How does COPD severity affect life expectancy. What role does smoking play in COPD prognosis. Can early diagnosis and lifestyle changes improve COPD outcomes. How is COPD classified and measured. What treatments are available for managing COPD symptoms.

Understanding COPD and Its Impact on Life Expectancy

Chronic Obstructive Pulmonary Disease (COPD) is a progressive lung condition that affects millions of people worldwide. While the diagnosis can be daunting, it’s crucial to understand that COPD doesn’t necessarily mean a shortened lifespan. The prognosis varies significantly from person to person, depending on various factors.

Dr. Albert A. Rizzo, chief medical officer for the American Lung Association, emphasizes that COPD is not a death sentence. Many individuals with COPD live into their 70s, 80s, or even 90s. However, the life expectancy can be influenced by the severity of the disease, overall health, lifestyle choices, and access to proper medical care.

COPD Severity Classification and Its Relation to Life Expectancy

The Global Initiative on Obstructive Lung Disease (GOLD) system is used to classify COPD severity. This classification is based on the forced expiratory volume (FEV1) test, which measures how much air a person can forcefully exhale in one second.

• GOLD 1: Mild COPD (FEV1 of 80% or more)
• GOLD 2: Moderate COPD (FEV1 50%-79%)
• GOLD 3: Severe emphysema/chronic bronchitis (FEV1 30%-49%)
• GOLD 4: Very severe COPD (FEV1 less than 30%)

Generally, a higher GOLD stage correlates with a higher risk of complications and mortality. However, it’s important to note that this is just one aspect of assessing COPD’s impact on life expectancy.

Symptom Severity and Exacerbation Risk

In addition to the GOLD stages, doctors also categorize patients based on their symptoms and risk of exacerbations (flare-ups). This categorization ranges from A to D, with D representing the highest symptom severity and exacerbation risk.

The Impact of Smoking on COPD Life Expectancy

Smoking is the leading cause of COPD and significantly affects life expectancy in COPD patients. Research has shown that the impact on life expectancy is much more pronounced in current and former smokers compared to those who have never smoked.

For male smokers aged 65 with COPD, the reduction in life expectancy varies based on the COPD stage:

• Stage 1: 0.3 years
• Stage 2: 2.2 years
• Stage 3: 5.8 years
• Stage 4: 5.8 years

This reduction is in addition to the 3.5 years of life expectancy lost due to smoking alone, regardless of COPD status. For women who are current smokers, the impact is even more severe, with a loss of about 5 years at Stage 2 and 9 years at Stage 4.

The BODE Index: A Comprehensive Measure of COPD Prognosis

The BODE Index is another tool used by healthcare professionals to assess life expectancy in COPD patients. This index takes into account multiple factors:

• Body mass index (BMI)
• Airflow Obstruction (measured by FEV1)
• Dyspnea (difficulty breathing)
• Exercise capacity (measured by a 6-minute walk test)

The BODE Index is considered more comprehensive than the FEV1 test alone, as it incorporates various aspects of the disease’s impact on overall health and functionality. A higher BODE score indicates a greater risk of mortality from COPD.

Treatment Options and Their Impact on COPD Prognosis

While there is currently no cure for COPD, various treatments can help manage symptoms and potentially improve life expectancy. Dr. Rizzo notes that researchers are still searching for medications that can slow down disease progression and reverse airway inflammation.

Current treatment options include:

• Bronchodilators: These medications, usually inhaled, help open airways and improve breathing.
• Corticosteroids: These can help control flare-ups, which is crucial as frequent hospitalizations are linked to higher mortality rates.
• Supplemental oxygen: For patients with consistently low oxygen levels, supplemental oxygen can be prescribed to improve quality of life and potentially extend lifespan.

How effective are these treatments in improving COPD prognosis? While they don’t cure the disease, proper management of symptoms and prevention of exacerbations can significantly impact a patient’s quality of life and potentially extend lifespan. Regular use of prescribed medications, especially those that help prevent flare-ups, can reduce the frequency of hospitalizations, which is a key factor in COPD prognosis.

The Importance of Early Diagnosis in COPD Management

Early diagnosis plays a crucial role in improving life expectancy for COPD patients. Dr. Rizzo estimates that approximately half of COPD patients had the disease for several years before being diagnosed. Many individuals mistakenly attribute symptoms like coughing and shortness of breath to other factors such as being overweight, out of shape, or continuing to smoke.

Early diagnosis allows for:

• Timely intervention and treatment
• Better management of symptoms
• Potential slowing of disease progression
• Improved quality of life

Is early diagnosis always possible? While it should be the goal, early diagnosis can be challenging due to the gradual onset of symptoms and the need for proper testing. Healthcare providers play a crucial role in recognizing potential COPD symptoms and ordering appropriate diagnostic tests, such as spirometry.

Lifestyle Changes and Their Impact on COPD Life Expectancy

In addition to medical treatments, lifestyle changes can significantly impact the life expectancy and quality of life for COPD patients. These changes include:

1. Smoking cessation: This is the single most important step a COPD patient can take to slow disease progression and improve life expectancy.
2. Regular exercise: Pulmonary rehabilitation programs can improve exercise capacity and quality of life.
3. Healthy diet: Proper nutrition can help maintain a healthy weight and support overall health.
4. Avoiding air pollutants: Minimizing exposure to indoor and outdoor air pollutants can help prevent exacerbations.
5. Vaccinations: Keeping up-to-date with flu and pneumonia vaccinations can prevent complications.

How much can these lifestyle changes improve COPD outcomes? While the impact varies from person to person, studies have shown that smoking cessation alone can significantly slow the rate of lung function decline. Regular exercise and pulmonary rehabilitation can improve exercise capacity and quality of life, potentially reducing the risk of hospitalizations and improving overall prognosis.

