Resuscitation for Cardiac Arrest Should Begin and End with Basic Life Support

Submitted by Michael R. Swift, RN, BSc, BSN, CEN, CCRN, TCRN

Tags: cardiac cardiac arrest epinephrine heart attack heart disease

Resuscitation for Cardiac Arrest Should Begin and End with Basic Life Support

Share Article:

Advanced Cardiovascular Life Support (ACLS) consists of a number of medical interventions used for people who have had a cardiac arrest or other cardiovascular emergency. ACLS is performed by trained healthcare personnel and is a higher level of care beyond Basic Life Support (BLS) which is “the foundation for saving lives after cardiac arrest [1].” In addition to BLS skills, ACLS utilizes medical interventions which include the insertion of intravenous (IV) lines; the administration of epinephrine (adrenaline); the usage of 100% oxygen; the placement of an advanced airway such as an endotracheal tube; and the collaboration of a team of healthcare professionals.

The American Heart Association (AHA) is the nation’s leading advocate for emergency cardiovascular care, BLS, and ACLS research and training. The AHA teaches that the BLS “Chain of Survival” is one that begins with recognizing a victim of an apparent cardiac arrest and notifying emergency medical services. The core skills of BLS are performing high-quality chest compressions, giving breaths (ventilation), and using an automatic external defibrillator (AED) [1]. Both BLS and ACLS are universally recognized and promoted as potentially life-saving interventions. Their use is considered the standard of care in healthcare [2] [3].

Individually and collectively, BLS and ACLS are also known as cardiopulmonary resuscitation (CPR) [4]. The primary goal of CPR says Marini and Wheeler (1997) is to “preserve neurologic function by rapidly restoring oxygenation, ventilation, and circulation to patients with arrested circulation [5].” In 2000, the AHA’s goals for patients receiving ACLS CPR aligned with their goals for those receiving BLS CPR. At that time, the AHA declared, “Cerebral resuscitation - returning the patient to the level of neurological functioning he or she had before the arrest - stands as the ultimate purpose of all resuscitative efforts [6].”

Far from achieving its ultimate purpose, the AHA’s CPR interventions have also failed to show steady progress in saving the lives of cardiac arrest patients. According to recent non-traumatic cardiac arrest survival data, the US out-of-hospital cardiac arrest (OHCA) survival to hospital discharge rate in 2012 was 11.4%. Nearly a decade later (2021), the OHCA survival rate stood at 9.1% [7]. Finding the ultimate goal of restoring baseline neurological function elusive, the AHA quietly revised its goals. It now emphasizes what it calls a return of spontaneous circulation or ROSC [8]. In the pursuit of ROSC, the AHA recommends epinephrine (adrenaline) in ACLS [3].

Epinephrine is a circulating endogenous hormone and an alpha and beta receptor agonist. Zaritsky and Chernow (1989) inform us that “Normal plasma epinephrine concentrations are in the range of 24-74 pg/ml [9].” Epinephrine stimulates smooth muscle vasoconstriction when it binds to alpha receptors. When it binds to beta receptors, it increases the strength and rate of heart contractions while also increasing myocardial oxygen demand [2] [9]. And while epinephrine produces little constriction of normal coronary arteries, it causes pronounced vasoconstriction in arteries with atherosclerotic endothelium [10]. In cardiac arrests not involving trauma, respiratory failure, congenital, endocrine, or toxicological causes, atherosclerotic coronary vessels are a common cause [3] [4] [11]. Thus, it is most likely an occlusion of one or more coronary vessels that lead to cardiac arrest [3] [11].

Epinephrine HCl has a long-standing and central role in ACLS. It is given at a dose of 1 mg every 3-5 minutes intravenously during cardiac arrest [8]. This is about 2000 times the normal concentration found in the plasma (Epinephrine 1 mg/5000 ml of blood volume = 0.0002 mg/ml = 200,000 pg/ml ÷ 100 pg/ml = 2000 pg/ml). Numerous studies have shown that even when this massive dose of epinephrine is effective in restoring a perfusing cardiac rhythm, it is also associated with severe cerebral and cardiac side effects [2] [12] [13] [14]. Moreover, even the AHA concedes that the administration of epinephrine does nothing to increase a patient’s long-term chances of survival after cardiac arrest [8]. This information alone should make us abandon the use of a drug which offers nothing of benefit to the patient that is superior to BLS CPR [3] [15] [16].

