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lecture 18 brickner

prevalence of CHD 4-9/1,000 live births with bicuspid aortic valves being most common abnormality @ 3% prevalence in general population
definition of CHD presence at birth of a gross structural abnormality of heart, great arteries or veins that can potentially have functional significance
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
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
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
severe hypertensive pulmonary resistance can even reverse shunt of PDA obvi it can also reverse any other L-R shunt like VSDs or ASDs
criterion for determining if L-R shunt is significant Qp (pulmonary flow) is 1.5-2x greater than Qs (systemic flow)
central cyanosis desaturation of arterial blood beginning from within lungs or heart (intracardiac R-L shunt, hypoventilation or V/Q mismatch)
peripheral cyanosis increased extraction of O2 by peripheral tissue in the presence of nl arterial O2 saturations (hypovolemia, shock, vasoconstriction from cold or meds)
how to evaluate a pt for possible CHD careful PEx, EKG, measuring arterial O2 sats, CXR then Echo and cardiac cath to positively confirm
5 Ts that cause baby to be cyanotic tetralogy of Fallot, tricuspid atresia, transposition of great arteries, truncus arteriosus, total anomalous pulmonary return
2 most common causes for cyanosis in adults Eisenmenger syndrome, tetralogy of Fallot
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)
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
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
most common type of VSD membranous portion of ventricular septum - near the AV and TV aka perimembranous defect
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
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
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
pts with VSD will all need prophylactic tx for? bacterial endocarditis
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
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
complication of PDA if not repaired risk of endocarditis or endarteritis (of PA)
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
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
complications of coarctation of aorta if not treated essentially same as those of prolonged HTN: stroke, premature CAD, endocarditis, aortic dissection ro rupture
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
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
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
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
compensatory change in pt with chronic cyanosis (Eisenmenger syndrome) erythrocytosis (Hct of 60% or more), inc red cell mass
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
Created by: sirprakes