Socioeconomic Factors and Access to Care in COPD Prognosis

An often overlooked aspect of COPD life expectancy is the role of socioeconomic factors and access to healthcare. Dr. Rizzo points out that individuals with COPD who lack access to healthcare and insurance are more likely to experience complications and earlier mortality, even if their initial diagnosis is similar to those with better access to care.

Factors that can impact COPD prognosis include:

• Access to regular medical care
• Ability to afford medications and treatments
• Living conditions and exposure to air pollutants
• Nutritional status
• Education about the disease and self-management techniques

How can these disparities be addressed? Improving access to healthcare, providing education about COPD management, and addressing social determinants of health are crucial steps in reducing disparities in COPD outcomes. Community health initiatives and policy changes aimed at improving air quality and reducing smoking rates can also play a significant role in improving overall COPD prognosis across different socioeconomic groups.

Ongoing Research and Future Directions

The field of COPD research is continually evolving, with new studies aiming to better understand the disease and improve treatment options. Current areas of research include:

• Investigating why some individuals are more susceptible to COPD than others
• Developing new medications to slow disease progression and reverse airway inflammation
• Studying the impact of gender, age, and socioeconomic status on COPD outcomes
• Exploring the potential of personalized medicine in COPD treatment

These ongoing research efforts hold promise for improving COPD prognosis and quality of life for patients in the future. As our understanding of the disease grows, so too does the potential for more effective treatments and management strategies.

In conclusion, while COPD is a serious and progressive disease, it’s important to remember that a diagnosis doesn’t automatically mean a significantly shortened lifespan. With proper management, early intervention, and lifestyle changes, many individuals with COPD can lead full and active lives. The key lies in working closely with healthcare providers, adhering to treatment plans, and making positive lifestyle changes to manage the disease effectively.

COPD: What’s My Life Expectancy?

Written by Kathryn Whitbourne

• COPD Severity and Life Expectancy
• Symptoms and Severity
• Smoking Plays a Role
• The BODE Index
• Can Medication Help?
• Early Diagnosis Can Make a Difference
• Make Lifestyle Changes
• More

There’s no one-size-fits-all answer when it comes to predicting someone’s life span with COPD. A lot depends on your age, health, lifestyle, and how severe the disease was when you were diagnosed, plus the steps you’ve taken to lessen the damage afterward.

“COPD is a disease with a lot of moving parts,” says Albert A. Rizzo, MD, chief medical officer for the American Lung Association. “It’s not a death sentence by any means. Many people will live into their 70s, 80s, or 90s with COPD.”

But that’s more likely, he says, if your case is mild and you don’t have other health problems like heart disease or diabetes. Some people die earlier as a result of complications like pneumonia or respiratory failure.

Doctors use a classification system called the Global Initiative on Obstructive Lung Disease (or GOLD) system to determine how severe your COPD is. It’s based on how much air you can forcefully exhale in 1 second after blowing into a plastic tube called a spirometer. You’ll also hear this called a forced expiratory volume (FEV1) test.

The classifications are based on results for an adult your same age, gender, and ethnic group but without COPD. So if your airflow was 80% of someone’s airflow who doesn’t have COPD, you’d be at GOLD or Stage 1. There four stages:

• GOLD 1: Mild COPD (FEV1 of 80% or more)
• GOLD 2: Moderate COPD (FEV1 50%-79%)
• GOLD 3: Severe emphysema/chronic bronchitis (FEV1 30%-49%)
• GOLD 4: Very severe COPD (FEV1 less than 30%)

In general, the higher your number on the GOLD system, the more likely you are to have problems with or even die from COPD.

Do you have trouble breathing? Have you been hospitalized for COPD flare-ups, which doctors call exacerbations? Doctors look at your symptoms and put you in one of four categories, A-D. The most serious would be GOLD D (high symptom severity and high exacerbation risk).

Smoking is the leading cause of COPD. One study found a small drop in life expectancy (about 1 year) for people with COPD who had never smoked. But there was a much larger reduction for current and former smokers. For men age 65 who smoke, the drop in life expectancy is:

• Stage 1: 0.3 years
• Stage 2: 2.2 years
• Stage 3: 5.8 years
• Stage 4: 5.8 years

This is in addition to the 3.5 years of life all smokers, whether they have COPD or not, lose to the habit.

The same study also found that women who were current smokers and at Stage 2 lost about 5 years of their lives at Stage 3 and 9 years of their lives at Stage 4.

Another system doctors use to measure life expectancy with COPD is the BODE Index, which stands for:

• Body mass: Are you obese or overweight?
• Airflow obstruction: How much air can you forcefully exhale from your lungs in 1 second (the FEV1 test).
• Dyspnea: How hard is it to breathe?
• Exercise capacity: How far can you walk in 6 minutes?

The higher your BODE score, the greater your risk for death from COPD. This test is considered more accurate than just the FEV1 score.

Right now there aren’t any medicines that cure COPD. “We are still looking for drugs that can slow down the disease process itself and reverse inflammation in the airways,” Rizzo says. But there are bronchodilators (medications usually taken through inhalers) that can open your airways and improve shortness of breath.

Corticosteroids can help control flare-ups. That’s important because more COPD hospitalizations are linked to a higher likelihood of death.

If you’re constantly low on oxygen, your doctor might prescribe supplemental oxygen. You’ll get a device you can take with you anywhere to help you breathe.

And you have to have access to care in the first place. Rizzo says more studies are looking at COPD in terms of gender, age, and socioeconomic status. Someone with COPD who doesn’t have access to health care and doesn’t have insurance is more likely to have complications and die early, even if their diagnosis is the same as someone from a higher income level.

An early diagnosis can also greatly improve your life expectancy. “Probably half the people with COPD had the disease for a number of years before they were diagnosed,” Rizzo says. “They didn’t bring it to the attention of their physician because they thought the cough and the shortness of breath were related to being overweight, out of shape, and still smoking.”

