Cardiac Flashcards
Wolf-Parkinson White
Accessory pathway in heart bypassing AV node
- -> ventricular pre-excitation
- -> shortened PR, delta wave, widened QRS
- Re-entrant tachycardia= narrowed QRS
Mitral regurgitation
Blowing holosystolic murmur over 5th LICS, midclavicular line
Radiates to axilla
- Can lead to CHF, pulmonary edema
Prevent by decreasing LV afterload
–> decreased systolic pressure driving blood into LA, increased forward stroke volume
Treat with arterial vasodilators
Isoproterenol
Beta agonist
- Increases cardiac contractility (B1)
- Decreases peripheral resistance (B2)
Phentolamine
Alpha receptor blocker
- -> subcutaneous vasodilation
- Used in NE-induced tissue necrosis (reverse effects of alpha agonist)
Tetralogy of Fallot
Abnormal neural crest cell migration featuring:
- VSD
- Overriding aorta
- Pulmonary stenosis
- R ventricular hypertrophy
Features:
- Blue baby
- Squat–> increase systemic pressure–> decrease R-> L shunt–> more blood to lungs
**Seen in 22q11 syndromes
Truncus arteriosis
Abnormal migration of neural crest cells
- Doesn’t divide into pulmonary trunk and aorta (only partial septum formation)
** seen in 22q11 syndromes
Transposition of great vessels
abnormal migration of neural crest cells
- RV–> aorta
- LV–> pulmonary artery
Symptoms:
- Irritable
- Machine-like murmur between scapulae (PDA)
- Severe cyanosis
- only survives with shunt (PDA, Atrial shunt)
- seen in infant of diabetic mother
Endocardial cushion defect
Membranous septal defect= AV septum defect–> L to R shunt–> pulmonary HTN–> Eisenmenger syndrome
Eisenmengers= blood reverses to R–> L shunt
- Cyanosis, clubbing, polycythemia
Patent foramen ovale
Failure of septum primum and secundum to fuse after birth
- Fusion driven by increase in pulmonary blood flow (decreased resistance)–> increased L atrial presssure–> pushes flap of septum primum closed over foramen ovale
- Normally develops into fossa ovalis
Patent foramen ovale–> increased risk of venous clots causing stroke (bypass pulmonary system)
Umbilical vein
Carries oxygenated blood from placenta–> ductus venosus–> IVC–> heart
- After birth: ligamentum teres hepaticus (within falciform ligament)
** Vitelline veins–> portal venous system
Umbilical arteries
Two: Connect internal iliac arteries (carrying fetal venous blood)–> to placenta
- become medial umbilical ligaments after birth
Ductus arteriosus
Connects pulmonary artery (RV) and aorta (LV)
- Patency ensures oxygenated blood reaches aorta
- At birth–> baby breathes O2–> decrease in prostaglandins–> ductus arteriosus closes–> ligamentum arteriosum
PDA= patent ductus arteriosus
- Maintained by indomethacin (essential to have PDA in babies with transposition of great vessels until surgical correction)
- See in congenital rubella infection
Ductus venosus
Carries oxygenated blood from umbilical vein–> IVC
After birth: ligamentum venosum
Notochord
Becomes nucleus pulposus of IV disc
Bulbus cordis
Base of Truncus arteriosus
Becomes smooth parts (outflow tracts) of L and R ventricle
Left horn of sinus venosus
Between SVC and IVC in early heart
Becomes coronary sinus
Right horn of sinus venosus
Between SVC and IVC in early heart
Becomes smooth part of R atrium
Right common cardinal vein, R anterior cardinal vein
Drain into sinus venosus
Become SVC
Wide split S2
Conditions delaying RV emptying:
- Pulmonic stenosis
- RBBB
Exaggerrated normal splitting
Fixed S2 splitting
Seen in ASD (patent foramen ovale)
ASD–> L–>R shunt
–> RA, RV volume increased
–> increased flow thru pulmonic valve
–> Eisenmenger if untreated (increased pulmonary vascular resistance)–> permanent damage–> shunt reverses R–>L
Paradoxixcal S2 splitting
Conditions delaying LV emptying: - Aortic stenosis - LBBB P2 sound occurs before A2 - On inspiration, splitting "paradoxically" eliminates as P2 delayed--> closer to A2
Hand grip maneuver
Increases systemic vascular resistance
- Increases: MR, AR, VSD, MVP
- Decreases: AS, HOCM
Valsalva, standing from sitting
Decreases venous return (less blood in LV)
- Increases MVP, HOCM
- Decreases most other murmurs
Rapid squatting
Increases venous return, preload (afterload with prolonged squatting)
- Decreases MVP, HOCM