Chapter 18 Acid-Base Balance and Blood Gas Analysis
Regulation of the hydrogen ion concentration
6. What is the normal plasma H+ concentration, the normal plasma HCO3− concentration, and the normal arterial pH of blood?
7. How is normal arterial pH maintained?
8. What are the buffering systems, and which system has the greatest contribution to the total buffering capacity of blood?
9. How does the bicarbonate buffering system work? What enzyme facilitates this reaction?
10. How does hemoglobin act as a buffer?
11. How does the ventilatory response work?
12. How does the renal response work?
13. How quickly can the buffering system, ventilation changes, and the renal response work?
Measurement of arterial blood gases
14. What is the relationship between a venous and arterial blood gas drawn from the same patient concurrently?
15. What errors can occur if heparin or air is present in an arterial blood gas sample?
16. What happens if there is a delay in analysis of the blood sample?
17. How does temperature affect the arterial blood gas (ABG)?
18. What does an anesthesia provider using alpha stat during cardiopulmonary bypass do to the ABG?
19. What does an anesthesia provider using pH stat during cardiopulmonary bypass do to the ABG?
Differential diagnosis of acid-base disturbances
20. What is the difference between a primary disturbance and a compensatory disturbance in acid-base status?
21. What adverse responses are associated with severe acidemia?
22. What adverse responses are associated with severe alkalemia?
23. What defines a primary respiratory acidosis or alkalosis?
24. What are the causes of a respiratory acidosis?
25. What is the compensatory response for a respiratory acidosis?
26. What is the treatment for a respiratory acidosis?
27. What are the causes of a respiratory alkalosis?
28. What is the compensatory response for a respiratory alkalosis?
29. What is the treatment for a respiratory alkalosis?
30. What defines a primary metabolic acidosis or alkalosis?
31. How is the anion gap calculated?
32. What are the causes of a metabolic acidosis?
33. What is the compensatory response for a metabolic acidosis?
34. Describe how the Stewart strong ion difference approach works.
35. What is the treatment for a metabolic acidosis?
36. What are the causes of a metabolic alkalosis?
37. What is the compensatory response for a metabolic alkalosis?
38. What is the treatment for a metabolic alkalosis?
39. How can an acute respiratory process be distinguished from a chronic process?
40. How is the Δgap determined?
41. How is the Winter’s formula used?
42. Diagram the algorithm for diagnosing an acid-base disorder.
Answers*
General definitions
1. A physiologic acid-base status optimizes enzyme function, myocardial contractility, and saturation of hemoglobin with oxygen. (334)
2. Bronsted defined an acid as a molecule that can act as a proton [H+] donor, and a base as a molecule that can act as a proton acceptor. In biologic molecules, weak acids or bases are molecules that can reversibly donate H+ or reversibly bind H+. (334)
3. Acidemia is defined as an arterial pH less than 7.35 and alkalemia is defined as an arterial pH greater than 7.45. (334)
4. An acidosis is the underlying process that lowers the pH, whereas an alkalosis is the process that raises the pH. A patient can have a mixed disorder with both an acidosis and an alkalosis, but can only be either acidemic or alkalemic. (334)
5. Base excess is usually defined as the amount of strong acid or strong base required to return 1 L of whole blood exposed in vitro to a PCO2 of 40 mm Hg to a pH of 7.4. The number is supposed to refer to the metabolic component of an acid-base disorder. It is most often used in the operating room as a surrogate marker for lactic acidosis to help determine the adequacy of volume resuscitation. (335)
Regulation of the hydrogen ion concentration
6. At 37° C, the normal plasma H+ concentration is 35 to 45 nmol/L. The normal plasma HCO3− concentration is 24 ± 2 mEq/L, and the normal arterial pH of blood is between 7.36 and 7.44. (335)
7. Normal arterial pH is maintained through three systems: buffers, ventilation changes, and renal response. The ventilatory response involves changes in alveolar ventilation and CO2 concentrations. The renal response involves reabsorption of bicarbonate ions or secretion of hydrogen ions. (335)
