Ventricular tachycardia may display a range of clinical presentations from asymptomatic to sudden death. Mechanisms postulated to produce VT include reentry, automaticity, and triggered activity, although most clinically significant forms of VT are believed to be due to reentry. The conditions for reentry - slow conduction and unidirectional block - are frequently found in ischemic heart disease. Diagnosis of VT may often be apparent from the physical examination and 12-lead ECG, but diagnostic uncertainty can usually be resolved by atrial recordings during VT to demonstrate VA dissociation. Occasionally, electrophysiologic studies are required. Hemodynamic stability or deterioration is not a reliable diagnostic criterion. Once the decision to treat VT has been made, a systematic procedure should be used. This should include documentation of the frequency of VT prior to treatment, use of drugs alone or in combination with therapeutic plasma levels, and objective measurement of response to therapy. Electrophysiologic studies are often helpful for establishing the mechanisms, confirming the diagnosis, and evaluating therapy.