Effects of inhaled nitric oxide for postoperative hypoxemia in acute type A aortic dissection: a retrospective observational study

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Abstract

Background

Postoperative hypoxemia in acute type A aortic dissection (AADA) is a common complication and is associated with negative outcomes. This study aimed to analyze the efficacy of low-dose (5–10 ppm) inhaled nitric oxide (iNO) in the management of hypoxemia after AADA surgery.

Methods

In this retrospective observational study, Medical records of patients who underwent AADA surgery at two institutions between January 2015 and January 2018 were collected. Patients with postoperative hypoxemia were classified as iNO and control groups. Clinical characteristics and outcomes were compared using a propensity score-matched (PSM) analysis.

Results

Among 436 patients who underwent surgical repair, 187 (42.9%) had hypoxemia and 43 were treated with low-dose iNO. After PSM, patients were included in the iNO treatment ( n = 40) and PSM control ( n = 94) groups in a 1:3 ratio. iNO ameliorated hypoxemia at 6, 24, 48, and 72 h after initiation, and shortened the durations of ventilator support (39.0 h (31.3–47.8) vs. 69.0 h (47.8–110.3), p < 0.001) and ICU stay (122.0 h (80.8–155.0) vs 179.5 h (114.0–258.0), p < 0.001). There were no significant between-group differences in mortality, complications, or length of hospital stay.

Conclusions

In this study, we found that low-dose iNO improved oxygenation in patients with hypoxemia after AADA surgery and shortened the durations of mechanical ventilation and ICU stay. No significant side effects or increase in postoperative mortality or morbidities were observed with iNO treatment. These findings warrant a randomized multicenter controlled trial to assess the exact efficiency of iNO for hypoxemia after AADA.

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Most cited references 24

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Presentation, Diagnosis, and Outcomes of Acute Aortic Dissection: 17-Year Trends From the International Registry of Acute Aortic Dissection.

Linda Pape, Mazen Awais, Elise Woznicki … (2015)

Diagnosis, treatment, and outcomes of acute aortic dissection (AAS) are changing.

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Inhaled nitric oxide for the adult respiratory distress syndrome.

Angel F. Lopez, U Pison, Rolf Rossaint … (1993)

The adult respiratory distress syndrome is characterized by pulmonary hypertension and right-to-left shunting of venous blood. We investigated whether inhaling nitric oxide gas would cause selective vasodilation of ventilated lung regions, thereby reducing pulmonary hypertension and improving gas exchange. Nine of 10 consecutive patients with severe adult respiratory distress syndrome inhaled nitric oxide in two concentrations for 40 minutes each. Hemodynamic variables, gas exchange, and ventilation-perfusion distributions were measured by means of multiple inert-gas-elimination techniques during nitric oxide inhalation; the results were compared with those obtained during intravenous infusion of prostacyclin. Seven patients were treated with continuous inhalation of nitric oxide in a concentration of 5 to 20 parts per million (ppm) for 3 to 53 days. Inhalation of nitric oxide in a concentration of 18 ppm reduced the mean (+/- SE) pulmonary-artery pressure from 37 +/- 3 mm Hg to 30 +/- 2 mm Hg (P = 0.008) and decreased intrapulmonary shunting from 36 +/- 5 percent to 31 +/- 5 percent (P = 0.028). The ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen (PaO2/FiO2), an index of the efficiency of arterial oxygenation, increased during nitric oxide administration from 152 +/- 15 mm Hg to 199 +/- 23 mm Hg (P = 0.008), although the mean arterial pressure and cardiac output were unchanged. Infusion of prostacyclin reduced pulmonary-artery pressure but increased intrapulmonary shunting and reduced the PaO2/FiO2 and systemic arterial pressure. Continuous nitric oxide inhalation consistently lowered the pulmonary-artery pressure and augmented the PaO2/FiO2 for 3 to 53 days. Inhalation of nitric oxide by patients with severe adult respiratory distress syndrome reduces the pulmonary-artery pressure and increases arterial oxygenation by improving the matching of ventilation with perfusion, without producing systemic vasodilation. Randomized, blinded trials will be required to determine whether inhaled nitric oxide will improve outcome.

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Lung dysfunction following cardiopulmonary bypass.

