The elucidation of precipitating factors, such as exertional or emotional stress, concurrent medica- tions or illness, and alleviating factors is important. The presence of a family history of SCD, ischemic heart disease, valvular heart disease, nonischemic cardiomyopathy (NICM), or HF raises concern for the presence of one of these disorders associated with VA. Obtaining a complete medication history is im- portant. Various antiarrhythmic and other medications can cause QT prolongation and torsades de pointes ; some medications can also induce Brugada type I electrocardiographic pat- tern and VF (www.brugadadrugs.org).S4.1-9,S4.1-10 Patients with bigeminy and trigeminy can present with effective bradycardia, an apical-radial pulse deficit and relative hypertension with a wide pulse pressure. Effective bradycardia from PVCs can result in inaccurate estimation of the heart rate. Although premature beats on auscultation of the heart can be detected, the physi- cal examination is focused largely on finding evidence of structural heart disease. Carotid bruits or diminished peripheral pulses may be indicators of atherosclerotic disease associated with ischemic heart disease. Jugular venous distention, rales, gallops, and peripheral edema provide evidence of HF. Auscultation may reveal cardiac murmurs consistent with valvular heart disease, such as aortic stenosis or mitral regurgitation, and may be as- sociated with HF and VA. A midsystolic click may indi- cate mitral valve prolapse that can be associated with Many VA are asymptomatic and detected only on an ECG or telemetry. Such cases highlight the need to search for evidence of underlying heart disease. Recommendation-Specific Supportive Text 1. Rapid, sustained VT may result in syncope sec- ondary to marked reduction in cardiac output, Table 6. Important Considerations in the Evaluation of Patients With Known or Suspected VA Component Assessment and Findings Relevant for VA and/or SCD Risk History 1. 