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Eric Niederhoffer, Ph.D. SIU-SOM

Biochemical basis of acidosis and alkalosis: e valuating acid base disorders. Eric Niederhoffer, Ph.D. SIU-SOM. Approach h istory physical examination d ifferentials clinical and laboratory studies compensation Respiratory a cidosis a lkalosis Metabolic acidosis alkalosis

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Eric Niederhoffer, Ph.D. SIU-SOM

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  1. Biochemical basis of acidosis and alkalosis: evaluating acid base disorders Eric Niederhoffer, Ph.D. SIU-SOM

  2. Approach history physical examination differentials clinical and laboratory studies compensation Respiratory acidosis alkalosis Metabolic acidosis alkalosis Special cases pregnancy children Outline

  3. Approach • History - subjective information concerning events, environment, trauma, medications, poisons, toxins • Physical examination - objective information assessing organ system status and function • Differentials - potential reasons for presentation • Clinical and laboratory studies - degree of changes from normal • Compensation - assessment of response to initial problem

  4. Reference ranges and points ParameterReference rangeReference point pH7.35-7.45 7.40 PCO2 33-44 mm Hg 40 mm Hg PO2 75-105 mm Hg HCO3- 22-28 mEq/L 24mEq/L Anion gap 8-16 mEq/L 12 mEq/L Osmolar gap <10 mOsm/L

  5. Delta ratio 𝛥 ratio = 𝛥Anion gap/𝛥[HCO3-] = (AG – 12)/(24 - [HCO3-])

  6. Compensation

  7. Respiratory acidosis • PCO2 greater than expected • Acute or chronic • Causes • excess CO2 in inspired air • (rebreathing of CO2-containing expired air, addition of CO2 to inspired air, insufflation of CO2 into body cavity) • decreased alveolar ventilation • (central respiratory depression & other CNS problems, nerve or muscle disorders, lung or chest wall defects, airway disorders, external factors) • increased production of CO2 • (hypercatabolic disorders)

  8. Racid acute A 65-year-old man with a history of emphysema comes to the physician with a 3-hour history of shortness of breath. pH 7.18 PO261 mm Hg PCO258 mm Hg HCO3-26 mEq/L History suggests hypoventilation, supported by increased PCO2 and lower than anticipated PO2. Respiratory acidosis (acute) due to no renal compensation.

  9. Description pH 7.18 PO2 61 mm Hg PCO2 58 mm Hg HCO3- 26 mEq/L 1-2 mEq/L increase in HCO3- for every 10 mm Hg increase in PCO2. PCO2 increase = 58-40 = 18 mm Hg. HCO3- increase predicted = (1-2) x (18/10) = 2-4 mEq/L add to 24 mEq/L (reference point) = 26-28 mEq/L

  10. Racid chronic A 56-year-old woman with COPD is brought to the physician with a 3-hour history of severe epigastric pain. pH 7.39 PO262 mm Hg PCO252 mm Hg HCO3-29 mEq/L History suggests hypoventilation, supported by increased PCO2. Respiratory acidosis (chronic) with renal compensation.

  11. Description pH 7.39 PO262 mm Hg PCO252 mm Hg HCO3-29 mEq/L 3-4mEq/L increase in HCO3- for every 10 mm Hg increase in PCO2. PCO2 increase = 52-40 = 12 mm Hg. HCO3- increase predicted = (3-4) x (12/10) = 4-5 mEq/L add to 24 mEq/L (reference point) = 28-29 mEq/L

  12. Respiratory alkalosis • PCO2 less than expected • Acute or chronic • Causes • increased alveolar ventilation • (central causes, direct action via respiratory center; hypoxaemia, act via peripheral chemoreceptors; pulmonary causes, act via intrapulmonary receptors; iatrogenic, act directly on ventilation)

  13. Ralk acute A 17-year-old woman is brought to the physician with a 3-hour history of epigastric pain and nausea. She admits taking a large dose of aspirin. Her respirations are full and rapid. pH 7.57 PO2104 mm Hg PCO225 mm Hg HCO3-23 mEq/L History suggests hyperventilation, supported by decreased PCO2. Respiratory alkalosis (acute) due to no renal compensation.

