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  1. 1. III. IntroductionCongestive heart failureCongestive heart failure (CHF) is a condition in which the hearts function as apump is inadequate to deliver oxygen rich blood to the body. Congestive heartfailure can be caused by: 1. diseases that weaken the heart muscle, 2. diseases that cause stiffening of the heart muscles, or 3. diseases that increase oxygen demand by the body tissue beyond the capability of the heart to deliver adequate oxygen-rich blood.The heart has two atria (right atrium and left atrium) that make up the upperchambers of the heart, and two ventricles (left ventricle and right ventricle) thatmake up the lower chambers of the heart. The ventricles are muscular chambersthat pump blood when the muscles contract. The contraction of the ventriclemuscles is called systole.Many diseases can impair the pumping action of the ventricles. For example, themuscles of the ventricles can be weakened by heart attacks or infections(myocarditis). The diminished pumping ability of the ventricles due to muscleweakening is called systolic dysfunction. After each ventricular contraction(systole) the ventricle muscles need to relax to allow blood from the atria to fillthe ventricles. This relaxation of the ventricles is called diastole.Diseases such as hemochromatosis (iron overload) or amyloidosis can causestiffening of the heart muscle and impair the ventricles capacity to relax and fill;this is referred to as diastolic dysfunction. The most common cause of this islongstanding high blood pressure resulting in a thickened (hypertrophied) heart.Additionally, in some patients, although the pumping action and filling capacity ofthe heart may be normal, abnormally high oxygen demand by the bodys tissues(for example, with hyperthyroidism or anemia) may make it difficult for the heartto supply an adequate blood flow (called high output heart failure).
  2. 2. In some individuals one or more of these factors can be present to causecongestive heart failure. The remainder of this article will focus primarily oncongestive heart failure that is due to heart muscle weakness, systolicdysfunction.Congestive heart failure can affect many organs of the body. For example:• The weakened heart muscles may not be able to supply enough blood to the kidneys, which then begin to lose their normal ability to excrete salt (sodium) and water. This diminished kidney function can cause the body to retain more fluid.• The lungs may become congested with fluid (pulmonary edema) and the persons ability to exercise is decreased.• Fluid may likewise accumulate in the liver, thereby impairing its ability to rid the body of toxins and produce essential proteins.• The intestines may become less efficient in absorbing nutrients and medicines.• Fluid also may accumulate in the extremities, resulting in edema (swelling) of the ankles and feet.Eventually, untreated, worsening congestive heart failure will affect virtually everyorgan in the body.
  3. 3. Picture of the heart and valves, left and right ventricles, left and right atriaDespite the paucity of epidemiologic work on congestive heart failure (CHF), thesalient features of the natural course of cardiac failure are understood. Theestimated 1983 incidence of CHF in the United States was 214,000 men and184,000 women. The estimate of prevalence was 2.3 million persons, with aremarkable increase with advancing age and higher rates in men than women atall ages. Overt heart disease plus age are the principal determinants of theincidence of CHF. Nearly 90% of patients with CHF have systemic hypertensionor coronary heart disease, or both, as the antecedent underlying condition.Diabetes mellitus increases the risk of CHF at all ages, particularly in women andthose treated with insulin. The prognosis after diagnosis of CHF is grim and isrelated to the degree of myocardial dysfunction. The challenge is to developmore effective drugs not only for the management of overt CHF, but also for theprevention of its progression
  4. 4. Heart failure is the clinical endpoint for a number of diseases resulting inmyocardial dysfunction. Ischemic cardiomyopathies due to coronary arterydisease and dilated cardiomyopathies, either idiopathic or familial, make up mostcases. Many other diseases can also lead to end-stage heart failure. Theseinclude valvular, congenital, metabolic, and inflammatory disorders.In terms of the pathology, cardiac remodeling is characterized by myocytichypertrophy, chamber dilatation, and changes in the composition of the matrix.The fibrotic heart ultimately becomes somewhat spherical, and, subsequently, itloses efficiency as a pump. Therefore, an important goal is to identify andfavorably intervene before terminal myocardial remodeling begins.IV. Structural OrganizationAnatomical back groundThe heart is a muscular pump that contains four chambers: right atrium, leftatrium, right ventricle and left ventricle. The two small atria make up the top of
  5. 5. the heart, and the two large ventricles make up the bottom of the heart. The rightatrium pumps blood to the right ventricle, and the left atrium pumps blood to theleft ventricle. A wall, called the septum, separates the right atrium and rightventricle, from the left atrium and left ventricle.Blood flows through the heart in the following manner: • The right atrium receives oxygen-poor blood from the body, and then pumps the blood through the tricuspid valve and into the right ventricle. • The right ventricle pumps the blood through the pulmonic valve and to the lungs, where it picks up more oxygen. • The left atrium receives the oxygen-rich blood from the lungs, and then pumps the blood through the mitral valve and into the left ventricle. • The left ventricle pumps blood through the aortic valve and to the rest of the body. • The blood supplies oxygen to the body and the cycle starts again.Anatomy examples: • Normal circulation through the heart • The human heart • Cross-section of heart at the level of the atria • Cross-section of heart at the level of the ventricles • The heart sits inside the pericardium • The heart valvesCoronary ArteriesThe coronary arteries supply oxygen to the heart muscle.
