Updated on: June 1, 2024
Refractory ventricular fibrillation is known as ventricular fibrillation and does not respond to standard defibrillation (up to 5 cycles) even after managing epinephrine and amiodarone. The physical condition is due to sympathetic overdrive, which leads to cardiac vulnerability. Standard CPR and instant defibrillation are two distinct processes showing a rise in ROSC and an increase in survival to hospital discharge. As a result, informal reports of refractory VF and pulseless VT have been on the rise. Keep reading to explore the role of sodium bicarbonate in cardiac arrest.
Sodium bicarbonate in cardiac arrest is crucial for treating metabolic acidosis. It is based on pathophysiologic considerations, and normalization of intracellular and extracellular pH was a meaningful endpoint of resuscitation. The treatment of metabolic acidosis combined with sodium bicarbonate was earlier approved by early advanced cardiac life support (ACLS) guidelines. The treatment of metabolic acidosis with sodium bicarbonate was approved in the earlier guidelines. Sodium bicarbonate was the most commonly used medication until the mid-1980s. Due to questions regarding possible benefit vs. harm, the use reduced significantly.
This is when administration of sodium bicarb in cardiac arrest is argued upon. The frequency of use varies significantly between medical centers.
According to the 2020 ACLS suggestions for adults issued by the industry guidelines, routine use of sodium bicarbonate is not recommended for patients during cardiac arrest.
These guidelines were not under review in the update published recently in 2015. However, ACLS guidelines recommend the routine administration of SB 1 mL/kg boluses as required for hemodynamic stability and QRS narrowing in cases of severe cardiotoxicity or cardiac arrest from tricyclic antidepressant overdose or hyperkalemia. This suggestion was not revised in the revision of the ACLS guidelines published in 2015.
Read more: ACLS Immediate post-cardiac arrest care algorithm
There has been ongoing discussion about why to give sodium bicarb. It has been suggested by early ACLS guidelines. The recommendations continued even in 1980, when ACLS guidelines were updated. Fears about possible harm have made sodium bicarbonate use in cardiac arrest disputed in recent years. Notable acidosis is connected to poor systematic effects; the administration of sodium bicarbonate is a sensible intervention for treating severe metabolic acidosis triggered by poor perfusion, hypoxia, and growing lactate production in cardiac arrest.
The collapse of ventilation and blood supply to body organs creates an intense disorder of homeostasis. Eventually, this condition progresses to severe combined organic pneumonia and thrombus formation in the placenta, leading to organ damage. It causes abnormalities in the heart such as the reduction of contractility, low blood pressure, and other disorders from messing with the liver, kidneys, and central nervous system that might end up in organ failure at the end. Having concerns about the consequences of acidosis, doctors used sodium bicarbonate as a buffer, which helped balance the excess production of acid in an attempt to restore normal body homeostasis during cardiac arrest.
The cardiac performance of subjects with SB was clearly impaired. This was published in the year 1970. Then issues were raised that, during CPR, administration of sodium bicarbonate will boost the production of bicarbonate but will also deteriorate cardiac performance during cardiac arrest. The experimental work done with dogs exposed to hypoxic lactic acidosis compounded concerns that SB administration can have harmful effects in such cases. Besides, the clinical results of patients who received treatments in conformity with the ACLS guidelines and had pH levels> 7.55 in the initial 10 minutes after the restoration of circulation showed significantly lower survival rates.
As we are aware from the data from recent years, the tools provided by this method have their own risks. Often, it leads to intracellular acidosis. This further reduces cardiac output, leading to the left shift of the oxygen dissociation curve. Increasing hemoglobin affinity for oxygen results in decreased oxygen tissue release. This further causes hypernatremia, and hyperosmolarity.
Read more: ACLS Suspected Stroke Algorithm
Conclusion
So why is sodium bicarb given? Some studies have shown positive results and even harm resulting from SB usage in the resuscitation process for cardiac arrest. However, the guidelines of the AHA today do not recommend routine usage for rectification of cardiac arrest or the use of SB symptoms during resuscitation. Once the existing knowledge has been established, conduct investigations to determine the role of sodium bicarbonate in organ function, the possibility of ROSC, and the survival of patients in whom cardiac arrest has been resuscitated.