18 min
SGEM#394: Say Bye Bye Bicarb for Pediatric In-Hospital Cardiac Arrest The Skeptics Guide to Emergency Medicine
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- Education
Reference: Cashen K, Reeder RW, Ahmed T, et al. Sodium bicarbonate use during pediatric cardiopulmonary resuscitation: a secondary analysis of the icu-resuscitation project trial. Pediatric Crit Care Med. 2022
Date: February 15, 2023
Guest Skeptic: Dr. Carlie Myers is Pediatric Critical Care Attending at Cincinnati Children’s Hospital Medical Center.
Case: A 6-month-old boy presents to the emergency department (ED) with three days of worsening cough, cold symptoms, and fever. Parents note that he has been progressively more tired and difficult to arouse. He is found to be in hypoxic respiratory failure and septic shock. Intravenous (IV) access is obtained. He is quickly intubated. Despite multiple fluid boluses, he remains hypotensive and is started on vasoactive support. His blood gas reveals a mixed respiratory and metabolic acidosis with a lactate of 5.0. Despite your best efforts, he has an episode of agitation leading to hypoxia and subsequent cardiac arrest. Your team begins high quality cardiopulmonary resuscitation (CPR). An arterial blood gas is obtained demonstrates a pH of 7.0, PaCO2 of 70, PaO2 of 28, HCO3– of 7, Base Deficit of -10, and Lactate 10.0.
A team member asks if you want to administer some sodium bicarbonate (1mEq/kg).
Background: We often manage patients in cardiac arrest in the ED or the intensive care unit (ICU). Apart from high-quality CPR and early defibrillation, many other interventions we try lack a strong evidence base. But that does not stop us from trying to save the patient’s life and may represent some intervention bias.[1] The SGEM has covered the use of epinephrine, vasopressin, methylprednisolone, and calcium for cardiac arrest in SGEM#238, SGEM#350, and SGEM#353. Today we are focusing on sodium bicarbonate.
Sodium bicarbonate has historically been used during CPR with the goal of alkalizing blood pH and treating metabolic acidosis. There are a few key assumptions about the use of sodium bicarbonate.
* Low pH decreases cardiac function and responsiveness to catecholamines.
* Sodium bicarbonate administration will increase the pH.
* The increase in pH will lead to improved responsiveness to catecholamines and cardiac function.
But it’s not that straightforward. Many of the studies supporting these claims were conducted on animal models or in vitro. [2] It is unclear if we see the same effects of acidosis and sodium bicarbonate in vivo.
HCO3– + H+ ↔ H2O + CO2
Rapid bicarbonate infusion can cause an imbalance in CO2 across the cell membrane. HCO3– + H+ converts to H2CO3 and then to CO2 +H20. Extracellular CO2 rises rapidly, it diffuses across cell membranes and the reverse reaction occurs H2O + CO2→ HCO3– + H+; therefore, creating intracellular acidosis.
There was a lack of evidence about the benefits and potential harm from using sodium bicarbonate in cardiac arrest [3], so it was removed from the American Heart Association’s (AHA) guidelines.
The latest guidelines from the AHA in 2020 state, “clinical trials and observational studies since the 2010 guidelines have yielded no new evidence that routine administration of sodium bicarbonate improves outcomes from undifferentiated cardiac arrest and evidence suggests that it may worsen survival and neurological recovery.” [4]
This association seems to hold true in the pediatric literature as well. [5-6]
Clinical Question: What is the association between sodium bicarbonate use and pediatric in-hospital cardiac arrest mortality and morbidity?
Reference: Cashen K, Reeder RW, Ahmed T, et al. Sodium bicarbonate use during pediatric cardiopulmonary resuscitation: a secondary analysis of the icu-resuscitation project trial. Pediatric Crit Care Med. 2022
Date: February 15, 2023
Guest Skeptic: Dr. Carlie Myers is Pediatric Critical Care Attending at Cincinnati Children’s Hospital Medical Center.
Case: A 6-month-old boy presents to the emergency department (ED) with three days of worsening cough, cold symptoms, and fever. Parents note that he has been progressively more tired and difficult to arouse. He is found to be in hypoxic respiratory failure and septic shock. Intravenous (IV) access is obtained. He is quickly intubated. Despite multiple fluid boluses, he remains hypotensive and is started on vasoactive support. His blood gas reveals a mixed respiratory and metabolic acidosis with a lactate of 5.0. Despite your best efforts, he has an episode of agitation leading to hypoxia and subsequent cardiac arrest. Your team begins high quality cardiopulmonary resuscitation (CPR). An arterial blood gas is obtained demonstrates a pH of 7.0, PaCO2 of 70, PaO2 of 28, HCO3– of 7, Base Deficit of -10, and Lactate 10.0.
A team member asks if you want to administer some sodium bicarbonate (1mEq/kg).
Background: We often manage patients in cardiac arrest in the ED or the intensive care unit (ICU). Apart from high-quality CPR and early defibrillation, many other interventions we try lack a strong evidence base. But that does not stop us from trying to save the patient’s life and may represent some intervention bias.[1] The SGEM has covered the use of epinephrine, vasopressin, methylprednisolone, and calcium for cardiac arrest in SGEM#238, SGEM#350, and SGEM#353. Today we are focusing on sodium bicarbonate.
Sodium bicarbonate has historically been used during CPR with the goal of alkalizing blood pH and treating metabolic acidosis. There are a few key assumptions about the use of sodium bicarbonate.
* Low pH decreases cardiac function and responsiveness to catecholamines.
* Sodium bicarbonate administration will increase the pH.
* The increase in pH will lead to improved responsiveness to catecholamines and cardiac function.
But it’s not that straightforward. Many of the studies supporting these claims were conducted on animal models or in vitro. [2] It is unclear if we see the same effects of acidosis and sodium bicarbonate in vivo.
HCO3– + H+ ↔ H2O + CO2
Rapid bicarbonate infusion can cause an imbalance in CO2 across the cell membrane. HCO3– + H+ converts to H2CO3 and then to CO2 +H20. Extracellular CO2 rises rapidly, it diffuses across cell membranes and the reverse reaction occurs H2O + CO2→ HCO3– + H+; therefore, creating intracellular acidosis.
There was a lack of evidence about the benefits and potential harm from using sodium bicarbonate in cardiac arrest [3], so it was removed from the American Heart Association’s (AHA) guidelines.
The latest guidelines from the AHA in 2020 state, “clinical trials and observational studies since the 2010 guidelines have yielded no new evidence that routine administration of sodium bicarbonate improves outcomes from undifferentiated cardiac arrest and evidence suggests that it may worsen survival and neurological recovery.” [4]
This association seems to hold true in the pediatric literature as well. [5-6]
Clinical Question: What is the association between sodium bicarbonate use and pediatric in-hospital cardiac arrest mortality and morbidity?
18 min