  14. Description pH 7.57 PO2 104 mm Hg PCO2 25 mm Hg HCO3- 23 mEq/L 1-2 mEq/L decrease in HCO3- for every 10 mm Hg decrease in PCO2. PCO2 decrease = 40-25 = 15 mm Hg. HCO3- decrease predicted = (1-2) x (15/10) = 2-3 mEq/L subtract from 24 mEq/L (reference point) = 21-22 mEq/L

  15. Ralk chronic A 81-year-old woman with a history of anxiety is brought to the physician with a 2-hour history of shortness of breath. She has been living at 9,000 ft elevation for the past 1 month. Her respirations are full at 20/min. pH 7.44 PO2 69 mm Hg PCO2 24 mm Hg HCO3-16 mEq/L History suggests hyperventilation, supported by decreased PCO2. Respiratory alkalosis (chronic) with renal compensation.

  16. Description pH 7.44 PO2 69 mm Hg PCO2 24 mm Hg HCO3-16 mEq/L 4-5mEq/L decrease in HCO3- for every 10 mm Hg decrease in PCO2. PCO2 decrease = 40-24 = 16 mm Hg. HCO3- decrease predicted = (4-5) x (16/10) = 6-8mEq/L subtract from 24 mEq/L (reference point) = 16-18 mEq/L

  17. Metabolic acidosis • Plasma HCO3- less than expected • Gain of strong acid or loss of base • Alternatively, high anion gap or normal anion gap metabolic acidosis • Causes • high anion-gap acidosis (normochloremic) • (ketoacidosis, lactic acidosis, renal failure, toxins) • normal anion-gap acidosis (hyperchloremic) • (renal, gastrointestinal tract, other)

  18. Macid high AG A 20-year-old man with a history of diabetes is brought to the emergency department with a 3-day history of feeling ill. He is non-adherent with his insulin. Urine ketones are 2+ and glucose is 4+. pH 7.26 Na+ 136 mEq/L PO2110 mm Hg K+ 4.8 mEq/L PCO219 mm Hg Cl- 101 mEq/L HCO3- 8mEq/L CO2, total 10 mEq/L Glucose 343 mg/dL Urea 49 mg/dL Creatinine1 mg/dL History suggests diabetic ketoacidosis. Metabolic acidosis with appropriate respiratory compensation.

  19. Description pH7.26 Na+ 136 mEq/L PO2110 mm Hg K+ 4.8 mEq/L PCO219 mm Hg Cl- 101 mEq/L HCO3- 8mEq/L Glucose 343 mg/dL Urea 49 mg/dL AG = 136-101-8=27 mEq/LCreatinine 1 mg/dL 1.2 mm Hg decrease in PCO2 for every 1 mEq/L decrease in HCO3-. HCO3-decrease = 24-8 = 16 mEq/L PCO2 decrease predicted = 1.2 x 16 = 19 mm Hg. subtract from 40 mm Hg (reference point) = 21 mm Hg

  20. Macid normal AG A 43-year-old man comes to the physician with a 3-day history of diarrhea. He has decreased skin turgor. pH 7.31 Na+134 mEq/L PO2-- mm Hg K+2.9 mEq/L PCO231 mm Hg Cl-113 mEq/L HCO3-16 mEq/L Urea74 mgl/dL Creatinine3.4 mmol/L History is limited. Metabolic acidosis with respiratory compensation.

