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NursyDaisy
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146040
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23 Notes
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2012-04-30 13:57:59
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Pathophysiology
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Alterations of Cardiovascular Function
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  1. Disease of the Arteries and Veins
    • Varicosities are areas of veins in which blood has pooled, usually in the saphenous veins. Varicosities may be caused by damaged valves as a result of trauma to the valve or by chronic venous distention involving gravity and venous constriction.
    • Chronic venous insufficiency is inadequate venous return over a long period of time that causes pathologic ischemic changes in the vasculature, skin, and supporting tissues.
    • Venous stasis ulcers follow the development of chronic venous insufficiency and probably develop as a result of the borderline metabolic state of the cells in the affected extremities.
    • Deep venous thrombosis results from stasis of blood flow, endothelial damage or Hypercoagulability. The most serious complication of deep venous thrombosis is pulmonary embolism.
    • Superior vena cava syndrome is a progressive occlusion of the superior vena cava that leads to venous distention in the upper extremities and head. Because this syndrome is usually caused by bronchogenic cancer, it is generally considered an oncologic emergency rather than a vascular emergency.
    • Hypertension is the elevation of systemic arterial blood pressure resulting from increases in cardiac output, total peripheral resistance, or both.
    • Hypertension can be primary, without a known cause, or secondary, caused by an underlying disease.
    • The risk factors for hypertension include a positive family history; male gender; advancing age; black race; obesity; high sodium intake; low magnesium, potassium or calcium intake; diabetes mellitus; cigarette smoking; and heavy alcohol consumption.
    • The exact cause of primary hypertension is unknown, although several hypotheses are proposed, including overactivity of the sympathetic nervous system; overactivity of the renin-angiotensin-aldosterone system; sodium and water retention by the kidneys; hormonal inhibition of sodium-potassium transport across cell walls; and complex interactions involving insulin resistance, inflammation, and endothelial function.
    • Clinical manifestations of hypertension result from damage of organs and tissues outside the vascular system. These include heart disease, renal disease, central nervous system problems, and musculoskeletal dysfunction.
    • Hypertension is managed with both pharmacologic and nonpharmacologic methods.
    • Orthostatic hypotension is a drop in blood pressure that occurs on standing. The compensatory vasoconstriction response to standing is replaced by a marked vasodilation and blood pooling in the muscle vasculature.
    • Orthostatic hypotension may be acute or chronic. The acute form is caused by a delay in the normal regulatory mechanisms. The chronic forms are secondary to a specific disease or are idiopathic in nature.
    • The clinical manifestations of orthostatic hypotension include fainting and may involve cardiovascular symptoms, as well as impotence and bowel and bladder dysfunction.
    • An aneurysm is a localized dilation of a vessel wall, to which the aorta is particularly susceptible.
    • A thrombus is a clot that remains attached to a vascular wall. Arteriosclerosis can generate thrombus formation through roughening of the intima that activates the clotting cascade. Thrombus formation may be discrete or diffuse.
    • An embolus is a mobile aggregate of a variety of substances that occludes the vasculature. Sources of emboli include clots, air, amniotic fluid, bacteria, fat, and foreign matter. These emboli cause ischemia and necrosis when a vessel is totally blocked.
    • The most common source of arterial thrombotic emboli is the heart as a result of mitral and aortic valvular disease and atrial fibrillation, followed by myxomas. Tissues affected include the lower extremities, the brain, and the heart.
    • Emboli to the central organs cause tissue death in lungs, kidneys, and mesentery.
    • The generation of air emboli requires a connection between the vascular compartment and a source of air.
    • Amniotic fluid may be forced into the bloodstream and generate an embolus during labor and childbirth.
    • Aggregates of bacteria in the vasculature may be large enough to form an embolus.
    • Fat emboli are caused mainly by trauma to the long bones, either through defective fat metabolism after trauma or through the release of fatty globules from bone marrow exposed by fracture.
    • The introduction of foreign matter into the vasculature can occur with trauma and also can occur in a hospital setting in which intravenous and intrarterial lines are being used.
    • Vasospastic disorders include Raynaud disease, involving arterioles of the extremities; Prinzmetal angina, involving coronary arteries; and Buerger disease, involving arteries of the hands and feet.
    • Arteriosclerosis is a thickening and hardening of the arteries, involving the intimal layer and leading to hypertension. It seems to be a part of the normal aging process, but it is a disease state when it occurs to the point of symptom development.
    • Arteriosclerosis raises the systolic pressure by decreasing arterial distensibility and lumen diameter.
    • Atherosclerosis is a form of arteriosclerosis and is the leading contributor to coronary artery disease (CAD) and cerebrovascular disease (CVD).
