Cardiology Flashcards
O2 sat in chambers of fetal circulation.
Where is O2 sat highest? Lowest?
PBF ~ 7 - 15% 2nd trimester
30% 3rd trimester (lung growth so increased PBF)
20% around 38 weeks (more O2 so constricts?)
66% CO RV vs 33% LV
Left - because receiving DV blood flow (from UVC oxygenated blood) primarily without mixing in much “used” deoxygenated blood + little bit of blood from lungs
Increase ductus venosus - dilates.
Decrease HR, RR, CO
Fetus goes in hibernation mode - relies on maternal thermoregulation, decrease GI absorption, decreased RR, decrease renal tubular absorption
Preferentially sends blood to head, heart, adrenal glands (by dilating ductus venosus to increase blood to RA -> LA via FO). Abd circumference decrease in FGR fetuses (b/c less BF to those organs) and elevated MCA (diastolic flow increased as more BF to brain)
Note-tricuspid valve very sensitive to hypoxemia (therefore, babies with HIE can have TR)
- Increase PBF via breathing RA (dilates pulm vessels and decrease PVR)
- Closure of FO (increase LA pressure due to increase pulm BF and PV return so then closes; also distal SVR will increase LA pressure)
- Closure of DA (oxygen exposure of ductal tissue with constrict it, decrease PGE production (detached from placenta) and metabolism (from lung that is working more), decrease bradykinin (helps vasoconstrict)
UV constricts - because decrease blood flow
UA constricts - because increase O2 content
How does DCC work?
- continued blood flow from UV to LA/LV so continued preload while 1) lungs are aeration and increasing pulm BF and 2) not an acute drop in SVR so myocardium has time to start to handle a larger blood volume load
What influences ventricular wall stress?
Conceptualize Frank Starling curve
Frank starling curve - effect of increased and decreased preload
Frank starling curve - effect of increased and decreased afterload
PS, hypertelorism, downward slanting palpebral fissures, low at ears, short stature, short webbed neck, Percy’s excavation, cryotorchidism, cognitive delays, lymphedema
Noonan - most common cause of HOCM kids < 4 although most common cardiac defect with Noonan is PS
1 cyanotic congenital heart disease in infancy/childhood
ToF
1 cyanotic CHD in first week of life
TGA
describe early formation of cardiac tube
early cardiac embryology
mediator of cardiac development
mediators of septation
mediators of L-R differentiation
when does cardiac septation occur?
8 weeks
heterotaxy - what occurs
L atrial isomerism
- describe
- complications
R atrial isomerism
- describe
- complications
Reverse differential - infant pre ductal is 50% an post-ductal is 70%. Describe the scenario.
d-TGA with inadequate atrial or ventricular mixing and elevated PVR or LVOT (eg CoA).
Most common type of VSD. Which VSD types are more likely to close?
perimembranous
those with a muscular region (perimembranous or muscular)
Congenital heart disease - XR described as egg on a string
Scimitar syndrome X ray
- describe Scimitar syndrome
- complications
PAVPR (an anomalous pulm vein to RV)
Can develop pphn, can have some R pulm hypoplasia
Other associated anomalies
Snowman appearance on XR (congenital heart defect - cyanotic heart lesion)
snowman TAPVR
Infant with TEF, vertebral anomalies and hydronephrosis has a cardiac defect. What is the most likely cardiac defect in this scenario.
VACTERL
VSD
High lying UAC vs low lying UAC - risks and benefits
High - less ischemic complications; same rate of HTN
Low - **; same rate of HTN
Morphological development of the heart
- what occurs at week 2
cardiac development starts at gastrulation (going from 2 to 3 germ layers) and mesodermal cells migrate toward embryonic disk.
When does the heart undergo looping? Describe.
around 3 - 4 weeks - linear tube begins to bend towards the R side; distinct chambers appear around this time and more looping to get ventricles side by side.
NKX2.5
TBX1
When does septation occur?
Around 5 weeks.
Septation of atria (primum septum, primum ostium, secundum septum, secundum ostium?)
Septation of ventricles
Septation of truncus
EKG changes with D-TGA
R axis deviation (R QRS - up in I and down in avF), RVH, may have RAH
NOTE: Varying degrees of AV block extending to complete heart block may be seen in L-transposition of the great arteries
EKG changes and murmurs in ToF
EKG: RVH (b/c of increased RVP as a result of PS)
EKG changes in TA
L superior QRS common (0 to -90)
Increased LV forces
Decreased RV forces
RAH with large P wave
Adenosine
- mode of action
- indications for use
- adverse effects
- transiently blocks AVN (may need higher dose if on caffeine)
- SVT
- hypotension, bronchoconstriction, wheezing
Amiodarone
- mode of action
- indications for use
- adverse effects
- K channel blocker -> slows conduction (+also a Na and Ca channel blocker, and B adreno blocker - negative inotropy, chronotropy)
- SVT that does not respond to adenosine, VT (stable)
- LFT, PFT, TFT monitoring; Give Ca prior
Digoxin
- mode of action
- indications for use
- adverse effects
- Some AV block (helpful w. other agents eg flecainide, sotalol)
- Use more fetal tachycardias
- Monitor concentrations, toxic at high levels, NOT in WPW (risk accelerating the antegrade accessory pathway)
Flecainide
- mode of action
- indications for use
- adverse effects
- Na channel blocker; min effect on conduction
- More fetal SVT
- Monitor levels, worse if renal dysfunction, NO refrigeration (precipitates) and milk ingestion alters absorption
Propranalol
- mode of action
- indications for use
- adverse effects
- BB
- Use if adenosine responsive tachycardia, first line in WPW and FT, possible LT therapy
- Glucose, BP
Sotalol
- mode of action
- indications for use
- adverse effects
- K channel blocker; some BB effect; slows conduction but less effective than amioradone
- Useful in combo with flecainide in refractory SVT
- Bradycaria, prolonged QT monitoring, cautiously use in myocardial dysfunction
Verapamil
- mode of action
- indications for use
- adverse effects
- Ca channel blocker (slows AV conduction)
- Contraindicated < 12 mo b/c associations with sudden death
Most common cardiac lesion in Turner syndrome
L sided lesions eg CoA (30% of Turners have CoA)
Bicuspid aortic valve (If CoA and BV -> sicker, need LT follow)
Most common cardiac lesion in Noonan syndrome
Pulm valve stenosis (RAS pathway). also HOCM (most “common” cause of HOCM during **)
Most common cardiac tri 13
Valve dysplasia
Brachial arches
4 -> R subclavian
6 -> PDA
Normal PR newborn
Normal QRS
Normal QTc
0.08 - 0.11 s
0.04 - 0.07 s
0.45 s (up until < 6 months)
Types of shock
Types of heart block
Review pressors
Review pressors
Review pressors
Frank starling curve
Causes neonate HTN
Causes of prolonged QTc
Recognize torsades
Management of complete AV block
reocgnize this EKG
Management of WPW SVT
Delta wave
WPW
prolonged QTc
