If you just do a Google search and type in ‘smoking’ or ‘lung cancer’, you will be barraged with never ending facts and numbers, like how one in every three Americans is affected by lung disease and how COPD is the third leading cause of death and if you get lung cancer the odds are 95% that you will die.
Chronic Obstructive Pulmonary Disease (COPD) is largely preventable. Yet it affects over 15 million Americans and is the fourth leading cause of death in the U.S. Although many diseases have seen a gradual decline in their associated mortality, COPD rates have increased. The term COPD is a broad one used to describe a set of symptoms, referring to persistent, slowly progressive obstruction of airflow and dyspnea, that is predominantly irreversible. It may be caused by chronic bronchitis, emphysema, or bronchiectasis.
People with COPD experience deterioration in functional status; therefore, improving function is a major goal of treatment. Nurses are often facilitators and coordinators of pulmonary rehabilitation. Evaluation of the effects of treatment is an essential aspect of providing quality care. Although some effects of COPD are permanent, you can do plenty to assist your patient in managing it, by educating him on how to gain back control of his health. This will help to decrease the depression, hopelessness, and pessimism that are commonly seen in patients with COPD.
Your specific nursing measures can help ease your patient’s breathing and prevent further deterioration, thus protecting the remaining lung function and offering a better quality of life.
(Please note that asthma as not been covered extensively In this study. Only the summarization has been covered.)
Definitions, Anatomy & Pathology Review
Chronic obstructive pulmonary disease (COPD) is a term that applies to patients with chronic bronchitis, bronchiectasis, emphysema and, to a certain extent, asthma. A brief review of normal functional anatomy will provide a background for the discussion of pathology.
The airway down to the bronchioles normally is lined with ciliated pseudo-stratified columnar cells and goblet cells. Mucus derives from mucus glands that are freely distributed in the walls of the trachea and bronchi. The cilia sweep mucus and minor debris toward the upper airway. Low humidity, anesthesia gases, cigarette smoking and other chemical irritants paralyze the action of these cilia. The mucociliary action starts again after a matter of time. This is why people awaken to “smokers cough.”
“Chronic obstructive pulmonary disease (COPD) is a term that applies to patients with chronic bronchitis, bronchiectasis, emphysema and, to a certain extent, asthma.”
Bronchi run in septal connective tissue, but bronchioles are suspended in lung parenchyma by alveolar elastic tissue. The elastic tissue extends throughout alveolar walls, air passages, and vessels, connecting them in a delicate web. Bronchiolar epithelium is ciliated, single-layered and columnar or cuboidal. Beyond the bronchioles the epithelium is flat and lined with a film of phospholipid (surfactant), which lowers surface tension and thereby helps to keep these air spaces from collapsing. Remember that the phospholipid develops during later gestation in utero. This is the reason why premature infant’s lungs cannot stay inflated without the addition of surfactant therapy. Macrophages are found in alveolar lining. Smooth muscles surround the walls of all bronchi, bronchioles, and alveolar ducts and when stimulated they shorten and narrow the passages. Cartilage lends rigidity and lies in regular horse-shaped rings in the tracheal wall. Cartilage is absent in bronchi less than 1 mm in diameter.
The terminal bronchiole is lined with columnar epithelium and is the last purely conducting airway. An acinus includes a terminal bronchiole and its distal structures. Five to ten acini together constitute a secondary lobule, which is generally 1 to 2 cm in diameter and is partly surrounded by grossly visible fibrous septa. Passages distal to the terminal bronchiole include an average of three but as many as nine generations of respiratory bronchioles lined with both columnar and alveolar epithelium. Each of the last respiratory bronchioles gives rise to about six alveolar ducts, each of these to one or two alveolar sacs, and finally each of the sacs to perhaps seventy-five alveoli. Alveolar pores (pores of Kohn) may connect alveoli in adjacent lobules.
