What are the mechanisms by which cardiac arrest leads to acidosis, how does intravenous sodium bicarbonate correct acidosis, why does it cause hypernatremia, and what treatments can correct hypernatremia in a patient who suffered cardiac arrest and was revived with sodium bicarbonate administration, developing subsequent seizures due to excessive neuromuscular excitability?

From the Guidelines

Cardiac arrest leads to acidosis due to anaerobic metabolism, and while sodium bicarbonate can correct acidosis, its use is not recommended routinely due to potential adverse effects, including hypernatremia, which can be corrected with hypotonic fluids and careful monitoring of electrolytes. The mechanisms by which cardiac arrest leads to acidosis involve anaerobic metabolism during oxygen deprivation, causing lactic acid buildup and carbon dioxide retention 1. Sodium bicarbonate is administered to correct this acidosis by providing bicarbonate ions that neutralize excess hydrogen ions, shifting the pH toward normal. However, this treatment causes hypernatremia because sodium bicarbonate contains sodium ions that increase serum sodium concentration, and it can also produce excess CO2, which may paradoxically contribute to intracellular acidosis 1. To correct the hypernatremia, treatment should include administration of hypotonic fluids like 5% dextrose in water or half-normal saline (0.45% NaCl) to dilute the excess sodium. Free water replacement helps restore normal sodium concentration while maintaining adequate hydration. Additionally, loop diuretics like furosemide might be considered to enhance sodium excretion through the kidneys, but careful monitoring of electrolytes, especially sodium levels, is essential during treatment to prevent overcorrection, which could lead to cerebral edema, particularly in patients who develop seizures due to excessive neuromuscular excitability 1. Key considerations in managing these patients include:

• Avoiding routine use of sodium bicarbonate in cardiac arrest unless in special situations like preexisting metabolic acidosis, hyperkalemia, or tricyclic antidepressant overdose 1
• Guiding bicarbonate therapy by bicarbonate concentration or calculated base deficit whenever possible to minimize the risk of iatrogenically induced alkalosis 1
• Considering alternative non–CO2-generating buffers for minimizing adverse effects of sodium bicarbonate, although clinical experience and outcome studies are limited 1.

From the FDA Drug Label

In cardiac arrest, a rapid intravenous dose of one to two 50 mL vials (44.6 to 100 mEq) may be given initially and continued at a rate of 50 mL (44. 6 to 50 mEq) every 5 to 10 minutes if necessary (as indicated by arterial pH and blood gas monitoring) to reverse the acidosis. Bicarbonate solutions are hypertonic and may produce an undesirable rise in plasma sodium concentration in the process of correcting the metabolic acidosis Intravenous sodium bicarbonate therapy increases plasma bicarbonate, buffers excess hydrogen ion concentration, raises blood pH and reverses the clinical manifestations of acidosis. Sodium bicarbonate in water dissociates to provide sodium (Na+) and bicarbonate (HCO3-) ions

The mechanisms by which cardiac arrest leads to acidosis are not directly stated in the provided drug labels. Intravenous sodium bicarbonate corrects acidosis by buffering excess hydrogen ion concentration and raising blood pH. It causes hypernatremia because bicarbonate solutions are hypertonic and may produce an undesirable rise in plasma sodium concentration. To correct hypernatremia, the labels do not provide a direct answer, but it can be inferred that monitoring and adjustment of fluid and electrolyte disturbances may be necessary. For a patient who suffered cardiac arrest and was revived with sodium bicarbonate administration, developing subsequent seizures due to excessive neuromuscular excitability, the labels do not provide a direct treatment, and clinical judgment should be used to manage the condition 2 2.

From the Research

Mechanisms of Acidosis in Cardiac Arrest

• Cardiac arrest leads to a lack of oxygen delivery to tissues, resulting in lactic acidosis and metabolic acidosis 3
• The mechanisms of acidosis occurring during cardiopulmonary arrest involve the accumulation of lactic acid and other acidic byproducts due to anaerobic metabolism 3

Correction of Acidosis with Sodium Bicarbonate

• Sodium bicarbonate (SB) has been used to correct metabolic acidosis (MA) in cardiac arrest patients, although its effectiveness is controversial 4, 5
• The administration of SB can improve acid-base status, but its impact on outcomes such as return of spontaneous circulation (ROSC) and neurologic survival is unclear 6

Hypernatremia caused by Sodium Bicarbonate

• Excessive administration of SB can cause hypernatremia, as well as other potential harms such as paradoxical respiratory acidosis, intracellular acidosis, hypokalemia, and hypocalcemia 7
• The overuse of SB can lead to these adverse effects, highlighting the need for careful consideration of its use in clinical practice 7

Treatments for Hypernatremia and Seizures

• In patients who have developed hypernatremia and seizures after SB administration, treatment may involve correcting the electrolyte imbalance and managing the seizures with anticonvulsant medications
• However, there is limited evidence available to guide the specific treatment of hypernatremia and seizures in this context, and further research is needed to determine the best approach 4, 7