Question: What is the difference between systolic heart failure and diastolic heart failure?

Answer: The heart has, basically, two large pumping chambers. One is the right ventricle which pumps blood into the lungs where the blood gets rid of carbon dioxide and picks up oxygen, and then the blood goes into the left side of the heart -- and the left ventricle, which is a much larger and stronger pumping chamber and pumps that fresh blood to the rest of the body. If either one of those chambers, or both chambers doesn't squeeze as well as it's supposed to, it can lead to a variety of different symptoms, and that's systolic heart failure -- right ventricular systolic failure, or left ventricular systolic failure. Diastolic failure is very different in that it affects mainly the left ventricle. When there are certain conditions -- and sometimes it just happens as we get older -- certain conditions where the ventricle doesn't relax and let blood fill it properly, in other words it's stiff or non-compliant, what happens in that circumstance is, the pressure of the blood in the ventricle goes up, it's reflected back into the left atrium -- the small chamber -- and then back in the lungs and even though it's not due to poor squeezing of the heart, the symptoms can be very similar, mainly breathlessness and fatigue. Heart failure does not mean the heart has stopped working. Rather, it means that the heart's pumping power is weaker than normal or the heart has become less elastic. With heart failure, blood moves through the heart's pumping chambers less effectively, and pressure in the heart increases, robbing your body of oxygen and nutrients. To compensate for reduced pumping power, the heart's chambers respond by stretching to hold more blood. This keeps the blood moving, but over time, the heart muscle walls weaken and are unable to pump as strongly. As a result, the kidneys often respond by causing the body to retain fluid (water) and sodium. The resulting fluid buildup in the arms, legs, ankles, feet, lungs, or other organs, is called congestive heart failure. High blood pressure brings on heart failure by causing left ventricular hypertophy, a thickening of the heart muscle that results in less effective muscle relaxation between heart beats. This makes it difficult for the heart to fill with enough blood to supply the bodys organs, especially during exercise, leading your body to hold onto fluids and your heart rate to increase. TACHYSDYSRHYTHMIA - an abnormal heart rhythm with rate greater than 100 beats per minute in an adult. An arrhythmia (ah-RITH-me-ah) is a problem with the rate or rhythm of the heartbeat. During an arrhythmia, the heart can beat too fast, too slow, or with an irregular rhythm. A heartbeat that is too fast is called tachycardia (TAK-ih-KAR-de-ah). A heartbeat that is too slow is called bradycardia (bray-de-KAR-de-ah). Most arrhythmias are harmless, but some can be serious or even life threatening. During an arrhythmia, the heart may not be able to pump enough blood to the body. Lack of blood flow can damage the brain, heart, and other organs. Valvular heart disease is characterized by damage to or a defect in one of the four heart valves: the mitral, aortic, tricuspid or pulmonary. The mitral and tricuspid valves control the flow of blood between the atria and the ventricles (the upper and lower chambers of the heart). The pulmonary valve controls the flow of blood from the heart to the lungs, 1

and the aortic valve governs blood flow between the heart and the aorta, and thereby the blood vessels to the rest of the body. The mitral and aortic valves are the ones most frequently affected by valvular heart disease. Normally functioning valves ensure that blood flows with proper force in the proper direction at the proper time. In valvular heart disease, the valves become too narrow and hardened (stenotic) to open fully, or are unable to close completely (incompetent). A stenotic valve forces blood to back up in the adjacent heart chamber, while an incompetent valve allows blood to leak back into the chamber it previously exited. To compensate for poor pumping action, the heart muscle enlarges and thickens, thereby losing elasticity and efficiency. In addition, in some cases, blood pooling in the chambers of the heart has a greater tendency to clot, increasing the risk of stroke or pulmonary embolism. The severity of valvular heart disease varies. In mild cases there may be no symptoms, while in advanced cases, valvular heart disease may lead to congestive heart failure and other complications. Treatment depends upon the extent of the disease. Tachycardia is a fast or irregular heart rhythm, usually more than 100 beats per minute and as many as 400 beats per minute. At these elevated rates, the heart is not able to efficiently pump oxygen-rich blood to your body. Tachycardia can occur in either the upper heart chambers (atrial tachycardia) or lower heart chambers (ventricular tachycardia). Causes of tachycardia include:

Heart-related conditions such as high blood pressure (hypertension) Poor blood supply to the heart muscle due to coronary artery disease (atherosclerosis), heart valve disease, heart failure, heart muscle disease (cardiomyopathy), tumors, or infections Other medical conditions such as thyroid disease, certain lung diseases, electrolyte imbalance, and alcohol or drug abuse Emotional stress or drinking large amounts of alcoholic or caffeinated beverages

What causes an arrhythmia? Arrhythmias may be caused by many different factors, including:

Coronary artery disease. Electrolyte imbalances in your blood (such as sodium or potassium). Changes in your heart muscle. Injury from a heart attack. Healing process after heart surgery. Irregular heart rhythms can also occur in "normal, healthy" hearts.

