Cardiology Flashcards
Cyanotic Heart Diseases:
- tetrology of fallot
- ebsteins anomaly
- truncus arteriosus
- TGA
- tricuspid atresia
- TAPVC
- hypoplastic L heart
- pulmonary atresia
Ebsteins Anomaly
Big R atrium with small ventricle + malfunctioning tricuspid. Sometimes ASD or PFO too.
Causes early cyanosis. Can also be asymptomatic if mild. May have arrhythmia (WPW).
Defects causing cyanosis in first few hours of life
- ebsteins anomaly
- TGA
- pulmonary atresia
- PHTN
Defects causing shock / catastrophy
- hypoplastic L heart
- coarctation of aorta (if severe)
- aortic stenosis (if severe)
Acyanotic Congenital Defects
L to R shunt:
- ASD
- VSD
- PDA
- AVSD
Obstructive:
- coarctation of aorta
- aortic stenosis
- pulmonic stenosis
Heart Defects Causing CHF
VSD
PDA
AVSD
lead to excessive pulmonary flow
Tetralogy of Fallot
VSD, over-riding aorta (above VSD), PA stenosis, RVH
Truncus Arteriosus
Single trunk from both ventricles
aorta, PA, coronaries
Tricuspid Atresia
No tricuspid valve (need ASD, VSD, PDA)
Transposition of great arteries
Aorta starts in RV
pulmonary artery starts in LV (left + right side totally separate, reliant on ASD + PDA)
Total anomalous pulmonary venous connections
Pulmonary veins not connected to LA, go to SVC instead (reliant on an ASD/PDA/PFO)
Most common cyanotic heart defects
may present with other things, but CAN be cyanotic
- tetralogy of fallot
- tricuspid atresia
- transposition of great arteries
- TAPVC
- truncus arteriosus
DDx for cyanosis
Resp: RDS, TTN, MAS, pneumonia, CLD
Cardiac: cyanotic heart defect
Heme: Sepsis, polycythemia, methaemoglobinemia
neurometabolic: meningitis, ICH, drugs, hypothermia, hypoglycemia
Differentiating Resp vs Cardiac Cyanosis
Resp: increased WOB, sepsis RFs, meconium, difficult labour, high CO2, abnormal CXR, improve with O2
Cardiac: famHx, normal L+D, no or mild tachypnea, N CO2, CXR with pulm blood flow or cardiac silhoutette, min response to O2
Persistent Pulmonary Hypertension Description
Failure of post-natal adaptation: RVF, R–>L shunting through PFO + DA
primary: soon after birth, normal lungs on xray
secondary: diseased lungs, pulmonary vasoconstriction from hypoxia/acidosis
Work-up for Congenital Heart Disease
- CXR
- ECG, Echo
- Pre (R arm) and post ductal (leg) saturation
- four limb BP (systolic >10 higher in upper body = coarctation)
- hyperoxic test (if cyanosis): 100% O2, repeat ABG after 10-15m, fail if <150
- cyanosis: ABG, lactate, Hb, WBC, glucose
Interpretation of Pre + Post ductal saturations
pre-ductal sat >3% above post = bad
Shunting through DA (R–>L)
PPHTN (sometimes), severe coarctation/AS, HLHS
higher post-ductal TGA
Transposition of Great Vessels Management
- intubation + O2
- IV fluids
- Amp + Gent
- PGE1 (prostaglandin)
- transport –> balloon atrial septostomy
- switch operation at 7 days old
Ventricular Septal Defect: Presentation
- murmur starts about 1wk when PVR declines enough for L->R shunt
- Murmur: holosystolic, loudest LLSB
- loss of S2 split, loud P2 (PTHN)
- very large may have no murmur
- CHF symptoms (at 3-4wks): resp distress, feeding difficulty/diaphoresis, FTT, hepatomegally
- if small will be asymptomatic or just murmur
VSD treatment
- CHF symptoms: diuretics, nutrition support
- if closing spont (many do): monitor for signs of PHTN
- surgery if sx no managed and to avoid PHTN (eisenmengers syndrome, shunt reverses R -> L, cyanosis)
Atrial Septal Defect Presentation
- shunt L –> R, low pressure, no sound
- murmur at pulm valve = systolic ejection murmur (from extra flow)
- wide fixed split S2
- CHF symptoms rare
- CHF + PHTN in 3rd or 4th decade possible
ASD managment
- most close spontaneously
- if large or CHF not responding to meds, surgical closure
Patent Ductus Arteriosus Presentation
Aorta –> PA
- more common in premies
- murmur: cont at L infraclav or LUSB
- bounding peripheral pulses
- hyperactive precordium
- tachycardia, +/- gallop, wide pulse pressure
Patent DA complications and management
small - no intervention
large –> PHTN
premies: indomethacin (prostaglandin synthase inhib)
surgery if unsuccessful or in child/adult
CHF pathophys/etiologies
- low O2 (severe anemia)
- hypermetabolic state ( hyperthyroid)
- High output (overflow)
- cardiomyopathy
CHF Ddx - Premies
Anemia
PDA or large VSD (L->R)
severely preterm
lung disease
CHF ddx - infants
VSD/AVSD
AS or CoA
myocarditis
AVM
CHF ddx - child
L side obstruction
cardiomyopathy
myocarditis
younger:
Kawasaki’s
L –> R shunt
AVM
older: rheumatic heart disease acute HTN thyrotoxicosis meds
DDx for difficult feeding + resp distress in infant
- CHD / CHF
- resp infection
- sepsis
- metabolic disorder
Innocent Murmur Characteristics
Soft blowing, vibratory systolic well localized vary /w position
Pathologic Murmur characterstics
loud
harsh
pansystolic, diastolic, late systolic, continuous
no change with position
Pan-systolic Murmur
MR, TR, VSD
Continuous Murmur
PDA (varies in intensity)
Systolic Ejection Murmur
PS (/w ASD sometimes), AS,
Several innocent murmurs too
early diastolic murmur
AR or PR
mid diastolic
MS, TS
Newborn with Loud S2 (not split)
pulmonary HTN
