lecture 18 brickner
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| prevalence of CHD | 4-9/1,000 live births with bicuspid aortic valves being most common abnormality @ 3% prevalence in general population
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| definition of CHD | presence at birth of a gross structural abnormality of heart, great arteries or veins that can potentially have functional significance
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| fetal blood flow | umbilical v. - liver - IVC - RA to LA through foramen ovale or to pulm a. into aorta through DA - LV to aorta - umbilical a. for oxygenation
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| role of placenta to fetal circulation | provides exchange for O2 in utero; relatively low resistance during preg but after it's absent after birth, neonate's SVR doubles
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| the direction of blood flow through a shunt is determined by the relative distal resistance | distal resistance is related to presence of intracardiac obstructions and levels of PVR and SVR
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| severe hypertensive pulmonary resistance can even reverse shunt of PDA | obvi it can also reverse any other L-R shunt like VSDs or ASDs
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| criterion for determining if L-R shunt is significant | Qp (pulmonary flow) is 1.5-2x greater than Qs (systemic flow)
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| central cyanosis | desaturation of arterial blood beginning from within lungs or heart (intracardiac R-L shunt, hypoventilation or V/Q mismatch)
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| peripheral cyanosis | increased extraction of O2 by peripheral tissue in the presence of nl arterial O2 saturations (hypovolemia, shock, vasoconstriction from cold or meds)
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| how to evaluate a pt for possible CHD | careful PEx, EKG, measuring arterial O2 sats, CXR then Echo and cardiac cath to positively confirm
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| 5 Ts that cause baby to be cyanotic | tetralogy of Fallot, tricuspid atresia, transposition of great arteries, truncus arteriosus, total anomalous pulmonary return
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| 2 most common causes for cyanosis in adults | Eisenmenger syndrome, tetralogy of Fallot
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| in ASD, pts are usually asymptomatic until age 40-50 b/c there is no pressure gradient btwn the atria | R atrial and ventricular enlargement occurs over time eventually leading to palpitations (from a-fib) and CHF (from poor performance of RV)
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| PEx of pt with ASD | FIXED SPLIT S2 b/c RV takes longer than nl to eject extra blood so PV closes much later - doesn't change with resp either. SEM over PV area due to increase flow through PA
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| CXR and EKG findings of pt with ASD | CXR: R sided CM with prominent pulmonary vasculature // EKG: RAD and incomplete RBBB b/c more R ventricular tissue must be depol and it takes longer than LV depol
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| most common type of VSD | membranous portion of ventricular septum - near the AV and TV aka perimembranous defect
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| PEx of pt with VSD | holosystolic murmur starting at 2-6 wks of life, typically with palpable thrill, will be loud if defect is large
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| CXR and EKG findings of pt with VSD | CXR: may be nl or CM involving pulm vessels and all chambers except RA // EKG: may be nl or show LVH or biventricular hypertrophy
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| which chambers are most affected by VSD? | LV actually becomes overloaded due to increased return from lungs, can result in CHF. RV overload can lead to pulm HTN and subsequent Eisenmenger syndrome
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| pts with VSD will all need prophylactic tx for? | bacterial endocarditis
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| PEx of pt with PDA | only systolic murmur if less than 6 wks old, o/w continuous murmur (sounds like dishwasher) as aorta pumps into PA during entire cycle. dilated PA may compress L recurrent laryngeal nerve causing hoarseness of voice
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| CXR and EKG fidnings of pt with PDA | CXR: nl or dilated PA, vessels and aorta. possible L sided CM // EKG: may be nl or LVH
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| complication of PDA if not repaired | risk of endocarditis or endarteritis (of PA)
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| PEx of pt with coarctation of aorta | decreased or absent pulses in BLE, BP is much higher in BUE than BLE, systolic murmur f listening to posterior left paravertebral area, possible murmur of bicuspid aortic valve in 50% of these pts, radial-femoral pulse delay
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| CXR and EKG findings of pt with coarctation of the aorta | CXR: enlarved LV, post-stenotic dilation of aorta ("3 sign"), rib notching in adults // EKG: may or may not show LVH
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| complications of coarctation of aorta if not treated | essentially same as those of prolonged HTN: stroke, premature CAD, endocarditis, aortic dissection ro rupture
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| why is blood shunted from R-L in TOF? | obstruction of R outflow tract (commonly by pulmonic valve stenosis) causes flow to move from R-L and go out of aorta
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| causes of cyanosis in pt with TOF | both R-L shunt and intermixing of desaturated RV blood with saturated LV blood AND fact that lung is not receiving as much blood to saturate and return to LV
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| PEx of pt with TOF | decrescendo SEM due to R sided outflow obstruction, clubbing of nails, cyanosis, single loud S2 (don't hear PV closing really), RV lift
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| CXR and EKG findings of pt with TOF | CXR: may see RV enlargement & thus classic boot-shaped heart, small pulm arteries and vascular markings // EKG: RVH typically
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| compensatory change in pt with chronic cyanosis (Eisenmenger syndrome) | erythrocytosis (Hct of 60% or more), inc red cell mass
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| stages of Eisenmenger pathophysiology/histology | early/reversible: medial hypertrophy, intimal proliferation and fibrosis // later/irreversible: dilation and thinning of vessels, "onion skinning" (plexiform) and fibrinoid necrosis // latest: total occlusion of pulm vessels
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