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Flashcards in Peds Cardiology Deck (170):

boot-shaped heart

tetrology of fallot


egg-on-a-strin gappearance

transposition of great vessels


-rib notching caused by the dilated intercostal arteries
-prominent aortic knob w/ narrowing of aorta and then dilated descending aorta

coarctation of the aorta


describe the normal heart sounds

S1 –Closing of tricuspid and mitral valves
-Beginning of systole

S2 – Closing of aortic and pulmonary valves
-End of systole

Diastole- cardiac filling- no heart sound


if you hear a blurred or “whishing” sound across S1, you would call that what type of murmur?
-where that sound across S2 would be called ___

an early systolic murmur

a late systolic murmur


most murmurs occur when?

during early systole


describe what a holosystolic murmur sounds like

heard where S1 and S2 should be but often obscure the sounds of the valve closures


describe the split heart sounds

Split S1: MV closing just before TV

Split S2: AV closing just before PV
*Physiologic S2 splitting is common with inspiration


is split S1 or S2 more common in pediatrics?

split S2 (common w/ inspiration) aka physiological splitting

*split S1 is NOT common--> commonly confused with S4


cause of S4

due to a stiffened left ventricle which is unable to eject the final amount of blood through the aortic valve

*not common in pediatrics


why is there a split S2 with inspiration?

Physiologically, the act of inspiration increases the amount of right ventricular filling. Because the right ventricle now has more blood to eject, the valve remains open just a bit longer after the aortic valve has closed, leading to a split S2 with inspiration

*This is an important concept to remember when we talk about some of the heart defects which result in overfilling of the right side of the heart


which valve closes before the other

left side valves close first (bc left side is more buff than right)


abnormal heart sounds

1. click- most common
2. S3
3. S4


when do you hear a "click"

common w/ stenotic valves

*"snap" during valve closure


what causes an S3

due to large atrial volume, delays the closure of mitral or tricuspid valve


what causes an S4

-Indicates a hypertrophic, stiff left ventricle
-Produces a gallop rhythm


why do children have innocent/functional murmurs

-due to their small cardiac size and, therefore, the small size of their cardiac outflow tracts, specifically the pulmonary artery, but also the left ventricular outflow tract.
-As blood travels from a larger “pipe” into a smaller one, it creates noise. Therefore, 100% of children will have an innocent murmur if their hearts are auscultated frequently enough. When cardiac output increases, the amount of blood squeezing into the “small pipe” from the big one will produce a murmur sound


when does cardiac output increase in peds?

1. fevers
2. anemia
3. exercise
4. hyperthyroidism

*causes murmurs to be louder


how can you decrease cardiac output

move the patient from a supine position to a sitting or standing position. In that brief period of time, the positional change will decrease venous return to the heart which decreases stroke volume and therefore cardiac output. This is the reason we get dizzy if we get up too fast!!


how can you tell if a patient has an innocent murmur?

(most patients are noted to have a cardiac murmur when they are seated): lie the patient supine and locate the place on their chest where the murmur is most audible, with your stethoscope still in place, move them to a seated position. If the murmur diminishes or resolves completely, the child most likely has an innocent murmur.

*Be sure to collect an appropriate history, which I will review shortly, to be sure of your diagnosis.


characteristics of innocent cardiac murmurs

1. Produces a musical, single frequency sound
2. Louder with increased cardiac output
3. Decreased cardiac output= decreased murmur sound

*laminar flow


what is a pathologic murmur

when blood travels across a constricted area


how do we tell if a murmur is pathologic?

-Our little test of moving them supine to sitting will not change the sound of the murmur if it is pathologic.
-Additionally, the constricted area will initiate the murmur sound and the sound will radiate in the same direction as the blood is flowing. We use this to help us determine the most likely cardiac defect.

*Will not diminish/resolve with cardiac output changes


what creates turbulent flow

Blood flow from high pressure area to low pressure across a defect

-Produces a varying frequency “whooshing” sound


describe the different grades of a mumur

Grade I- barely audible
Grade II- soft, easily audible
Grade III- loud, no thrill
Grade IV- loud, with thrill
Grade V- heard with edge of stethoscope, with thrill
Grade VI- heard without stethoscope

*grade 1-3 are somewhat subjective


document murmurs by:



innocent cardiac mumurs

1. peripheral pulmonary stenosis
2. Still's murmur
3. Pulmonary Ejection Murmur
4. Venous hum (only functional diastolic murmur)


what is a peripheral pulmonary stenosis murmur?

