Last updated: April 17, 2023
Refractory ventricular fibrillation (VF) is explained as ventricular fibrillation which does not respond to standard defibrillation (up to 5 cycles) even after the management of epinephrine and amiodarone. The physical condition is thought to be due to sympathetic overdrive leading to cardiac vulnerability. As standard CPR and instant defibrillation are the two procedures that have exhibited a rise in ROSC and an increase in survival to hospital discharge, it shows that informal reports of refractory VF/pulseless VT have been on the up (Drennan et al., 2020)1.
Sodium bicarbonate (SB) management has been observed as an important part of the administration of severe metabolic acidosis in cardiac arrest, because, based on pathophysiologic factors, normalization of extracellular and intracellular pH was considered a meaningful endpoint of resuscitation. Treatment of metabolic acidosis with sodium bicarbonate was approved by early advanced cardiac life support (ACLS) guidelines published in 1976, and the most commonly used medication for cardiac arrest until the mid-1980s was sodium bicarbonate. However, because of questions regarding possible benefit vs harm, SB use fell steadily to almost no use by 1991, according to one study from the UK. At this moment, sodium bicarbonate administration in cardiac arrest is disputed and an affair of continuous debate and frequency of use varies greatly between medical centers. The 2020 ACLS suggestions for adults issued by the American Heart Association (AHA) state that:
“Routine use of sodium bicarbonate is not recommended for patients in cardiac arrest”
(Bryan D. Hayes, 2021)
(class III recommendation, based on the level of evidence (LOE) B) and these guidelines were not under review in the update published in 2015. However, ACLS guidelines recommend administration of SB 1 mL/kg boluses as required for hemodynamic stability (adequate mean arterial blood pressure) and QRS narrowing in cases of severe cardiotoxicity or cardiac arrest from hyperkalemia or tricyclic antidepressant overdose (class IIb recommendation, LOE C), and this suggestion was not reviewed or revised in the revision of the ACLS guidelines published in 2015. 2
Discussions concerning possible benefits vs harm from the administration of Sodium Bicarbonate have been ongoing for years. SB administration was suggested by early ACLS guidelines issued in 1976. These recommendations were continued even in 1980 when ACLS guidelines were updated, but fears about possible harm made Sodium bicarbonate use in cardiac arrest progressively disputed in recent years. As notable acidosis is connected to serious poor systematic effects, sodium bicarbonate administration appears to be a sensible intervention for the treatment of severe metabolic acidosis triggered by hypoxia, poor perfusion, and growing lactate production in cardiac arrest.
The collapse of ventilation and blood supply to body organs in cardiac arrest generates an intense disorder of homeostasis. Serious combined metabolic respiratory acidosis and damaged oxygen tissue delivery proceed to cell damage, as seen from cardiac abnormality from reduced myocardial contractility, hypotension, and renal, hepatic and central nervous system injury that can lead to a multi-organ collapse. Due to fears concerning the lethal effects of acidosis, clinicians have used sodium bicarbonate as a buffer to balance the high acid production in an attempt to help the body recover normal homeostasis in cardiac arrest.
According to data published in 1970 concerns were raised that SB administration during cardiac arrest can deteriorate the output during cardiac arrest and increase the harmful effects of bicarbonates, including increased osmolality. An experimental animal study emphasized these concerns showing that administration of SB can have harmful effects in dogs with hypoxic lactic acidosis, and the clinical data represented that patients with cardiac arrest who were treated with SB in accordance with the ACLS guidelines had dramatically lower survival if pH> 7.55 in the first 10 min after resuscitation started.
According to the data revealed in recent years suggest that SB administration can have harmful effects during cardiac arrest, comprising hiked intracellular acidosis, reduced cardiac output, a shift of the oxygen dissociation curve to the left, with a grown affinity of hemoglobin for oxygen resulting in decreased oxygen tissue release, hypernatremia, and hyperosmolarity. 2
Even though many studies have represented minor/no benefit and perhaps harm from SB administration for swift rectification of academia accompanying cardiac arrest, and the current guidelines issued by the AHA do not recommend routine administration, SB is still in use for resuscitation in cardiac arrest. More studies are required to explain further the effects of SB on organs task, on the prospect of ROSC, and on survival in patients resuscitated from cardiac arrest. 2