Acute decompensated right heart failure potentially triggered by multiple factors including pulmonary vasodilator removal during plasma exchange: a case report

Abstract Background Plasma exchange (PE) removes high-molecular-weight substances and is sometimes used for antineutrophil cytoplasmic antibody-associated vasculitis (AAV) with alveolar hemorrhage. Hypotension during PE is rare, except in allergic cases. We report a case of shock likely caused by in...

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Main Authors: Takayuki Toki, Kazuyuki Mizunoya, Misa Itabashi, Naoki Nishikawa, Koji Hoshino, Hitoshi Saito, Yuji Morimoto
Format: Article
Language:English
Published: SpringerOpen 2025-01-01
Series:JA Clinical Reports
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Online Access:https://doi.org/10.1186/s40981-025-00765-0
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author Takayuki Toki
Kazuyuki Mizunoya
Misa Itabashi
Naoki Nishikawa
Koji Hoshino
Hitoshi Saito
Yuji Morimoto
author_facet Takayuki Toki
Kazuyuki Mizunoya
Misa Itabashi
Naoki Nishikawa
Koji Hoshino
Hitoshi Saito
Yuji Morimoto
author_sort Takayuki Toki
collection DOAJ
description Abstract Background Plasma exchange (PE) removes high-molecular-weight substances and is sometimes used for antineutrophil cytoplasmic antibody-associated vasculitis (AAV) with alveolar hemorrhage. Hypotension during PE is rare, except in allergic cases. We report a case of shock likely caused by increased pulmonary vascular resistance (PVR) during PE. Case presentation A 66-year-old man with pulmonary hypertension (PH) and glomerulonephritis was admitted with dyspnea. He had discontinued sildenafil prior to admission. Alveolar hemorrhage associated with AAV was suspected, and PE was performed. Soon after, he developed circulatory failure and hyperlactatemia. Echocardiography revealed right ventricular dilation, suggesting increased PVR. Inhaled nitric oxide (iNO) was administered, rapidly improving hyperlactatemia and oxygenation. The shock observed during PE was attributed to multiple factors, including the potential removal of sildenafil, which may have led to an increase in PVR. Conclusions The shock was attributable to acute right heart failure caused by an exacerbation of PH, possibly due to sildenafil removal via PE, although other contributing factors could not be excluded.
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institution Kabale University
issn 2363-9024
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spelling doaj-art-87992fd38aa842f38483f90aa53306362025-02-02T12:12:25ZengSpringerOpenJA Clinical Reports2363-90242025-01-011111510.1186/s40981-025-00765-0Acute decompensated right heart failure potentially triggered by multiple factors including pulmonary vasodilator removal during plasma exchange: a case reportTakayuki Toki0Kazuyuki Mizunoya1Misa Itabashi2Naoki Nishikawa3Koji Hoshino4Hitoshi Saito5Yuji Morimoto6Department of Anesthesiology and Critical Care Medicine, Hokkaido University HospitalDepartment of Anesthesiology and Critical Care Medicine, Hokkaido University HospitalDepartment of Anesthesiology and Critical Care Medicine, Hokkaido University HospitalDepartment of Anesthesiology and Critical Care Medicine, Hokkaido University HospitalDepartment of Anesthesiology and Critical Care Medicine, Hokkaido University HospitalDepartment of Anesthesiology and Critical Care Medicine, Hokkaido University HospitalDepartment of Anesthesiology and Critical Care Medicine, Hokkaido University HospitalAbstract Background Plasma exchange (PE) removes high-molecular-weight substances and is sometimes used for antineutrophil cytoplasmic antibody-associated vasculitis (AAV) with alveolar hemorrhage. Hypotension during PE is rare, except in allergic cases. We report a case of shock likely caused by increased pulmonary vascular resistance (PVR) during PE. Case presentation A 66-year-old man with pulmonary hypertension (PH) and glomerulonephritis was admitted with dyspnea. He had discontinued sildenafil prior to admission. Alveolar hemorrhage associated with AAV was suspected, and PE was performed. Soon after, he developed circulatory failure and hyperlactatemia. Echocardiography revealed right ventricular dilation, suggesting increased PVR. Inhaled nitric oxide (iNO) was administered, rapidly improving hyperlactatemia and oxygenation. The shock observed during PE was attributed to multiple factors, including the potential removal of sildenafil, which may have led to an increase in PVR. Conclusions The shock was attributable to acute right heart failure caused by an exacerbation of PH, possibly due to sildenafil removal via PE, although other contributing factors could not be excluded.https://doi.org/10.1186/s40981-025-00765-0Plasma exchangeComplicationsPulmonary vascular resistancePulmonary hypertensionSildenafil
spellingShingle Takayuki Toki
Kazuyuki Mizunoya
Misa Itabashi
Naoki Nishikawa
Koji Hoshino
Hitoshi Saito
Yuji Morimoto
Acute decompensated right heart failure potentially triggered by multiple factors including pulmonary vasodilator removal during plasma exchange: a case report
JA Clinical Reports
Plasma exchange
Complications
Pulmonary vascular resistance
Pulmonary hypertension
Sildenafil
title Acute decompensated right heart failure potentially triggered by multiple factors including pulmonary vasodilator removal during plasma exchange: a case report
title_full Acute decompensated right heart failure potentially triggered by multiple factors including pulmonary vasodilator removal during plasma exchange: a case report
title_fullStr Acute decompensated right heart failure potentially triggered by multiple factors including pulmonary vasodilator removal during plasma exchange: a case report
title_full_unstemmed Acute decompensated right heart failure potentially triggered by multiple factors including pulmonary vasodilator removal during plasma exchange: a case report
title_short Acute decompensated right heart failure potentially triggered by multiple factors including pulmonary vasodilator removal during plasma exchange: a case report
title_sort acute decompensated right heart failure potentially triggered by multiple factors including pulmonary vasodilator removal during plasma exchange a case report
topic Plasma exchange
Complications
Pulmonary vascular resistance
Pulmonary hypertension
Sildenafil
url https://doi.org/10.1186/s40981-025-00765-0
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