Starting in the right ventricle (R.V), blood travels into the pulmonary artery (P.A). As it reaches the bifurcation leading to each lung, the blood gets restricted down into these smaller outflow tracts, producing a murmur sound.


peripheral pulmonary stenosis is most common in what age group?

newborns-6 months

*may persist until age 15-18 months


where is a peripheral pulmonary stenosis murmur best heard?

-best heard in 2 ICS and axilla
-radiates to the back

-systolic ejection, harsh


what are the most common innocent murmur of childhood.

Still's murmur

heard in 2y/o+ (3-6yrs*)


what is a Still's murmur caused by?

blood traveling into the right outflow tract from the right ventricle. The sound is generated near the entrance to the pulmonary artery and travels along the pulmonary artery, therefore, it is heard along the left sternal border on the anterior chest.


describe a Still's murmur

-best heard between apex and LSB
-distinctive higher-pitched sound that is sometimes described as musical or vibratory (ie. bass guitar string vibrating)
-diminished/resolved murmur w/ moving from supine to sitting or turning head


describe a pulmonary ejection murmur

-heard typically in slightly older kids (3+)
-Systolic ejection
--diminished/resolved murmur w/ moving from supine to sitting (innocent)


what is the only innocent diastolic murmur

venous hum

*diastolic murmurs are always pathologic as the heart is supposed to only be filling with blood not pumping it anywhere


describe a venous hum murmur

-right and left infraclavicular areas
-age 2
-diminishes by turning pts head


what is a venous hum murmur caused by?

caused from blood that is returning to the heart via the subclavian and jugular veins creating noise in the right and left infraclavicular areas.


what are some genetic syndromes that are associated w/ cardiac defects?

1. Down's syndrome (trisomy 21)
2. Turners syndrome
3. Edwards syndrome (trisomy 18)
4. Marfans syndrome


many children with Down’s Syndrome have congenital cardiac defects that it is recommended that all neonates with Down’s Syndrome be evaluated by a cardiologist how soon?

in the first 4 weeks of life


Cardiac defects associated w/ Down's syndrome (trisomy 21)

50% have ASD, VSD, or AVSD


Cardiac defects associated w/ Turner's syndrome

20-40% have coarctation of the aorta


Cardiac defects associated w/ Edward's syndrome (trisomy 18)

99% have VSD


Cardiac defects associated w/ Marfan's syndrome

90% have MVP, aortic root ectasia (resulting in AR), predisposed to aortic dissection

*should be ruled out in sport screenings!


Marfan’s syndrome is more associated with __ due to ___ resulting in __

sudden cardiac death due to abnormal aortic roots resulting in aortic dissection


what are the Ghent nosology?

associated w/ Marfan's syndrome

1. hypermobile joints
2. long upper extremities compared to lower and
3. height much greater than genetic potential would predict.


Only __% of the population has congenital cardiac defects, so many of the murmurs you hear in children will likely be innocent.


BUT! not all congenital cardiac defects have murmurs associated with them. In fact, some of the more life-threatening cardiac defects do not


Describe the appropriate historical questions to elicit in evaluating a pediatric patient for congenital heart disease

1. Feeding difficulties**- feed only for short period
2. Sweating (diaphoresis) with feeds-- cannot tolerate breastfeeding
3. 1st degree relatives with cardiac problems
4. Poor growth/weight gain
5. Delayed gross motor skills-- due to exercise intolerance
6. Rapid breathing, ??neonate with cough-- if CHD shunts blood to lungs causes tachypnea
7. Gray cyanosis- (w/ feeding)
8. Cyanosis with exercise, exercise intolerance


why do peds w/ heard disease sometimes present w/ cough

-If their cardiac defect shunts blood into their lungs, they will have tachypnea and for that reason, I have “radar” for neonates with a complaint of cough.