    • Atherosclerosis is an inflammatory disease that beings with endothelial injury (smoking, hypertension, diabetes [insulin resistance], hyperhomocysteinemia, dyslipidemia, etc.) and progresses through several stages to become a fibrotic plaque.
    • Once a plaque has formed, it can rupture, resulting in clot formation and instability and vasoconstriction leading to obstruction of the lumen and inadequate oxygen delivery to tissues.
    • Peripheral artery disease is the result of atherosclerotic plaque formation in the arteries that supply the extremities, and it causes pain and ischemic changes in the nerves, muscles, and skin of the limb.
    • Coronary artery disease (CAD) is almost always the result of atherosclerosis that gradually narrows the coronary arteries or that ruptures and causes sudden thrombus formation and myocardial ischemia and even infarction. Many risk factors contribute to the onset and escalation of CAD, including dyslipidemia, smoking, hypertension, diabetes mellitus (insulin resistance), advancing age, obesity, sedentary lifestyle, psychosocial factors, hyperhomocysteinemia, and heavy consumption of alcohol.
    • The three risk factors most predictive of CAD are hypercholesterolemia, cigarette smoking, and hypertension.
    • Ischemic heart disease is most commonly the result of coronary artery disease and the resultant decrease in myocardial blood supply.
    • Angina pectoris is chest pain caused by myocardial ischemia.
    • Therapeutic interventions for CAD include use of vasodilators and medications to reduce cardiac workload (e.g., beta-blockers), as well as surgical procedures.
    • Atherosclerotic plaque progression can be gradual but sudden coronary obstruction due to thrombus formation cases the acute coronary syndromes. These include unstable angina and myocardial infarction.
    • Unstable angina results in reversible myocardial ischemia.
    • Myocardial infarction is caused by prolonged, unrelieved ischemia that interrupts blood supply to the myocardium. After about 20 minutes of myocardial ischemia, irreversible hypoxic injury causes cellular death and tissue necrosis.
    • Myocardial infarction is clinically classified as non-STEMI or STEMI based on electrocardiographic findings which suggest the extent of myocardial damage (subendocardial versus transmural).
    • An increase in plasma enzyme levels is used to diagnose the occurrence of myocardial infarction and indicate its severity. Elevations of the isoenzymes creatine kinas (CK-MB), troponins, and lactic dehydrogenase (LDH-1) are most predictive of a myocardial infarction.
    • Treatment of a myocardial infarction includes revascularization (thrombolytics or PCI), antithrombotics, ACE inhibitors, and beta-blockers. Pain relief and fluid management also are key components of care. Dysrhythmias and cardiac failure are the most common complications of acute myocardial infarction.
  2. Disorders of the Heart Wall
    • Inflammation of the pericardium, or pericarditis, may result from several sources (infection, drug therapy, tumors). Pericarditis presents with symptoms that are physically troublesome, but in and of themselves they are not life threatening.
    • Fluid may collect within the pericardial sac (pericardial effusion). Cardiac function may be severely impaired if the accumulation of fluid occurs rapidly and involves a large volume.
    • Cardiomyopathies are a diverse group of primary myocardial disorders that are usually the result of remodeling, neurohumoral responses, and hypertension. The cardiomyopathies are categorized as dilated (congestive), restrictive (rigid and noncompliant), and hypertrophic (asymmetric). The size of the cardiac muscle walls and chambers may increase or decrease depending on the type of cardiomyopathy, thereby altering contractile activity.
    • The hemodynamic integrity of the cardiovascular system depends to a great extent on properly functioning cardiac valves. Congenital or acquired disorders that result in stenosis, incompetence, or both can structurally alter the valves.
    • Characteristic heart sounds, cardiac murmurs, and systemic complaints assist in determined which valve is abnormal. If severely compromised function exists, a prosthetic heart valve may be surgically implanted to replace the faulty one.
    • Mitral valve prolapse (MVP) is a common finding, especially in young women. Although not grossly abnormal, the mitral valve leaflets do not position themselves properly during systole, Mitral valve prolapse may be a complete asymptomatic condition or can result in unpredictable symptoms. Afflicted valves are at greater risk for developing infective endocarditis.
    • Rheumatic fever is an inflammatory disease that results from a delayed immune response to a streptococcal infection in genetically predisposed individuals. The disorder usually resolves without seqeulae if treated early.
    • Severe or untreated cases of rheumatic fever may progress to rheumatic heart disease, a potentially disabling cardiovascular disorder.
    • Infective endocarditis is a general term for infection and inflammation of the endocardium, especially the cardiac valves. The most common cause of infective viridians streptococcus. In the mildest cases, valvular function may be slightly impaired by vegetations that collect on the valve leaflets. If left unchecked, severe valve abnormalities, chronic bacteremia, and systemic emboli may occur as vegetations break off the valve surface and travel through the bloodstream. Antibiotic therapy can limit the extension of this disease.
