What are the implications and management of hyperbicarbonatemia?

From the Guidelines

A high bicarbonate level of 37 is not immediately worrisome but requires careful evaluation and management based on its underlying cause and severity. The management of hyperbicarbonatemia primarily focuses on addressing the root cause rather than directly treating the elevated bicarbonate levels. For metabolic alkalosis, the most common cause of hyperbicarbonatemia, treatment includes:

• Correcting volume depletion with normal saline (0.9% NaCl) at rates of 100-200 mL/hour until euvolemia is achieved,
• Discontinuing diuretics if they're contributing to the condition, and
• Addressing potassium and chloride deficiencies with supplements such as potassium chloride 40-60 mEq/day divided into multiple doses 1. In severe cases (pH > 7.60 or bicarbonate > 40 mEq/L) with neurological symptoms, dilute hydrochloric acid (0.1-0.2 N HCl) may be administered through a central line at 100-200 mL/hour, or acetazolamide 250-500 mg IV/PO every 6 hours can be used to promote bicarbonate excretion. For respiratory acidosis-induced compensatory hyperbicarbonatemia, treating the underlying respiratory condition is essential, which may include bronchodilators, antibiotics for infections, or ventilatory support. Hyperbicarbonatemia can lead to decreased ionized calcium, hypokalemia, tissue hypoxia due to leftward shift of the oxyhemoglobin dissociation curve, and neurological symptoms including confusion and seizures, making prompt identification and management crucial for preventing complications. It's also important to note that the use of sodium bicarbonate therapy should be approached with caution, as it may be associated with sodium and fluid overload, an increase in lactate and Paco2, and a decrease in serum ionized calcium, as suggested by the surviving sepsis campaign guidelines 1. In contrast, the correction of acidemia due to metabolic acidosis has been associated with increased serum albumin, decreased protein degradation rates, and increased plasma concentrations of branched chain amino acids, highlighting the importance of maintaining optimal bicarbonate levels in certain patient populations 1.

From the Research

Implications of Hyperbicarbonatemia

• A high bicarbonate level of 37 can be indicative of metabolic alkalosis, a condition characterized by elevated pH and plasma bicarbonate levels above normal 2.
• Metabolic alkalosis can be caused by gastrointestinal hydrogen and chloride loss, or by renal causes, and requires both generation and maintenance of high levels of bicarbonate to persist 2.
• Severe metabolic alkalosis, with an arterial blood pH of 7.55 or higher, is associated with significantly increased mortality rates, especially in critically ill patients 3.

Management of Hyperbicarbonatemia

• The management of metabolic alkalosis involves correcting the underlying cause, such as fluid and electrolyte abnormalities, and may require the use of medications like acetazolamide to reduce serum bicarbonate levels 4, 5, 6.
• Acetazolamide has been shown to be effective in reducing serum bicarbonate levels and improving acid-base status in patients with metabolic alkalosis, with a rapid onset of action and long duration of effect 4, 5, 6.
• The choice of intravenous or oral acetazolamide may depend on the individual patient's needs and circumstances, with intravenous administration potentially resulting in more rapid decreases in bicarbonate levels 6.
• In some cases, correction of intravascular volume with sodium chloride may be necessary, especially in patients with chloride-responsive alkalosis 2.
• In severe cases, dialysis with a higher K+, Cl-, and low HCO3- bath may be necessary, especially in emergency situations with severe hypokalemia 2.

Key Considerations

• The diagnosis of metabolic alkalosis is established by noting pH, serum bicarbonate, and pCO2 elevation, and requires determination of intravascular volume, supine and standing blood pressure, and renin-angiotensin-aldosterone axis to establish the underlying cause 2.
• Factors that interfere with the kidney's ability to eliminate excess bicarbonate, such as volume contraction, low glomerular filtration rate, potassium deficiency, hypochloremia, aldosterone excess, and elevated arterial carbon dioxide, can promote the generation or impair the correction of metabolic alkalosis 3.