium plus potassium). A normal anion gap is approximately 8–16 mmol/L (12–20 mmol/L when potassium is used). Anion gap = Na – (HCO3 + Cl) Anion gap = 132 – (90 + 22) = 20 mmol/L
38. Which of the following conditions will cause an increased anion gap?
A. Diarrhea
B. Hypoaldosteronism
C. Hyperkalemia
D. Renal failure
• D. Renal failure
• An increased anion gap occurs when there is production or retention of anions other than bicarbonate or chloride (measured anions). For example, in renal failure, retention of phosphates and sulfates (as sodium salts) increases the anion gap. Other common causes of metabolic acidosis with an increased anion gap are diabetic ketoacidosis and lactate acidosis. The anion gap may also be increased in the absence of an acid–base disorder. Common causes include hypocalcemia, drug overdose, and laboratory error when measuring electrolytes.
39. Alcoholism, liver failure, and hypoxia induce acidosis by causing:
B. Increased excretion of bicarbonate
C. Increased retention of PCO2
D. Loss of carbonic anhydrase
• A. Depletion of cellular NAD+
•  Oxygen debt and liver failure block oxidative phosphorylation, preventing  NADH from being oxidized back to NAD+. Oxidation of ethanol to acetate results in accumulation of NADH. When NAD+ is depleted, glycolysis cannot proceed. It is regenerated by reduction of pyruvate to lactate, causing lactate acidosis.
40. Which of the following is the primary mechanism causing respiratory alkalosis?
A. Hyperventilation
B. Deﬁcient alveolar diﬀusion
C. Deﬁcient pulmonary perfusion
D. Parasympathetic inhibition
• A. Hyperventilation
• Hyperventilation via stimulation of the respiratory center (or induced by a respirator) is the mechanism of respiratory alkalosis. Causes include low PO2, anxiety, fever, and drugs that stimulate the respiratory center. Acute respiratory alkalosis is often uncompensated because renal compensation is not rapid. Uncompensated respiratory alkalosis is characterized by an elevated pH and a low PCO2 with normal bicarbonate
41. Which condition can result in acidosis?
A. Cystic ﬁbrosis
B. Vomiting
C. Hyperaldosteronism
D. Excessive O2 therapy
• D. Excessive O2 therapy
• When O2 saturation of venous blood is greatly elevated, Hgb cannot release O2. Oxyhemoglobin cannot bind CO2 or hydrogen ions and acidosis results. Pure O2 may cause neurological damage, leading to convulsion and blindness, especially in infants. It can induce respiratory failure by causing pulmonary hemorrhage, edema, and hyalinization. The other three conditions cause alkalosis. Vomiting and cystic ﬁbrosis cause loss of chloride, resulting in hypovolemia and intestinal bicarbonate absorption. Hyperaldosteronism causes hypokalemia; this results in increased renal H+ excretion and a shift of H+ into cells in exchange for K+.
42. Which of the following conditions is associated with an increase in ionized calcium (Cai) in the blood?
A. Alkalosis
B. Hypoparathyroidism
C. Hyperalbuminemia
D. Malignancy
• D. Malignancy
• Increased Cai occurs in hyperparathyroidism, malignancy, and acidosis. Cai is elevated in primary hyperparathyroidism due to resorption of calcium from bone. Many nonparathyroid malignancies create products called parathyroid hormone-related proteins that stimulate the parathyroid receptors of cells. Acidosis alters the equilibrium between bound and free calcium, favoring ionization. Hyperalbuminemia increases the total calcium by increasing the proteinbound fraction, but does not aﬀect the Cai.
