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200 Cards in this Set
- Front
- Back
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What % of children are born with congenital defects?
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.8%
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In what weeks of gestation is the heart at risk?
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2-8
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What are the three categories of heart defects?
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abnorm septation
abnorm blood vessels abnorm connections between chambers and blood vessels |
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What is the most common cardiac congenital defect?
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ventricular septal defect
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What diverts blood from the pulmonary circulation into the aorta?
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ductus arteriosus
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What kind of pressure is in the fetal pulmonary system?
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high
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What kind of pressure is in the fetal aorta?
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low
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How does peripheral vascular resistance change after birth?
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increases
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What closes the foramen ovale?
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fall in right atrial pressure, increased left atrial pressure,
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What two shunts connect the pulmonary and systemic circulation in a fetus?
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foramen ovale
ductus arteriosus |
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When does the ductus arteriosus close after birth?
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24-48 hours
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Which atrium has more trabeculation?
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right
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What separates the trabeculated from the smooth part of the right atrium?
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crista terminalis
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Where are ostium secundum defects?
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in the foramen ovale region
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Where are ostium primum defects?
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lower midseptum
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What is the most common ASD?
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ostium secundum
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Where are sinus venosum defects?
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proximal atrial septum, adjacent to vena cava
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What happens with persistent left to right shunt?
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pulmonary hypertension
can reverse the shunt cause cyanosis paradoxical embolization |
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What is paradoxical embolization?
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passage of embollus from right side of the heart to systemic circulation
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How big are osteum secundum defects?
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usually larger than 2 cm
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What are symptoms of osteum secundum in childhood?
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little to none
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What are the adult symptoms of osteum secundum?
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exertional dyspnea and fatigue
exertional cyanosis atrial fibrillation |
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What does exertional cyanosis occur?
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severe pulmonary hypertension, approaches systemic pressure
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Life expectancy of osteum secundum without surgery?
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40
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When do you fix an osteum secundum defect?
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between 2-5 years
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What are the symptoms of osteum primum?
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increased pulmonary blood flow and related effects
respiratory infections atrial fibrillation, heart block |
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Which ASD has a higher mortality?
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osteum primum
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Where do VSDs usually occur?
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membranous septum in preaortic area
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Where do perimembranous defects occur?
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membranous septum in preaortic area
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Where are muscular septal defects?
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below membranous septum of ventricle
often multiple |
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What are the pathological features of a VSD?
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normal pulmonary vascular resistance, but pulmonary artery pressure rises, pulmonary hypertension
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What are the clinical features of a VSD with pulmonary hypertension?
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exertional dyspnea and fatigue
respiratory infections CHF |
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What is Eisenmenger's complex?
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systemic pressure in the right ventricle
arterial unsaturation |
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What happens if there's systemic pressure in the right ventricle?
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breathlessness, fatigue, exertional chest pain
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What does a VSD sound like?
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loud, holosystolic murmer in fourth interspace
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How do you treat small VSDs?
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good dental hygiene to prevent endocarditis
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When do you operate on large VSDs?
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3-12 months
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What is an atrioventricular defect associated with?
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septal defect at the base of the heart
ostium primum and basal ventricular septal defect |
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What are the pathologic features of an atrioventricular defect?
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left to right shunt at both atria and ventricles
mitral and tricuspid regurgitation volume overload, pulmonary hypertension |
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When do symptoms of an atrioventricular defect start showing up?
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infancy
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What kind of symptoms do babies with an atrioventricular defect have?
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increased pulmonary blood flow
cardiac failure failure to thrive respiratory infections |
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How old do people with an AV defect live until?
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before 15 without surgery
mean age 2 |
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What are the chief causes of death in infancy in AV defect?
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heart failure and pneumonia
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How do you repair an AV defect?
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divide common AV valve into mitral and tricuspid, closing atrial and ventricular defects with a patch
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What happens in truncus arteriosus?
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single great vessel leaves the base of the heart through a single semilunar valve
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What happens in Type I Truncus Arteriosus?
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right and left pulmonary arteries arise from a common pulmonary artery, that arises from the truncus
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What happens in Type II Truncus Arteriosus?
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right and left pulmonary arteries both arise from the common truncus close to one another
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What is the most common type of Truncus Arteriosus?
