Effects of extrathoracic mechanical ventilation on pulmonary hypertension secondary to lung disease

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Abstract

Purpose

Biphasic cuirass ventilation (BCV) is a form of non-invasive extrathoracic positive and negative pressure mechanical ventilation. The present study was conducted to quantify our positive experience using BCV to dramatically improve gas exchange and cardiac function in patients with acute exacerbation of chronic respiratory failure and secondary pulmonary hypertension (PH).

Methods

BCV was applied for 2 weeks in 17 patients with PH caused by lung disease. Ventilation sessions were limited to 1 h per day to prevent exhaustion. To assess respiratory and circulatory effects, percutaneous arterial oxygen saturation (SpO ₂) was measured before and after each daily BCV session, and right heart catheter test [mean pulmonary artery pressure (mPAP), right atrium pressure (RAP), pulmonary artery occlusion pressure (PAOP) and cardiac index (CI)] and serum N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured before and after a series of BCV sessions.

Results

SpO ₂ transiently improved after each BCV session. After a series of BCV, mPAP decreased from 27.2 to 22.4 mmHg ( p = 0.0007). PAOP, CI and serum NT-proBNP levels decreased compared with baseline. No patients were treated with epoprostenol, iloprost, bosentan or sildenafil for PH.

Conclusion

BCV may improve circulatory function in patients with PH caused by lung disease.

Electronic supplementary material

The online version of this article (doi:10.1007/s00540-016-2172-7) contains supplementary material, which is available to authorized users.

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Most cited references 32

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Mild-to-moderate pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD); such a complication is associated with increased risks of exacerbation and decreased survival. Pulmonary hypertension usually worsens during exercise, sleep and exacerbation. Pulmonary vascular remodelling in COPD is the main cause of increase in pulmonary artery pressure and is thought to result from the combined effects of hypoxia, inflammation and loss of capillaries in severe emphysema. A small proportion of COPD patients may present with "out-of-proportion" pulmonary hypertension, defined by a mean pulmonary artery pressure >35-40 mmHg (normal is no more than 20 mmHg) and a relatively preserved lung function (with low to normal arterial carbon dioxide tension) that cannot explain prominent dyspnoea and fatigue. The prevalence of out-of-proportion pulmonary hypertension in COPD is estimated to be very close to the prevalence of idiopathic pulmonary arterial hypertension. Cor pulmonale, defined as right ventricular hypertrophy and dilatation secondary to pulmonary hypertension caused by respiratory disorders, is common. More studies are needed to define the contribution of cor pulmonale to decreased exercise capacity in COPD. These studies should include improved imaging techniques and biomarkers, such as the B-type natriuretic peptide and exercise testing protocols with gas exchange measurements. The effects of drugs used in pulmonary arterial hypertension should be tested in chronic obstructive pulmonary disease patients with severe pulmonary hypertension. In the meantime, the treatment of cor pulmonale in chronic obstructive pulmonary disease continues to rest on supplemental oxygen and a variety of measures aimed at the relief of airway obstruction.

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Lung fibrosis can be complicated by pulmonary hypertension, limiting exercise tolerance and life expectancy. Furthermore, vasodilators might cause deterioration in gas exchange. Our aim was to compare acute effects of sildenafil, nitric oxide, and epoprostenol in individuals with pulmonary hypertension secondary to lung fibrosis. We did a randomised controlled, open-label trial, in 16 individuals admitted to our hospital with pulmonary hypertension secondary to lung fibrosis. After inhalation of nitric oxide (10-20 ppm), we assigned patients to either maximum tolerated dose of intravenous epoprostenol (mean 8.0 ng/kg per min; n=8) or oral sildenafil (50 mg; n=8). Our primary objective was to assess pulmonary vasodilative potency (decrease in pulmonary vascular resistance index) of sildenafil by comparison with inhaled nitric oxide and infused epoprostenol. Analyses were by intention to treat. Pulmonary vascular resistance index was reduced by nitric oxide (-21.9%, 95% CI -14.1 to -36.2), epoprostenol (-36.9%, -24.4 to -59.6), and sildenafil (-32.5%, -10.2 to -54.1). However, ratio of pulmonary to systemic vascular resistance decreased only in individuals who received nitric oxide and sildenafil. Baseline measurement of multiple-inert-gas elimination showed right-to-left shunt flow (4.8%, 0.0-28.2) and little perfusion of low ventilation(V)/perfusion(Q) areas (0.1%, 0.0-13.0). Prostacyclin increased V/Q mismatch (shunt 16.8%, 10.8-35.9; low V/Q 3.8%, 0.0-13.0) and decreased arterial oxygenation. By contrast, nitric oxide (4.5%, 0.0-18.0; 0.0%, 0.0-17.3) and sildenafil (3.3%, 0.0-11.3; 0.0%, 0.0-12.4) maintained V/Q matching, with raised arterial partial pressure of oxygen (14.3 mm Hg, -1.7 to 31.3) noted for sildenafil. We recorded no adverse events. Sildenafil causes preferential pulmonary vasodilation and improves gas exchange in patients with severe lung fibrosis and secondary pulmonary hypertension.

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Author and article information

Contributors

Yoko Sato: +81-3-3353-8111 , yok.s@nifty.com

Noriyuki Saeki: nsaekimd@v07.itscom.net

Takuma Asakura: tasakura2@gmail.com

Kazutetsu Aoshiba: kaoshiba@tokyo-med.ac.jp

Toru Kotani: tkotani@anes.twmu.ac.jp

Journal

Journal ID (nlm-ta): J Anesth

Journal ID (iso-abbrev): J Anesth

Title: Journal of Anesthesia

Publisher: Springer Japan (Tokyo )

ISSN (Print): 0913-8668

ISSN (Electronic): 1438-8359

Publication date (Electronic): 18 April 2016

Publication date PMC-release: 18 April 2016

Publication date (Print): 2016

Volume: 30

Pages: 663-670

Affiliations

[ ]Department of Anesthesiology and Intensive Care Medicine, Tokyo Women’s Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666 Japan

[ ]Synthesis Shinkawabashi Hospital, 1-15 Shinkawadori, Kawasaki-Ku, Kawasaki, Kanagawa 210-0013 Japan

[ ]Nitta Central Clinic, 1-20-19 Yaguchi, Ohta-ku, Tokyo, 146-0093 Japan

[ ]Department of Respiratory Medicine, Tokyo Medical University Ibaraki Medical Center, 3-20-1 Chuo, Ami, Inashiki, Ibaraki 300-0395 Japan

Article

Publisher ID: 2172

DOI: 10.1007/s00540-016-2172-7

PMC ID: 4956720

PubMed ID: 27090795

SO-VID: 5d4d4d7d-c4de-48fc-bb71-451220dce4e3

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.