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Chapter 4

Chapter 4.  Arterial Blood Gas Assessments. Table 4-1. Normal Blood Gas Values. Box 4-1. Acid-Base Disturbance Classifications. This Chapter Provides the Following Review. The PCO 2 /HCO 3 /pH relationship—an essential cornerstone of ABG interpretations

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Chapter 4

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  1. Chapter 4  Arterial Blood Gas Assessments

  2. Table 4-1. Normal Blood Gas Values

  3. Box 4-1. Acid-Base Disturbance Classifications

  4. This Chapter Provides the Following Review • The PCO2/HCO3/pH relationship—an essential cornerstone of ABG interpretations • The six most common acid-base abnormalities seen in the clinical setting • The metabolic acid-base abnormalities • The hazards of oxygen therapy in the patient with chronic ventilatory failure with hypoxemia

  5. Figure 4-1. Nomogram of the PCO2/HCO3/pH relationship. -

  6. Figure 4-2. Acute ventilatory failure is confirmed when the reported PCO2, pH, and HCO3 values all intersect within the red-colored respiratory acidosis bar. For example, when the PCO2 is 60 mm Hg at a time when the pH is 7.28 and the HCO3 is 26 mEq/L, acute ventilatory failure is confirmed. -

  7. Figure 4-3. Acute alveolar hyperventilation is confirmed when the reported PCO2, pH, and HCO3 values all intersect within the red-colored respiratory alkalosis bar. For example, when the reported PCO2 is 25 mm Hg at a time when the pH is 7.55 and the HCO3 is 21 mEq/L, acute alveolar hyperventilation is confirmed.

  8. A Quick Clinical Calculation for Acute PaCO2 Changes in pH and HCO3

  9. Acute Increases in PaCO2(e.g., Acute Hypoventilation)

  10. Using the Normal ABG Values as a Baseline—pH 7.40, PaCO2 40, and HCO3 24: • For every 10 mm Hg the PaCO2 increases, the pH will decrease about 0.06 units and the HCO3 will increase about 1 mEq/L. • Or, for every 20 mm Hg the PaCO2 increases, the pH will decrease about 0.12 units and the HCO3 will increase about 2 mEq/L.

  11. Using the Normal ABG Values as a Baseline—pH 7.40, PaCO2 40, and HCO3 24 (Cont’d) • Thus if the patient’s PaCO2 suddenly were to increase to, say, 60 mm Hg, the expected pH change would be about 7.28 and the HCO3 would be about 26 mEq/L.

  12. Using the Normal ABG Values as a Baseline—pH 7.40, PaCO2 40, and HCO3 24 (Cont’d) • It should be noted, however, that if the patient’s PaO2 is severely low, lactic acid may also be present. • This results in a combined metabolic and respiratory acidosis. • In such cases the patient’s expected pH and HCO3 values would both be lower than expected for a particular PaCO2 level.

  13. Acute Decreases in PaCO2(e.g., Acute Hyperventilation)

  14. Using the Normal ABG Values as a Baseline—pH 7.40, PaCO2 40, and HCO3 24 • For every 5 mm Hg the PaCO2 decreases, the pH will increase about 0.06 units and the HCO3 will decrease about 1 mEq/L. • Or, for every 10 mm Hg the PaCO2 decreases, the pH will increase about 0.12 units and the HCO3 will decrease about 2 mEq/L.

  15. Using the Normal ABG Values as a Baseline—pH 7.40, PaCO2 40, and HCO3 24 (Cont’d) • Thus if the patient’s PaCO2 suddenly were to decrease to, say, 30 mm Hg, the expected pH change would be about 7.52 and the HCO3 would be about 22 mEq/L.

  16. Using the Normal ABG Values as a Baseline—pH 7.40, PaCO2 40, and HCO3 24 (Cont’d) • Again, it should be noted, however, that if the patient’s PaO2 is severely low, lactic acid may also be present. • In such cases the patient’s expected pH and HCO3 values would both be lower than expected for a particular PaCO2 level.

  17. Table 4-2. General Rule of Thumb for the Paco2/ HCO−3/pH Relationship

  18. The Six Most Common Acid-Base Abnormalities Seen in the Clinical Setting • Acute alveolar hyperventilation • Acute ventilatory failure • Chronic ventilatory failure with hypoxemia • Acute alveolar hyperventilation superimposed on chronic ventilatory failure • Acute ventilatory failure superimposed on chronic ventilatory failure

  19. Acute Alveolar Hyperventilation with Hypoxemia(Acute Respiratory Alkalosis) • pH: increased 7.55 • PaCO2: decreased 29 mm Hg • HCO3: decreased 22 mEq/L • PaO2: decreased 61 mm Hg* ABG Changes Example *When pulmonary pathology is present

  20. The most common cause of acute alveolar hyperventilation is:Hypoxemia

  21. Figure 4-4. Relationship of venous admixture to the stimulation of peripheral chemoreceptors in response to alveolar consolidation.