43. Which of the following conditions is associated with hypophosphatemia?
A. Rickets
B. Multiple myeloma
C. Renal failure
D. Hypervitaminosis D
• A. Rickets
• Rickets can result from dietary phosphate deﬁciency, vitamin D deﬁciency, or an inherited disorder of either vitamin D or phosphorus metabolism. Vitamin D–dependent rickets (VDDR) can be reversed by megadoses of vitamin D. Type 1 is caused by a deﬁciency in renal cells of 1-α-hydroxylase, an enzyme that converts 25 hydroxyvitamin D to the active form, 1,25 hydroxyvitamin D. Type 2 is caused by a deﬁciency in the vitamin D receptor of bone tissue. Vitamin D–resistant rickets (VDRR) is caused by a deﬁciency in the renal reabsorption of phosphate. Consequently, aﬀected persons (usually men because it is most commonly X-linked) have a normal serum calcium and a low Pi.
44. Which of the following tests is consistently abnormal in osteoporosis?
A. High urinary calcium
B. High serum Pi
C. Low serum calcium
D. High urine or serum N-telopeptide of
• D. High urine or serum N-telopeptide of
• Commonly used markers for other bone diseases such as serum or urinary calcium, inorganic phosphorus, total alkaline phosphatase (ALP), and vitamin D are neither sensitive nor specific for osteoporosis. Calcium and phosphorus are usually within normal limits. Although estrogen deficiency reduces formation of 1,25 hydroxyvitamin D (1,25 hydroxycholecalciferol), promoting postmenopausal osteoporosis, the 1,25 hydroxyvitamin D is low in only 30%–35% of cases, and low levels may be caused by other bone disorders. Serum markers for osteoporosis include both N-telopeptide of type 1 collagen (NTx) and C-telopeptide of type 1 collagen (CTx). These can be used to follow treatment with resorption antagonists (bisphosphonates) because they decrease significantly when therapy is successful
45. Which of the following is a marker for bone formation?
A. Osteocalcin
B. Tartrate resistant acid phosphatase (TRAP) C. Urinary pyridinoline and deoxypyridinoline D. Urinary C-telopeptide and N-telopeptide crosslinks (CTx and NTx)
• A. Osteocalcin
•  Biochemical markers for osteoporosis are classiﬁed as either markers for bone formation or resorption. Osteocalcin is a protein hormone that stimulates osteoblasts and increases bone mineralization. Pyridinoline is formed when hydroxylysine groups on adjacent ﬁbrils are joined together, and deoxypyridinoline when hydroxylysine and lysine groups are joined. These form crosslinks between the C and N terminal ends of one ﬁbril (which are nonhelical) and the helical portion of an adjacent ﬁbril. The resulting products are called C- and N-telopeptide crosslinks of type 1 collagen. Osteoclasts cause cleavage of these bonds, resulting in loss of both telopeptides—deoxypyridinoline and pyridinoline—in the urine. TRAP is an enzyme (produced by osteoclasts) that hydrolyzes phosphate in the hydroxyapatite matrix of the bone.
46. Which of the following tests is consistently abnormal in osteoporosis?
A. High urinary calcium
B. High serum Pi
C. Low serum calcium
D. High urine or serum N-telopeptide of type 1 collagen
• D. High urine or serum N-telopeptide of type 1 collagen
• Commonly used markers for other bone diseases such as serum or urinary calcium, inorganic phosphorus, total alkaline phosphatase (ALP), and vitamin D are neither sensitive nor specific for osteoporosis. Calcium and phosphorus are usually within normal limits. Although estrogen deficiency reduces formation of 1,25 hydroxyvitamin D (1,25 hydroxycholecalciferol), promoting postmenopausal osteoporosis, the 1,25 hydroxyvitamin D is low in only 30%–35% of cases, and low levels may be caused by other bone disorders. Serum markers for osteoporosis include both N-telopeptide of type 1 collagen (NTx) and C-telopeptide of type 1 collagen (CTx). These can be used to follow treatment with resorption antagonists (bisphosphonates) because they decrease significantly when therapy is successful.
