Diseases of the heart and circulatory system are the most common causes of death in industrialized countries. Few people escape having some damage to the heart and blood vessels in a lifetime.
Classifications of Heart Disease
There are many ways of classifying heart disease. The heart’s anatomy forms the basis for one grouping of heart pathology:
* Endocarditis means “inflammation of the lining of the heart.” Endocarditis may involve the lining of the chambers, but the term most commonly refers to inflammation of the endocardium on the valves and valvular disease.
* Myocarditis is inflammation of heart muscle.
* Pericarditis refers to inflammation of the serous membrane on the heart surface as well as that lining the pericardial sac. These inflammatory diseases are often caused by infection, but may also be secondary to other types of respiratory or systemic diseases.
Another classification of heart disease is based on causative factors:
* Congenital heart disease is a condition present at birth.
* Rheumatic heart disease originates with an attack of rheumatic fever in childhood or in youth.
* Coronary artery disease involves the walls of the blood vessels that supply the heart muscle.
* Heart failure is caused by deterioration of the heart tissues and is frequently the result of long-standing disorders, such as high blood pressure.
Congenital Heart Disease
Congenital heart diseases often are the result of defects in fetal development. Two of these disorders represent the abnormal persistence of structures that are part of the normal fetal circulation (Fig. 10-13 A). Because the lungs are not used until a child is born, the fetus has some adaptations that allow blood to bypass the lungs. The fetal heart has a small hole, the foramen ovale, in the septum between the right and left atria. This opening allows some blood to flow directly from the right atrium into the left atrium, thus bypassing the lungs. Failure of the foramen ovale to close is one cause of an abnormal opening known as an atrial septal defect (see Fig. 10-13 B). The ductus arteriosus in the fetus is a small blood vessel that connects the pulmonary artery and the aorta so that some blood headed toward the lungs will enter the aorta instead. The ductus arteriosus normally closes on its own once the lungs are in use. Persistence of the vessel after birth is described as patent (open) ductus arteriosus (see Fig. 10-13 C). The most common single congenital heart defect is a hole in the septum between the two ventricles, a disorder known as ventricular septal defect (see Fig. 10-13 D). In each of the above defects, part of the heart’s left side output goes back to the lungs instead of out to the body. A small defect remaining from the foramen ovale or a small patent ductus may cause no difficulty and is often not diagnosed until an adult is examined for other cardiac problems. More serious defects greatly increase the left ventricle’s work and may lead to heart failure. In addition, ventricular septal defect creates high blood pressure in the lungs, which damages lung tissue. Other congenital defects that tax the heart involve restriction of outward blood flow. Coarctation of the aorta is a localized narrowing of the aortic arch (see Fig. 10-13 E). Another example is obstruction or narrowing of the pulmonary trunk that prevents blood from passing in sufficient quantity from the right ventricle to the lungs. In many cases, several congenital heart defects occur together. The most common combination is that of four specific defects known as the tetralogy of Fallot. Socalled “blue babies” commonly have this disorder.
The blueness, or cyanosis, of the skin and mucous membranes is caused by a relative lack of oxygen. In recent years, it has become possible to remedy many congenital defects by heart surgery, one of the more spectacular advances in modern medicine. A patent ductus arteriosus may also respond to drug treatment. During fetal life, prostaglandins (hormones) keep the ductus arteriosus open. Drugs that inhibit prostaglandins can promote closing of the duct after birth.
Figure 10-13 Congenital heart defects. (A) Normal fetal heart showing the foramen ovale and ductus arteriosus. (B) Persistence of the foramen ovale results in an atrial septal defect. (C) Persistence of the ductus arteriosus (patent ductus arteriosus) forces blood back into the pulmonary artery. (D) A ventricular septal defect. (E) Coarctation of the aorta restricts outward blood flow in the aorta.
Rheumatic Heart Disease
A certain type of streptococcal infection, the type that causes “strep throat,” is indirectly responsible for rheumatic fever and rheumatic heart disease. The toxin produced by these streptococci causes a normal immune response. However, in some cases, the initial infection may be followed some 2 to 4 weeks later by rheumatic fever, a generalized inflammatory disorder with marked swelling of the joints. The antibodies formed to combat the toxin are believed to cause this disease. These antibodies may also attack the heart valves, producing a condition known as rheumatic endocarditis. The heart valves, particularly the mitral valve, become inflamed, and the normally flexible valve cusps thicken and harden. The mitral valve may not open sufficiently (mitral stenosis) to allow enough blood into the ventricle or may not close effectively, allowing blood to return to the left atrium (mitral regurgitation). Either condition interferes with blood flow from the left atrium into the left ventricle, causing pulmonary congestion, an important characteristic of mitral heart disease. The incidence of rheumatic heart disease has declined with antibiotic treatment of streptococcal infections. However, children who do not receive adequate diagnosis and treatment are subject to developing the disease.
Coronary Artery Disease
Like vessels elsewhere in the body, the coronary arteries that supply the heart muscle, can undergo degenerative changes with time. The lumen (space) inside the vessel may gradually narrow because of a progressive deposit of fatty material known as plaque in the lining of the vessels, usually the arteries.