Still, the AHA says that it recommends the use of epinephrine in ACLS because it can improve aortic diastolic blood pressure, coronary artery perfusion pressure, and the rate of ROSC [8]. To this, we should ask: Are these hemodynamic improvements beneficial to the patient, and if so, is there a trade-off? Then we should ask whether these changes can return the patient to the level of neurological functioning he or she had before the arrest. These questions should be asked because the original intent of ACLS and the use of epinephrine was to return the patient to their baseline neurological status [6]. And if ACLS and epinephrine are unable to do this, then their use is pointless. In fact, according to Calloway (2013), “On the basis of observational data and limited clinical trials, standard dose epinephrine does not increase and may actually reduce long-term survival and neurological recovery after CPR [17].”

Achieving ROSC only to leave the patient comatose and ventilator-dependent due to an anoxic brain injury is morally unjustifiable. In fact, 80% of cardiac arrest patients never wake up despite receiving standard CPR  [18].  So why does the AHA continue to promote epinephrine in cardiac arrest although it is no more effective in a patient’s recovery than a placebo [2]? Two reasons are sometimes offered for the continuation of this recommendation. One is that achieving ROSC in a cardiac arrest patient gives family members more time to say their final goodbyes. Another is that the extra survival time for these patients allows more time for organ and tissue donation [19]. Neither reason is morally sound or beneficial to the patient.

Alternatively, there may be other, less altruistic, reasons for achieving ROSC that are not mentioned by the AHA. For example, intensive care unit (ICU) admissions and skilled nursing facility (SNF) placement of cardiac arrest survivors with poor neurological outcomes provide revenue for hospitals, SNFs, and the myriad of physicians and other specialists that are needed to maintain them. In fact, according to a 2018 study, the healthcare costs after cardiac arrest in the United States is an estimated $33 billion per year [20]. Is it not plausible that this influences the emphasis on ROSC?

Also, the AHA is a 501(c) tax-exempt corporation with over $1.6 billion in reported assets [21]. Its 2021-2022 tax statement indicates that it received $880 million in total revenue for the fiscal year [21]. Consider now that most patients in whom initial ROSC is achieved are admitted to the ICU where they die within 24 hours from a subsequent cardiac arrest [8]. In order to survive their emergency room visit and get admitted to the ICU, however, ACLS training of healthcare workers (HCW) is needed to delay the patient’s death. Therefore, every 2 years ACLS recertification/renewal training is required for HCWs at a cost of about $200 per HCW. According to their tax records, the AHA’s CPR training activities for the 2021-2022 tax year - after expenses - generated $15 million in revenue for the organization [21]. Thus, revenue and jobs for the AHA and its affiliated partners could be another motivation for the AHA to push for ROSC through ACLS interventions.

In conclusion, the recommended administration of epinephrine in ACLS is of no proven benefit to the cardiac arrest patient [17]. The only tangible benefit of the ACLS interventions used on these patients is increased revenue for the AHA, hospitals, and healthcare providers. Meanwhile, the most important outcome needed from an ACLS intervention on a cardiac arrest patient - good neurological recovery - goes lacking. Epinephrine, which decreases cerebral microcirculation, virtually assures that the cardiac arrest patient will be unable to awaken from their post-resuscitation coma [19]. Most of these patients can expect to remain comatose, on a ventilator, and in a vegetative state until death [18]. Consequently, until the AHA can demonstrate a neurological benefit for cardiac arrest patients subjected to ACLS interventions, epinephrine use should be discontinued, and resuscitation for cardiac arrest patients should begin and end with basic life support.