47. Which of the following laboratory results is consistent with primary hypoparathyroidism?
A. Low calcium; high inorganic phosphorusPi
B. Low calcium; low Pi
C. High calcium; high Pi
D. High calcium; low Pi
• D. High calcium; low Pi
• Increased Cai occurs in hyperparathyroidism, malignancy, and acidosis. Cai is elevated in primary hyperparathyroidism due to resorption of calcium from bone. Many nonparathyroid malignancies create products called parathyroid hormone-related proteins that stimulate the parathyroid receptors of cells. Acidosis alters the equilibrium between bound and free calcium, favoring ionization. Hyperalbuminemia increases the total calcium by increasing the proteinbound fraction, but does not aﬀect the Cai.
48. What role do CTx and NTx play in the management of osteoporosis?
A. Increased urinary excretion is diagnostic of early stage disease
B. Increased levels indicate a low risk of developing osteoporosis
C. Decreased urinary excretion indicates a positive response to treatment
D. The rate of urinary excretion correlates with the stage of the disease
• C. Decreased urinary excretion indicates a positive response to treatment
• Markers for both bone formation and resorption are used to monitor treatment for osteoporosis. Serum and urinary measurements of CTx and NTx and urinary deoxypyridinoline are used to monitor medications such as biphosphonates that inhibit bone resorption. Levels fall with successful treatment. DEXA scan, an x-ray procedure based on subtraction of surrounding tissue, is the most sensitive diagnostic test for osteoporosis and can show bone loss as small as 1%. However, it takes months before a DEXA scan shows increased bone remodeling following treatment.
49. What role does vitamin D measurement play in the management of osteoporosis?
A. Vitamin D deﬁciency must be demonstrated to establish the diagnosis
B. Vitamin D is consistently elevated in osteoporosis
C. A normal vitamin D level rules out osteoporosis
D. Vitamin D deﬁciency is a risk factor for developing osteoporosis
• D. Vitamin D deﬁciency is a risk factor for developing osteoporosis
• Vitamin D assay is not used to diagnose osteoporosis. Vitamin D deﬁciency is a cause of secondary osteoporosis, and together with low PTH, calcium, and estrogen are important risk factors. If one or more of these is abnormal, then bone resorption or remodeling may be abnormal, predisposing one to osteoporosis. Deﬁciency of vitamin D also causes rickets (called osteomalaciain adults), a condition in which bones become soft owing to reduced deposition of hydroxyapatite.
50. Which statement best describes testing recommendations for vitamin D?
A. Vitamin D testing should be reserved only for those persons who demonstrate hypercalcemia of an undetermined cause
B. Vitamin D testing should be speciﬁc for the 1,25(OH)D3 form
C. Testing should be for total vitamin D when screening for deﬁciency
D. Vitamin D testing should not be performed if the patient is receiving a vitamin D supplement
• C. Testing should be for total vitamin D when screening for deﬁciency
• Vitamin D deﬁciency is far more common than vitamin D excess, and screening for vitamin D deﬁciency is advocated especially for dark-skinned persons and people who do not get adequate sunlight. Provitamin D is a steroid, and vitamin D is now considered a hormone rather than a vitamin. The hormone regulates transcription of over 200 genes and has pronounced eﬀects on both dendritic cells and T lymphocytes. Deﬁciency is associated with many chronic diseases including autoimmune diseases, cancers, hypertension, and heart disease. There are two forms of the vitamin, ergocalciferol (D2) and cholecalciferol (D3). Active D2 and D3 are formed when two hydroxyl groups are added, the ﬁrst being at the 25 position by the liver and the second at the α-1 position by the kidney. The majority of the circulating vitamin D is in the 25-hydroxylated form of D2 and D3, called 25(OH)D. The plasma 25(OH)D concentration is an expression of both dietary and endogenous vitamin D and is the most appropriate test for detecting nutritional vitamin D deﬁciency. Since the eﬀect on calcium is derived from the active 1,25 form of the vitamin, plasma 1,25(OH)D concentration is a more speciﬁc test for hypervitaminosis D.
