DETROIT – Tuesday is an ozone action day or Air Quality Alert for Metro Detroit, but what does that mean?

The Michigan Department of Environment, Great Lakes, and Energy has declared Tuesday, May 30, to be an action day for elevated levels of ozone. Pollutants are expected to be in the unhealthy for sensitive groups range.

Ozone action days are called when hot summer temperatures are expected to combine with pollution to create high amounts of ground-level ozone. Breathing high levels of ozone can trigger a variety of health problems, particularly in children, the elderly, and people with asthma or other lung diseases.

Where does it come from?

NOAA and the Environmental Protection Agency (EPA) partner in developing a national Air Quality Forecast (AQF) System. The goal of this partnership is to provide ozone, particulate matter, and other pollutant forecasts with enough accuracy and advance notice for people to take action to prevent or limit harmful effects from poor air quality.

State and local air quality agencies, as well as the private sector, are also essential partners in the national air quality monitoring network, EPA's national inventory of emissions data.

What causes "bad" Ozone?

“Bad” ozone is found at ground level. In cities, it’s made when emissions from vehicles, power plants, chemical plants, and other sources react with heat and sunlight. The hotter the day and the stronger the sun, the more ozone is formed. That's why ozone is usually worst on windless, hot summer afternoons. High levels of ozone are mainly a concern for people from April 1–September 30.

You’re most likely to find high levels of "bad" ozone in urban areas. You might hear it called “smog.” However, other areas can also have high ozone levels when winds blow pollution hundreds of miles from their original sources.

How does "bad" Ozone affect me?

Even at low levels, breathing ozone can cause chest pains, coughing, and throat irritation. It can also aggravate lung diseases like emphysema, bronchitis, and asthma. The more ozone pollution a person breathes, the more permanent damage it can do to her lungs.

Because it usually forms in hot weather, anyone who spends time outdoors in the summer may be affected - children, older people, outdoor workers, and people exercising may be particularly susceptible. The higher the ozone level, the more people who will experience health symptoms. Millions of Americans live in areas where ozone levels are higher than the national health standards, and should pay attention to ozone levels when the weather is hot and sunny.

How do I stay safe during an Air Quality Alert?

Follow these simple tips to stay safe when there is an air quality alert:

  • Stay inside if possible, particularly if you have respiratory concerns or other health problems, are a senior or child

  • If you must go out, try to limit the amount of time you are out to strictly essential activities

  • Minimize your use of items that increase pollution, such as cars, gas powered lawn mowers and other vehicles

  • Do not burn debris or other items during an air quality alert

  • Take the bus, carpool, telecommute, bike, or walk. You'll reduce traffic congestion and air pollution as well as save money.

  • If you plan to barbecue, use an electric starter or charcoal chimney instead of lighter fluid. Fumes from the fluid contribute to ozone formation.

  • Avoid drive-thru facilities or other situations where your vehicle idles for an extended period of time. You'll save money on gas and reduce pollution.

Who is most at risk?

Several groups of people are particularly sensitive to ozone, especially when they are active outdoors. This is because ozone levels are higher outdoors, and physical activity causes faster and deeper breathing, drawing more ozone into the body.

  • People with lung diseases, such as asthma, chronic bronchitis, and emphysema, can be particularly sensitive to ozone. They will generally experience more serious health effects at lower levels. Ozone can aggravate their diseases, leading to increased medication use, doctor and emergency room visits, and hospital admissions.

  • Children, including teenagers, are at higher risk from ozone exposure because they often play outdoors in warmer weather when ozone levels are higher, they are more likely to have asthma (which may be aggravated by ozone exposure), and their lungs are still developing.

  • Older adults may be more affected by ozone exposure, possibly because they are more likely to have pre-existing lung disease.

  • Active people of all ages who exercise or work vigorously outdoors are at increased risk.

  • Some healthy people are more sensitive to ozone. They may experience health effects at lower ozone levels than the average person even though they have none of the risk factors listed above. There may be a genetic basis for this increased sensitivity.

In general, as concentrations of ground-level ozone increase, more people begin to experience more serious health effects. When levels are very high, everyone should be concerned about ozone exposure.

What are the health effects?

Ozone affects the lungs and respiratory system in many ways. It can:

  • Irritate the respiratory system, causing coughing, throat soreness, airway irritation, chest tightness, or chest pain when taking a deep breath.

  • Reduce lung function, making it more difficult to breathe as deeply and vigorously as you normally would, especially when exercising. Breathing may start to feel uncomfortable, and you may notice that you are taking more rapid and shallow breaths than normal.

The risk of exposure to unhealthy levels of ground-level ozone is greatest during warmer months. Children, who often play outdoors in warmer weather, are at higher risk.

  • Inflame and damage the cells that line the lungs. Within a few days, the damaged cells are replaced and the old cells are shed—much like the way your skin peels after sunburn. Studies suggest that if this type of inflammation happens repeatedly, lung tissue may become permanently scarred and lung function may be permanently reduced.

  • Make the lungs more susceptible to infection. Ozone reduces the lung’s defenses by damaging the cells that move particles and bacteria out of the airways and by reducing the number and effectiveness of white blood cells in the lungs.

  • Aggravate asthma. When ozone levels are unhealthy, more people with asthma have symptoms that require a doctor’s attention or the use of medication. Ozone makes people more sensitive to allergens—the most common triggers for asthma attacks. Also, asthmatics may be more severely affected by reduced lung function and airway inflammation. People with asthma should ask their doctor for an asthma action plan and follow it carefully when ozone levels are unhealthy.

  • Aggravate other chronic lung diseases such as emphysema and bronchitis. As concentrations of ground-level ozone increase, more people with lung disease visit doctors or emergency rooms and are admitted to the hospital.

  • Cause permanent lung damage. Repeated short-term ozone damage to children’s developing lungs may lead to reduced lung function in adulthood. In adults, ozone exposure may accelerate the natural decline in lung function that occurs with age.


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Most of Minnesota and western Wisconsin had summery temperatures on Saturday, but dew points were not summery at all. Many locations had Saturday afternoon dew points in the 20s and 30s. Some spots in west-central Minnesota reported afternoon dew points in the teens for a while.

The combination of warm temps, low dew points/relative humidity and gusty winds prompted red flag warnings to be issued Saturday afternoon into Saturday evening for northwestern Minnesota and parts of north-central and west-central Minnesota:


Red flag warning until 9 p.m. Saturday

National Weather Service

Here are details of the west-central Minnesota portion of the Saturday red flag warning, plus a fire weather watch for Sunday:

URGENT - FIRE WEATHER MESSAGE National Weather Service Twin Cities/Chanhassen MN 133 PM CDT Sat May 27 2023 ...RED FLAG WARNING FROM THIS AFTERNOON THROUGH THIS EVENING FOR PORTIONS OF WEST-CENTRAL AND WESTERN MINNESOTA... ...FIRE WEATHER WATCH FOR PORTIONS OF WEST-CENTRAL AND WESTERN MINNESOTA FOR SIMILAR CONDITIONS ON SUNDAY... .Winds remain steady out of the south at 10-15mph with gusts from 20-25mph at times as humidities have fallen into the upper teens to lower 20s due to low dew points and warm temperatures. Critical fire weather conditions are expected and any fires that form will have the ability spread quickly. Similar conditions are expected on Sunday in a similar airmass, thus a Fire Weather Watch has been issued for tomorrow as well. MNZ041-042-047-048-054>056-064-280200- /O.NEW.KMPX.FW.W.0004.230527T1833Z-230528T0200Z/ /O.NEW.KMPX.FW.A.0003.230528T1800Z-230529T0200Z/ Douglas-Todd-Stevens-Pope-Lac Qui Parle-Swift-Chippewa- Yellow Medicine- 133 PM CDT Sat May 27 2023 ...RED FLAG WARNING IN EFFECT UNTIL 9 PM CDT THIS EVENING FOR LOW RELATIVE HUMIDITY AND SUSTAINED WINDS IN WEST-CENTRAL AND WESTERN MINNESOTA... ...FIRE WEATHER WATCH IN EFFECT FROM SUNDAY AFTERNOON THROUGH SUNDAY EVENING FOR LOW RELATIVE HUMIDITY AND SUSTAINED WINDS IN WEST-CENTRAL AND WESTERN MINNESOTA... The National Weather Service in Twin Cities/Chanhassen has issued a Red Flag Warning, which is in effect until 9 PM CDT this evening. a Fire Weather Watch has also been issued. This Fire Weather Watch is in effect from Sunday afternoon through Sunday evening. * AFFECTED AREA...West-central and western Minnesota. * WIND...South 10 to 15 mph with gusts 20 to 25 mph. * HUMIDITY...15 to 25 percent. * IMPACTS...any fires that develop will likely spread rapidly. Outdoor burning is not recommended. PRECAUTIONARY/PREPAREDNESS ACTIONS... A Red Flag Warning means that critical fire weather conditions are either occurring now, or will shortly. A combination of strong winds, low relative humidity, and warm temperatures can contribute to extreme fire behavior. A Fire Weather Watch means that critical fire weather conditions are forecast to occur. Listen for later forecasts and possible Red Flag Warnings.

The Minnesota Department of Natural Resources posts fire danger and burning restriction updates here.

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Air quality alert begins at noon on Sunday

The Minnesota Pollution Control Agency has issued an air quality alert for much of eastern Minnesota, beginning at noon on Sunday:


Air quality alert (orange) from noon Sunday through 8 p.m. Monday

Minnesota Pollution Control Agency

Here are the air quality alert details, from the MPCA:

The Minnesota Pollution Control Agency (MPCA) has issued an air quality alert for east central Minnesota, effective from noon on Sunday, May 28, through 8 p.m. on Monday, May 29. The affected area includes the Twin Cities metropolitan area, St. Cloud, Hinckley, Mankato, Albert Lea, Rochester, and the tribal nations of Prairie Island, Leech Lake, and Mille Lacs.

Ground-level ozone is expected to be high during the afternoon hours on Sunday and Monday, and air quality is expected to reach the Orange (unhealthy for sensitive groups) AQI category across east central and southeast Minnesota. Sunny skies, warm temperatures, and low humidity will create an environment favorable for two types of pollutants (Volatile Organic Compounds and Nitrogen Oxides) to react in the air to produce ground-level ozone. Ozone will be highest during the afternoon and early evening hours when sunshine is most abundant, and temperatures are highest. Air quality is expected to reach the Orange AQI category. This is considered unhealthy for sensitive groups. Ozone levels will be low during the overnight and morning. Air quality will improve on Tuesday, when a weather system will move across the state and bring increased moisture, clouds, and scattered thunderstorms to eastern Minnesota.

People whose health is affected by unhealthy air quality: There are people who are more likely to be affected when ozone pollution reaches an unhealthy level.

  • People who have asthma or other breathing conditions like chronic obstructive pulmonary disease (COPD), chronic bronchitis, and emphysema.

  • Children and teenagers.

  • People of all ages who are doing extended or heavy, physical activity like playing sports or working outdoors.

  • Some healthy people who are more sensitive to ozone even though they have none of the risk factors. There may be a genetic base for this increased sensitivity.

Health effects: Unhealthy ozone levels can aggravate lung diseases like asthma, emphysema, and COPD. When the air quality is unhealthy, people with these conditions may experience symptoms like difficulty breathing deeply, shortness of breath, throat soreness, wheezing, coughing, or unusual fatigue. If you are experiencing any of these symptoms, use your inhalers as directed and contact your health care provider.

Take precautions: Everyone should take precautions when the air quality is unhealthy.

  • Take it easy and listen to your body.

  • Limit, change, or postpone your physical activity.

  • If possible, stay away from local sources of air pollution like busy roads and wood fires.

  • If you have asthma, or other breathing conditions like COPD, make sure you have your relief/rescue inhaler with you.

  • People with asthma should review and follow guidance in their written asthma action plan. Make an appointment to see your health provider if you don’t have an asthma action plan.

Pollution reduction tips: Ozone is produced on hot, sunny days by a chemical reaction between volatile organic compounds and oxides of nitrogen.

  • Reduce vehicle trips and fill the gas tank at dawn or dusk.

  • Encourage use of public transport, or carpool, when possible.

  • Postpone use of gasoline-powered lawn and garden equipment on air alert days. Use battery or manual equipment instead.

  • Avoid backyard fires.

Dry weather through Monday in many areas

We’ll have a sun-splashed Sunday in Minnesota and Wisconsin. A ridge of high pressure aloft and a surface high-pressure system to our east will keep rain away.

The upper-level ridging breaks down a bit on Monday, and the surface high-pressure system will shift slightly eastward. Those events will allow a chance of scattered showers and thunderstorms to enter western Minnesota on Memorial Day.

The National Oceanic and Atmospheric Administration’s North American Mesoscale (NAM) forecast model shows the surface pressure pattern and the potential rain pattern from 4 a.m. Sunday to 10 p.m. Monday:


Simulated radar from 4 a.m. Sunday to 10 p.m. Monday

NOAA, via

On Tuesday, the chance of scattered showers and thunderstorms will spread across the remainder of Minnesota and into Wisconsin, then unsettled weather will linger through the remainder of the week.

You can find updated weather information for Minnesota and western Wisconsin on the MPR News network

The Saturday afternoon high temperature at Minneapolis-St. Paul International Airport was 84 degrees. The average May 27 Twin Cities high temp is just 73 degrees.

Sunday highs in the Twin Cities metro area will reach the low to mid 80s. Most of Minnesota and western Wisconsin will top out in the 80s on Sunday, with 70s near Lake Superior:


Sunday forecast highs

National Weather Service

Memorial Day highs will be mainly in the 80s as well:


Monday forecast highs

National Weather Service

Once again there will be 70s near Lake Superior.

Twin Cities metro area highs are projected to reach the upper 80s Tuesday through Friday. I wouldn’t be surprised to see a few spots in the metro area touch 90 degrees on Tuesday or Thursday.

There isn’t any really chilly weather in sight. The NWS Climate Prediction Center shows a tendency for above-normal temps in Minnesota and western Wisconsin next weekend and into the start of the following week:


Temperature outlook June 2 through June 6

NWS Climate Prediction Center

Programming note

You can hear my live weather updates on MPR News at 7:35 a.m., 9:35 a.m. and 4:39 p.m. each Saturday and Sunday.

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On May 31, the World Health Organization (WHO) and public health officials around the world will come together to share their resources and knowledge on ending or drastically reducing the use of cigarette smoking - one of deadliest and toxic habits which millions of people still continue to cling to despite repeated health warnings of its additive and adverse impacts on the human body.

The Sunday Observer spoke to Senior Professor of Forensic Medicine at the Sir John Kotelawala Defence University, Prof. Ravindra Fernando, who has spearheaded the campaigns to end smoking in Sri Lanka for several years in the various posts he has held as a experienced Toxicologist for his opinion as to what drives the smoking habit in people and how they can stop becoming addicted to it.


Q: As a Toxicologist tell us what do cigarettes contain that make them so unhealthy for us? And how do they make an impact on the respiratory system, making it difficult for us to breathe normally?

Prof. Ravindra Fernando

A. The short term and long term health consequences of inhaling these chemicals which are mostly harmful can be severe if not fatal . The gases inhaled from a cigarette causes constriction of the bronchi, numb the cilia, thickens the mucus-secreting membranes, dilates the distal airways, and destroys the alveolar walls. A particular component of a cigarette is carbon monoxide; this gas increases the risk for coronary artery disease. Smoking also impacts your cardiovascular health and also affects the health of those around who don’t smoke as well.. Risks that smokers face can include, stroke, heart disease including heart attacks.

Q: Who are those most vulnerable to the adverse impacts of tobacco smoking? Children? Elderly with lowered immunity?

A. Children as well as elderly with lowered immunity are most vulnerable.

Q: Are men and women affected equally?

A. Yes.

Q: Babies? Children? How vulnerable are they to such adverse impacts from tobacco smoke?

A. They are more vulnerable.

Q: What about pregnant women? Will toxic fumes from cigarettes affect their foetus?

A. Smoking doubles your risk of abnormal bleeding during pregnancy and delivery. This can put both you and your baby in danger. Smoking raises your baby’s risk for birth defects, including cleft lip, cleft palate, or both. A cleft is an opening in your baby’s lip or in the roof of her mouth (palate).

Q: Are persons with asthma also vulnerable?

A. In persons with asthma, an asthma attack can occur when something irritates your airways and “triggers” an attack. Your triggers might be different from other people’s triggers. So it is important to be aware that tobacco smoke is a common trigger for asthma, and that tobacco smoke—including secondhand smoke—is unhealthy for everyone, especially people with asthma.

Q: How many harmful chemicals are there in tobacco smoke?

A. There are more than 7,000 chemicals in tobacco smoke, at least 250 of which are known to be harmful, including hydrogen cyanide, carbon monoxide, and ammonia. Commercial tobacco smoke contains hundreds of harmful chemicals. As I just mentioned, there are more than 7,000 chemicals in commercial tobacco smoke, including hundreds of chemicals that are toxic and about 70 that can cause cancer. Here are just a few of the chemicals and toxins in commercial tobacco smoke: Benzene (Found in gasoline), Toluene (Used in paint thinners), Butane (Used in lighter fluid), Cadmium (Used in making batteries), Ammonia (Used in household cleaners), and Hydrogen Cyanide(Used in chemical weapons)

Q: Chronic Obstructive Pulmonary disease (COPD) is said to be one of the commonest outcomes of smoking with fatal results as well. What is COPD?