Cardiomyopathy (literally "heart muscle disease") is the measurable deterioration of the function of the myocardium (the heart muscle) for any reason, usually leading to heart failure; common symptoms are dyspnea (breathlessness) and peripheral edema (swelling of the legs). People with cardiomyopathy are often at risk of dangerous forms of irregular heart beat and sudden cardiac death. The most common form of cardiomyopathy is dilated cardiomyopathy.

Cardiomyopathy is a weakening of the heart muscle or a change in the heart muscle. It often occurs when the heart cannot pump as well as it should, or with other heart function problems. Most patients with cardiomyopathy have heart failure. Causes Common types of cardiomyopathy include:

Dilated cardiomyopathy is a condition in which the heart becomes weak and large. It cannot pump blood well enough. Many different medical problems can cause this type of cardiomyopathy. Hypertrophic cardiomyopathy (HCM) is a condition in which the heart muscle becomes thick. This thickening makes it harder for blood to leave the heart. This type of cardiomyopathy is usually passed down through families. Ischemic cardiomyopathy is caused by narrowing of the arteries that supply the heart with blood. Restrictive cardiomyopathy is a group of disorders in which the heart chambers are unable to properly fill with blood because the heart muscle is stiff. Peripartum cardiomyopathy occurs during pregnancy or in the first 5 months afterward.

Common causes of cardiomyopathy are:

Alcoholism and cocaine use Amyloidosis Chemotherapy drugs Coronary artery disease (ischemic cardiomyopathy) -- most common cause End-stage kidney disease Genetic defects High blood pressure (hypertension) Infections due to viruses -- HIV, Lyme disease, Chagas disease Nutritional deficiencies (such as selenium, thiamine, and calcium) Pregnancy Systemic lupus erythematosus

Congestive Heart Failure

The words "heart failure" sound alarming, but they do not mean that your heart has suddenly stopped working. Instead, heart failure means your heart is not pumping as well as it should to deliver oxygen-rich blood to your body's cells. Congestive Heart Failure happens when the heart's weak pumping action causes a buildup of fluid called congestion in your lungs and other body tissues. Congestive Heart Failure usually develops slowly. You may go for years without symptoms, and the symptoms tend to get worse with time. This slow onset and progression of Congestive Heart Failure is caused by your heart's own efforts to deal with its gradual weakening. Your heart tries to make up for this weakening by enlarging and by forcing itself to pump faster to move more blood through your body.

Who is at risk for developing Congestive Heart Failure, and what are its causes? According to a recent study, people over 40 have a 1 in 5 chance of developing Congestive Heart Failure in their lifetime. Nearly 5 million people in the United Statesmostly older adultsalready have Congestive Heart Failure, and the number of people with Congestive Heart Failure keeps rising. About 550,000 people develop Congestive Heart Failure each year. This is because people are living longer and surviving heart attacks and other medical conditions that put them at risk for Congestive Heart Failure. People who have other types of heart and vessel disease are also at risk for Congestive Heart Failure. Risk factors for Congestive Heart Failure include --Previous heart --Coronary artery --High blood pressure --Irregular heartbeat --Heart valve disease (especially of the aortic --Cardiomyopathy (disease of the --Congenital heart defects (defects you --Alcohol and drug abuse What are the attacks disease (hypertension) (arrhythmia) and mitral valves) heart muscle) are born with) symptoms?

Symptoms can help doctors find out which side of your heart is not working properly. If the left side of your heart is not working properly (left-sided heart failure), blood and fluid back up into your lungs. You will feel short of breath, be very tired, and have a cough (especially at night). In some cases, patients may begin to cough up pinkish, blood-tinged sputum. If the right side of your heart is not working properly (right-sided heart failure), the slowed blood flow causes a buildup of fluid in your veins. Your feet, legs, and ankles will begin to swell. This swelling is called edema. Sometimes edema spreads to the lungs, liver, and stomach. Because of the fluid buildup, you may need to go to the bathroom more often, especially at night. Fluid buildup is also hard on your kidneys. It affects their ability to dispose of salt (sodium) and water, which can lead to kidney failure. Once Congestive Heart Failure is treated, the kidneys' function usually returns to normal.

Renal failure or kidney failure (formerly called renal insufficiency) describes a medical condition in which the kidneys fail to adequately filter toxins and waste products from the blood. The two forms are acute (acute kidney injury) and chronic (chronic kidney disease); a number of other diseases or health problems may cause either form of renal failure to occur. Renal failure is described as a decrease in glomerular filtration rate. Biochemically, renal failure is typically detected by an elevated serum creatinine level. Problems frequently encountered in kidney malfunction include abnormal fluid levels in the body, increased acid levels, abnormal levels of potassium, calcium, phosphate, and (in the longer term) anemia as well as delayed healing in broken bones. Depending on the cause, hematuria (blood loss in the urine) and proteinuria (protein loss in the urine) may occur. Long-term kidney problems have significant repercussions on other diseases, such as cardiovascular disease.

