Ventricular Tachyarrhythmias

VTach/VFIB are uncommon but potentially fatal dysrhythmias requiring urgent diagnosis and management.

Risk increases with age owing to the higher incidence of structural and ischemic heart disease and cardiac failure.

Primary cause of sudden death and accounts for 75–80% of sudden cardiac death. Incidence in USA is about 300,000/y and similar in other developed nations.

Males at greater risk (46% vs. 34%).

Pts under 30 with HOCM, myocarditis, RV dysplasia, or long-QT syndrome are at higher risk for VTach/VFIB.

Cardiac and vascular surgery (up to 50% incidence) does not influence late mortality if LV function is preserved.

Low cardiac output after CABG (requiring pressors) predicts life-threatening VTach/VFIB within 72 h postop.

Cardiac ischemia.

Uncorrected electrolyte and/or acid-base disturbances, hypoxia, hypercarbia, hypothermia.

Use of class 1 and 3 antiarrhythmics, sympathomimetics, QT-prolonging drugs.

Placement of central venous catheters.

Electrolyte imbalance (particularly hypokalemia and hypomagnesemia), acid-base disturbances, hypoxia, hypotension, fluid overload, ongoing myocardial ischemia, and metabolic disturbances.

Use of IV epinephrine and other catecholamines/sympathomimetics.

Drugs that prolong QT (organophosphates, antipsychotics, tricyclics) may precipitate PVT, particularly in Brugada and other long-QT syndromes.

Poor cardiac function.

Modulation of neuroendocrine stress responses.

R-on-T phenomenon.

Chest pain, SOB, palpitations, presyncope, altered mental status.

VTach is caused by high-frequency electrical depolarization from a ventricular myocardial focus and is characterized by a widened QRS (>0.12 sec), high rate (>120 bpm) and variable morphology (MVT or PVT) and duration (sustained vs. nonsustained).

Atrioventricular dissociation may be present, where p waves may be seen with or without capture/fusion beats. This implies VTach rather than SVT with aberrant conduction.

MVT has a single QRS morphology and can evolve into PVT. Often reentrant etiology post-MI.

Torsade de pointes: Atypical PVT with beat-to-beat variation, prolonged QT, changing/twisting QRS axis around baseline.

VFIB: Nonperfusing broad complexes (fast, chaotic, irregular, and disorganized).

Ventricular ectopic beats can sometimes precede VTach.