European Journal of Cardiovascular Medicine

Airway diseases include several conditions such as asthma and chronic obstructive pulmonary disease (COPD). An acute exacerbation of obstructive airway disease refers to a sudden aggravation of respiratory symptoms in a patient already diagnosed with COPD or asthma.^[1] Pulmonary hypertension (PH) arising secondary to COPD is classified under group 3 of the WHO classification, which covers PH associated with lung diseases and/or hypoxemia.^[2]

PH is hemodynamically defined by an abnormal rise in pulmonary arterial pressure (PAP).^[3] The occurrence of PH among patients with COPD (COPD-PH) is clinically significant and largely correlates with disease severity. Moreover, specific genetic markers have been implicated in the development of PH in COPD.^[4] Evidence from patients with spirometric Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 4 indicates that up to 90% may present with abnormal mean pulmonary arterial pressure (mPAP) >20 mmHg, most often within the range of 20–35mmHg. Only about 1%–5% of COPD patients exhibit mPAP values exceeding 35–40 mmHg at rest.^[5]

Hemodynamically, PAP is determined by cardiac output, pulmonary vascular resistance (PVR), and pulmonary artery wedge pressure (PAWP). In COPD, resting PH arises mainly due to elevated PVR, whereas PH during exertion is chiefly the result of increased cardiac output in the presence of relatively “fixed” PVR, reflecting impaired recruitability and distensibility of pulmonary vessels.^[6] Hyperinflation contributes to raised PVR and PAWP,^[7,8] and increases PAP, especially during physical activity.⁷ Traditionally, elevated PVR in COPD has been attributed to hypoxic pulmonary vasoconstriction, vascular remodeling, emphysematous destruction of the pulmonary vascular bed, polycythemia, and hyperinflation. However, more recently, endothelial dysfunction and systemic inflammation have also been identified as important contributors to PH pathogenesis. Indeed, cigarette smoke–induced endothelial dysfunction is thought to represent the initiating step in the development of PH in COPD.^[9] There is a paucity of data about the about the characteristics of patients with acute exacerbations of obstructive airway diseases in our study setting.

OBJECTIVEs

• Effect of acute exacerbations of obstructive airway diseases on pulmonary artery systolic pressure in our tertiary care centre.
• To assess the effect of bronchodilation on changes in FEV₁ and FVC in patients with acute exacerbations of obstructive airway diseases in our tertiary care centre.

Study Design and Patients

This is a prospective study conducted with total of 50 patients with history of exacerbations of airway obstructive diseases attended OPD or admitted in the wards of Department of Pulmonary Medicine at J. J. M. Medical College (JJMMC), Davangere, Karnataka. A written informed consent was taken from all the patients participating in the study.

Inclusion Criteria

1. Age: ≥18 years
2. Gender: both males and females
3. Patients with asthma
4. Patients with COPD
5. Patients with cough and dyspnea
6. Post bronchodilator FEV₁/FVC <0.70 in spirometry

Exclusion Criteria

1. Pregnant women
2. Other chronic medical disorders like Systemic Lupus Erythematosus (SLE) or cancer
3. Suffering from any neurological or psychiatric illness
4. Patients not willing to sign informed consent form

Assessment Parameters

The demographic details, such as age, gender, history of smoking, tabaco consumption, and any allergies were recorded. The following clinical and hemodynamic characteristics were measured and assessed:

• Pulmonary Artery Systolic Pressure (PASP), mmHg
• Forced Expiratory Volume in 1 second (FEV₁), %
• Forced Vital Capacity (FVC), %
• FEV₁/FVC
• Partial pressure of oxygen (PaO₂)

The FEV1 and FVC were measured pre- and post-bronchodilator treatment

Statistical Analysis

Data were entered in Microsoft Excel 2021 and statistical analysis was done using IBM Statistical Software for Social Sciences (SPSS) version 22. Categorical variables were represented in the form of frequency, and percentage. Continuous variables were presented as descriptive statistics (Mean and Standard deviation). Independent sample t-test was done to compare the difference between pre- and post-bronchodilator treatment. p<0.05 was considered statistically significant

The mean age of patients was 50.86 year with majority being distributed in the age group of 41-50 years (26%). Male predominance (52%) was observed as compared to females (48%). 48% and 36% of patients were having history of smoking and alcohol abuse respectively. Furthermore, 42% of the patients having history of allergies (Table 1).

