**8.3 Pneumonia**

COPD predisposes the lungs to pneumonia as part of acute exacerbation or as discrete event. (Ewing & Torres,1999;Griffith & Mazurek,1991 as cited in Shapiro SD,2010)

#### **8.4 Systemic complications and co-morbidities**

Ischemic cardiac disease is more common in COPD and cardiac events are the single largest cause of mortality in this population (Ashley et al.,1975;Mannino et al,2003 as cited in Shapiro SD,2010). Arrhythmia, congestive heart failure and aortic aneurysm are more common. COPD may lead to a hypercoagulable state due to erythrocytosis and systemic inflammation(mediated via TNF-α, IL-6) posing greater risk of stroke, pulmonary embolism and deep vein thrombosis(Bhowmik et al,2000;Wouters et al.,2002 as cited in Shapiro SD,2010). Weight loss, osteoporosis, skin wrinkling, anemia, fluid retention and depression are some of the other systemic co-morbidities commonly associated with COPD. Major chronic diseases (e.g. congestive heart failure, dementia, ischaemic heart disease, stroke, diabetes, cancer, asthma, COPD, depression and hypertension) were associated with at least one of the other diseases in 60–90% of cases(Charlson et al.,2007 as cited in Shapiro SD,2010). A major question is whether coexisting chronic illnesses found in COPD subjects are merely related to common risk factors (e.g. aging, tobacco smoking and genetic predisposition) or are also consequences, at least in part, of the pulmonary and/or systemic inflammation that characterise COPD.

### **9. Diagnosis and laboratory work-up**

#### **9.1 Spirometry**

Objective measurement of airflow obstruction is the mainstay of workup for diagnosis, staging and follow-up of COPD(Petty,2001). The most important values measured are the forced expiratory volume in one second (FEV1) and the forced vital capacity (FVC) or the forced expiratory volume after 6 seconds, (FEV6 ), which is the recommended substitute for FVC(Enright et al.,2002 as cited in Shapiro SD,2010). COPD is confirmed when a patient, who has symptoms that are compatible with COPD, is found to have airflow obstruction (FEV1/FVC ratio less than 0.70 and an FEV1 less than 80 percent of predicted) and there is no alternative explanation for the symptoms and airflow obstruction (eg, bronchiectasis, vocal cord paralysis, tracheal stenosis). If airflow is abnormal, postbronchodilator testing should be performed. Correction of airflow to the normal range suggests a diagnosis of asthma and could exclude COPD. Because of variability in the FVC (or FEV6) measure, the FEV1/FVC ratio can establish a diagnosis of obstruction but is not useful to monitor disease progression(GOLD,2006). FEV1/FVC ratio is the basis for GOLD staging of COPD(see Table 2).


\*FEV1: forced expiratory volume in one second; \*\*FVC: forced vital capacity; \*\*\*Chronic respiratory failure: arterial partial pressure of oxygen (PaO2) less than 60 mm Hg (8.0 kPa) with or without arterial partial pressure of CO2 (PaCO2) greater than 50 mm Hg (6.7 kPa) while breathing air at sea level.

Table 2. Staging of severity of COPD (GOLD,2006)

Other spirometric findings include decreased inspiratory capacity and vital capacity, accompanied by increased total lung capacity, functional residual capacity, and residual volume are indicative of hyperinflation. The single breath carbon monoxide diffusing capacity (DLCO) decreases in proportion to the severity of emphysema because of the destruction of the alveoli and the loss of alveolar capillary bed.(Bates,1989)

### **9.2 Arterial blood gas**

134 Chronic Obstructive Pulmonary Disease – Current Concepts and Practice

Both resting and exercise mean pulmonary arterial pressures may be elevated. Prolonged pulmonary hypertension can give rise to chronic cor pulmonale in late stages. Alveolar hypoxia, respiratory acidosis, remodeling of the pulmonary vasculature with medial hypertrophy of muscular pulmonary arteries, increased viscosity of blood due to erythrocytosis, increased blood volume, left ventricular dysfunction and chronic pulmonary thromboembolic disease can all contribute to the pulmonary hypertension(Farber et al.,1982;Fletcher et al,1989 as cited in Shapiro SD,2010). Correction of hypoxia and acidosis

COPD predisposes the lungs to pneumonia as part of acute exacerbation or as discrete

Ischemic cardiac disease is more common in COPD and cardiac events are the single largest cause of mortality in this population (Ashley et al.,1975;Mannino et al,2003 as cited in Shapiro SD,2010). Arrhythmia, congestive heart failure and aortic aneurysm are more common. COPD may lead to a hypercoagulable state due to erythrocytosis and systemic inflammation(mediated via TNF-α, IL-6) posing greater risk of stroke, pulmonary embolism and deep vein thrombosis(Bhowmik et al,2000;Wouters et al.,2002 as cited in Shapiro SD,2010). Weight loss, osteoporosis, skin wrinkling, anemia, fluid retention and depression are some of the other systemic co-morbidities commonly associated with COPD. Major chronic diseases (e.g. congestive heart failure, dementia, ischaemic heart disease, stroke, diabetes, cancer, asthma, COPD, depression and hypertension) were associated with at least one of the other diseases in 60–90% of cases(Charlson et al.,2007 as cited in Shapiro SD,2010). A major question is whether coexisting chronic illnesses found in COPD subjects are merely related to common risk factors (e.g. aging, tobacco smoking and genetic predisposition) or are also consequences, at least in part, of the pulmonary and/or systemic inflammation that

