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Indian Journal of Critical Care Medicine
Medknow Publications on behalf of the Indian Society of Critical Care Medicine
ISSN: 0972-5229 EISSN: 1998-359x
Vol. 11, Num. 2, 2007, pp. 90-92

Indian Journal of Critical Care Medicine, Vol. 11, No. 2, April-June, 2007, pp. 90-92

Case Report

A rapid decrease in pulmonary arterial pressure by noninvasive positive pressure ventilation in a patient with chronic obstructive pulmonary disease

Pamukkale University Medical Faculty, Department of Pulmonary Diseases, Denizli
Correspondence Address:Pamukkale University Medical Faculty, Pulmonary Department, Kinikli, 20200, Denizli ndursunoglu@yahoo.com

Code Number: cm07014

Abstract

The natural history of chronic obstructive pulmonary disease (COPD) is characterized by progressive decrements in expiratory airflow, increments in end-expired pulmonary volume, hypoxaemia, hypercapnia and the progression of pulmonary arterial hypertension (PAH). Noninvasive positive pressure ventilation (NPPV) treatment is increasingly used for the treatment of acute and chronic respiratory failure in patients with COPD. NPPV can increase PaO2 and decrease PaCO2 by correcting the gas exchange in such patients. The acute effect of NPPV on decreasing PAP is seen in patients with respiratory failure, probably due to the effect on cardiac output. Here, a case with COPD whose respiratory acidosis and PAH rapidly improved by NPPV was presented and therefore we suggested to perform an echocardiographic assessment to reveal an improvement of PAH as well as respiratory acidosis, hypercapnia and hypoxemia with that treatment.

Keywords: Noninvasive positive pressure ventilation, chronic obstructive pulmonary disease, respiratory failure, pulmonary arterial pressure, echocardiography

Introduction

Pulmonary arterial hypertension (PAH) is the primary cardiovascular complication encountered in chronic obstructive pulmonary disease (COPD). The natural history of COPD is characterized by progressive decrements in expiratory airflow, increments in end-expired pulmonary volume, hypoxemia, hypercapnia and the progression of PAH. [1],[2] In patients with COPD, unfavorable prognostic factors include airway obstruction, ventilatory capacity, hypercapnia and PAH. [3] In particular, PAH in COPD leads to the development of right ventricular hypertrophy, dilation and failure, the so-called cor pulmonale, which indicates an advanced stage of respiratory disease. [1],[2] Furthermore, PAH can be a predictive factor for hospitalization for acute exacerbations in COPD patients. [4] Doppler echocardiography which is an inexpensive, easy and reproducible method, is commonly used to estimate mean and systolic pulmonary arterial pressure (PAP) and to diagnose PAH in patients with COPD.

The goals of therapy consist of attenuation of PAH, enhancement of right ventricular function, alleviation of clinical symptoms and improvement in survival. The agents that have been most extensively evaluated for these purposes include oxygen, vasodilators, theophylline and inotropic medications. Currently, noninvasive positive pressure ventilation (NPPV) treatment is increasingly used for the treatment of acute and chronic respiratory failure in patients with COPD. [5] NPPV can increase PaO2 and decrease PaCO2 by correcting the gas exchange in such patients. The acute effect of NPPV on decreasing PAP is seen in patients with respiratory failure, probably due to the effect on cardiac output. [6]

Here, a case with COPD whose respiratory acidosis and PAH rapidly improved by NPPV was presented.

Case Report

A 69-year-old man admitted with severe dyspnea, cough, expectoration of purulent sputum, cyanosis and tendency to sleep. He had a diagnosis of COPD and using NPPV and long-term oxygen therapy together with his medical treatment since the last three years. He had a history of 40 packs-year smoking and was an ex-smoker for 20 years. His medical history revealed systemic hypertension and usage of antihypertensive medication for 10 years.

Initial physical examination revealed that, he was semi-conscious, obese with barrel chest, dyspneic and using accessory respiratory muscles with supraclavicular, suprasternal and intercostal retractions heaves and had flapping tremor, chemosis in his conjuctivas and cyanosis in his nails and mucosa. His physical examination was as follows: body temperature 36.8°C, arterial blood pressure 154/72 mmHg, heart rate 96 beats/min, respiratory rate 40 breaths/min. Pulmonary auscultation revealed silent chest in both hemithoraces and inspiratory crackles in both basal areas. There were no heart murmurs, no peripheral edema, no jugular vein distention. The liver and spleen were not palpable. The abdomen was soft and flat without tenderness or rigidity. His hemogram, blood chemistries and hemostasis tests were within normal limits. Arterial blood gas (ABG) analysis in room air was as the following pH:7.23, PCO2 :79 mmHg, PO2 :39 mmHg, O2 sat%:73 % and HCO3 :34 mEq/L [Table - 1]. Chest radiography revealed bilateral hyperlucency, increased bronchovascular images of the lung fields and enlargement of right descending pulmonary artery. Pulmonary function tests revealed very severe bronchoconstriction; FVC: 560 ml(14%), FEV1: 450 ml (15%), FEV1/FVC: 80%, PEF: 990 ml (13%), FEF 25-75: 420 ml (14%). His ECG revealed sinus rhythm with incomplete right bundle brunch block and left anterior hemiblock. His echocardiography revealed very severe pulmonary hypertension with 60 mmHg mean and 75 mmHg systolic pulmonary arterial pressures by Doppler. He had right atrial (40 mm) and right ventricular (44 mm) enlargement and right ventricular hypertrophy with 10 mm of right ventricular free wall diameter. However, right ventricular ejection fraction of the patient was within normal limits (65%).