Also, doctors have to diagnose COPD correctly by ordering the right tests, he says.

Rizzo also points to studies under way figure out why some people are more likely to get COPD than others. A study started this year by the National Institutes of Health and supported by the American Lung Association will look at lung function in 25-35-year-olds (lung function reaches its peak in the mid-20s) and figure out what changes over the course of their lifetime. “We want to notice when an individual develops findings of COPD, what may have led to it, and what we can learn from that to improve survival,” he says.

While there isn’t a drug to take care of COPD, there are many lifestyle changes you can make that will slow disease progression and improve your chances of living a longer life. You can:

• Quit smoking. It’s the most important thing you can do to improve your life expectancy with COPD.
• Avoid secondhand smoke and other things that might irritate your lungs.
• Exercise.
• Control your weight.
• Stay up to date with vaccines, including COVID-19, seasonal flu, and pneumonia vaccines.

Once you’ve been diagnosed with COPD, follow your doctor’s advice to stop smoking, exercise, and take any medications prescribed. “And most important, stay active,” Rizzo says. “Walking is the best exercise for lungs, so walk on a regular basis.”

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What You Need to Know

How long a person may live with COPD depends on the severity of the symptoms. There are various ways to measure COPD stages, including by looking at complications such as difficulty breathing or blocked airflow.

Millions of adults in the United States have chronic obstructive pulmonary disease (COPD), and just as many are developing it. But many of them are unaware, according to the National Heart Lung and Blood Institute.

One question many people with COPD have is, “How long can I live with COPD?” There’s no way to predict the exact life expectancy, but having this progressive lung disease can shorten lifespan.

How much so depends on your overall health and whether you have other diseases such as heart disease or diabetes.

Researchers over the years have come up with a way to assess the health of someone with COPD. One of the most current methods combines spirometry lung function test results with a person’s symptoms. These result in labels that can help predict life expectancy and guide treatment choices in those with COPD.

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) is one of the most used systems of classifying COPD. GOLD is an international group of lung health experts who periodically produce and update guidelines for doctors to use in the care of people with COPD.

Doctors use the GOLD system to assess people with COPD in “grades” of the disease. Grading is a way to measure the severity of the condition. It uses the forced expiratory volume (FEV1), a test that determines the amount of air a person can forcefully exhale from their lungs in one second, to categorize the severity of COPD.

The most recent guidelines make FEV1 part of the assessment. Based on your FEV1 score, you receive a GOLD grade or stage as follows:

• GOLD 1: FEV1 of 80 percent predicted or more
• GOLD 2: FEV1 of 50 to 79 percent predicted
• GOLD 3: FEV1 of 30 to 49 percent predicted
• GOLD 4: FEV1 of less than 30 percent predicted

The second part of the assessment relies on symptoms such as dyspnea, or difficulty breathing, and degree and amount of acute exacerbations, which are flare-ups that may require hospitalization.

Based on these criteria, people with COPD will be in one of four groups: A, B, C, or D.

Someone with no exacerbations or one that didn’t require hospital admission in the past year would be in group A or B. This will also depend on an assessment of breathing symptoms. Those with more symptoms would be in group B, and those with less symptoms would be in group A.

People with at least one exacerbation that required hospitalization, or at least two exacerbations that did or didn’t require hospital admission in the past year, would be in Group C or D. Then, those with more breathing symptoms would be in group D, and those with less symptoms would be in group C.

Under the new guidelines, someone labeled GOLD Grade 4, Group D, would have the most serious classification of COPD. And they’ll technically have a shorter life expectancy than someone with a label of GOLD Grade 1, Group A.

Another measure that uses more than just the FEV1 to gauge a person’s COPD condition and outlook is the BODE index. BODE stands for:

• body mass
• airflow obstruction
• dyspnea
• exercise capacity

BODE takes an overall picture of how COPD affects your life. Though the BODE index is used by some physicians, its value may be lessening as researchers learn more about the disease.

Body mass

The body mass index (BMI), which looks at body mass based on height and weight parameters, can determine if a person is overweight or obese. BMI can also determine if someone’s too thin. People who have COPD and are too thin may have a poor outlook.

Airflow obstruction

This refers to the FEV1, as in the GOLD system.

Dyspnea

Some prior studies suggest that trouble breathing can affect outlook for COPD.

Exercise capacity

This means how well you’re able to tolerate exercise. It’s often measured by a test called the “6-minute walk test.”

One of the key features of COPD is systemic inflammation. A blood test that checks for certain markers of inflammation may be helpful.

Research published in the International Journal of Chronic Obstructive Pulmonary Disease suggests that the neutrophil-to-lymphocyte ratio (NLR) and eosinophil-to-basophil ratio significantly correlate to the severity of COPD.

The above article suggests a routine blood test can measure these markers in those with COPD. It also noted that the NLR may be particularly helpful as a predictor for life expectancy.

As with any serious disease, such as COPD or cancer, probable life expectancy is based largely on the severity or stage of the disease.

For example, in a 2009 study published in the International Journal of Chronic Obstructive Pulmonary Disease, a 65-year-old man with COPD who currently smokes tobacco has the following reductions in life expectancy, depending on stage of COPD:

• stage 1: 0.3 years
• stage 2: 2.2 years
• stage 3 or 4: 5.8 years

The article also noted that for this group, an additional 3.5 years were also lost to smoking compared with those who never smoked and didn’t have lung disease.

For former smokers, the reduction in life expectancy from COPD is:

• stage 2: 1.4 years
• stage 3 or 4: 5.6 years

The article also noted that for this group, an additional 0.5 years were also lost to smoking compared to those who never smoked and didn’t have lung disease.

For those who never smoked, the reduction in life expectancy is:

• stage 2: 0.7 years
• stage 3 or 4: 1.3 years

For former smokers and those who’ve never smoked, the difference in life expectancy for people at stage 0 and people at stage 1 wasn’t as significant, as opposed to those who were current smokers.

