heart Flashcards
acyanotic congenital heart disease
-Left-to-Right Shunt Lesions:
-Atrial Septal Defect (ASD)
-Ventricular Septal Defect (VSD)
-Atrioventricular Septal Defect (AV Canal)
-Patent Ductus Arteriosus (PDA)
-Qp:Qs > 1
ASD- atrial septal defect
-opening in the atrial septum permitting free communication of blood between the atria
-Seen in 10% of all CHD
-assoc with fetal alcohol syndrome
-3 major types:
-Secundum ASD – at the Fossa Ovalis, most common.
-Primum ASD – lower in position & is a form of ASVD, MV cleft -> 25% of down syndrome
-Sinus Venosus ASD – high in the atrial septum, associated w/partial anomalous venous return & the least common
ASD- SS
-Rarely presents with signs of CHF
-Most asymptomatic -> may have easy fatigability or mild growth failure.
-Cyanosis does not occur unless pulmonary HTN present
-Hyperactive precordium, RV heave, fixed widely split S2
-2-3/6 systolic ejection murmur @ LSB
-Mid-diastolic murmur heard over LLSB
-Systolic murmur is caused by increased FLOW across the pulmonary valve, NOT THE ASD
-Diastolic murmur is caused by increased flow across the tricuspid valve & this suggest high flow Qp:Qs is 2:1
-paradoxical embolism- DVT clot goes to brain instead of lungs
ASD: tx
-Surgical or catherization lab closure for secundum ASD w/ a Qp:Qs ratio >2:1.
-Closure is performed electively between ages 2-5 yrs to avoid late complications (wait for it to close on its own)
-amplatzer is used
-Surgical correction is done earlier in children w/ CHF or significant Pulm HTN
-Once pulmonary HTN w/ shunt reversal occurs this is considered too late.
-Mortality is < 1%.
-endocarditis prophylaxis NOT required for ASD
VSD- ventricular septal defect
-abnormal opening in ventricular septum
-allows free communication between RV and LV
-25% of CHD
-fetal alcohol syndrome and down syndrome
-pulmonary artery is the determinant of flow
-left to right shunt occurs secondary to pulmonary vascular resistance being < systemic vascular resistance -> NOT the higher pressure in LV
-leads to elevated RV & pulmonary pressures/volume -> hypertrophy of LA & LV
-if the pulmonary HTN develops the blood switch to R->L shunt -> eisenmenger!
-holosystolic murmur at the LLSB
-4 types:
-Perimembranous (or membranous) – MC
-Infundibular (subpulmonary or supracristal VSD) – involves the RV outflow tract.
-Muscular VSD – can be single or multiple.
-AVSD – inlet VSD, almost always involves AV valvular abnormalities
-fatigue, failure to thrive,
VSD- SS
-Small - moderate VSD, 3-6mm, are usually asymptomatic and 50% will close spontaneously by 2yo
-Moderate – large VSD, almost always have symptoms and will require surgical repair
-2-3/6 harsh holosystolic murmur heard along LLSB, more prominent with small VSD, maybe absent with a very Large VSD.
-Prominent P2, Diastolic murmur.
-CHF, FTT, Respiratory infections, exercise intolerance hyperactive precordium
-Symptoms develop 1-6mo
VSD- tx
-Small VSD - no surgical intervention, no physical restrictions, just reassurance -> periodic follow-up and endocarditis prophylaxis.
-Symptomatic VSD - Medical treatment initially with afterload reducers & diuretics
-Indications for Surgical Closure:
-Large VSD w/ medically uncontrolled symptomatology & continued FTT.
-Ages 6-12 mo w/ large VSD & Pulm. HTN
-Age > 24 mo w/ Qp:Qs ratio > 2:1.
-Supracristal VSD of any size, secondary to risk of developing AV insufficiency
-larger the VSD -> aortic annulus -> incompetency of aortic valve -> aortic insufficiency
atrioventricular septal defect- AVSD
-results from incomplete fusion of endocardial cushions, which form lower portion of atrial septum, membranous portion of ventricular septum and septal leaflets of triscupid and mitral valves.
-account for 4% OF ALL CHD
-downs syndrome (trisomy 21), seen in 20-25%
-COMPLETE FORM
-Low primum ASD continuous with a posterior VSD.
-Cleft in both septal leaflets of TV/MV.
-Results in a large L to R shunt at both levels.
-TR/MR, Pulm HTN w/ increase in PVR.
-INCOMPLETE FORM
-Any one of the components may be present.
-MC is primum ASD, cleft in the MV & small VSD.
-Hemodynamics are dependent on the lesions.
atrioventricular septal defect- SS
-Incomplete AVSD maybe indistinguishable from ASD - usually asymptomatic.
-CHF in infancy.
-Recurrent pulmonary infections.
-Failure to thrive.
-Exercise intolerance, easy fatigability.
-Late cyanosis from pulmonary vascular disease w/ R to L shunt -> cyanosis is indicative of blood not going through pulmonary circulation!
-Hyperactive precordium
-Normal or accentuated 1st hrt sound
-Wide, fixed splitting of S2
-Pulmonary systolic ejection murmur w/thrill
-Holosystolic murmur @ apex w/radiation to axilla
-Mid-diastolic rumbling murmur @ LSB
-Marked cardiac enlargement on CX-Ray
atrioventricular septal defect tx
-Surgery is always required.
