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Flashcards in CV surgery and congenital heart defects Deck (18):

CV surgery questions

-Aneurysm= 2x normal size
-Reasons to operate on an Ao aneurysm (type B only): persistent pain, mal perfusion, aortic rupture
-Ao aneurysms: type A includes ascending, type B only descending
-Ao stenosis: long latency period (w/o Sx), but once Sx appear 50% will be dead in 2 yrs


Classification of congenital heart defects (CHDs)

-Acyanotic (shunt) lesions: atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA)
-Obstructive lesions: pulmonic stenosis, aortic stenosis, coarctation of aorta
-Cyanotic lesions: transposition of great arteries, tetralogy of fallot


Physiology of left to right shunts

-Pulmonar artery pressure should be about 1/5th of systemic pressure
-Right heart/pulmonary circulation is low resistance, high capacitance
-Left heart/systemic circulation is high resistance, limited capacitance
-Left-right communication (defect): redirection of oxygenated blood from high resistance (systemic) to low resistance (pulmonary) circulation
-Redirection is based on resistance, not pressure


Atrial septal defect (ASD)

-Left-right atrial shunt
-Since the RV is more compliant than LV there is R heart volume overload
-There is RAE, prominent RV impulse, and possible dilated RV
-There is systolic ejection murmur (pulmonic- due to increased volume thru pulmonic valve) and split S2
-Late risks: paradoxic embolism, arrhythmias
-Rx: device closure


Ventricular septal defect (VSD) 1

-Can be pressure restrictive (pressure difference btwn ventricles is maintained- small hole) or pressure non-restrictive (pressure difference equalizes btwn ventricles as more blood enters RV- large hole)
-Pressure restrictive VSD: LVP>>RVP and there is harsh systolic ejection murmur


Ventricular septal defect (VSD) 2

-Pressure non-restrictive VSD: LVP=RVP, but PVR (pulmonary vascular resistance) is less than SVR, so there is L->R shunt
-Results in CHF, systolic murmur (blood going thru VSD from LV->RV since SVR>PVR) and diastolic murmur (increased flow from LA->LV)
-Can lead to pulmonary HTN and then the shunt reverses (since PVR>SVR)
-In a R-L shunt there is cyanosis (not all blood reaches lungs), and a loud P2


Clinical course of VSDs

-Unrestrictive VSDs will often need surgery in infancy to prevent CHF
-Late risks: endocarditis, Ao valve prolapse
-Rx: surgical closure


Patent ductus arteriosus (PDA)

-Prevalent in premature infants
-Closes due to increase in pO2 and decrease in prostaglandins (PGE1)
-Causes a shunt of oxygenated blood from Ao to pulm arteries (PVR-This leads to continuous murmur (both diastolic and systolic) b/c there is constantly blood moving from Ao to PA
-Risks: newborns at risk for CHF, respiratory failure and children at risk for endocarditis
-Rx: coil occlusion


Obstructive congenital heart defects

-Pulmonic stenosis, Ao stenosis, coarctation
-Ventricle must generate increased pressure, leading to compensatory hypertrophy, hyperplasia, post-steonitic arterial dilation
-Newborns are in high-output state (increased HR) and increased pressure requirement results in early circulatory failure


Pulmonary stenosis

-Obstruction to RV systolic ejection: RVH and PA dilation
-May be mild (ASx), moderate (exercise limitation), or severe
-Severe (RVP>LVP) may be comorbid with ASD (R->L atrial shunt) resulting in cyanosis
-PE: harsh systolic murmur @ upper sternal borders radiating to lungs, ejection click, possible hepatomegaly
-Can see PA enlargement and post stenotic dilation on CXR
-RVH (possible RAE) on ECG
-Rx: ballot catheter dilation


Aortic stenosis

-Dysplasia of Ao leaflets leads to limited valve motion
-Obstruction to LV systole: LVH and mitral insufficiency (secondary MR)
-Also mild (ASx), moderate (exercise limitation), and severe (LV failure)
-PE: harsh systolic murmur, ejection click, suprasternal thrill
-Rx: balloon catheter and surgery


Hypoplastic left heart syndrome (HLHS)

-Underdeveloped LV size, hyper plastic septum and LV wall
-Must keep PDA open
-Rx: Norwood procedure where they fuse Ao to RV and Rv does all the work


Coarctation of the Ao

-Narrowing of Ao causing a large gradient btwn Asc and Desc Ao
-High BP in UEs but low or normal in LEs
-May lead to increased renin-angiotensin activation (due to decreased renal perfusion), rib-notching (for collateral circulation)
-Neonatal coarctation: hypoplastic aortic isthmus
-Discrete coarctation: discrete narrowing of Ao
-Clinical course: may get CHF in newborn, and if there is PDA the lower extremities will get cyanosis due to PDA deoxygenated blood
-If severe coarctation want to keep PDA open (give PGE1) to promote blood flow to LEs
-Rx: surgical intervention


Tetralogy of Fallot 1

-4 things: VSD, pulm stenosis, RVH, overriding Ao (over the RV)
-There is mal-alignment of infundibular septum: unequal distribution of LV/RV outflow tracks
-This along w/ VSD and pulm stenosis lead deoxygenated blood to be shunted R->L to Ao leading to cyanosis
-Severity depends on pulm stenosis, b/c that dictates PVR and thus the amount of shunting


Tetralogy of Fallot 2

-Pts will have harsh systolic murmur (PS), decreased pulmonary arteries in CXR, along w/ boot-shaped heart on CXR, clubbing from chronic cyanosis
-Pts often squat when feeling out of breath to increase venous return and TPR
-Rx is surgical repair


Transposition of great arteries

-The aorta is connected to RV and PA connected to LV
-This means deoxygenated blood from RV goes to body continuously and causes cyanosis, and the oxygenated blood from LV keeps going to the lungs (circulation are in parallel, not in series)
-PDA must be open to live (or septal defect), so the blood from PA can get to the Ao
-Murmur not always present, increased pulmonary arteries on CXR
-Rx is creating an ASD for blood to mix and keeping PDA open (PGE1 administered immediately), then switch the Ao and PA


Loss of shunting

-Shunting should be absent 24hrs after birth, meaning if there is a difference in pO2 sat btwn UEs and LEs there is still shunting occurring (PDA)


Difference btwn SVR and PVR

-Normal PVR: 0-1
-Normal SVR: 10-20
-A PVR ≥3 is concerning