Success of Mechanical Circulatory Support as a Bridge to Treatment in Acute Right Ventricular Failure
Recommended Citation
Zahedi S, Parsons A, Vahabzadeh A, Franco-Palacios DJ. Success of Mechanical Circulatory Support as a Bridge to Treatment in Acute Right Ventricular Failure. Am J Respir Crit Care Med 2024; 209:A2212.
Document Type
Conference Proceeding
Publication Date
6-1-2024
Publication Title
Am J Respir Crit Care Med
Abstract
Right ventricular (RV) failure is associated with significant morbidity and mortality and carries inhospital mortality rates estimated to be 70-75%. RV failure may occur secondary to acute inferior myocardial infarction, decompensated heart failure, pulmonary embolism, or pulmonary hypertension. While medical therapy aimed at optimizing the contractility of the heart, paired with preload and afterload management are useful therapeutic modalities, in cases of significant right heart failure they are ineffective and mechanical support may be needed. A 40-year-old man with a past medical history of hypertension, polysubstance abuse and previous pulmonary embolism (PE) presented to the emergency department after being found wandering in the street confused. Patient was hypoxic, agitated, and hypotensive. A CT PE showed a large extrinsic thrombus in the distal left main PA and causing complete occlusion of the left lower lobe arteries as well as lobar and segmental thrombus in the right lower lobe. The main PA was dilated, and the RV wall was hypertrophic. Troponins were elevated (1800 ng/L). Echocardiogram showed moderate enlarged RV with diminished RV systolic function. RV systolic pressure was unable to be estimated. Patient was intubated in the ED and on high intensity heparin. His hypotension initially responded to IV fluids but later became hemodynamically unstable requiring rapid increase in norepinephrine. Due to worsening RV failure, he was placed on VA ECMO (fem-fem configuration) with rapid hemodynamic improvement and as a bridge to percutaneous thrombectomy. After pulmonary angiography revealed chronic thrombus attempts for thrombectomy were aborted. Inotropic support with milrinone and addition of afterload reduction with inhaled nitric oxide allowed for weaning off VA ECMO. Sildenafil and IV furosemide were started, and the patient was successfully decannulated. The initial concern was for acute on chronic PE. Although initially VA ECMO in this case was used for hemodynamic compensation to attempt percutaneous thrombectomy, it ultimately served as a bridge to PAH therapy in a patient presenting with new diagnosis CTEPH and RV failure. His urine was positive for cocaine. It is possible that patient RV failure was precipitated by acute cocaine toxicity inducing vasoconstriction in the setting of unknown chronic thromboembolic pulmonary hypertension. The patient will follow-up in the PH clinic to decide on appropriate vasodilator therapy and referral to a CTEPH center. VA ECMO's ability to provide rapid and complete off-loading of the right heart as a bridge to treatment should be considered in medically refractory cases and rapid cardiovascular decompensation.
Volume
209
First Page
A2212