-Treat congestive symptoms.
-Pulmonary banding maybe required in premature infants or infants < 5 kg.
-Correction is done during infancy to avoid irreversible pulmonary vascular disease.
-Mortality low w/incomplete 1-2% & as high as 5% with complete AVSD.
patent ductus arteriosus (PDA)
-Persistence of the normal fetal vessel that joins the PA to the Aorta.
-Normally closes in the 1st wk of life.
-10% of all CHD, seen in 10% of other congenital hrt lesions and can often play a critical role in some lesions.
-Female : Male ratio of 2:1
-Often associated w/ coarctation & VSD
-dx- pulse and BP differentials in lower and upper extremities
-TORCH infection PDA assoc with -> rubella
eisenmenger syndrome =
pulmonary HTN due to congenital heart defect
-once you get here its too late
PDA- hemodynamics
-As a result of higher aortic pressure, blood shunts L to R through the ductus from Aorta to PA.
-Extent of the shunt depends on size of the ductus & PVR:SVR.
-Small PDA, pressures in PA, RV, RA are normal
-Large PDA, PA pressures are equal to systemic pressures. In extreme cases 70% of CO is shunted through the ductus to pulmonary circulation.
-Leads to increased pulmonary vascular disease.
PDA- SS
-Small PDA’s are usually asymptomatic
-Large PDA’s can result in symptoms of CHF, growth restriction, FTT.
-Bounding arterial pulses
-Widened pulse pressure
-Enlarged heart, prominent apical impulse
-Classic continuous machinary systolic murmur
-Mid-diastolic murmur at the apex
-doppler echo - confirms
PDA- tx
-Indomethacin, inhibitor of prostaglandin synthesis can be used in premature infants -> if it doesnt close -> surgery
-PDA requires surgical or catheter closure.
-Closure is required treatment heart failure & to prevent pulmonary vascular disease.
-Usually done by ligation & division or intra vascular coil.
-Mortality is < 1%
obstructive heart lesions
-Pulmonary Stenosis.
-Aortic Stenosis.
-Coarctation of the Aorta.
pulmonary stenosis
-pulmonary valve or subpulmonary ventricular outflow tract
-7-10% of all CHD.
-Most cases are isolated lesions
-Maybe biscuspid or fusion of 2 or more leaflets.
-Can present w/or w/o an intact ventricular septum
-obstruction of pulmonary flow -> decrease valve SA, decrease flow from left side, decrease opening
-compensate with RV hypertrophy
-associated with Noonan’s syndrome, secondary to valve dysplasia (high hairline, triangular face, transparent wrinkled skin, prominent nasolabial folds)
pulmonary stenosis hemodynamics
-RV pressure hypertrophy -> RV failure.
-RV pressures maybe > systemic pressure.
-Post-stenotic dilation of main PA.
-W/intact septum & severe stenosis -> R-L shunt through PFO -> cyanosis.
-Cyanosis is indicative of Critical PS.
pulmonary stenosis - SS
-Depends on the severity of obstruction.
-Asymptomatic w/ mild PS < 30mmHg.
-Mod-severe: 30-60mmHg, > 60mmHg.
-Prominent jugular a-wave, RV lift.
-Split 2nd heart sound w/ a delay.
-Ejection click, followed by systolic murmur.
-Heart failure & cyanosis seen in severe cases
-higher the pressure in the ventricle the higher the resistance through the valve
pulmonary stenosis tx
-Mild PS no intervention required, close follow-up.
-Mod-severe – require relieve of stenosis.
-Balloon valvuloplasty, treatment of choice.
-Surgical valvotomy is also a consideration
-if critical keep the PFO open with prostaglandin E -> surgery
aortic stenosis
-at or near aortic valve
-causes systolic pressure gradient of > 10mmHg
-7% of CHD
-supravalvular stenosis is found in williams syndrome
-3 Types
-Valvular – MC
-Subvalvular(subaortic) – involves the left outflow tract.
-Supravalvular – involves the ascending aorta -> least common.
aortic stenosis hemodynamics
-Pressure hypertrophy of LV and LA
-staged based on valvular SA and pressures:
-Mild AS- 0-25mmHG
-Moderate AS- 25-50mmHg
-Severe AS- 50-75mmHg
-Critical AS- > 75mmHg
aortic stenosis: SS
-Mild AS may present with exercise intolerance, easy fatigabiltity, but usually asymptomatic.
-Moderate AS – Chest pain, dypsnea on exertion, dizziness & syncope.
-Severe AS – Weak pulses, left HF, Sudden Death.
-LV thrust at the Apex.
-Systolic thrill @ rt base/suprasternal notch.
-Ejection click, 3-4/6 systolic murmur @ RSB/LSB w/ radiation to the carotids.
aortic stenosis tx
-surgery does not offer a cure
-reserved for pts with sx and resting gradient of 60-80mmHg
-subaortic stenosis- reserved for gradients of 40-50mmHg bc rapidly progressive
-Balloon valvuloplasty- standard of tx for children
-Aortic insufficiency & re-stenosis is likely after surgery and may require valve replacement.
-Activity should not be restricted in Mild AS.
-Mod-severe AS -> no competitive sports
-AVR is standard for adults
