Chapter 13 Acid-Base Balance

1. Chapter 13Acid-Base Balance

2. Learning Objectives Describe how the lungs and kidneys regulate volatile and fixed acids. Describe how an acid’s equilibrium constant is related to its ionization and strength. State what constitutes open and closed buffer systems. Explain why open and closed buffer systems differ in their ability to buffer fixed and volatile acids. Explain how to use the Henderson-Hasselbalch equation in hypothetical clinical situations.

3. Learning Objectives (cont.) Describe how the kidneys and lungs compensate for each other when the function of one is abnormal. Explain how renal absorption and excretion of electrolytes affect acid-base balance. Classify and interpret arterial blood acid-base results. Explain how to use arterial acid-base information to decide on a clinical course of action.

4. Learning Objectives (cont.) Explain why acute changes in the blood’s carbon dioxide level affect the blood’s bicarbonate ion concentration. Calculate the anion gap and use it to determine the cause of metabolic acidosis. Describe how standard bicarbonate and base excess measurements are used to identify the nonrespiratory component of acid-base imbalances. State how Stewart’s strong ion difference approach to acid-base regulation differs from the Henderson-Hasselbalch approach.

5. Hydrogen Ion Regulation in Body Fluids • Acid-base balance is what keeps [H+] in normal range • For best results, keeps pH 7.35–7.45 • Tissue metabolism produces massive amounts of CO2, which is hydrolyzed into volatile acid H2CO3 CO2 + H2O → H2CO3 → H+ + HCO3– • Rx is catalyzed in RBCs by carbonic anhydrase • Lungs eliminate CO2; falling CO2 reverses Rx

6. Hydrogen Ion Regulation in Body Fluids (cont.) Ventilation ↑ CO2 + H2O ← H2CO3 ← HCO3–+H+ ↑ HHb → H+ + HCO3–

7. Hydrogen Ion Regulation in Body Fluids (cont.) Buffer solution characteristics A solution that resists changes in pH when an acid or a base is added Composed of a weak acid and its conjugate base (i.e., carbonic acid/bicarbonate: in blood exists in reversible combination as NaHCO3 and H2CO3 Add strong acid HCl + NaHCO3→ NaCl + H2CO3; buffered with only small acidic pH change Add base NaOH + H2CO3 → NaHCO3 + H2O; buffered with only slight alkaline pH change

8. The body must maintain the pH of fluids within a narrow range of: 7.25-7.35 7.30-7.40 7.35-7.45 7.40-7.50

9. Hydrogen Ion Regulation in Body Fluids (cont.) Bicarbonate & nonbicarbonate buffer systems Bicarbonate: composed of HCO3– and H2CO3 Open system as H2CO3 is hydrolyzed to CO2 Ventilation continuously removes CO2 preventing equilibration driving reaction to right HCO3– + H+→ H2CO3 → H2O + CO2 Removes vast amounts of acid from body per day

10. Hydrogen Ion Regulation in Body Fluids (cont.) Bicarbonate & nonbicarbonate buffer systems (cont.) Nonbicarbonate: composed of phosphate & proteins Closed system: no gas to remove acid by ventilation Hbuf/buf– represents acid & conjugate base H+ + buf–↔ Hbuf reach equilibrium, buffering stops Both systems: important to buffering fixed & volatile acids

11. Buffer Systems {Insert Figure 13-1}

12. pH of Buffer System:Henderson-Hasselbalch Equation Describes [H+] as ratio of [H2CO3]/[HCO3–] pH = 6.1 + log [HCO3–]/(PaCO2 × 0.03) pH is logarithmic expression of [H+]. 6.1 is the log of the H2CO3 equilibrium constant (PaCO2 × 0.03) is in equilibrium with, & directly proportional to blood [H2CO3] Blood gas analyzers measure pH & PaCO2; then use H-H equation to calculate HCO3–

13. What is the role of proteins in the acid-base regulation process? produces fixed (nonvolatile) acids produces volatile acids isohydric buffering produces carbonic acid

14. Hydrogen Ion Regulation in Body Fluids (cont.) Bicarbonate buffer system HCO3– can continue to buffer fixed acid H+ as long as ventilation is adequate to exhale volatile acid CO2 Ventilation H+ + HCO3–→ H2CO3 → H2O + CO2 Fixed acid HCO3– cannot buffer H2CO3 (volatile) acid In hypoventilation, H2CO3 accumulates; only nonbicarbonate system can serve as buffer

15. Hydrogen Ion Regulation in Body Fluids (cont.) Nonbicarbonate buffer system Hb is most important buffer in this system: it’s most abundant Can buffer any fixed or volatile acid As closed system, products of buffering accumulate & buffering may slow or stop (H+ + Buf-↔ HBuf). HCO3– and buf– exist in same blood system so Ventilation H+ + HCO3–→ H2CO3 → H2O + CO2 Fixed acid → H+ + Buf- ↔ HBuf