This process, called atherosclerosis, causes thickening and hardening of the vessels with a loss of elasticity (Fig. 10-14). The athero part of the name means “gruel,” because of the porridge-like material that adheres to the vessel walls. The vessels’ narrowing leads to ischemia, a lack of blood supply to the areas fed by those arteries. Degenerative changes in the arterial wall also may cause the inside vascular surface to become roughened, promoting blood clot (thrombus) formation. (see Fig. 10-14 C).
Figure 10-14 Coronary atherosclerosis. (A) Fat deposits (plaque) narrow an artery, leading to ischemia (lack of blood supply). (B) Plaque causes blockage (occlusion) of a vessel. (C) Formation of a blood clot (thrombus) in a vessel leads to myocardial infarction (MI).
Myocardial Infarction In the heart, thrombus formation results in a life-threatening condition known as coronary thrombosis. Sudden occlusion, or closure, of a coronary vessel with complete obstruction of blood flow is commonly known as a heart attack. Because the area of tissue damaged in a heart attack is described as an infarct, the medical term for a heart attack is myocardial infarction (MI) (Fig. 10-15). The oxygen- deprived tissue will eventually undergo necrosis (death). The symptoms of MI commonly include the abrupt onset of severe, constricting chest pain that may radiate to the left arm, back, neck or jaw. Patients may experience shortness of breath, sweating, nausea, vomiting, or pain in the epigastric region, which can be mistaken for indigestion. They may feel weak, restless, or anxious and the skin may be pale, cool and moist. The outcome of a myocardial infarction depends largely on the extent and location of the damage. Many people die within the first hour after onset of symptoms, but prompt, aggressive treatment can improve outcomes. Medical personnel make immediate efforts to relieve chest pain, stabilize the heart rhythm, and reopen the blocked vessel. Complete and prolonged lack of blood to any part of the myocardium results in tissue necrosis and weakening of the heart wall.
Angina Pectoris Inadequate blood flow to the heart muscle causes a characteristic discomfort, called angina pectoris, felt in the region of the heart and in the left arm and shoulder. Angina pectoris may be accompanied by a feeling of suffocation and a general sensation of forthcoming doom. Coronary artery disease is a common cause of angina pectoris, although the condition has other causes as well.
Abnormalities of Heart Rhythm Coronary artery disease or myocardial infarction often results in an abnormal rhythm of the heartbeat, or arrhythmia. Extremely rapid but coordinated contractions, numbering up to 300 per minute, are described as flutter. An episode of rapid, wild, and uncoordinated heart muscle contractions is called fibrillation, which may involve the atria only or both the atria and the ventricles.
Ventricular fibrillation is a serious disorder because there is no effective heartbeat. It must be corrected by a defibrillator, a device that generates a strong electrical current to discharge all the cardiac muscle cells at once, allowing a normal rhythm to resume. An interruption of electric impulses in the heart’s conduction system is called heart block. The seriousness of this condition depends on how completely the impulses are blocked. It may result in independent beating of the chambers if the ventricles respond to a second pacemaker.
Figure 10-15 Myocardial infarction (MI).
Treatment of Heart Attacks The death rate for heart attacks is high when treatment is delayed. Initial treatment involves cardiopulmonary resuscitation (CPR) and defibrillation at the scene when needed. The American Heart Association is adding training in the use of the automated external defibrillator (AED) to the basic course in CPR. The AED detects fatal arrhythmia and automatically delivers the correct preprogrammed shock. Work is underway to place machines in shopping centers, sports venues, and other public settings. Prompt transport by paramedics who are able to monitor the heart and give emergency drugs helps people to survive and reach a hospital. The next step is to restore blood flow to the ischemic areas by administering thrombolytic drugs, which act to dissolve the clots blocking the coronary arteries. Therapy must be given promptly to prevent permanent heart muscle damage. In many cases, a pulmonary artery catheter (tube) is put in place to monitor cardiac function and response to medication.
Supportive care includes treatment of chest pain with intravenous (IV) morphine. Healthcare workers monitor heart rhythm and give medications to maintain a functional rhythm. Oxygen is given to improve heart muscle function. Some patients require surgery, such as angioplasty to reopen vessels or a vascular graft to bypass damaged vessels; others may need an artificial pacemaker to maintain a normal heart rhythm. Recovery from a heart attack and resumption of a normal lifestyle is often possible if the patient follows his or her prescribed drug therapy plan and takes steps to reduce cardiac risk factors.
Heart failure is a condition in which the heart is unable to pump sufficient blood to supply the tissues with oxygen and nutrients. The heart’s chambers enlarge to contain more blood than the stretched fibers are able to pump. Blood backs up into the lungs, increasing blood pressure in the lungs. The ventricular muscles do not get enough blood, decreasing their ability to contract. Additional mechanisms cause the retention of fluid, leading to the name congestive heart failure (CHF). In an attempt to increase blood flow, the nervous system increases contraction of smooth muscle in the blood vessels, increasing blood pressure. Soon there is an accumulation of fluids in the lungs, liver, abdomen, and legs. People can live with compensated heart failure by attention to diet, drug therapy, and a balance of activity and rest.