Part of the ICU Pharmacology Hub — browse every related guide in one place.
The monitor alarms and the rate reads 180. The QRS is narrow, the rhythm is dead regular, and the patient is anxious, palpitating, maybe a little short of breath but talking to you. This is the classic picture of supraventricular tachycardia — an umbrella term for regular, fast rhythms that originate at or above the AV node, most commonly AV nodal re-entrant tachycardia (AVNRT). SVT is one of the few ICU rhythms where a bedside nurse, working within orders and protocol, moves through a fast, well-defined sequence: recognize it, decide if the patient is stable, try a vagal maneuver, and if that fails, give adenosine correctly. This guide walks that sequence and the physiology behind each step.
SVT is regular, narrow (QRS < 0.12 s in the typical case), and fast enough that P waves are usually lost in the preceding T wave. Rates commonly sit between 150 and 220. Two look-alikes deserve a mention. The first is sinus tachycardia, which has a clear cause (fever, pain, hypovolemia, anxiety, sepsis) and a visible P before every QRS — you treat the cause, not the rate. The second, and the dangerous one, is atrial fibrillation with a rapid ventricular response, which is irregular — if you look carefully at the R-to-R intervals and they march unevenly, this is not AVNRT and adenosine is not the tool. And any wide-complex regular tachycardia should be treated as ventricular tachycardia until proven otherwise, not assumed to be "SVT with aberrancy."
Before any maneuver or drug, answer one question: is the tachycardia causing hemodynamic instability? Signs of instability include hypotension, acutely altered mental status, signs of shock, ischemic chest discomfort, or acute heart failure — and a plausible link to the rate. An unstable patient in SVT does not get a slow trial of vagal maneuvers and drugs; they get prompt synchronized cardioversion under provider direction. The stable patient — uncomfortable but perfusing — is the one who walks down the vagal-then-adenosine ladder.
Vagal maneuvers increase parasympathetic tone at the AV node, slowing conduction enough to interrupt the re-entry circuit. The classic Valsalva — bearing down against a closed glottis — works, but the modified Valsalva is meaningfully more effective: have the seated patient strain for about 15 seconds, then immediately lay them flat and passively raise their legs to 45 degrees for 15 seconds. The postural change augments the reflex and converts a larger share of patients. Carotid sinus massage is a physician maneuver and is avoided in patients with carotid bruits or a history of stroke. Whatever the maneuver, have the patient on the monitor and a rhythm strip running so you capture the conversion.
Adenosine transiently blocks conduction through the AV node, breaking the re-entry loop and letting the sinus node retake control. Its half-life is measured in seconds — under 10 — which drives everything about how it is given. Because it is destroyed almost the instant it hits the bloodstream, it must reach the heart in one fast bolus.
| Step | What to do | Why |
|---|---|---|
| Access | Use the largest, most proximal IV — an antecubital or a central line is ideal | The drug must reach the AV node before it is metabolized |
| First dose | 6 mg rapid IV push | A slow push simply disappears before it works |
| Flush | Immediate 20 mL saline flush, often via a stopcock or the two-syringe technique | Chases the tiny drug volume into the central circulation |
| Escalate | If no conversion, 12 mg rapid push + flush; a second 12 mg may follow per protocol | Re-entry circuits vary in how much AV block they need |
Adenosine can precipitate bronchospasm, so it is used cautiously in severe asthma or COPD. Its effect is prolonged by dipyridamole and by carbamazepine, and blunted by methylxanthines like theophylline and caffeine, which may demand higher doses. Patients with a transplanted (denervated) heart are exquisitely sensitive and dosing is reduced. And critically: if the "SVT" is actually pre-excited atrial fibrillation (Wolff-Parkinson-White with an accessory pathway), AV-nodal blockers including adenosine can dangerously accelerate conduction down the bypass tract — another reason that an irregular or wide, bizarre rhythm changes the plan.
Pair this with the atrial fibrillation with RVR guide for the irregular imposter, the wide-complex tachycardia guide for the rhythm you must not mistake for SVT, and the synchronized cardioversion guide for the unstable pathway.
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