Types of CHF: Usually manifested by biventricular failure

One ventricle may precede the other One side may fail . the other side tries to compensate Prolonged strain . causes remaining side to fail

MOST COMMON FORM OF CHF: LEFT SIDED FAILURE SIGNS AND SYMPTOMS OF LEFT SIDED HEART FAILURE: Dyspnea - Because the impaired left ventricle cannot eject the increased circulating blood volume, the pressure in the pulmonary circulation increases, causing further shifting of fluid into the alveoli. The fluid-filled alveoli cannot exchange oxygen and carbon dioxide. Without sufficient oxygen, the patient experiences dyspnea and has difficulty getting enough sleep. Orthopnea, difficulty breathing when lying flat. They may need pillows to prop themselves up in bed, or they may sit in a chair and even sleep sitting up. Some patients have sudden attacks of dyspnea at night, a condition known as paroxysmal nocturnal dyspnea (PND). Fluid that accumulated in the dependent extremities during the day begins to be reabsorbed into the circulating blood volume when the patient lies down. Cough associated with left ventricular failure is initially dry and nonproductive. The cough may become moist over time. Large quantities of frothy sputum, which is sometimes pink (blood-tinged), may be produced, usually indicating severe pulmonary congestion (pulmonary edema). Crackles that do not clear with coughing are detected in the early phase of left ventricular failure. As the failure worsens and pulmonary congestion increases, crackles may be auscultated throughout all lung fields. At this point, oxygen saturation may decrease. Blood flow to the kidneys decreases, causing decreased perfusion and reduced urine output (oliguria). Renal perfusion pressure falls, which results in the release of renin from the kidney. Release of renin leads to aldosterone secretion and increased intravascular volume. However, when the patient is sleeping, the cardiac workload is decreased, P.951, improving renal perfusion, which may then lead to frequent urination at night (nocturia). As HF progresses, decreased CO may cause other symptoms. Decreased gastrointestinal perfusion causes altered digestion. Decreased brain perfusion causes dizziness, lightheadedness, confusion, restlessness, and anxiety due to decreased oxygenation and blood flow. As anxiety increases, so does dyspnea, increasing anxiety and creating a vicious cycle. Stimulation of the sympathetic system also causes the peripheral blood vessels to constrict, so the skin appears pale or ashen and feels cool and clammy.

Decreases in ejected ventricular volume cause the sympathetic nervous system to increase the heart rate (tachycardia), often causing the patient to complain of palpitations. The pulses become weak and thready. Without adequate CO, the body cannot respond to increased energy demands, and the patient becomes easily fatigued and has decreased activity tolerance. Fatigue also results from the 5

increased energy expended in breathing and the insomnia that results from respiratory distress, coughing, and nocturia. PULMONARY EDEMA: As the left ventricle's abilities are diminished, blood tends to pool and back-up behind it in the pulmonary (lung) circulation. This back-up is under increased pressure, as the right side of the heart is still pumping into this circulation. The result is fluid leakage into the lungs, a condition called pulmonary edema. Fluid retention in the body by the kidneys can also be a culprit in developing pulmonary edema. This situation translates into shortness of breath. The diagram below illustrates just how apparent this problem can develop in some patients: Pulmonary edema fluid accumulation in the lungs interfering with gas exchange in the alveoli, there is retrograde fluid accumulation in the left atrium and pulmonary vein, pulmonary capillaries and veins become engorged with blood, the lungs fill with fluid. Cor Pulmonale: Is a condition in which the heart is affected by lung damage. There is right ventricular enlargement secondary to malfunction of the lungs. pulmonary hypertension is present in cor pulmonale.

Heart failure is caused by any condition which reduces the efficiency of the myocardium, or heart muscle, through damage or overloading. As such, it can be caused by as diverse an array of conditions as myocardial infarction (in which the heart muscle is starved of oxygen and dies), hypertension (which increases the force of contraction needed to pump blood) and amyloidosis (in which protein is deposited in the heart muscle, causing it to stiffen). Over time these increases in workload will produce changes to the heart itself:

