This review, based on current evidence, highlights the pearls and pitfalls of LVOTO, including pathophysiology, presentation, diagnosis, and management in the emergency department (ED).

LVOTO is associated with obstruction of forward blood flow from the LV. The condition is associated with anatomic and physiological factors. Anatomic factors include those associated with reduced LV outflow tract size, while physiologic factors include exogenous inotropes, high endogenous sympathetic tone, tachycardia, and reduced preload or afterload. Patients with LVOTO are critically ill. Examination may reveal a new systolic murmur, cardiogenic pulmonary edema, and poor systemic perfusion. However, LVOTO can be a challenging diagnosis. Clinicians should consider LVOTO in those with refractory shock that worsens with conventional shock treatments (e.g., vasopressors for hypotension, inotropes for poor cardiac output, and diuresis for cardiogenic pulmonary edema). Ultrasound is the diagnostic modality of choice, with echocardiogram demonstrating high-velocity, late-peaking continuous-wave Doppler through the LV with classic dagger shape and LVOT pressure gradient ≥30 mmHg. Management is based on correcting the outflow obstruction by increasing LV size and prolonging filling time. This includes treating concomitant illness (e.g., sepsis), stopping inotropes and diuretics, volume resuscitation, increasing vascular resistance with phenylephrine or vasopressin, and managing tachyarrhythmias. Patients should be admitted to a critical care setting.