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VasopressorsBrands: Adrenalin

Epinephrine

Epinephrine — Potent Alpha-1, Beta-1, and Beta-2 Adrenergic Agonist

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💡 ICU High-Yield Summary: Potent direct alpha/beta agonist for anaphylactic shock, cardiac arrest, post-cardiac arrest shock, and refractory septic shock — powerful inotrope and bronchodilator with transient hyperlactatemia.
🫀 Compare this agent in the Vasopressors & Inotropes MasterclassOpen →🫁 Compare this agent in the Respiratory & Airway Pharmacology MasterclassOpen →⚡ Compare this agent in the Cardiac Arrest & Peri-Arrest Pharmacology MasterclassOpen →🚨 Compare this agent in the Anaphylaxis & Refractory Allergy Pharmacology MasterclassOpen →

🧬 Mechanism of Action & Target Pathway

Pan-Adrenergic Receptor Agonism

  1. Low dose (0.01–0.05 mcg/kg/min): Predominant Beta-1 and Beta-2 agonism → Increased CO, HR, and bronchodilation.
  2. High dose (>0.1 mcg/kg/min): Alpha-1 agonism predominates → Potent systemic vasoconstriction and MAP rise.
  3. Beta-2 hepatic stimulation accelerates glycolysis, causing transient type B hyperlactatemia.
Beta-1/Beta-2 Agonism (Low Dose) → Alpha-1 Agonism (High Dose) → Inotropy + Vasoconstriction

Pharmacokinetics & Pharmacodynamics (PK/PD) — Epinephrine

receptor occupancy
Target ParameterMAP ≥ 65 mmHg and ROSC in cardiac arrest
Half-Life (t1/2)1 to 2 minutes
Protein BindingMinimal
Primary EliminationRenal urine excretion of metabolites (VMA)
Metabolism Pathway:Hepatic MAO and COMT metabolism
Volume of Distribution Notes:Intravascular distribution

⚖️ ICU Clinical Reasoning

Why I Choose It (Indications & Strengths)

  • ✓First-line treatment for anaphylaxis; give IM epinephrine promptly in the anterolateral thigh unless IV epinephrine is specifically required in a monitored refractory setting.
  • ✓First-line vasopressor/inotrope in Cardiac Arrest (ACLS 1 mg IV q3–5 min).
  • ✓An additional vasoactive option in septic shock when norepinephrine-based therapy is insufficient; current sepsis guidance also allows epinephrine in selected patients with persistent hypoperfusion or escalating vasopressor needs.

Why I Don't (Limitations & Gaps)

  • ✕Profound tachyarrhythmias and myocardial ischemia.
  • ✕Causes non-hypoxic Type B hyperlactatemia (can obscure sepsis clearance).
  • ✕Splanchnic vasoconstriction.
⭐ Bedside Pearl: Epinephrine stimulates hepatic beta-2 receptors causing glycogenolysis and transient hyperlactatemia — do not confuse epinephrine-induced Type B hyperlactatemia with worsening tissue hypoperfusion!

💉 Dosing & Administration Protocols

Routine ICU Dosing

Septic-shock hypotension (current U.S. label): 0.05–2 mcg/kg/min IV infusion, titrated to the desired MAP and weaned gradually. Adult anaphylaxis: 0.3–0.5 mg IM in the anterolateral thigh; may repeat every 5–10 minutes as needed. Adult cardiac arrest: epinephrine 1 mg IV/IO every 3–5 minutes per AHA ALS guidance.

Renal Function Dosing

CrCl RangeDose Adjustment
Renal impairmentCurrent U.S. labeling does not provide a renal dose-adjustment table; titrate the infusion to hemodynamic response and monitor renal perfusion.

Dialytic Clearance (HD / CRRT)

Intermittent Hemodialysis (HD):No label-based dialysis-specific regimen is required; titrate to hemodynamic response rather than assuming dialysis clearance is clinically relevant.
Continuous Renal Replacement (CRRT):No CRRT-specific numeric regimen is established; titrate to hemodynamic response.

🩺 Organ Failure Considerations

Renal Failure & AKI

Current labeling does not provide a renal dose-adjustment algorithm for shock infusion; titrate to effect and monitor perfusion, arrhythmia and ischemic complications.

Hepatic Impairment & Cirrhosis

Rapidly metabolized; no universal hepatic dose-adjustment algorithm is provided in current labeling, so titrate to effect.

⚠️ Toxicity & Safety Warnings

Major Warnings

  • 🚨Tachyarrhythmias, myocardial ischemia, extravasation necrosis, severe hypertension.

🔄 Bedside Drug Interactions

Interacting DrugMechanismClinical ConsequenceMandatory ICU Action
Non-selective Beta-BlockersUnopposed alpha-1 stimulationSevere hypertension and bradycardiaUse alternative inotrope.

📊 Monitoring & TDM Protocols

Required Monitoring Parameters

  • ▪ Continuous arterial blood pressure
  • ▪ Heart rate and ECG rhythm
  • ▪ Serum lactate and blood glucose

Evidence Status

Current

Last Medically Reviewed

2026-08-28

Evidence Checked Through

2026-08-28

Notes: Direct claim-level source traceability is present; current status retained after the 2026-08-29 medication audit.

📚 Evidence Traceability & Guideline Citations

"Current labeling supports epinephrine infusion for septic-shock hypotension at 0.05–2 mcg/kg/min, titrated to MAP; AHA adult ALS recommends 1 mg every 3–5 minutes during cardiac arrest."

Source: Epinephrine Injection U.S. Prescribing Information, DailyMed 2026; AHA Adult Advanced Life Support guidance.View Reference ↗

🩺 Bedside Patient Scenarios

Anaphylactic Shock with Airway Edema

Scenario: Severe bronchospasm and hypotension after penicillin administration.

Bedside Decision: Administer Epinephrine 0.3 mg IM immediately in mid-outer thigh.

Rationale: Reverses bronchospasm via beta-2 and corrects vasodilation via alpha-1.

🎯 Exam Traps & Board Misconceptions

❌ Misconception:"A rise in lactate after starting epinephrine means the patient's septic shock is worsening."
✓ Reality: FALSE. Epinephrine stimulates hepatic beta-2 receptors causing non-hypoxic Type B hyperlactatemia.

Interpret lactate in the full clinical context; epinephrine can increase lactate through beta-adrenergic metabolic effects, so a rise is not by itself proof of worsening tissue hypoperfusion.

🫀 Physiology & Hemodynamics

Epinephrine

drug
SVR
↑Increased
Heart Rate
↑↑Strongly Increased
Contractility
↑↑Strongly Increased
Preload
↑Increased
Afterload
↑Increased
Cardiac Output
↑↑Strongly Increased
MAP
↑↑Strongly Increased
PVR
↑↓Variable
Myocardial O₂ Demand
↑↑Strongly Increased

Mechanism

Potent β1 + β2 + α1 agonism. Dose-dependent: lower doses β-dominant (inotropy/chronotropy), higher doses α-dominant (vasoconstriction).