emphysema | medical plaintalk

A baby enters to the world with collapsed, fluid filled lungs. Within 10 seconds, he gasps, takes a noisy breath and completes his transition to the outer world. From that point, he will inhale and exhale air over 8 million times a year until he takes his last breath at death. Breathing is his link to life, much as his umbilical cord was the link when he was in the womb. As long as his heart and lungs remain healthy and the muscles and bones his chest can move normally, he will maintain a comfortable, laissez-faire relationship with his breathing, seldom paying much attention to the never-ending process of taking in oxygen and getting rid of carbon dioxide. Strenuous physical activity will make him notice his breathing and he will learn the physical limits beyond which breathing harder and faster is ineffective. While he will experience discomfort with breathing at those limits, he will not feel fear or distress because he understands that his gasping for air is a normal response and that he will recover promptly when he rests.

Words used to describe trouble breathing

But when there is trouble somewhere in the respiratory system, the act of breathing becomes distressing in ways that and prompt a variety of different descriptions: “I feel short of breath.” “I can’t catch my breath.” “My chest is tight.” “I’m smothering.” “I’m suffocating.” “I can’t take a deep breath.” “I can’t breathe out all the way.” “Breathing is hard work.” “I need to more air.” Doctors use one word to encompass all of these descriptions – dyspnea, defined as abnormally uncomfortable awareness of breathing. Dyspnea is not a diagnosis but a symptom of many different types of respiratory problems. Diagnosis requires discovering where the trouble is in the normal chain of events that make up one breath.

The drive to breathe

The first part of a normal breath is the drive to breathe – a message from the brain to the muscles that increase the volume of the chest. The ribs move outward and the diaphragm between the chest and the abdomen moves down. The chest cavity expands, much like a fireplace bellows, sucking air down the trachea and the bronchial tubes into the lungs. In the next step, oxygen is absorbed into the blood and carbon dioxide is expelled from it. This gas exchange takes place in the spongy tissue of the lungs, in tiny air sacs called alveoli where red blood cells flow in single file though tiny capillaries. After 3-4 seconds, the muscles relax, the chest cavity diminishes in size and air rushes back out. Normal breathing goes on automatically, beneath conscious awareness unless the body demands more gas exchange because of increased exertion.

The drive to breathe increases when the body’s demand for oxygen goes up. “Hard breathing” from exertion is not distressing or indicative of illness unless it occurs in someone who has been very fit and previously more capable. Low oxygen pressure at high altitude also stimulates the breathing drive, but true dyspnea is a sign of altitude sickness and need for immediate treatment and evacuation to lower altitude because of fluid in the lungs. Anxiety and fever increase respiratory drive, as does hyperthyroidism, producing variable awareness of rapid breathing, but little discomfort.

The highway air movement follows

Moving air in and out of the lungs is the next part of normal breathing and a common source of true dyspnea. Infections, chronic inflammation from allergies, cigarette smoke or other environmental toxins can narrow and partially obstruct the trachea and the bronchi. Symptoms include coughing, wheezing and faster breathing to compensate for less air moved with each breath. Breathing “seems like hard work.” Sometimes bronchial spasm from inflammation makes it difficult for people to exhale fully. They have a sense of not being able to empty the air from their lungs and as a result get the feeling that they cannot inhale enough on their next breath. Asthma is the typical illness which causes this type of dyspnea.

Muscle disorders like Lou Gehrig’s disease, overall weakness from chronic illness, or paralysis from spinal cord problems can limit air transport by limiting chest wall movement. Obesity causes breathing problems because even normal muscle may not be strong enough to move the chest wall buried under heavy weight.

The deep reaches of the lungs where the work is done

Farther down into the lungs, dyspnea comes from impaired gas exchange and feels like air hunger – no matter how fast the breathing rate is, there still seems to be insufficient air. Lung infections like viral and bacterial pneumonia, and chronic inflammatory disorders that produce lung scarring are the typical culprits. Cough, fever and rapid onset of dyspnea are clues to pneumonia. Gradual onset of dyspnea is more common in the inflammatory scarring and in smoking related lung disease, which causes both obstruction to air flow and loss of the alveoli where gas exchange occurs.

Poor blood flow through the lungs can be the culprit

Normal breathing also depends on the heart, which is the pump that pushes blood through the lungs for gas exchange. A failing heart makes blood flow too sluggish for adequate gas exchange during each breath, causing a sense that air flow is inadequate and making breathing rate go up. People who have cardiac dyspnea also describe feeling suffocated or smothered, especially if fluid begins to leak from the blood into the lung tissue. Gravity influences the symptoms which worsen with lying down and improve with sitting up.

Pulmonary emboli, clots that form in the legs or pelvis and break off and travel upstream, can cause severe and sudden dyspnea by lodging in and blocking major blood vessels in the lungs. Air reaches the lung segment where the clot is lodged, but gas exchange doesn’t occur because no blood is getting through. Large clots can be fatal immediately.

Should you develop dyspnea, seek help and try to provide a good history of your symptoms. Symptom history is very important in diagnosis and accurate diagnosis is crucial to proper treatment. The goal of treatment, of course, is a return to the comfortable lack of awareness of breathing that should accompany you from cradle to grave.

Before birth the lungs are not inflated. Oxygen and carbon dioxide enter and exit through the mother’s blood via the placenta. In the first 10 seconds after birth, a dramatic changeover begins, and from that point until the last breath is drawn the lungs connect us to this world. The first gasping breath of a newborn baby signals the beginning of the body’s most vital and most tenuous relationship with this world – that with air, or more correctly with the 21% of air that is oxygen.

