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228 Cards in this Set
- Front
- Back
what is the #1 cause of death worldwide?
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heart disease
(40% of deaths in the US) (1.5x all cancers combined) |
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normal heart morphology
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250-300gm in women
300-350gm in men RV thickness = 0.3-0.5cm LV thickness = 1.3-1.5cm **usually measured 1-2cm below the tricuspid or mitral valve** |
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where do the coronary arteries arise?
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just distal to the aortic valve
|
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how can coronary arteries be dominant?
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the coronary artery that supplies the posterior descending branch is considered dominant
80% of patients are right dominant |
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what are the three major epicardial coronary arteries?
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1) left anterior descending (LAD) artery
2) left circumflex (LCX) artery 3) right coronary artery (RCA) |
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when does most blood flow through the coronary arteries occur?
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during ventricular diastole
|
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what parts of the heart are supplied by the left anterior descending artery?
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most of the apex
anterior left ventricle anterior 2/3 of septum |
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what parts of the heart are supplied by the left circumflex artery?
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lateral wall of left ventricle
posterior 1/3 of septum (20% of pts) |
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what parts of the heart are supplied by the right coronary artery?
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right ventricle
posterior 1/3 of septum (80% of pts) posterobasal left ventricle **occlusion of the right coronary artery can damage the left ventricle** |
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aging heart
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- can have reduction in size of LV cavity
- calcification of the mitral annulus and/or aortic valve (aortic valve calcification often causes stenosis) - fibrous thickening of valves (can mimic prolapsed mitral valve) - fewer myocytes (more fibrous tissue) compared to a younger person - amyloid of aging - lipofuscin granules |
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lipofuscin
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wear/tear pigment found in aging hearts (sign of oxidative injury)
a lot is found in atrophic hearts (brown atrophy) |
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congestive heart failure
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heart is unable to pump at the rate that is necessary for the requirements of metabolizing tissue, or can do so only from an elevated filling pressure
mortality is 50% in 5 years |
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what is the leading discharge diagnosis in hospitalized patients older than 65?
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congestive heart failure
causes 1 million hospitalizations per year (pts are living longer, so there are more hospitalizations) |
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what are the causes of CHF?
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1) most cases are deterioration of systolic dysfunction (contractile problems)
2) fewer cases have diastolic dysfunction (left ventricular hypertrophy) 3) iatrogenic causes (fluid overload can throw old ppl into heart failure) |
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cardiac hypertrophy
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increase in mass and size of heart often accompanied by the deposition of fibrous tissue (heart is 2-4x heavier than normal)
often precedes onset of CHF, as heart responds to increased mechanical work or to trophic signals more mass causes increased metabolic requirements and increased wall tension (both result in more O2 consumption) heart rate and contractility inc. O2 consumption (often present in hypertrophic states) |
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patterns of cardiac hypertrophy
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pressure overload
- concentric LV hypertrophy - caused by HTN and aortic stenosis - cavity is normal to reduced in size volume overload - caused by mitral/aortic valve regurg/insufficiency - hypertrophy & dilation with increased ventricular diameter - thickness doesn't correlate with pathology (pt could be compensated or decompensated) |
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how does the weight of the heart change in patients with hypertrophy?
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the weight increases to 2-3x normal in HTN, ischemic heart disease, aortic stenosis, mitral insufficiency, and dilated cardiomyopathy
the weight increases to 3-4x normal in aortic insufficiency and hypertrophic cardiomyopathy |
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molecular changes in cardiac hypertrophy
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with prolonged overload, re-expression of protein synthesis is similar to that in fetal heart development (ANP & BNP tries to dec blood volume)
alterations in handling of Ca may cause impaired contraction/relaxation apoptosis of myocytes |
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what is the end result of cardiac hypertrophy?
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hypertrophy is the balance between adaptation and potentially deleterious alterations
eventually the compensatory changes become an added cardiac burden degree of structural abnormality does not necessarily correlate with level of dysfunction |
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causes of left heart failure
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ischemic heart disease
hypertension (most common) aortic and mitral valve disease nonischemic myocardial disease |
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what is the most common cause of left heart failure?
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hypertension
|
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what causes the clinical presentations of left heart failure?
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congestion of pulmonary circulation
stasis of blood in left-sided chambers hypoperfusion of tissues |
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what is seen in the heart in left heart failure?
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LV hypertrophy, often dilation (volume overload)
secondary enlargement of left atrium; if there is resultant a-fib, pt can get stasis and thrombus with substantial risk of stroke microscopic: hypertrophy and fibrosis |
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what is seen in the lung in pts with left heart failure?
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congestion and edema (frothy and pink)
with time, get siderophages (heart failure cells) cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, rales |
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what is seen in the kidney in pts with left heart failure?
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decreased CO activates RAAS and causes retention of salt and water with subsequent expansion of blood volume
salt retention is counteracted by ANP released via atrial dilation (decreases blood volume) if perfusion deficit is severe, pre-renal azotemia can occur |
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what are heart failure cells?
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aka siderophages
hemosiderin-containing macrophages in the alveoli (most common in left heart failure and chronic lung congestion) a) in left heart failure, the left ventricle can not keep pace with the incoming blood from the pulmonary veins b) resulting backup causes increased pressure on the alveolar capillaries, and red blood cells leak out c) alveolar macrophages ingest the red blood cells, and become engorged with brownish hemosiderin |
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what is pre-renal azotemia?
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abnormally high levels of nitrogen-containing compounds
BUN and creatinine are elevated, but BUN is elevated out of proportion to creatinine (in renal azotemia, the increase is proportional) occurs following hemorrhage, shock, volume depletion, congestive heart failure, and narrowing of the renal artery |
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effects of left-sided congestive heart failure on the brain
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in advanced CHF, pt can get cerebral hypoxia and hypoxic encephalopathy
causes loss of attention span and restlessness |
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what is the most common cause of right heart failure?
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left heart failure (caused by back-up)
|
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what are the two causes of right heart failure?
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1) left heart failure (most common)
2) pure right failure with severe pulmonary hypertension (cor pulmonale) |
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what is seen in pts with pure right heart failure (cor pulmonale)?
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- right sided hypertrophy and dilation
- septum may bulge into left side, causing some LV dysfunction - minimal pulmonary congestion - engorgement of systemic and portal venous systems |
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what is the main difference between the two causes of right heart failure?
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in right heart failure caused by left heart failure, there is substantial pulmonary congestion
in pure right heart failure (caused by pulmonary HTN) there is minimal pulmonary congestion |
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what is seen in the liver/portal system in pts with right heart failure?