8. The buffering systems in blood include bicarbonate, hemoglobin, phosphate, and plasma proteins. The bicarbonate buffering system is the largest contributor and provides 50% of the total buffering capacity of the body. Hemoglobin is responsible for about 35% of the total buffering capacity, and phosphate and plasma proteins account for the remainder. (335)
9. Carbonic anhydrase facilitates the hydration of carbon dioxide in the plasma and in the erythrocytes into H2CO3, which spontaneously dissociates to H+ and HCO3−. The HCO3− that is formed then enters the plasma to function as a buffer, and the H+ that is generated is buffered by hemoglobin. (335)
10. In plasma, hemoglobin exists as a weak acid. It acts as a buffer by binding H+ generated by the bicarbonate buffering system. Carbon dioxide can also be transported by hemoglobin as carbaminohemoglobin. Deoxyhemoglobin has a greater affinity for carbon dioxide, so venous blood carries more carbon dioxide than arterial blood. (335-336)
11. Carbon dioxide diffuses across the blood-brain barrier to change CSF pH. Central chemoreceptors lie on the anterolateral surface of the medulla and respond to changes in CSF pH. Minute ventilation increases 1 to 4 L/min for every 1 mm Hg increase in PCO2. Peripheral chemoreceptors are at the bifurcation of the common carotid arteries and aortic arch. The peripheral chemoreceptors are sensitive to changes in PO2, PCO2, pH, and arterial perfusion pressure. They communicate with the central respiratory centers via the glossopharyngeal nerves. The stimulus from central and peripheral chemoreceptors to either increase or decrease alveolar ventilation diminishes as the pH approaches 7.4 such that complete correction or overcorrection is not possible. (336)
12. The kidneys correct for pH changes by reabsorbing filtered HCO3−, excreting titratable acids, and producing ammonia. (336-337)
13. The buffering system of the blood responds to changes in arterial pH almost instantly. Compensatory changes in alveolar ventilation in response to changes in arterial pH occur within minutes. Compensatory changes by the kidneys in response to changes in arterial pH require 12 to 48 hours and may not be maximal for up to 5 days. (335)
Measurement of arterial blood gases
14. Venous PCO2 is 4 to 6 mm Hg higher and pH 0.03 to 0.04 lower than arterial values. Venous blood cannot be used for estimation of oxygenation because venous PO2 is significantly lower than arterial PO2 and the relationship is not linear. (338)
15. Because heparin is acidic, excessive amounts of heparin in the syringe containing blood for arterial blood gas and pH analysis may result in a falsely decreased arterial pH reading. Air bubbles in the syringe containing blood for an arterial blood gas sample could result in the diffusion of oxygen and carbon dioxide between the air bubble and the blood in the syringe. Typically, this results in a decrease in the carbon dioxide tensions in the blood sample. The change in oxygen tension (either falsely higher or lower) depends on the patient’s PO2. (338)
16. A delay in analysis of the blood sample can lead to oxygen consumption and carbon dioxide production by the metabolically active white blood cells. Usually this error is small and can be reduced by placing the sample on ice. In some leukemia patients with markedly elevated white blood cell counts, this error can become significant. This is known as leukocyte larceny. (338)
17. Decreases in temperature decrease the partial pressure of a gas in solution even though the total gas content does not change. A blood gas with a pH of 7.4 and PCO2 of 40 mm Hg at 37° C will have a pH of 7.58 and PCO2 of 23 mm Hg at 25° C. The change in PO2 with respect to temperature depends on the degree that hemoglobin is saturated with oxygen, but as a guideline, the PO2 is decreased approximately 6% for every 1° C that the patient’s body temperature is below 37° C. (338)
18. The term alpha stat developed because as the patient’s pH was allowed to drift with temperature, the protonation state of histidine residues remained “static.” During cardiopulmonary bypass, an anesthesia provider using alpha stat would manage the patient based on an ABG measured at 37° C and strive to keep that pH at 7.4, while the patient’s true pH would be higher. (338)
19. pH stat requires keeping a patient’s pH static at 7.4 based on the core temperature. During cardiopulmonary bypass, an anesthesia provider using pH stat would manage the patient based on an ABG that is corrected for the patient’s temperature. This usually means adding carbon dioxide so that the patient’s temperature-corrected blood gas has a pH of 7.4. (338)
