Bicarbonate (\(\text{HCO}_3^-\)) is a negatively charged electrolyte in the blood that maintains the body’s acid-base balance. It acts as the primary buffer system, absorbing excess acid to prevent the blood’s pH from becoming too low (acidic) or too high (alkaline). The lungs and kidneys constantly regulate this molecule to keep the blood pH within a narrow, slightly alkaline range of 7.35 to 7.45. The kidneys control bicarbonate levels by excreting or reabsorbing it, while the lungs manage the acid component by controlling carbon dioxide levels. A measurement of high bicarbonate suggests this delicate balance has been disrupted, leading to an overly alkaline state.
Defining Elevated Bicarbonate
A high bicarbonate level signifies metabolic alkalosis, a condition where the blood and body tissues become too alkaline. This imbalance occurs due to either a gain of bicarbonate or a substantial loss of acid from the body. Bicarbonate is typically measured as part of a routine blood test, such as a Basic Metabolic Panel.
The normal reference range for bicarbonate in the blood is generally between 22 and 29 milliequivalents per liter (\(\text{mEq/L}\)), though this range can vary by laboratory. When the concentration rises above this upper limit, it is considered elevated, indicating metabolic alkalosis.
Factors That Cause High Bicarbonate
Elevated bicarbonate levels result from two primary physiological mechanisms: the loss of acid or the retention or addition of alkali (bicarbonate). The most common cause of acid loss is severe or prolonged vomiting, which removes high concentrations of hydrochloric acid from the stomach. This loss of acid causes the blood’s overall alkalinity to increase.
Acid loss can also occur in a hospital setting through nasogastric suctioning. In both scenarios, the loss of hydrogen ions leads to a compensatory rise in circulating bicarbonate.
Another frequent cause involves the use of certain medications, particularly loop and thiazide diuretics. These diuretics increase the excretion of sodium and chloride in the urine, which promotes the retention of bicarbonate in the kidneys. This mechanism is often coupled with volume contraction, or dehydration, which further concentrates the bicarbonate remaining in the blood.
Additionally, conditions causing excessive activity of the adrenal hormone aldosterone, such as hyperaldosteronism, can lead to bicarbonate retention. Aldosterone promotes the kidneys to save sodium while increasing the excretion of potassium and hydrogen ions, effectively raising the blood \(\text{pH}\).
Physical Effects of High Bicarbonate
When the blood becomes too alkaline due to high bicarbonate, it can affect the function of multiple organ systems, including the nerves, muscles, and heart. Mild metabolic alkalosis may not cause noticeable symptoms, but physical manifestations appear as the imbalance becomes more pronounced. A change in \(\text{pH}\) causes shifts in other electrolytes, notably a decrease in the concentration of free, ionized calcium and potassium in the blood.
The reduction in ionized calcium causes the nerves and muscles to become overly excitable, leading to symptoms like tingling sensations, muscle twitching, or painful muscle cramps. In severe cases, this hypocalcemia can trigger tetany, involving involuntary, sustained muscle spasms. The central nervous system may also be affected, resulting in confusion, lethargy, or disorientation. Severe alkalosis can also predispose an individual to abnormal heart rhythms (arrhythmias).
Addressing High Bicarbonate Levels
Identifying high bicarbonate usually begins with a blood test, frequently a Basic Metabolic Panel. Once metabolic alkalosis is confirmed, the primary goal of treatment is to identify and reverse the underlying cause of the imbalance. Treating the root cause is often sufficient to allow the body’s natural regulatory mechanisms to correct the bicarbonate levels.
If the cause is related to fluid loss from vomiting or diuretic use, treatment involves replacing lost water and electrolytes, specifically chloride, using intravenous saline solution. Replacing chloride helps the kidneys excrete the excess bicarbonate. For cases driven by hyperaldosteronism, medications that block the effects of aldosterone, such as spironolactone, may be used. In severe or symptomatic cases, a carbonic anhydrase inhibitor like acetazolamide may be administered to directly increase bicarbonate excretion by the kidneys.