Question

Response must:

• be in the form of a 100 to 250-word well-developed paragraph
• contain well-developed sentences, correct spelling, and proper grammar
• demonstrate your achievement of lesson objectives in your response
• include data, facts, key terminology, specific examples and direct quotations from the textbook and at least 1 other resource to support your main point
• include appropriate citation and a resource list for all sources used.

Case Scenario: Your patient, a 70-year-old male recently admitted to the hospital, has a pCO₂ of 64, pO₂ of 69, and pH of 7.4. He is short of breath and has rattles in the bases of both lungs.

1. Question: Give an admitting diagnosis based on blood gases. Defend your answer using specific facts, data, and other information drawn from the textbook and at least one other supplemental source.

Answer 1

Greetings of the day!

Answer:

The patient is having COPD.

because pCO₂ = 64, pO₂ = 69, short of breath and has rattles in the bases of both lungs.

COPD

Chronic obstructive pulmonary disease (COPD) is characterised by persistent airflow limitation that is usually progressive and associated with a chronic inflammatory response in the airways and lungs to noxious particles or gases. The persistent airflow limitation results from a combination of diffuse small airway disease and destruction of the lung parenchyma (emphysema).

Chronic bronchitis is inflammation of the lining of the bronchial tubes, which carry air to and from the air sacs (alveoli) of the lungs. It's characterized by daily cough and mucus (sputum) production.

Emphysema is a condition in which the alveoli at the end of the smallest air passages (bronchioles) of the lungs are destroyed as a result of damaging exposure to cigarette smoke and other irritating gases and particulate matter.

COPD is a chronic inflammatory process in the lower airways and the lung parenchyma caused by many factors that trigger and maintain inflammation. An imbalance between proteases and anti-proteases may be a contributory factor.

Tobacco smoke

The most important and modifiable aetiological factor for COPD is smoking.

Smokers have a higher prevalence of respiratory symptoms and lung function abnormality, a greater annual rate of decline in FEV1 , and higher death rates from COPD than nonsmokers. Women may have more symptoms than men for the same number of pack-years smoked. About 40–50% of lifelong smokers will develop COPD, compared with only 10% of never-smokers. Passive exposure to cigarette smoke may also contribute to respiratory symptoms and impaired lung function in schoolchildren. However, not all smokers develop clinically significant COPD, which suggests that genetic factors may modify individual risk. The proportion of the risk of COPD attributable to smoking has been estimated as 40–60%, depending on how many risk factors have been taken into account.

Although never-smokers are less likely to have COPD and have less severe COPD than ever-smokers, never-smokers nonetheless comprise about one-quarter of those classified with Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage II+ COPD.

Occupational airborne exposure

Several studies show that 30–40% of the general population report having been exposed to airborne pollutants at work (for further information, see chapters 7 and chapter 24). When the exposure is sufficiently intense or prolonged, occupational dust, chemicals and vapours can cause COPD independently of cigarette smoking. Studies of general populations and working groups show that about 15–20% of COPD cases are due to occupational exposure. In never-smokers, the fraction of COPD attributable to occupational exposure is estimated to be 30%. A variety of occupations may represent an increased risk of COPD, such as mining, agriculture, and textile, paper, wood, chemical, and food processing.

Outdoor and indoor pollution

A high level of urban air pollution is harmful to individuals with COPD, as it can result in exacerbations and a poorer quality of life (for further information on air pollution, see chapter 6). The role of outdoor air pollution in Europe in causing COPD is unclear. The relative importance of short-term, high peak exposures compared with long-term, low-level exposures is not known. Heavy indoor air pollution caused by the use of biomass fuel is a risk factor for the development of COPD.

Socioeconomic status

The risk of developing COPD is inversely related to socioeconomic status based on education or income. The effects of various indicators of socioeconomic status may differ between men and women, and socioeconomic status may also reflect factors such as nutrition, overcrowding and air pollution, as well as genetic determinants.

Early life environmental factors

Smoking mothers, frequent respiratory infections and asthma in childhood, and bronchial hyperreactivity are important risk factors for COPD. The proportion of the risk of COPD attributable to these early childhood events may be as great as that attributable to smoking (see also chapter 4).

Genetic factors

The best documented genetic risk factor for COPD is hereditary α₁-antitrypsin deficiency (see also chapter 3). However, in most populations, homozygous α₁-antitrypsin deficiency is found in fewer than five people per 10 000. Polymorphisms of many genes or combinations of genes may increase (or decrease) the risk of an individual developing COPD. Individual genes may be related to specific phenotypes of COPD. Single genes, such as the gene encoding matrix metalloproteinase (MMP)-12, may be related to decline in lung function. Genome-wide studies of gene expression and genetic variation have provided exciting new avenues for future investigation and potentially new approaches to risk prediction and therapy.

Clinical manifestations

The most important symptoms of COPD are breathlessness on exertion and chronic cough with or without phlegm. The dyspnoea usually worsens over time but is often not present in mild or moderate COPD. The cough may be dry or productive. Cough and phlegm often precede dyspnoea on exertion by many years. Other symptoms include wheezing and chest tightness. As the disease progresses and reaches the severe stages, fatigue, weight loss and anorexia may increase. To establish the diagnosis of COPD, lung function measurement by spirometry is necessary.