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Type I
right and left pulmonary arteries arise from a common pulmonary artery, that arises from the truncus |
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What happens in Type III Truncus Arteriosus?
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right and left pulmonary arteries arise separately from opposite sides of the common truncus
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What happens in Type IV Truncus Arteriosus?
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Not actually a type of truncus
right and left pulmonary arteries arise from patent ductus from descending aorta actually a form of pulmonary atresia with VSD |
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What accompanies a Truncus Arteriosus?
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VSD
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What do the clinical features of a Truncus Arteriosus depend upon?
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location and size of pulmonary arteries
whether the truncal valve is competent or not |
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How does the location and size of pulmonary arteries change the clinical outcome in Truncus Arteriosus?
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changes magnitude of blood flow into the lungs
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What happens if you have Truncus Arteriosus and hypoplastic pulmonary arteries?
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severe cyanosis
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What happens in Truncus Arteriosus with sizable pulmonary arteries and low pulmonary vascular resistance?
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high blood flow into the lungs, volume overload of the left heart chambers, CHF
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What is the important difference between Truncus Arteriosus and other left to right lesions?
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shunting from aorta to pulmonary arteries, even during diastole
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What does shunting from aorta to pulmonary arteries do in Truncus Arteriosus?
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decreased coronary artery flow, ischemia, death
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How do you fix Truncus Arteriosus?
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surgical closure of VSD, conduit from right ventricle to pulmonary arteries
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Why do patients with Truncus Arteriosus die young?
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CHF, respiratory infections
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What are the components of hypoplastic left heart syndrome?
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aortic valve atresia
mitral valve atresia mitral valve stenosis hypoplasia of the aortic arch atresia of the aortic arch |
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What causes hypoplasia of a cardiac vessel?
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malformations, impeded growth
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What causes atresia of a cardiac vessel?
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malformations or impeded growth
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What are the types of aortic valve atresia?
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with mitral valve hypoplasia
with mitral valve atresia |
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What is the most severe form of hypoplastic left heart syndrome?
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aortic orifice is covered by a membrane, ascending aorta is hypoplastic, small left ventricle with endocardial fibroelastis, dilated right atrium, patent foramen ovale
increased left atrial pressure and pulmonary artery hypertension |
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What are the clinical features of hypoplastic left heart syndrome?
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decreased perfusion, shock, vascular collapse, low BP, heart failure
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What is the goal of surgical therapy for hypoplastic left heart syndrome?
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maintaining adequate systemic perfusion
transect main pulmonary artery, anastamose proximal end of pulmonary artery to ascending aorta, connecting systemic artery or right artery to distal end of pulmonary artery |
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What happens in transposition of the great arteries?
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abnormal origin of pulmonary artery and aorta
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What happens in d-transposition?
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complete flip of arteries
pulmonary artery from left ventricle, aorta from right aorta generally in front of the pulmonary artery |
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What keeps complete transposition compatible with life?
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communication between pulmonary and systemic circulation
can be patent ductus, ASD, VSD |
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What happens embryologically with transposition?
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subpulmonary infundibulum (pulmonary outflow track) doesn't grow properly, end up with the vessels connected incorrectly
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What is the cardinal abnormality with transposition?
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arterial hypoxemia
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What are symptoms of transposition?
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cardiac dilation and failure
cyanosis, breathlessness at rest, respiratory failure |
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How do you treat transposition?
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enlarge the interatrial connection at first, allow more oxygenation
band pulmonary artery to control excess flow |
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What is the "atrial switch" operation?
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excision of most of the atrial septum, diversion of caval blood through pericardial or synthetic conduit or atrial flap to mitral valve, allows pulmonary and venous return into right and left ventricles respectively
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What is the Mustard procedure?
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excision of most of atrial septum, diversion of caval blood flow through pericardial or synthetic conduit
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What is the Senning procedure?
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atrial flap to mitral valve, allows pulmonary flow back to tricuspid valve
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What is the arterial switch operation?
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pulmonary artery and aorta are interchanged, need to reimplant coronary arteries to new aorta
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What is the Jantene operation?
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right and left pulmonary arteries arise from a common pulmonary artery, that arises from the truncus
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What happens in Tetralogy of Fallot?
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VSD, right ventricular flow obstruction, right ventricular hypertrophy, overriding aorta
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How is right ventricular flow in Tetraology of Fallot?
