Complexities, Benefits, Risks, and Clinical Implications of Sodium Bicarbonate Administration in Critically Ill Patients: A State-of-the-Art Review

Abstract

Sodium bicarbonate has been used in the treatment of different pathologies, such as hyperkalemia, cardiac arrest, tricyclic antidepressant toxicity, aspirin toxicity, acute acidosis, lactic acidosis, diabetic ketoacidosis, rhabdomyolysis, and adrenergic receptors' resistance to catecholamine in patients with shock. An ongoing debate about bicarbonate's efficacy and potential harm has been raised for decades because of the lack of evidence supporting its potential efficacy. Despite the guidelines' restrictions, sodium bicarbonate has been overused in clinical practice. The overuse of sodium bicarbonate could be because of the desire to correct the arterial blood gas parameters rapidly instead of achieving homeostasis by treating the cause of the metabolic acidosis. Moreover, it is believed that sodium bicarbonate may reverse acidosis-induced myocardial depression, hemodynamic instability, ventricular arrhythmias, impaired cellular energy production, resistance to catecholamines, altered metabolism, enzyme suppression, immune dysfunction, and ineffective oxygen delivery. On the other hand, it is crucial to pay attention to the potential harm that could be caused by excessive sodium bicarbonate administration. Sodium bicarbonate may cause paradoxical respiratory acidosis, intracellular acidosis, hypokalemia, hypocalcemia, alkalosis, impaired oxygen delivery, cerebrospinal fluid acidosis, and neurologic dysfunction. In this review, we discuss the pathophysiology of sodium bicarbonate-induced adverse effects and potential benefits. We also review the most recent clinical trials, observational studies, and guidelines discussing the use of sodium bicarbonate in different pathologies.

Keywords: acid–base balance; acute kidney injury; cardiac arrest; cerebrospinal fluid acidosis; diabetic ketoacidosis; high anion gap; lactic acidosis; metabolic acidosis; normal anion gap; resuscitation; rhabdomyolysis; sodium bicarbonate.

Figure 1

Pathophysiology of developing neurological dysfunction in patients with acute respiratory acidosis and after sodium bicarbonate administration. Sodium bicarbonate administration causes acute increase in arterial PCO₂. Since BBB is freely permeable to CO₂, high arterial PCO₂ causes CSF acidosis. CSF acidosis affects the release and uptake of neuromodulators and neurotransmitters and the activity of ion channels. Subsequently, this affects neural activity and the action potential. In contrast, acute metabolic acidosis causes mild changes in CSF pH; as a result, it causes mild neurological dysfunction. Abbreviations: PCO₂, partial pressure of carbon dioxide; CSF, cerebrospinal fluid; BBB, blood–brain barrier.

Figure 2

The Virchow–Robin Space surrounding a cortical artery. Virchow–Robin Space (green-dotted area) is a perivascular space surrounding arteries, arterioles, venules, and veins. Virchow–Robin Space passes to the brain parenchyma through the subarachnoid space and the subpial space (blue-dotted area). Virchow–Robin Space connects the CSF in the subarachnoid space to the IF in the brain parenchyma.