Two different circulations supply the lungs. The pulmonary arteries and veins are involved in gas exchange. The pulmonary arteries branch with the bronchi, dividing into capillaries at the level of the respiratory bronchiole, and supplying these as well as the alveolar ducts and alveoli. In the periphery of the lung, the pulmonary veins lie in the interlobular septa rather than accompanying the arteries and airways. The bronchial arteries are small and arise mostly from the aorta. They accompany the bronchi to supply their walls. In some cases of COPD, like bronchiectasis, extensive anastomoses develop between the pulmonary and bronchial circulations. This can allow major shunting and recirculation of blood, therefore contributing to cardiac overload and failure. Lymphatics run chiefly in bronchial walls and as a fine network in the pleural membrane. The lumina of the capillaries in the alveolar walls are separated from the alveolar lining surfaces by the alveolar-capillary membrane, consisting of thin endothelial and epithelial cells and a minute but expansile interstitial space. This interface between air and blood, only 2 microns in thickness, is the only place where gases may be exchanged effectively.
Diseases that make up COPD:
Chronic bronchitis is a clinical disorder characterized by excessive mucus secretion in the bronchi. It was traditionally defined by chronic or recurrent productive cough lasting for a minimum of three months per year and for at least two consecutive years, in which all other causes for the cough have been eliminated. Today’s definition remains more simplistic to include a productive cough progressing over a period of time and lasting longer and longer. Sometimes, chronic bronchitis is broken down into three types: simple, mucopurulent or obstructive. The pathologic changes consist of inflammation, primarily mononuclear, infiltrate in the bronchial wall, hypertrophy and hyperplasia of the mucus-secreting bronchial glands and mucosal goblet cells, metaplasia of bronchial and bronchiolar epithelium, and loss of cilia. Eventually, there may be distortion and scarring of the bronchial wall.
Asthma is a disease characterized by increased responsiveness of the trachea and bronchi to various stimuli (intrinsic or extrinsic), causing difficulty in breathing due to narrowing airways. The narrowing is dynamic and changes in degree. It occurs either spontaneously or because of therapy. The basic defect appears to be an altered state of the host, which periodically produces a hyperirritable contraction of smooth muscle and hypersecretion of bronchial mucus. This mucus is abnormally sticky and therefore obstructive. In some instances, the illness seems related to an altered immunologic state.
Histological changes of asthma include an increase in the size and number of the mucosal goblet cells and submucosal mucus glands. There is marked thickening of the bronchial basement membrane and hypertrophy of bronchial and bronchiolar smooth muscle tissue. A submucosal infiltration of mononuclear inflammatory cells, eosinophils and plugs of mucus blocks small airways. Patients who have had asthma for many years may develop cor pulmonale and emphysema.
Pulmonary emphysema is described in clinical, radiological and physiologic terms, but the condition is best defined morphologically. It is an enlargement of the air spaces distal to the terminal non-respiratory bronchiole, with destruction of alveolar walls.
Although the normal lung has about 35,000 terminal bronchioles and their total internal cross-sectional area is at least 40 times as great as that of the lobar bronchi, the bronchioles are more delicate and vulnerable. Bronchioles may be obstructed partially or completely, temporarily or permanently, by thickening of their walls, by collapse due to loss of elasticity of the surrounding parenchyma, or by influx of exudate. In advanced emphysema, the lungs are large, pale, and relatively bloodless. They do not readily collapse. They many contain many superficial blebs or bullae, which occasionally are huge. The right ventricle of the heart is often enlarged (cor pulmonale), reflecting pulmonary arterial hypertension. Right ventricular enlargement is found in about 40% of autopsies of patients with severe emphysema. The distal air spaces are distended and disrupted, thus excessively confluent and reduced in number. There may be marked decrease in the number and size of the smaller vascular channels. The decrease in alveolar-capillary membrane surface area may be critical. Death may result from infection that obliterates the small bronchi and bronchioles. There is often organized pneumonia or scarring of the lung parenchyma due to previous infections.
Classification of emphysema relies on descriptive morphology, requiring the study of inflated lungs. The two principal types are centrilobular and panlobular emphysema. The two types may coexist in the same lung or lobe.