What’s the upshot of these methods of predicting life expectancy? The more you can do to keep from progressing to a higher stage of COPD the better.

The best way to slow down the progression of the disease is to stop smoking if you smoke. Also, avoid secondhand smoke or other irritants such as air pollution, dust, or chemicals.

If you’re underweight, it’s helpful to maintain a healthy weight with good nutrition and techniques to increase food intake, such as eating small, frequent meals. Learning how to improve breathing with exercises such as pursed lip breathing will also help.

You may also want to participate in a pulmonary rehabilitation program. You’ll learn about exercises, breathing techniques, and other strategies to maximize your health.

And while exercise and physical activity may be challenging with a breathing disorder, it’s one of the best things you can do for the health of your lungs and the rest of your body.

Talk with your doctor about a safe way to start exercising. Learn the warning signs of breathing problems and what you should do if you notice a minor flare-up. You’ll want to follow any COPD medication therapy prescribed to you by your doctor.

The more you can do to improve your overall health, the longer and fuller your life can be.

Did you know?

COPD is the third leading cause of death in the United States, according to the American Lung Association.

Chronic obstructive pulmonary disease (COPD)

Ministry of Health of the Astrakhan Region

Center for Medical Prevention

Reminder for the public

B LUNGS

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the lungs, in which the airways are gradually blocked (their obstruction develops). This is due to chronic inflammation, which is usually caused by irritation of the bronchi and lungs by various substances that enter the body with air.

Most cases of COPD begin in people over 40 years of age. COPD leads to reversible (bronchospasm, swelling of the bronchial wall, impaired bronchial secretion), and irreversible (bronchial wall sclerosis, collapse of the small bronchi on expiration, pulmonary emphysema) changes in the respiratory system.

The systemic consequences of the disease are also formed. First of all, the skeletal muscles are affected, while the patient loses muscle mass and strength, which leads to limitation of physical activity. A patient with COPD has a higher risk of fractures and a decrease in bone density. COPD is a risk factor for the formation of cardiovascular changes, serves as a factor in the development of atherosclerosis of blood vessels and the heart.

COPD risk factors and mechanisms of development:

The main cause of COPD is tobacco smoke 80-90% cases (active and passive smoking). In order to calculate how dangerous smoking is for each patient, the PAKA coefficient was developed. To calculate this coefficient, you need to multiply the number of packs of cigarettes smoked per day (20 cigarettes per pack) by the number of years a person smokes. People who have a coefficient of 10 or higher have a very high risk of developing COPD, and the risk is greater, the higher the coefficient.

· Long-term inhalation of smoke from the combustion of biofuels (wood, coal for stove heating).

Presence of dust and chemicals at workplaces (found in miners, welders, workers in the metallurgical and chemical industries, etc.).

· Living in environmentally unfavorable conditions.

Frequent infections in childhood. Various infections (bacterial, viral) provoke the development of COPD exacerbation. Frequent viral diseases lead to a decrease in the level of immunity of the whole organism, and especially at the level of the bronchi, which contributes to the development of bacterial infections.

Main clinical signs of COPD:

900 10 1. Cough , both dry and with sputum that increases after a night’s sleep (the notorious “smoker’s cough”).

2. Progressive dyspnea , which appears due to obstruction of the passage of air through the bronchi. Difficulty breathing at first occurs only during fast walking, running and hard physical work. With a long course of the disease, shortness of breath begins to disturb even at rest, which leads to disability of the patient.

3. Wheezing in the chest when breathing (appear in later stages of the disease) and a feeling of tightness in the chest.

Obstructive pulmonary disease can develop in a person over many years, at first without manifesting itself. There are 4 stages of COPD severity:

I – mild;

II – moderate;

III – heavy;

IV – extremely severe.

Chronic obstructive pulmonary disease is a progressive disease! Most patients are treated in stages III and IV, when severe shortness of breath appears. In stages I and II, as a rule, there is no shortness of breath, but only a rare cough in the morning worries, so the patient does not go to the doctor. This is the trick of the disease. Most patients come late, valuable time for treatment is partially lost.

At each stage (I – IV) you can feel satisfactory (as usual) – this is the phase of remission or imaginary recovery, when the manifestations of the disease are minimal. But with hypothermia or for no apparent reason, an exacerbation may occur.

COPD is a chronic disease that cannot be cured but can be stopped.

In addition to the medication prescribed by your doctor, at all stages you must adhere to the following recommendations:

1. Quit smoking. Remember that smoking is a proven factor in the development of lung cancer. If you smoke, you should have an annual spirometry test and a simple exercise tolerance test that you can do yourself to help diagnose COPD. To do this, for 6 minutes, try to walk the maximum distance on level ground. A healthy person walks at least 600 m. If you walked less than 600 m during a 6-minute walk due to shortness of breath, consult a doctor – this may be the first symptom of COPD.

2. Avoid infectious diseases. Annual influenza vaccination is possible (in autumn, preferably in September or October).

3. Talk to your doctor about a rehabilitation program that improves respiratory muscle strength and endurance.

4. Avoid excessive exercise.

5. Do not interrupt the treatment prescribed by your doctor! Remember that the drugs you take to control COPD do not accumulate in your body and are not addictive!

BE HEALTHY! TAKE CARE OF YOURSELF!

