Metabolic alkalosis resident survival guide

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Marufa Marium, M.B.B.S[2]

Synonyms and keywords: Approach to Metabolic alkalosis, Metabolic alkalosis management, Metabolic alkalosis work-up


The normal physiological pH of blood is 7.35 to 7.45. An increase above this range is known to be Alkalosis. Metabolic Alkalosis is defined as a disease state where the blood pH is more than 7.45 due to secondary metabolic processes. The primary pH buffers in maintaining chemical equilibrium of physiological Blood pH are alkaline Bicarbonate ions(HCO3) and acidic carbon dioxide(CO2). When there is an increased amount of Bicarbonate(HCO3) in the body or a decreased amount of carbon dioxide or a loss of hydrogen ions, it causes alkalosis. Metabolic alkalosis occurs due to the trapping of Bicarbonate ions (HCO3) or loss of hydrogen ions in the body due to some metabolic causes for example- gastrointestinal loss of hydrogen ions, intracellular shifting of hydrogen ions, renal hydrogen loss, increased bicarbonate ions in extracellular compartment, diuretic induced alkalosis or contraction alkalosis. Patient with normal renal physiology will compensate this increased amount of bicarbonate through excretion. But impaired renal function secondary to chloride depletion, hypokalemia, hyperaldosteronism, reduced glomerular function rate, reduced effective arterial blood volume (EABV)) in heart failure or cirrhosis will lead to metabolic alkalosis. When the physiologic blood pH is above 7.45, it triggers the respiratory center to cause hypoventilation, thus decreased PCO2 leading to compensatory respiratory acidosis. The PCO2elevates from 0.5 to 0.7 mmHg per 1.0 mill mole elevation in plasma bicarbonate concentration. In severe Metabolic alkalosis PCO2 can reach 60 mmHg. The mortality rate with metabolic alkalosis is 45% with arterial blood pH 7.55 to 80% with arterial blood pH of 7.65. Treatment is usually supportive based on cause of the disease.


Life Threatening Causes

Life-threatening causes of severe metabolic alkalosis (pH 7.55 to 7.65) may result in death (45% to 80%) or permanent disability within 24 hours if left untreated.[1]

Common Causes


Shown below is an algorithm summarizing the diagnosis and treatment of Metabolic Alkalosis.[1]

History: • H/O Cystic fibrosis/Congenital adrenal hyperplasia/CHF/Uncontrolled HTN?
• Excess antacid consumption?
Calcium over supplementation?
Beta lactum antibiotic use?
• Recent or current diuretic use?
Vomiting or diarrhea?
• massive use of licorice?
• H/O recent hypercapneic respiratory failure?
Physical Examination: •General appearance: Restlessness/ Irritable/lethargic?
Skin: decreased or normal turgor?
HEENT: Headache/Dizziness?
CVS: Dysrhythmia/Tachycardia?
Respiratory: Hypoxemia, Compensatory hypoventilation, Pulmonary microatelactasis, Increased V/Q mismatch
GI: Nausea/vomiting/diarrhea?
GU: Urine output, frequency?
CNS: Confusion, loss of consciousness/Mental obtundation, Neuromuscular excitability/Muscle cramps, Tremor, tingling and numbness in extremities, Weakness?
Laboratory TestsABG(pH >7.45, HCO3 >26 mEq/L, PCO2 compensates for increased HCO3 by decreasing)
Basic metabolic panel
Serum Aldosterone And renin
Urine analysis, Urine pH, Urine Chloride and sodium
Chest X-ray
Abdominal USG/CT to rule out mass
Expanded EABV(No sign of volume depletion or Saline unresponsive)Treatment: Treat underlying cause.
Contracted EABV(sign of volume depletion or saline responsive)Treatment: Replace volume with NaCl if depleted, correct electrolyte imbalance, reduction of gastric secretion by H2 blocker or PPI, discontinue diuretics, Acetazolamide, NH4Cl and HCl should be reserved for severe cases.
Rule out by historyTreatment: According to cause with discontinuation of offending agents.
Renal failure with ingestion
• Acute correction of hypercapnea
Milk-alkali syndrome
HCO3 ingesion
GI loss(low urine Cl)
Renal loss(high urine Cl)
Gastric: Vomiting, NG suction
Lower bowel: Villous adenoma, chloridorrhea, laxative abuse
Non-reabsorbed ions: Penicillin
• =Impaired tubular transport: Loop and thiazide diuretics, Barrter's and Gitelman's disease, Hypomagnesaemia
High Renin, High aldosterone:• Malignant hypertension
renovascular hypertension
Renin secretin tumor
Low Renin, High aldosterone:• Aldosterone secreting tumor
Adrenal hyperplasia
Glucocorticoid remediable aldosteronism
Low Renin, Low Aldosterone:• Licorice
Liddle's syndrome
Enzyme deficiency


  • Maintenance of airway, breathing, circulation if there is an unstable patient.[10]
  • Correction of the underlying cause for HCO3 production.
  • Removal of inciting factors that reabsorb HCO3.
  • Patient should be monitored carefully with SaO2, vital signs monitor and EKG.
  • Consider respiratory support in hypoxemic patient.



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