Reduced contractility, or force of contraction, due to overloading of the ventricle. In health, increased filling of the ventricle results in increased contractility (by the FrankStarling law of the heart) and thus a rise in cardiac output. In heart failure this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin filaments in over-stretched heart muscle. A reduced stroke volume, as a result of a failure of systole, diastole or both. Increased end systolic volume is usually caused by reduced contractility. Decreased end diastolic volume results from impaired ventricular filling as occurs when the compliance of the ventricle falls (i.e. when the walls stiffen). Reduced spare capacity. As the heart works harder to meet normal metabolic demands, the amount cardiac output can increase in times of increased oxygen demand (e.g. exercise) is reduced. This contributes to the exercise intolerance commonly seen in heart failure. This translates to the loss of one's cardiac reserve. The cardiac reserve refers to the ability of the heart to work harder during exercise or strenuous activity. Since the heart has to work harder to meet the normal metabolic demands, it is incapable of meeting the metabolic demands of the body during exercise. Increased heart rate, stimulated by increased sympathetic activity in order to maintain cardiac output. Initially, this helps compensate for heart failure by maintaining blood

pressure and perfusion, but places further strain on the myocardium, increasing coronary perfusion requirements, which can lead to worsening of ischemic heart disease. Sympathetic activity may also cause potentially fatal arrhythmias. Hypertrophy (an increase in physical size) of the myocardium, caused by the terminally differentiated heart muscle fibres increasing in size in an attempt to improve contractility. This may contribute to the increased stiffness and decreased ability to relax during diastole. Enlargement of the ventricles, contributing to the enlargement and spherical shape of the failing heart. The increase in ventricular volume also causes a reduction in stroke volume due to mechanical and contractile inefficiency.

The general effect is one of reduced cardiac output and increased strain on the heart. This increases the risk of cardiac arrest (specifically due to ventricular dysrhythmias), and reduces blood supply to the rest of the body. In chronic disease the reduced cardiac output causes a number of changes in the rest of the body, some of which are physiological compensations, some of which are part of the disease process:

Arterial blood pressure falls. This destimulates baroreceptors in the carotid sinus and aortic arch which link to the nucleus tractus solitarius. This center in the brain increases sympathetic activity, releasing catecholamines into the blood stream. Binding to alpha-1 receptors results in systemic arterial vasoconstriction. This helps restore blood pressure but also increases the total peripheral resistance, increasing the workload of the heart. Binding to beta-1 receptors in the myocardium increases the heart rate and make contractions more forceful, in an attempt to increase cardiac output. This also, however, increases the amount of work the heart has to perform. Increased sympathetic stimulation also causes the hypothalamus to secrete vasopressin (also known as antidiuretic hormone or ADH), which causes fluid retention at the kidneys. This increases the blood volume and blood pressure. Reduced perfusion (blood flow) to the kidneys stimulates the release of renin an enzyme which catalyses the production of the potent vasopressor angiotensin. Angiotensin and its metabolites cause further vasocontriction, and stimulate increased secretion of the steroid aldosterone from the adrenal glands. This promotes salt and fluid retention at the kidneys, also increasing the blood volume. The chronically high levels of circulating neuroendocrine hormones such as catecholamines, renin, angiotensin, and aldosterone affects the myocardium directly, causing structural remodelling of the heart over the long term. Many of these remodelling effects seem to be mediated by transforming growth factor beta (TGF-beta), which is a common downstream target of the signal transduction cascade initiated by catecholamines and angiotensin II, and also by epidermal growth factor (EGF), which is a target of the signaling pathway activated by aldosterone Reduced perfusion of skeletal muscle causes atrophy of the muscle fibres. This can result in weakness, increased fatigueability and decreased peak strength - all contributing to exercise intolerance.

The increased peripheral resistance and greater blood volume place further strain on the heart and accelerates the process of damage to the myocardium. Vasoconstriction and fluid retention produce an increased hydrostatic pressure in the capillaries. This shifts of the balance of forces in 7

