Adrenaline is a potent **β₁/β₂/α₁ agonist** with **dose-dependent** inotropy, chronotropy, bronchodilation, and vasoconstriction.
It’s the **drug of choice for anaphylaxis**, a powerful **inopressor** for LCOS/post-CPB or refractory septic vasoplegia, and the standard **ALS** vasopressor.
Typical ICU/OR infusion **0.02–0.2 (up to 0.5) mcg/kg/min**; use central access and be vigilant for **arrhythmias, ischaemia, lactate rise, hypokalaemia**, and **extravasation injury.
# 1) Receptor-level action → clinical effects
**Primary receptors (dose-dependent):**
* **β₁ agonist** → ↑ inotropy, ↑ chronotropy, ↑ dromotropy → ↑ **CO**.
* **β₂ agonist** → **bronchodilation**, skeletal-muscle vasodilation, **↓ mast-cell mediator release**; metabolic effects (↑ glucose, **↓ K⁺** via cellular shift).
* **α₁ agonist** (more prominent at higher doses) → **arterial/venous vasoconstriction** → ↑ **SVR/MAP**.
**Clinical phenotype by dose (rule of thumb):**
* **Very low–low** (≤0.02–0.05 mcg/kg/min): β₁/β₂ dominant → ↑ CO, mild ↓ SVR.
* **Moderate** (0.05–0.2): balanced β + α → ↑ CO **and** ↑ SVR.
* **High** (>0.2): α₁ predominant → marked vasoconstriction; risk of ↑ afterload, ischaemia, lactate rise.
**Key bedside effects**
* **Heart:** powerful inotrope/chronotrope; may precipitate **AF/VT/VF**, ↑ myocardial O₂ demand → **ischaemia**.
* **Vessels:** dose-dependent vasoconstriction (skin/splanchnic) or vasodilation (muscle) → net MAP usually rises with moderate–high doses.
* **Lungs:** **bronchodilation**; cornerstone for **anaphylaxis**.
* **Metabolic:** **hyperglycaemia**, **lactataemia** (β-driven glycolysis; not always tissue hypoperfusion), **hypokalaemia** (β₂ shift).
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# 2) Vial strength, preparation & basic pharmacokinetics (+ disadvantages)
**Common presentations**
* **1 mg/mL** (1:1000) amp (IM use; can be diluted for infusions).
* **0.1 mg/mL** (1 mg in 10 mL; 1:10,000) prefilled syringe (IV bolus for ALS).
* Infusion mixes (ICU/OR): **4 mg in 50 mL** (80 mcg/mL) or **1 mg in 50 mL** (20 mcg/mL). Central line preferred.
**PK**
* **Onset IV:** < 1 min; **peak:** minutes; **offset:** 1–3 min after stop.
* **t½:** ~2–3 min; **metabolism:** MAO & COMT → inactive; **excretion:** renal metabolites.
**Disadvantages from PK/PD**
* Requires **continuous infusion**; narrow titration window.
* **Tachyarrhythmias**, **lactate rise**, **hyperglycaemia**.
* **Peripheral extravasation** can cause **ischaemic necrosis**.
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# 3) Practical dosing
## A. Anaesthesia / Cardiac theatre
**Indications:** post-CPB myocardial stunning/LCOS, anaphylaxis under anaesthesia, refractory hypotension with low CO.
* **Post-CPB/LCOS infusion:** start **0.02–0.05 mcg/kg/min**, titrate q2–5 min by 0.01–0.02; typical **0.02–0.2 mcg/kg/min** (higher if refractory).
* **Rescue bolus (careful):** 10–20 **mcg** IV aliquots (0.1–0.2 mL of 1:10,000) for transient hypotension while starting infusion.
* **Math example (70 kg @ 0.1 mcg/kg/min = 7 mcg/min):** with **80 mcg/mL** → **5.25 mL/h**.
## B. ICU
**Indications:** vasodilatory shock with low CO (septic/post-CPB vasoplegia), cardiogenic shock as an inopressor when dobutamine/milrinone insufficient.