Department

GBUZ JSC “CMP” – 2017

Chronic obstructive pulmonary disease and concomitant diseases

AH – arterial hypertension

ACE – angiotensin converting enzyme

BA – bronchial asthma

BB – β-blockers

CCB – calcium channel blockers

WHO – World Health Organization

GCS — glucocorticosteroids

DN – respiratory failure

VA – ventricular arrhythmias

VT – ventricular tachycardia

IHD – ischemic heart disease

MI – myocardial infarction

BMI – body mass index

LV – left ventricle

LS – medicines

LDC – cardiac arrhythmias

OP – osteoporosis

FEV ₁ – forced expiratory volume in 1 second

RL – lung cancer

DM – diabetes mellitus

CH – heart failure

CVD – cardiovascular diseases

AF – atrial fibrillation

COPD – chronic obstructive pulmonary disease

CHF – chronic heart failure

ECG – electrocardiogram

Chronic obstructive pulmonary disease (COPD), along with arterial hypertension (AH), coronary heart disease (CHD) and diabetes mellitus (DM), is the leading group of chronic noncommunicable diseases. They account for more than 40% of all causes of death. The World Health Organization (WHO) classifies COPD as a group of diseases with a high level of social burden. The disease is widespread in both economically developed and developing countries. The forecast compiled by WHO experts until 2020 indicates that COPD will not only become one of the most common human diseases, but will also become one of the leading causes of death. At the same time, a further decrease in mortality from myocardial infarction (MI), cancer, tuberculosis, etc. is expected.

The current concept of COPD, developed by WHO experts (GOLD, 2006), is based on the fact that it is among those that can be prevented (primary prevention), successfully treated (secondary prevention) and significantly extend the life expectancy of a sick person. The severity and prognosis of COPD are often determined by the extrapulmonary manifestations of the disease.

In clinical practice, it is necessary to distinguish between diseases that manifest themselves in the natural course of COPD. These include cardiovascular disease (CVD), osteoporosis (OP). Another clinical situation may develop in patients with long-term CVD, which are accompanied by obstructive disorders of the ventilation function of the lungs. Often, the appearance of shortness of breath in patients of this category is associated not so much with manifestations of heart failure (HF), but with a violation of the gas exchange function of the lungs or a combined dysfunction of both the lungs and the heart. Among the diverse clinical manifestations of COPD and concomitant diseases, it is necessary to distinguish the stages of the underlying disease, in which signs of a systemic disease appear.

The inflammatory process is initially localized in the respiratory tract and lung parenchyma, but at certain stages of the disease, its systemic inflammatory effects appear. Biomarkers of this process are an increase in blood levels of fibrinogen, C-reactive protein and a number of cytokines, an increase in ESR, and leukocytosis. Tobacco smoking is one of the aggressive risk factors for the development and progression of COPD, but it is also associated with the occurrence of a large group of comorbidities. Tobacco smoking leads to the appearance of pathological processes in the lungs and the development of systemic inflammatory reactions, systemic oxidative stress, dysfunction of the vascular endothelium, an increase in the activity of procoagulant factors, amplification of oncogenes, and other systemic changes. It is necessary to isolate the COPD phenotype with severe systemic inflammatory manifestations. The prognosis for this COPD phenotype is poor.

The most common comorbidities in COPD are cachexia, hypotrophy and atrophy of skeletal muscles, arterial hypertension, ischemic heart disease, heart failure, vasculopathy of the pulmonary circulation, infectious and oncological diseases of the respiratory tract. The prognosis is most unfavorable when COPD is combined with CVD.

Patients with severe forms of COPD are at high risk of sudden death. One of the causes of sudden death are cardiac arrhythmias (HRDs).

Supraventricular and ventricular arrhythmias are a common clinical problem in patients with COPD. Especially often, NRS are observed with hypoxemia and hypercapnia. Undoubtedly, the presence of concomitant coronary artery disease and HF plays an important role. Another important cause of arrhythmia episodes in patients with COPD is the intake of a number of drugs (PM): theophylline, digoxin, β-adrenergic receptor agonists (β-agonists).

The epidemiology of HRS in COPD patients and their association with deaths was studied by Danish scientists (Copenhagen City Heart Study). This unique study shows that COPD is associated with a high incidence of HRS. The frequency of development of atrial fibrillation (AF) depends on the violation of the ventilation function of the lungs. Thus, in COPD patients with no history of myocardial infarction, AF occurred 2 times more often with forced expiratory volume in 1 second (FEV ₁ ) <60%.

Sudden death in patients with COPD is relatively common during an exacerbation of the disease. Mortality was over 14%; logistic regression analysis revealed 4 independent risk factors: age, alveolar-arterial gradient above 41 mm Hg, ventricular tachycardia (VT), AF.

It should be noted that epidemiological studies on the issue of arrhythmias in patients with COPD are not enough, there are many unresolved issues, in particular the role of drugs prescribed to cardiological patients to control blood pressure and heart rate.

The pathogenesis of arrhythmias in patients with COPD is multifactorial. Drugs that are prescribed to patients with COPD, dysfunction of the autonomic conduction system of the heart, coronary artery disease, hypertension, dysfunction of the left and right ventricles, an increase in the level of catecholamines in the blood during the development of hypoxemia, hypokalemia, hypomagnesemia, respiratory acidosis can provoke the development of arrhythmia.

The most studied arrhythmogenic effects of theophylline and its derivatives. Arrhythmias such as sinus tachycardia, supraventricular extrasystole, AF, atrial tachycardia, ventricular arrhythmias (VA) are associated with the appointment of xanthine derivatives. The occurrence of both atrial and VA is directly dependent on the concentration of theophylline in the blood serum (its therapeutic window is in the range of 10-15 microns / l). The toxic effects of theophylline can be promoted by smoking, taking macrolides, antihistamines.

In the development of arrhythmogenic effects of theophylline, age plays a role, as well as concomitant diseases such as coronary artery disease, liver disease. Arrhythmogenic effects are primarily due to theophylline. Some of the LDCs were life threatening. So, VT, polytopic ventricular extrasystole develop even with a therapeutic concentration of theophylline. Particular attention should be paid to the period of exacerbation of COPD, when patients develop respiratory failure (RD), manifestations of hypoxemia increase. At the same time, the treatment programs include intravenous administration of theophylline, which creates conditions for the manifestation of its arrhythmogenic effect.