Centrilobular emphysema (CLE) or centriacinar emphysema affects respiratory bronchioles selectively. Fenestrations develop in the walls, enlarge, become confluent, and tend to form a single space as the walls disintegrate. There is often bronchiolitis with narrowing of lumina. The more distal parenchyma (alveolar ducts and sacs and alveoli) is initially preserved, then similarly destroyed as fenestrations develop and progress.
The disease commonly affects the upper portions of the lung more severely, but it tends to be unevenly distributed. The walls of the emphysematous spaces may be deeply pigmented. This discoloration may represent failure of clearance mechanisms to remove dust particles, or perhaps the pigment plays an active role in lung destruction. CLE is much more prevalent in males than in females. It is usually associated with chronic bronchitis and is seldom found in nonsmokers.
Panlobular emphysema (PLE) or panacinar emphysema is a nearly uniform enlargement and destruction of the alveoli in the pulmonary acinus. As the disease progresses, there is gradual loss of all components of the acinus until only a few strands of tissue, which are usually blood vessels, remain. PLE is usually diffuse, but is more severe in the lower lung areas. It is often found to some degree in older people, who do not have chronic bronchitis or clinical impairment of lung function. The term senile emphysema was formerly applied to this condition. PLE occurs as commonly in women and men, but is less frequent than CLE. It is a characteristic finding in those with homozygous deficiency of serum alpha-1 antitrypsin. It has also been found that certain populations of IV Ritalin abusers show PLE.
Bullae are common in both CLE and PLE, but may exist in the absence of either. Air-filled spaces in the visceral pleura are commonly termed blebs, and those in the parenchyma greater than 1 cm in diameter are called bullae. A valve mechanism in the bronchial communication of a bulla permits air trapping and enlargement of the air space. This scenario may compress the surrounding normal lung. Blebs may rupture into the pleural cavity causing a pneumothorax, and through a valve mechanism in the bronchopleural fistula a tension pneumothorax may develop.
Paracicatricial emphysema occurring adjacent to pulmonary scars represents another type of localized emphysema. When the air spaces distal to terminal bronchioles are increased beyond the normal size but do not show destructive changes of the alveolar walls, the condition is called pulmonary overinflation. This condition may be obstructive, because of air trapping beyond an incomplete bronchial obstruction due to a foreign body or a neoplasm. Many lung lobules may be simultaneously affected as a result of many check-valve obstructions, as in bronchial asthma. Pulmonary overinflation may also be nonobstructive, less properly called “compensatory emphysema”, when associated with atelectasis or resection of other areas of the lung.
Bronchiectasis means irreversible dilation and distortion of the bronchi and bronchioles. Saccular bronchiectasis is the classic advanced form characterized by irregular dilatations and narrowing. The term cystic is used when the dilatations are especially large and numerous. Cystic bronchiectasis can be further classified as fusiform or varicose.
Tubular bronchiectasis is simply the absence of normal bronchial tapering and is usually a manifestation of severe chronic bronchitis rather than of true bronchial wall destruction.
Repeated or prolonged episodes of pneumonitis, inhaled foreign objects or neoplasms have been known to cause bronchiectasis. When the bronchiectatic process involves most or all of the bronchial tree, whether in one or both lungs, it is believed to be genetic or developmental in origin.
Mucoviscidosis, Kartagener’s syndrome (bronchiectasis with dextrocardia and paranasal sinusitis), and agammaglobulinemia are all examples of inherited or developmental diseases associated with bronchiectasis. The term pseudobronchiectasis is applied to cylindrical bronchial widening, which may complicate a pneumonitis but which disappears after a few months. Bronchiectasis is true saccular bronchiectasis but without cough or expectoration. It is located especially in the upper lobes where good dependent drainage is available. A proximal form of bronchiectasis (with normal distal airways) complicates aspergillus mucus plugging.
Advanced bronchiectasis is often accompanied by anastomoses between the bronchial and pulmonary vessels. These cause right-to-left shunts, with resulting hypoxemia, pulmonary hypertension and cor pulmonale.
