Ventricular Tachycardia (VT)

Treat every wide-complex tachycardia as VT until proven otherwise - roughly 80% to 90% of wide-QRS tachycardias are VT. Features that favor it: AV dissociation, fusion or capture beats, QRS over 0.14 s with right bundle branch morphology or over 0.16 s with left bundle branch morphology, an RS interval over 100 ms in a precordial lead, and negative QRS concordance across the precordium.

Pulseless VT - defibrillate immediately, 150 to 200 J biphasic or 360 J monophasic, then 5 cycles of CPR at 30 compressions to 2 breaths, escalating energy with each successive shock. Epinephrine 1 mg IV every 3 to 5 minutes alongside. Each minute of delay costs roughly 10% of survival, and delaying 2 minutes or more drops survival from about 39% to 22%.

Unstable with a pulse - direct current cardioversion. If VT does not respond, or recurs after successful cardioversion, IV amiodarone maintains sinus rhythm.

Stable VT with structural heart disease - IV procainamide, amiodarone, or sotalol, whichever is available, with IV lidocaine as the alternative. Add an IV beta blocker when ischemia is the driver, and get the patient to coronary angiography and revascularization if the VT is ischemia-induced.

Stable idiopathic or outflow-tract VT - IV beta blockade and non-dihydropyridine calcium channel blockers are first choice. Give IV verapamil as a bolus through a large-bore cannula. Most outflow-tract VT terminates with adenosine.

Torsades and long QT - IV magnesium and mexiletine for long-QT-induced stable VT. When incessant VT comes from a short-long sequence and R-on-T, temporary pacing at a higher rate prevents it.

Fix the substrate you can fix - send potassium, magnesium, and calcium, and optimize all three in any patient in VT. The common triggers are myocardial ischemia, hypokalemia, hypomagnesemia, hypocalcemia, sepsis, and metabolic acidosis; cocaine, methamphetamine, and digitalis toxicity are the drug causes.

Preop ECG in sinus rhythm - it names the substrate: ischemia or prior infarct, long QT, hypertrophic cardiomyopathy, Brugada pattern, or arrhythmogenic right ventricular cardiomyopathy. Echocardiography grades LV function and screens for cardiomyopathy; cardiac MRI defines scar, infiltrative disease, ARVC, and myocarditis when echo is not enough.

Take a three-generation family history in a young patient - channelopathies present first with syncope, cardiac arrest, or sudden death, and guidelines call for a detailed three-generation history when one is suspected.

Patients with an ICD - they may present with device shocks. The device can also discharge inappropriately in response to rapid supraventricular rhythms, and sensing problems, lead migration, and battery failure occur as they do with pacemakers.

VT storm - three or more sustained episodes in 24 hours requiring intervention. Management is IV antiarrhythmics, IV beta blockers, and DC cardioversion along with sedation; refractory cases need intubation, mechanical circulatory support, and catheter ablation.

After ROSC - suspect acute myocardial infarction in every case of pulseless VT and get urgent coronary angiography and PCI where feasible; fibrinolytics during CPR are not recommended. Metabolic acidosis follows collapse quickly, though it does not develop significantly if the arrhythmia is terminated within 30 to 60 seconds.

Ventricular tachycardia (VT) is a wide-complex rhythm of ventricular origin: three or more consecutive beats above 100 per minute. Sustained VT lasts more than 30 seconds, or forces intervention sooner because of hemodynamic compromise; non-sustained VT is shorter and does not destabilize. Monomorphic VT holds one stable QRS shape and usually reflects reentry around myocardial scar, while polymorphic VT varies beat to beat and points to acute ischemia or a repolarization disorder - torsades de pointes is the long-QT form.

Ischemic heart disease is the most common substrate, followed by cardiomyopathy, channelopathies, and infiltrative disease. The rapid rate cuts diastolic filling, so preload and stroke volume fall and cardiac output collapses; coronary and cerebral hypoperfusion follow, and sustained VT can degenerate into ventricular fibrillation. VT and VF cause most sudden cardiac deaths.