This document provides an overview of acid-base disorders and hydrogen ion homeostasis in the body. It discusses normal hydrogen ion concentrations in extracellular fluid, lysosomes, urine and gastric acid. Buffering systems that help regulate hydrogen ion levels like the bicarbonate buffering system are also examined. Various acid-base disorders like metabolic acidosis, respiratory acidosis, and their causes and compensatory mechanisms are summarized as well.

1. Hydrogen Ion (An overview of acid base) John O’Connor RDE SSU BMS DEC 2007

2. Acid Base Disorders Hydrogen ion ( H + ) homeostasis Essential for life: e.g. mitochondrial function charge & shape of proteins ionisation of Ca ++ , Mg ++

4. Hydrogen ion units H + conc . as nanomoles per litre (nmol/L) H + as pH pH = 1/ log 10 H+ in mol/L e.g. 100 nmol/L = 1/ log 10 100 x 10 -9 pH = 1/log 10 -7 pH = 7

5. Carbon dioxide the major source of acid in the body CO 2 + H 2 O H 2 CO 3 H 2 CO 3 H + + HCO 3 -

10. Other buffers: haemoglobin CO 2 Cl - Cl - CO 2 + H 2 O H 2 CO 3 H + + HCO - 3 HCO - 3 Hb - HbH CO 2 from tissue respiration Carbonate dehydratase erythrocyte

11. Other buffers: haemoglobin CO 2 Cl - Cl - CO 2 + H 2 O H 2 CO 3 H + + HCO - 3 HCO - 3 Hb - HbH CO 2 loss in alveoli Carbonate dehydratase erythrocyte

13. Reabsorption of filtered bicarbonate Glomerulus Tubule Proximal tubular cell Na + HCO 3 - H + + HCO 3 - HCO 3 - + H + H 2 CO 3 H 2 CO 3 CO 2 + H 2 O Na + Na + Na + HCO 3 - CO 2 + H 2 O

14. Renal hydrogen ion excretion Glomerulus Tubule Tubular cell Na + HPO 4 2- H + + HPO 4 2- HCO 3 - + H + H 2 PO 4 H 2 CO 3 CO 2 + H 2 O Na + Na + Na + HCO 3 - Dihydrogen phosphate in urine

15. Renal ammonium excretion

23. PaCO 2 Relationship between arterial H + and partial pressure of CO 2 Metabolic acidosis Metabolic alkalosis

24. Case 1 Elderly man admitted with confusion SOB, cough + sputum Known to A&E staff as type I diabetic Hydrogen ion 66 nmo./L (pH 7.18) pCO 2 7.4 kPa (55.5 mmHg)

25. PaCO 2 Relationship between arterial H + and partial pressure of CO 2 Metabolic acidosis Metabolic alkalosis

26. Case 1 Elderly man admitted with confusion SOB, cough + sputum Known to A&E staff as type I diabetic Hydrogen ion 66 nmo./L (pH 7.18) pCO 2 7.4 kPa (55.5 mmHg) Acidotic with a respiratory component But does pCO 2 explain severity of acidosis ? Why has he not compensated for high pCO 2 ? This suggests there is a non-respiratory component

28. Case 2 Young woman admitted post head injury # skull & cerebral contusions respiratory rate 38/min 3 days later blood gases were: Hydrogen ion 36 nmol/L (pH 7.44) pCO 2 3.9 kPa (29.3 mmHg) Derived bicarbonate 19 mmol/L Normal values: H + 35-46 nmol/L (pH 7.35 - 7.45) pCO 2 4.5 - 5.7 kpa pO 2 10 - 12 kpa HCO 3 - 20-24 mmol/L

29. PaCO 2 Relationship between arterial H + and partial pressure of CO 2 Metabolic acidosis Metabolic alkalosis

30. Case 2 Young woman admitted post head injury # skull & cerebral contusions respiratory rate 38/min 3 days later blood gases were: Hydrogen ion 36 nmol/L (pH 7.44) pCO 2 3.9 kPa (29.3 mmHg) Derived bicarbonate 19 mmol/L Compensated respiratory alkalosis pCO 2 is reduced due do hyperventilation secondary to the head injury

32. Case 3 60y man admitted with severe abdo pain started 2.5 hrs earlier Clinically shocked, distended abdomen, no femoral pulses. Hydrogen ion 90 nmol/L (pH 7.05) pCO 2 3.5 kPa (26.3 mmHg) pO 2 12 kPa (90 mmHg) Derived bicarbonate 7 mmol/L

33. PaCO 2 Relationship between arterial H + and partial pressure of CO 2 Metabolic acidosis Metabolic alkalosis

36. Case 4 A young woman, 8 hrs post asprin OD Hydrogen ion 30 nmol/L (pH 7.53) pCO 2 2.0 kPa (15.0 mmHg)

37. PaCO 2 Relationship between arterial H + and partial pressure of CO 2 Metabolic acidosis Metabolic alkalosis

38. Case 4 A young woman, 8 hrs post asprin OD Hydrogen ion 30 nmol/L (pH 7.53) pCO 2 2.0 kPa (15.0 mmHg) Patient is alkalotic pCO 2 very low, yet hydrogen ion only mildly reduced ? Compensated respiratory alkalosis But salicylate OD causes: 1. Hyperventialtion - respiratory alkalosis 2. Metabolic poisoning - non-respiratory acidosis

46. Inhibits hepatic gluconeogenesis and elevates the ratio of hydroxybutyric acid to acetoacetic acid. Acetic acid is converted by coenzyme A to acetyl-coenzyme A, which, in turn, is used for lipolysis, in the formation of ketone bodies, and in the citric acid cycle . Low insulin levels and increased glucagon, catecholamine, growth hormone, and cortisol levels inhibit the hepatic metabolism of acetyl-coenzyme A by the citric acid cycle and triglyceride synthesis, thereby further enhancing ketogenesis. .