In addition to relieving patient suffering, research is needed to help reduce the enormous economic and social burdens posed by chronic diseases such as osteoporosis, arthritis, diabetes, Parkinson’s and Alzheimer’s diseases, cancer, heart disease, and stroke.”
Treatments for CHF:
Heart failure caused by an excessive workload is curable by treating the primary disease, such as anemia or thyrotoxicosis or hypertension or diabetes. Also, curable are forms caused by anatomical problems such as a heart valve defect. These defects can be surgically corrected.
However, for the common forms of heart failure due to damaged heart muscle no known cure (like a heart attack that damages the heart muscle where the attack took place on the organ) but prevention of it happening again can take place in many cases through treatment of the disease or illness with being compliant in following up with your doctor for the disease or illness and being compliant in following doctor’s orders. The worst thing you can do is ignore it. The treatment seeks to improve patients quality of life and length of survival through lifestyle change and drug therapy.
Patients can minimize the effect t of heart failure by controlling the risk factors for heart disease they may have. Obvious steps include: Don’t smoke or quit smoking, lose weight if necessary, abstaining from alcohol, and making those dietary changes to reduce the amount of salt and fat consumed Regular, modest exercise is also helpful for many patinets, though the amount and intensity should be carefully monitored by a physician.
Even with lifestyle changes, most heart failure patients must take medication. Many patients receive 2 or more meds. Types of medication given: ACE inhibitors, Digitalis, Diuretics, Hydralazine, and Nitrates.
These are some of the meds given for heart failure. Not all medications are suitable for patients, and more than one drug may be needed. Always review the list your pharmacist provides in the action, side effects, with instructions of how to take the drug to make it most effective in your body with what to look for while on this medication to keep you the patient most informed on what you should know.
Results of studies over the years have placed more emphasis on the use of drugs known as angiotensin converting enzymes (ACE) inhibitors. Several studies have indicated that ACE inhibitors improve survival among heart failure patients and may slow perhaps even prevent the loss of the heart pumping activity. This drug prevents the transfer of your enzyme Angiotensin 1 to convert to Angiotensin 2 which prevents the vessels in your body to do vasoconstriction which prevents the pressure in the bloodstream to raise = high B/P (hypertension). This prevents stress to the heart, due to high B/this causes blood to get to the heart slowly and more difficult causing the heart to pump harder but the ACE inhibitor with allowing vasodilation (opening of vessels) keeping pressure down to make the job easier= less stress on the heart. Originally these medications where for patients in the treatment of hypertension but they help patients with heart failure, among other things, decreasing the pressure inside the blood vessels causing the heart to do its job easier.
Digitalis increases the force of the heart’s contractions, helping to improve circulation in the body.
Diuretics are for reducing the amount of fluid in the bloodstream and body by releasing them via the kidneys and having us void the excess out in our urine, these are useful for patients with fluid retention.
Those who aren’t prescribed or cannot take these meds already mentioned may be given a hydralazine medication and/or a drug in the Nitrate classification, each of which help relax tension in the blood vessels to improve blood flow. Also, both Hydralazine and Nitrates function is they cause vasodilation in the vessels improving blood flow to the heart.
Sometimes heart failure is life threatening. Usually, this happens when drug therapy and lifestyle changes fail to control its symptoms. In such cases, a heart transplant may be the only treatment option. However, candidates for transplantation often have to wait months or even years before a suitable donor heart is found.
Studies over the years indicate that some transplant candidates improve during this waiting period through drug treatment and other therapy, and can be removed from the transplant list.
Transplant candidates who do not improve sometimes need mechanical pumps, which are attached to the heart. Called left ventricular assist device (LVADs), the machine takes over part or virtually all of the heart’s blood-pumping activity. However, current LVADs are not permanent solutions for heart failure but are considered bridges to transplantation. Worldwide, about 3,500 heart transplants were performed annually. The vast majority of these are performed in the United States (2,000-2,300 annually). Cedars Sinai Medical Center in Los Angeles, California has performed the most heart transplants in the last three consecutive years performing 95 transplants in 2012 alone. About 800,000 people have a Class IV heart defect indicating a new organ. The degrees of CHF are I, II, III and IV. In learning more about CHF with heart transplants (including becoming a candidate for one) go to wwwtransplantexperience.com or even hearttransplant.com.