Breathing is something we do without thinking, adjusting rate and depth of respiration to the demand for oxygen by the tissues. Healthy hearts and lungs rise to the demand, increasing blood flow as needed. In a sedentary person, exercising muscle has to be trained in order to be able to utilize the increased oxygen delivered. Unhealthy lungs, however, fail to meet the increased demands of exertion, and may eventually fail to meet oxygen demands at rest. Then, breathing is always rapid and even speaking is laborious.

Decoding lung symptoms

A huge number of problems affect the airways, but only a limited number of symptoms result. They are: 1. shortness of breath, especially with exertion. 2. cough – either dry and unproductive, or productive of sputum which is either clear, red and frothy, yellow or green, foul smelling, or bloody. 3. chest pain, often associated with the chest wall movement. 4. wheezing. In addition, lung tumors can cause a variety of peculiar symptoms outside the lungs – the most common is weight loss; the most exotic are peculiar neurological symptoms.

Because the lung is a living record of the air inhaled over time, a complete patient history is the first step in decoding symptoms. The second step is almost always an imaging study. X-rays, CT and MRI scans are so good at revealing chest pathology that a skilled chest examination is a dying art. Technology also uncovers lung scars and nodules in patients who have no symptoms. Bronchoscopies and biopsies define abnormalities further. Often, but not always, such findings are benign, evidence of old encounters with fungus spores or of unknown cause. Autopsies also uncover unsuspected lung pathology like mild to moderate emphysema (see side bar) and evidence of long term exposure to pollution and smoke. Lungs of modern city dwellers are speckled with black particles from polluted air. Smokers’ lungs are black and shiny, as if smeared with tar. Smoking avoidance would be the single most effective way to improve many people’s respiratory problems, but a pristine lung at the end of a long life would still be a virtual impossibility. Breathing is often very dirty work.

The bronchial tree – air’s roadway

The work of breathing begins with muscular contraction. The diaphragm, a muscular sheet lying horizontally between the abdomen and the chest, contracts downward and expands the chest cavity. The short muscles between the ribs – the intercostals – assist by pulling the chest walls outward. Like a bellows, this chest expansion pulls air into the lungs by means of negative pressure. Air rushes from the nose into the trachea, down hollow tree-like branches called bronchi, into tinier branches called bronchioles, and finally into millions of tiny expandable sacs called alveoli. The bronchial tree is elastic, expanding on inhalation and collapsing back to baseline diameter on exhalation. In asthmatics, the fine muscles in these tubular walls respond irritably to allergens and constrict the passages. Inflammation from infection or inhalation of toxic substances and even rapid breathing of cold dry air can also trigger tightening of the bronchi, called bronchospasm. Airflow resistance rises in bronchospasm, making the sufferers of asthma and bronchitis cough and wheeze. Treatment of both conditions aims at dilating the airways by using drugs that relax the smooth muscle fiber and at reducing inflammation of the bronchial lining with steroids and antibiotics.

The alveoli – where the work gets done

Air flow rushing down the bronchial tree dead ends in the alveoli, expanding them until they resemble very soft Styrofoam. Fine capillaries course through the thin walls of the alveoli, picking up oxygen and delivering carbon dioxide for exhalation. Airborne particles settle out in the moist alveoli, though they only get that far by surviving the cough reflex and the cilia -the tiny hair-like projections that constantly sweep dust and foreign bodies up and out of the bronchial tree. Alveoli are also the site of pneumonia – infections with either bacteria or viruses that set up shop in thin alveolar fluid. The organisms excite inflammation and increased secretions, which impair gas exchange and cause shortness of breath, fever and coughing. Patients with pneumonia look and feel terrible. Pneumonia can also involve the pleura, the lining over the lung, adding the misery of pleuritic pain with each breath, and causing fluid to accumulate between the lung and chest wall – a problem called a pleural effusion.

Fluid accumulation in the chest

Pleural effusions sometimes accompany heart failure. Less often, they are blood tinged accompaniments of pulmonary emboli – clots that reach the lung from leg and pelvic veins. Small clots in the lung block oxygen exchange in their vicinity; large ones kill suddenly, with no warning, by blocking major blood vessels bringing blood to the lungs. Shortness of breath and coughing producing blood tinged sputum are warnings to be heeded, particularly if they occur after a prolonged period of bedrest or sitting without getting up – situations that promote clot formation in the legs.

Sputum- the stuff that gets coughed up

Blood-tinged sputum can be less serious a symptom, since it is a common result of a bloody nose above. But when associated with cough and weight loss, it is a telltale sign of lung cancer. Yellow and green sputum usually indicate infection. If foul smelling, it may come from a lung abscess. Pink frothy sputum is a sign of edema in the lungs, usually from heart failure, but also from altitude sickness, and is always accompanied by severe shortness of breath.

The last breath

At the end of life, breathing usually ceases not because the lungs fail, but because the drive to breathe that made the newborn gasp its first breath ceases. All those breaths in between are like footprints left behind. Use them well.

Addendum: Alveoli Gone Wrong

Over a lifetime, especially when chronic airway disease impedes airflow, the alveoli change. They merge making larger spaces with fewer capillaries for air exchange. When severe, even getting enough oxygen in at rest is difficult. This condition is called emphysema, most commonly a problem in chronic smokers, but also a genetic disease in rare people. Oxygen delivered by a mask helps the symptoms for a while, but the condition inevitably progresses.

If alveoli rupture, as they can in emphysema or in congenital conditions that produce enlarged pockets, they leak air into the chest cavity. Air builds up between the lung and the inner chest wall an emergency condition called a pneumothorax that is very painful and potentially life threatening, requiring insertion of a chest tube to drain the air and restore negative pressure to keep the lung inflated. Similarly, a penetrating wound in the chest wall sucks air into the chest cavity, collapsing the lung. Covering the chest wound tightly to prevent air from entering can save a life.

Posted by medical plaintalk

Posted by medical plaintalk