Objective measurement of airflow obstruction is the mainstay of workup for diagnosis, staging and follow-up of COPD(Petty,2001). The most important values measured are the forced expiratory volume in one second (FEV1) and the forced vital capacity (FVC) or the forced expiratory volume after 6 seconds, (FEV6 ), which is the recommended substitute for FVC(Enright et al.,2002 as cited in Shapiro SD,2010). COPD is confirmed when a patient, who has symptoms that are compatible with COPD, is found to have airflow obstruction (FEV1/FVC ratio less than 0.70 and an FEV1 less than 80 percent of predicted) and there is no alternative explanation for the symptoms and airflow obstruction (eg, bronchiectasis, vocal cord paralysis, tracheal stenosis). If airflow is abnormal, postbronchodilator testing should be performed. Correction of airflow to the normal range suggests a diagnosis of

by long-term oxygen therapy and pulmonary vasodilators may slow this process.

event. (Ewing & Torres,1999;Griffith & Mazurek,1991 as cited in Shapiro SD,2010)

**8.2 Pulmonary hypertension and Cor pulmonale** 

**8.4 Systemic complications and co-morbidities** 

**8.3 Pneumonia** 

characterise COPD.

**9.1 Spirometry** 

**9. Diagnosis and laboratory work-up** 

Arterial blood gases reveal mild or moderate hypoxemia without hypercapnia in the early stages of COPD. In the later stages of the disease, hypoxemia tends to become more severe and may be accompanied by hypercapnia with increased serum bicarbonate levels(Bates,1989). The changes in ABG represent ventilation perfusion mismatch, which may be worsened during exercise, sleep and episodes of exacerbation.

### **9.3 Alpha1-antitrypsin level**

Of the approximately 75 different alleles for alpha1-antitrypsin (AAT) deficiency variants, 10-15 are associated with serum levels below the protective threshold of 11 µmol/dL. The most common severe variant is the Z allele, which accounts for 95% of the clinically recognized cases of severe AAT deficiency. The diagnosis of severe AAT deficiency is confirmed when the serum level falls below the protective threshold value (ie, 3-7 µmol/dL). Specific phenotyping is reserved for patients in whom serum levels are 7-11 µmol/dL or when genetic counseling or family analysis is needed.

#### **9.4 Sputum evaluation**

In patients with stable chronic bronchitis, the sputum is mucoid and the predominant cells are macrophages(Miravitlles,2002;Sethi et al.,2002 as cited in Shapiro SD,2010). With an exacerbation, the sputum becomes purulent, with excessive neutrophils and a mixture of organisms visualized through Gram staining. *Streptococcus pneumoniae* and *Haemophilus influenzae* are pathogens frequently cultured during exacerbations.

Current Overview of COPD with Special Reference to Emphysema 137

Treatment of COPD encompasses health promotion, prevention, control of symptoms and exacerbations, rehabilitation and palliation. Treatment plan needs to be individualized according to the stage and characteristics of the disease, age, co-morbidities in each patient. Global Initiative for Chronic Obstructive Lung Disease (GOLD) recommends that pharmacologic and nonpharmacologic therapies should be added in a stepwise fashion to control symptoms, decrease exacerbations, and improve patient function and quality of life (GOLD,2006). Patient should be educated about the disease and should be encouraged to participate actively in therapy and understand the need of proper dosing and timing of

ATS Statement (1995) recommended symptomatic management after the patient presented to the healthcare system with specific complaints(ATS,1995). However, new evidence suggests that the "pre-symptomatic" phase individuals progressively loose lung function in these years and also have poorer prognosis in terms of cardiac outcomes and hence earlier and more aggressive diagnosis and appropriate treatment of these previously unidentified individuals can help, not only by slowing progression but also by improving symptomatic

Mainstays of drug therapy of stable COPD are bronchodilators, primarily beta agonists and anticholinergics, and inhaled glucocorticoids, given alone or in combination depending upon the severity of disease and response to therapy. Attention to co-morbidities like heart disease, depression, osteoporosis and rehabilitation for acceptable quality of life is also important. Reduction of risk factors like cigarette smoking and occupational exposure should be a central feature of every comprehensive treatment plan. The only medical therapies that clearly reduce disease progression and mortality are smoking cessation and

Smoking cessation is the single most effective therapy for the majority of COPD patients(Anthonisen et al,1994;Department of Health and Human Services(US),2008). The transition from smoking to nonsmoking status involves following five stages: precontemplation, contemplation, preparation, action, and maintenance. Smoking intervention programs include self-help, group, physician-delivered, workplace, and community programs. Setting a target date to quit may be helpful. Physicians and other

≥65% 50–64% 36–49% ≤35%

≥350 250–349 150–249 ≤149

Parameter 0 Points 1 Point 2 Points 3 Points **B**ody: BMI >21 ≤21 — —

**D**yspnea: MMRC score 0-1 2 3 4

BMI, body mass index; FEV1, forced expiratory volume in 1 second. Table 3. BODE Index for Staging COPD (Celli et al.,2004)

medications as well as proper inhaler technique is essential.

**O**bstruction: FEV1 (%

**E**xercise: 6-minute walk distance (meters)

predicted)

**11. Treatment** 

control(GOLD,2006).

supplemental oxygen (NOTT,1980).

**11.1 Cessation of cigarette smoking** 