Another surgical procedure for heart failure that is available in America is cardiomyoplasty. This is a surgical procedure in which healthy muscle from another part of the body is wrapped around the heart to provide support for the failing heart. Most often the latissimus dorsi muscle is used for this purpose. A special pacemaker is implanted to make the skeletal muscle contract. The electrical stimulator icauses the back muscle to contract, pumping the blood from the heart (this allows the heart to do its job more effectively).
Complications of CHF:
Through the Mayo clinic as a reference regarding complications their website stated: “If you have heart failure, your outlook depends on the cause and the severity, your overall health, and other factors such as your age. Complications can include:
- Kidney damage or failure. Heart failure can reduce the blood flow to your kidneys, which can eventually cause kidney failure if left untreated. Kidney damage from heart failure can require dialysis for treatment.
- Heart valve problems. The valves of your heart, which keep blood flowing in the proper direction through your heart, may not function properly if your heart is enlarged, or if the pressure in your heart is very high due to heart failure.
- Liver damage. Heart failure can lead to a buildup of fluid that puts too much pressure on the liver. This fluid backup can lead to scarring, which makes it more difficult for your liver to function properly.
- Stroke. Because blood flow through the heart is slower in heart failure than in a normal heart, it’s more likely you’ll develop blood clots, which can increase your risk of having a stroke.Tips on CHF:Closely follow your doctor’s instructions, being compliant with the instructions and taking your meds.Control your weight in making it easier for your heart, that’s in failure, to function better (less stress).Limit or stop alcohol consumption as your doctor informs you. The best defense against heart failure is PREVENTION! Almost all the cardiac risk factors can be controlled of eliminated (smoking, obese, high cholesterol, high B/P, diabetes).
- Going to the doctor can be stressful but know he is there for you. It is hard to remember everything you want to ask the doctor with everything you hear at your visit. It helps to prepare a list of questions you may have and bring it with you at your appointment to address to the doctor your concerns. In doing this it helps you with your appointment so you can record the answers by listing them on the paper you have. Before you leave the doctor’s office, be sure you understand your condition and its treatment, including any medications your taking this doctor ordered for you with him or her knowing any other medications you may be on through a different doctor to prevent side effects or adverse reactions but if you forget this about the medications there is always your pharmacist you can ask than your M.D. later. With you knowing this information you will see why it is so vital for you doing all these actions or inter- ventions for your disease that the doctor ordered and you’re more out to follow them as well.
- Of course, stop smoking permanently if actively smoking.
- Watch what you eat and how much. Watch the diet intake of cholesterol and sodium that can cause a negative impact on the heart by causing stress to the organ through either high B/P=high sodium that causes vasoconstriction or high cholesterol frequently=blockage in an artery and both cause diminishing of oxygenated blood getting to the heart. Without oxygen to our tissues or cells this causes tissue & cellular starvation. What is starvation to the heart=chest pain (what we call angina). Take a brittle diabetic, the furthest area from the heart is the feet the first area to experience starvation is the toes, foot or lower extremity which is why this is usually the first to be amputated if necessary (you usually see an upper extremity amputated due to trauma).
- Immediately call your doctor of any significant change in your condition, such as an intensified shortness of breath or swollen feet or weight gain of 3lbs or more within one week.
- See your doctor regularly in evaluating your CHF.
- Some people’s symptoms and heart function will improve with proper treatment. However, heart failure can be life-threatening. People with heart failure may have severe symptoms, and some may require heart transplantation or support with an artificial heart device.”
