Dyspnea (trouble breathing): A symptom with many causes

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.

Posted by medical plaintalk

Physician turned medical writer.

Iron: Too Little and Too Much

Poison is in everything, and no thing is without poison. The dosage makes it either a poison or a remedy.
Paracelsus. Swiss-German physician (1493-1541)

Iron is present in abundant quantities in the earth’s core and crust, in the sun, the stars and meteorites – and inside all living things. In humans, iron carries oxygen to all the body’s cells, carries carbon dioxide back to the lungs, enables many chemical reactions related to energy production, and binds oxygen inside for use in muscle cells. It is a vital nutrient – a substance that must be part of the diet, but also one which the body cannot excrete except by losing blood and skin cells. Both too little iron and too much iron present us with problems.

Where the body puts iron

Iron is absorbed from food in the upper part of the small intestine. Specialized proteins
carry it in the blood and store it in the liver and other organs. Ten percent of total body
iron is attached to myoglobin in muscles, 25 percent is stored in the liver and in specialized cells throughout the body, and the major portion, 65 percent, is bound to hemoglobin inside red blood cells. Hemoglobin-bound iron is constantly recycled as old red blood cells are destroyed and new ones are made.

Iron absorption from food – a tightly regulated process

Iron must be bound to proteins or it excites free radical damage in cells. When all of the protein binding sites for hemoglobin in the body are filled, the liver sends a signal to the small intestine to decrease the amount of iron taken in from food. This regulation of iron absorption is a very sensitive and tightly regulated process in which a message is sent to the intestines conveying how much iron is already in the body. That amount determines how much or how little iron is absorbed from food. This feedback loop is necessary because, beyond minor blood loss and regular shedding of skin and bowel cells, the body has no way to get rid of extra iron. Most health problems related to iron come from too little iron in the diet, from too much iron, delivered intravenously in the form of blood transfusions, or from genetic defects in the feedback loop that tells the intestines how much iron to take in.

Too Little Iron

Deficiency of iron in the body causes weakness, fatigue, and shortness of breath because of inability to carry enough oxygen in the blood and failure to produce required energy. Skin and nail beds are pale because mature red blood cell production is limited (iron deficiency anemia). Dizziness and fainting upon standing up can occur.
Iron deficiency comes about because dietary iron is insufficient to make up normal losses of iron through menstrual blood loss , or abnormal losses that might occur chronically, such as from an unsuspected stomach inflammation, an intestinal tumor or abnormally heavy menstrual bleeding.

Who becomes iron deficient?

Dietary iron deficiency is very common, especially in people who restrict calories, avoid meat or have poor diets. Women of childbearing age, children and the elderly of both sexes are the most at risk. Dietary deficiency can also be aggravated by increased need for iron, as in pregnancy and childhood growth. While many foods contain iron, it is better absorbed from animal sources like beef, chicken liver, fish and mollusks than from plant based sources like spinach and beans. Iron absorption also requires an acid environment, which acid relieving drugs block.

Iron deficiency in post-menopausal women or in men of any age group always raises suspicion of low grade, unsuspected blood loss, which usually comes from the gastrointestinal tract. Causes are gastritis (often from use of anti-inflammatory drugs), ulcers, colitis, diverticulitis, tumors and rare vascular malformations are all causes. Black, tarry and metallic smelling stool is often a clue.

Replenishing iron stores

Treatment of iron deficiency requires improving diet and finding and correcting sources of blood loss. Iron is better absorbed by the stomach from food than it is from pills. Red meat is the best source. But iron supplements are necessary when iron deficiency has caused symptoms. Several different versions of iron supplements may have to be tried – ferrous sulfate is the most commonly prescribed, but can be hard on the stomach. Ferrous gluconate may cause less nausea and stomach upset. Ferrous fumarate contains more iron per pill. The addition of Vitamin C to the diet helps absorption of iron supplements and iron can also be delivered by injection if dietary methods and oral suuplements fail.

Too Much Iron

Iron overload is called hemochromatosis and its symptoms come from damage to the cells in which iron is stored once the normal iron binding proteins can hold no more. The damage is very slow and cumulative and the liver and the heart bear the brunt. Testicles and thyroid gland are also storage sites. Skin storage may cause the patient to look inappropriately tanned, but weakness, lassitude, weight loss, shortness of with breath and abdominal pain typically bring the patient to the doctor.

Transfusion-related iron overload

Hemochromatosis can be caused by repetitive transfusions of blood. Transfusion related hemochromatosis afflicts patients with bone marrow diseases such as myelofibrosis and multiple myeloma. Repeated transfusions are the treatment for severe anemia in these patients and each unit of packed red blood cells delivers enough iron for six months. Iron overload begins to develop quickly.

Hereditary hemochromatosis

Hemochromatosis can also be caused by a genetic problem in which too much iron is absorbed. This hereditary version of hemochromatosis occurs in about 5 in 1000 people in the US. Caucasians are more susceptible than other races. While men and women are affected equally, men typically develop symptoms in their 30s or 40s, a decade or two earlier than women, because women are able to shed iron on a monthly basis until menopause.

Hemochromatosis is treated by regular bleeding, performed in the same way that blood donations are collected. But bleeding is not suitable treatment for patients whose severe anemia is the problem that forces them to receive repeated blood transfusions. The only option for them is chelation of the iron with drugs that bind iron in the blood and carry it out of the body, a difficult and time consuming process, but one that lengthens survival time. A new oral drug may soon make the process easier. At this time in medical history though, using iron as a remedy is easier than treating iron as a poison.

Posted by medical plaintalk

Physician turned medical writer.