A characteristic of COPD is exacerbations or episodes of acute worsening of the respiratory symptoms. The most common causes of exacerbations are viral or bacterial infections. Increased air pollution also appears to precipitate exacerbations of COPD. Some patients are particularly prone to exacerbations while others are not. Two or more exacerbations during the previous year is the most important indicator of a future exacerbation.

Exacerbations accelerate the decline in lung function that characterises COPD, resulting in reduced physical activity, poorer quality of life, and an increased risk of death; they are also responsible for a large proportion of the healthcare costs attributable to COPD.

Patients with COPD often suffer from other diseases (comorbidities). The comorbidities may share common risk factors with COPD, in particular cigarette smoking. They may also represent extrapulmonary manifestations or complications of COPD, such as muscle dysfunction due to inactivity. Comorbidities may be secondary to treatment of COPD; for example, osteoporosis due to oral corticosteroid treatment. The most common comorbidities in COPD are ischaemic heart disease, anxiety and depression, osteoporosis, skeletal muscle dysfunction, gastro-oesophageal reflux, anaemia, lung cancer, diabetes and metabolic syndrome. Comorbidities contribute to the overall severity and manifestations of the disease. They can occur in mild, moderate or severe COPD and they increase the risks of hospitalisation and mortality of COPD independently.

The clinical effects of COPD show considerable inter-individual variation, depending on which respiratory symptoms predominate, the frequency of exacerbations, the level and rate of lung function decline and the amount of emphysema, as well as comorbidities. Various subtypes of the disease are often termed phenotypes of COPD.

People with COPD are also likely to experience episodes called exacerbations, during which their symptoms become worse than the usual day-to-day variation and persist for at least several days.

A characteristic of COPD is exacerbations or episodes of acute worsening of the respiratory symptoms. The most common causes of exacerbations are viral or bacterial infections. Increased air pollution also appears to precipitate exacerbations of COPD. Some patients are particularly prone to exacerbations while others are not. Two or more exacerbations during the previous year is the most important indicator of a future exacerbation.

Exacerbations accelerate the decline in lung function that characterises COPD, resulting in reduced physical activity, poorer quality of life, and an increased risk of death; they are also responsible for a large proportion of the healthcare costs attributable to COPD.

Patients with COPD often suffer from other diseases (comorbidities). The comorbidities may share common risk factors with COPD, in particular cigarette smoking. They may also represent extrapulmonary manifestations or complications of COPD, such as muscle dysfunction due to inactivity. Comorbidities may be secondary to treatment of COPD; for example, osteoporosis due to oral corticosteroid treatment. The most common comorbidities in COPD are ischaemic heart disease, anxiety and depression, osteoporosis, skeletal muscle dysfunction, gastro-oesophageal reflux, anaemia, lung cancer, diabetes and metabolic syndrome. Comorbidities contribute to the overall severity and manifestations of the disease. They can occur in mild, moderate or severe COPD and they increase the risks of hospitalisation and mortality of COPD independently.

The clinical effects of COPD show considerable inter-individual variation, depending on which respiratory symptoms predominate, the frequency of exacerbations, the level and rate of lung function decline and the amount of emphysema, as well as comorbidities. Various subtypes of the disease are often termed phenotypes of COPD.

ABG ANALYSIS

COPD’s pathology includes loss of tissue elasticity, emphysematous bullae, small airway obstruction, and destruction of lung parenchyma. Persons with COPD are typically separated into one of two catagories: “pink puffers” (normal PaCO₂, PaO₂ > 60 mmHg) or “blue bloaters” (PaCO₂ > 45 mmHg, PaO₂ < 60 mmHg). Pink puffers have severe emphysema, and characteristically are thin and free of signs of right heart failure. Blue bloaters, on the other hand, have frequent episodes of right heart failure, and produce copious sputum resulting in coughing and respiratory infections. Blue bloaters presents more of a chronic bronchitis picture although they too may exhibit emphysematous changes.

Pink puffers (normal PaCO₂, PaO₂ > 60 mmHg) have emphysematous lung tissue destruction. Diffusing capacity is decreased by destroyed pulmonary capillaries. ABG’s are near normal due to compensatory hyperventilation. The only subtle changes typically are a PaO₂ slightly depressed (often in the mid 70’s, resulting in mild pulmonary vasoconstriction), and a low-normal PaCO₂.

Blue bloaters (PaCO₂ > 45 mmHg, PaO₂ < 60 mmHg) suffer from pulmonary hypoxic vasoconstriction from the marked hypoxia and respiratory acidosis. This in turn leads to right ventricular hypertrophy and cor pulmonale. The right heart failure then leads to systemic venous congestion, peripheral edema, hepatic congestion, and ascites. Secondary erythrocytosis may occur, spurred by the hypoxia. Changes on ABG’s are much more pronounced.

