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Q1: A 28-year-old man walks in with a regular narrow-complex tachycardia at 190 bpm, BP 110/70. Talk me through your immediate management. (2 min)
Stable SVT. ABCDE, oxygen if hypoxic, IV access, continuous monitoring, defibrillator at bedside, 12-lead ECG. Step 1 — modified Valsalva (REVERT): semi-recumbent 45 degrees, 15-second forced strain to ~40 mmHg, then supine with legs raised to 45 degrees for 15 seconds. If unsuccessful: adenosine 6 mg rapid IV bolus, then 12 mg if necessary (57.4% then 93.4%; ~30 seconds to termination). Warn that adverse effects occurred in 36%, lasted less than 1 minute, and were usually mild. If adenosine should be avoided (asthma — bronchoconstriction in both asthmatics of a 26-patient series) or fails: IV verapamil 5 mg then 7.5 mg if necessary. If still in SVT: IV amiodarone (PSVT 61% in one CCU series) or synchronised DC cardioversion. If he becomes unstable: synchronised DC cardioversion. [1][2][12]
Q2: The adenosine doesn't work and he becomes wheezy. What happened and what now? (3 min)
Two issues. First, wheeze after adenosine matches the reported bronchoconstriction in both asthmatics of a 26-patient intravenous series — alternative treatments should be considered in asthmatics; take a drug/asthma history first. Second, ineffectiveness is often a technique failure — adenosine must be given as a rapid bolus. Now: stop adenosine, treat bronchospasm, and switch to IV verapamil 5 mg then 7.5 mg if necessary. If he deteriorates: synchronised DC cardioversion. Long-term: catheter ablation (AVNRT 95% acute / 93% long-term). [11][1][7]
Q3: His ECG in sinus rhythm shows a short PR, delta wave and broad QRS. What is the diagnosis, and what is the dangerous scenario I must know about? (2 min)
Wolff-Parkinson-White (WPW) syndrome — a manifest accessory pathway (bundle of Kent) bypassing the AV node (delta wave, short PR, broad QRS). The dangerous scenario is pre-excited atrial fibrillation: an irregular wide-complex tachycardia; AV-nodal blockers can increase the ventricular rate and have caused VF. Electrical cardioversion is first-line for pre-excited AF and antidromic AVRT. Definitive: accessory-pathway catheter ablation (treatment of choice after sudden-death survival; first long-term option for 88% in a 17-country registry). Community SCD rate 0.0015 per patient-year; no SCD among those asymptomatic at diagnosis, so routine EPS is not required in asymptomatic patients.
Q4: What is tachycardiomyopathy, and which SVTs cause it? (2 min)
Tachycardiomyopathy is reversible ventricular systolic dysfunction caused by an incessant (or very frequent) tachycardia — it resolves with rate control or ablation. The key teaching: always look for an incessant tachycardia in unexplained heart failure. The SVT substrates are: focal atrial tachycardia (the classic cause), permanent junctional reciprocating tachycardia (PJRT) — a concealed, slowly-conducting accessory pathway causing an incessant long-RP tachycardia, often in children/young adults — and, less commonly, incessant AVRT or atrial flutter with rapid rates. Diagnosis is by ambulatory ECG and EPS; treatment is catheter ablation of the focus/pathway, after which the cardiomyopathy typically recovers.
Q5: How does the modified Valsalva work, and what trial established it? (1 min)
The modified Valsalva (REVERT protocol) increases vagal tone to transiently slow AV-nodal conduction and break the re-entrant circuit. The patient strains against a closed glottis at ~40 mmHg for 15 seconds in the semi-recumbent position, then is laid flat with the legs passively raised to 45 degrees for 15 seconds — the leg-lift augments venous return, provoking a reflex vagal surge on release. The REVERT trial (Appelboam et al., Lancet 2015) showed return to sinus rhythm at 1 minute in 93 of 214 (43%) vs 37 of 214 (17%) with a standard semi-recumbent Valsalva (40 mm Hg, 15 s strain in both groups).