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increased size and weight (congestive hepatomegaly)
chronic passive congestion - congested red center of lobule - paler periphery - "nutmeg liver" central hypoxia can cause centrilobular necrosis (if prolonged and severe, cardiac sclerosis/cirrhosis occurs from loss of hepatocytes) pressure backs up through portal venous system causing congestive splenomegaly and sinusoidal dilation as well as ascites |
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what is seen in the kidney of pts with right heart failure?
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more renal congestion than is seen in left heart failure
fluid retention, edema, azotemia |
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what is seen in the CNS of pts with right heart failure?
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in advanced CHF, can get cerebral hypoxia and hypoxic encephalopathy
causes loss of attention span and restlessness |
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what happens in the body cavities of pts with right heart failure?
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pleural and pericardial effusions (especially common are rt-sided pleural effusions)
ascites |
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what is seen in the subQ tissue of pts with rt heart failure?
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dependent edema
- pedal and pretibial in ambulatory pts - back and sacral areas in ambulatory pts ***pitting edema*** |
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congenital heart disease
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most arise from faulty embryogenesis during wks 3-8
the most severe are incompatible with intrauterine survival, but range from severe problems at birth to no clinical problems until late adulthood seen in 1% of live births (more in premies and stillborns) |
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pathogenesis of congenital heart disease
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main known causes are sporadic genetic abnormalities
recognizable genetic or environmental influences in about 10% - genetic: trisomies (esp. 21), turner syndrome - environment: rubella most are multifactorial |
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genetics of congenital heart disease
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heart is one of the first organs to form and develop
different defects in a family may have a common genetic defect b/c of common developmental pathways - errors in mesenchymal tissue migration - extracellular matrix abnormalities - situs and looping defects determining laterality |
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how many congenital heart defects are caused by errors of mesenchymal tissue migration?
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15% of CHD are anomalies in outflow tract(s)
can be failure of fusion or failure of septation may be due to abnormal development of neural crest-derived cells |
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a region of what chromosome has a large role in the development of the conotruncus?
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chromosome 22
deletions in this region are present in 15-50% of the congenital heart defects - these deletions are also associated with other types of abnormalities |
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extracellular matrix abnormalities that cause congenital heart disease
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endocardial cushion defects
AV septal defect in Down's syndrome (trisomy 21) |
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what is the most common genetic cause of congenital heart disease?
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down's syndrome (trisomy 21)
|
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what are the three major categories of congenital heart diseases?
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1) left-to-right shunts
2) right-to-left shunts 3) obstructions |
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what is a shunt?
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abnormal communication between chambers or blood vessels
direction of flow depends on pressure differentials |
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right to left shunts
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shunted blood bypasses the lung and is not oxygenated
Sx: cyanosis, clubbing, polycythemia, paradoxical emboli |
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left to right shunts
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increase in pulmonary flow causes low resistance, low pressure right-sided structures to be exposed to higher pressures
pulmonary HTN, then right ventricular hypertrophy, and subsequently right CHF when right pressure rises enough, the shunt switches direction once significant irreversible pulmonary HTN, cardiac disease is considered irreparable |
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obstruction
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abnormal narrowing of chambers, valves, or vessels
- valve stenosis - atresias - coarctation |
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what are the different left-to-right shunts?
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atrial septal defects (ASDs)
patent foramen ovale (PFO) ventricular septal defect (VSD) patent ductus arteriosus (PDA) atrioventricular septal defect (AVSD) |
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atrial septal defects
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L to R shunt
pulmonary blood flow is 2-4x normal (tolerated very well) irreversible pulmonary HTN occurs in <10% of pts usually asymptomatic from a functional point of view (may cause a murmur) until adulthood or late adulthood (symptoms are rare younger than 30yo) three types: 1) secundum (90%) 2) primum (5%) 3) sinus venosus (5%) Tx: surgery (low mortality) - post-op survival is "normal" |
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secundum atrial septal defect
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90% of ASDs
deficient or fenestrated (swiss cheese) fossa ovale, near the mid septum most are isolated abnormalities, but if there is another defect the other is usually more dominant |
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primum atrial septal defect
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5% of ASDs
adjacent to AV valves usually associated with cleft anterior mitral leaflet (partial AVSD) |
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sinus venosus
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ASD near the entrance of the superior vena cava
commonly associated with anomalous connection of right pulmonary veins to superior vena cava or right atrium |
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patent foramen ovale
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L to R shunt (present in 20% of ppl)
important in fetal life to allow oxygenated blood from the placenta to bypass the non-oxygenated lungs if it remains open, a R to L shunt can form if there is a significant rise in RV pressure; this shunt can either be sustained and permanent or temporary (caused by cough or bowel movement) |
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what are the three physiological fetal shunts? where are they?
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1. Ductus arteriosus
… protects lungs against circulatory overload … allows the right ventricle to strengthen … hi pulmonary vascular resistance, low pulmonary blood flow … carries mostly med oxygen saturated blood 2. Ductus venosus … fetal blood vessel connecting the umbilical vein to the IVC … blood flow regulated via sphincter … carries mostly hi oxygenated blood 3. Foramen ovale … shunts highly oxygenated blood from right atrium to left atrium |
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ventricular septal defect
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incomplete closure of ventricular septum (most common congenital heart abnormality)
frequently associated with other abnormalities depending on size, range from severe problems at birth to spontaneous closure (mostly seen in small muscular septal defects) most are single holes, but can occasionally appear as "swiss cheese" |
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what is the most common congenital heart abnormality?
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ventricular septal defect
|
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how are ventricular septal defects classified?
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size and location
90% involve membranous septum remainder are below pulmonary valve (infundibular VSD) or in muscular septum **small muscular VSDs are most likely to spontaneously close; others remain patent** |
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clinical features of VSDs
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50% of small muscular defects close spontaneously and remainder are well tolerated for yrs
large membranous or infundibular VSDs remain patent, with significant L-R flow - pts can have RV hypertrophy and pulmonary HTN from birth; even if they don't it will develop with time in any large VSD - large ones have murmur and heart failure from birth (want to fix before pulmonary disease becomes irreversible) |
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patent ductus arteriosus
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persistence after birth of communication btwn pulmonary (pulmonary artery) and arterial systems (aorta); forms a L-R shunt
isolated in 90% of cases Sx: continuous, harsh murmur, but functionally asymptomatic during childhood since it is a L-R shunt, more blood flow goes through pulmonary arteries and lungs and the shunt eventually switches to R-L should be closed ASAP if isolated, but if necessary for life can be maintained with PgE |
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atrioventricular septal defect (AVSD)
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L-R shunt caused by abnormal development of the AV canal
- superior and inferior endocardial cushions fail to fuse - incomplete closure of AV septum - inadequate formation of AV valves |
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what is a partial atrioventricular septal defect?