51. The serum level of which of the following laboratory tests is decreased in both VDDR and VDRR?
A. Vitamin D
B. Calcium
C. Pi
D. Parathyroid hormone
• C. Pi
• Persons with VDDR and VDRR have a low Pi. However, persons with VDDR have decreased serum calcium, as well. Parathyroid hormone (PTH) is increased in persons with VDDR because calcium is the primary stimulus for PTH release, but not in persons with VDRR. Vitamin D levels vary depending upon the type of rickets and the vitamin D metabolite that is measured. 1,25(OH)D, the active form of vitamin D, is low in type 1 but high in type 2 VDDR. It may be either normal or low in VDRR.
52. Which of the following is the most accurate measurement of Pi in serum?
A. Rate of unreduced phosphomolybdate formation at 340 nm
B. Measurement of phosphomolybdenum blue at 680 nm
C. Use of aminonaptholsulfonic acid to reduce phosphomolybdate
D. Formation of a complex with malachite green dye
• A. Rate of unreduced phosphomolybdate formation at 340 nm
• The colorimetric method (Fiske and SubbaRow) used previously for Pi reacted ammonium molybdate with Pi, forming ammonium phosphomolybdate (NH4)3[PO4(MoO3)12]. A reducing agent, aminonaptholsulfonic acid (ANS), was added, forming phosphomolybdenum blue. The product was unstable and required sulfuric acid, making precipitation of protein a potential source of error. These problems are avoided by measuring the rate of formation of unreduced phosphomolybdate at 340 nm.
53. What is the percentage of serum calcium that is ionized (Cai)?
A. 30%
B. 45%
C. 60%
D. 80%
• B. 45%
• Calcium exists in serum in three forms: protein bound, ionized, and complexed (as undissociated salts). Only Cai is physiologically active. Protein bound and Cai each account for approximately 45% of total calcium, and the remaining 10% is complexed.
54. Which of the following conditions will cause erroneous Cai results? Assume that the samples are collected and stored anaerobically, kept at 4°C until measurement, and stored for no longer than 1 hour.
A. Slight hemolysis during venipuncture
B. Assay of whole blood collected in sodium oxalate
C. Analysis of serum in a barrier gel tube stored at 4°C until the clot has formed
D. Analysis of whole blood collected in sodium heparin, 20 U/mL (low-heparin tube)
• B. Assay of whole blood collected in sodium oxalate
• Unlike Pi, the intracellular calcium level is not signiﬁcantly diﬀerent from plasma calcium, and calcium is not greatly aﬀected by diet. Whole blood collected with 5–20 U/mL heparin and stored on ice no longer than 2 hours is the sample of choice for Cai. Blood gas syringes preﬁlled with 100 U/mL heparin should not be used because the high heparin concentration will cause low results. Citrate, oxalate, and ethylenediaminetetraacetic acid (EDTA) must not be used because they chelate calcium. Serum may be used provided that the sample is iced, kept capped while clotting, and assayed within 2 hours (barrier gel tubes may be stored longer).
55. Which of the following conditions is associated with a low serum magnesium?
B. Hemolytic anemia
C. Hyperparathyroidism
D. Pancreatitis
• D. Pancreatitis
• Low magnesium can be caused by gastrointestinal loss, as occurs in diarrhea and pancreatitis (loss of Mg and Ca as soaps). Hyperparathyroidism causes increased release of both calcium and magnesium from bone. Addison’s disease (adrenocorticosteroid deﬁciency) may be associated with increased magnesium accompanying hyperkalemia. Hemolytic anemia causes increased release of magnesium as well as potassium from damaged red blood cells (RBCs).
