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Inj. Adenosine - MD Anaesthesiology Exam Notes
1. Basics
| Feature | Detail |
|---|---|
| Class | Endogenous purine nucleoside / Antiarrhythmic (unclassified - not in Vaughan-Williams) |
| Availability | 3 mg/mL injection (2 mL, 4 mL vials); preservative-free, sterile |
| Trade name | Adenocard (previously); now generic |
| Chemical | 6-amino-9-β-D-ribofuranosyl-9-H-purine |
| Endogenous source | Present in all body cells; released during hypoxia, inflammation, acute cellular injury |
2. Mechanism of Action
Adenosine acts on G-protein coupled A1 receptors on the extracellular surface of cardiac cells.
Dual mechanism:
-
Direct effect (via Gi/Go proteins):
- Activates inward-rectifier K+ channels (IK,ACh) - similar to acetylcholine
- Increased K+ conductance → hyperpolarization of membrane potential
- Shortens atrial APD, decreases atrial contractility
- Slows conduction in SA node and AV node
-
Indirect (anti-adrenergic) effect:
- Antagonizes catecholamine-stimulated adenylate cyclase
- Decreases cAMP accumulation
- Inhibits ICaL (L-type Ca2+ current) and pacemaker current (If) in SA node cells
- Decreases Vmax
Net cardiac effects:
- Transient AV nodal block (A-H interval prolongation) - 1st, 2nd, or 3rd degree, lasting seconds
- Slows sinus rate initially, then reflex tachycardia follows
- His-Purkinje system is NOT directly affected
- Normal accessory pathways are NOT blocked (unlike AV node)
- Unusual accessory pathways with long conduction/decremental properties MAY be blocked
"Adenosine interacts with G-protein coupled A1 receptors present on the extracellular surface of cardiac cells and activates K+ channels (IK,Ach)... The increase in K+ conductance shortens the atrial APD, hyperpolarizes the membrane potential, and decreases atrial contractility." - Braunwald's Heart Disease, 15e
3. Pharmacokinetics
| Parameter | Value |
|---|---|
| Elimination half-life | 1 to 6 seconds (< 10 seconds clinically) |
| Metabolism | Rapid - by vascular endothelium and erythrocytes |
| Routes of elimination | (a) Phosphorylation → AMP; (b) Deamination → inosine; (c) Cellular reuptake via nucleoside transport system |
| Metabolites | Incorporated into high-energy phosphate pool (AMP, ADP, ATP) |
| Distribution | Cleared on first pass through circulation |
| Excretion | Metabolites excreted renally |
Key point: Most effects are exerted during first passage through the circulation. This is why rapid IV bolus + flush is mandatory.
4. Indications
Primary (Therapeutic):
-
SVT - Drug of first choice for acute termination of:
- AV nodal reentrant tachycardia (AVNRT) - nearly 100% effective
- AV reentrant tachycardia (AVRT) - orthodromic type
- PSVT with or without accessory bypass tract (WPW, Lown-Ganong-Levine)
- Sinus node reentry tachycardia, atrial tachycardias (transiently)
-
RVOT-VT (Right Ventricular Outflow Tract VT): Terminates adrenergically-driven VTs (catecholamine-sensitive VTs originating in RVOT); idiopathic left septal VT rarely responds
-
Pediatric SVT: Safe and effective including neonates
Diagnostic (Unmasking):
- Differentiating wide-QRS tachycardia: Terminates SVT with aberrancy; reveals underlying atrial mechanism in AF/flutter (does not terminate AF/flutter, only produces transient AV block)
- WPW ablation: Differentiating AV nodal from accessory pathway conduction during EP study
- Stress testing: IV adenosine infusion used as a pharmacological stress agent for myocardial perfusion imaging (causes coronary vasodilation)
"Doses of 12 mg or less terminate 92% of SVTs, usually within 30 seconds." - Braunwald's Heart Disease, 15e
5. Dosing
Adults (≥50 kg):
| Step | Dose | Route | Flush |
|---|---|---|---|
| Initial | 6 mg | Rapid IV push over 1-2 sec | 20 mL NS immediately |
| If no response in 1-2 min | 12 mg | Rapid IV push | 20 mL NS immediately |
| If still no response | 12 mg (repeat once) | Rapid IV push | 20 mL NS immediately |
| Maximum single dose | 12 mg | ||
| Maximum total dose | 18 mg (doses >18 mg unlikely to revert and should not be used) |
Pediatric (<50 kg):
| Step | Dose | Max |
|---|---|---|
| Neonate | 0.05-0.1 mg/kg; increase by 0.05-0.1 mg/kg q2 min | Max single dose: 0.3 mg/kg |
| Child | 0.1 mg/kg initial | Max: 6 mg |
| Child repeat | 0.2 mg/kg, then 0.3 mg/kg q2 min | Max: 12 mg per dose |
Special populations (reduced dose):
- Central venous access: Start with 3 mg (faster delivery to heart)
- Heart transplant recipients (denervated, supersensitive): Start with 1-3 mg
- Dipyridamole co-administration: Start with 1-3 mg (potentiates adenosine)
Administration technique:
- Use the most proximal IV access available (antecubital or above)
- Use a two-way stopcock with adenosine syringe + 20 mL NS syringe
- Push adenosine first, immediately followed by 20 mL NS flush
- Must be rapid - drug is cleared in seconds; slow injection = drug degraded before reaching heart
6. Drug Interactions
| Drug | Interaction | Action |
|---|---|---|
| Methylxanthines (theophylline, caffeine, aminophylline) | Competitive antagonists at A1 receptor - BLOCK adenosine effects | Increase adenosine dose; may need 12 mg as starting dose |
| Dipyridamole | Blocks nucleoside transport (reuptake blocker) - POTENTIATES adenosine | Reduce dose to 1-3 mg |
| Carbamazepine | Blocks adenosine uptake - POTENTIATES | Reduce dose |
| Digoxin | Enhanced depressant effects on SA/AV nodes | Use with caution |
| Beta-blockers | Additive AV nodal depression | Use with caution |
| Verapamil/Diltiazem | Additive nodal effects | Use with caution |
| Atropine | Does NOT block adenosine (unlike vagal effects) | Atropine ineffective against adenosine-induced bradycardia |
7. Adverse Effects
Side effects occur in ~40% of patients but are transient (< 1 minute):
Common (benign, self-limiting):
- Flushing (most common)
- Dyspnea / chest tightness (feel of impending doom - warn patient!)