  6. 6. The heart has three main coronary arteries: • Right coronary artery: supplies the right ventricle • Left coronary artery: supplies the left ventricle • Posterior circumflex artery: supplies the posterior aspect of both ventriclesAnatomy examples: • Coronary angiogram • Front view of the heart and coronary arteries • Back view of the heart and coronary arteriesCardiac Conduction SystemAn electrical impulse stimulates the muscle fibers in the heart to contract. Theimpulse spreads through the heart in a very organized manner, so that the atriacontract first, followed by the ventricles.The electrical impulse proceeds in the following manner: • The electrical impulse originates at the sinoatrial (SA) node, which is located in the wall of the right atrium. o The SA node is the hearts natural pacemaker: it regulates the heart rate. • The impulse proceeds through the atria, stimulating them to contract. • After the atria are stimulated to contract, the atrioventricular (AV) node slows the electrical impulse before it proceeds to the ventricles. This pause allows the ventricles to fill with blood before they contract. o The AV node is located between the atria and the ventricles. • After the pause, the impulse then proceeds through the ventricles, stimulating them to contract.
  7. 7. Anatomy examples: • The cardiac conduction system • EKG showing electrical activity of heart.V. Confimatory testDiagnosisPhysicians can often make a preliminary diagnosis of heart failure with only a medicalhistory and careful physical examination. An English study suggests, in fact, that the
  8. 8. condition may be under-diagnosed. The following signs along with a history of heartdisease strongly suggest heart failure:• Enlarged heart.• Irregular heart sounds.• Abnormal sounds in the lungs.• Swelling or tenderness of the liver.• Fluid retention.• Elevation of pressure in the veins of the neck.Confirming these findings definitely or determining the severity of the condition,however, is difficult. Further tests are usually needed.LaboratoryBoth blood and urine tests are used to check for malfunctions of the liver and kidneys andto detect signs of diabetes.Blood tests can also be used to evaluate the following:• Cholesterol and lipid levels.• Anemia.• Thyroid disease.Urine tests can also be used to assess:• Albumin. The presence of this protein in the urine is usually a sign of kidney disease, but even tiny amounts (microalbumin) signal an increased risk for heart failure in people with and without diabetes.VI. Sign, Symptoms and complicationSigns and SymptomsIrrespective of the etiology, the first manifestation of congestive heart failure(CHF) is usually tachycardia. An obvious exception to this finding occurs incongestive heart failure due to a primary bradyarrhythmia or complete heart
  9. 9. block. As the severity of congestive heart failure increases, signs of venouscongestion usually ensue. Left-sided heart failure is generally associated withsigns of pulmonary venous congestion, whereas right-sided heart failure isassociated with signs of systemic venous congestion. Marked failure of eitherventricle, however, can affect the function of the other, leading to systemic andpulmonary venous congestion. Later stages of congestive heart failure arecharacterized by signs and symptoms of low cardiac output. Generally,congestive heart failure with normal cardiac output is called compensatedcongestive heart failure, and congestive heart failure with inadequate cardiacoutput is considered decompensated.Signs of congestive heart failure vary with the age of the child.2 Signs ofpulmonary venous congestion in an infant generally include tachypnea,respiratory distress (retractions), grunting, and difficulty with feeding. Often,children with congestive heart failure have diaphoresis during feedings, which ispossibly related to a catecholamine surge that occurs when they are challengedwith eating while in respiratory distress.Right-sided venous congestion is characterized by hepatosplenomegaly and,less frequently, edema or ascites. Jugular venous distention is not a reliableindicator of systemic venous congestion in infants because the jugular veins aredifficult to observe. Also, the distance from the right atrium to the angle of the jawmay be no more than 8-10 cm, even when the individual is sitting upright.Uncompensated congestive heart failure in an infant primarily manifests asa failure to thrive. In