1. Acid Base Imbalances

2. Acid-Base Regulation  Body produces significant amounts of carbon dioxide & nonvolatile acids daily  Regulated by: Renal excretion of acid (H+ combines with phosphate or ammonia, which are excreted) Renal excretion of acid (H+ combines with phosphate or ammonia, which are excreted) Respiratory excretion of CO2 Respiratory excretion of CO2 Buffer systems (hemoglobin, phosphate, bicarbonate, proteins) Buffer systems (hemoglobin, phosphate, bicarbonate, proteins)

4. Measurement  Arterial: Normal pH 7.36-7.44; normal HCO3 25; normal pCO2 40 Normal pH 7.36-7.44; normal HCO3 25; normal pCO2 40  Peripheral venous: pH is 0.02-0.04 lower than arterial pH is 0.02-0.04 lower than arterial HCO3 is 1-2 mEq/L higher than arterial HCO3 is 1-2 mEq/L higher than arterial pCO2 is 3-8 mmHg higher, depending on peripheral extraction and use of O2 pCO2 is 3-8 mmHg higher, depending on peripheral extraction and use of O2

5. Respiratory Acidosis

6. Definition  Decreased pH due to pulmonary CO2 retention (hypoventilation causes hypercapnea)  CO2 retention causes increased H2CO3 production – causes acidemia  Serum HCO3 is normal acutely, and increases as compensation occurs

7. Causes  Increase in PaCO2  Anything which causes a decrease in minute ventilation has the potential to cause respiratory acidosis Airway Airway CNS depression CNS depression Pulmonary disease Pulmonary disease Hypoventilation of neuromuscular conditions Hypoventilation of neuromuscular conditions

8. Symptoms  CO2 narcosis: Headache, blurred vision Headache, blurred vision Asterixis, tremors, weakness Asterixis, tremors, weakness Confusion, somnolence Confusion, somnolence  If prolonged: Signs of increased ICP Signs of increased ICP Papilledema Papilledema

9. Compensation  Acutely: intracellular proteins buffer intracellular proteins buffer HCO3 is formed by the intracellular buffers HCO3 is formed by the intracellular buffers Compensation is insignificant Compensation is insignificant  Chronically Renal retention of HCO3 is the primary buffering system Renal retention of HCO3 is the primary buffering system Onset: 6-12 hrs, takes days to complete Onset: 6-12 hrs, takes days to complete

10. Compensation  Acute: HCO3 increases 1 mEq/L for every 10 mmHg rise in PCO2 HCO3 increases 1 mEq/L for every 10 mmHg rise in PCO2 Insignificant effect on pH Insignificant effect on pH  Chronic: HCO3 increases 3.5-5 mEq/L for every 10mmHg rise in PCO2 HCO3 increases 3.5-5 mEq/L for every 10mmHg rise in PCO2 Can almost normalize pH Can almost normalize pH Usually results in hypochloremia Usually results in hypochloremia

11. Management  Must increase minute ventilation  Must also improve ventilation Bronchodilators, postural drainage, antibiotics (i.e. treat underlying cause) Bronchodilators, postural drainage, antibiotics (i.e. treat underlying cause)  Role of hypoxic drive???

12. Respiratory Alkalosis

13. Causes  Increased minute ventilation Leads to low pCO2, high pH Leads to low pCO2, high pH If acute, HCO3 is normal If acute, HCO3 is normal If chronic, HCO3 will drop due to renal comp. If chronic, HCO3 will drop due to renal comp.  Causes: CNS diseases, hypoxemia, anxiety, hypermetabolic states, toxic states, hepatic insufficiency, assisted ventilation CNS diseases, hypoxemia, anxiety, hypermetabolic states, toxic states, hepatic insufficiency, assisted ventilation

14. Symptoms  Mimic hypocalcemia  Depend on degree, acuity & cause  Due to irritability of CNS & PNS, and increased cerebral vascular resistance Paresthesias of lips, extremities; lightheadedness, dizziness, muscle cramps, carpopedal spasms Paresthesias of lips, extremities; lightheadedness, dizziness, muscle cramps, carpopedal spasms

15. Management  Treat underlying cause i.e. remove stimulus i.e. remove stimulus  Treat symptoms E.g. benzos, pain medication, rebreathing mask (allows CO2 retention) E.g. benzos, pain medication, rebreathing mask (allows CO2 retention)

16. Metabolic Alkalosis

17. Definition  Low pH due to increased HCO3 or decreased H+  Requires loss of H+ or retention of HCO3  Must know PCO2… elevation of HCO3 could be due to renal compensation for chronic respiratory acidosis

18. Causes  Increased HCO3 reabsorption due to volume, K+ or Cl- loss  Loss of H+ and Cl- from vomiting and NG suctioning can lead to HCO3 retention  Renal impairment of HCO3 excretion

19. Causes  Hypovolemic Vomiting/suction, diuretics, adenomas Vomiting/suction, diuretics, adenomas  Euvolemic/Hypervolemic Exogenous mineralocorticoids, ectopic ACTH, Cushing’s, severe hypoK, adenoCA Exogenous mineralocorticoids, ectopic ACTH, Cushing’s, severe hypoK, adenoCA  Unclassified Milk-alkali syndrome, IV PCN rx, metabolism of organic acid anions, massive transfusion, nonparathyroid hypercalcemia Milk-alkali syndrome, IV PCN rx, metabolism of organic acid anions, massive transfusion, nonparathyroid hypercalcemia

20. Treatment  Treat underlying causes  Replace losses  May be saline-responsive or saline resistant

21. Metabolic Acidosis

22. Mechanism  Increased production of acids  Decreased renal excretion of acids  Loss of alkali

23. Alcoholic Ketoacidosis  Normal glucose  High ketones  Drinking binge; starvation

24. Lactic Acidosis  2 different forms; l- and d-  Increased production vs. decreased elimination  Systemic Sepsis, hypovolemia, hypoxia Sepsis, hypovolemia, hypoxia  Localized E.g. bowel ischemia, metformin, HIV meds E.g. bowel ischemia, metformin, HIV meds

25. Treatment  Correct underlying cause  Reduce O2 demand  Ensure adequate O2 delivery to tissues  HCO3 Given to improve hemodynamic consequences of acidosis Given to improve hemodynamic consequences of acidosis

26. Summary  Look at pH  Look at pCO2 and HCO3  Look at patient!!  Treat the patient, not the numbers