1,2,3: Use of Ang II in a HM3

Vasodilatory shock is characterized by peripheral vasodilation, hypotension and preserved cardiac output. Management involves identifying and treating the underlying cause and reestablishing adequate blood pressure. Contemporary vasopressors include catecholamines and vasopressin, and their use is l...

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Bibliographic Details
Published in:The Journal of heart and lung transplantation Vol. 40; no. 4; p. S532
Main Authors: Andrade, A., Gavrilos, G., Pillarella, J., Narang, N., Sciamanna, C., Pauwaa, S., Macaluso, G., Cotts, W., Tatooles, A., Pappas, P.
Format: Journal Article
Language:English
Published: Elsevier Inc 01-04-2021
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Summary:Vasodilatory shock is characterized by peripheral vasodilation, hypotension and preserved cardiac output. Management involves identifying and treating the underlying cause and reestablishing adequate blood pressure. Contemporary vasopressors include catecholamines and vasopressin, and their use is limited by adverse effects. Adjunctive use of Angiotensin II (Ang II) has been shown to increase mean arterial pressure (MAP) in patients with vasodilatory shock. We describe the first successful use of Ang II in a patient with a HM3 left ventricular assist device (VAD). 58-year-old gentleman with long-standing NICM, LV EF 20-25%, atrial fibrillation (AF), CKD stage III, recent COVID-19, presented with an ST elevation myocardial infarction and progressed to refractory cardiogenic shock. He was supported with inotropes and an intra-aortic balloon pump and implanted with a HM3. VAD course was complicated by right ventricular dysfunction, respiratory failure, and renal failure, necessitating initiation of continuous dialysis. Patient developed sepsis due to clostridium dificile colitis and pneumonia that progressed to refractory vasodilatory shock on post-op day 20. He was supported on HM3 at 5600 rpm, inotropes and escalating doses of pressors. He developed AF with rapid ventricular response, limiting further uptitration, thus, Ang II was initiated. Initial dose was 20 ng/kg/min, with a robust response in MAPs from 60s to 80s mmHg in 2 minutes. Within 24 hours he was weaned off of Ang II and within 72 hours, he was weaned off of all pressors (Table). He was subsequently transitioned to HD and weaned off of inotropic and ventilatory support. Treatment options for patients with catecholamine-resistant vasodilatory shock are limited. In patients with refractory vasodilatory shock supported with durable LVAD therapies, information on the use of Ang II is limited. In our patient with multi-system organ failure and impending death, we were able to utilize Ang II to provide hemodynamic stability and rescue him from septic shock.
ISSN:1053-2498
1557-3117
DOI:10.1016/j.healun.2021.01.2121