Clinical cardiogenic shock is characterized by tissue hypoperfusion resulting from cardiac dysfunction. Severe left ventricular (LV) dysfunction (usually from myocardial infarction) is the most common cause; however, arrhythmias, acute valvular dysfunction,ventricular rupture, or ventricular septal defect may also result in shock. Hemodynamic criteria for cardiogenic shock include a systolic blood pressure o90 mm Hg, a cardiac index o2.2 L/min/m 2 , and a pulmonary capillary wedge pressure 418 mm Hg. 1 Pharmacotherapy has primarily consisted of inotropic and vasopressor support. Unfortunately, the use of these agents may increase myocardial oxygen consumption, result in arrhythmogenesis, or decrease renal and splanchnic blood flow. To date, mechanical options for patients with drug refractory have included intra-aortic balloon pump (IABP) counterpulsation and percutaneous LV assist devices. Although percutaneous LV assist devices provide superior hemodynamic support compared with IABP, the use of these devices does not appear to improve early survival in patients with cardiogenic shock. 2 Complications associated with these devices include arterial damage, limb ischemia, sepsis, coagulopathy/bleeding, and stroke. 3 In this issue of HeartRhythm, Eitel et al 4 entice us to consider temporary LV pacing in patients with QRS prolongation due to left bundle branch morphology, drug-refractory cardiogenic shock, and asynchronous LV contraction. The study includes a small number of eclectic patients, is uncontrolled, and reveals no statistically significant findings. Nevertheless, it may portend a promising therapeutic adjunct in a clinical scenario where many, possibly the majority, of affected patients die. The potential for long-term survival following cardiogenic shock emphasizes the importance of improving short-term survival, which remains unacceptably low despite optimal intensive care. 4,5 Today, cardiac resynchronization therapy (CRT) is well studied and widely embraced. It is important, however, to remember that the first clinical report of biventricular (BiV) pacing was followed by uncontrolled studies (such as that of Eitel et al) demonstrating marked short-term improvements in hemodynamics and symptoms. 6