Epinephrine, also known as adrenaline, is a naturally occurring hormone used as a medication during life-threatening emergencies. In resuscitation, it is a standard component of advanced cardiac life support protocols. Cardiac arrest occurs when the heart stops effectively pumping blood, leading to a collapse of circulation and the absence of a pulse. Immediate intervention, including cardiopulmonary resuscitation (CPR), is required to manually circulate blood and oxygen. Epinephrine is administered to support these manual efforts and attempt to restore a functional heart rhythm.
Epinephrine’s Role in Restarting Circulation
The beneficial effects of epinephrine during resuscitation are primarily driven by its interaction with alpha-adrenergic receptors. This interaction causes intense, widespread peripheral vasoconstriction, which is the narrowing of arteries in non-central areas. This powerful squeezing action forces blood out of the periphery and back toward the core circulation. By constricting these vessels, epinephrine increases the overall pressure within the major arteries, particularly the aorta.
This increased pressure drives blood flow to the heart muscle during the chest relaxation phase of CPR. The measurement for this effect is the Coronary Perfusion Pressure (CPP), defined as the pressure difference between the aorta and the right atrium. Adequate blood flow delivers oxygen and energy substrates necessary for the heart to potentially restart. Research indicates that a CPP above 15 millimeters of mercury (mmHg) is associated with successful resuscitation.
The standard dose is administered every three to five minutes to maintain central vasoconstriction and maximize CPP. Epinephrine also interacts with beta-adrenergic receptors, increasing heart rate and contractility. However, in a non-beating heart, alpha-adrenergic vasoconstriction remains the drug’s most important immediate action. This manipulation of vascular tone is the central purpose of administering the drug during the initial phase of resuscitation.
Achieving Return of Spontaneous Circulation
The immediate desired outcome of CPR and epinephrine is the Return of Spontaneous Circulation (ROSC). ROSC is the successful restoration of a sustained heart rhythm strong enough to produce a pulse and generate blood pressure. Epinephrine increases the likelihood of achieving this immediate goal in both in-hospital and out-of-hospital cardiac arrests. This short-term success is a prerequisite for a patient surviving the event.
The drug’s ability to raise the CPP above the threshold is the direct mechanism leading to higher rates of ROSC. For patients with non-shockable rhythms, such as asystole or pulseless electrical activity, epinephrine is important because defibrillation is not an option. In these circumstances, the drug is one of the few interventions available to improve the heart’s environment. Patients who receive epinephrine have a higher rate of achieving ROSC and subsequent survival to hospital admission.
Despite improved immediate resuscitation rates, this short-term gain does not always translate into a positive long-term outcome. While epinephrine increases the number of people who have their heart restarted, the overall effect on survival to hospital discharge is less pronounced. This disparity highlights the complexity of post-resuscitation care and the drug’s varied physiological effects. The limitations of this short-term benefit lead to the controversy surrounding the drug’s continued use.
The Unintended Consequences of Epinephrine Use
While epinephrine’s alpha-adrenergic effects are beneficial during the arrest, they carry significant unintended consequences that can impair recovery. The drug’s beta-adrenergic stimulation increases the heart muscle’s need for oxygen, which is detrimental after the heart restarts. Once circulation is restored, the revived heart faces an increased workload due to the drug-induced increase in heart rate and contractility. This increased myocardial oxygen demand can exacerbate injury, potentially leading to post-resuscitation cardiac dysfunction.
A major concern revolves around the drug’s effect on microcirculation, particularly in the brain. The intense vasoconstriction that improves pressure in large central vessels can paradoxically impair blood flow in smaller capillaries and arterioles. This microcirculatory dysfunction reduces the delivery of oxygen and nutrients to the brain tissue, even after a pulse is restored. This effect can persist after administration, leading to a prolonged period of reduced tissue perfusion.
This microcirculatory impairment creates a trade-off where improved immediate survival may come at the cost of neurological function. Evidence suggests that while epinephrine increases the chance of ROSC, it may negatively impact the rate of survival with favorable neurological outcomes. The reduced cerebral microcirculation can cause ischemic damage, or brain injury from insufficient blood flow, despite the re-establishment of normal blood pressure. This complex interaction is the primary reason epinephrine remains a subject of ongoing research and debate.