Prevalence of Sodium Bicarbonate-Induced Alkalemia in Cardiopulmonary Arrest Patients^{(July/August)}

¹ Clinical Pharmacist, Emergency Medicine, Baptist Medical Center Downtown, Jacksonville, FL; Clinical Assistant Professor of Pharmacy Practice, University of Florida, Jacksonville; Guest Lecturer, College of Allied Health and Nursing, Nova Southeastern University, Ft. Lauderdale, FL
² Clinical Pharmacist, Critical Care, Department of Pharmacy, Mayo Clinic, Jacksonville
³ Biostatistician, Biostatistics Unit, Mayo Clinic
⁴ Physician, Internal Medicine, Department of Internal Medicine, Mayo Clinic

^* To whom correspondence should be addressed. E-mail: matthew.geraci{at}bmcjax.com.

	Abstract

BACKGROUND: Intravenous sodium bicarbonate (SB) administration during cardiopulmonary arrest (CPA) is intended to counteract lactic acidosis due to hypoxia, poor perfusion, and anaerobic metabolism. Despite a lack of documented efficacy and a level III recommendation from the American Heart Association, SB is widely used during resuscitation events. SB has both theoretical and measurable adverse effects. Excess or poorly timed administration during a CPA may elevate a patient's pH, inducing alkalemia. Despite decades of controversy surrounding use of this drug, the prevalence of SB-induced alkalemia has not been previously documented.

OBJECTIVE: To estimate the prevalence of SB-induced alkalemia in inpatients after CPA and to investigate the pattern of SB administration.

METHODS: Medical records were retrospectively reviewed with attention to SB administration and arterial blood gas (ABG) data. After application of inclusion and exclusion criteria to 264 CPA patients, the study group comprised 88 patients. When measured, if PCO₂ and pH were above normal limits after SB administration, we concluded that SB contributed to the alkalemia.

RESULTS: Twenty-seven (31%) patients received SB without any ABG data, and 70 (79%) patients received at least one empiric SB dose. Of the 61 patients with ABG data, alkalemia occurred in 10, a prevalence of 16%. Administration of SB increased pH in only 9 (15%) other CPA patients and had no effect in the 42 (69%) remaining patients.

CONCLUSIONS: Administration of SB during CPA was causally linked with inducing alkalemia in 16% of patients. Early collection of ABG samples may assist in optimizing pH during CPA and thus reduce unwarranted empiric use of SB.

Key Words: alkalemia, alkaline agent, buffer therapy, cardiopulmonary arrest, resuscitation, sodium bicarbonate.

Reprints:Dr. Geraci, Baptist Medical Center Downtown, Department of Pharmacy, 800 Prudential Dr., Jacksonville, FL 32207, fax 904/202-8001, matthew.geraci@bmcjax.com