The next group of drugs that are widely used in the treatment of COPD are β-agonists. The most widely used salbutamol in the form of metered inhalation, as well as intravenously. Little is taken into account that salbutamol administered through a nebulizer is prescribed in a fairly high dose of 2.5 to 5 mg, and in especially severe cases, its dose can be even higher. At high doses, salbutamol affects the activity of the sinus node: the relationship between the time parameters of the phases of electrophysiological activity and rest changes. Salbutamol increases the time of impulse conduction through the atrioventricular node, reducing the refractory time of the excitability of the node, as well as the myocardium. This allows us to attribute salbutamol to drugs of proarrhythmic action. However, a meta-analysis of data from 33 randomized, placebo-controlled studies that studied the effects of β-agonists in COPD showed that a single use of drugs leads to an increase in the number of heartbeats by an average of 9in 1 min. Their other effects were a decrease in the level of potassium in the blood by an average of 0.36 mmol / l and chlorine by 0.18-0.54 mmol / l. β-Agonists are associated with undesirable effects in the work of the heart; this is mainly due to their influence on the occurrence of sinus tachycardia. Potentially, this group of drugs should be considered as drugs that give the following undesirable effects: they reveal or aggravate myocardial ischemia, heart failure, cardiac arrhythmias and can cause sudden death. Side effects of β-agonists occur most often in patients with concomitant CVD.

In recent years, attention has been drawn to the side effects of long-acting β-agonists. When the QT interval is prolonged on the electrocardiogram (ECG) for more than 0.45 ms, the arrhythmogenic effect of β-agonists may appear. If the duration of the QT interval exceeds 0.45 ms, it is not recommended to use β-agonists for a long time, it is better to refuse their further use.

Prolongation of the QT interval initially occurs in patients with congenital disorders in the conduction system of the heart, idiopathic conduction disorders are also possible. Prolongation of the Q-T interval occurs with hypokalemia, hypomagnesemia, hypocalcemia, hypothyroidism, anorexia. The duration of the QT interval is increased by quinidine, amiodarone, sotalol, disopyramide, antimicrobials (macrolides, pentamidine, fluoroquinolones), antihistamines and psychotropic drugs.

Relatively little is known about the association between DN in patients with COPD and left ventricular (LV) dysfunction and VA. A direct relationship was found between the severity of DN manifestations and LV diastolic dysfunction, while blood gas parameters and the clinical picture did not correlate with the frequency of arrhythmia episodes. It is recommended to make a diagnostic assessment of episodes of VA that occurred against the background of LV diastolic dysfunction, since they may be latent myocardial ischemia (its painless forms) and overload of the right ventricle during the formation of cor pulmonale. It should be emphasized that with the development of arrhythmia, the clinical manifestations of DN always increase.

A special place in COPD patients is occupied by multifocal atrial tachycardia, which is associated to a large extent with the development of DN. The prognosis of the course of COPD with the appearance of this type of arrhythmia is considered to be unfavorable.

Treatment programs for HRS in patients with COPD have a number of features. Important points in them are the correction of violations of acid-base balance, as well as hypokalemia, hypomagnesemia, oxygen therapy. An important place is occupied by measures aimed at the prevention or treatment of myocardial ischemia. It is necessary to exclude the appointment of drugs that can lengthen the QT interval. These include macrolides, antifungals, antihistamines. It is recommended to abandon the appointment of theophylline and its derivatives if the ECG shows a prolongation of the QT interval.

Antiarrhythmic therapy varies greatly depending on the severity of clinical manifestations of COPD, concomitant diseases and a number of individual patient reactions. Patients who have asymptomatic VA recorded on the ECG, as a rule, do not need antiarrhythmic drugs. With the development of clinical symptoms (hemodynamic collapse, myocardial ischemia, acute left ventricular failure), cardioversion is indicated. The drugs of choice are subclass IA antiarrhythmic drugs: quinidine, novocainamide, and disopyramide. In 2006, the American and European Society of Cardiology developed joint guidelines for the treatment of AF in patients with obstructive pulmonary disease. In these recommendations, great importance is given to the fight against hypoxemia, acidemia; preference is given to the use of non-dihydropyridine calcium channel blockers (CCBs): diltiacem, verapamil. Theophylline, β-agonists, β-blockers (BB), adenosine should be avoided. With supraventricular tachycardia, it is advisable to use CCB, amiodarone, cardiac glycosides, flecainide. The greatest antiarrhythmic effect is achieved with intravenous administration of verapamil. With multifocal atrial tachycardia, it is preferable to prescribe verapamil, as well as metoprolol (of all BBs, it has the least effect on bronchial smooth muscle tone).

The combination of hypertension and COPD is common in clinical practice. Difficulties in managing patients in this category are primarily due to the fact that some antihypertensive drugs can cause bronchospasm, aggravating the course of bronchial asthma (BA) and COPD. An extremely cautious prescription of BB is recommended, to a lesser extent, caution applies to angiotensin-converting enzyme (ACE) inhibitors. When managing patients with COPD and signs of DN, drug treatment of hypertension should be combined with oxygen inhalations and attempts should be made to improve ventilation parameters of external respiration function. More active respiratory support is also possible, which is non-invasive ventilation of the lungs, as well as combined inhalation therapy with β-agonists and glucocorticosteroids (GCS), which allows controlling the course of hypertension.

If patients have signs of reversible airway obstruction, then BBs are highly likely to contribute to bronchoconstriction and, moreover, to the development of resistance to the action of β-agonists.

