1. 25 y.o. male 2 weeks of presyncope and fatigue Supine HR 70bpm, Standing HR 116bpm ABG: pH 7.54, pCO2 47, PO2 92, HCO3 34 A Case

2. Objectives 1.Review pathophysiology of metabolic alkalosis 2.Discuss an approach to metabolic alkalosis 3.Outline treatments for metabolic alkalosis

3. Pathophysiology Two Necessities for Metabolic Alkalosis 1.Initiation Factor – increase HCO3 2.Maintenance Factor -process suppressing normal renal response

4. Pathophysiology What are these processes? 1.Decreased ECV (especially with hypoCl-) H 2 O + CO 2 Blood Tubule Na + H+H+ K+K+ HCO 3 - + H + H 2 CO 3 CO 2 + H 2 O 3HCO 3 - Proximal Convoluted Tubule

5. Pathophysiology 2.Hypokalemia Extracellular K+K+ H+H+ Intracellular

6. Pathophysiology 3.Aldosterone Blood Tubule K+K+ H+H+ Cl - HCO 3 - + H + H 2 CO 3 CO 2 + H 2 O HCO 3 H 2 O + CO 2 H+H+ Intercalated Cell

7. An Approach History: -vomiting, diarrhea, diuretic use, family hx, alkali load? P/E: -volume status (cap. refill, skin turgor, postural hypotension/tachycardia, BP) -syndromic features (Cushingoid) Note: Don’t forget to do a cardiac exam to exclude arrhythmias caused by electrolyte abnormalities.

8. Chloride Sensitive Obtain a spot urine chloride If urine Cl- < 20 mEq/L: GI Losses: -Vomiting/NG -Villous adenoma (secretory diarrhea) Renal Losses: -Remote diuretic use -Post hypercapnea (with associated decreased EABV) -Non-reabsorbable anions (eg: penicillin)

9. Chloride Insensitive If Urine Cl- > 20 mEq/L, obtain serum K+: Normal Serum K+: -Alkali load (citrate, acetate, lactate) -Milk-Alkali Syndrome (CRF from hyperCa with alkali) Decreased Serum K+: Check volume status

10. Chloride Insensitive: Volume status Hypertension -Primary hyperaldosteronism -Malignant hypertension -Renin secreting tumour -Cushing’s Syndrome -Liddle’s Disease (AD ENaC mutation) -Congenital Adrenal Hyperplasia

11. Chloride Insensitive: Volume Status Normotension/Hypotension -Current diuretic use -HypoK+/Mg2+ -Bartter’s Syndrome

12. Come again? Metabolic Alkalosis Urine Cl- <20mEq/LUrine Cl- >20mEq/L GI Loss Vomit/NG Villous Adenoma Renal Loss Remote diuretic use Post hypercapnea Non-reabsorbable anions Normal K+ Alkali load Decreased K+ Hypertension Primary hyperaldo Malignant HTN Renin secreting tumour Cushing’s Syndrome Liddle’s Disease CAH Normo/Hypotension Recent diuretic use HypoK+/Mg2+ Bartter’s Syndrome

13. Treatment Chloride Sensitive: Volume replacement with NaCl solution (except in those with edema) Chloride Insensitive: Correct underlying cause Block aldosterone activity Severe Metabolic Alkalosis (pH >7.6) IV HCl Dialysis

14. QUESTIONS?