    • Human immunodeficiency virus (HIV) is associated with cardiac abnormalities, including myocarditis, endocarditis, pericarditis, and cardiomyopathy. Left heart failure is the most common clinical manifestation.
  3. Manifestations of Heart Disease
    • A dysrhythmia (arrhythmia) is a disturbance of heart rhythm. Dysrhythmias range in severity from occasional missed beats or rapid beats to disturbances that impair myocardial contractility and are life threatening.
    • Dysrhythmias can occur because of an abnormal rate or impulse generation or the abnormal conduction of impulses.
    • Heart failure is an inability of the heart to supply the metabolism with adequate circulatory volume and pressure.
    • Right ventricular failure is usually the result of chronic pulmonary hypertension caused by left heart failure or chronic hypoxic lung disease.
    • Left heart failure (congestive heart failure) can be divided into systolic and diastolic heart failure.
    • The most common causes of left ventricular failure are myocardial infarction, fluid overload, hypertension, or valvular disease.
    • Systolic heart failure is caused by increased preload, decreased contractility, or increased afterload. These processes result in an increased left ventricular end-diastolic pressure that results in increased pulmonary venous pressures and pulmonary edema.
    • In addition to the hemodynamic changes of left ventricular failure, there is a neuroendocrine response that tends to exacerbate and perpetuate the condition.
    • The neuroendocrine mediators of congestive heart failure (CHF) include the sympathetic nervous system and the renin-angiotensin-aldosterone system; thus diuretics, beta-blockers, and angiotensin-converting enzyme (ACE) inhibitors are important components of the pharmacologic therapy.
    • Diastolic heart failure is a clinical syndrome characterized by the symptoms and signs of heart failure, a preserved ejection fraction, and abnormal diastolic function.
    • Diastolic dysfunction means that the left ventricular end-diastolic pressure is increased, even if volume and cardiac output are normal.
  4. Shock
    • Shock is a widespread impairment of cellular metabolism involving positive feedback loops that places the individual on a downward physiologic spiral leading to multiple organ dysfunction syndrome.
    • Types of shock are carcinogenic, Hypovolemic, neurogenic, anaphylactic, and septic. Multiple organ dysfunction syndrome can develop from all types of shock.
    • The final common pathway in all types of shock is impaired cellular metabolism – cells switch from aerobic to anaerobic metabolism. Energy stores drop, and cellular mechanisms relative to membrane permeability, action potentials, and lysozyme release fail.
    • Anaerobic metabolism results in activation of the inflammatory response, decreased circulatory volume, and decreasing pH.
    • Impaired cellular metabolism results in cellular inability to use glucose because of impaired glucose intake, resulting in a shift to glycogenolysis, gluconeogenesis, and lipolysis for fuel generation.
    • Glycogenolysis is effective for about 10 hours. Gluconeogenesis results in the use of proteins necessary for structure, function, repair, and replication that leads to more impaired cellular metabolism.
    • Gluconeogenesis contributes to lactic acid, uric acid, and ammonia buildup, interstitial edema, and impairment of the immune system, as well as general muscle weakness leading to decreased respiratory function and cardiac output.
    • Cardiogenic shock is decreased cardiac output, tissue hypoxia, and the presence of adequate intravascular volume.
    • Hypovolemic shock is caused by loss of blood or fluid in large amounts. The use of compensatory mechanisms may be vigorous, but tissue perfusion ultimately decreases and results in impaired cellular metabolism.
    • Neurogenic shock results from massive vasodilation, causing a relative hypovolemia, even though cardiac output may be high, and results in impaired cellular metabolism.
    • Anaphylactic shock is caused by physiologic recognition of a foreign substance. The inflammatory response is triggered, and a massive vasodilation with fluid shift into the interstitium follows. The relative hypovolemia leads to impaired cellular metabolism.
    • Septic shock begins with impaired cellular metabolism caused by uncontrolled septicemia. The infecting agent triggers the inflammatory and immune responses. This inflammatory response is accompanied by widespread changes in tissue and cellular function.
    • Multiple organ dysfunction syndrome (MODS) is the progressive failure of two or more organ systems after a severe illness or injury. It can be triggered by chronic inflammation, necrotic tissue, severe trauma, burns, adult respiratory distress syndrome, acute pancreatitis, and other sever injuries.
    • MODS involves the stress response; changes in the vascular endothelium resulting in microvascular coagulation; release of complement, coagulation, and kinin proteins; and numerous inflammatory processes. Consequences of all these mediators are a misdistribution of blood flow, hypermetabolism, hypoxic injury, and myocardial depression.
    • Clinical manifestations of MODS include inflammation, tissue hypoxia, and hypermetabolism. All organs can be affected including the kidney, lung, liver, gastrointestinal tract and central nervous system.

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