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primum atrial septal defect combined with a cleft anterior mitral leaflet from MI
|
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what is a complete atrioventricular septal defect?
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large, combined AVSD with a large, common AV valve
essentially a hole in the center of the heart through which all four chambers can communicate >1/3 are caused by Down syndrome correctable |
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what are the congenital right-to-left shunts?
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tetralogy of fallot (TOF)
transposition of the great arteries (TGA) truncus arteriosus (TA) tricuspid atresia (triA) total anomalous pulmonary venous connection/return (TAPVC) |
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what are the four cardiovascular features of tetralogy of fallot?
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1) ventricular septal defect
2) obstruction of right ventricular outflow tract (subpulmonary stenosis) 3) aorta overrides VSD (overriding aorta) 4) right ventricular hypertrophy |
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what is the most common form of cyanotic congenital heart disease?
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tetralogy of fallot
|
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tetralogy of fallot
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R-L shunt that results from the anterosuperior displacement of the infundibular septum
pt can survive into adulthood, even if untreated (though Tx is necessary) with increasing subpulmonary stenosis, get smaller, thin-walled pulmonary arteries and aorta increases in diameter (as the child and the heart grow the condition worsens, but the stenosis protects the pulmonary vasculature therefore RV failure is rare) Tx: surgical repair is usual, though it can be complicated if the pt has pulmonary artery atresia |
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what is the shape of the heart in Xrays of pts with tetralogy of fallot?
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the heart is enlarged and boot-shaped b/c of the right ventricular hypertrophy
|
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describe the ventricular septal defect in tetralogy of fallot
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large VSD with aortic valve forming the superior border
**causes an overriding defect of aorta and both ventricles** |
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what causes pulmonary obstruction in tetralogy of fallot?
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due to narrowing of infundibulum, often accompanied by pulmonary artery stenosis (atresia which involves pulmonary arteries occurs but is rare; in this case a patent ductus arteriosus is necessary for survival)
|
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what determines the direction of blood flow in tetralogy of fallot?
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severity of RV outflow obstruction
mild obstruction - resembles VSD - L-R shunt - aka pink tetralogy severe obstruction - R-L shunt - aka classic tetralogy (pt may be cyanotic at birth) |
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transposition of great arteries (TGA)
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aorta arises from the right ventricle and pulmonary artery arises from left ventricle; the aorta is anterior and to the right of the pulmonary artery (usually behind and to the left) leading to dissociation/separation of pulmonary and aortic circulations
R-L shunt caused by abnormal formation of truncal and aortopulmonary septa incompatible with post-natal life unless a shunt is present RV hypertrophy occurs early b/c it functions as the systemic ventricle; LV is thin and atrophic w/o surgery, most pts die in months |
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what shunts are present in pts with transposition of the great arteries that allows post-natal life?
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ventricular septal defect (35% of pts) - may be a stable shunt
patent ductus arteriosus or patent foramen ovale (65% of pts) - unstable shunts, so require interventional shunt within days |
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what is the Tx for transposition of the great arteries?
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surgery to transect and switch the great vessels
also need to fix the coronary arteries |
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truncus arteriosus
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R-L shunt formed by failure of the embryological truncus arteriosus to separate into that aorta and the pulmonary artery
single artery receives blood from both ventricles pt must have underlying ventricular septal defect Sx: early cyanosis, early pulmonary HTN |
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tricuspid atresia
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complete occlusion of the tricuspid valve because of unequal division of AV canal in embryo leads to R-L shunt
- mitral valve is large - almost always have RV hypoplasia - circulation occurs via ASD or PFO - pt also has VSD pt is cyanotic at birth mortality is high in first wks-mos |
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total anomalous pulmonary venous connection (TAPVC)
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no pulmonary veins directly enter the left atrium because in the embryo the common pulmonary vein fails to develop or becomes atretic causing the primitive systemic veins to remain patent
veins usually drain into the left innominate vein or coronary sinus pt needs an ASD or PFO to get pulmonary venous blood into the left atrium RA - hypertrophied RV - hypertrophied LA - hypoplastic LV - usually normal dilated pulmonary trunk |
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what are the obstructive congenital heart anomalies?
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1) coarctation of aorta
2) pulmonary stenosis/atresia 3) aortic stenosis/atresia |
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coarctation of the aorta
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congenital obstruction of the aorta
male:female ratio is 2:1 common in Turner syndrome (X0) infantile form - hypoplasia of arch proximal to a PDA - symptomatic in early childhood adult form - ridgelike infolding of the aorta just opposite a closed ductus arteriosus (ligamentum arteriosum), distal to arch vessels - asymptomatic until adulthood pt may have other anomalies or the coarctation may be solitary untreated, eventually leads to cardiomegaly, LV hypertrophy, and left CHF |
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what are the symptoms of aortic coarctation?
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with PDA, pt is often cyanotic at birth
- needs intervention to survive neonatal period - cyanosis of lower body without PDA, pt is often asymptomatic until adulthood - upper limb HTN - low BP, weak pulses, signs of arterial insufficiency in lower limbs - development of collateral circulation with costal notching |
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pulmonary stenosis/atresia
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obstruction of pulmonary artery
isolated or with other anomalies pt develops RV hypertrophy can be mild or severe can have post-stenotic dilation of pulmonary artery uless there is subpulmonary stenosis (when the trunk is not dilated and may be hypoplastic if valve is atretic, there is no communication btwn RV and lung, therefore hypoplastic RV and ASD blood enters lung through a PDA |
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valvular aortic stenosis/atresia
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hypoplastic, thickened cusps that may be abnormal in number (2 instead of 3); isolated lesion in 80%
if severe stenosis/atresia, pt has hypoplastic LV and ascending aorta and needs PDA to allow blood into aorta and coronaries pt may have LV endocardial fibroelastosis hypoplastic left heart syndrome (usually fatal in first weeks) |
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subaortic stenosis
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thickened ring or collar of dense endocardial fibrosis tissue below the level of the aortic cusps
|
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supravalvular stenosis
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inherited form caused by mutated elastin gene
wall of ascending aorta is thickened, causing luminal constriction |
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aortic stenosis and atresia
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3 varieties:
1) valvular stenosis/atresia 2) subaortic stenosis 3) supravalvular stenosis LV hypertrophy in response to obstruction stenosis is usually well-tolerated unless it's very severe |
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ischemic heart disease (coronary heart disease)
|
80-90% of all CV deaths
diminished coronary perfusion relative to heart's metabolic demands involves O2 insufficiency >90% is due to reduction in coronary flow secondary to atherosclerotic obstruction |
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what factors aggravate ischemic heart disease?