16. Which one of the following blood buffers systems is classified as a bicarbonate buffer (open buffer system)? Hemoglobin Erythrocyte Organic phosphates Plasma proteins

17. Acid Excretion Buffers are temporary measure; if acids were not excreted, life-threatening acidosis would follow Lungs Excrete CO2, which is in equilibrium with H2CO3 Crucial: body produces huge amounts of CO2 during aerobic metabolism (CO2 + H2O → H2CO3) In addition, through HCO3– eliminate fixed acids indirectly as byproducts are CO2 & H2O Remove ~24,000 mmol/L CO2 removed daily

18. Acid Excretion (cont.) Kidneys Physically remove H+ from body Excrete <100 mEq fixed acid per day Also control excretion or retention of HCO3– If blood is acidic, then more H+ are excreted & all HCO3– is retained (vice versa ) While lungs can alter [CO2] in seconds, kidneys require hours/days to change HCO3– & affect pH

19. Acid Excretion (cont.) Basic kidney function Renal glomerulus filters the blood by passing water, electrolytes, and nonproteins through semipermeable membrane. Filtrate is modified as it flows through renal tubules HCO3– is filtered through membrane, while CO2 diffuses into tubule cell, where it’s hydrolyzed into H+, which is then secreted into renal tubule H+ secretion increases in the face of acidosis i.e., hypoventilation or ketoacidosis increases secretion

20. Acid Excretion (cont.) Basic kidney function (cont.) Reabsorption of HCO3– For every H+ secreted, an HCO3– is reabsorbed Reacts in filtrate, forming H2CO3 which dissociates into H2O & CO2 CO2 immediately diffuses into cell, is hydrolyzed, & H+ is secreted into filtrate, HCO3– diffuses into blood Thus, HCO3– has effectively been moved from filtrate to blood in exchange for H+ If there is excess HCO3– that does not react with H+, it will be excreted in urine

21. Acid Excretion (cont.)

22. Acid Excretion (cont.)

23. Acid Excretion (cont.) Basic kidney function (cont.) Role of urinary buffers in excretion of excess H+ Once H+ has reacted with all available HCO3–, excess reacts with phosphate & ammonia If all urinary buffers are consumed, further H+ filtration ends when pH falls to 4.5 Activation of ammonia buffer system enhances Cl– loss & HCO3– gain

24. Acid-Base Disturbances • Normal acid-base balance • Kidneys maintain HCO3– of 22-26 mEq/L • Lungs maintain CO2 of 35-45 mm Hg • These produce pH of 35-45 (H-H equation) pH = 6.1 + log (24/(40 × 0.03) → pH = 7.40 • Note pH determined by ratio of HCO3– to dissolved CO2 • Ratio of 20:1 will provide normal pH (7.40) • Increased ratio results in alkalemia • Decreased ratio results in acidemia

25. Acid-Base Disturbances (cont.) Primary respiratory disturbances PaCO2 is controlled by the lung, changes in pH caused by PaCO2 are considered respiratory disturbances Hyperventilation lowers PaCO2, which raises pH; referred to as respiratory alkalosis Hypoventilation (PaCO2) decreases the pH; called respiratory acidosis

26. Acid-Base Disturbances (cont.)

27. Acid-Base Disturbances (cont.)

28. To maintain a normal pH range of 7.35–7.45, the ratio of HCO3– to dissolved CO2 should be: 10:1 15:1 20:1 30:1

29. Acid-Base Disturbances (cont.) Primary metabolic disturbances Involve gain or loss of fixed acids or HCO3– Both appear as changes in HCO3– as changes in fixed acids will alter amount of HCO3– used in buffering

30. Acid-Base Disturbances (cont.) • Primary metabolic disturbances (cont.) • Decrease in HCO3– results in metabolic acidosis • Increase in HCO3– results in metabolic alkalosis • Compensation: Restoring pH to normal • Any primary disturbance immediately triggers compensatory response • Any respiratory disorder will be compensated for by kidneys (process takes hours to days) • Any metabolic disorder will be compensated for by lungs (rapid process, occurs within minutes)

31. Acid-Base Disturbances (cont.) • Compensation: Restoring pH to normal (cont.) • Respiratory acidosis (hypoventilation) • Renal retention HCO3– raises pH toward normal • Respiratory alkalosis • Renal elimination HCO3–lowers pH toward normal • Metabolic acidosis • Hyperventilation ↓CO2, raising pH toward normal • Metabolic alkalosis • Hypoventilation ↑CO2, lowering pH toward normal

32. Acid-Base Disturbances (cont.) The CO2 hydration reaction’s effect on [HCO3–] Large portion of CO2 is transported as HCO3– As CO2 increases, it also increases HCO3– In general, effect is increase of ~1 mEq/L HCO3– for every 10 mm Hg increase in PaCO2 An increase in CO2 of 30 would increase HCO3– by ~3 mEq/L

33. Acid-Base Disturbances (cont.)

34. Clinical Acid-Base States

35. Clinical Acid-Base States (cont.) Respiratory acidosis (alveolar hypoventilation) Any process that raises PaCO2 > 45 mm Hg & lowers pH below 7.35 Increased PaCO2 produces more carbonic acid Causes Anything that results in VA that fails to eliminate CO2 equal to VCO2 . .