* **Start:** **0.02–0.05 mcg/kg/min**; **range:** **0.02–0.5 mcg/kg/min**.
* Combine with **norepinephrine** when SVR is very low; or with **inodilator** (dobutamine/milrinone) if afterload high and contractility poor.
## C. Life-threatening emergencies (for completeness)
* **Adult cardiac arrest (ALS):** **1 mg IV** (1:10,000) every 3–5 min cycles.
* **Anaphylaxis (adult):** **0.5 mg IM** (1:1000) mid-outer thigh; repeat q5 min PRN. Refractory → **IV infusion** (e.g., 1–4 mcg/min then titrate) under monitoring.
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# 4) Special populations — dosing cautions
### Pregnancy
* First-line for **anaphylaxis** in pregnancy (maternal life priority); can reduce uterine blood flow at high IV doses—use **IM first** when appropriate and titrate IV carefully intra-op.
### Lactation
* Minimal oral bioavailability for infant; short t½; single/emergency doses acceptable.
### Hepatic impairment
* Widely metabolised extrahepatically; **no formal adjustment**—**titrate to effect**.
### Renal impairment
* Metabolites renally excreted but inactive; **no adjustment**. Watch perfusion and urine output.
### Obesity
* Start with **IBW/AdjBW-based** rates to avoid overshoot; titrate to haemodynamics.
### Paediatrics
* **Anaphylaxis IM:** **0.01 mg/kg** (1:1000), max **0.5 mg**.
* **Infusion:** **0.02–1 mcg/kg/min** titrated in specialist setting.
* **Cardiac arrest:** **0.01 mg/kg IV** (1:10,000 = 0.1 mL/kg).
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# 5) Drug interactions (clinically key)
* **MAO inhibitors / TCAs / SNRIs:** **exaggerated pressor** and arrhythmic responses → start at **very low doses** or avoid.
* **Non-selective β-blockers** (e.g., propranolol): **unopposed α₁ vasoconstriction** → severe hypertension/bradycardia; bronchospasm risk persists (β₂ blocked).
* **Halogenated volatiles (esp. halothane):** myocardial sensitisation → **ventricular arrhythmias**.
* **Digoxin:** arrhythmia risk ↑.
* **Insulin/oral hypoglycaemics:** hyperglycaemia from epi may necessitate higher insulin.
* **Inhaled β₂-agonists:** additive hypokalaemia—monitor K⁺.
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# 6) Significant complications & management
| Complication | Mechanism / Features | Management |
| ------------------------------------------------------ | ---------------------------------------------------- | ------------------------------------------------------------------------------------------------------------------------------------------------ |
| **Tachyarrhythmias (AF/VT/VF)** | β₁ excess, esp. hypoxia/acidosis | Reduce/stop; correct K⁺/Mg²⁺; antiarrhythmics/defibrillate per ACLS. |
| **Myocardial ischaemia** | ↑ MVO₂ + ↑ afterload | Lower dose; add inodilator; ensure adequate MAP/CPP and treat pain/anaemia. |
| **Severe hypertension / limb or mesenteric ischaemia** | α₁ vasoconstriction at high dose | Titrate down; reconsider target MAP; balance with inodilator. |
| **Lactataemia** (β-driven) | Accelerated glycolysis—not necessarily hypoperfusion | Interpret with context; check ScvO₂/echo; don’t chase lactate alone. |
| **Hypokalaemia** | β₂-mediated intracellular shift | Monitor K⁺; replace if needed. |
| **Hyperglycaemia** | Glycogenolysis/gluconeogenesis | Adjust insulin. |
| **Extravasation necrosis** | Intense local α₁ vasoconstriction | **Stop infusion, leave cannula**, **phentolamine 5–10 mg** in 10–15 mL saline infiltrated around site; warm compress; surgical review if severe. |
| **Pulmonary oedema** | Afterload ↑ + tachycardia | Reduce dose; diuretics/vasodilator if appropriate; optimise ventilation. |
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