A. Chronic obstructive pulmonary disease (COPD) refers to a group of diseases that cause airflow blockage and breathing-related problems. COPD includes emphysema and chronic bronchitis. With COPD, less air flows through the airways—the tubes that carry air in and out of your lungs—because of one or more of the following:

The airways and tiny air sacs in the lungs lose their ability to stretch and shrink back.

The walls between many of the air sacs are destroyed.

The walls of the airways become thick and inflamed (irritated and swollen).

The airways make more mucus than usual, which can clog them and block airflow.

Q: Symptoms?

A. In the early stages of COPD, there may be no symptoms, or you may only have mild symptoms. As COPD worsens, the symptoms may become more severe. Symptoms of COPD include:

A cough that lingers for a long time and doesn’t go away completely, or a cough that produces a lot of mucus

Shortness of breath, especially with physical activity

Wheezing (a whistling sound when you breathe)

Tightness in the chest

Q: “Second hand smoking”? For our readers’ benefit can you explain what it is and how it affects the health of even those who do not smoke? By inhaling these fumes will he/she also suffer from the same complications that the smoker is likely to suffer from?

A. Secondhand smoke (SHS) is smoke from burning tobacco products, like cigarettes, cigars, or pipes. Secondhand smoke exposure occurs when people breathe in smoke breathed out by people who smoke or from burning tobacco products. There is no safe level of exposure to secondhand smoke; even brief exposure can cause serious health problems and be deadly.

Completely eliminating smoking is the only way to fully protect people who do not smoke from secondhand smoke exposure.

Q: Yet, Smokeless tobacco products such as Babul, Beedi, Mawa, Pampara, and Gurkha are still available in the market. Are they better or worse than smoking cigarettes or cigars?

A. They also contain nicotine and other harmful substances.

Q: Who are those most vulnerable to secondhand smoking? Children? Elderly with lowered immunity?

A. People who do not smoke who are exposed to secondhand smoke, even for a short time, can suffer harmful health effects. In adults who do not smoke, secondhand smoke exposure can cause coronary heart disease, stroke, lung cancer, and other diseases. It can also result in premature death. Children as well as elderly with lowered immunity are most vulnerable.

Q: What is the safest distance to be to avoid inhaling the fumes of second hand smoking?

A. Do not smoke or allow others to smoke in your home or car. Opening a window does not protect you from smoke. Look for restaurants and other places that do not allow smoking. “No-smoking sections” in the same restaurant with “smoking sections” do not protect adequately from secondhand smoke—even if there is a filter or ventilation system.

Make sure your children’s day care centres and schools are tobacco-free. For schools, a tobacco-free campus policy means no tobacco use or advertising on school property is allowed by anyone at any time.

This includes off-campus school events. Teach children to stay away from secondhand smoke.

Q: Can cigarette smoke remain in the environment even after the smoker has stopped smoking? If so, for how long and in what way?

A. Yes, it can remain for several minutes.

Q: A Global School based survey conducted nearly a decade ago revealed that more than 6,000 children (10-14 years old) and 17,2500 adults (15+ years old) reportedly continue to use tobacco each day and that the smoking prevalence among aged 13-15 years in Sri Lanka was believed to be around 2 percent Is the number the same today? Or has it increased?

A. Yes, there is no significant increase of smokers in Sri Lanka.

Q: Yet smokeless tobacco products such as Babul, Beedi, Mawa, Pampara, and Gurkha are still available in the market. What are the health impacts of these smokeless products? Are they better or worse than smoking cigarettes or cigars?

A. They are also harmful as they have toxic products.

Q: Can cigarette smoke remain in the environment even after the smoker has stopped smoking? If so, for how long and in what way?

A. Yes, it can remain for several minutes.

Q: A Global School based survey conducted nearly a decade ago revealed that more than 6,000 children (10-14 years old) and 17,2500 adults (15+ years old) reportedly continue to use tobacco each day and that the smoking prevalence among aged 13-15 years in Sri Lanka was believed to be around 2 percent Is the number the same today? Or has it increased?

A. No new data available. I think it is the same.

Q: So what is the best solution to halt a further spread of dangerous drugs and smoking among school children and teenagers?

A. Reduction of the nomber of smokers in the community.

Q: This year’s theme is “We need food, not tobacco”. What is the significance of this global theme in our Lankan contest given that commercial tobacco cultivation is one of the highest revenue earners for our badly hit economy?

A. The 2023 global campaign aims to raise awareness about alternative crop production and marketing opportunities for tobacco farmers and encourage them to grow sustainable, nutritious crops. It will also aim to expose the tobacco industry’s efforts to interfere with attempts to substitute tobacco growing with sustainable crops, thereby contributing to the global food crisis. In my personal opinion I strongly feel that tobacco growing should be substituted with food and other economical crops, in order to ensure that we have a healthy future generation . This is what our healthy policy makers MUST prioritise.

Q: What are the gaps you see in our health system with regard to reducing the prevalent soaring rates of smoking in the country?

A. I reiterate, harmful effects of smoking should be highlighted in every forum. Efforts at conveying this message of reducing smoking and its harmful impacts ,to the community is extremely important.

Q: Currently, there are several myths swirling around smoking, which drive smoking among young people. Which of these do you wish to dispel?

A. The myth that smoking is important to project your personality should be dispelled. Also that it is not additive and can be easily stopped if one wanted to. My message to them is that smoking is addictive. Once you take that first smoke ,the majority crave for more and find it difficult to give it up until they become chain smokers. There is a widespread assumption that smoking behaviour is largely established by the age of 18 years. As a result, smoking prevention has focused almost exclusively upon youth. However, recent trends suggest that young adulthood may be an important—and largely overlooked—period in the development of regular smoking behaviour. The myth of enjoying smoking should be dispelled.

Q: Your message to all smokers out there who want to kick the habit and those about to take their first puff?

A. Stop smoking NOW. It is harmful.

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Hypercapnia can be caused by various underlying respiratory conditions, such as chronic obstructive pulmonary disease (COPD), which may prevent a person’s lungs from either taking in enough oxygen or expelling (breathing out) enough CO2.

In mild hypercapnia, the body can often regulate itself, temporarily altering breathing by gasping or taking deeper breaths. Chronic cases, however, usually require medical intervention.

Consistently increased levels of CO2 in the bloodstream can be harmful over time, increasing the pH of your blood and affecting the health of the lungs, respiratory system, and other major systems in the body.

Symptoms of hypercapnia

Symptoms of hypercapnia can vary in severity and depend on the underlying issue.

Mild symptoms of hypercapnia commonly include:

  • flushed skin
  • drowsiness or inability to focus
  • mild headaches
  • feeling disoriented or dizzy
  • shortness of breath
  • being abnormally tired or exhausted

If these symptoms persist beyond a few days, see your doctor.

Severe symptoms

The symptoms of severe hypercapnia can be life threatening and require immediate medical attention.

See your doctor right away if you have one or more of the following symptoms, especially if you have COPD.

  • unexplained feelings of confusion
  • abnormal feelings of paranoia or depression
  • abnormal muscle twitching
  • irregular heartbeat
  • hyperventilation
  • seizures
  • panic attack
  • passing out

Causes of hypercapnia

Hypercapnia can have several causes, including:

  • COPD is a term describing a group of progressive lung conditions that make it harder to breathe. Chronic bronchitis and emphysema are two common examples of COPD.
  • COPD is often caused by smoking or breathing harmful air in polluted environments. Over time, COPD causes the alveoli (air sacs) in your lungs to lose their ability to stretch as they take in oxygen.
  • COPD can also destroy the walls between these alveoli. This compromises the airflow in and out of the lungs, making it harder to take in oxygen and get rid of CO2.

Nerve and muscular problems

Nerve and muscular conditions that can lead to hypercapnia include:

  • Guillain-Barré syndrome: This is an autoimmune disorder in which the immune system attacks healthy cells.
  • Amyotrophic lateral sclerosis (ALS): This is a degenerative disease affecting the brain and spinal cord.
  • Encephalitis: This is inflammation of the brain.
  • Muscular dystrophies: These are conditions causing muscles to weaken over time.

Genetic causes

In rare cases, hypercapnia can be caused by a genetic condition in which your body doesn’t produce enough of a protein called alpha-1-antitrypsin.

This protein comes from the liver and is used by your body to keep the lungs healthy.

What else can cause hypercapnia?

Other causes for hypercapnia include:

  • sleep apnea
  • obesity
  • complications from asthma
  • drug overdose
  • activities that impact breathing, such as scuba diving
  • being on a ventilator

Who’s at risk for hypercapnia?

Some risk factors for hypercapnia, especially as a result of COPD, include:

  • smoking cigarettes, cigars, or pipes
  • age, as many conditions that cause hypercapnia are progressive and usually don’t begin to show symptoms until after age 40
  • having asthma, especially if you smoke
  • breathing in fumes or chemicals in workplace environments, such as factories, warehouses, or electrical or chemical plants

A late diagnosis of COPD or another condition that causes hypercapnia can also increase your risk.

See your doctor at least once per year for a full physical examination to make sure you’re keeping an eye on your overall health.

How is hypercapnia diagnosed?

If your doctor thinks you have hypercapnia, they’ll likely test your blood and breathing to diagnose the issue and the underlying cause.

An arterial blood gas test is commonly used to diagnose hypercapnia.

This test can assess the levels of oxygen and CO2 in your blood, determine your blood’s pH, and make sure your oxygen pressure is healthy.

Your doctor may also test your breathing using spirometry.

In this test, you breathe forcefully into a tube.

An attached spirometer measures how much air your lungs contain and how forcefully you can blow that air out.

X-rays or CT scans of your lungs can also help your doctor see if you have emphysema or other related lung conditions.

What treatment options are available?

If an underlying condition is causing your hypercapnia, your doctor will set up a treatment plan for the symptoms of your condition.

Your doctor will likely recommend you stop smoking or limit your exposure to fumes or chemicals if they’ve caused COPD-related hypercapnia.


If you are hospitalized for severe symptoms, you may be put on a ventilator to make sure you can breathe properly.

You may also be intubated, which is when a tube is inserted through your mouth into your airways to help you breathe.

These treatments allow you to get consistent oxygen to balance your CO2 levels.

This is especially important if you have an underlying condition or if you’ve experienced respiratory failure and can’t breathe very well on your own.


Some medications can help you breathe better, including:

  • bronchodilators, also known as inhalers, which help your airway muscles work properly
  • Inhaled or oral corticosteroids, which help keep airway inflammation to a minimum
  • antibiotics for respiratory infections, such as pneumonia or acute bronchitis


Some therapies can also help treat symptoms and causes of hypercapnia.

For example, with oxygen therapy, you carry a small device that delivers oxygen straight into your lungs.

Pulmonary rehabilitation allows you to change your diet, exercise routine, and other habits to make sure that you’re contributing positively to your overall health.

This can reduce your symptoms and the possible complications of an underlying condition.


Some cases may require surgery to treat or replace damaged airways or lungs.

In lung volume reduction surgery, your doctor removes damaged tissue to allow your remaining healthy tissue to expand and bring in more oxygen.

In a lung transplant, a damaged lung is removed and replaced by a lung from an organ donor.

Both surgeries can be serious, so talk with your doctor about these options to see if they’re right for you.

Can hypercapnia be prevented?

If you have a respiratory condition causing hypercapnia, getting treatment is the best way to prevent hypercapnia.

Lifestyle measures, such as quitting smoking, losing weight, or exercising regularly, can also reduce your risk of hypercapnia significantly.

Getting treated for COPD or another underlying condition that can cause hypercapnia will significantly improve your long-term health and prevent future episodes.

If you need long-term treatment or surgery, listen closely to your doctor’s instructions so your treatment plan or recovery from surgery is successful.

They’ll advise you on symptoms to look out for and what to do if they occur.

With proper care, people with hypercapnia can live healthy, active lives.

Frequently asked questions

What happens when CO2 levels are too high?

When CO2 levels in the bloodstream are too high, it can lead to various symptoms, ranging from mild to potentially life threatening.

Mild symptoms may include headaches, dizziness, and fatigue.

In more severe cases, you may experience difficulty breathing, irregular heartbeat, seizures, or respiratory failure.

Severe symptoms of hypercapnia require immediate medical attention.

What happens to the body during hypercapnia?

Hypercapnia occurs when oxygen and CO2 levels become imbalanced in the bloodstream.

This imbalance changes the pH balance of your blood, making it too acidic.

This condition is called metabolic acidosis.

Metabolic acidosis can put excess strain on the kidneys, which can lead to kidney disease or failure.

What is the difference between hypercarbia, hypercapnia, and hypoxemia?

Hypercarbia and hypercapnia are terms describing conditions where there are excess amounts of CO2 in the bloodstream.

While slight differences exist between the two conditions, their names are often used interchangeably.

Hypoxemia refers to having low oxygen levels in the bloodstream, which can cause harm to healthy tissues in the body.

Hypercarbia, hypercapnia, and hypoxemia can co-occur but are not always related.


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FDA approves Recarbio to treat hospital-acquired and ventilator-associated bacterial pneumonia

Clinical Review: Acute Respiratory Distress Syndrome

Stress And Distress During Pregnancy: How To Protect Both Mother And Child

Respiratory Distress: What Are The Signs Of Respiratory Distress In Newborns?

Emergency Paediatrics / Neonatal Respiratory Distress Syndrome (NRDS): Causes, Risk Factors, Pathophysiology

Prehospital Intravenous Access And Fluid Resuscitation In Severe Sepsis: An Observational Cohort Study

Pneumology: Difference Between Type 1 And Type 2 Respiratory Failure

Difference Between Hypoxaemia, Hypoxia, Anoxia And Anoxia

Anoxia: What It Is, What The Symptoms Are, And How To Treat The Patient

Hypocapnia: Definition, Symptoms, Causes, Diagnosis, Values, Treatment



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COPD is characterized by progressive damage to the lungs and breathing difficulty over time among affected individuals, with a host of clinical signs manifesting as the diesease progresses.

In a symposium at the 2023 American Thoracic Society International Conference, taking place May 20-24 in Washington, DC, researchers presented abstracts exploring the prediction of COPD and markers of progression.

Predicting Future Lung Health With Baseline Lung Function

Overall lung health is typically determined by measuring forced expiratory volume in 1 second (FEV1), with a decline in FEV1 increasing the risk of COPD over time. However, baseline FEV1 as a predictor of long-term respiratory disease and overall health outcomes has not been well studied, according to the first abstract presented at the session.1

The researchers hypothesized that low or high baseline FEV1 (LLF or HLF) could be an indicator of future lung health for younger patients and tested the theory in a cohort of 532 Lovelace Smokers Cohort (LSC) participants between 40 and 60 years of age.

All patients had a post bronchodilator FEV1/forced vital capacity (FVC) ≥ 0.7 and were stratified into a HLF group (mean FEV1 of 105% predicted) and a LLF group (mean FEV1 of 73% predicted). Eleven years later, 56 patients from the HLF and 24 participants from the LLF groups were assessed, with a mean follow-up of 5.5 years.

Those in the HLF group saw an FEV1 decline of 30 ml/year vs 20 ml/year in the LLF group. Individuals in the LLF group had a higher COPD incidence compared with the HLF group (9% vs 3%) and a higher risk of death (18% vs 6%). The LLF group also had higher rates of diabetes (13% vs 4%) and chronic bronchitis (36% vs 25%).

After adjustment, those with LLF at baseline were at higher risks of COPD, diabetes, hypertension, cardiovascular disease, and mortality. The findings support using spirometry in smokers who are not obstructed monitor health over time.

The Impact of Respiratory Exacerbations on Lung Function in Those With Normal Spirometry

Among individuals with normal spirometry, the effect of respiratory disease exacerbations is not as clear, according to the authors of another abstract.2 The study explored the association of exacerbations with lung function decline in patients in the COPDGene study with at least 10 pack-years of smoking history who had normal lung function (FEV1/FVC <0.7 and/or FEV1 predicted < 80%) at enrollment.

In the study population (n = 2628), all of whom had normal lung function at enrollment, 1 exacerbation per year was associated with COPD at a 5-year follow-up visit, with an odds ratio of 1.32 (95% CI, 1-1.74, P = .045). Severe exacerbations per year did not show a statistically significant association with COPD at visit 2, however.

“Exacerbations between visit 1 and visit 2 were associated with increased mortality, but the relationship between respiratory exacerbations and mortality is not significantly affected by having COPD at visit 2,” the authors wrote.

Overall, they concluded that respiratory exacerbations in individuals with normal spirometry resulted in lung function decline and COPD, but also predicted mortality without progression to COPD first.

Factors Impacting COPD-Specific Mortality in a Novel Risk Model

Authors of another abstract presented during the symposium wrote that while prognostic risk scores for COPD exist, most model mortality overall and not COPD-specific mortality.3 They developed CausalCoxMGM, a novel method “that learns causal probabilistic graphical models of heterogeneous clinical datasets containing continuous, categorical, and censored variables.”