  22. Figure 4-5. The PaO2 and PaCO2 trends during acute alveolar hyperventilation.

  23. Box 4-2. Pathophysiologic Mechanisms That Lead to a Reduction in the Paco2

  24. Acute Ventilatory Failure with Hypoxemia(Acute Respiratory Acidosis) • pH: decreased 7.21 • PaCO2: increased 79 mm Hg • HCO3: increased (slightly) 28 mEq/L • PaO2: decreased 57 mm Hg ABG Changes Example

  25. Chronic Ventilatory Failure with Hypoxemia(Compensated Respiratory Acidosis) pH: normal 7.38 PaCO2: increased 66 mm Hg HCO3: increased (significantly) 35 mEq/L PaO2: decreased 63 mm Hg ABG Changes Example

  26. Box 4-3. Respiratory Diseases Associated with Chronic Ventilatory Failure during the Advanced Stages

  27. Figure 4-6. The PaO2 and PaCO2 trends during acute or chronic ventilatory failure.

  28. Acute Ventilatory Changes Superimposed on Chronic Ventilatory Failurez • Acute alveolar hyperventilation superimposed on chronic ventilatory failure • Acute ventilatory failure superimposed on chronic ventilatory failure

  29. Acute Alveolar Hyperventilation Superimposed on Chronic Ventilatory Failure(Acute Hyperventilation on Compensated Respiratory Acidosis) pH: increased 7.53 PaCO2: increased 51 mm Hg HCO3: increased 37 mEq/L PaO2: decreased 46 mm Hg ABG Changes Example

  30. Table 4-3. Examples of Acute Changes in Chronic Ventilatory Failure

  31. Acute Ventilatory FailureSuperimposed on Chronic Ventilatory Failure(Acute Hypoventilation on Compensated Respiratory Acidosis) pH: decreased 7.21 PaCO2: increased 110 mm Hg HCO3: increased 43 mEq/L PaO2: decreased 34 mm Hg ABG Changes Example

  32. Table 4-3. Examples of Acute Changes in Chronic Ventilatory Failure

  33. Lactic AcidosisMetabolic Acidosis • Because acute hypoxemia is commonly associated with respiratory disorders, acute metabolic acidosis (caused by lactic acid) often further compromises respiratory acid-base status.

  34. Lactic AcidosisMetabolic Acidosis (Cont’d) pH: decreased 7.21 PaCO2: normal or decreased 35 mm Hg HCO3: decreased 19 mEq/L PaO2: decreased 34 mm Hg ABG Changes Example

  35. Figure 4-1. Nomogram of the PCO2/HCO3/pH relationship.

  36. Metabolic Acid-Base Abnormalities

  37. Metabolic Acidosis pH: decreased 7.26 PaCO2: normal 37 mm Hg HCO3: decreased 18 mEq/L PaO2: normal 94 mm Hg (or decreased if lactic (or 52 mm Hg if acidosis is present) lactic acidosis is present) ABG Changes Example

  38. . Anion Gap • The anion gapis used to determine if a patient’s metabolic acidosis is caused by either: • the accumulation of fixed acids (e.g., lactic acids, keto acids, or salicylate intoxication), or • an excessive loss of HCO3

  39. Anion Gap (Cont’d) • The law of electroneutrality states that the total number of plasma positively charged ions (cations) must equal the total number of plasma negatively charged ions (anions) in the body fluids. • To calculate the anion gap, the most commonly measured cations are sodium (Na+) ions.

  40. Anion Gap (Cont’d) • The most commonly measured anions are chloride (Cl−) ions and bicarbonate (HCO3) ions. • The normal plasma concentrations of these cations and anions are as follows: Na+: 140 mEq/L Cl−: 105 mEq/L HCO3: 24 mEq/L

  41. Anion Gap (Cont’d) • Mathematically, the anion gap is the calculated difference between the Na+ ions and the sum of the HCO3 and Cl− ions: Anion gap = [Na+] − ([Cl−] + [HCO3]) = 140 − 105 + 24 = 140 − 129 = 11 mEq/L

  42. Anion Gap (Cont’d) • The normal range for the anion gap is 9 to 14 mEq/L. • An anion gap greater than 14 mEq/L represents metabolic acidosis.

  43. Anion Gap (Cont’d) • An elevated anion gap is frequently caused by the accumulation of fixed acids—for example: • Lactic acids • Keto acids • Salicylate intoxication

  44. Anion Gap (Cont’d) • This is because the H+ ions that are generated by the fixed acids chemically react with—and are buffered by—the plasma HCO3 • This action causes • The HCO3 concentration to decrease and • The anion gap to increase

  45. Anion Gap (Cont’d) • Clinically, when the patient exhibits both metabolic acidosis and an increased anion gap, the respiratory care practitioner must investigate further to determine the source of the fixed acids. • This needs to be done in order to appropriately treat the patient.

  46. Anion Gap (Cont’d) • For example, metabolic acidosis caused by: • Lactic acids justifies the need for oxygen therapy—to reverse the accumulation of the lactic acids, or • Ketone acids justifies the need for insulin—to reverse the accumulation of the ketone acids.

  47. Anion Gap (Cont’d) • It is interesting that metabolic acidosis caused by an excessive loss of HCO3does not cause the anion gap to increase. • For example, in renal disease or severe diarrhea

  48. Anion Gap (Cont’d) • This is because as the HCO3 concentration decreases, the Cl− concentration usually increases to maintain electroneutrality. • In short, for each HCO3 ion that is lost, a Cl− anion takes its place • Law of electroneutrality

  49. Anion Gap (Cont’d) • This action maintains a normal anion gap. • Metabolic acidosis caused by a decreased HCO3level is commonly called hyperchloremic metabolic acidosis.

  50. Summary • When metabolic acidosis is accompanied by an increased anion gap, the most likely cause of the acidosis is fixed acids. • Lactic acids • Keto acids • Salicylate intoxication

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