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- increased cardiac energy demand (hypertrophy)
- decreased blood pressure - increased heart rate - hypoxia/hypoxemia |
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what are the four basic manifestations of ischemic heart disease?
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1) myocardial infarction (MI)
2) angina pectoris 3) chronic ischemic disease with heart failure 4) sudden cardiac death |
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stable (typical) angina pectoris
|
most common type
increased O2 demand outstrips ability of stenosed arteries to deliver nutrients; reduction of perfusion to a critical level, rendering the heart vulnerable to further ischemia if O2 demand is increased plaque is stable and not disrupted relieved by rest and/or nitroglycerin - nitro achieves effect by dilation of peripheral vasculature - can tx by dilating coronary arteries, but they are probably already maximally dilated |
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unstable (crescendo) angina pectoris
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sudden change in plaque morphology induces partially occlusive platelet aggregation or thrombus and/or vasoconstriction leading to severe but transient reduction in flow
pain occurs with progressive frequency and is brought on by progressively less effort and lasts progressively longer (often occurs at rest) harbinger of subsequent acute MI in many pts |
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sudden cardiac death
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frequently, a disrupted plaque and partial thrombus have led to regional ischemia that induces fatal arrhythmia
|
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what are the acute coronary syndromes?
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myocardial ischemia
unstable angina sudden cardiac death **frequently initiated by unpredictable and abrupt conversion of a stable plaque to an unstable lesion via erosion, ulceration, fissuring, rupture or hemorrhage** **usually thrombosis is superimposed** |
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pathogenesis of ischemic heart disease?
|
1.) fixed coronary obstructions
2.) plaque change 3.) inflammation 4.) coronary thrombus 5.) vasoconstriction |
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fixed coronary obstructions in ischemic heart disease
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>90% of IHD pts have significant coronary atherosclerosis in at least one vessel
usually lesions decrease the cross section of one of the major vessels by at least 75% - compensatory vasodilation is no longer sufficient - causes symptomatic ischemia on exercise if stenosis is 90% or more, ischemia occurs at rest |
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where do fixed coronary artery obstructions tend to occur?
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within the first few cm of left anterior descending artery and left circumflex artery
anywhere in right coronary artery |
|
plaque change in ischemic heart disease
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initiating event is usually disruption of a previously partially stenotic plaque, followed by thrombosis
- hemorrhage into atheroma can expand its volume - plaque can rupture or fissure, exposing thrombogenic plaque contents - fissures most often occur at junction of fibrous cap and adjacent vessel wall - plaque can ulcerate, exposing thrombogenic subendothelium |
|
what factors influence plaque change in ischemic heart disease?
|
structure/composition of plaque
adrenergic stimulation |
|
what is the structure of disrupted atherosclerotic plaques?
|
disrupted lesions are usually eccentric, have a large core of debris and lipid with many macrophages, and have a thin fibrous cap
|
|
what property of the fibrous cap of an atherosclerotic plaque predisposes it to rupture?
|
decreased collagen
- increased degradation - decreased synthesis |
|
what are the most dangerous atherosclerotic lesions?
|
mildly to moderately stenotic lesions (<70%) b/c they don't induce angina before disruption
they tend to have a thin fibrin cap, with little inflammation |
|
why are high-grade lesions not as risky as low-grade lesions?
|
- composition is less complex (more collagen is present)
- since they limit the blood flow, they cause less mechanical stress - slow progression allows for development of collateral artery branches - pt's heart is pre-conditioned |
|
what is the effect of adrenergic stimulation on plaque disruption?
|
physical stress on the plaque in hypertension or vasospasm
stimulation on waking (peak time for MI is 6AM-noon) emotional stress - marked increase in incidence of sudden death associated with disasters |
|
what is the peak time for MIs to occur?
|
6am-noon
|
|
inflammation in ischemic heart disease
|
initial lesion needs interaction btwn endothelial cells & wbcs, leading to accumulation of T cells and macrophages in arterial wall
late plaque destabilization and rupture involve secretion of metalloproteinases inflammatory markers for atherosclerosis ultra-sensitive C-reactive protein |
|
ultra-sensitive C-reactive protein
|
>3mg/L indicates a high risk for CV disease
1-3mg/L indicates moderate risk for CV disease <1mg/L indicates low risk for CV disease |
|
coronary thrombus
|
total occlusion by a thrombus associated with disrupted plaque causes acute transmural MI
incomplete occlusion causes unstable angina, subendocardial infarcts or sudden death thrombosis activates growth-related signals in smooth muscle, which can contribute to growth of plaque |
|
vasoconstriction in ischemic heart disease
|
decreases lumen size and can increase mechanical forces leading to plaque rupture
stimulated by: - adrenergic agonists - platelet contents - impaired secretion of endothelial relaxing factors - inflammatory mediators |
|
angina pectoris
|
symptoms complex of paroxysmal, usually recurrent attacks of substernal/precordial chest discomfort/pain caused by transient (15sec-15min) myocardial ischemia that falls short of inducing cell necrosis
three patterns: 1) stable/typical 2) prinzmetal/variant 3) unstable/crescendo |
|
prinzmetal (variant) angina
|
uncommon
occurs at rest with no relation to activity, HR, or BP caused by coronary artery spasm usually relieved by vasodilators or calcium channel blockers |
|
what type of angina pectoris is also known as preinfarction angina?
|
unstable (crescendo) angina
|
|
what is the leading cause of death in the US?
|
myocardial infarction (MI)
about 1.5 million MIs/yr - 1/3 of these pts die |
|
what are the types of myocardial infarction?
|
1) transmural
2) subendocardial (non-transmural) |
|
transmural MI
|
more common than subendocardial MI
full thickness in distribution of a single coronary vessel plaque change + complete, occlusive thrombosis |
|
subendocardial MI
|
infarction is limited to inner 1/3-1/2 of cardiac wall, but can extend beyond the territory of a single vessel, affecting the areas that have poorest perfusion
usually caused by diffuse stenosing atherosclerosis and flow reduction, not by plaque disruption or thrombosis severe global hypotension can cause circumferential subendocardial infarcts also occurs after lytic therapy - save some muscle that would otherwise be damaged in a plaque rupture |
|
incidence and risk factors for myocardial infarction
|
same risk factors for atherosclerosis
frequency increases with age - 10% in pts <40yo - 45% in pts <65yo women are usually protected during reproductive years, but after menopause their risk increases rapidly (IHD is overwhelming COD in elderly women) |
|
coronary artery occlusion
|
caused by sudden plaque change
exposure of subendothelial collagen or plaque content induces platelet adhesion, aggregation, and activation stimulation of vasospasm by platelet aggregation activation of extrinsic path of coagulation cascade coronary artery can completely occlude in minutes 10% of transmural MI are not thrombotic (vasospasm, emboli, vasculitis, amyloidosis, hematologic disorders) |
|
what platelet aggregators are released in response to sudden plaque change?