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impeded at the infindibulum, pulmonary valve may be stenotic
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What happens to the pulmonary artery in TOF?
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becomes hypoplastic
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What is the pathogenesis of TOF?
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underdevelopment of the infundibulum, causing the aortico-pulmonary septum to be displaced to the right with failure to join the ventricular septum, results in anterior position of right ventricular outlet septum, narrowing of right ventricular outflow
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What is the prime clinical feature of TOF?
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cyanosis
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What are the clinical features of TOF?
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cyanosis, clubbed fingers and toes, polycythemia, syncope, cerebral damage, convulsions
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What do surgical techniques for TOF try to accomplish?
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closure of septal defect, relief of right ventricular outflow problems
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What are symptoms of congenital heart problems related to?
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cyanosis or CHF
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What causes cyanosis?
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inadequate oxygen content of arterial blood
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What causes CHF?
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inadequate total systemic/regional blood flow to meet the system's demands
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What are the responses to congenital heart defects?
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hypertrophy, dilation, atrophy
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Where is the tricuspid valve?
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between the right atrium and right ventricle
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Where is the mitral valve?
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between the left atrium and left ventricle
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What is the function of the atrium?
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to collect blood returning to the heart from the periphery or from the lungs, acts as a booster pump to "prime" ventricles
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What do the atria contribute to total Cardiac Output?
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20%
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How is the atrium filled?
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passively during diastole
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How thick is the left ventricle?
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6-11 mm
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What is the systolic BP in the aorta?
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90-150 mmHg
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What is the systolic BP in the pulmonary artery?
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15-25 mmHg
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How thick is the right ventricle?
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2-4 mm
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For how long does cardiac muscle contract?
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about 200 ms
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What is the conduction system muscle like?
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few myofibrils, weak contraction, automaticity (rhythmic generation of action potentials)
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What is the cardiac muscle like?
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striated, latticework of fibers, myofibrils with actin-myosin filaments that slide during contraction
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What is the cardiac muscle syncytium like?
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intercalated discs are dark lines, cell membranes that separate cardiac cells, facilitates the spread of action potentials via gap junctions
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What separates the atria and ventricles?
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nondonductive fibrous tissue
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Where does the electrical impulse travel from the atria to the ventricles?
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AV node only!
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What happens after the mitral valve opens?
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diastolic filling, slight increase in stroke volume
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What happens once end-diastolic volume is reached?
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isovolumetric contraction, increased intraventricular pressure
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What happens when the aortic valve opens?
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ejection, rise in stroke volume, then fall
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What happens when end-systolic volume is reached?
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isovolumetric relaxation, drop in intraventricular pressure
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What is the order of events in the cardiac cycle?
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mitral valve opens, diastolic illing, end-diastolic volume, isovolumetric contraction, aortic valve opens, ejection, end systolic volume, isovolumetric relaxation
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How do you calculate CO?
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liters of blood pumped/minute
SV x HR |
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How does the autonomic NS change HR?
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affects SA node, can adjust both HR and CO in one beat
affects intrinsic contractility of muscle fibers |
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How does cardiac filling affect stroke volume?
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increases
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How does increasing preload change muscle fibers?
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increases initial muscle length without changing the final contraction length, so long as it occurs after a constant afterload
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How does increased afterload change SV and CO?
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decreases SV and CO if preload remains constant, shortening peak isometric tension that develops equals the load upon it
negative effect on muscle fiber shortening |
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Where can you have increased afterload?
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systolic BP, aortic valve, coarctation of hte aorta, sub-aortic obstruction, supra-aortic obstruction
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How does NE affect the heart?
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enhances contractility, increases SV and CO
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How do you measure contractility?
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imaging, EKG, MRI, nuclear imaging, angiography of Lv to determine EF
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How do you calculate EF?
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EF = SV/EDV
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What is a normal EF?
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>55%
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How do you determine end diastolic PV?
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fill the LV with progressively more volume
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What happens to the LV when you reach a volume beyond 150-170 ml?
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steep rise in pressure
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What is the end systolic PV curve?
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systolic pressure achieved during LV contraction at each filling volume
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How does the sympathetic system affect heart rate?
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positive chronotropic
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How does the sympathetic system affect cardiac action potentials?
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decreases duration of cardiac action potentials, minimizes effect of high heart rates on diastolic filling time
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How does the sympathetic system affect action potential conduction?