Table 1: Demographic characteristics

The mean (±SD) PASP, PaO₂, and FEV₁/FVC of eligible patients enrolled in to the study were found to be 40.78 (±15.29), 78.76 (±10.41), and 0.82 (±0.39) respectively (Table 2).

Table 2: Descriptive statistics

In patients with exacerbation of obstructive airway diseases there was a statistically significant (p<0.001) increase in FEV₁ and FVC values were observed post-bronchodilation as compared to pre-bronchodilation (Table 3).

Table 3: Comparison of FEV₁ and FVC between pre- and post-bronchodilation

Values are expressed as mean ± SD; n=50  

In this prospective study, we sought to evaluate the impact of bronchodilation on FEV₁ and FVC changes in patients presenting with acute exacerbations of obstructive airway diseases, as there is limited data regarding the characteristics of such patients in our tertiary care setting.

The mean age of study participants was 51 years, with the majority falling within the 41–50-year age group. These results were consistent with findings reported in earlier studies. For instance, Manjhi et al., in a cross-sectional observational study, documented a mean patient age of 66.42 years, with most cases occurring in the 60–69-year age group.^[10] In our cohort, 52% of patients were male and 48% were female, which aligns with the male predominance described by Manjhi et al. in their observations.^[10]

Clinical guidelines for COPD diagnosis recommend performing spirometry after administering an adequate dose of an inhaled bronchodilator to minimize measurement variability.^[11,12] Similarly, our study demonstrated a statistically significant improvement (p<0.001) in both FEV₁ and FVC after bronchodilator administration compared to baseline (pre-bronchodilator) values. Calverley et al. emphasized that bronchodilator responsiveness can be highly variable, noting that over half of patients initially classified as reversible by ATS/GOLD criteria could be categorized differently upon repeat testing.^[13]

Population-based research also indicates that post-bronchodilator spirometry reduces COPD prevalence estimates. For example, in the PLATINO study, bronchodilator testing decreased the overall prevalence of FEV₁/FVC% <0.70 from 21.7% to 14%.^[14] Hansen et al., in their study comprise of 985 COPD patients, reported that bronchodilator responsiveness, along with baseline FEV₁, was a positive prognostic marker. However, when baseline FEV₁ was replaced with post-bronchodilator FEV₁, bronchodilator reversibility lost its prognostic significance.^[15]

Burrows highlighted the complex association between bronchodilator response and clinical outcomes in obstructive lung disease.^[16] He suggested that inconsistencies among studies,^[17,18] may result from differences in initial lung function assessments, methods of measuring bronchodilator response, and varying asthma prevalence within populations. His observation that mortality is linked to age and reduced post-bronchodilator FEV₁ provides partial justification for using post-bronchodilator spirometry values in defining COPD.^[16]

This study outcomes demonstrated that obstructive airway disease has a significant impact on pulmonary arterial systolic pressure. Bronchodilation leads to improvements in forced expiratory volume and forced vital capacity, thereby enhancing overall pulmonary function in patients experiencing acute exacerbations. Consequently, post-bronchodilator measurements of forced expiratory volume and forced vital capacity may serve as valuable predictors of lung function in patients with acute exacerbations of obstructive airway diseases.

limitations

This study has a few limitations. First, it was carried out in a single tertiary care hospital, which may restrict the applicability of the findings to other healthcare settings. Second, the sample size was relatively small, and inclusion of a larger cohort would be necessary to draw more definitive conclusions. Third, right heart catheterization was not performed, which might have aided in identifying additional cases. Lastly, the possibility of observer bias could not be entirely ruled out.

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