Inhaled nitric oxide preserves ventricular function during resuscitation using a percutaneous mechanical circulatory support device in a porcine cardiac arrest model: an echocardiographic myocardial work analysis
Abstract Background Resuscitation using a percutaneous mechanical circulatory support device (iCPR) improves survival after cardiac arrest (CA). We hypothesized that the addition of inhaled nitric oxide (iNO) during iCPR might prove synergistic, leading to improved myocardial performance due to lowe...
Main Authors: | , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
BMC
2021-04-01
|
Series: | BMC Cardiovascular Disorders |
Subjects: | |
Online Access: | https://doi.org/10.1186/s12872-021-01992-w |
_version_ | 1819199984334012416 |
---|---|
author | Christoph Nix Rashad Zayat Andreas Ebeling Andreas Goetzenich Uma Chandrasekaran Rolf Rossaint Nima Hatam Matthias Derwall |
author_facet | Christoph Nix Rashad Zayat Andreas Ebeling Andreas Goetzenich Uma Chandrasekaran Rolf Rossaint Nima Hatam Matthias Derwall |
author_sort | Christoph Nix |
collection | DOAJ |
description | Abstract Background Resuscitation using a percutaneous mechanical circulatory support device (iCPR) improves survival after cardiac arrest (CA). We hypothesized that the addition of inhaled nitric oxide (iNO) during iCPR might prove synergistic, leading to improved myocardial performance due to lowering of right ventricular (RV) afterload, left ventricular (LV) preload, and myocardial energetics. This study aimed to characterize the changes in LV and RV function and global myocardial work indices (GWI) following iCPR, both with and without iNO, using 2-D transesophageal echocardiography (TEE) and GWI evaluation as a novel non-invasive measurement. Methods In 10 pigs, iCPR was initiated following electrically-induced CA and 10 min of untreated ventricular fibrillation (VF). Pigs were randomized to either 20 ppm (20 ppm, n = 5) or 0 ppm (0 ppm, n = 5) of iNO in addition to therapeutic hypothermia for 5 h following ROSC. All animals received TEE at five pre-specified time-points and invasive hemodynamic monitoring. Results LV end-diastolic volume (LVEDV) increased significantly in both groups following CA. iCPR alone led to significant LV unloading at 5 h post-ROSC with LVEDV values reaching baseline values in both groups (20 ppm: 68.2 ± 2.7 vs. 70.8 ± 6.1 mL, p = 0.486; 0 ppm: 70.8 ± 1.3 vs. 72.3 ± 4.2 mL, p = 0.813, respectively). LV global longitudinal strain (GLS) increased in both groups following CA. LV-GLS recovered significantly better in the 20 ppm group at 5 h post-ROSC (20 ppm: − 18 ± 3% vs. 0 ppm: − 13 ± 2%, p = 0.025). LV-GWI decreased in both groups after CA with no difference between the groups. Within 0 ppm group, LV-GWI decreased significantly at 5 h post-ROSC compared to baseline (1,125 ± 214 vs. 1,835 ± 305 mmHg%, p = 0.011). RV-GWI was higher in the 20 ppm group at 3 h and 5 h post-ROSC (20 ppm: 189 ± 43 vs. 0 ppm: 108 ± 22 mmHg%, p = 0.049 and 20 ppm: 261 ± 54 vs. 0 ppm: 152 ± 42 mmHg%, p = 0.041). The blood flow calculated by the Impella controller following iCPR initiation correlated well with the pulsed-wave Doppler (PWD) derived pulmonary flow (PWD vs. controller: 1.8 ± 0.2 vs. 1.9 ± 0.2L/min, r = 0.85, p = 0.012). Conclusions iCPR after CA provided sufficient unloading and preservation of the LV systolic function by improving LV-GWI recovery. The addition of iNO to iCPR enabled better preservation of the RV-function as determined by better RV-GWI. Additionally, Impella-derived flow provided an accurate measure of total flow during iCPR. |
first_indexed | 2024-12-23T03:25:01Z |
format | Article |
id | doaj.art-41efa150763e46bd97cdd5c6bbbcf795 |
institution | Directory Open Access Journal |
issn | 1471-2261 |
language | English |
last_indexed | 2024-12-23T03:25:01Z |
publishDate | 2021-04-01 |
publisher | BMC |
record_format | Article |