The clinical efficacy of selective β1-blockers was studied in a meta-analysis, in randomized, placebo-controlled, double-blind studies. We analyzed data on a single use of cardioselective BBs and their effect on FEV ₁ , and also evaluated the effectiveness of short-acting β-agonists. Decreased FEV ₁ was 7.9%, however, a good response to taking bronchodilators was obtained. At the same time, it was concluded that cardioselective BBs do not cause a noticeable deterioration in ventilation function in broncho-obstructive syndrome. However, it should be noted that these were patients with mild to moderate severity of bronchial obstruction. It is advisable to use this subgroup of BBs in the treatment of patients with COPD in combination with hypertension and coronary artery disease.

ACE inhibitors can cause a dry, nonproductive cough, and some patients may even develop a typical asthma attack. ACE inhibitors cannot be considered as a first-line treatment for hypertension in patients with COPD. Angiotensin II receptor blockers are acceptable. They do not cause coughing, and cases of iatrogenic asthma have not been described with their use. In terms of their efficacy and safety, angiotensin II receptor blockers can be comparable to CCBs.

Diuretics are another group of drugs that are widely used in the treatment of hypertension. However, long-term use of them can lead to such undesirable manifestations as hypokalemia, hypomagnesemia, which can be aggravated by the constant use of β-agonists and corticosteroids. Another problem that can be exacerbated by the use of diuretics in patients with COPD is the development of metabolic alkalosis. Decompensated forms of it can lead to an increase in the degree of hypoxemia. Of the existing drugs with a diuretic effect, it is recommended to prescribe low doses of hydrochlorothiazide (up to 25 mg).

The leading role in the treatment of hypertension in COPD patients is occupied by CCBs. Derivatives of dihydropyridine – amlodipine nifedipine, nicardipine – have found wide application. It should be noted their positive effect on the regulation of bronchial smooth muscle tone, suppression of mast cell degranulation and potentiation of the dilatation effect of β-agonists. It is possible to combine CCB as ionotherapy or in combination with low doses of thiazide diuretics.

IHD and COPD often coexist. Often, COPD is detected in patients who have had a myocardial infarction, and is more often observed in tobacco smokers. In the same group of patients with comorbidity, higher mortality and a higher percentage of patients with pulmonary heart disease are noted. There is evidence that coronary artery disease of varying severity occurs in many patients with COPD. These data should also be taken into account in situations where patients with emphysema are being prepared for surgery to reduce the lung tissue. If an assessment of the coronary reserve is not carried out, then it is unlikely that it will be possible to achieve positive results of surgical intervention. The presence of COPD increases the risk of death in patients with coronary artery disease by 50%. With the addition of HA, the risk of sudden death increases even more. Decreased FEV ₁ increases the probability of death of a patient with comorbidity by 14% by 10%. A long-term observation of 20 thousand patients showed that even chronic bronchitis is a risk of developing coronary artery disease.

Of great importance in COPD is the development of hypoxemia, which significantly worsens the course of coronary artery disease. The decrease in blood oxygen saturation to 80% is especially detrimental. The most dangerous combination of hypoxemia with hypercapnia. Treatment programs for patients in this category necessarily include oxygen inhalation. Long-term oxygen therapy (inhalations for more than 15 hours a day) significantly increases the survival rate of patients with a combination of COPD and coronary artery disease. It should be noted that they need oxygen inhalation, especially at night, when there is a deterioration in respiratory function and a decrease in coronary reserve.

Drug therapy in the combined course of coronary artery disease and COPD is one of the most urgent tasks, but there are still no reports of studies on the adequate choice of drugs in patients of this category. In COPD, salbutamol, salmeterol, formoterol and their combinations with corticosteroids are most often prescribed. Sympathomimetics have a significant effect on the myocardium due to the development of hypokalemia, hypomagnesemia, and an increase in oxygen debt. With the use of these drugs, the development of arrhythmias is associated, which can also occur with the use of theophylline. Preference is given to combined preparations, which include small doses of β-agonists and corticosteroids, and due to this, their maximum effect on the tone of the smooth muscles of the respiratory tract is achieved. Of the existing bronchodilator drugs, cardiotoxic properties are least pronounced in tiotropium bromide.

BBs, which are classified as basic drugs in the treatment of coronary artery disease, are prescribed to patients with COPD with great caution or they are completely abandoned. Metoprolol is considered to be the drug of choice if there is an urgent need to prescribe a BB. Priority is given to combined α,β-blockers: labetalol, carvedilol.

Chronic heart failure (CHF) aggravates the prognosis of patients with COPD. It appears in more than 20% of them and, as a rule, is due to the presence of concomitant coronary artery disease, hypertension, type 2 diabetes, OP. Diagnosis of CHF presents difficulties, as it is largely masked by manifestations of acute or chronic DN. In the period of exacerbation of COPD, the development of LV diastolic dysfunction is characteristic. In DN and HF, the clinical manifestations can be very similar. In both cases, the leading place is occupied by shortness of breath, the intensity of which increases with physical exertion. However, some features in its clinical manifestation can be noted. The diagnostic algorithm includes the study of oxygen pulse at rest and during exercise, X-ray examination of the chest organs, ECG and echocardiography data. Biochemical markers of CHF are an increase in the level of brain natriuretic hormone, which is highly specific for patients with CHF. A decrease in LV ejection fraction, characteristic of CHF, is an important sign by which five-year survival of patients can be predicted. According to a number of authors, among patients who were admitted to the hospital with newly diagnosed signs of CHF, the prevalence exceeded 55%.

One of the methods that have been developed in recent years in the treatment of patients in this category are non-invasive ventilation and long-term treatment with oxygen inhalation. Against this background, conventional therapy, which is prescribed in the treatment of CHF, gives a noticeably greater effect, at least the immediate prognosis for removing the patient from the exacerbation of DN and HF is more favorable.

