Supraventricular Tachycardia (SVT)

Start with the 12-lead - regular and narrow with no visible P waves points to AVNRT or AVRT. Irregular with absent P waves is atrial fibrillation, irregular with flutter waves is atrial flutter, and irregular with multiple P wave morphologies is multifocal atrial tachycardia. Each is treated differently, so name the rhythm before you treat it.

Stable patient, vagal first - Valsalva or carotid sinus massage, then adenosine. European Society of Cardiology guidance puts vagal maneuvers and adenosine first-line for both diagnosis and treatment, with beta blockers and calcium channel blockers second-line.

Adenosine dosing - 6 mg IV through a peripheral line followed by a 20 mL saline flush for rapid delivery, with subsequent doses starting at 12 mg. Drop the initial dose to 3 mg if the line accesses the central circulation, if the patient is on dipyridamole or carbamazepine, or in a cardiac transplant recipient.

Adenosine as a diagnostic - it slows AV nodal conduction enough to unmask flutter or atrial tachycardia underneath. Record a continuous ECG through the push: it separates true resistance, meaning a non-AV-nodal rhythm, from a transient effect caused by the very short half-life.

Warn the patient before you push - flushing, lightheadedness, nausea, sweating, numbness, and a sense of impending doom are common and brief. The serious effects are AV block, prolonged asystole, PACs and PVCs, hypotension, and cardiac ischemia.

Antidromic AVRT - adenosine is used only when the diagnosis is certain.

Unstable patient - urgent synchronized cardioversion. For PSVT in adults start at 100 to 120 J biphasic (100 to 200 J monophasic) and escalate; in pediatric SVT start at 0.5 J/kg and double if needed.

Wide-complex and unsure - in a hemodynamically stable wide-QRS tachycardia where SVT cannot be separated from VT, adenosine is useful both diagnostically and therapeutically.

Preop workup - 12-lead ECG, echocardiography, thyroid function testing, and routine bloods; review the medication list and rule out digoxin toxicity, a classic cause. Establish hemodynamic stability and whether ischemic heart disease or heart failure sits underneath.

Pediatrics - adenosine carries a class I recommendation for hemodynamically stable pediatric SVT, and refractory cases may need a higher dose. Untreated pediatric SVT progresses to cardiogenic shock and heart failure.

Why not to let it ride - frequent PSVT causes tachycardia-induced cardiomyopathy. In a patient with coronary disease it can present as myocardial infarction, and in known heart failure as an acute exacerbation.

Supraventricular tachycardia (SVT) is any arrhythmia originating at or above the bundle of His; the 2015 ACC/AHA definition specifically excludes atrial fibrillation. Most episodes are reentrant - a circuit inside the AV node (AVNRT), one using an accessory pathway (orthodromic or antidromic AVRT), or circuits within atrial myocardium or around the sinus node. Less often the mechanism is enhanced or abnormal automaticity, or triggered activity.

Paroxysmal SVT (PSVT) starts and stops abruptly and gives a regular narrow-complex tachycardia, which separates it from atrial fibrillation, atrial flutter, and multifocal atrial tachycardia. Above 150 beats per minute the P waves hide and the specific rhythm is hard to name. Beyond otherwise healthy patients, PSVT follows myocardial infarction, rheumatic heart disease, mitral valve prolapse, pneumonia, chronic lung disease, pericarditis, and digoxin toxicity.