Differential diagnosis of acid-base disturbances
20. A primary disturbance in acid-base status is the initial deviation in the arterial pH secondary to either respiratory or metabolic causes. A compensatory response occurs in an attempt to reverse the alteration in the arterial pH. Typically the compensatory response is not able to completely reverse the deviation in arterial pH. (339)
21. Acidemia usually leads to decreased myocardial contractility. Respiratory acidosis may produce more rapid and profound myocardial dysfunction than metabolic acidosis because of the rapid entry of carbon dioxide into the cardiac cells. In the brain, this rapid rise in carbon dioxide can lead to confusion, loss of consciousness, or seizures. (339)
22. Severe alkalemia can lead to decreased cerebral and coronary blood flow due to arteriolar vasoconstriction. The consequences are more prominent with respiratory than with metabolic causes because of the rapid movement of carbon dioxide across cell membranes. Acute hyperventilation can produce confusion, myoclonus, asterixis, depressed consciousness, and seizures. (339)
23. A primary respiratory acidosis is accompanied by a PCO2 above normal, usually greater than 43 mm Hg. A primary respiratory alkalosis is accompanied by a PCO2 below normal, usually lower than 37 mm Hg. (339-340)
24. Respiratory acidosis may occur secondary to increased carbon dioxide production, decreased carbon dioxide elimination, or from rebreathing or absorption. Causes of increased carbon dioxide production include: malignant hyperthermia, sepsis, or overfeeding. Causes of decreased carbon dioxide elimination include: CNS depressants, decreased skeletal muscle strength, or intrinsic pulmonary disease. Causes of rebreathing or absorption include: exhausted soda lime, incompetent one-way valves, or laparoscopic surgery. (339)
25. Over the course of hours to days, the kidneys will compensate for the acidosis by increased hydrogen ion secretion and bicarbonate reabsorption. The hallmark of a chronic respiratory acidosis is an elevated PCO2 with a near normal pH. (339-340)
26. The treatment for a respiratory acidosis is treatment of the underlying disorder. The use of mechanical ventilation to decrease an acutely increased PCO2 may be necessary if the pH is less than 7.2. (340)
27. Respiratory alkalosis may occur with increased minute ventilation or decreased carbon dioxide production. Causes of increased minute ventilation relative to carbon dioxide production include: CNS disease, pain and anxiety, sepsis, liver disease, pregnancy, or hypoxemia. Causes of decreased carbon dioxide production include: hypothermia and skeletal muscle paralysis. (340)
28. Respiratory alkalosis is compensated for by decreased reabsorption of bicarbonate ions from the renal tubules and increased urinary excretion of bicarbonate. (340)
29. Treatment for a respiratory alkalosis should be directed at correcting the underlying cause. Mild alkalemia usually does not require treatment. During general anesthesia, the minute ventilation may be decreased in order to decrease the elimination of carbon dioxide. (340)
30. A metabolic acidosis is present when accumulation of any acid other than carbon dioxide results in a pH lower than 7.35. The HCO3− concentration is usually less than 22 mEq/L. A metabolic alkalosis is present when the pH is higher than 7.45 due to gain of bicarbonate ions or loss of hydrogen ions. The HCO3− concentration is usually greater than 26 mEq/L. (340-342)
31. The anion gap is the difference between the measured cations (sodium) and measured anions (chloride and bicarbonate). A normal gap value is 8 to 12 mEq/L and is mostly composed of albumin. A patient with a low serum albumin will have a lower anion gap. Each 1 g/dL decrease in serum albumin below 4.4 g/dL will lower the actual concentration of unmeasured anions by 2.3 to 2.5 mEq/L. (341)
32. The causes of a metabolic acidosis are divided into anion gap and nonanion gap causes. An increase in the anion gap occurs when the anion replacing bicarbonate is not one that is routinely measured. The most common unmeasured anions are lactic and keto-acids. Other common anions include: methanol, ethylene glycol, uremia, paraldehyde, and aspirin. Metabolic acidosis with a normal anion gap occurs when chloride replaces the lost bicarbonate, such as with bicarbonate-wasting processes in the kidney (renal tubular acidosis) or gastrointestinal tract (diarrhea). Aggressive fluid resuscitation with normal saline will induce a nongap metabolic acidosis because the chloride administration impairs bicarbonate reabsorption in the kidneys. (341)
