The intensivist who is competent in advanced CCE may perform a comprehensive assessment of cardiac anatomy and function using multiple views and Doppler assessment. Measurement of stroke volume and cardiac output using Doppler is a routine part of the advanced CCE examination, and allows the intensivist to quantitate hemodynamic function of the patient in shock. A pericardial effusion with systolic collapse of the right atrium, diastolic collapse of the RV, and mitral valve inflow decrease by 25% during inspiration (in spontaneously breathing patients) is consistent with tamponade physiology.1–3 Myocardial ischemia manifests with segmental wall motion abnormality, with different segments corresponding to specific coronary artery involvement.4 Ventricular rupture is diagnosed by color Doppler inspection of an ischemic segment, in association with pericardial effusion. Valvular abnormalities leading to shock include ruptured chordae or papillary muscle (mitral apparatus) or severe damage to the aortic valve resulting in a flail leaflet, both being associated with severe valvular regurgitation. Severe mitral or aortic valve stenosis may cause shock as a primary event, or complicate management of hemodynamic failure from other cause. Doppler analysis allows quantitative measurement of the severity of valvular stenosis and regurgitation. For example, the severity of aortic stenosis may be assessed qualitatively with 2D imaging by examining the aortic valve anatomy and motion. In addition, aortic valve area may be assessed quantitatively by the continuity principle using spectral Doppler analysis of the LV outflow tract (LVOT) and the aortic valve.5 Quantitative measurement of valve function is routine for the PCCM clinician trained in advanced level CCE. Acute RV myocardial infarction results in RV dilatation in association with decreased endomyocardial thickening of the RV free wall and the inferior wall of the LV.4 Acute cor pulmonale due to increased pulmonary vascular impedance (eg, acute pulmonary embolism, ARDS) is diagnosed by the presence of both RV dilation (RV end-diastolic area/LV end-diastolic area > 1) and intraventricular septal dyskynesia.6 Vasodilatory shock (eg, sepsis) can result in an LV of normal, decreased, or enlarged size depending on load conditions and contractile function. A decreased systemic vascular resistance can be identified using Abbas formula: mitral regurgitation peak velocity/LVOT velocity time integral < 0.2.7 Shock due to hyperdynamic LV function with LV intracavitary pressure gradient occurs in the hypotensive, hypovolemic patient who is overly diuresed while receiving inotropes. This entity presents with hyperdynamic LV function, a late peaking dagger-shaped intracavitary spectral Doppler signal that is usually found in mid-ventricle with higher peak velocity at the site of obstruction as compared with LVOT, and systolic anterior mitral valve leaflet motion. Finally, screening for rupture of an abdominal aortic aneurysm in a hypotensive patient can be rapidly achieved using the cardiac transducer.