They applied the model to individuals in phase 1 and 2 of the COPDGene study to learn the clinical, imaging, and blood-derived gene expression features that are linked to overall and adjudicated COPD-related mortality.

Four features were associated with overall and COPD-specific mortality: age, 6-minute walk distance (6MWD), resting oxygen saturation, and the standard deviation of lung attenuation from CT imaging.

Features linked to COPD-specific mortality in the phase 1 group were FEV1/FVC and ATS/ERS classification of COPD severity. Factors contributing to overall mortality were body mass index, heart rate, duration of smoking, and overall health status. In the phase 2 group, 6MWD was linked to COPD-specific mortality and overall mortality, while age and airway wall thickness were linked COPD-specific mortality. The gene expression markers NELL2 and GRB10 were directly linked to overall mortality in the phase 2 cohort, and NRG1 was directly linked to COPD-specific mortality.

The authors concluded that the novel method could identify key features linked to COPD-specific mortality, overall mortality, or both.

Additional markers, including gene expressions and microbiome profiles, were explored in abstracts presented at the session, emphasizing a need for more research in this area and the exploration of additional markers for COPD and other lung conditions.


1. Tesfaigzi Y, Brown MN, Liu C, et al. The FEV1 as a predictor of future health in young non-obstructed smokers. Abstract presented at: American Thoracic Society International Conference; May 20-24, 2023; Washington, DC. Accessed May 23, 2023.

2. Fortis S, Strand M, Bhatt SP, et al. Respiratory exacerbations and lung function decline in people with normal spirometry and smoking exposure. Abstract presented at: American Thoracic Society International Conference; May 20-24, 2023; Washington, DC. Accessed May 23, 2023.

3. Lovelace TC, Benos PV. Disentangling predictors of overall and COPD-specific mortality with probabilistic graphical models. Abstract presented at: American Thoracic Society International Conference; May 20-24, 2023; Washington, DC. Accessed May 23, 2023.

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 EROS real-world outcomes data show prompt initiation of BREZTRI is associated with a reduced risk of future exacerbations in people living with COPD1

EXACOS-CV US data highlights increased risk of severe cardiovascular events following an acute COPD exacerbation2

Results from the EROS real-world retrospective study showed that initiating fixed-dose triple-combination therapy BREZTRI AEROSPHERE® (budesonide/glycopyrronium/formoterol fumarate) within 30 days of a qualifying moderate or severe exacerbation in patients with COPD (chronic obstructive pulmonary disease) is associated with a decreased risk of future exacerbations by 24% vs. delaying treatment by one to six months, and by 34% vs. delaying treatment six months to one year.1

The EROS study is the first real-world evidence analysis of BREZTRI in more than 2,400 patients with COPD from a claims database registry, and was presented today as a late-breaking abstract at the ATS 2023 International Conference in Washington, DC, hosted by the American Thoracic Society. AstraZeneca's presence at ATS 2023 also includes new data from TEZSPIRE and FASENRA.

Professor Charlie Strange, MD, Medical University of South Carolina, US and investigator in the EROS study, said: "A key treatment goal in COPD is to avoid exacerbations that may lead to increased risk of future exacerbations, possible hospitalization or even death. The EROS real-world data build on the body of clinical evidence that BREZTRI is effective in reducing COPD exacerbation rates and can significantly reduce the risk of future exacerbations if used as soon as a patient’s COPD symptoms worsen.”

Another late-breaking presentation at ATS 2023, the EXACOS-CV US retrospective cohort study using the HealthCore Integrated Research Database of people with COPD showed the risk of an acute severe cardiovascular (CV) event (including stroke, heart failure, pulmonary embolism, arrhythmia, or heart attack) increased by 32% in the first 30 days following a single acute moderate or severe COPD exacerbation, compared to those without a prior COPD exacerbation. According to the results, the risk of CV events was highest in the first 90 days following the COPD exacerbation, the risk remained elevated for one year, and each subsequent COPD exacerbation was associated with an even higher risk of acute CV events (>2 times increased CV risk following two or three COPD exacerbations).2 These results suggest that patients with COPD should be considered at risk of cardiopulmonary events following an acute exacerbation, even those who are newly-diagnosed.

Robert Fogel, Vice President, Global Medical Affairs, Respiratory & Immunology, AstraZeneca, said: “As the third leading cause of death worldwide3, improving outcomes for patients must be an urgent priority for physicians and healthcare systems. The EROS and EXACOS-CV studies increase our understanding of the significant cardiopulmonary risk COPD patients face as well as the opportunity to reduce COPD exacerbations through more proactive treatment with BREZTRI.”

AstraZeneca Respiratory & Immunology pipeline and portfolio highlighted in more than 50 abstracts at ATS 2023

Key additional data from AstraZeneca at ATS include:

  • Two post hoc analyses from the NAVIGATOR Phase III trial demonstrating efficacy of TEZSPIRE in patients with severe, uncontrolled asthma irrespective of prior omalizumab use; and in improving rhinosinusitis symptoms measured with SNOT-22 in patients who also have a history of comorbid nasal polyps.4,5
  • Real-world evidence from the retrospective RANS trial supporting the strong clinical efficacy of FASENRA specifically in patients with severe eosinophilic asthma and nasal polyps; and a post-hoc analysis of five FASENRA Phase III/IIIb trials showing an increased rate of achieving clinical remission in patients with severe eosinophilic asthma and concomitant nasal polyps.6,7

BREZTRI AEROSPHERE® (budesonide/glycopyrronium/formoterol fumarate) Important Safety Information

  • BREZTRI is contraindicated in patients who have a hypersensitivity to budesonide, glycopyrrolate, formoterol fumarate, or product excipients
  • BREZTRI is not indicated for treatment of asthma. Long-acting beta2-adrenergic agonist (LABA) monotherapy for asthma is associated with an increased risk of asthma-related death. These findings are considered a class effect of LABA monotherapy. When a LABA is used in fixed-dose combination with ICS, data from large clinical trials do not show a significant increase in the risk of serious asthma-related events (hospitalizations, intubations, death) compared with ICS alone. Available data do not suggest an increased risk of death with use of LABA in patients with COPD
  • BREZTRI should not be initiated in patients with acutely deteriorating COPD, which may be a life-threatening condition
  • BREZTRI is NOT a rescue inhaler. Do NOT use to relieve acute symptoms; treat with an inhaled short-acting beta2-agonist
  • BREZTRI should not be used more often than recommended; at higher doses than recommended; or in combination with LABA-containing medicines, due to risk of overdose. Clinically significant cardiovascular effects and fatalities have been reported in association with excessive use of inhaled sympathomimetic drugs
  • Oropharyngeal candidiasis has occurred in patients treated with orally inhaled drug products containing budesonide. Advise patients to rinse their mouths with water without swallowing after inhalation
  • Lower respiratory tract infections, including pneumonia, have been reported following ICS. Physicians should remain vigilant for the possible development of pneumonia in patients with COPD as the clinical features of pneumonia and exacerbations frequently overlap
  • Due to possible immunosuppression, potential worsening of infections could occur. Use with caution. A more serious or fatal course of chickenpox or measles can occur in susceptible patients
  • Particular care is needed for patients transferred from systemic corticosteroids to ICS because deaths due to adrenal insufficiency have occurred in patients during and after transfer. Taper patients slowly from systemic corticosteroids if transferring to BREZTRI
  • Hypercorticism and adrenal suppression may occur with regular or very high dosage in susceptible individuals. If such changes occur, consider appropriate therapy
  • Caution should be exercised when considering the coadministration of BREZTRI with long-term ketoconazole and other known strong CYP3A4 Inhibitors. Adverse effects related to increased systemic exposure to budesonide may occur
  • If paradoxical bronchospasm occurs, discontinue BREZTRI immediately and institute alternative therapy
  • Anaphylaxis and other hypersensitivity reactions (eg, angioedema, urticaria or rash) have been reported. Discontinue and consider alternative therapy
  • Use caution in patients with cardiovascular disorders, especially coronary insufficiency, as formoterol fumarate can produce a clinically significant cardiovascular effect in some patients as measured by increases in pulse rate, systolic or diastolic blood pressure, and also cardiac arrhythmias, such as supraventricular tachycardia and extrasystoles
  • Decreases in bone mineral density have been observed with long-term administration of ICS. Assess initially and periodically thereafter in patients at high risk for decreased bone mineral content
  • Glaucoma and cataracts may occur with long-term use of ICS. Worsening of narrow-angle glaucoma may occur, so use with caution. Consider referral to an ophthalmologist in patients who develop ocular symptoms or use BREZTRI long term. Instruct patients to contact a healthcare provider immediately if symptoms occur
  • Worsening of urinary retention may occur. Use with caution in patients with prostatic hyperplasia or bladder-neck obstruction. Instruct patients to contact a healthcare provider immediately if symptoms occur
  • Use caution in patients with convulsive disorders, thyrotoxicosis, diabetes mellitus, and ketoacidosis or unusually responsive to sympathomimetic amines
  • Be alert to hypokalemia or hyperglycemia
  • Most common adverse reactions in a 52-week trial (incidence ≥ 2%) were upper respiratory tract infection (5.7%), pneumonia (4.6%), back pain (3.1%), oral candidiasis (3.0%), influenza (2.9%), muscle spasms (2.8%), urinary tract infection (2.7%), cough (2.7%), sinusitis (2.6%), and diarrhea (2.1%). In a 24-week trial, adverse reactions (incidence ≥ 2%) were dysphonia (3.3%) and muscle spasms (3.3%)
  • BREZTRI should be administered with extreme caution to patients being treated with monoamine oxidase inhibitors and tricyclic antidepressants, as these may potentiate the effect of formoterol fumarate on the cardiovascular system
  • BREZTRI should be administered with caution to patients being treated with:
    • Strong cytochrome P450 3A4 inhibitors (may cause systemic corticosteroid effects)
    • Adrenergic drugs (may potentiate effects of formoterol fumarate)
    • Xanthine derivatives, steroids, or non-potassium sparing diuretics (may potentiate hypokalemia and/or ECG changes)
    • Beta-blockers (may block bronchodilatory effects of beta-agonists and produce severe bronchospasm)
    • Anticholinergic-containing drugs (may interact additively). Avoid use with BREZTRI
  • Use BREZTRI with caution in patients with hepatic impairment, as budesonide and formoterol fumarate systemic exposure may increase. Patients with severe hepatic disease should be closely monitored 


BREZTRI AEROSPHERE is indicated for the maintenance treatment of patients with chronic obstructive pulmonary disease (COPD).


Not indicated for the relief of acute bronchospasm or for the treatment of asthma.

Please see full BREZTRI Prescribing Information, including Patient Information.

You may report side effects related to AstraZeneca products.

TEZSPIRE® (tezepelumab-ekko) Important Safety Information


Known hypersensitivity to tezepelumab-ekko or excipients.


Hypersensitivity Reactions

Hypersensitivity reactions were observed in the clinical trials (eg, rash and allergic conjunctivitis) following the administration of TEZSPIRE. Postmarketing cases of anaphylaxis have been reported. These reactions can occur within hours of administration, but in some instances have a delayed onset (ie, days). In the event of a hypersensitivity reaction, consider the benefits and risks for the individual patient to determine whether to continue or discontinue treatment with TEZSPIRE.

Acute Asthma Symptoms or Deteriorating Disease

TEZSPIRE should not be used to treat acute asthma symptoms, acute exacerbations, acute bronchospasm, or status asthmaticus.

Abrupt Reduction of Corticosteroid Dosage

Do not discontinue systemic or inhaled corticosteroids abruptly upon initiation of therapy with TEZSPIRE. Reductions in corticosteroid dose, if appropriate, should be gradual and performed under the direct supervision of a physician. Reduction in corticosteroid dose may be associated with systemic withdrawal symptoms and/or unmask conditions previously suppressed by systemic corticosteroid therapy.

Parasitic (Helminth) Infection

It is unknown if TEZSPIRE will influence a patient’s response against helminth infections. Treat patients with pre-existing helminth infections before initiating therapy with TEZSPIRE. If patients become infected while receiving TEZSPIRE and do not respond to anti-helminth treatment, discontinue TEZSPIRE until infection resolves.

Live Attenuated Vaccines

The concomitant use of TEZSPIRE and live attenuated vaccines has not been evaluated. The use of live attenuated vaccines should be avoided in patients receiving TEZSPIRE.


The most common adverse reactions (incidence ≥3%) are pharyngitis, arthralgia, and back pain.


There are no available data on TEZSPIRE use in pregnant women to evaluate for any drug-associated risk of major birth defects, miscarriage, or other adverse maternal or fetal outcomes. Placental transfer of monoclonal antibodies such as tezepelumab-ekko is greater during the third trimester of pregnancy; therefore, potential effects on a fetus are likely to be greater during the third trimester of pregnancy.


TEZSPIRE is indicated for the add-on maintenance treatment of adult and pediatric patients aged 12 years and older with severe asthma.

TEZSPIRE is not indicated for the relief of acute bronchospasm or status asthmaticus.

Please see full Prescribing Information, including Patient Information and Instructions for Use.

You may report side effects related to AstraZeneca products by clickinghere.

FASENRA® (benralizumab) Important Safety Information


Known hypersensitivity to benralizumab or excipients.


Hypersensitivity Reactions

Hypersensitivity reactions (eg, anaphylaxis, angioedema, urticaria, rash) have occurred after administration of FASENRA. These reactions generally occur within hours of administration, but in some instances have a delayed onset (ie, days). Discontinue in the event of a hypersensitivity reaction.

Acute Asthma Symptoms or Deteriorating Disease

FASENRA should not be used to treat acute asthma symptoms, acute exacerbations, or acute bronchospasm.

Reduction of Corticosteroid Dosage

Do not discontinue systemic or inhaled corticosteroids abruptly upon initiation of therapy with FASENRA. Reductions in corticosteroid dose, if appropriate, should be gradual and performed under the direct supervision of a physician. Reduction in corticosteroid dose may be associated with systemic withdrawal symptoms and/or unmask conditions previously suppressed by systemic corticosteroid therapy.

Parasitic (Helminth) Infection

It is unknown if FASENRA will influence a patient’s response against helminth infections. Treat patients with pre-existing helminth infections before initiating therapy with FASENRA. If patients become infected while receiving FASENRA and do not respond to anti-helminth treatment, discontinue FASENRA until infection resolves.


The most common adverse reactions (incidence ≥ 5%) include headache and pharyngitis.

Injection site reactions (eg, pain, erythema, pruritus, papule) occurred at a rate of 2.2% in patients treated with FASENRA compared with 1.9% in patients treated with placebo.


A pregnancy exposure registry monitors pregnancy outcomes in women exposed to FASENRA during pregnancy. To enroll call 1-877-311-8972 or visit

The data on pregnancy exposure from the clinical trials are insufficient to inform on drug-associated risk. Monoclonal antibodies such as benralizumab are transported across the placenta during the third trimester of pregnancy; therefore, potential effects on a fetus are likely to be greater during the third trimester of pregnancy.


FASENRA is indicated for the add-on maintenance treatment of patients with severe asthma aged 12 years and older, and with an eosinophilic phenotype.

  • FASENRA is not indicated for treatment of other eosinophilic conditions
  • FASENRA is not indicated for the relief of acute bronchospasm or status asthmaticus

Please see full Prescribing Information, including Patient Information and Instructions for Use.

You mayreport side effects related to AstraZeneca products.



COPD refers to a group of lung diseases, including chronic bronchitis and emphysema, that cause airflow blockage and breathing-related problems.8 It affects an estimated 391 million people around the world and is the third leading cause of death globally.3,9


The EROS (Exacerbations and Real-World Outcomes) study is a retrospective analysis of real-world outcomes in 2,409 COPD patients appearing in the MORE2 Registry® claims database in the US to examine whether prompt initiation of BREZTRI following an exacerbation lowers risk of future exacerbations compared to delayed and very delayed initiation.1 In the study, qualifying exacerbations included: one moderate exacerbation while on maintenance treatment, the second of two moderate events without any maintenance treatment, and severe events defined as COPD hospitalizations.


EXACOS-CV US (EXACerbations and their OutcomeS – CardioVascular) is a retrospective cohort study of 355,978 patients 40 years and older who were diagnosed with COPD between 1 January 2012 and 31 December 2019. The study used US administrative claims data from the Healthcare Integrated Research Database, managed by Carelon Research (formerly HealthCore), to investigate a correlation between cardiovascular events and moderate-to-severe COPD exacerbations.2


BREZTRI AEROSPHERE (budesonide/glycopyrronium/formoterol fumarate) is a single-inhaler, fixed-dose triple-combination of formoterol fumarate, a LABA, glycopyrronium bromide, a LAMA, with budesonide, an ICS, and delivered in a pressurized metered-dose inhaler. BREZTRI AEROSPHERE is approved to treat COPD in more than 50 countries worldwide including the US, EU, China and Japan, and is currently being studied in Phase III trials for asthma.