|
TxA2
serotonin platelet factor 3 platelet factor 4 these factors stimulate vasospasm |
|
myocardial response to coronary artery occlusion
|
outcome is dependent on severity and duration of flow deprivation
cessation of aerobic glycolysis within seconds and loss of contractility in 1-2 minutes severe ischemia for 20-30 minutes causes irreversible damage - permanent damage if perfusion severely reduced for 2-4 hrs - rationale for window before irreversible changes in thrombolytic therapy in humans, necrosis progresses over 6 hrs, 12 if there are collaterals |
|
what parts of the heart are commonly affected by MIs?
|
- all transmural MIs involve at least a part of the LV
- 15-30% of those affecting posterior wall and posterior septum extend into RV - isolated RV infarction is only 1-3% LAD is affected in 40-50% of thrombi RCA is affected in 30-40% of thrombi LCX is affected in 15-20% of thrombi less frequent in the left main coronary, diagonal branches of LAD, and marginal branches of LCX |
|
morphology of MIs
|
transmurals involve nearly the entire perfusion zone of the affected vessel, with a rim of preserved subendocardial tissue, supplied by blood in the heart cavities
infarcts can extend in next days-weeks - see older infarcts at the center, with more recent changes at the periphery |
|
gross morphology of MI
|
<12 hrs, no gross changes unless the tissue is marinated in triphenyltetrazolium chloride (dehydrogenases are depleted in damaged area, so it does not pick up dye)
12-24 hrs: red-blue appearance due to stagnated blood progressive delineation: muscle becomes yellow-tan and soft 10-14 days: peripheral hyperemic zone of vascular granulation tissue eventually involutes to fibrous scar |
|
what is seen in infarcted tissue microscopically 4-12 hrs after infarction?
|
long & thin wavy fibers at periphery
vacuolization or myocytolysis in peripheral reversible ischemic fibers, especially viable subendothelium beginning stages of coagulative necrosis |
|
what is seen in infarcted tissue microscopically 1 day after infarction?
|
definite coagulative necrosis
pyknosis hypereosinophilic muscle fibers edema scattered neutrophils |
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what is seen in infarcted tissue microscopically 2-3 days after infarction?
|
acute inflammation peaks
|
|
what is seen in infarcted tissue microscopically 5-10 days after infarction?
|
macrophages remove necrotic myocytes
|
|
what is seen in infarcted tissue microscopically 2-4 weeks after infarction?
|
prominent granulation tissue forms
|
|
what is seen in infarcted tissue microscopically 6 wks after infarction?
|
well-advanced scarring (fibroblast proliferation causes collagen deposition)
|
|
therapeutic interventions for acute MI
|
idea is to rescue ischemic but not necrotic tissue to limit the size of the infarct
benefit depends on rapidity of occlusion relief 3-4 hours after onset of symptoms is the critical time 1) thrombolysis 2) percutaneous transluminal coronary angioplasty (PTCA) 3) coronary arterial bypass graft (CABG) |
|
thrombolysis for treatment of MI
|
streptokinase/tPA dissolves thrombus via activation of the fibrinolytic system
affects thrombus, but not the underlying plaque |
|
percutaneous transluminal coronary angioplasty (PTCA)
|
Tx for acute MI
can eliminate/disrupt thrombus and relieve some of the underlying plaque obstruction plaque ruptures at the weakest point and oftern hemorrhages into adjacent wall media dissects and stretches with obstruction relief, which creates an unstable plaque |
|
why is reperfused myocardium hemorrhagic?
|
injured vasculature is leaky
|
|
what are contraction bands?
|
intensely eosinophilic transverse bands composed of contracted sarcomeres in critically damaged myocytes
|
|
reperfusion injury
|
cell damage to a small amount of cells after infarcted tissue has been reperfused with blood
free radicals from wbcs can cause apoptosis and endothelial swelling at the capillary level |
|
what is stunned myocardium?
|
difficulty of temporarily infarcted cells to recover after reperfusion of ischemic myocardium
may result in reversible heart failure that benefits from temporary cardiac assistance |
|
what is cardiac preconditioning?
|
repetitive short-lived severe ischemia (repetitive angina or silent ischemia) protecting myocardium from greater subsequent ischemic insult
|
|
coronary artery bypass graft (CABG)
|
usually not Tx for acute situations, unless there is a complication of angioplasty
most often is an "elective" procedure |
|
symptoms of MI
|
chest pain, radiating down left arm
rapid, weak pulse diaphoresis dyspnea 10-15% are silent (picked up by changes in EKG) |
|
when do most MI deaths occur?
|
1/2 occur within the first hour, often b/c the pt never reaches a hospital
if pts get to hospital, death rate has decreased from 30% to between 7-13% since the 60s |
|
what cardiac markers are typically used to test for MI?
|
marker - rise - peak - normalize
CK-MB - 2-4hrs - 24hrs - 72hrs troponin - 2-4hrs - 48hrs - 7-10days |
|
why are there cardiac markers that indicate MIs?
|
intracellular molecules (creatine kinase and troponins) leak out of fatally injured cells via damaged cell membranes
|
|
creatine kinase (MI diagnosis)
|
old cardiac marker, but still used
3 isoenzymes from 2 dimers (M&B) CK-MM: skeletal muscle and heart CK-BB: brain, lung CK-MB: mainly heart CK-MB rises 2-4 hrs after MI, peaks at 24hrs, and normalizes at 72 hours myocardial damage is likely when total CK>190U/L, CK-MB>24U/L, CK-MB>6% of total |
|
troponins (MI diagnosis)
|
not normally detectable in the blood
appear 2-4 hrs after MI, peak at 48hrs, normalize at 7-10 days cardiac and skeletal muscle troponin I and T have differences in amino acid sequences, so assays (esp. for T) can be made specific for the cardiac form since it has a longer t1/2 than CK, it is useful if CK is normal |
|
what is the effect of reperfusion on CK and Tn levels?