severe cases, failure to thrive may be followed by signs ofrenal and hepatic failure.In older children, left-sided venous congestion causes tachypnea, respiratorydistress, and wheezing (cardiac asthma). Right-sided congestion may result inhepatosplenomegaly, jugular venous distention, edema, ascites, and/or pleuraleffusions. Uncompensated congestive heart failure in older children may havefatigue or lower-than-usual energy levels. Patients may complain of coolextremities, exercise intolerance, dizziness, or syncope.Clinical findings may include hypotension, cool extremities with poor peripheralperfusion, a thready pulse, and decreased urine output. Chemical evidence ofrenal and liver dysfunction may be present, as well as a diminished level of
  10. 10. consciousness. Children with uncompensated congestive heart failure,particularly older children, generally have a lower cardiac output than what mostexperienced clinicians would estimate on the basis of the clinical signs.Signs and symptoms of congestive heart failure include the following: • Tachycardia • Venous congestion o Right-sided  Hepatomegaly  Ascites  Pleural effusion  Edema  Jugular venous distension o Left-sided  Tachypnea  Retractions  Nasal flaring or grunting  Rales  Pulmonary edema • Low cardiac output o Fatigue or low energy o Pallor o Sweating o Cool extremities o Poor growth o Dizziness o Altered consciousness o SyncopeVII. TreatmentSurgical
  11. 11. Heart transplantationWhen progressive end-stage heart failure occurs despite maximal medicaltherapy, the criterion standard for therapy has been heart transplantation. SinceChristiaan Barnard performed the first orthotopic heart transplantation in 1967,the world has seen tremendous advancement in the field of cardiactransplantation.Compared with patients who receive only medical therapy, transplant recipientshave fewer rehospitalizations, marked functional improvements, enhancedquality of life, more gainful employment, and longer lives with 50% surviving to 10years.11 Heart transplantation is associated with a 1-year survival rate of 83%,which decreases in a linear manner by approximately 3.4% per year. Carefulselection of donors and recipients, as well as efforts to minimize potentialperioperative dangers (ischemic times, pulmonary hypertension, mechanicalsupport, cardiogenic shock), are critical to ensure good outcomes.The single greatest advancement in ensuring long-term function of the allograft isthe development of immunologic modulators. Pioneered by Dr Norman Shumwayat Stanford University, steroids and antipurine metabolites including azathioprineand mycophenolate mofetil (MMF) have been widely used.Central to the current immunosuppression regimens are calcineurin inhibitors,cyclosporine, and tacrolimus. These drugs inhibit cellular pathways responsiblefor the production of interleukin (IL)-2 and subsequent T-cell activation. Theyinhibit the nuclear translocation of cytoplasmic factors needed to bind to the IL-2gene promoter. Immunosuppressive regimens have evolved from cyclosporin toa predominant use of tacrolimus.Triple drug therapy consisting of steroids, calcineurin inhibitors, and MMF hasbecome standard initial immunotherapy after heart transplantation.12 Additionalagents, such as antithymocyte globulin, rapamycin, and IL-2 receptorantagonists, also have important roles in modern immunosuppression protocols.The Achilles heel in the long-term success of heart transplantation is thedevelopment of coronary graft atherosclerosis, the cardiac version of chronicrejection. Coronary graft atherosclerosis is uniquely different from typical
  12. 12. coronary artery disease in that it is diffuse and usually not amenable torevascularization. Furthermore, although heart transplantation is a feasiblesolution for patients with end-stage heart disease, its use is limited by aninadequate donor supply.In the United States, fewer than 2500 heart transplantation procedures areperformed each year.13 Each year, an estimated 10-20% of patients die whileawaiting a heart transplant. Of the 5 million people with heart failure,approximately 30,000-100,000 have such advanced disease that they wouldbenefit from transplantation or mechanical circulatory support.14 This disparitybetween the number of patients needing transplants and the availability of heartdonors has refocused efforts to find other ways to support the severely failingheart.VIII. Reference
  13. 13.