56. When measuring calcium with the complexometric dye o-cresolphthalein complexone, magnesium is kept from interfering by: A. Using an alkaline pH B. Adding 8-hydroxyquinoline C. Measuring at 450 nm D. Complexing to EDTA
• o-Cresolphthalein complexone can be used to measure either magnesium or calcium. Interference in calcium assays is prevented by addition of 8-hydroxyquinoline, which chelates magnesium. When magnesium is measured, ethyleneglycol bistetraacetic acid (EGTA) or EDTA is used to chelate calcium. Two other dyes that can be used for both magnesium and calcium assays are calmagite and methylthymol blue. Arsenazo III dye is commonly used to measure calcium. It is more speciﬁc for Ca+2 than the others, and does not require addition of a Mg+2 chelator
57. Which electrolyte measurement is least aﬀected by hemolysis?
A. Potassium B. Calcium C. Pi D. Magnesium
• B. Calcium
• Potassium, phosphorus, and magnesium are the major intracellular ions, and even slight hemolysis will cause falsely elevated results. Serum samples with visible hemolysis (20 mg/dL free Hgb) should be redrawn.
58. Which of the following conditions is associated with hypokalemia?
B. Hemolytic anemia
C. Digoxin intoxication
D. Alkalosis
• D. Alkalosis
• Addison’s disease (adrenocortical insuﬃciency) results in low levels of adrenal corticosteroid hormones, including aldosterone and cortisol. Because these hormones promote reabsorption of sodium and secretion of potassium by the collecting tubules, patients with Addison’s disease display hyperkalemia and hyponatremia. Hemolytic anemia and digoxin intoxication cause release of intracellular potassium. Alkalosis causes potassium to move from the extracellular ﬂuid into the cells as hydrogen ions move from the cells into the extracellular ﬂuid to compensate for alkalosis.
59. Which of the following conditions is most likely to produce an elevated plasma potassium?
A. Hypoparathyroidism
B. Cushing’s syndrome
C. Diarrhea
D. Digitalis overdose
• D. Digitalis overdose
•  Digitalis toxicity causes potassium to leave the cells and enter the extracellular ﬂuid, resulting in hyperkalemia. Renal failure, hemolytic anemia and Addison’s disease are other frequent causes of hyperkalemia. Hypoparathyroidism indirectly causes hypokalemia by inducing alkalosis via increased renal retention of phosphate and bicarbonate. Cushing’s syndrome (adrenal cortical hyperfunction) results in low potassium and elevated sodium. Diarrhea causes loss of sodium and potassium.
60. Which of the following values is the threshold critical value (alert or action level) for low plasma potassium?
A. 1.5 mmol/L
B. 2.0 mmol/L
C. 2.5 mmol/L
D. 3.5 mmol/L
• C. 2.5 mmol/L
• The reference range for potassium is 3.6–5.4 mmol/L. However, values below 2.5 mmol/L require immediate intervention because below that level there is a grave risk of cardiac arrhythmia, which can lead to cardiac arrest. The upper alert level for potassium is usually 6.5 mmol/L, except for neonatal and hemolyzed samples. Above this level, there is danger of cardiac failure.
61. Which electrolyte is least likely to be elevated in renal failure?
A. Potassium
B. Magnesium
C. Inorganic phosphorus
D. Sodium
• D. Sodium
•  Reduced glomerular ﬁltration coupled with decreased tubular secretion causes accumulation of potassium, magnesium, and inorganic phosphorus. Poor tubular reabsorption of sodium oﬀsets reduced glomerular ﬁltration. Unﬁltered sodium draws both chloride and water, causing osmotic equilibration between ﬁltrate, serum, and the tissues. In renal disease, serum sodium is often normal, although total body sodium is increased owing to ﬂuid and salt retention.
62. Which of the following is the primary mechanism for vasopressin (ADH) release?
A. Hypovolemia
B. Hyperosmolar plasma
C. Renin release
D. Reduced renal blood ﬂow
• B. Hyperosmolar plasma
• ADH is released by the posterior pituitary in response to increased plasma osmolality. Normally, this is triggered by release of aldosterone caused by ineﬀective arterial pressure in the kidney. Aldosterone causes sodium reabsorption, which raises plasma osmolality; release of ADH causes reabsorption of water, which increases blood volume and restores normal osmolality. A deﬁciency of ADH (diabetes insipidus) results in dehydration and hypernatremia. An excess of ADH (syndrome of inappropriate ADH release [SIADH]) results in dilutional hyponatremia. This may be caused by regional hypovolemia, hypothyroidism, central nervous system injury, drugs, and malignancy.