If you are needing any guidance in how to lose weight through using all 4 food groups, with assistance in what to eat now to lose weight till in therapeutic range for your height than eating food from the market or needing to understand how the body works with food and metabolism with where activity comes into play go to healthyusa.tsfl.com and see what we can provide you in answering all these questions for you through Dr. Anderson and myself as your coach free. SO LIVE AS HEALTHY AS POSSIBLE IN YOUR ROUTINE HABITS, YOUR DIETING OF THE 4 FOOD GROUPS, MAINTAINING YOUR WEIGHT IN A THEREPEUTIC RANGE (look as calculating BMI online for free to find out what your weight range for your height is), and BALANCING REST WITH EXERCISE TO HELP DECREASE THE CHANCE OF GETTING HEART FAILURE. Go to healthyusa.tsfl.com to learn what Dr. Anderson through his book of “Dr. A.’s Healthy Habits” and me (for free) as your health coach could provide you with. Just take a view of what can be offered to you for no price with no hacking go to healthyusa.tsfl.com and take a peek;) Join me like many who are trying to live life healthier with making America a healthier home and we all should take part to help the health care system to be more effective for our society. Recommended to anyone with disease before changing your diet, activity/exercise program review with your doctor to get clearance to maintain your safety.
Heart failure can be ongoing (chronic), or your condition may start suddenly (acute).
Heart failure signs and symptoms may include by the MAYO CLINIC are:
- Shortness of breath (dyspnea) when you exert yourself or when you lie down
- Fatigue and weakness
- Swelling (edema) in your legs, ankles and feet
- Rapid or irregular heartbeat
- Reduced ability to exercise
- Persistent cough or wheezing with white or pink blood-tinged phlegm
- Increased need to urinate at night
- Swelling of your abdomen (ascites)
- Sudden weight gain from fluid retention
- Lack of appetite and nausea
- Difficulty concentrating or decreased alertness
- Sudden, severe shortness of breath and coughing up pink, foamy mucus
- Chest pain if your heart failure is caused by a heart attack
- To diagnose heart failure, your doctor will first ask you questions about your medical symptoms and history. Your doctor will want to know:
- if you have any other health conditions such as diabetes, kidney disease, angina, high blood pressure, or other heart problems.
- if you smoke
- if you drink alcohol and how much you drink
- what medications you are takingYour doctor will also perform a complete physical exam. Your doctor will look for signs of heart failure as well as any other illnesses that may have caused your heart to weaken.
- After the physical exam, your doctor may also order some of these tests:
- For the diagnosing of the CHF the MAYO clinic states the following:
- Blood tests. Your doctor may take a sample of your blood to check your kidney, liver and thyroid function and to look for indicators of other diseases that affect the heart.
- A blood test to check for a chemical called N-terminal pro-B-type natriuretic peptide (NT-proBNP) may help in diagnosing heart failure if the diagnosis isn’t certain when used in addition to other tests.
- Chest X-ray. X-ray images help your doctor see the condition of your lungs and heart. In heart failure, your heart may appear enlarged and fluid buildup may be visible in your lungs. Your doctor can also use an X-ray to diagnose conditions other than heart failure that may explain your signs and symptoms.
- Electrocardiogram (ECG). This test records the electrical activity of your heart through electrodes attached to your skin. Impulses are recorded as waves and displayed on a monitor or printed on paper.
- This test helps your doctor diagnose heart rhythm problems and damage to your heart from a heart attack that may be underlying heart failure.
- Echocardiogram. An important test for diagnosing heart failure is the echocardiogram. An echocardiogram helps distinguish systolic heart failure from diastolic heart failure in which the heart is stiff and can’t fill properly.The echocardiogram also can help doctors look for valve problems or evidence of previous heart attacks, other heart abnormalities, and some unusual causes of heart failure.
- Your ejection fraction is measured during an echocardiogram and can also be measured by nuclear medicine tests, cardiac catheterization and cardiac MRI. This is an important measurement of how well your heart is pumping and is used to help classify heart failure and guide treatment.
- An echocardiogram uses sound waves to produce a video image of your heart. This test can help doctors see the size and shape of your heart and how well your heart is pumping.