-Infants have a high threshold for reflexive coughing until they are about 3 months old, so they need significant lung pathology such as bronchiolitis or pertussis before they will cough, not just a mild URI.


human eyes cannot detect skin color changes until oxygen saturation is ____ and even then the child will not be “blue” just somewhat ashen or gray especially around the lips/mouth.

in the low 80’s,

**It is very easy to miss this on exam unless you are specifically looking for it. In older children, the caregiver may report grayish lips with exercise or inability to tolerate exercise that their peers can do.


the cardiac exam includes what 7 essential elements

1. Color- Consider Pulse Oximetry
2. Respiratory effort/rate
3. Auscultate
4. Palpate chest for thrills, heaves
5. Compare brachial/femoral pulses
6. Check blood pressure-right arm
7. Clubbing of fingers/toes (chronic low O2?)
8. Edema (CHF?)


It is currently standard of practice to screen all neonates in the newborn nursery with ___ between 24 hours of age and discharge in order to detect critical congenital cardiac defects

pulse oximetry


how is pulse oximetry obtained in neonate?

-obtained from right hand and either foot and is consider normal if over 95% and not more than 3% difference between upper/lower extremity.

* At our altitude, a slightly lower pulse ox may be used as the cutoff.


____ screens for children with significant shunting of blood into the right side of their heart down into their lungs

Observing respiratory rate


how should you check pulses in a neonate

-Comparing amplitude and timing of the brachial pulse to the femoral pulse screens for coarctation of the aorta, as does checking the blood pressure specifically from the right arm against either thigh.

*femoral pulses are weaker and delayed compared with the right radial pulse


how does CHF present in infants

-In adults, the fluid ends up in their feet and legs.

-In infants, it will travel to dependent areas such as their sacrum, but that may not be obvious with their chubby behinds!
*Look for it in their face, specifically around their eyes.


the heart is unable to pump blood out efficiently and it backs up into systemic circulation



significant differences in the chest x-rays of adult vs. children (less than 2y/o)

1. infants are born with a more prominent right ventricle due to fetal circulation- on CXR bc of rotation of the heart, most of the hearts silhouette is RV
(only 10% of the curve seen along the left side of the heard is LV)
2. hearts of young children look very large in their chest cavity on CXR and it is easy to think you are seeing an enlarged heart when you aren’t. It is normal for children less than 2 y/o to have normal heart silhouettes which are taking up 50% of their chest cavity on x-ray vs. the 1/3 rule used in adults
3. infants are born with a large thymus gland overlying their upper mediastinum and giving it an enlarged appearance


Office work-up/referral tips

1) All children with a 3/6 or greater murmur, or holosystolic murmur, need pediatric cardiology referral--> likely underlying cardiac defect
2) If history/exam is + in les than 2m/o, get pediatric cardiology consult ASAP (ie. call)
3) If older and stable, can screen with EKG, refer if abnormal

**Don't order an echo in PCP


when would you expect a PFO murmur and when should you call/refer to cardiology?

-It is not uncommon to hear a Grade 1-2 murmur in an infant less than 3 weeks old as the foramen ovale is still open.
-If the history and remaining exam are reassuring, it is acceptable to observe and bring the infant back weekly to recheck and see if there are any concerning symptoms/signs developing.

-If the murmur hasn’t resolved by 4 weeks of age, call the pediatric cardiologist for guidance


what should you do if you are concerned about a murmur in an older child and aren’t sure of your positional change exam, but their history seems benign?

screen them w/ EKG:
-if it is abnormal: refer to cardiology
-if it is normal: observe


in pediatric EKGs, ___ is common until age 3

RV dominance


how does RV dominance present on a pediatric EKG

1. Dominant S in Lead I
2. Dominant R in lead III


how does RVH present on a pediatric EKG

1. deep S waves in V6
2. tall R waves in V1


how does LVH present on a pediatric EKG

1. Tall R waves in Lead II, aVF, V5, V6


How to get to a proper cardiac dx in peds

1. physiology of cardiac lesion
2. physics of fluid flow and sound travel
3. reasoning


AHA guidelines suggest antibiotic prophylaxis to protect agains bacterial endocarditis. They are needed for:

1. Prosthetic valve
2. Previous bacterial endocarditis
3. Congenital heart disease:
-Unrepaired cyanotic CHD
-Completely repaired but with prosthetic device, only in first 6 months after surgery
-Repaired CHD, but with residual defects
-Cardiac transplantation patients who develop cardiac valve abnormality


what procedures are indicated for SBE prophylaxis?