TEZSPIRE (tezepelumab) is being developed by AstraZeneca in collaboration with Amgen as a first-in-class human monoclonal antibody that inhibits the action of TSLP, a key epithelial cytokine that sits at the top of multiple inflammatory cascades and is critical in the initiation and persistence of allergic, eosinophilic and other types of airway inflammation associated with severe asthma, including airway hyperresponsiveness.10,11 TEZSPIRE  is approved in the US, EU, Japan and other countries for the treatment of severe asthma.12-14


NAVIGATOR is a Phase III, randomized, double-blinded, placebo-controlled trial to evaluate the efficacy and safety of TEZSPIRE (210mg every four weeks) compared to placebo added to SoC in adults and adolescents with severe, uncontrolled asthma.15 Two post hoc analyses from the NAVIGATOR trial evaluated the effect of TEZSPIRE on the annualized asthma exacerbation rate (AAER) over 52 weeks with and without prior omalizumab, and changes in total and domain SNOT-22 scores from baseline to week 52 in patients with a history of nasal polyps.4,5

Amgen collaboration
In 2020, Amgen and AstraZeneca updated a 
2012 collaboration agreement for TEZSPIRE. Both companies will continue to share costs and profits equally after payment by AstraZeneca of a mid single-digit inventor royalty to Amgen. AstraZeneca continues to lead development and Amgen continues to lead manufacturing. All aspects of the collaboration are under the oversight of joint governing bodies. Under the amended agreement, Amgen and AstraZeneca will jointly commercialize TEZSPIRE in North America. Amgen will record product sales in the US, with AZ recording its share of US profits as Collaboration Revenue. Outside of the US, AstraZeneca will record product sales, with Amgen recording profit share as Other/Collaboration revenue.


FASENRA (benralizumab) is a monoclonal antibody that binds directly to IL-5 receptor alpha on eosinophils and attracts natural killer cells to induce rapid and near-complete depletion of eosinophils via apoptosis (programmed cell death).16 FASENRA is currently approved as an add-on maintenance treatment for severe eosinophilic asthma in the US, EU, Japan and other countries, and is approved for self-administration in the US, EU and other countries.

FASENRA was developed by AstraZeneca and is in-licensed from BioWa, Inc., a wholly-owned subsidiary of Kyowa Kirin Co., Ltd., Japan.  

AstraZeneca in Respiratory & Immunology

Respiratory & Immunology, part of AstraZeneca BioPharmaceuticals is a key disease area and growth driver to the Company.

AstraZeneca is an established leader in respiratory care with a 50-year heritage and a growing portfolio of medicines in immune-mediated diseases. The Company is committed to addressing the vast unmet needs of these chronic, often debilitating, diseases with a pipeline and portfolio of inhaled medicines, biologics and new modalities aimed at previously unreachable biologic targets. Our ambition is to deliver life-changing medicines that help eliminate COPD as a leading cause of death, eliminate asthma attacks and achieve clinical remission in immune-mediated diseases.


AstraZeneca is a global, science-led biopharmaceutical company that focuses on the discovery, development, and commercialization of prescription medicines in Oncology, Rare Diseases, and BioPharmaceuticals, including Cardiovascular, Renal & Metabolism, and Respiratory & Immunology. Based in Cambridge, UK, AstraZeneca operates in over 100 countries and its innovative medicines are used by millions of patients worldwide. Please visit and follow the Company on Twitter @AstraZenecaUS.


Media Inquiries

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  1. Pollack, M, Tkacz, J, Schinkel, J. et al. Exacerbations and real-world outcomes (EROS) among patients with COPD receiving single inhaler triple therapy of budesonide/glycopyrrolate/formoterol fumarate [Poster Discussion]. Presented at the American Thoracic Society International Conference 2023 (19-24 May)
  2. Daniels, K, Tave, A., Neikirk, A., et al. Incidence of acute cardiovascular events following acute exacerbation of chronic obstructive pulmonary disease in a large US claims database [Thematic Poster Session]. Presented at the American Thoracic Society International Conference 2023 (19-24 May).
  3. World Health Organization. The Top 10 Causes of Death. Accessible at: [last accessed May 2023]
  4. Menzies-Gow, A, Colice, G, Ambrose, C, et al. Efficacy of tezepelumab in patients with severe, uncontrolled asthma by prior omalizumab use: a post hoc analysis of the phase 3 NAVIGATOR study. [Mini Symposium] Presented at the American Thoracic Society International Conference 2023 (19-24 May)
  5. Spahn, J, Jacobs, J, Hoyte, F, et al. Tezepelumab efficacy by SNOT-22 domain scores in patients with severe, uncontrolled asthma and comorbid nasal polyps in the phase 3 NAVIGATOR study. [Poster Discussion] Presented at the American Thoracic Society International Conference 2023 (19-24 May)
  6. Le TT, et al. Real-World Evidence of Benralizumab in Patients with Severe Eosinophilic Asthma and Nasal Polyps: Initial Results of the RANS Study. [Poster discussion]. Presented at the American Thoracic Society International Conference 2023, 23 May 2023, 14:15-16:15 EST
  7. Louis R, et al. Approaching clinical remission in severe asthma: An analysis of patients with chronic rhinosinusitis with nasal polyps (CRSwNP) treated with benralizumab across five clinical trials. [Poster discussion]. Presented at the American Thoracic Society International Conference 2023, 23 May 2023, 9:00-16:15 EST
  8. GOLD. Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2023. [Online]. Available at: [last accessed May 2023]
  9. Adeloye D, Song P, Zhu Y, et al. Global, regional, and national prevalence of, and risk factors for, chronic obstructive pulmonary disease (COPD) in 2019: a systematic review and modelling analysis. Lancet Respir Med. (2022) Vol 10(5); 447-458
  10. Corren J, et al. Tezepelumab in adults with uncontrolled asthma [supplementary appendix; updated April 18, 2019]. N Engl J Med. 2017;377:936-946.
  11. Varricchi G, et al. Thymic Stromal Lymphopoietin Isoforms, Inflammatory Disorders, and Cancer. Front Immunol. 2018;9:1595.
  12. AstraZeneca plc. Tezspire (tezepelumab) approved in the US for severe asthma. Available at: [Last accessed: May 2023].  
  13. AstraZeneca plc. Tezspire approved in the EU for the treatment of severe asthma. 2022. Available at: [Last accessed: May 2023].  
  14. AstraZeneca plc. Tezspire approved in Japan for the treatment of severe asthma. Available at: [Last accessed: May 2023]. 
  15. Menzies-Gow A, et al.  Tezepelumab in Adults and Adolescents with Severe, Uncontrolled Asthma. N Engl J Med. 2021;384: 1800-1809. DOI: 10.1056/NEJMoa2034975. 
  16. AstraZeneca. Fasenra Summary of Product Characteristics. Available at: [Last accessed: May 2023].


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Undiagnosed and overdiagnosed chronic obstructive pulmonary disease (COPD) are common in primary health care (PHC) settings when COPD is defined with use of postbronchodilator airflow obstruction, according to systematic review and meta-analysis findings published in BMJ Open Respiratory Research.

Investigators sought to quantify COPD underdiagnosis and overdiagnosis in PHC settings where postbronchodilator airflow obstruction was used to establish a diagnosis of COPD.

The researchers systematically searched the Medline (OVID) and Embase electronic databases through January 4, 2022, for relevant studies published in English. The search yielded 21 cross-sectional prevalence studies with 3959 cases of spirometry-defined COPD, with all studies reporting data on undiagnosed COPD, and 9 articles also providing data on COPD overdiagnosis. In addition, 5 COPD case series were found that reported on 7381 confirmed COPD cases in 10,142 patients; these provided data relating only to COPD overdiagnosis. Most of the studies (n=23) recruited adults aged at least 40 years of age, with an average mean age of 59.1 years (95% CI, 47.9-68.5; range, 46.8-72 years).

The 21 cross-sectional studies had a variable baseline prevalence of spirometry-defined COPD, and the proportion of spirometry-defined COPD undiagnosed in this population varied substantially by risk category (I2 = 97.1%). In 3 adequately sized studies of individuals who smoked and showed COPD symptoms, 14% to 26% of patients had spirometry-confirmed COPD that was not documented in their health records. Moreover, this problem was greater among those who smoked and had only a clinician diagnosis of chronic bronchitis (25.6%; 95% CI, 23.2%-28.1%), such that a concurrent COPD diagnosis was not documented in a quarter of medical records.

This review highlights that underdiagnosis and overdiagnosis of COPD is a complex and multifaceted problem, and the magnitude of this issue is expected to worsen given even further reductions in spirometry use post-COVID-19.

In studies involving individuals who smoked who had spirometric evidence of COPD, regardless of symptoms, but did not have a COPD diagnosis, the pooled prevalence estimate was 16% (95% CI, 14%-18%). The investigators further found that in patients receiving inhaled therapies for obstructive lung diseases, COPD and/or fixed airflow obstruction in patients with asthma was undiagnosed in 25% of patients (95% CI, 22%-28%).

Among 8 heterogeneous cross-sectional studies of adequate sample size, 6 found that 26% to 52% of patients did not have postbronchodilator airflow obstruction on spirometry, despite a probable intent to manage COPD.

The baseline prevalence of spirometry-confirmed COPD varied between 50% and 75% in the adequately powered COPD case series. Among these patients, 25% to 50% had no evidence of airflow obstruction on postbronchodilator spirometry and would be considered overdiagnosed.

In citing study limitations, the researchers noted that excluding articles published in languages other than English at the title/abstract phase could have limited the generalizability of their findings. In addition, the studies were not directly assessed for publication bias and in all but 2 studies, the age spectrum of COPD was not considered.

“This review highlights that underdiagnosis and overdiagnosis of COPD is a complex and multifaceted problem, and the magnitude of this issue is expected to worsen given even further reductions in spirometry use post-COVID-19,” stated the investigators. “There is an underlying need for greater awareness and action by both at-risk patients and health care providers about reporting and documenting symptoms and then objectively investigating for a potential COPD diagnosis.

Disclosure: Some of the study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.

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Cannabis smoking is not associated with an elevated risk of chronic obstructive pulmonary disease (COPD) even among those possessing a clinically high risk for developing the disease, according to a study, Impact of Marijuana Smoking on COPD Progression in a Cohort of Middle-Aged and Older Persons, published in the journal of the COPD Foundation. 

COPD, which refers to a group of diseases that cause airflow blockage and breathing-related problems including emphysema and chronic bronchitis, makes breathing difficult for the 16 million Americans with this disease. 

Older Adults, Longterm Smokers

Researchers at the University of California Los Angeles (UCLA) evaluated the relationship between cannabis use and the development of COPD in a cohort of older subjects who either smoked cannabis now or who smoked cigarettes on a regular basis in the past.

The researchers determined that neither former nor current cannabis smoking was associated with evidence of COPD progression or its development.

Background: Limited data are available regarding the impact of marijuana smoking impact on the development or progression of COPD in middle-aged or older adults with a variable history of tobacco cigarette smoking.

Methods: Researchers divided ever-tobacco smoking participants in the Subpopulations and Intermediate Outcomes in COPD Study (SPIROMICS) into three groups based on self-reported marijuana use: current, former or never marijuana smokers (CMS, FMS or NMS, respectively). Longitudinal data were analyzed in participants with ≥2 visits over a period of ≥52 weeks.

Measurements: Researchers then compared CMS, FMS and NMS, and those with varying amounts of lifetime cannabis use. Mixed effects linear regression models were used to analyze changes in spirometry, symptoms, health status and radiographic metrics. All models were adjusted for age, sex, race and baseline tobacco smoking amount.

Spirometry tests are commonly used to help diagnose lung conditions, like asthma and COPD, by measuring the amount of air someone can breathe out in one forced breath. This is done with a device called a spirometer, which has a mouthpiece the patient can breathe into.

“In [this] cohort of ever-tobacco smokers of ≥20 pack-years with established COPD or at risk of developing COPD followed over an average of more than four years, a history of current and/or former smoking of marijuana of any cumulative lifetime amount was not found to be associated with a significantly deleterious impact on progression of COPD,” the authors reported.

“Among ever-tobacco smokers in the same cohort without COPD at enrollment, self-reported current and/or former concomitant marijuana smoking, including heavy marijuana smoking, was not found to be associated with an increased risk of subsequently developing COPD.”

The findings are consistent with prior studies concluding that cannabis inhalation, even long-term, is not positively associated with COPD, lung cancer, or irreversible airway damage, per the study.

Younger Adults: Similar Findings, Different Study

A similar longitudinal study was undertake  recently at the University of Queensland, Australia and published in Respiratory Medicine with a cohort of 1173 young adults between 21 and 30 who smoked cannabis, tobacco, both or nothing over 9 years found an association between tobacco smokers and reduced airflow. Those who smoked cigarettes alone, or cigarettes with cannabis, had reductions in their airflow, though cannabis did not add to these reductions; smoking cannabis alone did not reduce airflow or seem to impact lung functioning. Even after 9 years of use, cannabis smoke exposure did not seem to impact the lungs.

Photo: American Lung Association


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(ABC 6 News) – The Minnesota Pollution Control Agency (MPCA) has issued an air quality alert for southern Minnesota, from 12 p.m. through 8 p.m. Tuesday, May 23. The affected area includes the Twin Cities metropolitan area, St. Cloud, Rochester, Mankato, Marshall, and the tribal nations of Mille Lacs, Upper Sioux, and Prairie Island.

Ground-level ozone is expected to be high during the afternoon hours on Tuesday, and air quality is expected to reach the Orange (unhealthy for sensitive groups) AQI category across southern Minnesota. Southerly winds are transporting pollutants into the state. Sunny skies, warm temperatures, and low humidity will allow these pollutants to react in the air to produce ground-level ozone. Ozone will be highest during the afternoon and early evening hours when sunshine is most abundant, and temperatures are highest. Air quality is expected to reach the Orange AQI category. This is considered unhealthy for sensitive groups.

People whose health is affected by unhealthy air quality:  There are people who are more likely to be affected when ozone pollution reaches an unhealthy level.

  • People who have asthma or other breathing conditions like chronic obstructive pulmonary disease (COPD), chronic bronchitis, and emphysema.
  • Children and teenagers.
  • People of all ages who are doing extended or heavy, physical activity like playing sports or working outdoors.
  • Some healthy people who are more sensitive to ozone even though they have none of the risk factors. There may be a genetic base for this increased sensitivity.

Health effects: Unhealthy ozone levels can aggravate lung diseases like asthma, emphysema, and COPD. When the air quality is unhealthy, people with these conditions may experience symptoms like difficulty breathing deeply, shortness of breath, throat soreness, wheezing, coughing, or unusual fatigue. If you are experiencing any of these symptoms, use your inhalers as directed and contact your health care provider.

Take Precautions: Everyone should take precautions when the air quality is unhealthy.

  • Take it easy and listen to your body.
  • Limit, change, or postpone your physical activity.
  • If possible, stay away from local sources of air pollution like busy roads and wood fires.
  • If you have asthma, or other breathing conditions like COPD, make sure you have your relief/rescue inhaler with you.
  • People with asthma should review and follow guidance in their written asthma action plan. Make an appointment to see your health provider if you don’t have an asthma action plan. 

Pollution reduction tips: Ozone is produced on hot, sunny days by a chemical reaction between volatile organic compounds and oxides of nitrogen.

  • Reduce vehicle trips and fill-up the gas tank at dawn or dusk.
  • Encourage use of public transport, or carpool, when possible.
  • Postpone use of gasoline powered lawn and garden equipment on air alert days. Use battery or manual equipment instead.
  • Avoid backyard fires.

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(MENAFN- EIN Presswire)

AirPhysio helps to clear blocked airways and remove mucus from the lungs to facilitate easier breathing

AirPhysio lung clearance device product shot

All-natural solution alleviates lung and respiratory conditions

The beauty of AirPhysio is that it is completely drug and chemical free so does not require a prescription.” - Daniel SeldonSYDNEY, NSW, AUSTRALIA, May 22, 2023/ / -- For anyone who suffers from a lung or respiratory condition, there's an innovative award-winning Australian device that can help alleviate their symptoms.

airphysio is an all-natural Oscillating Positive Expiratory Pressure mucus clearance device that is suitable for anyone suffering from conditions such as asthma, cystic fibrosis, chronic bronchitis, chronic obstructive pulmonary disease (COPD), bronchiectasis, emphysema, respiratory syncytial virus (RSV), pneumonia or even the common cold or flu.

Listed on the Australian Register of Therapeutic Goods, the device uses the same airway clearance techniques that doctors have been utilising on patients in hospitals for years. Simple and easy to use, the air physiotherapy mechanical device is an effective lung training tool that loosens and mobilises thick, stubborn mucus in the airways which makes it hard to breathe.

How AirPhysio works

AirPhysio helps to clear blocked airways and clear mucus from the lungs. Breathing through the device creates a positive pressure which causes a stainless-steel ball to vibrate. This turbulence helps to loosen mucus, enabling the user to cough and expel it out naturally.

While results vary from person to person, based on their physical fitness and severity of disease, with continued use, the device has the potential to slow down the progression of respiratory conditions such as asthma, COPD, bronchiectasis, and cystic fibrosis.

Daniel Seldon from aussie pharma direct who distribute AirPhysio, says that the device offers sufferers another tool in their toolkit to tackle these conditions.