- Stress test. Stress tests measure how your heart and blood vessels respond to exertion. You may walk on a treadmill or pedal a stationary bike while attached to an ECG machine. Or you may receive a drug intravenously that stimulates your heart similar to exercise. Sometimes the stress test can be done while wearing a mask that measures the ability of your heart and lungs to take in oxygen and breathe out carbon dioxide.If your doctor also wants to see images of your heart while you’re exercising, he or she may order a nuclear stress test or a stress echocardiogram. It’s similar to an exercise stress test, but it also uses imaging techniques to visualize your heart during the test.
- Stress tests help doctors see if you have coronary artery disease. Stress tests also determine how well your body is responding to your heart’s decreased pumping effectiveness and can help guide long-term treatment decisions.
- Cardiac computerized tomography (CT) scan or magnetic resonance imaging (MRI). These tests can be used to diagnose heart problems, including causes of heart failure.In a cardiac MRI, you lie on a table inside a long tube-like machine that produces a magnetic field. The magnetic field aligns atomic particles in some of your cells. When radio waves are broadcast toward these aligned particles, they produce signals that vary according to the type of tissue they are. The signals create images of your heart.
- In a cardiac CT scan, you lie on a table inside a doughnut-shaped machine. An X-ray tube inside the machine rotates around your body and collects images of your heart and chest.
- Coronary angiogram. In this test, a thin, flexible tube (catheter) is inserted into a blood vessel at your groin or in your arm and guided through the aorta into your coronary arteries.
- A dye injected through the catheter makes the arteries supplying your heart visible on an X-ray. This test helps doctors identify narrowed arteries to your heart (coronary artery disease) that can be a cause of heart failure. The test may include a ventriculogram — a procedure to determine the strength of the heart’s main pumping chamber (left ventricle) and the health of the heart valves.
Myocardial biopsy. In this test, your doctor inserts a small, flexible biopsy cord into a vein in your neck or groin, and small pieces of the heart muscle are taken. This test may be performed to diagnose certain types of heart muscle diseases that cause heart failure.
Tune in tomorrow for part 3 of CHF treatment, complications & tips.
“Heart failure is serious. But there is hope. With the right treatment, you can lead an active life.”
The definition of heart failure, it occurs when the heart loses its ability to pump enough blood through the body. Usually, the loss in pumping action is a symptom of an underlying heart problem, such as hypertension and CAD = coronary artery disease. The term heart failure suggests a sudden and complete stop of heart activity but actually the heart does not suddenly or abruptly stop. Instead the way it works is heart failure usually develops over time, years. The heart first compensates with the disease or illness the individual has but, just like a car, after wear and tear the heart goes into decompensating to heart failure due to the heart decline. How serious is this condition? It varies from person to person depending on factors like an individual with obesity & unhealthy versus a person in healthier condition. All people diagnosed or not diagnosed with heart failure lose a pumping capacity of the heart happens as they age but diagnosed with heart failure makes the engine of the body a challenge in doing its function properly. The pump loss is more significant in the person with heart failure and often results from a heart attack (actual scaring to the tissue=death to that tissue area) or from other diseases that can damage the heart. The severity of the condition determines the impact it has on a person’s life. At the other end, extremes, treatment often helps people lead full lives if the person follows the meds ordered by the doctor including the diet and activity/exercise the doctor orders to the patient with heart failure (compliance so important). There are different levels of heart failure but even the mildest form is a serious health problem, which must be treated. If not the pump (the heart) will just get worse in doing its function properly. To improve the chance of living longer in an individual with heart failure, patients must take care of themselves, see their physician (cardiologist) on a regular basis, and closely follow treatments (as ordered) with knowing what heart failure actually to understanding how the disease works (is the failure on the right side or left side? Which in time will effect the other side in time). In knowing what side the failure is on will make you understand what signs and symptoms to expect.