|
peak of both accelerates (will be less than 24/48 hrs respectively)
|
|
consequences of MI
|
in-hospital death at 10%
complications occur in 75% - contractile dysfunction of LV - arrhythmias - myocardial rupture - pericarditis - infarct extension/expansion - thrombus - ventricular aneurysm - papillary muscle dysfunction - late heart failure as a rule, the larger the infarct, the more likely there will be complications |
|
on what factors is long-term prognosis dependent?
|
quality of residual LV function
extent of vascular obstruction in vessels perfusing viable tissue mortality in the first year is 30% (including those that die before reaching ER) 3-4% mortality for subsequent years |
|
contractile dysfunction of LV after MI
|
can result in varying degrees of LV failure, hypotension, pulmonary congestion & edema
cardiogenic shock occurs in 10-15%, associated with large infarcts (>40% of LV) - 70% mortality - 2/3 of in-hospital deaths |
|
what is the cause of 2/3 of in-hospital deaths related to MI?
|
cardiogenic shock due to contractile dysfunction of LV
associated with large infarcts that involve >40% of the LV |
|
arrhythmias as a consequence of MI
|
common
causes most sudden death results from conduction disturbances or myocardial irritability parts of the AV conduction system are in an inferoseptal location |
|
myocardial rupture as a consequence of MI
|
weakening of the necrotic, inflamed tissue
most common location is the free LV wall with hemopericardium and cardiac tamponade (generally btwn 3-7 days after MI) IV septal rupture creates L-R shunt papillary muscle is least common site (causes acute, severe mitral regurgitation) |
|
when does pericarditis occur as a consequence of MI?
|
day 2 or 3
|
|
ventricular aneurysm as a consequence of MI
|
late complication from anteroseptal infarct
heals with a thin scar that bulges during systole |
|
why does an MI cause papillary muscle dysfunction?
|
only causes papillary muscle dysfunction if they are in the affected area
first causes ischemia and then fibrosis |
|
chronic ischemic heart disease
|
progressive heart failure as a result of ischemic myocardial damage
usually pt has a previous MI or bypass surgery in hx - post-infarction decompensation due to exhaustion of compensatory hypertrophy of viable tissue occasionally no history of MI, but severe obstructive CAD |
|
morphology of chronic ischemic heart disease
|
heart is heavy with LV hypertrophy and dilation
moderate to severe stenosing atherosclerosis often scars of old infarcts hypertrophy of remaining viable fibers may have thrombi and/or patchy endocardial fibrous thickening subendocardial vacuolization and fibrosis |
|
clinical features of chronic ischemic heart disease
|
insidious onset of CHF in pts with past MIs or angina
Dx of exclusion of other causes of heart failure |
|
sudden cardiac death
|
unexpected cardiac death early after onset of symptoms or in absence of symptoms
most caused by acute MI - in younger pts, look for other causes death is usually caused by arrhythmia |
|
pathogenesis of sudden cardiac death
|
some are hereditary
often caused by primary electrical abnormalities - channelopathies (most important) - long QT syndrome (prototype) |
|
what are channelopathies?
|
AD inheritance of mutations in genes needed for normal ion channel fcn
either genes coding for ion channels or accessory proteins needed for functioning of the channels most important cause of arrhythmias that lead to death in pts with sudden cardiac death |
|
morphology of sudden cardiac death
|
80-90% have coronary stenosis, usually severe (75-90% occlusion)
1/2 have plaque disruption 1/4 have acute MI pts commonly have old MIs similar to severe chronic ischemia |
|
how can a physician improve the prognosis of pts that are susceptible to sudden cardiac death?
|
implanting a pacemaker or automatic cardioverter defibrillator
|
|
what are the minimum criteria for dx of systemic (left-sided) hypertensive heart disease?
|
LV hypertrophy, usually concentric, in absence of other CV pathology
Hx or pathological evidence of elevated BP |
|
what is the minimum BP that is required to produce LV hypertrophy?
|
no minimum
even mild elevations, if prolonged, can induce LV hypertrophy it is an adaptive response to pressure overload |
|
gross morphology of compensated systemic (left-sided) hypertensive heart disease
|
circumferential LV hypertrophy without dilation
wt increase is disproportionate to cardiac size LV>2cm and wt may exceed 500gm eventually LV gets stiff, impairs diastolic filling, and causes subsequent left atrial enlargement |
|
microscopic morphology of compensated systemic (left-sided) hypertensive heart disease
|
increase in myocyte diameter
cell and nuclear enlargement intersitial fibrosis |
|
clinical features of compensated systemic (left-sided) hypertensive heart disease
|
- may be asymptomatic
- EKG or echo evidence of LV hypertrophy - atrial fibrillation - BP control can prevent/cause regression of hypertrophy |
|
pulmonary (right-sided) hypertensive heart disease (cor pulmonale)
|
RV hypertrophy and dilation
potential heart failure secondary to pulmonary HTN (cor pulmonale) caused by disorders of the lung or pulmonary vasculature; by definition, excludes RV hypertrophy and dilation caused by congenital heart disease or caused by left-sided heart disease can be acute (after massive PE) or chronic (secondary to prolonged overload b/c of obstruction of pulmonary vasculature) |
|
morphology of acute pulmonary (right-sided) hypertensive heart disease (cor pulmonale)
|
caused by massive PE
marked dilation of right ventricle without hypertrophy (no time) normal crescentic shape of RV changes to dilated ovoid |
|
morphology of chronic pulmonary (right-sided) hypertensive heart disease (cor pulmonale)
|
secondary to prolonged overload b/c of obstruction of pulmonary vasculature
- wall thickens up to 1cm or more (may resemble thickness of LV) - thickened muscle bundles in outflow tract or thickened muscle connecting septum to anterior RV papillary muscle if severe, can compress LV or cause tricuspid regurgitation loss of normal fatty component of RV |
|
stenosis
|
failure of a valve to open completely, with impedance of forward blood flow
|
|
incompetence
|
failure of a valve to close completely, with reversal of flow
|
|
insufficiency
|
failure of a valve to close completely, with reversal of flow
|
|
regurgitation
|
failure of a valve to close completely, with reversal of flow
|
|
functional regurgitation
|
valve becomes incompetent due to ventricular dilation, causing papillary muscles to be pulled down and outward and preventing co-aptation of otherwise normal valve leaflets
can also be caused by dilation of aortic or pulmonary annulus |
|
how quickly do valvular diseases present?
|
can be rapid, if a cusp is destroyed by an infection, but more often results gradually over years
|
|
what is the most frequent valvular disease?
