Non-invasive Thoracic Impedance Changes in COVID-19 Pulmonary Infection
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SHORT COMMUNICATION
Non-invasive Thoracic Impedance Changes in COVID-19 Pulmonary Infection Sunil Kapur 1 & Michael O. Sweeney 1 & William Sauer 1 & Calum A. MacRae 1 Received: 29 May 2020 / Accepted: 1 October 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Keywords Thoracic impedance . Implantable cardiac defibrillator . Covid-19
Abbreviations TI Thoracic impedance ICD Implantable cardiac defibrillator COVID-19- Coronavirus disease 19 HF Heart failure EC Electrical cardiometry EIT Electrical impedance tomography Severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) causes coronavirus disease 2019 (COVID-19), a systemic illness with respiratory tract abnormalities [1]. Thoracic impedance (TI) is a capability of implantable cardiac defibrillators (ICDs) that reflects complex biophysical characteristics in the chest. Dynamic changes in TI have been shown to reflect changes in pulmonary interstitial fluid in heart failure (HF) patients [2, 3]. We sought to determine if COVID-19related pulmonary changes could result in changes in TI as measured by ICDs. Consecutive patients followed by the Brigham and Women’s Cardiac Electrophysiology Device Clinic who were evaluated for COVID between March 15 and April 15, 2020, were identified and divided into two cohorts: those with severe pulmonary disease requiring hospitalization and those without who were managed out of hospital. Those diagnosed with COVID-19 via PCR testing and an implanted device with TI monitoring capability were selected. Patients were excluded from this study if they had evidence of decompensated heart failure, recent device implant, advanced renal failure ± dialysis (chronic kidney disease class 4 or 5 Editor-in-Chief Enrique Lara-Pezzi oversaw the review of this article * Sunil Kapur [email protected] 1
Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, USA
with an estimated glomerular filtration rate (GFR) of < 30 mL/ min), or pulmonary embolism. With these criteria, the study consisted of 3 hospitalized and 8 nonhospitalized patients. Study approval was obtained from the Mass General Brigham Institutional Review Board. Among the hospitalized cohort, patient 1 is a 73-year-old gentleman with ischemic cardiomyopathy (LVEF 30%). He was admitted on February 2, 2020, for heart failure exacerbation. The patient was optimized with diuresis/medication during which a reduction of central venous pressure from 31 of 12 mmHg. NT-proBNP (reference < 1800 pg/mL) decreased from 20,609 pg/mL to baseline of 4124 pg/mL. The patient had improvement and was discharged on March 3. The patient reported fevers and chills starting March 5 and shortness of breath on March 8. He presented to the hospital on March 10 and was hypoxic at 92% saturation on room air. COVID testing was positive on March 11 and again on March 12. On March 16, he developed worsening hypoxia and was intubated. Chest CT showed parenchymal lung disease consistent with COVID. He recovered with intensive level care over the c
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