series | BMC Cardiovascular Disorders |
spelling | doaj.art-41efa150763e46bd97cdd5c6bbbcf7952022-12-21T18:01:52ZengBMCBMC Cardiovascular Disorders1471-22612021-04-0121111710.1186/s12872-021-01992-wInhaled nitric oxide preserves ventricular function during resuscitation using a percutaneous mechanical circulatory support device in a porcine cardiac arrest model: an echocardiographic myocardial work analysisChristoph Nix0Rashad Zayat1Andreas Ebeling2Andreas Goetzenich3Uma Chandrasekaran4Rolf Rossaint5Nima Hatam6Matthias Derwall7Department of Anesthesiology, Medical Faculty, RWTH University Hospital Aachen, RWTH Aachen UniversityDepartment of Thoracic and Cardiovascular Surgery, Medical Faculty, RWTH University Hospital Aachen, RWTH Aachen UniversityDepartment of Anesthesiology, Medical Faculty, RWTH University Hospital Aachen, RWTH Aachen UniversityDepartment of Anesthesiology, Medical Faculty, RWTH University Hospital Aachen, RWTH Aachen UniversityAbiomed, Inc.Department of Anesthesiology, Medical Faculty, RWTH University Hospital Aachen, RWTH Aachen UniversityDepartment of Thoracic and Cardiovascular Surgery, Medical Faculty, RWTH University Hospital Aachen, RWTH Aachen UniversityDepartment of Anesthesiology, Medical Faculty, RWTH University Hospital Aachen, RWTH Aachen UniversityAbstract Background Resuscitation using a percutaneous mechanical circulatory support device (iCPR) improves survival after cardiac arrest (CA). We hypothesized that the addition of inhaled nitric oxide (iNO) during iCPR might prove synergistic, leading to improved myocardial performance due to lowering of right ventricular (RV) afterload, left ventricular (LV) preload, and myocardial energetics. This study aimed to characterize the changes in LV and RV function and global myocardial work indices (GWI) following iCPR, both with and without iNO, using 2-D transesophageal echocardiography (TEE) and GWI evaluation as a novel non-invasive measurement. Methods In 10 pigs, iCPR was initiated following electrically-induced CA and 10 min of untreated ventricular fibrillation (VF). Pigs were randomized to either 20 ppm (20 ppm, n = 5) or 0 ppm (0 ppm, n = 5) of iNO in addition to therapeutic hypothermia for 5 h following ROSC. All animals received TEE at five pre-specified time-points and invasive hemodynamic monitoring. Results LV end-diastolic volume (LVEDV) increased significantly in both groups following CA. iCPR alone led to significant LV unloading at 5 h post-ROSC with LVEDV values reaching baseline values in both groups (20 ppm: 68.2 ± 2.7 vs. 70.8 ± 6.1 mL, p = 0.486; 0 ppm: 70.8 ± 1.3 vs. 72.3 ± 4.2 mL, p = 0.813, respectively). LV global longitudinal strain (GLS) increased in both groups following CA. LV-GLS recovered significantly better in the 20 ppm group at 5 h post-ROSC (20 ppm: − 18 ± 3% vs. 0 ppm: − 13 ± 2%, p = 0.025). LV-GWI decreased in both groups after CA with no difference between the groups. Within 0 ppm group, LV-GWI decreased significantly at 5 h post-ROSC compared to baseline (1,125 ± 214 vs. 1,835 ± 305 mmHg%, p = 0.011). RV-GWI was higher in the 20 ppm group at 3 h and 5 h post-ROSC (20 ppm: 189 ± 43 vs. 0 ppm: 108 ± 22 mmHg%, p = 0.049 and 20 ppm: 261 ± 54 vs. 0 ppm: 152 ± 42 mmHg%, p = 0.041). The blood flow calculated by the Impella controller following iCPR initiation correlated well with the pulsed-wave Doppler (PWD) derived pulmonary flow (PWD vs. controller: 1.8 ± 0.2 vs. 1.9 ± 0.2L/min, r = 0.85, p = 0.012). Conclusions iCPR after CA provided sufficient unloading and preservation of the LV systolic function by improving LV-GWI recovery. The addition of iNO to iCPR enabled better preservation of the RV-function as determined by better RV-GWI. Additionally, Impella-derived flow provided an accurate measure of total flow during iCPR.https://doi.org/10.1186/s12872-021-01992-wLeft ventricular assist devicePercutaneous mechanical circulatory supportCardiac arrestCardiopulmonary resuscitationLeft ventricular unloadingNitric oxide |
