04.28 - Valve Disease 2 (Nichols) Flashcards
4 Components of Tetrology of Fallot
PROVe: Pulmonic Stenosis, RV Hypertorphy, Overriding Aorta, Ventricular Septal Defect
6 Cyanotic Congenital Heart Defects
TOF, Transposition, Truncus Arteriosus, Total Anomalous Pulmonary Venous Return, Tricuspid Atresia, Hypoplastic Left Heart
90% of ASD’s are
Ostium Secundum Defects
ASD vs VSD: in which does Pulmonary HTN occur more quickly
VSD
ASD vs VSD: which has increased risk for infective endocarditis
VSD due to jet lesions
Clinical severity of TOF depends largely on
Degree Pulmonary Outflow Obstruction (if mild –> Condition is more benign)
Clubbing of the tips of fingers and toes, Polycythemia, Paradoxical Embolization
Severe systemic cyanosis (Right-to-Left Shunts)
Common congenital heart defect in females with Turner
Coarction of Aorta
Defect in lowest part of atrial septum
Ostium Primum ASD
Does Libman-Sacks Endocarditis often embolize?
No
Eisenmenger Syndrome
When a Left-to-Right shunt reverses do to increased Pulmonary hypertension
Harsh, “machinery-like” murmurs
PDA
In Calcific Aortic Stenosis, onset of symptoms =
Time for valve replacement
In more than half of cases, Coarction of Aorta is accompanied by
Bicuspid Aortic Valve
In whom is Libman-Sack Endocarditis most common
Young Black Females (same as SLE?)
Large, boot-shaped heart
Tetrology of Fallot
Location of Ostium Secundum vs Ostium Primum
Ostium Secundum is Fossa Ovalis, Primum is near AV valve
Marantic Endocarditis: common or rare
Common
Markedly enlarged intercostal and internal mammary arteries
Postductal Coarction without PDA
Midsystolic Click =
Mitral Valve Prolapse
Morphologic changes in Ostium Secundum ASD
RA and RV dilation, RV hypertrophy, Dilation of Pulmonary Artery (increased volume load)
Most common cause of cyanotic congenital heart disease
Tet of Fallot
Most common congenital cardiac anomaly at birth
VSD
Most common defects to be first diagnosed in adults
ASD’s (VSD’s more common at birth, but many close spontaneously)
Murmur in PDA
Harsh, “machinery-like” murmur
Once significant pulmonary HTN develops, the structural defects of congenital HD
are considered irreversible
Ostium Primum ASD’s can be related to
Mitral and Tricuspid valve abnormalities
Paradoxical embolus
Venous embolus that enters systemic circulation (thru patent septum or foramen ovale)
Percent of VSDs that occur in isolation
20-30 (Most are associated with other malformations)
Prevalence of Probe-patent Foramen Ovale
20%
Pulmonary HTN in TOF
No, because Pulmonic Outflow Stenosis protects pulmonary vasculature
Result of Left-to-Right Shunts
Increase pulmonary resistance –> RV Hypertrophy and eventually failure or shunt reversal
Right-to-Left shunting in TOF also increases risk of
Infective Endocarditis and Systemic Embolization
RV Failure in TOF
Rare, no Pulmonary HTN
Sinus Venosus ASD’s are often accompanied by
Anomalous drainage of pulmonary veins into RA or SVC
Site of approx 90% of VSD’s
Basal (membranous) region (last part of septum to develop)
Size of chambers of TOF
Left side normal, RV hypertrophy
Tiny (1-2mm) verrucous (wartlike) vegetations lined up on line of valve closure
Acute Rheumatic Valvulitis
Top 3 Congenital Hart Malformations
VSD, ASD, Pulmonary Stenosis
Typical sequelae of Cyanotic Heart Disease
Polycythemia; Hypertrophic Osteoarthropathy
What is nuclear dust
Basophilic debris
What leads to radiographically visible “notchin” of the ribs
Postductal Coarction without PDA
What size are vegetations of Libman-Sacks Endocarditis
Intermediate (bigger than Acute Rheumatic, smaller than Infective Endocarditis)
What type of defect is Ostium Secundum
ASD
When are you most likely to Eisenmenger Syndrome
Children with congenital heart disease with septal defects, and chronic left-to-right sunts
When do ASD’s become symptomatic
Adulthood
When does Postductal Coarction without PDA present
Usually asymptomatic, and may remain unrecognized until adult
When does Preductal Coarction with PDA usually present
Early in life, most infants don’t survive neonatal period
When is survival possible in Transposition
Shunt such as VSD
When will Paraxodical embolism occur
If right sided pressures increase: Pulmonary HTN or Valsalva