favour of interstitial fluid formation as the increased pressure forces additional fluid out of the blood, into the tissue. This results in edema (fluid build-up) in the tissues. In right-sided heart failure this commonly starts in the ankles where venous pressure is high due to the effects of gravity (although if the patient is bed-ridden, fluid accumulation may begin in the sacral region.) It may also occur in the abdominal cavity, where the fluid build-up is called ascites. In left-sided heart failure edema can occur in the lungs - this is called cardiogenic pulmonary oedema. This reduces spare capacity for ventilation, causes stiffening of the lungs and reduces the efficiency of gas exchange by increasing the distance between the air and the blood. The consequences of this are shortness of breath, orthopnoea and paroxysmal nocturnal dyspnea. The symptoms of heart failure are largely determined by which side of the heart fails. The left side pumps blood into the systemic circulation, whilst the right side pumps blood into the pulmonary circulation. Whilst left-sided heart failure will reduce cardiac output to the systemic circulation, the initial symptoms often manifest due to effects on the pulmonary circulation. In systolic dysfunction, the ejection fraction is decreased, leaving an abnormally elevated volume of blood in the left ventricle. In diastolic dysfunction, end-diastolic ventricular pressure will be high. This increase in volume or pressure backs up to the left atrium and then to the pulmonary veins. Increased volume or pressure in the pulmonary veins impairs the normal drainage of the alveoli and favors the flow of fluid from the capillaries to the lung parenchyma, causing pulmonary edema. This impairs gas exchange. Thus, left-sided heart failure often presents with respiratory symptoms: shortness of breath, orthopnea and paroxysmal nocturnal dyspnea. In severe cardiomyopathy, the effects of decreased cardiac output and poor perfusion become more apparent, and patients will manifest with cold and clammy extremities, cyanosis, claudication, generalized weakness, dizziness, and syncope The resultant hypoxia caused by pulmonary edema causes vasoconstriction in the pulmonary circulation, which results in pulmonary hypertension. Since the right ventricle generates far lower pressures than the left ventricle (approximately 20 mmHg versus around 120 mmHg, respectively, in the healthy individual) but nonetheless generates cardiac output exactly equal to the left ventricle, this means that a small increase in pulmonary vascular resistance causes a large increase in amount of work the right ventricle must perform. However, the main mechanism by which leftsided heart failure causes right-sided heart failure is actually not well understood. Some theories invoke mechanisms that are mediated by neurohormonal activation. Mechanical effects may also contribute. As the left ventricle distends, the intraventricular septum bows into the right ventricle, decreasing the capacity of the right ventricle. Systolic dysfunction Heart failure caused by systolic dysfunction is more readily recognized. It can be simplistically described as failure of the pump function of the heart. It is characterized by a decreased ejection fraction (less than 45%). The strength of ventricular contraction is attenuated and inadequate for creating an adequate stroke volume, resulting in inadequate cardiac output. In general, this is caused by dysfunction or destruction of cardiac myocytes or their molecular components. In congenital diseases such as Duchenne muscular dystrophy, the molecular structure of individual myocytes is affected. Myocytes and their components can be damaged by inflammation (such as in myocarditis) or by infiltration (such as in amyloidosis). Toxins and pharmacological agents (such 8

as ethanol, cocaine, and amphetamines) cause intracellular damage and oxidative stress. The most common mechanism of damage is ischemia causing infarction and scar formation. After myocardial infarction, dead myocytes are replaced by scar tissue, deleteriously affecting the function of the myocardium. On echocardiogram, this is manifest by abnormal or absent wall motion. Because the ventricle is inadequately emptied, ventricular end-diastolic pressure and volumes increase. This is transmitted to the atrium. On the left side of the heart, the increased pressure is transmitted to the pulmonary vasculature, and the resultant hydrostatic pressure favors extravassation of fluid into the lung parenchyma, causing pulmonary edema. On the right side of the heart, the increased pressure is transmitted to the systemic venous circulation and systemic capillary beds, favoring extravassation of fluid into the tissues of target organs and extremities, resulting in dependent peripheral edema. Diastolic dysfunction Heart failure caused by diastolic dysfunction is generally described as the failure of the ventricle to adequately relax and typically denotes a stiffer ventricular wall. This causes inadequate filling of the ventricle, and therefore results in an inadequate stroke volume. The failure of ventricular relaxation also results in elevated end-diastolic pressures, and the end result is identical to the case of systolic dysfunction (pulmonary edema in left heart failure, peripheral edema in right heart failure.) Diastolic dysfunction can be caused by processes similar to those that cause systolic dysfunction, particularly causes that affect cardiac remodeling. Diastolic dysfunction may not manifest itself except in physiologic extremes if systolic function is preserved. The patient may be completely asymptomatic at rest. However, they are exquisitely sensitive to increases in heart rate, and sudden bouts of tachycardia (which can be caused simply by physiological responses to exertion, fever, or dehydration, or by pathological tachyarrhythmias such as atrial fibrillation with rapid ventricular response) may result in flash pulmonary edema. Adequate rate control (usually with a pharmacological agent that slows down AV conduction such as a calcium channel blocker or a beta-blocker) is therefore key to preventing decompensation. Left ventricular diastolic function can be determined through echocardiography by measurement of various parameters such as the E/A ratio (early-to-atrial left ventricular filling ratio), the E (early left ventricular filling) deceleration time, and the isovolumic relaxation time. It is impossible to make a diagnosis over the internet, but I can address some possibilities. All of these organs can interact with each other. Lung problems can affect heart function, even to the point of causing right-sided heart failure, also called cor pulmonale. Valve regurgitation can also affect cardiac function; mild regurgitation usually is not sufficient to cause problems alone, but would make other problems worse. Ventricular hypertrophy, over time, will also impair heart function. Right-sided heart failure will cause an enlarged liver, called for passive congestion of the liver. Liver problems can cause an enlarged spleen and fluid retention in the abdomen, which would be perceived as an enlarged abdomen. The liver enzymes are only mildly elevated, which can be due to the fatty liver or the passive congestion. The ferritin is only slightly elevated. There is a disease process called hemochromatosis which is due to iron overload and can affect liver and heart function, but the ferritin levels are typically much higher and associated with an elevated serum iron and percent saturation. A 9

