Alterations in the Cardiovascular System 3

Two types of coronary heart disease are?
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Terms in this set (50)
Four anginal characteristics that increase risk for myocardial infarction.Angina that occurs at rest. Is of a new onset. Increased intensity. Increased duration.Silent Myocardial IschemiaAbsence of anginal pain. Diabetes mellitus is often associated.Variant AnginaCoronary artery spasms cause this type of angina. Usually occurs during rest or with minimal exercise and frequently occurs nocturnally.Unstable anginaPersistent and severe. Associated with rest or minimal activity. Lasts longer than twenty minutes if not treated. Has been present for one month or longer. Unstable plaque associated.Acute Myocardial InfarctionKnown as a heart attack. Characterized by ischemic death of myocardial tissue. Area of attack is determined by coronary artery.Other symptoms of M.I.Gastrointestinal complaints, nausea, vomitting, epigastric distress, fatigue and weakness. Skin is often pale, cool and moist. Hypotension and lowered cardiac output. Death within one hour of onset.Major characteristics of plaques for an M.I.Size of lipid rich core. Lack of stabilizing smooth muscle cells. Presence of inflammation with plaque breakdown. Stability and thickness of the fibrous cap.Plaque disruptionLipid core provides a stimulus for platelet aggregation and thrombus formation.Transmural infarctionInvolves the full thickness of the ventricular wall and most commonly occur when there is obstruction of a single artery.Subendothelial infarctionInvolves the inner one third to one half of the ventricular wall and occur more frequently in presence of severely narrowed arteries.How quickly after MI occurs is there loss of contractible function?60 seconds after onset.How quickly does irreversible myocardial cell death occur with severe ischemia?Occurs after twenty to forty minutes of severe ischemia.Necrotic ZoneAbsolute lack of blood flowZone of Injured CellsSome of which will recoverOuter ZoneCells are ischemic and can be salvaged in blood flow can be re-established.What happens to the area of necrosis 2 to 3 days after infarction?Acute inflammatory response develops. White blood cells increase. Neutrophils increase. Temperature increases.What happens to the area of necrosis 3-7 days after infarction?Center of infarcted area is soft and yellow. Rupture of ventricle interventricle septum, or the valve structure usually occurs at this time.How quickly is necrotic tissue replaced?By the 7th week. Replaced by scar tissue. Scar tissue lacks the ability to contract and initiate action potentials.Heart failureFailure of heart to pump appropriately.Cardiac reserveAbility of the heart to increase it's output during increased activity. There is a large cardiac reserve in athletes and a small cardiac reserve in people with heart attacks.High output heart failureUncommon type of heart failure that is caused by an excessive need for cardiac output. Can be caused by severe anemia.Low output heart failureDisorders that impair the pumping ability of the heart. Ischemic heart disease and cardiomyopathy.Right sided heart failure.Major clinical feature is that pulmonary congestion is minimal but the engorgement of the systemic and hepatic venous systems is pronounced.Right sided heart failure is usually caused by?Left sided heart failure, in which an increase in pulmonary blood volume eventually produces an increase burden on the right side.cor pulmonale means?When the right heart failure occurs in response to chronic pulmonary disease.Describe edema associated with right sided heart failure.Peripheral edema in the lower extremities when the person's upright and in the area over the sacrum when the individual is supine.Right heart failure causes congestion of the?The viscera. Organs associated are the liver, spleen, G.I. tract, and sometimes the jugular veins.Left sided heart failureImpairment of left ventricular function. There is a decrease in ejection of blood into the systemic circulation, an increase in left ventricular and left atrial end-diastolic pressures, and congestion of the pulmonary circulation.Pulmonary edema often occurs at night. why?The person has been reclining for some time and the gravitational forces have been removed from the circulatory system.Pulmonary edemaLife threatening condition in which capillary fluid moves into the alveoli. The accumulated fluid in the alveoli and airways causes lung stiffness, impairs lung expansion, and impairs gas exchange. This results in the hemoglobin leaving the lungs without being fully oxygenated.Properties of right sided heart failureAbdominal discomfort and anorexia. Ascites. Fatigue. Hepatomegaly, enlarged liver. Jugular vein distension. Swollen ankles.Properties of left sided heart failureAcute pulmonary edema. Fatigue. Dyspnea.Myocardial hypertrophyLong term compensatory mechanism. Starts early on. Cardiac muscle responds to increase in work demands by hypertophy. Hypertrophy increased contractile ability at first. Eventually results in thinning of ventricular wall thickness and loss of contractile ability.Heart valvesFunction in promoting directional flow of blood through the chambers of the heart. Valves that are easily affected are the mitral and aortic valves. Dysfunction to valves can be caused by congenital disorders, trauma, ischemic changes, inflammation.StenosisNarrowing of valve opening. Failure of leaflets to open correctly. Significant stenosis causes increase resistance to blood flow to occur.Stenosis can lead to...Distention of chamber that empties through valve. Increased work load of chamber that empties through valve. Impaired filling of chamber that is to receive blood through valve.Heart valve incompetence or regurgitant.Backward flow of blood when valve closed. Blood flow back into left ventricle when aortic valve affected. Blood flow back into left atrium when mitral valve affected.Mitral valve regurgitationIncomplete closure of mitral valve. Some blood moves into left ventricle, and some blood flows back into left atrium. Occurs due to rheumatic heart disease most often. Well tolerated, can be asymptomatic even if severe. Can lead to increased left atrial pressure and eventual pulmonary congestion.Aortic valve stenosisaortic valve between left ventricle and aorta. Results in increased resistance to ejection of blood into aorta. Increases work of left ventricle, blood ejected into systemic circulation drops. Caused by rheumatic fever most commonly. Must be one fourth of normal before critical impact on cardiac function, eventual drop in cardiac output.Aortic valve regurgitationAllows blood to flow back from aorta into left ventricle. Left ventricle enlarges, accommodates blood flowing from lungs and blood backflow. Cause by rheumatic fever most commonly. Asymptomatic until late. Eventual failure of left ventricle due to straining.