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increases rate of action potential conduction, esp in AV node
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How does the sympathetic system affect cardiac contractility?
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increases it at any given preload
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How does the sympathetic system affect cardiac relaxation?
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increases rate of cardiac relaxation (positive lusitropic) which helps to minimize effect of high heart rates on diastolic filling time
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What is atherosclerosis?
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inflammatory disease of elastic and muscular arteries from accumulation of lipids in wall of arteries beneath sites of endothelial injury, thrombosis and scarring weaken and destroy the artery wall
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What is an atheroma?
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raised intimal and subintimal local lesion with a core of cholesterol and cholesterol esters covered by a fibrous plaque
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What is arteriosclerosis?
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hardening of arteries, includes calcification, atherosclerosis, etc
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What is the earliest visible lesion in atherosclerosis?
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fatty streak
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What is in the fatty streak?
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lipid-laden macrophages, lipid-laden smooth-muscle cells in the intima
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What is the relationship between the fatty streak and advanced lesions?
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inconsistent, sometimes they progress, some disappear
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How does the plaque affect the layers of the artery?
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elevated above it, replaces much of the intima and some of the media, disrupts media's structure
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What is in the margins of the plaque?
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proliferating smooth muscle cells, CT, base is often neovascularized
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How long does the plaque take to develop?
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2-3 decades after the fatty streak
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How are plaques in coronary arteries different?
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contain more CT than atheromatous debris
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What are some complications of a plaque?
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calcification, ulceration, thrombosis and vascular occlusion, hemorrhage, rupture, aneurysm
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What are preferntial sites fo atherosclerosis?
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intimal irregularities, sites of turbulent flow
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What do plaques look like in coronary and cerebral arteries?
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segmental radially and longitudinally
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How doe vessels compensate for atherosclerotic obstruction?
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increased arterial diameter, formation of collateral vessels
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How does exercise affect atherosclerosis?
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causes vasoconstriction at sites of atherosclerosis
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What causes localized vasoconstriction?
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decreased local NO-prostacyclin secretion, increased endothelin production at sites of atherosclerosis in coronary/muscular arteries
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What are characteristics of stable atherosclerotic lesions?
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circumferential, avascular, collagen rich, lipid poor
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What are characteristics of unstable atherosclerotic lesions?
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eccentric, protruding, lipid-rich, easily ulcerated, vascular
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Where does the atherosclerotic plaque initially develop?
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external to the lumen
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How does CD40 affect atherosclerosis?
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activated platelets display CD40L, triggers inflammation, antibodies to CD40-CD40L by anti-CD40L antibodies inhibit initiation and progression of experimental atherosclerosis, can destabilize clots
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What are levels of CD40L in patients with unstable angina?
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high soluble and membrane-bound CD40L
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What viruses have been found in plaques?
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herpesvirus, CMV, C. pneumoniae, antibodies to H. pylori
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What happens when platelets are exposed to collagen?
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release aDP, aggregate
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What happens when tissue thrombospondin contacts plasma?
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activates extrinsic coagulation
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How do endothelial cell derived PGI2 levels affect platelets?
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reduction promotes platelet aggregation
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What is the early effect on plasminogen activator
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endothelial cell derived plasminogen activator is depleted
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What do adherent platelets release?
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Platelet Factor 3, Platelet Factor 4, TxA2
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What does Platelet Factor 3 do?
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initiates intrinsic coagulation
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What does Platelet Factor 4 do?
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antiheparin
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What does TxA2 do?
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vasoconstriction and platelet aggregation
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What is deposited in early endothelial injury?
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thrombin, fibrin, lipids from platelets, red cells
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What does PDGF do in late endothelial injury?
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causes proliferation of smooth muscle cells in the subintima
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What do smooth muscle cells do for late endothelial injury?
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increases glycosaminoglycans, enlarges, obstructing, space-occupying lesion
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What do fibroblasts do for late endothelial injury?
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increases collagen, enlarges, obstructing, space-occupying lesion
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What are trapped in damaged arterial wall?
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lipids in media
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How do LDL levels affect atherosclerosis?
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increased LDL blood levels like in LDL receptor deficiency disease, increased rate of infiltration into arterial wall
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What is Virchow's inhibition theory?
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hypertension, with heightened perfusion of lipids into arterial wall, accelerates development of atherosclerosis
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Which cells increase uptake of lipids in hypertension?
