Metabolic alkalosis refers to an increase in extracellular fluid alkalinity and/or the loss of hydrogen ions (H+), leading to an elevated pH. It is primarily characterized by a rise in blood plasma bicarbonate (HCO3-) concentration.
Etiology
Excessive Loss of Acidic Substances
Severe vomiting and prolonged gastrointestinal decompression can cause the loss of hydrogen ions (H+), chloride ions (Cl-), and potassium ions (K+) in gastric fluids. In such cases, intestinal and pancreatic HCO3- is not neutralized by H+, leading to its absorption into the bloodstream, which results in hypochloremic and hypokalemic alkalosis. The use of loop diuretics or thiazide diuretics can inhibit the active reabsorption of Cl- and passive reabsorption of Na+ in the renal loop, promoting increased secretion of H+ and K+ by distal tubules and collecting ducts. This leads to significant loss of H+ through the kidneys and increased reabsorption of HCO3-. Elevated levels of adrenal cortical hormones, particularly aldosterone, can stimulate renal excretion of H+ and promote H+ excretion through sodium (Na+) retention and potassium (K+) excretion, causing hypokalemic alkalosis.
Excessive Intake of Alkaline Substances
Patients with peptic ulcers may take excessive amounts of sodium bicarbonate (NaHCO3), or excessive NaHCO3 may be introduced through intravenous infusion. Sodium lactate, sodium acetate, or large transfusions of citrate-anticoagulated blood can also result in alkalosis. These organic acid salts are converted to NaHCO3 through oxidation in the body, leading to contraction alkalosis.
Intracellular Shift of H+
Hypokalemia can lead to the movement of potassium ions (K+) from intracellular to extracellular spaces and the concurrent shift of H+ into cells, causing metabolic alkalosis. In this context, potassium depletion in renal tubular cells reduces the K+-Na+ exchange, which is replaced by increased H+-Na+ exchange. This process leads to greater H+ excretion and HCO3- reabsorption, with urine becoming acidic, a phenomenon referred to as paradoxical aciduria.
Respiratory compensation for metabolic alkalosis occurs relatively quickly. A reduction in plasma H+ concentration suppresses the respiratory center, leading to slower and shallower breathing, which decreases CO2 exhalation. This results in an increase in plasma carbonic acid (H2CO3) levels, restoring the HCO3-/H2CO3 ratio to near-normal and moderating blood pH elevation. Renal compensation, being slower, involves reduced activity of carbonic anhydrase and glutaminase in renal tubular epithelial cells, leading to decreased secretion of H+ and ammonium ions (NH4+) and reduced reabsorption of HCO3-. This decreases blood HCO3- concentration.
Clinical Manifestations
Mild metabolic alkalosis often presents without obvious symptoms, as clinical signs may be masked by underlying conditions. Neuromuscular effects include symptoms of central nervous system excitation such as restlessness, mental confusion, or delirium. Facial and limb muscle twitching, hyperactive tendon reflexes, and carpopedal spasms are also observed. Alkalosis may suppress the respiratory center, leading to slow, shallow breathing and reduced ventilation. Cardiac effects include various arrhythmias, decreased blood pressure, and even cardiac arrest in severe cases.
Diagnosis
A preliminary diagnosis can be made based on the medical history, and blood gas analysis can confirm the diagnosis and its severity. During the compensatory phase, blood pH may remain near normal; however, HCO3- concentration and base excess (BE) are elevated to some extent. In uncompensated cases, blood pH and HCO3- concentration are significantly increased, while arterial partial pressure of carbon dioxide (PaCO2) is typically normal.
Blood gas analysis in metabolic alkalosis reveals an elevated pH, as well as increased values for actual bicarbonate (AB), standard bicarbonate (SB), and buffer base (BB). AB exceeds SB, BE shows a greater positive value, and PaCO2 is secondarily elevated.
Treatment
Treatment focuses on addressing the underlying cause. For metabolic alkalosis caused by the loss of gastric fluids, isotonic saline or glucose saline infusion restores extracellular fluid volume and replenishes chloride ions (Cl-). This dilution lowers HCO3- concentration, which is then excreted in urine, correcting mild hypochloremic alkalosis. Hypokalemia commonly accompanies metabolic alkalosis and can be managed with potassium chloride supplementation. Potassium replenishment promotes the intracellular uptake of K+, which exchanges with intracellular H+, thereby increasing extracellular H+ concentration. Potassium supplementation also enhances renal excretion of HCO3-, accelerating the resolution of alkalosis.
In cases of severe alkalosis, a 0.1 to 0.2 mol/L dilute hydrochloric acid solution may be used. For such treatment, 100 mL of 1 mol/L hydrochloric acid is mixed into 1,000 mL of 0.9% NaCl or 5% glucose solution and administered via a central venous catheter at a rate of 25 to 50 mL per hour. Blood gas analysis and electrolyte levels are monitored every 4 to 6 hours, and treatment may be repeated the next day if necessary.