Abstract Body: Case Presentation
Case 1: An 83-year-old female without medical history developed cardiogenic shock due to anterior STEMI. Post-LAD stenting and IABP placement, her cardiac index decreased from 2.2 to 1.2 L/min/m2; dobutamine was ineffective.
Case 2: A 77-year-old female with history of hypertension had a 30-second syncope at her husband’s funeral, then developed hypotension requiring norepinephrine, which worsened after treatment; she then complained of chest pain.
Treatment and Management
Case 1: Due to the status post cardiac cath after AMI, initial concerns were tamponade or decompensated AHF, which were addressed by POCUS showing only trace pericardial effusion and slightly decreased LVEF with normal CVP and PCWP. Urgent Formal echo revealed LVEF 45%, apical akinesis, small LV cavity, and LVOT obstruction (pressure gradient, PG 41 mmHg). Dobutamine was discontinued and IABP was removed. She was started on metoprolol, phenylephrine, and given IV fluid resuscitation.
Case 2: She had high troponin (699 ng/L) without EKG change; Takotsubo cardiomyopathy was suspected due to recent stress. Urgent Echo showed LVEF 30%, apical ballooning with severe mitral regurgitation(MR), and LVOT obstruction (PG 144 mmHg, image 1). She had a clean cardiac cath later. After transitioning to phenylephrine, her LVOT PG decreased to 42 mmHg, but MR persisted, she continued in cardiogenic shock on maximum pressor support and had a PEA arrest on day 3; After ROSC, an Impella device was placed immediately.
Outcome and Follow-Up
Case 1: The patient's hemodynamics improved rapidly, leading to ICU discharge on day 2.
Case 2: After 3-day Impella support, she was hemodynamically stable, and was discharged to rehabilitation 1 week later.
Teaching Points
Clinicians must consider LVOT obstruction in patients with shock unresponsive to conventional management. Timely echocardiography to evaluate for systolic anterior motion of the mitral valve and LVOT gradient is integral. High-risk patients include those with MI with apical akinesis, stress cardiomyopathy, and septic shock. Inotropes, IABP, hypovolemia, and low systemic vascular resistance exacerbate the shock state in LVOT obstruction. Management should include beta-blockers, volume expansion, and vasopressors targeting SVR (phenylephrine, vasopressin). For severe cases, ECMO or percutaneous LVAD may offer temporary support by unloading the LV and bypassing the obstruction.