“The beauty of AirPhysio is that it is completely drug and chemical free so does not require a prescription,” says Seldon.“It is not an inhaler, nebuliser, spirometer, spray, or puffer so is safe to use. It doesn't require refills or batteries, and causes no unpleasant side effects like headache, nausea, or dizziness.

“This Australian innovation puts the power back into the hands of the user and is an invaluable tool for anyone suffering from congestive lung diseases and laboured breathing conditions," he says.

There are four different types of AirPhysio which cater to different lung capacities.

low lung capacity is designed for people affected by lung or respiratory conditions such as asthma, cystic fibrosis, chronic bronchitis, COPD, bronchiectasis, emphysema, and RSV. It also aids in the recovery from pneumonia, colds and flu and is suitable for individuals with respiratory muscle weakness and low lung capacity due to advanced age.

Average Lung Capacity is ideal for teenagers and adults who want to improve their day-to-day breathing and lung capacity.

AirPhysio for Children is designed to help children breathe easier so they can live, play, and learn without being impacted by congested lungs. Suitable for ages five and up, it's ideal for children who are affected by respiratory conditions such as asthma, the common cold, flu, pneumonia, bronchiectasis, cystic fibrosis, and COPD.

AirPhysio Sports is for professional, elite, and amateur sportspeople aged 13 and over. AirPhysio Sports is a drug-free performance enhancer and lung expansion device that helps users achieve personal best results and a competitive edge by optimising lung capacity and increasing 02 and CO2 gas transfer to reduce recovery time.


Jenny Westdorp
Pivotal Communication
+61 413 334 425

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The breath of life refers to the act of breathing, which is fundamental to survival and sustained life. From a scientific standpoint, it involves the exchange of gases between the external environment and our internal organs, which takes place through the respiratory system.

Breathing is an involuntary biological process that is essential to the functioning of the body. Normally, it is automatic, and we do not have to consciously think about it. However, many people practice specific breathing exercises or techniques, such as yoga or meditation, to improve their overall health and wellbeing.

In this article, we will explore what the breath of life is, its significance for humans, and the benefits of improving our breathing patterns. We will also address some common questions related to the topic.

What Happens When You Take a Breath?

When we inhale, oxygen-rich air enters our lungs and moves into the bloodstream, providing cells with the energy they need to carry out their functions. At the same time, carbon dioxide, which is a waste product of cellular metabolism, is released from the body through exhalation.

The respiratory system, which consists of the lungs, airways, and muscles, plays a crucial role in this process. As we breathe in, the air is filtered, warmed, and humidified by the nose, throat, and bronchial passages. This ensures that the air entering the lungs is clean and at the right temperature and humidity level.

This exchange of gases is what allows oxygen to reach our cells, fueling our body’s processes, and helping us stay alive.

What Are the Different Types of Breathing?

There are several types of breathing, each of which serves a particular purpose. Here are some examples:

  • Abdominal breathing: also known as diaphragmatic breathing, this technique involves breathing deeply from the belly, rather than the chest. It can help reduce stress, improve oxygenation, and promote relaxation.
  • Alternate nostril breathing: a yoga practice that involves breathing in and out through one nostril at a time, while blocking the other with the finger. This technique can help balance the nervous system and promote relaxation.
  • Box breathing: a technique that involves inhaling for four counts, holding the breath for four counts, exhaling for four counts, and holding for four counts. It can help improve focus, reduce anxiety, and promote relaxation.
  • Pursed-lip breathing: a technique that involves inhaling through the nose and exhaling through pursed lips, as if blowing out a candle. It can help improve lung function, reduce shortness of breath, and promote relaxation.
  • What Are the Benefits of Good Breathing?

    Good breathing patterns are associated with several health benefits. These include:

  • Improved respiratory function: practicing deep breathing exercises can help improve lung capacity, oxygenation, and ventilation.
  • Reduced stress and anxiety: breathing techniques that promote relaxation, such as deep breathing or alternate nostril breathing, can help reduce stress and anxiety levels.
  • Improved mental clarity and focus: certain breathing techniques, such as box breathing, can help improve focus, attention, and cognitive performance.
  • Reduced pain and tension: deep breathing exercises can help reduce muscle tension, pain, and soreness.
  • Improved sleep: relaxation techniques that involve deep breathing can help promote better sleep quality and reduce insomnia.
  • How Does Breathing Affect the Nervous System?

    Breathing is closely linked to the autonomic nervous system, which controls many involuntary functions of the body, such as heart rate, digestion, and respiration.

    The autonomic nervous system is divided into two branches: the sympathetic nervous system, which is responsible for the fight-or-flight response, and the parasympathetic nervous system, which promotes rest and relaxation.

    Slow, deep breathing stimulates the parasympathetic nervous system and triggers the relaxation response, reducing stress and anxiety levels. Conversely, rapid breathing can activate the sympathetic nervous system and trigger the fight-or-flight response, increasing anxiety, and stress levels.

    How Can I Improve My Breathing?

    There are several ways to improve your breathing patterns and promote better respiratory function. Here are some tips:

  • Practice deep breathing: focus on breathing slowly and deeply from the belly, rather than shallowly from the chest. You can start by inhaling for four counts and exhaling for four counts, and gradually increase the length of your inhale and exhale as you feel more comfortable.
  • Engage in physical activity: regular exercise can help improve lung capacity and function, and promote better breathing patterns overall.
  • Avoid triggers of respiratory problems: if you have respiratory problems, such as asthma or allergies, avoid triggers that can exacerbate your symptoms, such as tobacco smoke, pollution, or allergens.
  • Practice relaxation techniques: techniques that promote relaxation, such as deep breathing, progressive muscle relaxation, or mindfulness meditation, can help reduce stress and anxiety levels and improve overall respiratory function.
  • How Can Breathing Help With Pain Management?

    Deep breathing exercises can help reduce pain and tension in the body by promoting relaxation and reducing muscle stiffness.

    By directing your attention to your breath, you can also distract yourself from pain sensations and improve your ability to cope with discomfort.

    Additionally, practicing deep breathing exercises can help stimulate the release of endorphins, which are natural painkillers produced by the body.

    Can Breathing Help With Sleep Problems?

    Deep breathing exercises can help promote relaxation and reduce anxiety levels, which can, in turn, improve sleep quality and reduce insomnia.

    By focusing on your breath, you can also quiet your mind and soothe racing thoughts, which can be a common problem for people with sleep disorders.

    Lastly, practicing regular deep breathing exercises can help regulate your circadian rhythms, which are responsible for regulating your sleep-wake cycle.

    Can Breathing Help With Digestive Problems?

    Breathing exercises can help improve digestion by promoting relaxation and reducing stress levels.

    Stress can interfere with the digestive process by causing the muscles in the digestive tract to contract, leading to bloating, gas, and other digestive problems.

    By practicing deep breathing exercises, you can reduce stress levels, promote relaxation, and help the muscles in your digestive tract relax and function properly.

    Can Breathing Help With Heart Health?

    Healthy breathing patterns are associated with several heart health benefits, including:

  • Reduced heart rate: slow and deep breathing can help reduce heart rate and promote relaxation.
  • Lower blood pressure: breathing techniques that promote relaxation can help lower blood pressure and reduce the risk of heart disease and stroke.
  • Better oxygenation: practicing deep breathing exercises can help improve oxygenation, which can reduce the risk of heart disease and other cardiovascular problems.
  • What Are Some Common Breathing Disorders?

    Breathing disorders can be caused by a variety of factors, including lung disease, allergies, and asthma.

    Some common breathing disorders include:

  • Asthma: a chronic respiratory disease characterized by inflammation and narrowing of the airways, leading to difficulty breathing.
  • Chronic obstructive pulmonary disease (COPD): a group of lung diseases, including chronic bronchitis and emphysema, that make it difficult to breathe.
  • Interstitial lung disease: a group of lung diseases that involve scarring and inflammation of the lung tissue, leading to difficulty breathing.
  • Sleep apnea: a sleep disorder characterized by episodes of interrupted breathing during sleep, leading to poor sleep quality and other health problems.
  • Can Breathing Techniques Help With Breathing Disorders?

    Breathing techniques, such as deep breathing or pursed-lip breathing, can help improve respiratory function and reduce symptoms associated with breathing disorders.

    Additionally, physical exercise can also help improve lung function and reduce the risk of complications associated with breathing disorders.

    However, it is important to consult with a healthcare professional before starting any breathing exercises, as some techniques may not be suitable for people with certain respiratory conditions.

    What Are the Key Takeaways?

    The breath of life is essential to our survival and sustained life. Breathing involves the exchange of gases between the external environment and our internal organs, which takes place through the respiratory system.

    Good breathing patterns are associated with several health benefits, including improved respiratory function, reduced stress and anxiety, and improved mental clarity and focus.

    There are several ways to improve your breathing patterns, including practicing deep breathing, engaging in physical activity, avoiding respiratory triggers, and practicing relaxation techniques.

    Breathing exercises can also help reduce symptoms associated with breathing disorders and promote better respiratory function overall.

    If you are experiencing breathing problems or have a respiratory condition, it is important to consult with a healthcare professional before starting any breathing exercises.

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    More than one-third of patients with chronic obstructive pulmonary disease (COPD) have metabolic syndrome (MetS), and those with this comorbidity are at higher risk for stroke, coronary artery disease, and mortality, according to study findings reported in Therapeutic Advances in Respiratory Disease.

    Metabolic syndrome is a common comorbidity of COPD. Researchers in Thailand sought to assess the prevalence of MetS in those with COPD as well as associated factors and clinical consequences after 5 years in this patient population.

    The investigators conducted a prospective, observational study from June 2015 to November 2020 of patients at least 40 years of age with stable COPD at Songklanagarind Hospital in Thailand. A total of 115 patients with COPD were included (mean age, 73 years; 90% male), of whom 43 patients (37.4%) were diagnosed with MetS. Participants’ COPD diagnosis was based on the Global Initiative for Chronic Obstructive Lung Disease 2015 guidelines; MetS was defined using the International Diabetes Federation’s global definition of MetS. The primary outcome was MetS prevalence in patients with COPD. Secondary outcomes were associated factors and clinical consequences of MetS after 5 years.

    Compared with the participants who had COPD without MetS, those with COPD and MetS had a higher rate of obesity (29.8 ± 3.0 kg/m2 vs 21.5 ± 3.1 kg/m2, respectively; P <.001), chronic bronchitis-type COPD (87% vs 9.7%; P <.001), and C-reactive protein (CRP) levels greater than 0.6 mg/L (58.1% vs 12.5%; P <.001). Multivariate analysis showed that chronic bronchitis-type COPD and high CRP levels in COPD (>0.6 mg/L) were significant potential predictors of MetS development in patients with COPD.

    Screening for MetS in patients with COPD may facilitate earlier, proper management and prevention of clinical consequences.

    Stroke, coronary artery disease, and mortality occurred significantly more frequently in patients with COPD and MetS vs those without MetS (34.9% vs 6.9%; 53.5% vs 4.2%; and 20.9% vs 2.8%, respectively). In multivariate analysis, stroke, coronary artery disease, exacerbation, and mortality were significant clinical consequences of MetS in patients with COPD: stroke (relative risk [RR], 15.36; 95% CI, 2.13-110.67); coronary artery disease (RR, 45.43; 95% CI, 4.61-447.07); exacerbation (RR, 1.95; 95% CI, 1.40-2.70); and mortality (RR, 48.01; 95% CI, 1.12-2049.43).

    Patients with COPD with MetS vs without MetS also had a significantly higher use rate of long-acting muscarinic antagonists (34.9% vs 20.8%, P =.041) and a significantly higher annual exacerbation rate (2.0 vs 1.0).

    Limitations include the single-center design and confounding factors such as family history of cardiovascular disease and physical inactivity, which also affect the consequences of MetS. In addition, female patients were 8% of the study population.

    “These findings could alert pulmonologists to the importance of MetS in COPD patients,” stated the researchers. “Screening for MetS in patients with COPD may facilitate earlier, proper management and prevention of clinical consequences.”

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    The Lincoln-Lancaster County Health Department has issued a health advisory for sensitive groups due to smoke from wildfires occurring in Alberta and British Colombia, Canada.

    Smoke may periodically reach levels that are unhealthy for children, older adults and those with asthma, lung disease, other respiratory conditions or heart disease.

    “Northerly winds combined with heavy smoke being generated by large wildfires in Canada are likely to result in levels of smoke in the air that are unhealthy for sensitive groups. Smoke impacts are most likely through early Friday afternoon, but could linger into Saturday,” says Gary Bergstrom, Air Quality Program Supervisor for the health department.

    Bergstrom said when tiny particles and gases in smoke are inhaled, they can cause asthma attacks, worsen chronic bronchitis and emphysema, and cause chest pain in some people with heart disease.

    he advises those at risk to reduce strenuous physical activity while outside, take plenty of breaks and watch for symptoms such as coughing, shortness of breath, difficulty breathing, or chest pain. People with asthma should follow their asthma action plans and have quick relief medicine readily available.

    More information about the Air Quality Index is available at

    (Photo: National Weather Service )

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    Asthma and COPDYou can't breathe when you exert yourself, and you suffer from episodes of coughing. There are two likely causes for this: you could have asthma, or you could have Chronic Obstructive Pulmonary Disease (COPD), such as emphysema or chronic bronchitis.

    Because asthma and COPD have a number of similarities, it can be difficult to distinguish between them. However, after taking into account your symptoms, medical history, a physical examination and results of medical tests, your doctor can determine if either of these chronic diseases are at the root of your poor health.


    Both asthma and COPD may cause shortness of breath and cough. A daily morning cough that produces phlegm is particularly characteristic of chronic bronchitis, a type of COPD. Episodes of wheezing and chest tightness (especially at night) is more common with asthma.

    In addition, patients with asthma are more likely to have allergies such as allergic rhinitis (hay fever) or atopic dermatitis (eczema).

    History of Smoking

    COPD is almost always associated with a long history of smoking, while asthma occurs in non-smokers as well as smokers. Smoking can also make asthma worse; and smokers are particularly likely to suffer from a combination of both asthma and COPD.

    Differing Treatments

    Although it may take some time and effort, it is important to distinguish between asthma and COPD. The treatment for the two conditions is different, and you will greatly benefit from an accurate diagnosis and appropriate treatment plan. Whether you have asthma, COPD, or both, make sure you see your doctor regularly.

    Reviewed: 9/28/20

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    &lt;p&gt;David Sacks / Getty Images&lt;/p&gt;

    David Sacks / Getty Images

    Medically reviewed by Michael Menna, DO

    Sepsis is the body’s extreme physical response to infection or injury, causing a dangerous whole-body immune reaction (inflammatory response). Pregnant people, adults over 65, infants, and those with compromised immunity or chronic disease are at more risk of developing it. About 1.7 million people in the United States develop sepsis every year, leading to approximately 350,000 deaths.

    The symptoms of sepsis vary based on severity and type. In some cases, it leads to septic shock, a potentially fatal condition in which blood pressure drops and multiple organ systems fail. Septic shock is a medical emergency that must be treated in the intensive care unit (ICU). Though this condition is challenging, in-hospital treatments can reverse the course of sepsis in many cases.

    Sepsis Symptoms

    Since sepsis is a whole-body inflammatory response, it can take many different shapes. The symptoms can resemble those of other infections or diseases, especially in their early course. They vary based on the location and type of infection or injury that’s causing the condition. The symptoms of sepsis include:

    • Fever

    • Chills

    • Sweaty, warm, or clammy skin

    • Rapid, shallow breathing

    • Shortness of breath

    • Elevated heart rate

    • Weak pulse

    • Confusion, and/or disorientation

    • Severe lethargy (lack of energy) or agitation

    • Severe pain or discomfort, with the location dependent on the site of injury or infection

    • Rash, typically small patches of red or discolored skin

    • Difficulty urinating and/or a lack of urine

    Whatever form it takes, sepsis is a medical emergency. Get immediate help and call 9-1-1 if you suspect you or a loved one has sepsis. Since this condition progresses rapidly, prompt medical attention is critical. In severe cases, or if untreated, this can lead to septic shock, which can cause:

    • Cardiac failure

    • Lasting organ and tissue damage

    • Organ failure in multiple systems, known as multi-organ dysfunction syndrome (MODS)

    • Dangerously low blood pressure

    What Causes Sepsis?

    Sepsis is a system-wide immune or inflammatory response triggered by an infection or traumatic injury. To defend the body, the immune system releases proteins, called cytokines, into the blood. In sepsis cases, the injury or infection is so severe that these chemicals spread and flood the system, causing what’s called a cytokine storm. This can result in blood clots and leaky vessels, which can damage tissues and organs.

    A wide range of infections and medical conditions can cause sepsis, the most common of which are:

    • Bacterial infections: The most common cause of sepsis is infection of bacteria, primarily Staphylococcus aureus (staph), Escherichia coli (E. coli), and Streptococcus pyogenes (S. pyogenes).

    • Viruses: Sepsis can also be a response to a viral infection, such as influenza or COVID-19.

    • Post-surgery complications: Many cases of sepsis arise due to infection following surgery, or even a cut or wound.