33. Compensatory responses for a metabolic acidosis include increased alveolar ventilation from carotid body stimulation and renal tubule secretion of hydrogen ions into urine. Chronic metabolic acidosis is associated with loss of bone mass because buffers present in bone are used to neutralize the nonvolatile acids. (341)
34. The strong ion approach distinguished six primary acid-base disturbances (strong ion acidosis and alkalosis, nonvolatile buffer acidosis and alkalosis, and respiratory acidosis and alkalosis) as opposed to the four differentiated by the Henderson-Hasselbalch equation (metabolic acidosis and alkalosis, and respiratory acidosis and alkalosis). The more complex Stewart approach may be similar to the traditional Henderson-Hasselbalch approach if changes in albumin concentration are accounted for in the measurement of the anion gap. (341)
35. Treatment for metabolic acidosis is based on whether an anion gap is present or not. Intravenous administration of sodium bicarbonate can be given for a nongap acidosis because the problem is bicarbonate loss. Management of an anion gap acidosis should be guided by diagnosis and treatment of the underlying cause in order to remove the nonvolatile acids in the circulation. (342)
36. Causes of a metabolic alkalosis are based on whether the underlying cause is chloride responsive or chloride resistant. Chloride responsive causes include: renal loss from diuretics, GI loss from vomiting, or alkali administration. Chloride resistant causes include: hyperaldosteronism, refeeding syndrome, and profound hypokalemia. (342)
37. Compensatory responses for a metabolic alkalosis include increased reabsorption of hydrogen ions and decreased secretion of hydrogen ions by renal tubule cells, and alveolar hypoventilation. (342)
38. Treatment of a metabolic alkalosis should be aimed at reducing the acid loss by stopping gastric drainage or fluid repletion with saline and potassium chloride, which allows the kidneys to excrete excess bicarbonate ions. Occasionally, a trial of acetazolamide may be useful in causing a bicarbonaturia. (342)
39. Acute respiratory acidosis can be distinguished from a chronic respiratory acidosis by the degree of elevation of HCO3−. The renal effects to compensate for a respiratory acidosis take 12 to 48 hours to take effect and are reflected by a more marked increase in the plasma HCO3− concentration. During an acute process, the pH changes 0.08 for every 10 mm Hg change in PCO2 from 40 mm Hg. During a chronic process, the pH changes 0.03 for every 10 mm Hg change in PCO2 from 40 mm Hg. (342-343)
40. If an anion gap is present, then a Δgap should be determined. The Δgap is the excess anion gap added back to the serum bicarbonate level. It is used to determine if another concurrent metabolic process is present along with an anion gap metabolic acidosis. If the Δgap is less than 22 mEq/L, then a concurrent nongap metabolic acidosis exists. If the Δgap is greater than 26 mEq/L, then a concurrent metabolic alkalosis exits. (342-343)
41. The Winter’s formula is used to determine whether an appropriate respiratory compensation is present for the metabolic acidosis. If measured PCO2 is greater than calculated from the Winter’s formula, then the compensation is not adequate and respiratory acidosis is also present. If the measured PCO2 is less than calculated, then a respiratory alkalosis is present. For a metabolic acidosis, the calculated PCO2 equals the serum HCO3− concentration multiplied by 1.5 plus 8. For a metabolic alkalosis, the calculated PCO2 equals the serum HCO3− concentration multiplied by 0.7 plus 21. (342-343)
42. Step 1: Determine oxygenation
Step 2: Determine acidemia (pH < 7.35) or alkalemia (pH > 7.45)
Step 3: Determine whether the etiology is from a respiratory (PCO2 change from 40) or metabolic (HCO3− – change from 24 mEq/L) process
Step 4: If there is a respiratory abnormality, then assess whether the process is acute or chronic. If there is a metabolic acidosis, then skip to step 5. If there is a metabolic alkalosis, then skip to step 7.