spellingShingle | Christoph Nix Rashad Zayat Andreas Ebeling Andreas Goetzenich Uma Chandrasekaran Rolf Rossaint Nima Hatam Matthias Derwall Inhaled nitric oxide preserves ventricular function during resuscitation using a percutaneous mechanical circulatory support device in a porcine cardiac arrest model: an echocardiographic myocardial work analysis BMC Cardiovascular Disorders Left ventricular assist device Percutaneous mechanical circulatory support Cardiac arrest Cardiopulmonary resuscitation Left ventricular unloading Nitric oxide |
title | Inhaled nitric oxide preserves ventricular function during resuscitation using a percutaneous mechanical circulatory support device in a porcine cardiac arrest model: an echocardiographic myocardial work analysis |
title_full | Inhaled nitric oxide preserves ventricular function during resuscitation using a percutaneous mechanical circulatory support device in a porcine cardiac arrest model: an echocardiographic myocardial work analysis |
title_fullStr | Inhaled nitric oxide preserves ventricular function during resuscitation using a percutaneous mechanical circulatory support device in a porcine cardiac arrest model: an echocardiographic myocardial work analysis |
title_full_unstemmed | Inhaled nitric oxide preserves ventricular function during resuscitation using a percutaneous mechanical circulatory support device in a porcine cardiac arrest model: an echocardiographic myocardial work analysis |
title_short | Inhaled nitric oxide preserves ventricular function during resuscitation using a percutaneous mechanical circulatory support device in a porcine cardiac arrest model: an echocardiographic myocardial work analysis |
title_sort | inhaled nitric oxide preserves ventricular function during resuscitation using a percutaneous mechanical circulatory support device in a porcine cardiac arrest model an echocardiographic myocardial work analysis |
topic | Left ventricular assist device Percutaneous mechanical circulatory support Cardiac arrest Cardiopulmonary resuscitation Left ventricular unloading Nitric oxide |
url | https://doi.org/10.1186/s12872-021-01992-w |
work_keys_str_mv | AT christophnix inhalednitricoxidepreservesventricularfunctionduringresuscitationusingapercutaneousmechanicalcirculatorysupportdeviceinaporcinecardiacarrestmodelanechocardiographicmyocardialworkanalysis AT rashadzayat inhalednitricoxidepreservesventricularfunctionduringresuscitationusingapercutaneousmechanicalcirculatorysupportdeviceinaporcinecardiacarrestmodelanechocardiographicmyocardialworkanalysis AT andreasebeling inhalednitricoxidepreservesventricularfunctionduringresuscitationusingapercutaneousmechanicalcirculatorysupportdeviceinaporcinecardiacarrestmodelanechocardiographicmyocardialworkanalysis AT andreasgoetzenich inhalednitricoxidepreservesventricularfunctionduringresuscitationusingapercutaneousmechanicalcirculatorysupportdeviceinaporcinecardiacarrestmodelanechocardiographicmyocardialworkanalysis AT umachandrasekaran inhalednitricoxidepreservesventricularfunctionduringresuscitationusingapercutaneousmechanicalcirculatorysupportdeviceinaporcinecardiacarrestmodelanechocardiographicmyocardialworkanalysis AT rolfrossaint inhalednitricoxidepreservesventricularfunctionduringresuscitationusingapercutaneousmechanicalcirculatorysupportdeviceinaporcinecardiacarrestmodelanechocardiographicmyocardialworkanalysis AT nimahatam inhalednitricoxidepreservesventricularfunctionduringresuscitationusingapercutaneousmechanicalcirculatorysupportdeviceinaporcinecardiacarrestmodelanechocardiographicmyocardialworkanalysis AT matthiasderwall inhalednitricoxidepreservesventricularfunctionduringresuscitationusingapercutaneousmechanicalcirculatorysupportdeviceinaporcinecardiacarrestmodelanechocardiographicmyocardialworkanalysis |