    • Traumatic injury: Since injuries also trigger strong immune reactions, they can also set off sepsis.

    Most commonly, however, sepsis is triggered by an infection of the urinary tract, lungs, kidneys, or stomach.

    Risk Factors

    The chances of developing sepsis increase if you have a weakened immune system. There are several risk factors for this condition:

    • Age over 65

    • Younger age, especially infancy

    • Diabetes

    • Lung disease

    • Leukemia, lymphoma, or other types of cancer

    • Human immunodeficiency virus (HIV) or acquired immunodeficiency syndrome (AIDS)

    • Long-term antibiotic use

    • Recent surgery or infection

    • Recent organ or bone marrow transplant


    Since sepsis is a medical emergency, diagnosis of the condition occurs as you are being stabilized in the hospital. In addition to assessing your medical history and any test results, your healthcare provider may use the following several diagnostic tests:

    • Complete blood count (CBC): This panel of blood tests is used to count different types of white blood cells, liver function, and measure clotting ability. This helps support diagnosis and establish severity.

    • Serum lactate: This blood test measures the amount of lactic acid in your system, which is produced by your muscles and red blood cells; elevated levels can be a sign of sepsis.

    • Cultures and other tests: Additional tests, including blood, urine (urinalysis), saliva, or microscopic evaluation of samples from suspected sites of infection may be used to determine the underlying cause of the sepsis.

    • Arterial blood gas: This test measures the levels of oxygen and carbon dioxide in the blood. Low oxygen levels and high carbon dioxide levels can be a sign of sepsis.

    • Imaging: In some cases, healthcare providers may employ imaging techniques, such as chest X-ray or computerized tomography (CT) scan, to assess infection in the lungs.

    Stages of Sepsis

    Based on their evaluation, your healthcare will stage the disease:

    • Sepsis: The mildest form causes systemic inflammatory response syndrome (SIRS). This is defined by two of the following: a body temperature above 100.4º Fahrenheit (F) or below 96.8º F, heart rate above 90 beats per minute, rapid breathing (taking over 20 breaths a minute), white blood cell count above 12,000 per cubic milliliter (ml) or below 4,000.

    • Severe sepsis: Severe sepsis occurs when one or more organs are showing signs of damage; blood pressure drops dangerously low, and the lack of oxygen damages tissues in the body. Mental confusion, severe abdominal pain, muscle cramping, lethargy, and breathing difficulties result.

    • Septic shock: The most advanced and severe form of sepsis is septic shock. This is when, despite treatment, blood pressure remains dangerously low. This type can cause organ failure in multiple systems and can be fatal.

    Treatments for Sepsis

    As noted, sepsis is a medical emergency, with treatment typically taken on in the intensive care unit (ICU) of a hospital. The goals are three-fold: to stop the spread of infection, protect organs that are being damaged, and stop blood pressure from dropping. This involves several procedures.

    Stabilizing Respiration

    If you present with suspected sepsis, the first goal is to stabilize your breathing. Levels of oxygen in the blood and breathing are carefully monitored, and you’ll be placed on a respirator to ensure you’re at stable levels.

    Establishing Venous Access

    Alongside work to preserve breathing ability, healthcare providers will also work to gain access to your veins. This is done primarily by connecting a central venous catheter tube to major veins in your chest. This intravenous (IV) tube will be inserted into your vein and used to deliver specialized fluids and medications to your body.

    Intravenous Fluids

    Sepsis causes a loss of fluid and blood from the vessels, known as hypovolemia, which can lead to shock. The central venous catheter is used to deliver fluid and medications called vasopressors, which serve to raise blood pressure. The solutions used are typically either crystalloid—a kind of saline solution—or contain albumin, a protein produced in the liver.

    Antibiotic Therapy

    Using the IV, high doses of antibiotics or antimicrobial medicines are introduced to kill bacteria and fight off any infection. Specific approaches depend on the individual case, but if bacterial infection is suspected, healthcare providers use broad-spectrum antibiotics or combinations of them that can take on a wider range of cases. Antibiotics that may be used include:

    If a fungus is causing sepsis, treatment depends on your underlying health factors as well as the type of infection. The following antifungal medications may be considered:

    Related:When Would You Need Antibiotics?

    Other Therapies

    If initial treatments aren’t yielding results, several other medications may be attempted to stabilize blood pressure and reduce the inflammatory response:


    In severe cases, tissue and organ damage from sepsis can be so severe as to warrant surgery. This may mean amputation of an infected limb, or using methods to drain fluids from infected areas.


    At its core, preventing sepsis means maintaining good health, being vigilant about any chronic diseases or infections, and being aware of the signs and symptoms of the condition. Strategies for prevention include:

    • Keeping up to date on vaccinations

    • Washing your hands properly to prevent infection

    • Cleaning and covering any cuts you have on the skin

    • Seeking care for any chronic conditions you have

    • Knowing the signs and symptoms of sepsis

    • Seeking immediate, emergency care if you suspect you or a loved one has sepsis

    Related Conditions

    By its nature, sepsis is associated with a range of infections and injuries. In particular, conditions that affect immune responses often are comorbid, meaning they arise at the same time. The most common of these include:

    • Type 2 diabetes mellitus: A disease that affects the body’s ability to process sugars, diabetes mellitus has been found in 17% of sepsis cases.

    • Congestive heart failure: Congestive heart failure, in which the heart muscles aren’t pumping enough blood, can be triggered by changes in cardiac structure and function due to sepsis.

    • Cardiovascular conditions: Conditions affecting the health of arteries, including coronary artery disease (diseased arteries in the heart) and peripheral artery disease (diseased arteries in the rest of the body), and other cardiac issues are seen in 32% of sepsis cases.

    • End-stage renal disease: The systemic damage caused by sepsis can also cause kidneys to fail, known as end-stage renal disease, which has been found in approximately 23% of people hospitalized for sepsis.

    • Chronic obstructive pulmonary disease (COPD): COPD refers to a group of diseases affecting the lungs, including emphysema and chronic bronchitis; about one in five (20%) of those with sepsis experience this condition.

    • Dementia: Sepsis is also associated with dementia—a condition that impacts memory, thinking, and decision-making—and researchers found about 11.3% of people with sepsis have dementia.

    Living With Sepsis

    Depending on the individual case, and with prompt medical attention, sepsis can be effectively treated. Full recovery is expected for many people. However, this condition can progress rapidly; it’s fatal in 15% of sepsis cases without shock, which rises to 56% due to septic shock. Mortality due to sepsis can be impacted by the presence of other diseases.

    Those who’ve had sepsis may also experience lingering effects, which may require additional care. These include:

    • Insomnia, a difficulty getting to or staying asleep

    • Panic attacks, hallucinations, and nightmares

    • Muscle and joint pain

    • Reduced cognitive (mental) function

    • Loss of self-esteem

    • Organ failure, especially kidney or lung problems

    • Loss of a limb (to prevent the spread of infection)

    Those who have had sepsis treatment may have a reduced ability to take care of themselves. To promote recovery at home, there are several steps you can take:

    • Setting achievable goals for yourself, such as making sure you bathe or climb stairs independently

    • Prioritizing rest

    • Seeking support from family and friends

    • Keeping a journal logging your experiences, milestones, and feelings

    • Eating a well-balanced diet, which emphasizes carbohydrates, lean proteins, healthy fats, fruits, vegetables, and hydration

    • Try to incorporate regular physical activity and exercise into your lifestyle

    • Learning as much as you can about sepsis

    • Ensuring regular medical monitoring

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    The Airway Clearance Devices System Market is expected to reach US$ 589.3 million in 2022 and is projected to increase at a CAGR of 6.2% to US$ 1,137.8 million between 2022 and 2032. To cleanse the lungs of extra mucus, airway clearance devices are utilised. The chronic obstructive pulmonary disease (COPD) is characterised by an excessive mucus production that leads to mucus buildup in the airways. It causes shortness of breath, emphysema, chronic bronchitis, coughing, and wheezing.

    There are few types of airway clearance devices system, namely: positive expiratory pressure devices, intrapulmonary percussive ventilation, oral high-frequency oscillation, high-frequency chest wall oscillation, flutter devices, and incentive spirometry. Positive expiratory pressure devices is an alternative to conventional physiotherapy, and it consists of the one-way valve to which expiratory resistance is applied.

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    Intrapulmonary percussive ventilation devices combine internal thoracic percussion and aerosol inhalations. Oral high-frequency oscillation is worked on the principle of high frequency and low volume of oscillations, and it is developed from the technique of jet ventilation with high frequency.

    High-frequency chest wall oscillation devices is a mechanical device which works on the principle of positive pressure air pulse on the lungs by means of air pulse generator and inflatable chest. Flutter devices is a combination of high-frequency oscillations with positives expiratory pressure therapy. Incentive spirometry is used to measure inspiratory effort by using air volume and air flow.

    Airway Clearance Devices System Market: Drivers and Restraints

    Conventional methods like chest physiotherapy used for bronchial drainage in different types of respiratory dysfunction. However traditional chest physiotherapy is time-consuming and labour intensive both for non-hospitalized and hospitalized patients. On the counterpart, airway clearance devices systems increasing the compliance with patients and is the less time-consuming process.

    Reduced cost and independent application are other reason for changing the preference of patient population from conventional chest physiotherapy to airway clearances devices system market. All these factors influencing the burgeoning growth of the airway clearances devices system.

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    Others factors like decreased respiratory complications and demand for devices over conventional methods drives the growth of the airway clearance devices system market. Limited availability of evidence based data for effectiveness of devices act as a restraint on the growth of the airway clearance devices system market

    Airway Clearance Devices System Market: Market Overview

    Global Airway Clearance Devices System market has witnessed a robust growth due to increasing demand due to improving respiratory drainage and reduced infections. Airway Clearance Devices System market has a presence of many regional players which have a huge market share in emerging countries operating at regional or country level.

    The future of Airway Clearance Devices System market anticipated with double CAGR during forecasting period.

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    Airway Clearance Devices System Market: Region-Wise Overview

    Global Airway Clearance Devices System market segmented into following regions North America, Latin America, Western Europe, Eastern Europe, Asia-Pacific, Japan and the Middle East and Africa. North America is dominant in the Global Airway Clearance Devices System market mainly due to increased acceptances by patient population.

    In North America, particularly the USA is dominating due to the high penetration. Economic conditions in the APAC region are set to drive the Airway Clearance Devices System market to new heights. European and APAC are fastest growing region due to rising awareness of Airway Clearance Devices System Market.

    Growth in the Middle East and African region is considerably less when compared to the other regions. However, North America would maintain its position in the Airway Clearance Devices System market, though, we are anticipating emerging economies such India, China, Brazil, to have the highest growth rate in Airway Clearance Devices System market.

    Airway Clearance Devices System Market: Key Participants

    The key participants in the Airway Clearance Devices System market mainly include Monaghan Medical Corporation, Koninklijke Philips N.V., Vortran Medical Technology and others. Companies are mainly focused on R&D to strengthen core competencies of the company’s product portfolio.

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    The research report presents a comprehensive assessment of the market and contains thoughtful insights, facts, historical data, and statistically supported and industry-validated market data. It also includes projections using a suitable set of assumptions and methodologies. The research report provides analysis and information according to market segments such as geographies, application, and industry.

    Key Segments Profiled In The Airway Clearance Devices System Industry Survey

    Product Type:

    • Positive Expiratory Pressure
    • Intrapulmonary Percussive Ventilation
    • Oral High-Frequency Oscillation
    • High-Frequency Chest Wall Oscillation
    • Flutter
    • Incentive Spirometry

    End User:

    • Hospitals
    • Clinics
    • Ambulatory Surgical Centers

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    Future Market Insights, Inc. (ESOMAR certified, Stevie Award – recipient market research organization and a member of Greater New York Chamber of Commerce) provides in-depth insights into governing factors elevating the demand in the market. It discloses opportunities that will favor the market growth in various segments on the basis of Source, Application, Sales Channel and End Use over the next 10-years.

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    Fact Check: Post Does NOT Show Martha Stewart Promoting A Line Of 'C0PD Gummies'

    Not Martha's

    Does American television personality Martha Stewart advertise "C0PD Gummies" sold under her name? No, that's not true: Her website does not contain any information about such a product. The video does not sync with the audio, suggesting someone edited fake or impersonator audio over authentic video. The facebook post uses a common dodge to try to evade fact checking and platform restrictions on false content: Leetspeak, which is the substitution of numerals similar to letters. In this case, the post uses zeroes for the letter O.

    The story originated from a post published on Facebook on May 10, 2023. The caption said:

    Martha Stewart - For years I've watched countless friends and family suffer from ???????????????? and some even pass.. I regret not being able to help sooner so I've decided to release my newest ???????????????? ????????????????????????????. Just 2 pieces each day will help ease the symptoms of ???????????????? such as:

    ???? Click "Learn More" To Get Your Exclusive Discount!

    The post contained a video of Martha Stewart (or a very similarly-looking person) promoting the product. The audio closely resembles her voice and manner of speaking, but could be an impersonator or the product of audio deep fake technology.

    This is what the post looked like on Facebook at the time of writing:

    Screen Shot 2023-05-15 at 3.02.44 PM.png

    (Source: Facebook screenshot taken on Mon May 15 19:02:44 2023 UTC)

    However, a search for the term "COPD gummies" on Stewart's official website produces no results:

    Screen Shot 2023-05-15 at 4.09.34 PM.png

    (Source: Marthastewart screenshot taken on Mon May 15 20:09:34 2023 UTC)

    The link from the post on Facebook (archived here) led to an unrelated Kentucky-based company.

    According to the CDC website, chronic obstructive pulmonary disease (COPD) is a "group of diseases that cause airflow blockage and breathing-related problems," including emphysema and chronic bronchitis frequently resulting from smoking. The treatment of COPD includes quitting tobacco products, pulmonary rehabilitation, medicine, supplemental oxygen and preventative measures against lung infections, not "COPD gummies."

    Martha Stewart, known for her multiple entrepreneurial endeavors, does promote gummies. However, those are CBD gummies. Despite a similar-sounding name, CBD has nothing to do with COPD.

    CBD products contain cannabidiol from marijuana, and the official promo video on Stewart's website implies that her gummies may potentially help against stress. The CDC website says that CBD products will not make people high but emphasizes that its effects, benefits and risks are not fully understood by scientists at this point.

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    Global chronic obstructive pulmonary disease (COPD) treatment market is estimated to be valued at US$ 17,510.15 million in 2023 and is expected to exhibit a CAGR of 4.9% during the forecast period (2023-2030). Coherent Market Insights announces the publication of its most recently generated research report titled, “Chronic Obstructive Pulmonary Disease (COPD) Treatment Market – Forecast to 2030″, which offers a holistic view of the Chronic Obstructive Pulmonary Disease (COPD) Treatment market through systematic segmentation that covers every aspect of the target market.

    Chronic obstructive pulmonary disease includes chronic bronchitis, in which the bronchi (large air passages) are inflamed and scarred, and emphysema, in which the alveoli (tiny air sacs) are damaged. Chronic obstructive pulmonary disease (COPD) presents itself with mild, moderate, and severe symptoms. Treatment of chronic obstructive pulmonary disease (COPD) involves stepwise non-pharmacological and pharmacological interventions.

    Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. Symptoms include breathing difficulty, cough, mucus (sputum) production and wheezing. It is typically caused by long-term exposure to irritating gases or particulate matter, most often from cigarette smoke. 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 is characterized by daily cough and mucus (sputum) production.

    Chronic Obstructive Pulmonary Disease (COPD) Treatment with 100+ market data Tables, Pie Chat, Graphs and Figures spread through Pages and easy to understand detailed analysis. The information is gathered based on modern floats and requests identified with the administrations and items. Chronic Obstructive Pulmonary Disease (COPD) Treatment Market report includes historic data, present market trends, environment, technological innovation, upcoming technologies and the technical progress in the related industry.

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    ‣ 2030 Updated Report Introduction, Overview, and In-depth industry analysis.
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    Market Overview:

    This all-encompassing study was created in collaboration with core business professionals, as well as a specialized assessment inspection group, to lend Chronic Obstructive Pulmonary Disease (COPD) Treatment market report a comprehensive representation of current market conditions, enabling its intended owner to make critical business decisions with confidence. The Chronic Obstructive Pulmonary Disease (COPD) Treatment market objective of this detailed guide is to assist our valued customers to develop plans that will re-calibrate existing business practices, allowing them to reach previously unattainable business success. This comprehensive analysis will include information on prospective mergers & acquisitions, as well as revenues recorded by various Chronic Obstructive Pulmonary Disease (COPD) Treatment market players. A thorough study of this industry’s segmentation will help lead to a better comprehension of the various elements that influence Chronic Obstructive Pulmonary Disease (COPD) Treatment market.

    Segmentation Analysis:

    The Chronic Obstructive Pulmonary Disease (COPD) Treatment market report includes a detailed section on the exact segmentation of this industry. Segmentation is as follows – type and applications. With respect to type, this segment is further classified under (type here). On the basis of applications, the Chronic Obstructive Pulmonary Disease (COPD) Treatment market is divided among (applications here). This is done to ensure that a comprehensive detailing of the Chronic Obstructive Pulmonary Disease (COPD) Treatment market is examined and presented, to ensure that our respective clients are able to utilize our generated data to make the most informed business decisions possible.