|
acquired stenosis of mitral or aortic valves (2/3)
|
|
what are the mechanisms that cause valvular insufficiency?
|
disease of valve cusps
damage to supporting structures (annulus, papillary muscles, ventricular free wall) can be acute or chronic |
|
what are the most common chronic valve diseases?
|
1) mitral stenosis from rheumatic heart disease
2) mitral insufficiency from mitral valve prolapse (myxomatous degeneration) 3) aortic stenosis from calcification of normal or congenitally bicuspid valve 4) aortic insufficiency from dilation of ascending aorta (HTN or aging) |
|
valve degeneration caused by calcification
|
dystrophic calcification process without significant lipid deposition or cell proliferation
1) wear & tear with dystrophic calcification 2) chronic injury secondary to hyperlipidemia, HTN, or inflammation valves have osteoblast-like cells making bone matrix proteins and promoting calcium deposition |
|
calcific aortic stenosis
|
aortic stenosis is the most frequent valve abnormality (can be congenital or acquired)
acquired - calcification induced by wear/tear of congenitally bicuspid valve (presents in 50s-60s) or calcification of normal valves with aging (presents in 70s-80s) |
|
what is senile calcific aortic stenosis?
|
dystrophic calcification of normal aortic valves that occurs with aging
presents in 70s-80s |
|
morphology of calcific aortic stenosis
|
heaped up calcifications within cusps protrude into sinus of Valsalva, preventing opening of cusps
distortion primarily seen at base; free cusp edge is not involved - no fusion of commissures until very late (distinguish from rheumatic valvular disease) mitral valve is usually normal but can have extension of aortic calcification onto anterior leaflet and/or have annular calcification |
|
clinical course of calcific aortic stenosis
|
narrowing causes inc. in pressure gradient across stenotic valve (LV pressure may reach 200mmHg)
concentric LV hypertrophy that causes LV to be prone to ischemia Sx: angina and syncope, with eventual decompensation and CHF once symptomatic, 50% die in 5 yrs w/o intervention; if pt has CHF, 50% die in 2 yrs |
|
calcification of congenital bicuspid aortic valve
|
aortic valve is normally tricuspid (bicuspid occurs in 1% of the population)
causes 50% of aortic stenosis in adults one cusp is usually larger with a raphe from incomplete embryologic separation OR can be acquired from fusion of commissure in rheumatic disease raphe is the major site of calcification valve may become incompetent predisposing factor for infective endocarditis |
|
mitral annular calcification
|
calcification in the ring of the mitral valve
irregular, hard, occasionally ulcerated nodules 2-5mm behind the leaflets usually doesn't affect function, but if nodules ulcerate a thrombus can form and embolize (also provides a site for infective endocarditis) common in women>60yo myxomatous mitral valve elevated LV pressure |
|
myxomatous degeneration of mitral valve
|
aka mitral valve prolapse
floppy valve balloons back into the LA during systole most common valve disease in the west (present in 3% of adults, usually young women) |
|
what is the most common valve disease in the west?
|
myxomatous degeneration of mitral valve (aka mitral valve prolapse)
|
|
what is the morphology of mitral valve prolapse?
|
- intercordal ballooning
- leaflets are enlaged, thick and rubbery - tendinous cords are elongated and thin (can rupture) - annular dilation (rare in other causes of mitral insufficiency) - attenuation of fibrosa layer of valve with thickening of spongiosa layer with deposition of myxomatous material |
|
what are the secondary valve changes in mitral valve prolapse?
|
- fibrous thickening of the leaflets
- thickening of LV endocardial surface where valve hits - thickening of LA endocardium from the prolapse back into atrium - thrombi form on atrial surface of leaflet - calcification at the base of the posterior leaflet |
|
pathogenesis of mitral valve prolapse
|
developmental anomaly of connective tissue
common in Marfan syndrome and in some other herditary CT disorders |
|
clinical features of mitral valve prolapse
|
usually asymptomatic; picked up on physical exam as a midsystolic click
3% develop complications: - infective endocarditis - mitral insufficiency - stroke/systemic infarct from thromboembolism - arrhythmia |
|
rheumatic fever
|
acute immunologically mediated multisystem disease, occuring a few weeks after group A strep throat
acute rheumatic carditis, which complicates the active phase of rheumatic fever, may progress to chronic valve deformities |
|
how frequent is rheumatic fever?
|
occurs in about 3% of cases of strep pharyngitis
pts who do get it are prone to reactivation of disease with subsequent throat infections |
|
what major findings are common in rheumatic fever?
|
1) migratory polyarthritis of large joints
2) carditis 3) subcutaneous nodules 4) erythema marginatum of skin 5) sydenham chorea (involuntary purposeless rapid movements of extremities) |
|
Dx of rheumatic heart/valve disease by Jones criteria
|
evidence of preceding group A strep infection
two major findings OR one major and two minor findings **minor manifestations are nonspecific sx's like fever, arthralgia, acute phase reactants** |
|
pathogenesis of rheumatic heart/valve disease
|
antibodies form against M proteins of S. pyogenes cross-react with heart antigens
CD4 cells specific for S. pyogenes peptides also react against heart proteins and produce cytokines that activate macrophages |
|
what are aschoff bodies?
|
foci of swollen eosinophilic collagen surrounded by lymphocytes, some plasma cells and plump macrophages
pathognomic for rheumatic fever (found in the endo-, myo-, and pericardium in acute disease) |
|
what are anitschkow cells?
|
macrophages with abundant cytoplasm and with a central nucleus having chromatin in a central, thin, wavy ribbon
aka caterpillar cell pathognomic for rheumatic fever |
|
acute rheumatic fever
|
aschoff bodies
anitschkow cells in endo-, myo-, and pericardium in acute disease pericarditis with fibrinous or serofibrinous exudate (bread & butter exudate) that resolves w/o sequelae myocarditis especially in interstitial perivascular tissue endocarditis or valve involvement - fibrinoid necrosis w/in cusps or along tendinous cords - 1-2mm vegetations along lines of closure - subendocardial thickened lesions in LA (MacCallum plaques) |
|
what are MacCallum plaques?
|
subendocardial thickened lesions in left atrium
seen in acute rheumatic fever |
|
chronic rheumatic heart disease
|
- deforming fibrosis, particularly of the valve leaflets
- mitral valve always deformed, but involvement of other valves may be more important clinically - mitral leaflet thickening (commissure fusion; short, thick, fused tendinous cords; fibrous bridging across commissure and calcification) |
|
what is fish mouth (buttonhole) stenosis?