Types of Heart Failure
The term congestive heart failure (CHF) is often used to describe all patients with heart failure. In reality, congestion=the buildup of fluids in the heart for not pumping correctly, just like pipes in a home not working properly=back up of water in the pipes, happens with CHF also to the fluids (blood) backing up in the lungs. This is just one feature of the condition and does not occur in all patients. There are two main categories of heart failure although within each category, symptoms and effects may differ from patient to patient. The two categories are: 1-Systolic heart failure (systolic is the top number of your blood pressure=the heart at work). This occurs when the heart’s (muscle-myocardium) ability to contract (pump=being active) decreases, particularly starting on the L side of the heart where the muscle of the heart is greatest (myocardium=heart muscle). The heart cannot pump blood with enough force to push a sufficient amount out of the heart into the circulation through the aorta. The aorta is a artery (vessel) that leaves the L lower chamber of the heart (left side of the heart=highly oxygenated rich blood). Due to the heart not using enough force pushing the blood forward in the aorta this causes the blood to back up and cause it to go back up into the L lower to the L upper chamber that goes further back up into the pulmonary vein into the lungs=congestion in the lungs due to the heart failure.
2-Diastolic heart failure (diastolic is the bottom number of your blood pressure which is the pressure when the heart is at rest). This failure occurs when the heart has a problem relaxing. The heart cannot properly fill with blood because the muscle of the heart due to trying so hard to compensate over a long period of time with disease (ex. High B/P, Obesity, etc…) strains the heart in doing its function that failure finally starts that the muscle of the heart (myocardium) becomes stiff. This causes the heart to lose its ability to relax to allow proper filling of the heart in upper and lower chambers=back up of the blood. This failure starts on the right side of the heart causing the blood to back up away from the heart and may lead this blood that is highly concentrated with carbon dioxide to accumulation especially in the feet, ankles and legs. Some patients may have lung congestion.
Causes of Heart Failure:
As stated, the heart loses some of its blood pumping ability as a natural consequence of aging. How- ever, a number of other factors can lead to a potentially life-threatening loss of pumping activity.
As a symptom of underlying heart disease, heart failure is closely associated with the major risk factors for coronary heart disease: smoking, high cholesterol levels, hypertension (persistent high blood pressure), diabetes= abnormal blood sugar levels, and obesity. A person can change or eliminate those risk factors and thus lower their risk of developing or aggravating their heart disease and heart failure through healthy habits performed routinely, proper dieting, and balancing rest with exercise.
Among prominent risk factors, hypertension-HTN (high blood pressure) and diabetes are PARTICULARLY IMPORTANT. Uncontrolled HTN increases the risk of heart failure by 200 %, compared to those who do not have hypertension. Moreover, the degree of risk appears directly related to the severity of the high blood pressure.
Persons with diabetes have about a two to eight fold greater risk of heart failure than those without diabetes. Women with diabetes have a greater risk of heart failure than men with diabetes. Part of the risk comes from the diabetes association with other risk factors for heart disease such as high cholesterol or obesity or other risk factors. However, the disease process of diabetes also damages the heart muscle.
The presence of coronary disease is among the greatest risks for heart failure. Muscle damage and scarring caused by a heart attack greatly increase the risk of heart failure. Cardiac arrhythmias, or irregular heartbeats, also raise heart failure risk. Any disorder that causes abnormal swelling or thickening of the heart sets the stage for heart failure.
In some people, heart failure arises from problems with heart valves, the flap-like structures that help regulate blood flow through the heart. Infections in the heart are another source of increased risk for heart failure.
A single risk factor may be sufficient to cause heart failure, but a combination of factors dramatically increases the risk. Advanced age adds to the potential impact of any heart failure risk.
Finally, genetic abnormalities contribute to the risk for certain types of heart disease, which in turn may lead to heart failure. However, in most instances, a specific genetic link to heart failure has not been identified.
SO LIVE AS HEALTHY AS POSSIBLE IN YOUR ROUTINE HABITS, YOUR DIETING OF THE 4 FOOD GROUPS, MAINTAINING YOUR WEIGHT IN A THEREPEUTIC RANGE (look as calculating BMI online for free to find out what your weight range for your height is), and BALANCING REST WITH EXERCISE TO HELP DECREASE THE CHANCE OF GETTING HEART FAILURE.
CHF part 2 tomorrow and learn what the signs and symptoms with how its diagnosed, how its treated with tips on the disease (most importantly prevention).
“To keep the body in good health is a duty… otherwise we shall not be able to keep our mind strong and clear.”