1. Dental procedures involving gingival tissues, oral mucosa, periapical region of teeth
*None needed for routine fillings

2. Procedures on respiratory tract, infected skin or musculoskeletal tissue

*No longer recommended for GI/GU procedures, including hysterectomy


SBE prophylaxis medications

1. Amoxicillin, Adults 2g (Peds 50mg/kg) 1 hour before

If PCN-allergic:
1. Clindamycin- Adults 600mg (Peds 20mg/kg ) 1 hour before
2. Cephalexin- Adults 2g (Peds 50mg/kg)
3. Azithromycin/Clarithromycin- Adults 500mg (Peds 15mg/kg)


All would-be athletes, starting in __ , are required to have a “sports” physical performed and be cleared for play.

middle school


what is the purpose of the sports clearance

to perform a history and exam looking for evidence of cardiac pathology, neurologic risk factors and musculoskeletal disorders which may put them at risk for an adverse event during sports or put other players at risk

* From a cardiac standpoint, we are most concerned with the risk of Sudden Cardiac Death.


Despite our best attempts at screening, it is important to realize that only __% of patients who experienced SCD actually had a history suggestive of pathology



what is the leading cause of SCD in children

hypertrophic cardiomyopathy

*accounts for 36% of deaths


how does hypertrophic cardiomyopathy lead to SCD/syncope?

-the intraventricular septum becomes thickened causing the LV outflow tract to be narrowed.
-These patients depend on a large end-diastolic ventricular volume to stretch the outflow tract wide enough to maintain good cardiac output.
-During exercise, diastolic fill time is shortened due to increased heart rate. For patients with HCM, this doesn’t allow the necessary stretching of their LV outflow tract and they have decreased cardiac output at a time when exercise is demanding more. They will have near syncopal or syncopal episodes and may have SCD with their 1st episode of syncope


who is hypertrophic cardiomyopathy most common in?

males of african descent


Most common causes of SCD

1. Hypertrophic cardiomyopathy
2. Arrythmias, specifically prolonged QT syndrome
3. Aortic stenosis
4. Anomalous coronary arteries


what sports are riskiest for a SCD/ cardiac event

basketball and football

*other sports list on UTD


what is the treatment for HCM?

1. Beta blockers- slow HR to allow better ventricular filling
2. prohibited from basketball and football/ intense physical activity


why is prolonged QT syndrome dangerous?

QT interval becomes prolonged resulting in ventricular arrythmia and syncope, followed by torsades de pointes (a form of ventricular tachycardia) which is usually followed by ventricular fibrillation and death


why is anomalous coronary arteries dangerous?

Imagine a coronary artery coming off the aorta down near the valve and between the aorta and pulmonary artery. Obviously with exercise, this coronary artery would get compressed between the two large outflow tracts. A patient with this will have a syncopal episode and potentially SCD.


Patients with cardiac syncope will usually have a history of:

-sudden syncope, not the vaso-vagal syncope of feeling lightheaded, vision fading, nausea and then fainting.

*These patients often hurt themselves because their syncope comes completely without warning and they are unable to protect themselves the way a person with a vaso-vagal episode will by sitting down, trying to lie down, etc.


The focus of history taking around the risk of SCD is:

1. looking for syncopal or near-syncopal episodes
2. chest pain which occur with exercise.


The AAP recommended in 2010 that providers use the ____ to screen athletes prior to clearance for sports

Pre-participation physical evaluation version 4 (PPE-4)


the PPE-4 history and exam focuses on:

-The history focuses on cardiorespiratory diseases, previous orthopedic injuries, current skin infections, history of neurologic disorders, including head trauma, and family history of cardiac death.

