metabolic alkalosis
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Etiology
- chloride-responsive (urine Cl- < 10-15 meq/L)
- contraction alkalosis (volume depletion) most common[5]
- vomiting/NG suction: upper GI loss of HCl
- thiazide & loop diuretics: renal loss of HCl
- cirrhosis or heart failure may cause hypervolemia with hypotension due to low effective arterial volume[2]
- cystic fibrosis
- villous adenoma
- congenital chloridorrhea
- nephrotic syndrome
- chloride-resistant (urine Cl- > 15-20 meq/L) [much less common]
- 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
- normotensive or hypotensive
- hypertensive
- pCO2 higher than expected
- pCO2 lower than expected
Clinical manifestations
- respiratory compensation with hypoventilation
- weakness
- muscle cramps
- hyperreflexia
- dysrhythmias
- hypertension suggests chloride-resistance (see etiology)
- hypotension more common
- hypervolemia may occur with hypotension (cirrhosis, heart failure) or hypertension (hyperaldosteronism, renin-secreting tumor)
Laboratory
- arterial blood gas
- electrolytes
- serum bicarbonate: increased HCO3-
- serum K+: hypokalemia
- serum chloride: hypocloremia
- serum aldosterone: may be increased
- urine chloride
* Predicted pCO2 (respiratory) compensation for pure metabolic alkalosis (PaCO2, arterial)
- pCO2 (mm Hg) +/- 5 = 0.9 x HCO3- (meq/L) + 15
- pCO2 increases 0.7 mm Hg for each 1 meq/L rise in [[[A18927|HCO3-]]]
- response is limited by hypoxemia[2]
Management
- correct underlying disorder
- remove renin-secreting tumor
- remove aldosterone-secreting tumor
- discontinue offending agents
- correct hypovolemia
- chloride-responsive (saline-responsive) alkalosis
- normal saline to correct hypovolemia
- NaCl tablets
- treat hypokalemia with KCl
- acetazolamide 250-500 mg PO or IV every 8 hours
- CHF with edema present
- cor pulmonale
- hepatic cirrhosis
- post-hypercapnic state
- reduction of gastric HCl loss
- chloride-resistant alkalosis
- discontinue offending agents
- correct Mg+2 deficiency
- correct K+ deficits
- amiloride, triamterene or spironolactone
- treatment of severe metabolic alkalosis (pH > 7.55)
- particularly if contraindication to NaCl administration
- 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) [[[A18927|HCO3-]]]
- replace 1/2 the deficit in the 1st 12 hours, & the remainder in the following 24 hours
- hemodialysis
* LBM: lean body mass in kg.
More general terms
References
- ↑ Manual of Medical Therapeutics, 28th ed, Ewald & McKenzie (eds), Little, Brown & Co, Boston, 1995, pg 62-63
- ↑ 2.0 2.1 2.2 2.3 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 - ↑ Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000 Feb;11(2):369-75. PMID: https://www.ncbi.nlm.nih.gov/pubmed/10665945
- ↑ Shin HS. Value of the measurement of urinary chloride in hypokalaemic metabolic alkalosis. PMID: https://www.ncbi.nlm.nih.gov/pubmed/20377781
- ↑ 5.0 5.1 5.2 5.3 5.4 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: https://www.ncbi.nlm.nih.gov/pubmed/19322184
- ↑ Berend K et al Physiological Approach to Assessment of Acid-Base Disturbances. N Engl J Med 2014; 371:1434-1445. October 9, 2014 <PubMed> PMID: https://www.ncbi.nlm.nih.gov/pubmed/25295502 <Internet> http://www.nejm.org/doi/full/10.1056/NEJMra1003327
- ↑ 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: https://www.ncbi.nlm.nih.gov/pubmed/21849227
- ↑ Soifer JT, Kim HT. Approach to metabolic alkalosis. Emerg Med Clin North Am. 2014 May;32(2):453-63. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/24766943