Efstratios Apostolakis, Kriton S. Filos, Efstratios Koletsis … (2015)

It is well known by now that during open heart surgery many detrimental factors are involved in lung injury. The influence mainly of cardiopulmonary bypass (CPB), anesthesia, hypothermia, operation itself, as well as medication and transfusion, can cause a diffuse injury in the lungs, which most often leads to a postoperative pulmonary edema and abnormal gas exchange. We performed an unrestricted search of Pubmed Medline and EMBASE from 1966 through 2008. Clinical, experimental, basic science, and review papers were included. The hypothesis that a systemic inflammatory reaction takes place after the use of CPB, could explain most of these effects influences in the lung. On the other hand, the release of various pro-inflammatory cytokines like TNF-á, IL-1, IL-2, IL-6, IL-8, and endotoxin during CPB can lead to the entrapment of neutrophils in the pulmonary capillaries. Consequently, the following chain of reactions is likely to occur: an endothelial cell swelling, plasma and protein extravasation into the interstitial tissue, release of proteolytic enzymes, congestion of the alveoli with plasma, erythrocytes and inflammatory debris. In this review we highlight the possible pathophysiological mechanisms implicated in the observed postoperative lung dysfunction.

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Author and article information

Contributors

Yang Liu:

ORCID: http://orcid.org/0000-0003-4361-3264

liuyang3722@163.com

Min Yu: minyudr@163.com

Journal

Journal ID (nlm-ta): J Cardiothorac Surg

Journal ID (iso-abbrev): J Cardiothorac Surg

Title: Journal of Cardiothoracic Surgery

Publisher: BioMed Central (London )

ISSN (Electronic): 1749-8090

Publication date (Electronic): 22 January 2020

Publication date PMC-release: 22 January 2020

Publication date Collection: 2020

Volume: 15

Electronic Location Identifier: 25

Affiliations

[1 ]ISNI 0000 0004 0368 8293, GRID grid.16821.3c, Department of Cardiovascular Surgery, Shanghai General Hospital, , Shanghai Jiao Tong University School of Medicine, ; No. 100 Haining Road, Shanghai, 200080 China

[2 ]ISNI 0000 0000 9255 8984, GRID grid.89957.3a, Department of Cardiovascular Surgery, Shanghai General Hospital, , Nanjing Medical University, ; Shanghai, 200080 China

[3 ]ISNI 0000 0004 0369 1660, GRID grid.73113.37, Department of Rheumatology and Immunology, Changzheng Hospital, , Second Military Medical University, ; 415 Fengyang Road, Shanghai, 200000 China

[4 ]ISNI 0000 0000 9255 8984, GRID grid.89957.3a, Department of Central laboratory, Nanjing First People’s Hospital, , Nanjing Medical University, ; NO.68 Changle Road, Nanjing, 210006 China

[5 ]ISNI 0000 0004 0369 1660, GRID grid.73113.37, Department of Cardiovascular Surgery, Changhai Hospital, , Second Military Medical University, ; Shanghai, 200433 China

[6 ]Department of Critical Care Medicine, Naval medical Center of PLA, Shanghai, 200433 China

Author information

Yang Liu http://orcid.org/0000-0003-4361-3264

Article

Publisher ID: 1069

DOI: 10.1186/s13019-020-1069-6

PMC ID: 6977331

PubMed ID: 31969173

SO-VID: 638d702e-233e-4a07-8239-b322b4430d9c

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 31 March 2019

Date accepted : 7 January 2020

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;

Award ID: 81873524

Award ID: 81770411

Award Recipient : Min Yu

Funded by: National Natural Science Foundation of China (CN)

Award ID: 81300094

Award Recipient : Min Yu

Funded by: China Postdoctoral Science Foundation funded project

Award ID: 2018M633709

Funded by: Clinical Research Plan of Shanghai Hospital Development Center

Award ID: 16CR3086B

Award Recipient : Min Yu

Custom metadata

ScienceOpen disciplines: Surgery

Keywords: postoperative hypoxemia,acute type a aortic dissection,inhaled nitric oxide,propensity analysis

Data availability:

ScienceOpen disciplines: Surgery

Keywords: postoperative hypoxemia, acute type a aortic dissection, inhaled nitric oxide, propensity analysis

Effects of inhaled nitric oxide for postoperative hypoxemia in acute type A aortic dissection: a retrospective observational study

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Most cited references 24

Presentation, Diagnosis, and Outcomes of Acute Aortic Dissection: 17-Year Trends From the International Registry of Acute Aortic Dissection.

Inhaled nitric oxide for the adult respiratory distress syndrome.

Lung dysfunction following cardiopulmonary bypass.

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