Step 5: If there is a metabolic abnormality, determine the anion gap
Step 7: Determine whether there is adequate respiratory compensation for the metabolic process. (342-343)
Other information provided by the arterial blood gas
43. The dead space to tidal volume (VD/VT) ratio is the fraction of each tidal volume that is involved in dead space ventilation. Normal VD/VT is less than 0.3 and is mostly due to anatomic dead space. An increased dead space will decrease the efficiency of ventilation. Patients with a pulmonary embolus or chronic obstructive pulmonary disease are examples of patients who may have an increased VD/VT ratio. (343)
44. Arterial hypoxemia is caused by a low PO2 in the inhaled gases, hypoventilation, or venous admixture with or without a decreased mixed venous oxygen content. An increase in the venous admixture involves blood that passes from the pulmonary circulation to the systemic circulation without passing by ventilated alveoli. These right-to-left shunts can be intrapulmonary (atelectasis, pneumonia, one-lung ventilation) or intracardiac (congenital heart disease). (344)
45. The alveolar gas equation estimates the partial pressure of alveolar oxygen (PAO2) by using barometric pressure, water vapor pressure, the inspired oxygen content, and PCO2. (344-345)
46. The A-a gradient formula calculates the difference in oxygen partial pressure between alveolar (PAO2) and arterial (PaO2) blood. Calculation of the gradient provides an estimate of venous admixture as the cause of hypoxia. Normally, the A-a gradient is less than 15 mm Hg while breathing room air due to shunting via the thebesian and bronchial veins. Increased inspired FIO2 can lead to a larger gradient: up to 60 mm Hg while breathing FIo2 of 1.0 in healthy patients. The A-a gradient can also provide an assessment of the patient’s shunt fraction. To estimate the amount of shunt present, the shunt fraction is approximately 1% of cardiac output for every 20 mm Hg difference in the A-a gradient when the PaO2 is higher than 150 mm Hg. (344-345)
47. The PaO2/FIO2 (P/F) ratio is an alternative to the A-a gradient to communicate the degree of hypoxia. Patients with acute respiratory distress syndrome (ARDS) should have a P/F ratio below 200. (345)
Cardiac output estimates
48. Normal mixed venous PO2 (Pvo2) is 40 mm Hg. A true mixed venous PO2 should reflect blood from the superior and inferior vena cava. It is usually obtained from the distal port of an unwedged pulmonary artery catheter. Many physicians use the trend from a venous PO2 obtained from the superior vena cava as a surrogate number. If tissue oxygen consumption is unchanged, then changes in Pvo2 will reflect direct changes in cardiac output. (345)
49. The Fick equation is used to calculate cardiac output if PaO2, Pvo2, and hemoglobin are known. It basically states that the delivery of oxygen in the veins must equal the delivery of oxygen in the arteries minus the oxygen that is consumed (VO2). (345-346)
50. The arteriovenous difference is the difference between the arterial and mixed venous oxygen content. The number is a good estimate of the adequacy of oxygen delivery. The normal arteriovenous difference is 4 to 6 mL of O2/dL of blood. When tissue oxygen consumption is constant, an increased arteriovenous difference means that there is higher oxygen extraction, which can be seen with decreased cardiac output or congestive heart failure. A lower arteriovenous difference means there is lower extraction or higher cardiac output, which can occur during cyanide poisoning or sepsis. (346)