mildly elevated ferritin can be due to liver disease, any inflammatory process, such as rheumatoid arthritis, or thyroid disease. The next step depends upon which specialists you have already seen. If you have not yet seen a Pulmonologist or a Cardiologist, that would be the next step. What is jugular vein distention? The jugular veins carry blood from the head to the superior vena cava (the main vein of the upper body), which empties into the heart. The external jugular vein is closest to the skin and can sometimes be seen as a rope-like bulge on the side of the neck. Bulging of the external jugular vein is known as jugular vein distention. The height of the bulge measured from the top of the clavicle, or collar bone, is an indirect indicator of the central venous pressure, the pressure in the right atrium (the heart chamber that receives blood returning from the body). Jugular vein distention is affected by the position of your body. If the height is greater than 3 to 4 centimeters when measured while you are in bed with your head elevated 45 degrees, this may signal vascular or heart disease. Smaller amounts of jugular vein distention can occur in people without heart or vascular disease. Increased blood volume, which can occur with heart failure, or anything that interferes with filling of the right atrium or movement of the blood into the right ventricle, can increase the central venous pressure and the amount of jugular vein distention. For example, jugular vein distention may be raised by a narrowing or blockage of the superior vena cava, which can interfere with blood return to the heart. It can also be caused by constrictive pericarditis (infection of the lining that surrounds the heart) and cardiac tamponade (filling of the sac around the heart with blood or other fluid), both of which restrict the volume of the heart. Right-sided heart failure is another cause of elevated jugular vein distention. Jugular vein distention can accompany serious vascular and heart conditions. Seek immediate medical care (call 911) for chest pain or pressure, shortness of breath, pale skin or pallor, bluish coloration of the lips or fingernails, profuse sweating, difficulty breathing or rapid breathing (tachypnea), rapid heart rate (tachycardia), increasing fatigue or weakness (loss of strength), or change in level of consciousness. If your jugular vein distention is persistent, worsens, or otherwise causes you concern, seek prompt medical care. Heart failure is an illness in which the pumping action of the heart becomes less and less powerful. When this happens, blood does not move efficiently through the circulatory system and starts to back up, increasing the pressure in the blood vessels and forcing fluid from the blood vessels into body tissues. Symptoms depend on which area of the body is most involved in the reduced pumping action.

When the left side of the heart (left ventricle) starts to fail, fluid collects in the lungs (pulmonary edema). This extra fluid in the lungs (pulmonary congestion) makes it more difficult for the airways to expand as a person

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inhales. Breathing becomes more difficult and the person may feel short of breath, particularly with activity or when lying down.

When the right side of the heart (right ventricle) starts to fail, fluid begins to collect in the feet and lower legs. Puffy leg swelling (edema) is a sign of right heart failure, especially if the edema is pitting edema. With pitting edema, a finger pressed on the swollen leg leaves an imprint. Non-pitting edema is not caused by heart failure.

As the right heart failure worsens, the upper legs swell and eventually the abdomen collects fluid (ascites). Weight gain accompanies the fluid retention and is a reliable measure of how much fluid is being retained.

Although heart failure is a serious medical condition, there are many causes and the outcome can vary from person to person. Heart failure may develop gradually over several years, or more quickly after a heart attack or a disease of the heart muscle. Congestive heart failure (CHF) is generally classified as systolic or diastolic heart failure and becomes progressively more common with increasing age. In addition, patients with risk factors for heart disease are more likely to develop congestive heart failure. Systolic heart failure: This condition occurs when the pumping action of the heart is reduced or weakened. A common clinical measurement is ejection fraction (EF). The ejection fraction is a calculation of how much blood is ejected out of the left ventricle (stroke volume) divided by the maximum volume remaining in the left ventricle at the end of diastole, or when the heart is relaxed after filling with blood. A normal ejection fraction is greater than 55%. Systolic heart failure is diagnosed when the ejection fraction has significantly decreased below the threshold of 55%. Diastolic heart failure: This condition occurs when the heart can contract normally but is stiff, or less compliant, when it is relaxing and filling with blood. The heart is unable to fill with blood properly, which produces backup into the lungs and heart failure symptoms. Diastolic heart failure is more common in patients older than 75 years of age, especially in patients with high blood pressure, and it is also more common in women. In diastolic heart failure, the ejection fraction is normal or increased. Heart failure affects 2% of the adult population. In the United States, nearly four million people have heart failure. Each year about 550,000 new cases are diagnosed. The condition is more common among African Americans than Caucasians.