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endothelial cells, smooth muscle cells, macrophages
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What happens to lipid filled smooth muscle cells?
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necrosis and proliferation, local release of lipids
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What is the unifying theory?
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increased plasma LDL causes injury to endothelium
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How do monocytes cause atherosclerosis?
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adhere to vascular endothelium, penetrate it, form lesions during atherogenesis facilitated by endotehlial cell adhesion molecules
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What are CRP levels and amyloid A protein levels in people with unstable angina?
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CRP and amyloid A are elevated
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How does CRP predict myocardial injury?
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elevated predicts future MI
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What signals an irreversible injury?
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smooth muscle cell migration into the subintima
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What is the LDL cut off for atherosclerosis?
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80 mg/dl
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What is the LDL cutoff for symptomatic atherosclerosis?
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160 mg/dl
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What is the relationship between plasma HDL and atherosclerosis?
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inverse
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What changes HDL levels?
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exercise increases them
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How do plasma cholesterol levels change probability of atherosclerosis?
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higher cholesterol, higher atherosclerosis
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What is a foam cell?
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monocyte that traps lipids, but cannot completely degrade them, ultimately lyses and releases contents locally
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What happens if you have gradual occlusion of an artery?
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leads to cerebral ischemia, myocardial ischemia, and renal ischemia
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What happens if you have sudden occlusion of an artery?
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leads to thrombosis, MI, cerebral infarction, embolism (stroke or renal infarct)
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What happens if you have hemorrhage due to atherosclerosis?
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leakage or rupture of an aortic aneurysm, rupture of cerebral artery aneurysm, bleeding from atherosclerotic arteries
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How does age affect atherosclerosis?
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begins in the first decade, coronary lesions in teh second decade, cerebral lesions in the third decade
aorta > coronaries > cerebrals |
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How does gender affect atherosclerosis?
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CHD develops more quickly in males and is more common in middle aged males than females
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How does diabetes affect atherosclerosis?
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accelerates it, increases extent of lesions, more frequent necrosis and thrombosis, may affect platelet and fibrinolytic functions also
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How does race affect atherosclerosis?
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more common in whites than blacks/Asians, but Asians have more severe cerebral artery atherosclerosis
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How does hypertension affect atherosclerosis?
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accelerates it, increases perfusion of lipids into wall, damages endothelium, induces smooth muscle cell lysosomes, local release of acid hydrolases
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How does cigarette smoking affect atherosclerosis?
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increased, dose-related, fatal coronary heart disease, alters fatty streaks, more rapid deposition of lipids, increased ADP-induced platelet aggregation
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How do plasma lipids affect atherosclerosis?
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increased LDL increases risk
elevated plasma Lipoprotein A also increases risk |
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How does homocystine affect atherosclerosis?
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elevated levels create an independent risk factor similar to hypertension and smoking
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How does CRP change atherosclerosis?
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when elevated, enhances inflammation and lipid accumulation in atherosclerotic lesions
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What is ischemic heart disease?
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group of related syndromes from insufficient supply of oxygenated blood to meet the demands of the myocardium
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What is the single most common cause of death in the US?
|
ischemic heart disease
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What is the most common cause of ischemic heart disease?
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atherosclerosis
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What conditions other than atherosclerosis can cause CHD?
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diseases of coronary arteries or their ostia, aortic valvular disease, tachycardia, hypertension/ventricular hypertrophy, anemia, shock, exercise
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What causes IHD?
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diminished coronary perfusion relative to myocaridal demand
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How does coronary obstruction contribute to IHD?
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plaque formation reduces lumen's area, resulting in decreased blood flow
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At what point is the atherosclerosis too big for functioning?
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>75% reduction in cross sectional area
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Where in the coronaries does atherosclerosis occur?
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multiple major coronary arteries, proximally
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What is acute plaque change?
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acute alterations due to increased mechanical stresses
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What causes acute plaque change?
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adrenergic stimulation causing vasospasma or hypertension, susceptible plaque structure (eccentric, large core of necrotic debris and lipid, high density of macrophages, thin fibrous cap)
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How are plaques altered?
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hemorrhage into the plaque, increasing volume and obstruction
erosion or ulceration with exposure of subendothelial basement membrane rupture fissure at junction of fibrous cap and normal arterial wall |
