A 35-year-old pregnant woman at 8 weeks gestation comes to the emergency department due to persistent nausea and vomiting. The patient has had intermittent nausea for the past week and vomiting for the past 3 days. Now, she is unable to tolerate solids or liquids. Temperature is 36.7 C (98 F), blood pressure is 90/64 mm Hg, pulse is 108/min, and respirations are 14/min. Mucous membranes are dry and capillary refill time is delayed. Cardiac examination shows sinus tachycardia and no murmurs. The abdomen is nontender and nondistended. Compared to her baseline, which of the following sets of serum electrolyte concentration abnormalities are most likely present in this patient?
Hypokalemic, hypochloremic metabolic alkalosis | |
Common etiologies |
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Pathophysiology |
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Management |
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RAAS = renin-angiotensin-aldosterone system. | |
This patient has had severe vomiting (suggestive of hyperemesis gravidarum) and now has multiple signs of volume depletion (eg, dry mucous membranes, delayed capillary refill time, tachycardia). Vomiting causes a significant loss of gastric H+ from the body, which leads to increased serum HCO3− (metabolic alkalosis). There is also loss of water and salt (relatively more Cl− is lost than Na+ due to high gastric quantity of HCl), leading to volume depletion that perpetuates the metabolic alkalosis and causes other electrolyte abnormalities.
Intravascular volume depletion decreases renal perfusion, resulting in activation of the renin-angiotensin-aldosterone system. Aldosterone stimulates Na+ reabsorption and a lesser degree of passive Cl− reabsorption in the distal tubules of the kidneys in an effort to increase blood volume. The relatively greater loss of Cl− compared to Na+ from both the stomach and kidneys leads to a large Cl− deficit and characteristic hypochloremia.
The aldosterone-mediated increase in Na+ reabsorption comes at the expense of increased K+ and H+ excretion via the principal and alpha intercalated cells in the collecting duct. This leads to hypokalemia and exacerbation of the metabolic alkalosis. Chloride depletion then perpetuates the metabolic alkalosis because low tubular Cl− concentration impairs HCO3− excretion via the pendrin pump on beta intercalated cells.
If the hypovolemia persists, it also provides nonosmotic stimulus for the secretion of antidiuretic hormone (ADH). The ADH secretion is considered appropriate because the body's priority is to restore itself to euvolemia; however, it leads to free water retention with hyponatremia and more profound hypochloremia.
Educational objective:
Severe vomiting characteristically causes hypokalemic, hypochloremic metabolic alkalosis. The metabolic alkalosis is initiated by loss of gastric H+ from the body, worsened by hypovolemia-induced activation of the renin-angiotensin-aldosterone system, and perpetuated by profound gastric and renal losses of Cl− that lead to hypochloremia and impaired renal HCO3− excretion. Hypokalemia primarily results from aldosterone-mediated renal K+ losses.