63. Which of the following conditions is associated with hypernatremia?
A. Diabetes insipidus
B. Hypoaldosteronism
C. Burns
D. Diarrhea
• B. Hypoaldosteronism
• Diabetes insipidus results from failure to produce ADH. Because the collecting tubules are impermeable to water in the absence of ADH, severe hypovolemia and dehydration result. Hypovolemia stimulates aldosterone release, causing sodium reabsorption, which worsens the hypernatremia. Burns, hypoaldosteronism, diarrhea, and diuretic therapy are common causes of hyponatremia.
64. Which of the following values is the threshold critical value (alert or action level) for high plasma sodium?
A. 150 mmol/L
B. 160 mmol/L
C. 170 mmol/L
D. 180 mmol/L
• B. 160 mmol/L
• The adult reference range for plasma sodium is approximately 135–145 mmol/L. Levels in excess of 160 mmol/L are associated with severe dehydration, hypovolemia, and circulatory and heart failure. The threshold for the low critical value for sodium is 120 mmol/L. This is associated with edema, hypervolemia, and circulatory overload. Alert levels must also be established for potassium, bicarbonate, calcium, pH, PO2, glucose, bilirubin, hemoglobin, platelet count, and prothrombin time. When a sample result is below or above the low or high alert level, respectively, the physician must be notiﬁed immediately.
65. Which of the following conditions is associated with total body sodium excess?
A. Renal failure
B. Hyperthyroidism
C. Hypoparathyroidism
D. Diabetic ketoacidosis
• A. Renal failure
• Total body sodium excess often occurs in persons with renal failure, congestive heart failure, and cirrhosis of the liver. When water is retained along with sodium, total body sodium excess results rather than hypernatremia. Heart failure causes sodium and water retention by reducing blood ﬂow to the kidneys. Cirrhosis causes obstruction of hepatic lymphatics and portal veins, leading to local hypertension and accumulation of ascites ﬂuid. Renal failure results in poor glomerular ﬁltration and isosmotic equilibration of salt and water.
66. Which of the following conditions involving electrolytes is described correctly?
A. Pseudohyponatremia occurs only when undiluted samples are measured
B. Potassium levels are slightly higher in heparinized plasma than in serum
C. Hypoalbuminemia causes low total calcium but does not aﬀect Cai
D. Hypercalcemia may be induced by low serum magnesium
• C. Hypoalbuminemia causes low total calcium but does not aﬀect Cai
• When serum albumin is low, the equilibrium between bound and Cai is shifted, producing increased Cai. This inhibits release of PTH by negative feedback until the Cai level returns to normal. Potassium is released from platelets and leukocytes during coagulation, causing serum levels to be higher than plasma. Pseudohyponatremia is a measurement error caused by diluting samples containing excessive fat or protein. The colloids displace plasma water, resulting in less electrolytes being delivered into the diluent. Only ion-selective electrodes that measure whole blood or undiluted serum are unaﬀected. Magnesium is needed for release of PTH, and PTH causes release of calcium and magnesium from bone. Therefore, hypocalcemia can be associated with either magnesium deﬁciency or magnesium excess.
67. Which of the following conditions is associated with hyponatremia?
A. Diuretic therapy
B. Cushing’s syndrome
C. Diabetes insipidus
D. Nephrotic syndrome
Diuretics lower blood pressure by promoting water loss. This is accomplished by causing sodium loss from the proximal tubule and/or loop. Addison’s disease, syndrome of inappropriate ADH release, burns, diabetic ketoacidosis, hypopituitarism, vomiting, diarrhea, and cystic ﬁbrosis also cause hyponatremia. Cushing’s syndrome causes hypernatremia by promoting sodium reabsorption in the collecting tubule in exchange for potassium. Diabetes insipidus and nephrotic syndrome promote hypernatremia by causing water loss.