COPD refers to diseases characterized by an inflammatory reaction of the airways. Its persistence, frequent episodes of exacerbations are the cause of the progression and increase in the severity of the disease. In COPD, infectious diseases of the lower respiratory tract have a negative impact on the course of the disease. Among them, the main place is occupied by pneumonia, and the role of gram-negative pathogens is also significant, among which the Pseudomonas aeruginosa has a leading role. In mild forms of COPD, pathogens such as pneumococci, Haemophilus influenzae, Moraxella and a number of other pathogens take the 1st place. Recently, much attention has been paid to atypical pathogens, as well as legionella. In the fight against infectious diseases of the respiratory tract in patients with COPD, an ever-increasing role is played by vaccination, which increases resistance to such pathogens as influenza virus, pneumococcus, Haemophilus influenzae.

Another clinical problem is the combination of COPD and asthma. The combined course of these diseases is present in almost 10% of patients with COPD. Initially, the patient may be observed for COPD, but as it progresses, asthma may join it. However, the opposite picture is more often observed – COPD joins the long-term BA. This is especially true for patients with severe asthma, in whom the terminal airway is often involved in the inflammatory process. With external similarities in the treatment programs for COPD and BA, there are differences that relate to the choice of doses of corticosteroids and sympathomimetics. A special place in the treatment program for COPD is occupied by M-anticholinergics (tiotropium bromide). Recently, the combination of COPD and BA has been identified as a special phenotype, which is characterized by a severe, sometimes disabling, course.

In the presence of COPD, there is a high risk of developing oncological diseases, primarily lung cancer (LC). Tobacco smoking is a risk factor for the development of these two diseases. Occupational hazards play an important role in the occurrence of both LC and COPD: industrial pollutants, the nanoparticle production industry, etc. Patients with COPD should be included in the screening program for the early diagnosis of LC, especially if they smoke tobacco products and work in enterprises with harmful working conditions . This form of comorbidity has a significant impact on the choice of methods for the treatment of LC, both surgical and combined, based on the use of chemotherapy and radiation therapy.

The fight against the epidemic outbreak of tuberculosis is of great importance for Russian health care. Its high prevalence and mortality remain. The increasing multiple resistance of Mycobacterium tuberculosis to drugs is of great concern. The combination of tuberculosis and COPD has a negative impact on the course of each of these diseases. It is possible that the high percentage of drug resistance in mycobacteria is largely due to the fact that patients do not receive adequate treatment for COPD. After treatment of patients with acute forms of tuberculosis or exacerbation of its chronic forms, patients, as a rule, remain with COPD for the rest of their lives. This group of patients is especially prone to exacerbation of latent forms of tuberculosis in the progressive course of COPD. Some drugs, including inhaled corticosteroids, may worsen the tuberculous process. When these two forms of lung pathology are combined, the risk of developing LC is especially high.

COPD is one of the diseases in which comorbidity has a very high prevalence. Almost all patients have not one, but several diseases of the respiratory system. The most frequent is the combination of COPD and BA, and a rather severe course of each of the diseases is noted. If patients with COPD suffer from pneumonia, then there is always an exacerbation of the underlying disease and further aggravation of its course.

Systemic reactions in patients with COPD develop under the influence of inflammatory activity of lung tissue cells, tissue hypoxia, adverse effects of shortness of breath on metabolism, as well as risk factors such as smoking, industrial pollutants, genetic factors predisposing to the development of systemic reactions. One of the markers of the systemic inflammatory response is C-reactive protein. There is evidence of the diagnostic and prognostic value of this protein in COPD. Its high level in the blood correlates with the severity of inflammation, and its dynamics can be used to judge the course of exacerbation of COPD and the prognosis of the disease.

Systemic manifestations in patients with COPD include skeletal muscle changes. Patients acquire a haggard, cachectic appearance; noticeable hypotrophy of skeletal muscles (shoulder girdle, arms, chest, abdominals, lower extremities). Respiratory muscles: diaphragm, intercostal and fusiform muscles, muscles of the upper shoulder girdle – are involved in the pathological process much later. However, with the development of respiratory muscle fatigue syndrome, signs of DN rapidly increase. Modern rehabilitation programs include exercises that can increase both strength and endurance of skeletal muscles. Specific training regimen programs are complemented by exercises designed for the respiratory muscles.

Changes in nutritional status complete the picture of systemic manifestations in patients with COPD. Their life expectancy with a body mass index (BMI) of less than 20 is 2 times lower than with a BMI of more than 29. An integral assessment of systemic manifestations in COPD can be represented by parameters that are called BODE in the Latin abbreviation, where “B” means BMI, “ O” – obstructive violations of the ventilation function of the lungs, “D” – the severity of shortness of breath, “E” – tolerance to physical activity, which is established in the test with a 6-minute walk (see figure). Figure 1. Group of BODE features in COPD. Thus, with a decrease in height, BMI, an increase in lung obstruction, an increase in the severity of dyspnea and a decrease in exercise tolerance, qualitative changes occur in the course of COPD.

In recent years, when studying systemic manifestations of COPD, attention has been paid to the signs of OP, the role of the endocrine system and metabolic syndrome in patients of this category.

Metabolic disorders in the musculoskeletal system in patients with COPD are attributed to the systemic effects of this disease. Epidemiological studies of the prevalence of bone metabolism disorders in COPD patients revealed OP in 30-60%, osteopenia in 35-72%. There are data on the role of corticosteroids in the development of metabolic disorders in the bone tissue of patients with COPD and BA.

Treatment programs for OP, including vitamin D, calcitonin, drugs containing calcium, of course, apply to patients with COPD, the course of which was complicated by impaired bone metabolism. Methods for the prevention and early diagnosis of bone metabolism disorders are among the most important sections of the plan of an individual treatment program.

In recent years, a group of COPD patients with metabolic syndrome has been identified. This combination is characterized by a high incidence of CVD, especially hypertension. This triad is more common in women. A feature of patients in this category is often nocturnal respiratory arrest. During sleep apnea, oxygen saturation in the blood decreases significantly.