    Competitive Analysis:

    The Chronic Obstructive Pulmonary Disease (COPD) Treatment market will include a thorough examination of this industry’s competitors, their respective company overviews and description, an analysis of their product portfolios, financials, etc. We even include supply-chain analysis, a PEST analysis, market probability scenarios, Porter’s Five Forces analysis, and even various market expansion strategies. This information will enable our clients to utilize this essential data and enable them to make the most-suitable business decisions that will improve their company’s footprint in this industry.

    By Top Companies: AstraZeneca Plc, Orion Corporation, Mylan N.V., Boehringer Ingelheim, Teva Pharmaceutical Industries Ltd., GlaxoSmithKline plc, Novartis AG, Sunovion Pharmaceuticals, Inc., and CHIESI Farmaceutici SpA

    Detailed Segmentation:

    By Drug Class: Bronchodilators (Beta 2-Agonists, Anticholinergics, Theophyllines), Phosphodiesterase Type 4 Inhibitors, Steroids, Others

    By Route of Administration: Oral, Inhalation

    By Distribution Channel: Hospital Pharmacies, Retail Pharmacies, Online Pharmacies

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    Regional Coverage:

    Our Chronic Obstructive Pulmonary Disease (COPD) Treatment market research report has been curated to derive a comprehensive analysis, including this industry’s footprint, as well as sales demographics of all respective regions and countries involved. These regions are covered as follows –

    • North America (USA and Canada)
    • Europe (UK, Germany, France and the rest of Europe)
    • Asia Pacific (China, Japan, India, and the rest of the Asia Pacific region)
    • Latin America (Brazil, Mexico, and the rest of Latin America)
    • Middle East and Africa (GCC and rest of the Middle East and Africa)

    Features of the Chronic Obstructive Pulmonary Disease (COPD) Treatment Market Report

    ⮞In-depth Chronic Obstructive Pulmonary Disease (COPD) Treatment industry data presented in an easy-to-understand format

    ⮞Clear-cut market segmentation of the Chronic Obstructive Pulmonary Disease (COPD) Treatment industry, detailing key aspects of each sub-segment

    ⮞Well-analysed key market player profiles along with their corresponding strategies

    ⮞The precise analysis of potential regional and country-wise sales opportunities

    ⮞In-depth Intel concerning existing as well as potential trends in the Chronic Obstructive Pulmonary Disease (COPD) Treatment market

    ⮞Industry drivers and restraints of the Chronic Obstructive Pulmonary Disease (COPD) Treatment market have the potential to influence each of its segments and regions of operation.

    ⮞A precise comprehension of expansion strategies, new product launches, as well as potential acquisitions for various engaged companies.

    ⮞This report offers an amalgam of well-articulated literature, along with graphical representations of numerous related market variables.

    Key questions answered in the report:

    ⮞What is the growth potential of the Chronic Obstructive Pulmonary Disease (COPD) Treatment Food market?

    ⮞Which product segment will take the lion’s share?

    ⮞Which regional market will emerge as a pioneer in the years to come?

    ⮞Which application segment will experience strong growth?

    ⮞What growth opportunities might arise in the Chronic Obstructive Pulmonary Disease (COPD) Treatment industry in the years to come?

    ⮞What are the most significant challenges that the Chronic Obstructive Pulmonary Disease (COPD) Treatment market could face in the future?

    The Major Points Covered in the Table of Contents:

    Overview: This part provides a summary of the report, as well as a broad overview of the Chronic Obstructive Pulmonary Disease (COPD) Treatment Market, to offer an understanding of the nature and contents of the research study.

    Market Analysis: The research forecasts the market share of key segments of the Chronic Obstructive Pulmonary Disease (COPD) Treatment Market with accuracy and reliability. This study may be used by industry participants to make strategic investments in key growth areas of the Chronic Obstructive Pulmonary Disease (COPD) Treatment Market.

    Analysis of Leading Players’ Strategies: This report can be used by market participants to acquire a competitive advantage over their rivals in the Chronic Obstructive Pulmonary Disease (COPD) Treatment Market.

    Regional Growth Analysis: The report covers all of the key areas and countries. The regional analysis will assist market players in tapping into untapped regional markets, developing unique regional strategies, and comparing the growth of all regional markets.

    Market Forecasts: Report purchasers will get access to precise and validated estimations of the entire market size in terms of both value and volume. The study also includes estimates for the Chronic Obstructive Pulmonary Disease (COPD) Treatment Market in terms of consumption, production, sales, and other factors.

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    Chronic obstructive pulmonary disease (COPD) is a complex and constantly evolving pathology, which is characterized by a progressive and constant limitation of the available air volume (airflow obstruction).1 COPD could become the third leading cause of death for the population by 2030.1 The Global Initiative for Chronic Obstructive Lung Disease (GOLD) identifies COPD as:

    a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.2

    GOLD estimates that the number of patients who will die of COPD in 2060 will be approximately 5.4 million deaths annually, compared to 3.2 million deaths in 2015 annually.3 In the USA, the incidence of the disease involves 10.2–20.9% of the population, in Europe, despite a trend of reduction in mortality and a decreased difference between men and women, the percentage of findings remains high (3–26.1%).3 Some data from Africa, few and not covering all geographical areas, show COPD detection rates of 1.6–23.8%; in Latin America, the percentage is between 30% and 31.1%.3 In China, the percentage is about 8.6% (data from 2018), and highly variable and incomplete values for other Asian regions, with an average of 3.5–6.7%.3

    COPD is considered as the fifth cause of burden on the economy of the various states due to recurring hospitalizations and pharmacological treatments.4 Probably, this global economic aggravation derives from the fact that this pathology does not involve only the pulmonary area but develops many dysfunctions and physiological alterations involving the whole-body system.4 Although emphysema and chronic bronchitis are responsible for triggering the chronicity of the disease, the patient does not always go to hospital for respiratory reasons, but for important cardiac problems, fractures, the onset of lung tumours, mood disorders, muscle complex that prevent independence and severe metabolic alterations.1,5 Furthermore, it is not always possible to correctly assess the severity of COPD, as there is only a moderate relationship between pulmonary adaptation and the reduction in the patient’s quality of life.6 COPD is a systemic disease, and as such it is expressed with multiple symptoms, such as insomnia and drowsiness, dry mouth, anorexia, pain (local or from multiple involved areas), nausea, constipation, gastric reflux, dysphagia, sleep apnea, cough, fatigue and shortness of breath, wheezing and dyspnea, temporomandibular disorders and urinary incontinence.2,5,7–10 Some symptoms related to the presence of COPD and which have a negative impact on the mortality and morbidity of patients, are the finding of anxiety and depression, with values ranging from 8% up to a maximum of 80% of patients.1,5,11 Functional and structural alterations of the skeletal muscles (almost all patients), lack of coordination and an increase in accidental falls cause a decrease in active movement, leading to a decline in quality of life, an increase in mortality and in the number of hospitalizations.12–14

    The article reviews the adaptation of the skeletal muscles, with greater attention to the adaptations of the diaphragm, trying to highlight the relationship between the non-physiological variations that the main respiratory muscle undergoes and the neuromotor impairment found in COPD. The text could be an important reflection from a clinical and rehabilitation point of view to direct greater care to the function and adaptation of the diaphragm muscle.

    Peripheral Skeletal Muscle Adaptation in the Presence of COPD

    Patients with COPD experience skeletal muscle alterations, causing an increase in the rate of morbidity and mortality, as well as in disease exacerbation events and in the number of hospitalizations.15 Respiratory disease does not always perfectly reflect peripheral muscle adaptation.13,14 The following figures highlight, for the same patient, a slower pathological adaptation of the lungs of an average degree, compared to an accentuated sarcopenic adaptation (Figures 1 and 2).

    Figure 1 Moderate functional obstruction on respiratory function tests of a 70-year-old patient. X-ray picture of emphysema with pulmonary hyperinflation and thinning of the vascular pattern (arterial deficiency) with hypertension of the small circulation documented by the dilatation of the descending branch of the right pulmonary artery (arrow).

    Figure 2 MRI of the same patient with moderate degree of obstruction, but evident sarcopenia. In the cross section of the subject’s leg it is possible to notice a reduced muscle mass (light gray area), and a pronounced area of subcutaneous and intramuscular fat (dark gray area).

    Muscle functional impairment is found more with emphysematous patients than with chronic bronchitis, and for about 55% of patients with stable COPD; this process probably occurs faster than the pathological adaptation of the lungs.13,14 There are different causes, single or superimposable, which can induce skeletal muscle dysfunction. Cigarette smoke, the presence of diabetes, malnutrition, advanced age, polluted air and a sedentary lifestyle combine to produce non-physiological muscular behaviors.16,17 COPD is a further cause of muscle dysfunction. We can find systemic inflammation, oxidation, multiple drug intake, nocturnal and diurnal hypoxia, hypercapnia. The patient often presents co-morbidities such as polyneuropathy, osteoporosis, cardiovascular pathologies, bronchiectasis, obstructive sleep apnea, chronic kidney disease, anxiety and depression, nonalcoholic fatty liver disease, nonspecific pain and gastroesophageal reflux.5,9,11,18–20 These co-morbidities negatively affect muscle adaptation.

    Changes in Muscles in COPD: Males versus Females

    Females with COPD suffer a loss of lean mass in a greater percentage than males, and with a lower value of the expressed strength.21 Limb musculature undergoes a phenotypic transition in patients, with a tendency for loss of number and volume of aerobic fibers or type I fibers, and an increase in anaerobic fibers or type II fibers, compared to age-matched healthy subjects.21 Women have slightly fewer type IIx fibers (more glycolytic muscle cells than type II fibers), and a higher number of hybrid fibers. The latter information highlights a difficulty of the musculature in women to implement a correct regeneration and with more dilated times (compared to men).21 Women lose more muscle mass and are weaker than men. In patients with COPD, we can find sarcopenia, decrease in mass and strength, and concomitant atrophy, weakness and disappearance of lean material.22 Skeletal muscle areas, particularly of the extremities, have reduced capillary architecture, and increased mitochondrial and ribosomal dysfunction.14,23

    Stable Disease vs Exacerbation

    Exacerbation of respiratory symptoms causes an increase in non-physiological adaptations of skeletal muscles. The expression of muscle strength after 3 days of hospitalization, compared to stable patients, is lower; after 5 days of hospitalization, muscle strength is reduced by 5%, compared to outpatients.24 Hospitalization reduces muscle strength not only in the lower limbs, but also in the upper limbs; this decrease is greater for patients subject to multiple exacerbations during the year.24 The acute phase of the disease causes a reduction in the lean mass of the parasternal/intercostal muscles, which in parallel reflect the decrease in leg volumes; chest muscle weakness corresponds to spirometric severity.25,26 The severity of the presence of sarcopenia/atrophy in patients with COPD determines a worse prognosis, with increased mortality.16,25,27 We do not know the detailed pathological reasons that cause such muscular adaptations, and further studies will be necessary to better understand the therapeutic procedure.

    Balance Impairment

    Non-physiological muscle adaptation in patients with COPD, as measured by surface electromyography (sEMG) and electromyographic activity (EMG) under stress, determines a decrease in neuromotor coordination and early fatigue.28–32 This impaired neuro-coordination of the limbs and trunk during active motor activity of patients causes accidental falls and increased fear of falling, creating a behavioral framework that further degenerates into motor dysfunction, physical deconditioning and increased mortality.33 Patients with COPD have an approximately 51% higher rate of falling than healthy people of the same age.34 Females are more prone to accidental falls than males.34 During the acute phase, with hospitalization, the percentage of falls increases up to 55% of patients, and always with a higher finding value than in non-COPD and hospitalized elderly subjects (35%).34 The risk of falls in COPD is not related to forced expiratory volume in the 1st second (FEV1).34 Impaired neuro-coordination causes a disturbance of body balance during daily activities, a decrease in limb and trunk control during walking, regardless of the degree of severity of lung function.34,35

    There are several reasons given in order to understand the problem of lack of balance. The same causes that lead to muscle dysfunction, mentioned above, are pointed out as important genesis of balance deterioration.35 Other causes leading to an increase in the incidence of falls could be related to the presence of depression and anxiety, the use of portable oxygen devices, dyspnoea, altered biomechanics of the chest, decreased muscle elasticity, reduced neurocognitive function, obesity.16,34–38 A possible decline in the components that help maintain balance, the vestibular area and the proprioceptive system, can increase the number of accidental falls.16,39 Visual dysfunctions in COPD patients would not result in a balance disorder.40

    Patients with COPD and neuromuscular dysfunctions show a slower recovery in restoring the center of body balance, in the presence of external stresses, and with accentuated trunk rigidity.41 There is greater body sway during limb movements, a slower pace than in people of the same age but not with COPD: the pattern of movement and gait in patients is altered.41,42

    Another possible cause that would determine a dysfunction of balance, placing COPD among the chronic pathologies with the highest incidence of accidental falls (behind only osteoarthritis), comes from the non-physiological adaptation of the diaphragm muscle.40,42,43

    Diaphragm Muscle Adaptation in the Presence of COPD

    Currently, we do not have sufficient clinical attention directed to the diaphragm muscle in COPD patients; diaphragmatic dysfunction is present at every stage of the disease.3

    Effect of Dynamic Hyperinflation

    The maximal inspiratory pressure (PImax) is lower than in healthy subjects, as is the transdiaphragmatic pressure (Pdi) generated by the diaphragm.40,44 The contractile fibers are shortened, giving an inspiratory attitude and a flatter morphology.44 This morphological dysfunction corresponds to a lower functionality and expressed strength; the latter reflects the presence of hyperinflation and dyspnoea.44 Figure 3 highlights a diaphragm of a COPD patient in an inspiratory attitude, with flattening of the diaphragm; in the healthy subject, the right area is about 1.9 centimeters higher.45

    Figure 3 Chest x-ray of a COPD patient showing pulmonary hyperinflation characterized by parenchymal hyperdiaphania and flattening of the diaphragm.

    In COPD patients, the elasticity of the lung parenchyma decreases exponentially with the chronicity of the disease. In obese patients, in particular (especially in the android form), lipofibroblasts can accumulate in the lung tissue, secreting pro-inflammatory substances (adipocytokines) and transform into myofibroblasts, increasing pulmonary fibrosis.46 As the disease progresses, the chest expands to a lesser extent, the intercostal musculature will become stiffer, and the respiratory accessory musculature will be more ineffective.47 The diaphragm will be forced to work harder to overcome the resistances of the more rigid chest, with consequent morphological change (more “flat”), structural change (shorter fibers), positional change (inspiratory attitude), phenotypic change (phenotypic shift) and functional (greater stiffness).

    The diaphragm undergoes a flattening with mechanical disadvantages. There is a reduction of its area of apposition, a decline in the coordination between the diaphragm itself and the rib muscles, an increase in the radius of curvature (less ability to maintain the tension produced).3,44,48 The phrenic nerve undergoes myelin damage, with a slowing of the conduction velocity, with higher neuropathy values for subjects with hyperinflation and, in particular, for the left phrenic area.48,49 Neuropathic adaptations correlate positively with FEV1.49 Such neuropathy is a direct indicator of the risk of accidental falls.50

    Change in Contractile Function and Fiber Phenotype

    The diaphragm undergoes an unphysiological phenotypic adaptation, with an increase in type I fibers and a decline in type II fibers. Such metabolic change appears to occur faster than the phenotypic change of limb musculature.44

    Contractile fibers show signs of atrophy, myolysis, sclerosis and fibrosis.44,47 We can find a decline in endoplasmic reticulum function, which dysfunction causes an accumulation of intracellular calcium (Ca2+).51 The accumulation of Ca2+ in the sarcoplasm is cytotoxic for the cell, stimulating biochemical reactions that can lead to apoptosis.52 Furthermore, Ca2+ can bind to inorganic phosphorus (Pi), slowing and preventing the formation of actomyosin bridges, causing a weaker diaphragmatic contraction.44,53 The force expressed by the diaphragm is about 35% lower in patients, in particular, in patients with severe COPD.3

    The amount of myosin decreased by about 50% less than in healthy subjects, with a decreased Ca2+ binding sensitivity, with further decline in contractile strength.44 The amount of the nebulin protein is reduced, making the muscle fiber more fragile to mechanical stress.44,54 Another sarcomeric protein, titin, does not seem to decrease in quantity, but undergoes a decline in elastic capacity, negatively altering the mechanotransductive capacity of the fiber (less regenerative capacity and greater stiffness).44

    The volume of fibers, both glycolytic and oxidative, has a reduced volume (atrophy) of about 40–60% compared to healthy subjects, with increases in the ubiquitin-proteasome pathway. There is an accumulation of sarcomere area Z proteins, a misalignment of the sarcomeres and loss of serial sarcomeres (about 10–15% of the total), typical of a myopathy.3,14,44,55 There are several pathways that disrupt diaphragm fiber structure and function in the presence of oxidative stress and inflammation. Activation of the canonical nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway, the activation of the non-canonical NF-κB pathway, and activation of the myostatin-mothers against decapentaplegic homolog 3 (Smad3) pathway.56

    The fiber is shortened by about 28% compared to healthy subjects, with an increase in collagenous tissue.3,57 The regeneration capacity of the fibers is reduced (increased myostatin values), as is the ability of the satellite cells to repair the various muscle components.3,44 FEV1 is inversely related to diaphragm hypotrophy.44

    Changes in Blood and Lymph Supply

    We do not know the adaptation of the lymphatic vessels of the diaphragm in the presence of COPD. Generally, with inflammation involving the body system, from the chest to the abdomen, the diaphragm undergoes lymphangiogenesis.58

    The blood volume and capillary scaffolding affecting the diaphragm musculature appear to be preserved and, despite the increase in the number of type I fibers, the diaphragm shows reduced endurance capacity.44 It appears that the patient stops physical activity due to diaphragmatic weakness, despite an increase in phrenic electrical activity; dyspnea is the response to diaphragm fatigue and not necessarily to pathological pulmonary adaptation.3,59

    Diaphragm weakness, hypotrophy (diaphragm thickening fraction), reduced range of motion, are correlated with symptom exacerbation and re-hospitalization.60 The diaphragm predicts the possible exacerbation of symptoms in COPD patients, and it becomes essential to evaluate the diaphragm for an in-depth clinical assessment.60

    Another step forward that the clinician should take is to consider the importance of the diaphragm as a determinant for the neuromotor expression of the patient with COPD.