68. Which of the following laboratory results is usually associated with cystic ﬁbrosis?
A. Sweat chloride greater than 60 mmol/L
B. Elevated serum sodium and chloride
C. Elevated fecal trypsin activity
D. Low glucose
• A. Sweat chloride greater than 60 mmol/L
• Cystic ﬁbrosis causes obstruction of the exocrine glands including the sweat glands, mucus glands, and pancreas. Newborns with pancreatic involvement demonstrate fecal trypsin deﬁciency, which may be detected by a low fecal chymotrypsin or immunoreactive trypsin result. However, these tests require conﬁrmation. Serum sodium and chloride levels are low. More than 98% of aﬀected infants have elevated sweat sodium and chloride and low serum levels. Sweat chloride in excess of 60 mmol/L conﬁrms the clinical diagnosis. Some persons with the disease have insulin deﬁciency and elevated blood glucose. Genetic tests are available to detect several mutations that occur at the cystic ﬁbrosis transmembrane conductance regulator (CFTR) locus on chromosome 7.
69. When performing a sweat chloride collection, which of the following steps will result in analytical error?
A. Using unweighed gauze soaked in pilocarpine nitrate on the inner surface of the forearm to stimulate sweating
B. Collecting more than 75 mg of sweat in 30 minutes
C. Leaving the preweighed gauze on the inside of the arm exposed to air during collection
D. Rinsing the collected sweat from the gauze pad using chloride titrating solution
• C. Leaving the preweighed gauze on the inside of the arm exposed to air during collection
• The sweat chloride procedure requires the application of pilocarpine to stimulate sweating, and the use of iontophoresis (application of 0.16-mA current for 5 minutes) to bring the sweat to the surface. After iontophoresis, the skin on the inner surface of the forearm is washed with deionized water and dried, and a preweighed pair of 2-in.2 pads is taped to the skin. During the 30-minute collection of sweat, the gauze must be completely covered to prevent contamination and loss of sweat by evaporation. The Gibson–Cooke reference method for sweat chloride uses the Schales and Schales method (titration by Hg[NO3]2 with diphenylcarbazone indicator) to assay 1.0 mL of sweat eluted from the gauze with 5 mL of water. A Cotlove chloridometer is often used to measure sweat chloride. The sweat is eluted from the gauze with the titrating solution to facilitate measurement. Alternatively, a macroduct collection system may be used that does not require weighing. A minimum mass of 75 mg sweat is required for collection in gauze and 15 μL sweat for collection in macroduct tubing.
70. Which electrolyte level best correlates with plasma osmolality?
A. Sodium
B. Chloride
C. Bicarbonate
D. Calcium
• A. Sodium
• Sodium and chloride are the major extracellular ions. Chloride passively follows sodium, making sodium the principal determinant of plasma osmolality.
71. Which formula is most accurate in predicting plasma osmolality?
A. Na + 2(Cl) + BUN + glucose
B. 2(Na) + 2(Cl) + glucose + urea
C. 2(Na) + (glucose ÷ 18) + (BUN ÷ 2.8)
D. Na + Cl + K + HCO3
• C. 2(Na) + (glucose ÷ 18) + (BUN ÷ 2.8)
• Calculated plasma osmolality is based upon measurement of sodium, glucose, and urea. Because sodium associates with a counter ion, two times the sodium estimates the millimoles per liter of electrolytes. Some laboratories multiply by 1.86 instead of 2 to correct for undissociated salts. Dividing glucose by 18 converts from milligrams per deciliter to millimoles per liter. Dividing blood urea nitrogen (BUN) by 2.8 converts from milligrams per deciliter BUN to millimoles per liter urea.
 Author: DeanRegentJoshua ID: 303092 Card Set: Blood Gases pH and Electrolytes Updated: 2015-05-25 08:05:47 Tags: Blood Gases pH Electrolytes Folders: Clinical Chemistry Description: lifted from Chemistry/Apply knowledge of fundamental biological characteristics/Acid–base/1 Show Answers: