Cardio Flashcards
Most common cyanotic heart defect in kids
TOF
TOF
Genetic and enviro factors Assoc with 22q deletions Cyanosis lips, extremities, HSM LLSB Increased preload Increased SVR Boot shaped heart, increased pulm vasc markings
Tetralogy: VSD Pulm stenosis RVH overriding aorta
Holosystolic murmurs
MR, TR, VSD
TGA
No blood oxygenation without PDA, ASD, or VSD. Early and severe cyanosis. Single S2.
“Egg and string” CXR
Must have PDA.
NSAIDs contraindicated (cause PDA closure)
Requires two-step surgery, each sx carrying 50% mortality
Pulsus alternans
LV systolic dysfunction
Pulsus bigeminus
Sign HOCM
Pulsus bisferiens
AR
Pulsus parvus et tardus
AS
Pulsus paradoxus
Tamponade and tension pneumo
Hypoplastic Left Heart Syndrome
LV hypoplasia, mitral valve atresia, aortic valve lesions
Absent pulses with single S2, increased RV impulse
Gray (vs blue) cyanosis
CXR-globular heart with pulm edem. Echo most diagnostic
Tx: 3 separate sx or transplant. Each sx has high mortality
Truncus arteriosus
Sxs within few days of life. Severe SOB, early and freq resp infxns.
CXR-cadiomegaly, increased pulm markings
Single S2 (only 1 semilunar valve) and SEM (valve leaflets usu abnormal in functionality)
Most serious sequelae is pulmonary HTN-develops in 4/12
TAPVR
No venous return between pulm veins and LA-oxygenated blood to SVC. W or w/o obstruction of venous return
VSD
Presents w SOB w/resp distress, high pitched HSM over LLSB, loud pulmonic S2.
Increased vascular markings
Small lesions usu close in first 1-2 years life
Larger or more symptomatic lesions req sx
ASD
Twice as comm in women
Vast majority close spontaneously. Sx or transcath closure x’d for all symptomatic pts
Can have arrhythmia, poss paradoxical emboli
ASD-primum defect associated with what?
Concomitant MV abnormalities
ASD-secundum defect
Most common type ASD
Located in center of atrial septum
ASD-sinus venosus defect
Least common type ASD
PDA
Usu closes when PO2 >50mmHg
Normal finding in first 12 hours life; pathological after 24 hrs
Increased pressure, bounding pulses, high incidence of resp infxns
IE most comm complication later in life
ECG may show LVH due to high SVR
Indomethacin closes; prostaglandind keep open
Pear-shaped heart on CXR
Pericardial effusion
Boot shaped heart on CXR
TOF
Jug handle appearance (heart) on CXR
Primary pulmonary artery hypertension
3-like appearance of heart on CXR
coarc
Coarc-presentation
Severe CHF, resp distress, differential pressures and pulses between upper and lower extremities
Causes obstructed systemic circulation
Hypoplastic left heart
Critical aortic valve stenosis (congenital–bicuspid)
Severe coarc
Interruption of aortic arch
Heart defects causing high pulmonary flow
I.e. Left to right shunts
VSD
ASD
Large PDA
Eisenmenger syndrome
Originally left to right shunt….then right side hypertrophies and has more pressure than left side, so shunt reverses and becomes right-to-left.
RFs congenital heart disease
Maternal drug use in prengnancy: lithium, booze Maternal diabetes Maternal PKU Intrauterine infections, e.g. RUBELLA Prematurity
In summary: it’s all mom’s fault.
What do you want to ask about in hx to rule out/in congenital heart defects?
Cyanosis! Worse on feeding, crying?
Grey color changes
Sweating or resp distress on feeding or crying
Squatting when breathless (older children)
Collapse/syncope
