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Epinephrine in Cardiac Arrest

Epinephrine in Cardiac Arrest
Strong evidence supports the use of epinephrine as a first-line vasopressor during cardiac arrest.
Stimulates alpha-adrenergic receptors, causing vasoconstriction to improve coronary and cerebral perfusion pressures.
Standard dose is one milligram administered intravenously or intraosseously every three to five minutes.
Increases likelihood of return of spontaneous circulation (ROSC).
Recommended by advanced cardiac life support (ACLS) guidelines.

Vasopressin and Methylprednisolone
Vasopressin acts on V1 receptors to cause vasoconstriction without increasing myocardial oxygen demand.
May be combined with methylprednisolone and epinephrine to improve ROSC in specific cases.
Not a substitute for epinephrine; serves only as an adjunct therapy.
Evidence for its benefit is weaker, leading to a Class 2b recommendation.
Current guidelines suggest cautious use in select scenarios.

High-Dose Epinephrine
High-dose epinephrine refers to doses greater than one milligram per administration.
Excessive vasoconstriction impairs microcirculation and tissue perfusion.
Associated with worse neurological recovery and no survival benefit.
Studies show increased ROSC rates but poor long-term outcomes.
Classified as a Class Three Harm intervention by the American Heart Association.

Vasopressin and Methylprednisolone
Short-Term Outcomes: The VAM-IHCA trial showed improved ROSC rates with vasopressin and methylprednisolone.
Forty-two percent of patients achieved ROSC compared to thirty-three percent in the placebo group.
Vasopressin enhances vasoconstriction to improve coronary and cerebral perfusion.
Methylprednisolone may modulate inflammation and stabilize hemodynamics.
Statistically significant short-term benefits were observed.

Vasopressin and Methylprednisolone
Long-Term Outcomes: No significant improvement in survival to hospital discharge or neurological outcomes at six months.
No clear advantages in quality of life or long-term survival at one year.
Adverse effects like hyperglycemia and hypernatremia were similar between groups.
Limited evidence for routine use in clinical practice.
Suggested for specific cases under Class 2b recommendations.

High-Dose Epinephrine
Excessive stimulation of alpha-adrenergic receptors causes severe vasoconstriction.
Impairs microcirculation, reducing tissue perfusion and worsening ischemia.
Overstimulates beta-adrenergic receptors, increasing heart rate and myocardial oxygen demand.
Exacerbates myocardial ischemia and reduces recovery potential post-resuscitation.
Leads to poor neurological outcomes due to impaired cerebral microcirculation.

Clinical Implications
Focus on achieving both ROSC and favorable long-term neurological outcomes.
Standard-dose epinephrine remains the preferred vasopressor during ACLS.
Avoid high-dose epinephrine due to risks outweighing short-term benefits.
Use vasopressin and methylprednisolone cautiously as adjuncts in specific cases.
Follow evidence-based guidelines to optimize resuscitation efforts.