  1. American Heart Association, Basic Life Support Provider Manual, Dallas: American Heart Association, 2020.
  2. J. Jung, J. Rice and S. Bord, "Rethinking the role of epinephrine in cardiac arrest: the PARAMEDIC2 trial," Ann Transl Med, vol. 6(Suppl 2), no. S129, 2018.
  3. B. Long and A. Koyfman, "Emergency Medicine Myths: Epinephrine in Cardiac Arrest," The Journal of Emergency Medicine, vol. 52, no. 6, pp. 809-814, 2017.
  4. R. O'Connor, "Cardiac Arrest and Cardiopulmonary Resuscitation," in The Merck Manual (20th ED.), Kenilworth, Merck Sharp & Dohme, 2018, p. 539.
  5. J. Marini and A. Wheeler, Critical Care Medicine: The Essentials (2nd ED.), Baltimore: Williams & Wilkins, 1997.
  6. American Heart Association, ACLS Provider Manual, Dallas: American Heart Association, 2000.
  7. American Heart Association, "Heart Disease and Stroke Stats - 2023 Update: A Report from the American Heart Association," Circulation, vol. 147, no. 8, 2023.
  8. American Heart Association, Advanced Cardiovascular Life Support, Dallas: American Heart Association, 2020.
  9. A. Zaritsky and B. Chernow, "Catecholamines and Other Inotropes," in Essentials of Critical Care Pharmacology, Baltimore, Williams & Wilkins, 1989, pp. 236-254.
  10. B. Jensen, P. Swigart, M. Laden, T. DeMarco, C. Hoopes and P. Simpson, "The Alpha-1D is the Predominant Alpha-1-Adrenergic Receptor Subtype in Human Epicardial Coronary Arteries.," Journal of the American College of Cardiology, vol. 54, no. 13, pp. 1137-1145, 2009.
  11. M. Sorenson, L. Quinn and D. Klein, Pathophysiology: Concepts of Human Disease, New York: Pearson, 2019.
  12. G. Ristagno, W. Tang, L. Huang, A. Fymat, Y. Chang, S. Sun, C. Castillo and M. Weil, "Epinephrine reduces cerebral perfusion during cardiopulmonary resuscitation," Critical Care Medicine, vol. 37, no. 4, pp. 1408-15, 2009.
  13. G. Ristagno, S. Sun, W. Tang, C. Castillo and M. Weil, "Effects of epinephrine and vasopressin on cerebral microcirculatory flows during and after cardiopulmonary resuscitation," Critical Care Medicine, vol. 35, no. 9, pp. 2145-9, 2007.
  14. O. Oghifobibi, A. Toader, M. Nicholas, B. Nelson, N. Alindogan, M. Wolf and e. al., "Resuscitation with epinephrine worsens cerebral capillary no-reflow after experimental pediatric cardiac arrest: an in vivo multiphoton microscopy evaluation," Journal of Cerebral Blood Flow & Metabolism, vol. 42, no. 12, pp. 2255-2269, 2022.
  15. F. Dumas, W. Bougouin, G. Geri, L. Lamhaut, A. Bougle, F. Daviaud and e. al., "Is epinephrine during cardiac arrest associated with worse outcomes in resuscitated patients?," Journal of the American College of Cardiology, vol. 64, no. 22, pp. 2360-7, 2014.
  16. T. Olasveengen, L. Wik, K. Sunde and P. Steen, "Outcome when adrenaline (epinephrine) was actually given vs. not given - post hoc analysis of a randomized clinical trial," Resuscitation, vol. 83, pp. 327-332, 2012.
  17. C. Calloway, "Epinephrine for Cardiac Arrest," Curr Opin Cardiol, vol. 28, no. 1, pp. 36-42, 2013.
  18. H. Lurie, E. Nemergut, D. Yannopoulos and M. Sweeney, "The Physiology of Cardiopulmonary Resuscitation.," Anesthesia & Analgesia, vol. 122, no. 3, pp. 767-778, 2016.
  19. M. Welsford, J. Buick, I. Drennan, S. Lin and P. Atkinson, "#Epi: There is no place for the use of intravenous epinephrine as a standard component of cardiac arrest resuscitation care.," Canadian Journal of Emergency Medicine, vol. 21, no. 3, pp. 324-329, 2019.
  20. A. Damluji, S. Pomenti, T. Zhang, M. Cohen, R. Mitrani, M. Moscucci and R. Meyerburg, "Health Care Costs After Cardiac Arrest in the United States.," Circulation: Arrhythmia and Electrophysiology, vol. 11, no. 4, pp. 1-10, 13 Apr 2018.
  21. American Heart Association, "American Heart Association, Inc. Financial Highlights," American Heart Association, 2021-2022.