Sodium bicarbonate (\(\text{NaHCO}_3\)) is an alkalizing agent, or buffer, used to neutralize acid in the body. Historically, medical professionals administered this drug during cardiac arrest—when the heart stops pumping blood—to stabilize the patient’s internal chemical environment during resuscitation efforts. However, its use in this emergency setting is highly specific and often controversial, leading to strict medical guidelines governing its application.
The Problem of Acidosis in Cardiac Arrest
The immediate lack of circulation during a cardiac arrest quickly leads to severe metabolic acidosis. Without oxygen, the body’s cells switch from efficient aerobic metabolism to a less efficient anaerobic process, resulting in a buildup of lactic acid in the bloodstream and tissues.
This accumulation of acid lowers the blood’s pH, which directly harms the heart muscle’s function. Acidosis reduces the effectiveness of heart contractions and interferes with how heart cells respond to electrical impulses and life-saving medications. The acidity can also inhibit the function of catecholamines, such as epinephrine, which are administered to stimulate the heart during resuscitation. The theoretical benefit of sodium bicarbonate was to counteract this systemic acidosis, improving the heart’s responsiveness and increasing the chances of successful resuscitation.
Standard Dosing and Current Guidelines
When sodium bicarbonate is administered, the standard dose is 1 milliequivalent per kilogram (mEq/kg) of the patient’s body weight, given intravenously as a rapid injection. Repeat doses of half the original amount may be considered every 10 minutes for the duration of the resuscitation effort.
Despite the physiological problem of acidosis, current Advanced Cardiac Life Support (ACLS) guidelines from the American Heart Association (AHA) do not recommend the routine administration of sodium bicarbonate during cardiac arrest. Evidence suggests that widespread use does not improve patient survival rates or neurological outcomes. Consequently, its use is restricted to specific circumstances where the potential benefit outweighs the known risks.
Risks of Routine Administration
Medical guidelines advise against the routine use of sodium bicarbonate due to its potential to cause paradoxical intracellular acidosis. While the drug buffers acid in the bloodstream (extracellular space), the chemical reaction produces carbon dioxide (\(\text{CO}_2\)). In cardiac arrest, poor blood flow limits the lungs’ ability to eliminate this generated \(\text{CO}_2\).
Carbon dioxide crosses cell membranes, including those of the heart muscle cells, unlike the bicarbonate ion itself. Inside the cells, this gas reacts with water, forming carbonic acid, which makes the heart cells and other tissues more acidic. This intracellular hypercarbic acidosis can further depress the heart’s function and counteract the intended benefit.
The drug’s high concentration of sodium also presents a risk, as administration can lead to hypernatremia (high sodium in the blood). This can cause fluid shifts and increase the blood’s osmolarity, potentially harming brain cells.
Furthermore, the alkaline nature of sodium bicarbonate means it should not be mixed with other resuscitation drugs, such as epinephrine or calcium. If administered through the same intravenous line, the bicarbonate can chemically inactivate these medications. The drug also contributes to increased vascular resistance, which can reduce blood flow to the heart muscle.
Specific Situations Requiring Bicarbonate
While routine use is not supported, there are specific exceptions where sodium bicarbonate is recommended because its mechanism addresses the underlying cause of the arrest. One exception is cardiac arrest caused by severe hyperkalemia (high potassium in the blood). In this scenario, sodium bicarbonate helps shift potassium back into the cells, stabilizing the heart.
Sodium bicarbonate is also recommended for patients experiencing cardiotoxicity or cardiac arrest due to an overdose of tricyclic antidepressants (TCAs). The \(\text{NaHCO}_3\) works by increasing the blood’s alkalinity and providing sodium, which helps overcome the TCA effect of blocking the heart’s sodium channels. For TCA overdose, the dose is 1 to 2 mEq/kg, repeated as needed to maintain heart stability and a specific blood pH target.
Sodium bicarbonate may be considered in cases where the patient has metabolic acidosis that has not responded to other treatments and is contributing to the cardiac arrest. This application is guided by blood gas analysis, which measures the patient’s acid-base status. In these circumstances, the potential benefit in reversing a specific chemical abnormality outweighs the risks associated with routine use.