Causes

Complications

COPD can cause many complications, including:

• Respiratory infections. People with COPD are more likely to catch colds, the flu and pneumonia. Any respiratory infection can make it much more difficult to breathe and could cause further damage to lung tissue.
• Heart problems. For reasons that aren't fully understood, COPD can increase your risk of heart disease, including heart attack
• Lung cancer. People with COPD have a higher risk of developing lung cancer.
• High blood pressure in lung arteries. COPD may cause high blood pressure in the arteries that bring blood to your lungs (pulmonary hypertension).
• Depression. Difficulty breathing can keep you from doing activities that you enjoy. And dealing with serious illness can contribute to the development of depression.

Prevention

Identification and reduction of exposure to risk factors are important steps in the prevention and treatment of COPD. All individuals who smoke should be encouraged to quit regardless of their disease status. In addition, smokers without COPD should be offered smoking-cessation advice.

Preventing passive smoking in fetal and early life is important to reduce the risk of COPD in adult life. Smoking cessation is the most cost-effective form of both primary and secondary intervention in COPD. On a global scale, reduction of exposure to smoke from indoor biomass combustion, particularly among women and children, is important to reduce the prevalence of COPD.

Prevention of COPD exacerbations is important: influenza and pneumococcal vaccination as well as treatment with inhaled long-acting bronchodilators and inhaled corticosteroids all work to reduce exacerbations and hospitalisations for COPD.

Management

A COPD management programme includes the following four components: assessment and monitoring of disease; reduction of risk factors; management of stable COPD; and management of exacerbations. The goals of COPD management are to relieve symptoms, prevent disease progression, improve exercise tolerance, improve health status, prevent and treat complications and exacerbations, reduce mortality and prevent or minimise side-effects from treatment.

Important components of management are smoking cessation, medical treatment with bronchodilators as well as inhibitors of inflammation, physical exercise and, in advanced disease, oxygen therapy (see chapter 28).

Early rehabilitation after exacerbations is important (see chapter 29). The most effective component of pulmonary rehabilitation is physical exercise.

In the future, better classification of the different phenotypes of COPD is likely to enable implementation of personalised treatment, in which the characteristics of the patient together with the severity of the disease are the keys to choosing the best treatment option.

Comorbidities should be assessed at all stages of COPD. Differential diagnosis can often be difficult, as comorbidities with symptoms commonly seen in COPD may be overlooked, for instance heart failure or lung cancer causing breathlessness or depression presenting with fatigue. In general, any comorbiditity should be treated as in patients who do not have COPD.

Prognosis

COPD is a chronic, progressive disease showing great variation in its natural history. Spirometry providing data on FEV ₁ and FVC is the most common measure of disease progression. A large cohort of patients with COPD of GOLD stage II+ followed up every 6 months for 3 years showed a mean annual decline in FEV ₁ of 33 mL. An annual decline in FEV ₁ >40 mL was seen in 38% of the patients, while 8% showed an average annual increase of 20 mL. Current smoking and emphysema are related to more rapid decline in FEV ₁ .

In addition to rapid decline in FEV ₁ , factors that indicate a poor prognosis in established COPD are frequent exacerbations, respiratory insufficiency, nutritional status and comorbidities.

Smoking cessation is the most important intervention that affects the prognosis of the disease.

Future developments

There is a great deal of room for improvement in COPD care in Europe, and current trends suggest the following developments are possible and desirable.

• More accurate data on illness, exacerbations, natural history, cost and deaths, particularly in eastern Europe, will provide a stronger foundation for fighting COPD.
• Studies of the effectiveness of current prevention, education, medication, rehabilitation and terminal care will help to spread best practice and drive higher standards of COPD care.
• New therapeutic modalities will inhibit the decline in lung function.
• As smoking remains the key risk factor for COPD, several measures will reduce the burden of disease: more effective smoking cessation interventions and techniques to prevent people from starting to smoke; better surveillance of harmful occupational exposures; and protection in early childhood against harmful exposure and events that affect the lung.
• Governments, industry and the general public need to be made aware of the high burden of COPD in Europe. European countries should implement common strategies for effective prevention, diagnosis and treatment of this disabling and life-threatening disease.

Research needs

Research is needed in six key areas related to COPD.

• As smoking rates in Europe are declining, the relative importance of other risk factors to COPD will increase. There is a need to know how this will affect the clinical manifestations and prognosis of the disease.
• Although spirometry is a prerequisite in COPD studies, more extensive characterisation of disease than that offered by spirometry is required. Novel imaging techniques and biomarkers offer the potential to characterise subgroups, or phenotypes, of COPD.
• Limited data are available about the prevalence, incidence and natural history of various phenotypes of COPD, and their economic burden on European societies.
• Our knowledge of the pathogenesis of COPD and how this can be modified is still limited. Novel molecular and genetic techniques offer promising possibilities for gaining important knowledge on disease mechanisms, which opens up possibilities for development of new drugs.
• Cohort studies should be conducted to assess the long-term natural history of COPD and its phenotypes.
• The lungs are extremely exposed to the environment. There are few data on how global warming will affect the risk factors for, and eventually the incidence of, COPD.