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Heart failure affects 1% of people age 50 years or older, about 5% of those age 75 years or older, and 25% of those age 85 years or older. Heart failure is the most common reason for Medicare patients to be admitted to the hospital. As the number of elderly people continues to rise, often from the successful treatment of other types of heart disease, the number of people diagnosed with this condition will likely increase. The rate of death from heart failure is about 10% after one year. About half of those with congestive heart failure die within five years after their diagnosis. These statistics vary widely; a patient's exact diagnosis and response to therapy play a large role in patient survival. Any questions about diagnoses and therapy should be discussed with the treating physician. Advances in research are providing more options and improving outcomes for people with congestive heart failure.

Ventricular assist devices (VAD) help your heart pump blood from the main pumping chamber of your heart (the left ventricle) to the rest of your body. These pumps may be implanted in your body or connected to a pump outside your body. A ventricular assist device has three parts:

A pump. The pump weighs 1 to 2 pounds. It is placed in your belly if you will need it permanently, or it may also be used outside of your body when you are waiting for a permanent pump or a heart transplant. An electronic controller. The controller is like a small computer that controls how the pump works. Two batteries. The batteries are carried outside your body. They are connected to the pump with a cable that goes into your belly

You will need general anesthesia when your VAD is implanted. This will make you unconscious and unable to feel pain during the procedure. During surgery to implant the pump, the heart surgeon opens the middle of your chest with a surgical cut and then separates your breastbone. This allows the surgeon to reach your heart. Next, the surgeon will make space for the pump under your skin and tissue in the upper part of your belly wall. Then, the surgeon will place the pump in this space. A tube will connect the pump to your heart. Another tube will connect the pump to your aorta or one of your other major arteries. Another tube will be passed through your skin to connect the pump to the controller and batteries. The VAD will take blood from your left ventricle through the tube that leads to the pump. Then the device will pump the blood back out to one of your arteries and through your body. Surgery usually lasts 4 to 6 hours.

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You may need a VAD if you have severe heart failure that cannot be controlled with medicine or a special pacemaker. You may be on a waiting list for a heart transplant. Some patients who get a VAD are very ill and may already be on a heart-lung bypass machine. Not every patient with severe heart failure is a good candidate for this procedure A heart transplant is surgery to remove a person's diseased heart and replace it with a healthy heart from a deceased donor. Most heart transplants are done on patients who have end-stage heart failure. Heart failure is a condition in which the heart is damaged or weak. As a result, it can't pump enough blood to meet the body's needs. "End-stage" means the condition is so severe that all treatments, other than a heart transplant, have failed. What is coronary artery bypass graft (CABG) surgery? According to the American Heart Association 427,000 coronary artery bypass graft (CABG) surgeries were performed in the United States in 2004, making it one of the most commonly performed major operations. CABG surgery is advised for selected groups of patients with significant narrowings and blockages of the heart arteries (coronary artery disease). CABG surgery creates new routes around narrowed and blocked arteries, allowing sufficient blood flow to deliver oxygen and nutrients to the heart muscle. How does coronary artery disease develop? Coronary artery disease (CAD) occurs when atherosclerotic plaque (hardening of the arteries) builds up in the wall of the arteries that supply the heart. This plaque is primarily made of cholesterol. Plaque accumulation can be accelerated by smoking, high blood pressure, elevated cholesterol, and diabetes. Patients are also at higher risk for plaque development if they are older (greater than 45 years for men and 55 years for women), or if they have a positive family history for early heart artery disease. The atherosclerotic process causes significant narrowing in one or more coronary arteries. When coronary arteries narrow more than 50 to 70%, the blood supply beyond the plaque becomes inadequate to meet the increased oxygen demand during exercise. The heart muscle in the territory of these arteries becomes starved of oxygen (ischemic). Patients often experience chest pain (angina) when the blood oxygen supply cannot keep up with demand. Up to 25% of patients experience no chest pain at all despite documented lack of adequate blood and oxygen supply. These patients have "silent" angina, and have the same risk of heart attack as those with angina. When a blood clot (thrombus) forms on top of this plaque, the artery becomes completely blocked causing a heart attack. **If you have coronary artery disease (CAD), the arteries that supply blood and oxygen to the heart muscle become hardened and narrowed. If lifestyle changes and medicines don't help, your doctor may recommend coronary artery bypass surgery. 13

