Mechanism of Hypokalemia from Vomiting
Vomiting causes hypokalemia primarily through renal potassium losses driven by metabolic alkalosis and secondary hyperaldosteronism, not through direct loss of potassium in gastric fluid. 1
Primary Mechanisms
Metabolic Alkalosis and Renal Potassium Wasting
The key mechanism is metabolic alkalosis, which develops when gastric acid (HCl) is lost through vomiting, leaving behind bicarbonate in the circulation 1
Metabolic alkalosis directly increases renal potassium excretion through enhanced activity of the sodium epithelial channel (ENaC) in the cortical collecting duct, which increases potassium secretion via the ROMK2 channel to maintain electrical neutrality 1
The alkalosis itself upregulates ENaC activity, which is aldosterone-sensitive, creating a self-perpetuating cycle of potassium loss 1
Secondary Hyperaldosteronism from Volume Depletion
Volume depletion from vomiting activates the renin-angiotensin-aldosterone (RAA) system, causing increased aldosterone secretion that promotes sodium retention and potassium excretion 1, 2
This secondary hyperaldosteronism is particularly important in patients with high-output gastrointestinal losses, where sodium and water depletion paradoxically increases renal potassium losses 3, 2
Correcting volume depletion first is essential, as hypoaldosteronism from sodium depletion increases renal potassium losses 3
Increased Distal Sodium Delivery
Volume contraction from vomiting increases proximal sodium reabsorption initially, but the metabolic alkalosis causes bicarbonate to reach the distal tubule 1
Increased sodium-bicarbonate delivery to the cortical collecting duct enhances sodium uptake through ENaC, with consequent increased potassium excretion to maintain electroneutrality 1
Clinical Implications
Why Gastric Potassium Content is Irrelevant
Gastric fluid contains relatively little potassium (approximately 5-10 mEq/L), making direct gastrointestinal losses a minor contributor 4
The magnitude of hypokalemia seen with vomiting far exceeds what could be explained by direct potassium loss alone, confirming that renal wasting is the dominant mechanism 5, 4
Associated Electrolyte Disturbances
Hypomagnesemia frequently coexists with vomiting-induced hypokalemia and must be corrected concurrently, as magnesium depletion causes dysfunction of potassium transport systems and increases renal potassium excretion 3, 2
The combination of metabolic alkalosis, hypokalemia, and volume depletion creates a characteristic pattern that distinguishes vomiting from other causes of hypokalemia 4
Diagnostic Approach
Laboratory Findings
Arterial pH will be elevated (alkalosis) in vomiting-induced hypokalemia, distinguishing it from diarrhea (which causes acidosis) 4
Urine potassium will be inappropriately elevated (typically >20 mEq/L) despite hypokalemia, confirming renal losses rather than extrarenal causes 4
Urine chloride will be low (<20 mEq/L) in volume-depleted patients with vomiting, reflecting chloride depletion and secondary hyperaldosteronism 4
Treatment Considerations
Addressing the Root Cause
Correct volume depletion with normal saline first, as this addresses the secondary hyperaldosteronism driving renal potassium losses 3, 2
Treating the metabolic alkalosis by restoring chloride helps reduce the stimulus for renal potassium wasting 1
Potassium chloride is the preferred replacement form because it addresses both the potassium deficit and the chloride depletion that perpetuates alkalosis 6, 7
Common Pitfalls
Never supplement potassium without checking and correcting magnesium first, as hypomagnesemia is the most common reason for refractory hypokalemia in vomiting patients 3, 2
Failing to address volume depletion allows continued activation of the RAA system and persistent renal potassium wasting despite supplementation 3, 2
Using potassium preparations without chloride (such as potassium citrate or gluconate) fails to correct the chloride deficit and may be less effective 6