Bronchodilator therapy, systemic corticosteroid, intravenous antibiotic treatment and NPPV were initiated with a fraction of inspired oxygen of 2 L, a positive end-expiratory pressure of 4 cm H2O and a pressure-support level of 8 cm H2O with bilevel positive airway pressure (BIPAP) (Respironics Inc; Murrysville, PA). So, BIPAP treatment with nasal and oro-nasal masks has been continued with the increased pressure supports to 18/5 cmH2O. Afterwards, his mental status improved and tendency to sleep gradually diminished, his ABG analysis and mean and systolic PAPs were dramatically improved at the 11th day of NPPV treatment [Table - 1].

Discussion

The prevalence of PAH increases as COPD worsens and the development of PAH and cor pulmonale appears to affect survival of patients with COPD. Potential causes proposed to explain the development of PAH in COPD include gas exchange abnormalities, destruction of the pulmonary vascular bed, alterations in respiratory mechanics, changes in intrinsic pulmonary vessel tone and increased blood viscosity. In acute attacks of COPD, NPPV allows time for other conventional therapy to work, thus reversing the progression of respiratory failure and reducing morbidity and mortality and also improvements occur in minute ventilation, respiratory rate and transdiaphragmatic activity. [4] NPPV can improve pH relatively rapidly, at one hour after instituting ventilation. [7]

Doppler echocardiography is a well-tolerated, efficient evaluation method that can be used at NPPV initiation in acute COPD patients. It is recommended as a useful tool for early detection of hemodynamic alterations due to NPPV application in patients with acute ventilatory failure. [8] In our case, BIPAP treatment with nasal mask improved patient's mental status, respiratory acidosis, hypercapnia and hypoxemia. Our patient had compansated cor pulmonale without heart failure but with right atrial and right ventricular enlargement, right ventricular hypertrophy and normal right ventricular ejection fraction. So, an acute decompansation could occur in such a patient. It is very important to decrease PAP in patients with COPD in order to prevent progression to heart failure, the so-called decompansated cor pulmonale. Hence, NPPV is a successful treatment modality to decrease PAP more rapidly compared with medical therapy. In our patient, mean and systolic PAPs were dramatically improved at the 11 th day of NPPV treatment as well. An echocardiographic assessment of right heart structure and functions is a simple, noninvasive and reproducible method in patients with COPD. The subcostal approach successfully detected adequate Doppler signals in a large proportion of COPD patients. [9] Although ultrasound examination of the heart is technically difficult in patients with hyperinflation of the lungs, it could be obtained suitable images in up to 80-97% of patients. [10]

As a result, an echocardiographic assessment should be performed to the patients having NPPV treatment in COPD acute attacks, in order to reveal an improvement of PAH as well as respiratory acidosis, hypercapnia and hypoxemia with that treatment. Long-term results of NPPV on PAP are not available and further research in patients with COPD is needed.

References

1.Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. American Thoracic Society. Am J Respir Crit Care Med 1995;152:S77-121.  Back to cited text no. 1  [PUBMED]  
2.BTS guidelines for the management of chronic obstructive pulmonary disease. The COPD Guidelines Group of the Standards of Care Committee of the BTS. Thorax 1997;52:S1-28.  Back to cited text no. 2  [PUBMED]  
3.Weitzenblum E, Hirth C, Ducolone A, Mirhom R, Rasaholinjanahary J, Ehrhart M. Prognostic value of pulmonary artery pressure in chronic obstructive pulmonary disease. Thorax 1981;36:752-8.  Back to cited text no. 3  [PUBMED]  
4.Giaid A, Saleh D. Reduced expression of endothelial nitric oxide synthase in the lungs of patients with pulmonary hypertension. N Engl J Med 1995;333:214-21.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Turkington PM, Elliott MW. Rationale for the use of non-invasive ventilation in chronic ventilatory failure. Thorax 2000;55:417-23.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Diaz O, Iglesia R, Ferrer M, Zavala E, Santos C, Wagner PD, et al. Effects of noninvasive ventilation on pulmonary gas exchange and hemodynamics during acute hypercapnic exacerbations of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1997;156:1840-5.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Brochard L, Mancebo J, Wysocki M, Lofaso F, Conti G, Rauss A, et al. Noninvasive ventilation for acute exacerbation of COPD. N Engl J Med 1995;333:817-22.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Confalonieri M, Gazzaniga P, Gandola L, Aiolfi S, Della Porta R, Frisinghelli A, et al. Haemodynamic response during initiation of non-invasive positive pressure ventilation in COPD patients with acute ventilatory failure. Respir Med 1998;92:331-7.  Back to cited text no. 8  [PUBMED]  
9.Tramarin R, Torbicki A, Marchandise B, Laaban JP, Morpurgo M. Doppler echocardiographic evaluation of pulmonary artery pressure in chronic obstructive pulmonary disease. A European multicentre study. Working Group on Noninvasive Evaluation of Pulmonary Artery Pressure. European Office of the World Health Organization, Copenhagen. Eur Heart J 1991;12:103-11.  Back to cited text no. 9    
10.Danchin N, Cornette EA, Henriquez A, Godenir JP, Ethevenot G, Polu JM, et al. Two dimensional echocardiographic assessment of the right ventricle in patients with chronic obstructive lung disease. Chest 1987;92:229-33.  Back to cited text no. 10    

Copyright 2007 - Indian Journal of Critical Care Medicine


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