|
fibrous bridging across commissure and calcification of mitral leaflets
seen in chronic rheumatic heart disease |
|
microscopic morphology of chronic rheumatic heart disease
|
diffuse fibrosis
often see neovascularization Aschoff bodies replaced by scar |
|
what is the most frequent cause of mitral stenosis?
|
chronic rheumatic heart disease
causes 99% of cases |
|
what is the prevalence of valve involvement in chronic rheumatic heart disease?
|
mitral only in 65-70% of pts
mitral/aortic in 25% of pts can involve tricuspid valve; pulmonary valve involvement is rare |
|
what is the pathological course of chronic rheumatic heart disease?
|
with mitral valve stenosis, left atrium dilates and may contain thrombi
eventually lung changes and RV hypertrophy develop |
|
clinical course of rheumatic fever/heart disease
|
starts 10d-6wks after strep pharyngitis
usually occurs in children 5-15 years old, but 20% of first attacks are in adults culture negative but antibodies to strep enzymes in serum (streptolysin O and DNAse B) arthritis is more common in adults than children (fever plus one large joint after another is painful and swollen for days) - may develop arrhythmias, esp in mitral stenosis - thromboembolic complications - infective endocarditis |
|
describe carditis in rheumatic fever
|
friction rubs, weak heart sounds, tachycardia, arrhythmias
1% of pts die from acute fulminant rheumatic fever myocarditis may cause cardiac dilation to point of mitral valve insufficiency or heart failure if attacks are recurrent, carditis gets worse |
|
when does rheumatic valve disease present?
|
decades after the initial attack of rheumatic fever
|
|
infective endocarditis
|
colonization or invasion of valves or endocardium by an organism
bulky, friable vegetations made up of organisms (mostly bacterial) and thrombotic debris often causes destruction of underlying tissue |
|
acute endocarditis
|
destructive infection by a virulent organism, frequently of a previously normal valve
50% mortality in days-weeks, even with treatment usually requires surgery usually caused by S. aureus |
|
subacute endocarditis
|
destructive infection caused by organisms of lower virulence (commonly S. viridans) that often involves previously abnormal valves
insidious onset untreated, it can last wks to mos, but most recover with antibiotics |
|
what valve abnormalities are predisposing factors for infective endocarditis
|
rheumatic heart disease
floppy mitral valve degenerative artificial valves |
|
what host factors are predisposing factors for infective endocarditis?
|
immunosuppression/deficiency
neutropenia diabetes EtOH IV drug abuse |
|
what organisms commonly cause infective endocarditis on abnormal valves?
|
native bacteria (Strep viridans 50-60% of pts)
|
|
what organisms commonly cause infective endocarditis in normal or deformed valves?
|
Staph aureus (10-20%)
- esp. in IV drug users |
|
what kind of organisms cause infective endocarditis in prosthetic valves?
|
coagulase-negative Staph (e.g. Staph epidermidis)
|
|
what conditions predispose pts to seeding of blood by microbes?
|
- obvious infection elsewhere
- dental/surgical work with transient bacteremia - unrecognized infection - IV drug abuse |
|
morphology of infective endocarditis
|
- fibrin, inflammatory cells, organisms
- fungal vegetations tend to be larger than bacterial vegetations - aortic and mitral valves are the most common sites (right side may be involved in drug users) - vegetations can be single or multiple; can involve one or more valves - can erode into adjacent myocardium, producing ring abscess, and eroding cusp - systemic emboli often produce septic infarcts - subacute endocarditis usually causes less valvular destruction - often granulation tissue at base of vegetation - eventual fibrosis, calcification, chronic inflammation |
|
clinical course of infective endocarditis
|
fever
- rapidly developing in acute endocarditis - chills and weakness - may be slight or absent in elderly with subacute disease - accompanying mild fatigue, flu-like symptoms, wt loss murmurs - 90% of left-sided lesions - can be mistaken for abnormal valve murmur ring abscess and septic emboli in acute endocarditis rare - microemboli in the retina, subungual hemorrhage, petechiae |
|
nonbacterial thrombotic endocarditis (marantic vegetations)
|
- sterile, no organisms
- loosely attached masses of fibrin, platelets, other blood elements on valve leaflets - usually on normal valves - no inflammation - can be found on either side of heart - 1-5mm, single or multiple lesions located on line of closure or cusps - don't cause damage to valve, but can embolize - often seen in debilitated pts (e.g. CA pts) |
|
pathogenesis of nonbacterial thrombotic endocarditis
|
pt often has concomitant PE or venous thrombosis (hypercoaguable state)
often associated with mucin-producing adenocarcinomas (mucin has a procoagulant effect) also associated with other malignancies/hypercoagulable states, and with endocardial trauma (i.e. heart catheter) |
|
libman-sacks endocarditis
|
SLE endocarditis
occasional occurrence - sterile granular vegetations on mitral, aortic, tricuspid valves (can cause regurgitation) - single or multiple, 1-4mm lesions frequently on the undersurface of AV valves (can be scattered on valves, cords, and endocardium) - fine, granular eosinophilic material; may have hematoxylin bodies - often intense fibrinoid necrosis type valvulitis adjacent to vegetation - can result in fibrosis and valve deformity |
|
carcinoid heart disease
|
1/2 ot pts with carcinoid syndrome have lesions on right endocardium and valves (mostly on RV)
plaque-like endocardial fibrous thickenings of cardiac chambers, right-sided valves, and occasionally IVC and pulmonary artery |
|
morphology of carcinoid heart disease
|
plaque-like endocardial fibrous thickenings of cardiac chambers, right-sided valves, and occasionally IVC and pulmonary artery
fibrous intimal thickenings of smooth muscle and sparse collagen mucopolysaccharide matrix that expands endocardium underlying structures are intact |
|
pathogenesis of carcinoid heart disease
|
there is a relationship btwn the levels of serotonin and severity of lesions
confined to right heart, since lungs can inactivate serotonin and bradykinin pts treated with 5-HT analogues for migraine have similar (rare) left-sided lesions (also occurs with fen-phen, with pulmonary carcinoid, and with patent foramen ovale) |
|
clinical features of carcinoid heart disease
|
tricuspid insufficiency > pulmonary insufficiency (if there is pulmonary insufficiency, there there is always tricuspid insufficiency as well)
may also get right-sided stenoses |
|
complications of artificial valves
|
- about 60% develop serious complications in 10yrs
- thrombotic complications are the major ones (can obstruct valve or embolize) - pts on long-term anticoagulation, so they can have bleeding problems - infective endocarditis, often with ring abscess - structural deterioration of biological prostheses - hemolysis, mechanical obstruction, overgrowth by fibrous tissue |