CV path Flashcards
R -> L shunt
early cyanosis, blue baby
urgent surgical correction and/or maintenance of PDA
R -> L shunt causes
5 T's Truncus arteriosus (1 vessel) Transposition (2 switched vessels) Tricuspid atresia (3=Tri) Tetrology of Fallot (4=tetra) TAPCR (5 letters in name)
D-transposition of great vessels
not compatible w/life w/o shunt (VSD, PDA, PFO)
tricuspid atresia
absence of tricuspid valve and hypoplastic RV
requires both ASD and VSD for viability
tetralogy of fallot
d/t anterosuperior displacement of infundibular septum
MCC of early childhood cyanosis
PROVe
Pulmonary infundibular stenosis (prognostic)
Right ventricular hypertrophy (boot shape on CXR)
Overriding aorta
VSD
TAPVR
total anomalous pulmonary venous return
pulmonary vv drain into right heart circulation
associated with ASD and PSD to allow for R->L shunting to maintain CO
L->R shunt
late cyanosis -> blue kids
VSD>ASD>PDA
VSD
MC congenital cardiac defect
most self resolve
if large enough may lead to LV overload and HF
ASD
loud S1
wide fixed split of S2
ostium secundum defects most common (isolated)
ostium primum defects (other cardiac anomalies)
distinct from foramen ovale in that septa are missing rather then unfused
PDA
assocaited with continuous machine like murmur
eisenmenger syndrome
uncorrected L->R shunt -> increased pulmonary flow -> pulmonary HTN -> RVH occurs to compensate -> shunt becomes R -> L -> cyanosis, clubbing, polycythemia
coarctation of aorta
bicuspid aortic valve
turners
HTN in upper extremities and weak pulse in lower
erosion of ribs by collateral aa
alcohol exposure in utero
VSD
PDA
ASD
tetralogy of fallot
congenital rubella
septal defects
PDA
pulmonary a stenosis
downs
AV septal defect (endocardial cushion defect)
ASD
VSD
DM
transposition of great vessels
marfans
MVP
thoracic aortic aneurysm and dissection
aortic regurg
prenatal lithium exposure
ebstein anomaly
septal and post leaflets of tricuspid displaced toward apex
turners
bicuspid aortic valve
coarctation of aorta
williams syndrome
supravalvular aortic stenosis
22q11
truncus arteriosis
tetraology of fallot
mockenberg
medial calcific sclerosis uncommon affects medium sized aa calcification of elastic lamina of aa -> vascular stiffening w/o obstruction pipestem appearance on XRAY does NOT obstruct blood flow intima NOT involved
obliterative endarteritis of vasa basorum
thoracic aortic aneurysm d/t tertiary syphilis
aortic dissection
intimal tear
associated w/HTN, bicuspid aortic valve, inherited CT dis
Stanford type A aortic dissection
proximal
involves ascending aorta
surgery
stanford type B aortic dissection
distal
involves descending aorta and/or arch
ascending aorta NOT involved
Tx medically w/beta blockers, then vasodilators
prinzmental angina
aka variant secondary to coronary a spasm transient ST elevation triggers: tabacco, cocaine, triptans Tx: CCBs, nitrates, smoking cessation
coronary steal
distal to coronary stenosis vessels maximally dilated at baseline
administration of vasodilators dialtes normal vessels and shunts blood toward well-perfused ares -> decreased flow to heart
used in pharm stress test
MI
LAD>RCA>circumflex
MI gross 0-4 hrs
none
MI light 0-4 hrs
none
MI complications 0-4 hrs
arrhythmia
HF
cardiogenic shock
MI 4-24 hr gross
dark mottling
pale w/tetrazolium stain
MI 4-24 hr light
early coagulative necrosis
release of necrotic cell contnets into blood
edema
hemorrhage
wavy fivers
neutros
reperfusion injury may cause contraction bands
MI 4-24 hrs complications
arrhythmia
HF
cardiogenic shock
MI 1-3 days gross
hyperemia
MI 1-3 days light
extensive coagulative necorsis
acute inflammation w/neutros
MI 1-3 days complications
post MI fibrinous pericarditis
MI 3-14 days gross
hyperemic border around central yellow-brown softening
maximally yellow and soft by 10 days
MI 3-14 days light
macros
granulation tissue at margins
MI 3-14 days complications
free wall rupture -> tamponade; papillary mm rupture -> mitral regurg -> interventricular septal rupture d/t macro mediated degradation
LV pseudoaneurysm
MI 2 wks- 2mo gross
recanalized aa
gray-white scar
MI 2wks-2mo light
contracted scar complete
MI 2wk-2mo complications
dressler syndrome HF arrhythmias true ventricular aneurysm risk of mural thrombus
Dx of MI first 6 hrs
EKG gold standard
ST elevation (transmural) or depression (subendo)
hyperacute/peaked T waves
T wave inversion
new LBBB
pathologic Q waves
poor R wave progression (evolving or old transmural infarct
cardiac troponin I
rises after 4hrs and is high for 7-10 days
most specific
CK-MB
rises after 6-12 hrs
return to normal in 48hrs
transmural infarcts
ST elevation
increased necrosis
affects entire wall
subendocardial infarcts
d/t ischemic necrosis
anteroseptal MI
LAD
V1-2
anteroapical MI
distal LAD
V3-4