    Role of the Diaphragm in Neuromotor Function and Balance

    The diaphragm is an important muscle not only in the respiratory field, but also in the neuromotor field.61 The areas that manage the breath and non-respiratory actions of the diaphragm, and which serve as an informational crossroads between the brain areas and the spinal cord, are located in the pons, midbrain and medulla, ie, the central pattern generator (CPG).61 Within the CPG, we find the pre-Bötzinger complex (preBötC), the caudal ventral group (VRGc), the rostral ventral group (VRGr), the parabrachial/Kölliker-Fuse complex and the nucleus of the solitary tract (NTS) of the vagus nerve (Figures 4).61

    Figure 4 The figure illustrates an MRI image without contrast, highlighting, in a sagittal plane, the midbrain area, pons and medullary area. This anatomical area encloses the kernel of the respiratory network.

    Proprioceptive Response from the Diaphragm

    The movement of the diaphragm generates a Pdi, which is the difference between gastric and intrapleural pressure.62 These pressure changes and redistribution of body fluids activate multiple body receptors (mechanoreceptors, visceroceptors, chemoreceptors, baroreceptors, etc.), which are part of the exteroceptive and interoceptive system; the latter two fall within the definition of proprioception.63

    The diaphragm itself carries phrenic afferents from mechanoreceptors (30–45% sensory-type fibers), which are activated by specific stimuli (animal studies). Type IA fibers are activated during the exhalation phase (lengthening of muscle fibers) and during constant contraction and in the presence of fatigue.64 Type Ib fibers (Golgi tendon organs and simil-Pacinian corpuscles) send information during an increase in the contractile stress of the diaphragm (physical activity), during inspiration. Type III–IV fibers, myelinated and unmyelinated (type C fibers), respectively, and with a smaller diameter than the previous fibers (type IA), are activated by unphysiological breathing patterns and by the presence of metabolites related to contractile fatigue.64

    The unmyelinated fibers, the most representative of the diaphragm, can have components of a sympathetic type, and on an animal model, they send information in the presence of diaphragmatic fatigue with vasoconstrictive functions; type III fibers are not activated by diaphragmatic contractile fatigue.64,65 Studies on cadavers show that the right phrenic nerve has catecholaminergic axons and has a larger diameter, while the left phrenic nerve lacks them and has a smaller overall diameter; the reasons are not known.66

    There are only a few dozen spindles of the diaphragm but, despite this evident diversity compared to the skeletal muscles of the limbs and trunk, they are sufficient to exert an adequate afferential influence towards the central nervous system.67 In a healthy subject, before the diaphragm performs a complete movement of inspiration, low-threshold cutaneous receptors (Merkel, Ruffini) are stimulated.68,69 These receptors send afferents to the cortex (somatosensory opercular area or primary somatosensory cortex or area S1).61 The S1 area is important to prepare the body system to adequately manage proprioceptive stimulations, activating the insula and the anterior cingulate cortex.70 In particular, the right insula is fundamental for the conception of the self, that is, the correct elaboration of the bodily stimuli for the expression of the final movement (and the emotional aspect) with respect to our adequacy in executing this movement in the context in which where we are, at a given moment.71 When the diaphragm contracts to complete the inspiration, all the stimulated body receptors and the few diaphragmatic receptors will send information to the midbrain area (about 95% of the information) and to the spinal trigeminal nucleus, via spinothalamus pathways (laminae I–X).61,72,73 The nucleus of the solitary tract (NTS) in the midbrain will receive the major afferential information, while only a small portion of the receptor inputs will go to the spinal trigeminal nucleus or trigeminal nucleus caudalis.61,74 Likewise, the afferents of the vagus nerve from the crural area of the diaphragm (and from the phrenoesophageal ligaments), stimulated by the respiratory movement, will arrive at the NTS.75 The NTS will reciprocally exchange the information received with the cerebellum (from all cerebellar nuclei) and with the vestibular area.76,77 The trigeminal nucleus caudalis will exchange information with the vagal system (NTS), with the cerebellum (paramedian lobule) and with the vestibular area.78–81 The processing of the data obtained from this neurological network will be sent by the NTS towards the limbic area (periaqueductal gray area, amygdala, thalamus, pituitary) and towards the primary motor cortex or M1 (motor coordination) and the supplementary motor area of the cortex o SMA (movement planning and learning).61,73,82–84

    Descending excitatory information will be sent from the limbic area and motor cortex M1-SMA to the NTS.61,83,85,86 Finally, NTS sends inhibitory information to the rostral ventrolateral medullary area or premotor area of the sympathetic system.61,79,87 NTS will involve the CPG and phrenic neurons.66 Inhibition of the sympathetic area will produce an increase in the activity of the parasympathetic system, affecting neuromotor expression, with increases in strength and coordination (in particular, with slow and deep breaths).61,86,88

    Intra-Abdominal Pressure and Posture

    The diaphragm is essential not only for the force expressed, but also for maintaining body posture during daily activities, controlling the position of the lumbodorsal area allows for better control of limb movement.66 The inspiration causes an increase in intra-abdominal pressure (IAP), thanks also to the activation of the abdominal muscles (in particular, the transversus muscle), and the descent of the pelvic floor.61,89 The contraction of the diaphragm precedes the movements of the limbs, that is, for the anticipatory postural regulation.89 This pre-contraction allows the various spinal and cortical centers to have information before deciding what movement to make. The greater the demand for muscle strength in the limbs (lifting a load or pedaling), the wider the excursion of the diaphragm will be; in this way, there will be a better stabilization of the trunk (greater IAP) and an optimization of the coordination of the limbs.89,90 If the IAP is insufficient, for example, due to shallower breathing, postural control problems, balance alterations and limb dysfunctions will occur.89,91 IAP creates a hydraulic effect for the stabilization of the lumbodorsal column with a reduction of the electrical activity of the deep back muscles; the latter event occurs because the posterior spinal musculature is not used to maintain posture.9,91 The movement of the diaphragm during postural tasks is not correlated with the contraction function for respiration. The diaphragm is a structure that encompasses two identities and with non-homogeneous movements.91 If the need to create balance (a demanding bodily action) increases, this situation will decrease the ability of the diaphragm to express itself as a respiratory muscle.91 Likewise, the diaphragmatic contraction that precedes voluntary (about 20 milliseconds before muscle activity of the limbs), and non-voluntary movements, is independent of respiratory function.92,93

    It is the contraction of the diaphragm that informs the central nervous system of body position and postural needs (by sending information from body receptors); this proprioceptive information is conveyed towards the cortex by the activity of the diaphragm.92,93

    The Postural Diaphragm

    The parasympathetic system plays an important role in the proper functioning of the diaphragm and neuro coordination.61 COPD patients show an increase in the sympathetic system (sympathoexcitation), and this increase predicts a decrease in exercise tolerance and a poor prognosis.94,95 This chronic sympathoexcitation is inversely related to PImax.95 During an exacerbation, there is a discrepancy between the activity of the sympathetic and parasympathetic systems.

    Lung filling/emptying stimulates mechanoreceptors, such as rapid-adapting pulmonary stretch receptors (RARs), slow-adapting pulmonary stretch receptors (SARs), and C-type fibers. In particular, RARs send signals via the vagus nerve to the NTS to favor diaphragm activation.96 Lung hyperinflation and emphysema stimulate more RARs and type C fibers.97,98 Overstimulation of these receptors could cause a release of local pro-inflammatory substances, causing bronchoconstriction and perpetuating a pathological pulmonary environment.95,99 During an exacerbation, the parasympathetic system increases.

    Generally, vagal hyperactivation is measured indirectly by the decrease in heart rate variability (HRV).100 In reality, HRV does not correctly reflect vagus nerve involvement.101 The parasympathetic system is more active in acute phases at the pulmonary level, but not at the systemic level. In fact, the parasympathetic system in the acute phases fails to activate the diaphragm more.60 Data confirm that in the exacerbation phases, the COPD patient is more at risk of falling.34 There is a relationship between diaphragm weakness and the risk of falls.

    We know that electromyography of the spinal muscles and that of the external obliques and rectus abdominis is increased compared to healthy subjects; this should be an indirect clue to the dysfunction of the diaphragm as a postural muscle.41 We know that the ability to manage proprioceptive information in the COPD patient is impaired, and this alteration is connected to diaphragmatic dysfunction in the role of postural muscle.40,87 The diaphragm remains in a shortened condition, and with reduced excursion capacity in COPD patients.3,25 Another relationship between diaphragm weakness and fall risk.

    The diaphragm is unable to adequately solicit the spino-cortical and cortico-spinal neurological pathways, as its contractile capacity is decreased; the result is a balance impairment, increased risk of accidental falls and increased mortality/morbidity. We can strongly speculate that the impaired postural balance, the neuro-motor incoordination of the trunk and limbs, could be related to the diaphragm.

    We know that rehabilitation inspiratory training improves postural balance in patients.33 The same literature is very sparse on the relationship between diaphragm training and neuro-coordination response in COPD patients.33

    In light of the above, the clinician and rehabilitation field and scientific research should place greater emphasis on the assessment and training of the diaphragm, not only with the goal of slowing the progression of the disease or helping the patient in the acute phases, but as a target to prevent the occurrence of accidental falls.


    Chronic obstructive pulmonary disease (COPD) causes deterioration of the airways, with persistent and non-reversible airflow limitation. COPD could become the third leading cause of death for the population by 2030. There are several causes that lead to structural and functional alterations of the lungs, many of which could be counteracted before developing the disease, such as lifestyle and increased attention in avoiding some daily habits, such as physical activity and cigarette smoking, respectively.

    The skeletal muscles of the trunk, the limbs and the diaphragm muscle undergo non-physiological adaptations over time, which worsen the patient’s clinical picture and lead to an increase in accidental falls. The article reviewed the literature concerning the pathological adaptation of the diaphragm, placing emphasis on the spino-cortical and cortico-spinal neurological relationships that influence the management of proprioceptive information, and how diaphragmatic dysfunction can alter the neuro-coordination of the COPD patient. A greater interest of the clinician and the physiotherapist should be directed towards the diaphragm to counteract the genesis of unwanted falls.

    Ethics Statement

    The people involved in the figures to accompany the article have consented to the publication of the images.


    The article has been funded by the Italian Ministry of Health.


    The authors report no conflicts of interest in this work.


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    Syed Shahzad Razi, MD, FACS, board-certified, fellowship trained thoracic surgeon, and Robert S. Lebovics, MD, FACS, leading otolaryngologist, will further advance care and services for patients with breathing disorders.

    Hackensack Meridian JFK University Medical Center announced today the appointment of two renowned experts in diseases of the lungs and trachea to its team of physician leaders at the Advanced Lung & Airway Center. The Center, which treats patients with both cancerous and non-cancerous conditions that affect breathing, welcomed Syed Shahzad Razi, MD, FACS, a board-certified, fellowship-trained thoracic surgeon, and Robert S. Lebovics, MD, FACS, a leading otolaryngologist and academic researcher with expertise in infectious and inflammatory disorders.

    “We are delighted to welcome Dr. Razi and Dr. Lebovics to our team of experts at JFK University Medical Center who treat patients with breathing disorders,” said Faiz Y. Bhora, MD, FACS, Professor and Regional Chair of Surgery, Central Region, Hackensack Meridian Health and Hackensack Meridian School of Medicine, who leads the Advanced Lung & Airway Center. “These outstanding clinical leaders, both of whom have extensive knowledge and many years of experience, will help us further advance care for lung and airway disorders, which are often complex and require comprehensive evaluation and specialized procedures.” I have been privileged to have been part of Dr. Razi’s early training and have worked with Dr. Lebovics for over a decade, and HMHN is fortunate to recruit these outstanding clinicians. They will be part of a Department of Surgery that is regionally recognized for the breath and quality of surgical services that we provide.  

    “I am honored to be part of the JFK team that is devoted to diseases of the lung and airway,” said Dr. Lebovics.  “There are many forms of airway diseases that include cancerous and non-cancerous disorders of the windpipes that affect speech and breathing. These diseases that are often misdiagnosed as other lung conditions such as asthma, chronic bronchitis or emphysema. An accurate diagnosis is essential to ensure proper and timely treatment with a personalized care plan for each patient.”

    “I look forward to applying my experience in thoracic surgery to help patients being treated at the Advanced Lung & Airway Center at JFKUMC as well as Raritan Bay Medical Center and Old Bridge Medical Center,” said Dr. Razi.  “Sometimes breathing disorders are caused by prolonged intubation, tracheostomy or auto-immune disorders.  Cancers include tumors of the lung and esophagus and can also be caused by tumors from other regions of the body to the lungs.  I am proud to be part of the team at JFKUMC which has the experience and expertise to  diagnose and manage these complex conditions.” 

    “We are thrilled to have Dr. Razi and Dr. Lebovics join our team of surgeons at JFK University Medical Center,” said Amie Thornton, president, chief hospital executive, JFK University Medical Center.  “This is another example of how our patients in the community can receive the top care close to home.”

    Syed Shahzad Razi, MD, FACS
    Dr. Syed Shahzad Razi has extensive experience in surgeries of the airway, chest wall, diaphragm, esophagus and stomach, lung, mediastinum (area between the lungs), and pleura (tissue that covers the lungs and lines the chest cavity), as well as in robotic surgery. He is Board Certified by the American Board of Surgery and the American Board of Thoracic Surgery. He completed his Thoracic Surgery Fellowship at Jackson Memorial Hospital / University of Miami Hospital, Miami, FL, and his General Surgery Residency at Bronx-Lebanon Hospital Center, Bronx, NY. He also completed a General Surgery Internship at the University of Connecticut Medical Center, Farmington, CT. He earned his Medical Degree from Sindh Medical College, Karachi, Pakistan. Prior to joining Hackensack Meridian Health, Dr. Razi served as an attending thoracic surgeon at Memorial Healthcare System in Florida. Dr. Razi has extensive volunteer, research, and editorial experience in thoracic surgery and in subjects relating to the respiratory and foregut system (esophagus to duodenum). Additionally, Dr. Razi has experience as a medical student mentor at Florida International University.

    Robert S. Lebovics, MD, FACS
    Dr. Robert S. Lebovics is an internationally known otolaryngologist (specialist in surgical and medical management of conditions of the head and neck) with expertise in infectious and inflammatory disorders of both adults and children. He focuses on autoimmune and inflammatory diseases affecting the upper airways and head and neck region. He employs endoscopic techniques in the OR for repair of the larynx, trachea and large bronchi, using balloons, cryotherapy, and injections, as well as implanting stents for both benign and malignant disease. He received his medical degree from the State University of New York Downstate Medical Center in Brooklyn, NY, and completed otolaryngology training at the Albert Einstein/Montefiore Hospital Medical Center in the Bronx, NY. For almost nine years after his residency, Dr. Lebovics was Chief of the Clinical Otolaryngology Service at the National Institutes of Health in Bethesda, Maryland, where he worked with the National Institute of Deafness and Communication Disorders. At NIH he interfaced in the medical frontiers of gene therapy, immunotoxins for treating head and neck cancer, and techniques of surgical rehabilitation for both the larynx/trachea and the sinonasal tract. Concurrently Dr. Lebovics maintained a faculty appointment at Georgetown University where he regularly lectured and taught new physicians. Dr. Lebovics joined the hospital service that later became the Mount Sinai West (MSW) and Mount Sinai-St. Luke’s (MSSL) Hospitals.

    He is a member of various medical organizations, including being a Fellow of the American College of Surgeons and a Fellow of the American Academy of Otolaryngology - Head and Neck Surgery. He served for two years as the Secretary/Treasurer and later president of the New York Laryngological Society, and currently serves as a police surgeon for the NYPD. He is also on the Medical Advisory Board for the Vasculitis Foundation based in Kansas City.

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