scholarly journals The Significance of Elevated Brain Natriuretic Peptide Levels in Chronic Obstructive Pulmonary Disease

2005 ◽  
Vol 33 (5) ◽  
pp. 537-544 ◽  
Author(s):  
E Bozkanat ◽  
E Tozkoparan ◽  
O Baysan ◽  
O Deniz ◽  
F Ciftci ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Brain Natriuretic Peptide ◽  
Pulmonary Disease ◽  
Natriuretic Peptide ◽  
Forced Expiratory Volume ◽  
Gas Analysis ◽  
Arterial Oxygen ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Arterial Blood

We investigated the clinical significance of brain natriuretic peptide (BNP), a cardiac hormone, in chronic obstructive pulmonary disease (COPD). Subjects were 38 patients with stable COPD, of whom 20 had cor pulmonale (CP), and 22 were healthy individuals. Plasma BNP levels were measured and pulmonary arterial pressure (PAP) was estimated by echocardiography. Arterial blood gas analysis, forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) were also recorded. BNP levels of patients with COPD were higher than those of controls (48.2 ± 37.5 and 9.3 ± 3.0 pg/ml). Patients with CP had a higher mean BNP level with respect to those without CP (73.9 ± 35.8 and 21.0 ± 10.2 pg/ml, respectively). BNP levels correlated with PAP ( r = 0.68), partial arterial oxygen pressure ( r = −0.70), FEV1 ( r = −0.65) and FVC ( r = −0.52). We have concluded that BNP determination has a role in the diagnosis of CP in patients with COPD.

Elevated levels of brain natriuretic peptide in acute hypoxaemic chronic obstructive pulmonary disease

1992 ◽  
Vol 83 (5) ◽  
pp. 529-533 ◽  
Author(s):  
Chim C. Lang ◽  
Wendy J. Coutie ◽  
Allan D. Struthers ◽  
D. Paul Dhillon ◽  
John H. Winter ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Pulmonary Disease ◽  
Natriuretic Peptide ◽  
Plasma Levels ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Arterial Partial Pressure ◽  
Atrial Natriuretic

1. Studies in vitro have recently shown that both atrial natriuretic peptide and brain natriuretic peptide have pulmonary vasorelaxant activity. The purpose of the present study was to evaluate for the first time whether plasma levels of brain natriuretic peptide are elevated in chronic obstructive pulmonary disease. Plasma levels of brain natriuretic peptide and atrial natriuretic peptide were therefore measured in 12 patients admitted with acute hypoxaemic chronic obstructive pulmonary disease [arterial partial pressure of O2, 6.2 ± 0.4 kPa; arterial partial pressure of CO2, 6.9 ± 0.1 kPa; forced expiratory volume in 1 s, 0.6 ± 0.07 litre (27 ± 3% of predicted)]. All but three patients had oedema on admission. 2. Plasma levels of both brain natriuretic peptide and atrial natriuretic peptide were elevated in patients with chronic obstructive pulmonary disease (31.4 ± 4.1 pmol/l and 45.0 ± 8.1 pmol/l, respectively) compared with healthy control subjects (1.7 ± 0.8 pmol/l and 8.0 ± 3.5 pmol/l, respectively). Thus, plasma levels of brain natriuretic peptide and atrial natriuretic peptide in patients with chronic obstructive pulmonary disease were increased by 18.5- and 5.6-fold respectively compared with healthy control subjects. 3. There was a significant inverse correlation between the plasma level of brain natriuretic peptide and the arterial partial pressure of O2 (r = −0.65, r2 = 0.42, P = 0.03), but not between the plasma atrial natriuretic peptide level and the arterial partial pressure of O2 (r2 = 0.07, not significant). The arterial partial pressure of CO2 did not correlate with the plasma level of either brain natriuretic peptide or atrial natriuretic peptide. 4. Thus, plasma levels of brain natriuretic peptide were proportionately higher than those of atrial natriuretic peptide in patients with hypoxaemic chronic obstructive pulmonary disease. Unlike those of atrial natriuretic peptide, plasma levels of brain natriuretic peptide were correlated with the degree of hypoxaemia. Further studies are required to investigate the release and clearance of brain natriuretic peptide in chronic obstructive pulmonary disease, as well as its pulmonary vasodilator activity in vivo.

scholarly journals Meal Induced Oxygen Desaturation and Dyspnea in Chronic Obstructive Pulmonary Disease

1998 ◽  
Vol 5 (5) ◽  
pp. 361-365 ◽  
Author(s):  
Norman Wolkove ◽  
Li Yi Fu ◽  
Ashok Purohit ◽  
Antoinette Colacone ◽  
Harvey Kreisman
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Arterial Oxygen Saturation ◽  
Care Facility ◽  
Forced Expiratory Volume ◽  
Oxygen Desaturation ◽  
Arterial Oxygen ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Severe Copd

OBJECTIVE: To study arterial oxygen saturation (SpO2) obtained by pulse oximetry and dyspnea during active eating (AE) and passive eating (PE) in patients with severe chronic obstructive pulmonary disease (COPD).DESIGN: Patients were studied on two consecutive days with AE and PE, which occurred in random order. SpO2was recorded for 20 mins before and during eating, and dyspnea was recorded by the patient using a 10 cm visual analogue scale before and upon completion of eating.SETTING: Subjects were in-patients at an intermediate care facility who were hospitalized for pulmonary rehabilitation or for convalescence after an exacerbation of COPD.POPULATION STUDIED: Thirty-five patients with severe COPD (forced expiratory volume in 1 s [FEV1] less than 50% predicted, FEV1to forced vital capacity ratio less than 65%) were studied. Mean age was 70.5±7.1 years.MAIN RESULTS: Mean SpO2decreased significantly (P<0.05) from 91.7±3.4% to 90.1±4.0% during AE, and 91.7±3.2% to 90.8±3.6% during PE. Mean lowest SpO2was lower and percentage of time with SpO2less than 90% was greater during eating compared with corresponding control periods during both AE and PE. Dyspnea increased significantly (P<0.05) from 1.4±1.2 to 3.3±2.3 cm during AE, and from 1.5±1.5 to 2.4±2.2 cm during PE. The increase in dyspnea was significantly greater during AE than PE.CONCLUSIONS: Eating is an activity that can adversely affect SpO2and increase dyspnea in patients with severe COPD. Oxygen desaturation and particularly increased dyspnea may at least in part relate to the recruitment of upper extremity muscles during eating.

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