  21. Description pH 7.31 Na+ 134 mEq/L PO2 -- mm Hg K+ 2.9 mEq/L PCO231 mm Hg Cl- 113 mEq/L HCO3-16 mEq/L Urea 74 mg/dL Creatinine3.4 mg/dL AG = 134-113-16=5 mEq/L 1.2 mm Hg decrease in PCO2 for every 1 mEq/L decrease in HCO3-. HCO3-decrease = 24-16 = 8mEq/L PCO2 decrease predicted = 1.2 x 8 = 10 mm Hg. subtract from 40 mm Hg (reference point) = 30 mm Hg

  22. Metabolic alkalosis • Plasma HCO3- greater than expected • Loss of strong acid or gain of base • Causes (2 ways to organize) • loss of H+ from ECF via kidneys (diuretics) or gut (vomiting) • gain of alkali in ECF from exogenous source (IV NaHCO3 infusion) or endogenous source (metabolism of ketoanions) • or • addition of base to ECF (milk-alkali syndrome) • Cl- depletion (loss of acid gastric juice) • K+ depletion (primary/secondary hyperaldosteronism) • Other disorders (laxative abuse, severe hypoalbuminaemia)

  23. Urinary Chloride • Spot urine Cl- less than 10 mEq/L • often associated with volume depletion • respond to saline infusion • common causes - previous thiazide diuretic therapy, vomiting (90% of cases) • Spot urine Cl-greater than 20 mEq/L • often associated with volume expansion and hypokalemia • resistant to therapy with saline infusion • causes: excess aldosterone, severe K+deficiency, current diuretic therapy, Bartter syndrome

  24. Malkhigh Urine Cl- An 83-year-old woman is brought to the physician with a 1-week history of weakness and poor appetite. pH 7.58 Na+145 mEq/L PO260 mm Hg K+ 1.9 mEq/L PCO256 mm Hg Cl-86 mEq/L HCO3-52 mEq/L Urine Cl-74 mEq/L History is limited. Metabolic alkalosis with respiratory compensation. The cause is unknown, most likely excess adrenocortical activity, current diuretic therapy, or idiopathic.

  25. Description pH 7.58 Na+ 145 mEq/L PO2 60 mm Hg K+ 1.9 mEq/L PCO256 mm Hg Cl- 86 mEq/L HCO3-52 mEq/L Urine Cl- 74 mEq/L 0.6-0.75 mm Hg increase in PCO2 for every 1 mEq/L increase in HCO3-. HCO3-increase = 52-24 = 28 mEq/L PCO2 increase predicted = 0.6-0.75 x 28 = 17-21 mm Hg. add to 40 mm Hg (reference point) = 57-61 mm Hg

  26. Malklow Urine Cl- An 24-year-old woman is brought to the physician with a 3-month history of weakness and fatigue. Blood pressure is 90/60 mm Hg. pH 7.52 Na+137 mEq/L PO278 mm Hg K+2.6 mEq/L PCO249 mm Hg Cl-90 mEq/L HCO3-39 mEq/L Urine Cl- 5mEq/L History and physical examination suggests bulimia. Metabolic alkalosis with respiratory compensation. The cause is most likely bulimia.

  27. Description pH 7.52 Na+137 mEq/L PO278 mm Hg K+2.6 mEq/L PCO249 mm Hg Cl-90 mEq/L HCO3-39 mEq/L Urine Cl- 5mEq/L 0.6-0.75 mm Hg increase in PCO2 for every 1 mEq/L increase in HCO3-. HCO3-increase = 39-24 = 15 mEq/L PCO2 increase predicted = 0.6-0.75 x 15 = 9-12 mm Hg. add to 40 mm Hg (reference point) = 49-52 mm Hg

  28. Special Cases • Pregnancy – hyperventilation (respiratory alkalosis), hyperemesis (metabolic alkalosis or acidosis), maternal ketosis (metabolic acidosis) • Children – low bicarbonate reserve (N=12-16 mEq/L), low acid excretion reserve, inborn errors in metabolism, diabetes, and poisoning (all metabolic acidosis)

  29. Review Questions • What is an effective approach to acid base problems? • What are the normal ranges and reference points? • What are the anion and osmolar gap? • What is compensation? • What are the characteristics of respiratory acidosis and alkalosis? • What are the characteristics of metabolic acidosis and alkalosis? • What is the utility of spot urine Cl-? • What kinds of acid base conditions present during pregnancy and infancy?

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