Non-Invasive Administration of Inhaled Nitric Oxide in Critically Ill Adults and its Effects on Right Ventricular Function - a Cohort Study.
CCCF ePoster library. Tremblay J. Oct 4, 2017; 198165; 87 Disclosure(s): Nothing to disclose.
Dr. Jan-Alexis Tremblay
Dr. Jan-Alexis Tremblay
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Non-Invasive Administration of Inhaled Nitric Oxide in Critically Ill Adults and its Effects on Right Ventricular Function - a Cohort Study.

Tremblay, Jan-Alexis, MD1; Albert, Martin, MD2; Beaubien-Souligny, William, MD3; Elmi-Sarabi, Mahsa, MSc4; Denault, André, MD, PhD4,5




1Department of Medicine, Division of Critical Care, Université de Montréal, Montréal, Canada; 2Department of Medicine, Division of Critical Care, Hôpital Sacré-Coeur, Montréal, Canada; 3Department of Medicine, Division of Nephrology, Université de Montréal, Montréal, Canada; 4Department of Anesthesiology and Division of Critical Care, Montreal Heart Institute, Université de Montréal, Montréal, Canada; 5Division of Critical Care, Centre Hospitalier de l’Université de Montréal, Montreal, Canada.


In patients with acute right ventricular (RV) failure, decreasing RV afterload by administering inhaled vasodilators represents an interesting therapeutic approach, which has for now only been described in conjunction with endotracheal intubation1-4, whereas positive pressure mechanical ventilation and sedation can both be hemodynamically deleterious in such patients5.  
We aimed to assess the hemodynamic effects of non-invasively administering inhaled nitric oxide (iNO) in critically ill patients with acute RV failure, as well as demonstrate the feasibility and explore the safety profile of this approach.
This is a retrospective cohort study in which we evaluated the clinical course of all hemodynamically unstable patients with RV failure in whom iNO was initiated without intubation and mechanical ventilation in the intensive care unit (ICU) of our two centers between 2013 and 2017. The primary outcome was modifications in RV function parameters after starting iNO, and secondary outcomes included ICU length of stay, mortality, and occurrence of specific side effects (acute kidney injury as per the RIFLE6 definition, significant bleeding prompting clinical intervention and persistent headache in the patient or nursing staff).
18 patients were included in the analysis, 12 (67%) received iNO after cardiac surgery (mean EuroscoreII 19 ± 14) and 6 (33%) received iNO in a non-surgical context. Median [Q1; Q3] iNO concentration was 20 [20; 20] ppm and therapy duration was 24 [12; 46] hours. Most patients received iNO through nasal prongs (66.7%) or high flow nasal cannula (27.8%). Within one hour and compared to just before initiation of therapy, iNO reduced mean pulmonary artery pressure (PAP) from 28.4 to 25.3 mmHg (P=0.01), central venous pressure (CVP) from 17.5 to 13.1 mmHg (P<0.001), the ratio of mean PAP on mean arterial pressure7 from 39% to 33% (P<0.001) and the RV function index8 (systolic PAP/indexed cardiac output) from 23.2 to 18.6 (P=0.03). The pulmonary artery pulsatility index9, 10 ((systolic PAP - diastolic PAP)/CVP) increased from 1.45 to 2.24 (P=0.002), as did the indexed cardiac output from 2.0 to 2.6 l/min/m2 (P=0.004). These rapid hemodynamic changes were not associated with significant modifications of vasopressor and inotrope doses. ICU mortality was 27.78% and median ICU length of stay was 7 [5; 9] days. Two significant bleeding episodes and one acute kidney injury occurred during iNO therapy but none was felt to be attributable to iNO. No headache was reported by the patients or nursing staff.
Non-invasively administered iNO was associated with favourable hemodynamic effects in ICU patients with acute RV failure. This is the first report regarding such a therapeutic approach for these clinically challenging patients. Our results suggest the safety and feasibility of this therapy for which further prospective study is warranted.  

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