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metabolic alkalosis

Etiology: 1) chloride-responsive (urine Cl- < 10-15 meq/L) a) contraction alkalosis (volume depletion) most common [5] a) vomiting/NG suction: upper GI loss of HCl b) thiazide & loop diuretics: renal loss of HCl c) cirrhosis or heart failure may cause hypervolemia with hypotension due to low effective arterial volume [2] b) cystic fibrosis c) villous adenoma d) congenital chloridorrhea e) nephrotic syndrome 2) chloride-resistant (urine Cl- > 15-20 meq/L) [much less common] a) hypertensive - primary hyperaldosteronism - Cushing's syndrome - renal artery stenosis - glucocorticoid/mineralocorticoid therapy - renin-secreting tumor - inhibitors of 11-beta hydroxysteroid dehydrogenase - licorice ingestion - tobacco chewing - Liddle's syndrome - diuretics & K+ depletion - hypercalcemia - hypoparathyroidism b) normotensive or hypotensive - Bartter's syndrome - Gitelman's syndrome - gentamicin [2] 3) pCO2 higher than expected a) COPD & diuretics b) ARDS & diuretics 4) pCO2 lower than expected a) CHF & diuretics b) cirrhosis & diuretics c) hyperemesis Clinical manifestations: 1) respiratory compensation with hypoventilation 2) weakness 3) muscle cramps 4) hyperreflexia 5) dysrhythmias 6) hypertension suggests chloride-resistance (see etiology) 7) hypotension more common 8) hypervolemia may occur with hypotension (cirrhosis, heart failure) or hypertension (hyperaldosteronism, renin-secreting tumor) Laboratory: 1) arterial blood gas a) increased pH (pH > 7.44) b) increased pCO2 2) electrolytes a) serum bicarbonate: increased HCO3- b) serum K+: hypokalemia c) serum chloride: hypocloremia 3) serum aldosterone: may be increased 4) urine chloride a) < 25 meq/L (chloride-responsive) [5] b) > 40 meq/L (chloride-resistant) [5] c) diuretic use may initially cause a rise in urine chloride followed by a decline to < 25 meq/L [5] * Predicted pCO2 (respiratory) compensation for pure metabolic alkalosis (PaCO2, arterial) 1) pCO2 (mm Hg) +/- 5 = 0.9 x HCO3- (meq/L) + 15 2) pCO2 increases 0.7 mm Hg for each 1 meq/L rise in [HCO3-] 3) response is limited by hypoxemia [2] Management: 1) correct underlying disorder a) remove renin-secreting tumor b) remove aldosterone-secreting tumor c) discontinue offending agents d) correct hypovolemia 2) chloride-responsive (saline-responsive) alkalosis a) normal saline to correct hypovolemia b) NaCl tablets c) treat hypokalemia with KCl d) acetazolamide 250-500 mg PO or IV every 8 hours - CHF with edema present - cor pulmonale - hepatic cirrhosis - post-hypercapnic state e) reduction of gastric HCl loss - proton-pump inhibitor - lansoprazole - omeprazole - H2-receptor antagonist - ranitidine - cimetidine 3) chloride-resistant alkalosis a) discontinue offending agents - thiazides - loop diuretics b) correct Mg+2 deficiency c) correct K+ deficits d) amiloride, triamterene or spironolactone 4) treatment of severe metabolic alkalosis (pH > 7.55) a) particularly if contraindication to NaCl administration - heart failure - renal failure b) HCl solution - 150 mL of 1.0 N HCL in 1 L H2O (H+ 130 meq/L) - administer through central line @< 0.2 meq/kg/hr - do not infuse directly into the right atrium - H+ deficit: - 0.5 x LBM* (measured - desired) [HCO3-] - replace 1/2 the deficit in the 1st 12 hours, & the remainder in the following 24 hours c) hemodialysis * LBM: lean body mass in kg.

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alkalosis

References

  1. Manual of Medical Therapeutics, 28th ed, Ewald & McKenzie (eds), Little, Brown & Co, Boston, 1995, pg 62-63
  2. Medical Knowledge Self Assessment Program (MKSAP) 14, 15, 16, 17, 18, 19. American College of Physicians, Philadelphia 2006, 2009, 2012, 2015, 2018, 2021. - Medical Knowledge Self Assessment Program (MKSAP) 19 Board Basics. An Enhancement to MKSAP19. American College of Physicians, Philadelphia 2022
  3. Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000 Feb;11(2):369-75. PMID: 10665945
  4. Shin HS. Value of the measurement of urinary chloride in hypokalaemic metabolic alkalosis. PMID: 20377781
  5. Zietse R, Zoutendijk R, Hoorn EJ. Fluid, electrolyte and acid-base disorders associated with antibiotic therapy. Nat Rev Nephrol. 2009 Apr;5(4):193-202. PMID: 19322184
  6. Berend K et al Physiological Approach to Assessment of Acid-Base Disturbances. N Engl J Med 2014; 371:1434-1445. October 9, 2014 PMID: 25295502 http://www.nejm.org/doi/full/10.1056/NEJMra1003327
  7. Gennari FJ. Pathophysiology of metabolic alkalosis: a new classification based on the centrality of stimulated collecting duct ion transport. Am J Kidney Dis. 2011 Oct;58(4):626-36. Review. PMID: 21849227
  8. Soifer JT, Kim HT. Approach to metabolic alkalosis. Emerg Med Clin North Am. 2014 May;32(2):453-63. Review. PMID: 24766943