The surgery uses a piece of a vein from the leg or artery from the chest or wrist. The surgeon attaches this to the coronary artery above and below the narrowed area or blockage. This allows blood to bypass the blockage. Some people need more than one bypass. You may need bypass surgery for various reasons. Another procedure for CAD, angioplasty, may not have widened the artery enough. In some cases, the angioplasty tube can't reach the blockage. A bypass also can close again. This happens in more than 10 percent of bypass surgeries, usually after 10 or more years. Coronary angioplasty (AN-jee-oh-plas-tee) is a procedure used to open narrow or blocked coronary (heart) arteries. The procedure restores blood flow to the heart muscle. As you age, a waxy substance called plaque (plak) can build up inside your arteries. This condition is called atherosclerosis (ath-er-o-skler-O-sis). Atherosclerosis can affect any artery in the body. When atherosclerosis affects the coronary arteries, the condition is called coronary heart disease (CHD) or coronary artery disease. Over time, plaque can harden or rupture (break open). Hardened plaque narrows the coronary arteries and reduces the flow of oxygen-rich blood to the heart. This can cause chest pain or discomfort called angina (an-JI-nuh or AN-juh-nuh). If the plaque ruptures, a blood clot can form on its surface. A large blood clot can mostly or completely block blood flow through a coronary artery. This is the most common cause of a heart attack. Over time, ruptured plaque also hardens and narrows the coronary arteries. Angioplasty can restore blood flow to the heart. During the procedure, a thin, flexible catheter (tube) with a balloon at its tip is threaded through a blood vessel to the affected artery. Once in place, the balloon is inflated to compress the plaque against the artery wall. This restores blood flow through the artery. Doctors may use the procedure to improve symptoms of CHD, such as angina. The procedure also can reduce heart muscle damage caused by a heart attack.

If you have been diagnosed with heart failure, you should consider talking to your doctor about cardiac resynchronization therapy (CRT). CRT, which is sometimes referred to as "biventricular pacing," is a form of therapy for congestive heart failure caused by dilated cardiomyopathy. Several studies now document the remarkable benefits conferred by CRT on appropriately selected patients with heart failure. CRT uses uses a specialized pacemaker to re-coordinate the action of the right and left ventricles in patients with heart failure. In approximately 30% of patients with heart failure, an abnormality in the heart's electrical conducting system
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(called an "intraventricular conduction delay" or bundle branch block) causes the two ventricles to beat in an asynchronous fashion. That is, instead of beating simultaneously, the two ventricles beat slightly out of phase. This asynchrony greatly reduces the efficiency of the ventricles in patients with heart failure, whose hearts are already damaged. CRT re-coordinates the beating of the two ventricles by pacing both ventricles simultaneously. This differs from typical pacemakers, which pace only the right ventricle. When the work of the two ventricles is coordinated, the heart's efficiency increases, and the amount of work it takes for the heart to pump blood is reduced. Studies with CRT have demonstrated its ability to improve the symptoms, the exercise capacity, and the feeling of well-being of many patients with moderate to severe heart failure. Studies have also shown that CRT can improve both the anatomy and function of the heart - tending to reduce the size of the dilated left ventricle, and therefore improving the left ventricular ejection fraction. Perhaps most importantly, CRT can improve the survival of patients with heart failure.
INEFFECTIVE TISSUE PERFUSION NURSING INTERVENTIONS: Administer oxygen therapy per nasal cannula at 2-6 LPM as ordered.

Rationale: Oxygen therapy corrects hypoxemia and alleviates client's need for air. Semi Fowler's or High Fowler's position

Rationale: To promote greater ling expansion. Evaluate ABG analysis results

Rationale: Any alteration in the ABG components may indicate signs of respiratory failure. Auscultate lung fields at least every 4 hours for crackles and wheezes in dependent lung fields Rationale: Respiratory distress and presence of adventitious breath sounds are indicative of pulmonary congestion. Observe for increased rate of respirations

Rationale: It could be indicative of falling arterial pH. EXCESS FLUID VOLUME NURSING INTERVENTIONS: Administer diuretics as ordered.

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Rationale: Helps rid body fluids and sodium. Set an appropriate rate of fluid intake/infusion throughout 24 hour period.

Rationale: To prevent peaks/valleys in fluid level and thirst.

Weigh daily or on a regular schedule, as indicated.

Rationale: Provides a comparative baseline and evaluates the effectiveness of diuretic therapy when used. Record intake and output accurately.

Rationale: To determine fluid balance. Place in a semi-Fowler's position, as appropriate.

Rationale: To facilitate movement of diaphragm, thus improving respiratory effort. ACTIVITY INTOLERANCE NURSING INTERVENTIONS: Assist client with self - care activities as needed

Rationale: To conserve energy and protect the client from injury Keep supplies and personal articles within easy reach

Rationale: Articles within reach minimizes client's effort Provide a quiet environment and uninterrupted rest periods

Rationale: Restores energy needed for activity and cellular regeneration Encourage range of motion exercise such as Moving client's arms and legs as far as they can comfortably go in any direction

Rationale: A simple exercise can enhance circulation thus improving clients wellness Gradually increase client's level of activity if tolerated well

Rationale: To promote tolerance to certain activities Give client information that provides daily/weekly progress

Rationale: To sustain motivation

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