- Headache
- Nausea
- Lightheadedness
- Chest pain/pressure
Cardiac (expected, transient):
- Transient asystole/sinus arrest (lasts 3-15 seconds - this is the therapeutic effect and is self-terminating)
- Sinus bradycardia
- AV block (1st, 2nd, 3rd degree - all transient)
- PVCs on termination
Serious / Clinically Important:
- Atrial fibrillation (12% in one study) - due to shortening of atrial refractoriness. DANGEROUS in WPW because AF + rapid accessory pathway conduction can cause VF
- Bronchospasm - significant risk in asthmatics (adenosine activates A2B receptors on mast cells/bronchi)
- Hypotension (with high-dose infusions)
- Re-initiation of tachycardia (due to short duration of action) - repeat dosing or switch to CCB (verapamil)
8. Contraindications
Absolute:
- 2nd or 3rd degree AV block (without functioning pacemaker)
- Sick sinus syndrome (without pacemaker)
- Severe reactive airway disease / active bronchospasm / asthma
- Hypersensitivity to adenosine
- AF/flutter with WPW - AV blockade may increase conduction through accessory pathway → VF
Relative:
- Long QT syndrome
- Severe COPD
- Concomitant dipyridamole use (reduce dose instead)
9. Anaesthesia-Specific Considerations
| Scenario | Notes |
|---|---|
| Controlled hypotension | Adenosine infusion (50-200 mcg/kg/min) can produce controlled hypotension intraoperatively, though not a routine agent |
| Cardiac surgery | Used during EP studies; role in cardioplegia enhancement (adenosine preconditioning) |
| Cardiac transplant patients | Denervated heart - supersensitive response; start with 1 mg |
| In theatre SVT | Drug of choice for perioperative SVT; fast-acting, doesn't impair contractility |
| No effect on contractility | Unlike verapamil, adenosine does NOT cause prolonged hemodynamic compromise |
| Preferred over verapamil when: | - Patient on IV beta-blockers pre-op - Poorly compensated heart failure - Severe hypotension - Neonates |
| Verapamil preferred when: | - Patient on theophylline (blocks adenosine) - Active bronchoconstriction - Poor IV access |
| Renal impairment | No dose adjustment required (metabolized outside kidney) |
| Pregnancy | Safe and effective |
10. Comparison: Adenosine vs Verapamil for SVT
| Feature | Adenosine | Verapamil |
|---|---|---|
| Onset | Seconds | 1-2 minutes |
| Duration | < 10 seconds | 30-60 minutes |
| Contractility | Not affected | Negative inotrope |
| Use in heart failure | Safe | Caution |
| Use in hypotension | Safe | Risky |
| Use in asthma | Contraindicated | Safe |
| Use in theophylline patient | Needs higher dose | First choice |
| Bradycardia | Transient | Prolonged possible |
| Preferred in neonates | Yes | No |
| Can cause AF | Yes (12%) | No |
11. Quick Exam Mnemonics
"ADENOSINE works in SVT":
- A - A1 receptor activation (G-protein coupled)
- D - Decreases AV conduction (transient block)
- E - Endogenous nucleoside
- N - Nucleoside transport blocked by dipyridamole (potentiates)
- O - Open K+ channels → hyperpolarization
- S - Short half-life (< 10 seconds)
- I - Inhibits cAMP via anti-adrenergic effect
- N - Not blocked by atropine
- E - Effective in 92% of SVTs at ≤12 mg
Dose remember: "6 then 12 then 12" (adults); "0.1 then 0.2 then 0.3 mg/kg" (peds, max 6/12/12 mg)
12. Key Exam Points (High-Yield)
- Adenosine is NOT classified in Vaughan-Williams system
- Half-life < 10 seconds - shortest of any antiarrhythmic
- Drug of choice for acute AVNRT/AVRT - nearly 100% effective
- Works by A1 receptor → K+ channel activation + anti-adrenergic effect
- Theophylline BLOCKS (need higher dose); Dipyridamole POTENTIATES (need lower dose)
- NOT blocked by atropine
- Does NOT affect normal accessory pathways
- Can terminate RVOT-VT (catecholamine-sensitive VT)
- In WPW + AF - adenosine is dangerous (may precipitate VF)
- Warn patient about transient chest pain and dyspnea before injecting
- Causes AF in 12% - due to shortening of atrial refractoriness
- Administration: proximal vein, fast push, 20 mL NS flush immediately
- Heart transplant patients: start at 1-3 mg (supersensitive denervated heart)
- Does not impair myocardial contractility - advantage over CCBs
- Meta-analysis (2025): 12 mg initial dose may have better first-attempt conversion vs 6 mg stepwise approach - guideline reassessment ongoing
Sources: Braunwald's Heart Disease 15e | Fuster & Hurst's The Heart 15e | Miller's Anesthesia 10e | Roberts & Hedges' Clinical Procedures in Emergency Medicine | Harriet Lane Handbook 23e
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