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Clinical Pharmacology Case 12 — Complete Answer
Case Summary
58-year-old male, history of asthma, coronary heart disease, hypertension. Presents with rapid heartbeat, shortness of breath, fear of death. ECG: reciprocal AV supraventricular tachycardia at 230 bpm, scar fields on posterior-diaphragmatic wall of left ventricle. BP 130/80 mmHg, muted heart tones, pronounced tachycardia, no wheezing.
Station 1
1. Diagnosis
Paroxysmal Supraventricular Tachycardia (PSVT) — specifically reciprocal (re-entrant) AV nodal tachycardia at 230 bpm, in a patient with underlying coronary artery disease (evidenced by posterior-diaphragmatic scar), asthma, and hypertension.
2. P-medication (Drug of Choice)
Adenosine — the drug of first choice for prompt conversion of paroxysmal SVT to sinus rhythm (efficacy 90–95%).
Why not verapamil? Verapamil is the second option; it can cause hemodynamic deterioration in patients with poor LV function (scar fields suggest prior MI). Why not β-blockers? Contraindicated due to history of asthma. Why not digoxin? Slower onset; not suitable for acute termination.
3. Dosage Form
Adenosine — IV solution for injection (6 mg/2 mL ampoule, rapid intravenous bolus via a large peripheral vein or central vein)
4. Dosage
- Initial dose: 6 mg IV rapid bolus (over 1–2 seconds), followed immediately by 20 mL saline flush
- If no conversion in 1–2 minutes: repeat at 12 mg IV bolus
- May give a second 12 mg dose if necessary (maximum total dose ~30 mg)
Station 2
5. Pharmacokinetics
| Parameter | Detail |
|---|---|
| Half-life | < 10 seconds (extremely short) |
| Onset | Virtually immediate (seconds) |
| Duration | Seconds — self-terminating action |
| Metabolism | Taken up and degraded by red blood cells and vascular endothelium (not hepatic) |
| Distribution | Does not accumulate; no organ toxicity concerns |
| Interactions | Effect reduced by theophylline/caffeine (adenosine receptor blockers); effect potentiated by dipyridamole (adenosine uptake inhibitor) |
6. Mechanism of Action
Adenosine is an endogenous nucleoside that acts on A1 adenosine receptors in cardiac tissue:
- Activates inward rectifier K⁺ current (IKAdo) → marked hyperpolarization of AV nodal cells
- Inhibits calcium current (ICa-L) → suppresses calcium-dependent action potentials
- Net effect: direct inhibition of AV nodal conduction and prolongation of AV nodal refractory period
- This terminates re-entrant SVT by blocking the AV node as a limb of the re-entrant circuit, converting to sinus rhythm
Lesser effect on the SA node at standard doses.
7. Prescription
Rp:
Adenosine 6 mg/2 mL sol. inject. — amp. No. 3
D.S.: Administer 6 mg (2 mL) IV rapid bolus over 1–2 seconds,
followed immediately by 20 mL 0.9% NaCl flush.
If no response within 1–2 min, repeat 12 mg IV rapid bolus.
Under continuous ECG monitoring.
Station 3
8. Duration of Treatment
Adenosine is used as a single acute intervention — not for chronic/maintenance therapy. Duration of pharmacological effect is only seconds. Once SVT is terminated, no continued adenosine is given. Long-term arrhythmia prevention (if recurrent SVT) is managed with oral agents (e.g., verapamil, flecainide) or radiofrequency catheter ablation.
9. Side Effects
| Frequency | Side Effect |
|---|---|
| ~20% | Flushing |
| >10% | Shortness of breath / chest burning (may relate to bronchospasm — important in this asthmatic patient; however the effect lasts only seconds) |
| Common | Transient high-grade AV block (brief) |
| Less common | Atrial fibrillation, headache, hypotension, nausea, paresthesias |
| Rare | Ventricular proarrhythmia |
Note: In this asthmatic patient, the bronchospasm side effect may transiently occur but resolves within seconds due to adenosine's ultra-short half-life. This is clinically acceptable for a single acute termination dose.
10. Contraindications
| Contraindication | Reason |
|---|---|
| Second- or third-degree AV block (without pacemaker) | Can worsen conduction block |
| Sick sinus syndrome (without pacemaker) | Profound sinus bradycardia/arrest |
| Wolff-Parkinson-White with pre-excited AF | Can accelerate conduction via accessory pathway → VF |
| Theophylline / aminophylline use | Competitively blocks adenosine receptors, markedly reducing efficacy |
| Severe hypotension | Adenosine can cause transient hypotension |
| Dipyridamole use | Potentiates adenosine → extreme/prolonged block |
| Relative: Asthma | Risk of bronchospasm (but ultra-short half-life makes it generally acceptable for acute use when no alternative exists) |
Key clinical point: β-blockers (e.g., metoprolol, atenolol) are absolutely avoided here due to the patient's asthma history. Adenosine, despite the bronchospasm risk, is still preferred because its action lasts only seconds.
— Katzung's Basic and Clinical Pharmacology, 16th Edition, pp. 381–382
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