36. Clinical Acid-Base States (cont.)

37. Clinical Acid-Base States (cont.) . • Respiratory acidosis (cont.) • Compensation is by renal reabsorption of HCO3– • Partial compensation: pH improved but not normal • Full compensation: pH restored to normal • Correction (goal is to improve VA) • May include: • Improved bronchial hygiene & lung expansion • Non-invasive positive pressure ventilation, endotracheal intubation & mechanical ventilation • If chronic condition with renal compensation, lowering PaCO2 may be detrimental for patient

38. Clinical Acid-Base States (cont.) . . • Respiratory alkalosis (alveolar hyperventilation) • Lowers arterial PaCO2 decreases carbonic acid, thus increasing pH • Causes (see Box 13-4) • Any process that increases VA so that CO2 is eliminated at rate higher than VCO2. • Most common cause is hypoxemia • Anxiety, fever, pain • Clinical signs: early paresthesia; if severe, may have hyperactive reflexes, tetanic convulsions, dizziness

39. Clinical Acid-Base States (cont.) Respiratory alkalosis (cont.) Compensation is by renal excretion of HCO3– Partial compensation returns pH toward normal Full compensation returns pH to high normal range Correction Involves removing stimulus for hyperventilation i.e., hypoxemia: give oxygen therapy

40. Clinical Acid-Base States (cont.) . • Alveolar hyperventilation superimposed on compensated respiratory acidosis (chronic ventilatory failure) • Typical ABG for chronic ventilatory failure: • pH 7.38, PaCO2 58 mm Hg, HCO3– 33 mEq/L • Severe hypoxia stimulates increased VA, lowers PaCO2, potentially raising pH on alkalotic side • i.e. pH 7.44, PaCO2 50 mm Hg, HCO3– 33 mEq/L • Appears to be compensated metabolic acidosis • Only medical history & knowledge of situation allow correct interpretation of this ABG

41. Clinical Acid-Base States (cont.) Metabolic acidosis Low HCO3–, with a low pH Causes: Increased fixed acid accumulation Lactic acidosis in anaerobic metabolism Excessive loss of HCO3– Diarrhea Anion gap can help identify cause

42. Clinical Acid-Base States (cont.) • Increased anion gap metabolic acidosis • Normal anion gap = 9 to 14 mEq/L • As fixed acids increase, they dissociate & H+ binds with HCO3–, leaving unmeasured anion behind • Increasing anion gap • Normal anion gap metabolic acidosis • HCO3– loss does not cause increased gap • As HCO3– is lost, it is offset by gain in Cl– • Also called hyperchloremic acidosis

43. Clinical Acid-Base States (cont.)

44. Clinical Acid-Base States (cont.) . • Compensation for metabolic acidosis • Hyperventilation is main compensatory mechanism • Acidosis activates CNS receptors, signaling need to increase VE • Compensation happens very quickly • Lack of compensation implies ventilatory defect • Symptoms • Patients often complain of dyspnea due to hyperpnea • Kussmaul’s respiration seen with ketoacidosis • Neurologic response may range from lethargy to coma

45. What would the anion gap be for a metabolic acidosis caused by the loss of bicarbonate (HCO3– )? 12-16 mEq/L 3-6 mEq/L 9-14 mEq/L 6-10 mEq/L

46. Clinical Acid-Base States (cont.) Medical intervention to correct metabolic acidosis If pH is >7.2, no correction is required Hyperventilation usually brings it above this level pH below 7.2 can cause serious cardiac arrhythmias In severe acidosis, treat with IV NaHCO3

47. Calculate the anion gap for a patient with the following electrolytes results: 160 mEq/L for Na+, 108 mEq/L or Cl–, and 27 mEq/L for HCO3– . 11 mEq/L 25 mEq/L 8 mEq/L 30 mEq/L

48. Clinical Acid-Base States (cont.) Metabolic alkalosis Increased [HCO3–], with elevated pH Causes: Due to increased buffer baseor loss of fixed acids Loss of fixed acids occurs during vomiting (HCl) Often, it is iatrogenic due to diuretic use or gastric drainage

49. Clinical Acid-Base States (cont.) Metabolic alkalosis Compensation Hypoventilation, despite ensuing hypoxemia Metabolic alkalosis blunts hypoxemic stimulation of ventilation PaO2 as low as 50 mm Hg with continued compensation Correction Restore normal fluid volume, K+, and Cl– levels In severe alkalosis, may give dilute HCl in central line

50. If an anion gap yields a result of 25 mEq/L, what can be done for the patient to bring the anion gap back to normal? treat with intravenous NaHCO2 hypoventilation is required hyperventilation is required restrict fluid intake