Heart Failure: The Price of Success

In 1953, surgeon John Gibbon undertook the first successful open heart surgery using a heart-lung machine, a pump that performs both heart and lung functions while the heart is stopped for repairs. The pump ushered in a new era of cardiac surgery and made it possible to correct heart problems that had up until then caused premature disability and death.

In the years that followed Dr. Gibbon’s groundbreaking surgery, materials science, technology and pharmacology advanced rapidly, allowing surgery and medication to be used to treat a wider variety of heart problems, including heart attacks. Today we live in an age of coronary artery bypass surgery, clot-busting drugs, and stents that prop open diseased coronary arteries. Advancements such as these have reduced death rates from heart attacks substantially; nonetheless, heart disease remains the number one killer of men and women in the United States, and heart failure – the constellation of symptoms that come from poorly contracting heart muscle – is now the leading cause of hospitalization for patients over the age of sixty-five. With all of the progress that has been made in cardiovascular care, how can this be?

Why is there more heart failure now than in the past?

The answer is simple. Mortality rates are lower in the immediate aftermath of heart attacks because of the ability to dissolve clots and prop arteries open. Drugs and lifestyle management may be slowing the progression of the coronary artery disease that causes heart attacks. As a result of these advances, people no longer die as often in the earlier phases of a very long disease process which often ends in failure of the heart muscle to contract as strongly as it needs to.

If you liken cardiovascular care to home repairs, then the major advances in care have taken place in areas roughly equivalent to plumbing and electrical maintenance. Angioplasties, coronary artery bypasses, and stents are used to keep the pipes open; electronic pacemakers provide power, triggering muscle contractions in an organized fashion, while defibrillators restart the power when there are outages. A house with functional plumbing and electrical systems remains habitable remains habitable long enough for the underlying structural elements of the building, like the roof, ceilings, walls, and floors, to begin to fail. In the heart, the underlying structural element is muscle. When the muscular structure of the heart begins to fail, the signs and symptoms of heart failure appear.

Signs and symptoms

Heart muscle fibers that begin to contract less efficiently reduce the heart’s pumping capacity, preventing adequate blood flow to the major organs. The body reacts to this deficient blood flow by increasing the volume of blood in the body. It accomplishes this by retaining more salt and water, but when this happens, the blood’s increased volume stretches the failing heart muscle and damages it even further. The more the heart stretches, the less efficiently it pumps; the less efficiently it pumps, the more the body tries to boost blood flow by retaining fluids.

This vicious cycle results in what is known as congestion. Congestion occurs when the tissues, including the lungs, becoming filled with excess fluid. This fluid buildup causes swelling in the legs and abdomen and a shortness of breath. Fatigue and an inability to tolerate exercise are the heart failure patient’s constant companions. Gravity causes fluid to collect in the lower half of the body while the patient is standing or sitting, and when he lies down, it becomes redistributed, accumulating in the lungs where it can cause a telltale shortness of breath that is symptomatic of a deteriorating heart.

Causes

Age is an important contributing factor in the development of heart failure because the longer people live, the more time there is for coronary artery disease and the problems that contribute to it to take their toll on the heart muscle. Coronary artery disease deprives areas of the heart of blood and oxygen, leaving behind damaged muscle that contracts poorly and moves blood inefficiently. Smoking, excessive alcohol use, diabetes, hypertension, obesity, and lack of exercise contribute not only to coronary artery disease, but also to weakening the heart muscle directly. Less common factors involved in heart failure include viral infections that affect the heart and a variety of rare metabolic conditions that disrupt heart muscle fibers. Heart valve disease, when left untreated, can ultimately damage the heart by dilating it or causing it to thicken. However, valve disease is much less prevalent since the development of successful antibiotic treatments for childhood streptococcus infections.

Treatment

The quality and length of life heart failure patients can expect depends on how closely they adhere to the treatment plans provided by their doctors. Salt-restricted diets are a very important part of a heart failure treatment plan, and the mainstays of drug treatment plans are medications that prevent salt retention, get rid of excess water, improve the ability of the heart muscle to contract, and decrease blood pressure. Heart failure treatment treads a fine line between causing the patient’s body to retain too much and too little fluid. Drying a heart failure patient out too much can push the kidneys into failure. Too little and the lungs are liked soaked sponges, unable to exchange carbon dioxide for oxygen efficiently. The margin of error in fluid balance gets smaller and smaller as the disease progresses and this tightening window contributes to high hospital readmission rates for congestive heart failure patients. Physicians must monitor their patients’ weight, symptoms, electrolytes, and kidney functions more and more closely and start adding tests like chest X-rays and echocardiograms.

A variety of innovative devices and surgical procedures have been designed to cinch up dilated, failing hearts but have not succeeded in producing adequate results. Some success is being reported from the use of multiple pacemakers, which allow different segments of the heart to be stimulated in a defined order that improves the sequence of muscular contraction enough to generate greater cardiac output. Currently, bi-ventricular pacing—the separate pacing of both sides of the heart–is the most promising addition to the heart failure treatment arsenal. Cardiac transplantation remains the most difficult, expensive, and uncommon solution for a heart that has reached the end of its functional life.

Heart failure may eventually be overcome by artificial pumping devices or methods of stimulating the production of new cardiac muscle, but in the meantime, prevention is still the most desirable treatment option. Not smoking, maintaining a healthy weight and good exercise habits, sticking to a balanced diet of fresh foods, getting adequate sleep, and managing stress well are all cheap and valuable ways to invest in your heart’s health.

Posted by medical plaintalk

Physician turned medical writer.

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