-The exam focuses on skin, MSK, cardiac and neurologic.


never clear an athlete for sports if you hear a murmur or anything about their history is suggestive of cardiac pathology or a FH of cardiac pathology. It is safest for them (and you) to refer them to a cardiologist for a complete evaluation. Additionally, if a caregiver or athlete reports that they had to see a cardiologist before "for that murmur" what should you do?

send them back to the cardiologist for eval and clearance

HCM is often a condition that is evolving as the intraventricular septum thickens and the athlete could be more at risk in a later year than they were when they were younger.


describe the SVR and PVR of blood in-utero

high PVR- not much blood flow to lungs
low SVR


describe the critical time periods for cardiac changes

48 hrs- change in oxygenation close--close PDA from pulmonary artery side first

4-7 days- PDA closes all the way across (anatomically closes)

4-6 weeks- pulmonary artery lining thins out and decrease in PVR and get good blood flow to lungs


how does the foramen ovale close?

closes w/ increased SVR from umbilical cord clamping


a huge coarctation of the aorta of the newborn presents when

4-7 days of life as PDA closes


CXR and EKG findings for coarctation of the aorta of the newborn

-Enlarged heart/cardiomegaly
-increased pulmonary vascular markings

-RAD due to RVH


effects of coarctation of the aorta on the heart

enlarged LA, RV, and LV


PE findings of coarctation of the aorta in the newborn

-check femoral pulses against brachial
-check pulse ox between upper and lower extremity ---3% difference
-murmur at 2nd ICS- radiates to L axilla


sx of coarctation of the aorta of the newborn

1. poor perfusion
2. poor feeding
3. Shocky lookings-- bc can't breath
4. lethargic
5. normal femoral pulses


tx of coarctation of the aorta of the newborn

1. fluid bolus (increase BP)
2. give oxygen
3. labs
4. give prostaglandins E1 to open PDA
5. septic workup


sx/PE of coarctation of the aorta late presentation

1. increase BP in right arm
2. HA due to increased blood flow in carotids
3. murmur- 2nd ICS that radiates to left axilla
4. enlarged LV
5. leg discomfort
6. epistaxis
7. decreased femoral pulses compared to right radial pulse


CXR and EKG findings of coarctation of the aorta late presentation

-rib notching (collateral circulation of intercostal arteries)
-scalloping of AA

-LAD due to LVH


treatment of coarctation of the aorta early presentation

-balloon angioplasty to open PDA
-surgical repair


when does hypoplastic left heart syndrome present?

often detected pre-natally

-presents in 48 hrs of life (when PDA starts to close)


what is hypoplastic L heart syndrome

*left side of heart is underdeveloped

-small LV, MV atresia
-causes RV enlargement


PE of hypoplastic L heart syndrome

- NO murmur


CXR and EKG findings of hypoplastic L heart syndrome

-increased pulmonary vascular markings

-RAD due to RVH


treatment of hypoplastic L heart syndrome

-give PGE1 from birth
-surgery 1st week of life and 2 more later in life (last around 4y/o)


when do VSD present

-4-6 weeks old when PVR decreases and they shunt L--> R = increased blood in lungs


Sx/PE of VSD

1. tachycardia
2. increased RR (increased blood in lungs)
3. ashen color (esp. around lips)
4. coughing
5. poor feeding w/ sweating
6. fussy
7. fluid in lungs
8. murmur at 4th ICS-pansystolic
9. enlarged LV


what direction is blood shunted with VSD?

L--> R because RVpressure is less than LV pressure


CXR and EKG findings for VSD

-increased pulmonary vascular markings (pulm. edema)

-LAD due to LVH


treatment of VSD

1. see back 3-4 weeks of age--> if murmur is still there get echo w/ cardiologist

VSD w/ CHF manifestations: meds and surgery
*need to be over 25lbs for anesthesia and surgery


What is Eisenmenger Syndrome

-inside lining of lungs change to become more resistant to BF--> leads to PHTN (irreversible)
-R--> L shunt (cyanotic lesion)


what cardiac disease have a risk of Eisenmenger Syndrome

1. VSD
2. PDA


Sx/PE of ASD

1. RVH
2. migraine HA
3. TIA
4. murmur- 2nd ICS w/ widely split fixed S2


CXR and EKG findings of ASD

-increased pulmonary vascular markings
-normal RVH

-normal or RAD


tx of ASD

1. can leave alone or cardiac cath --coil embolization procedure


Sx/PE of pulmonary stenosis

1. RVH and RA enlargment
2. narrowed pulmonary valves
3. murmur 2nd ICS that radiates to BACK (the smaller the louder)
4. tachypnea (presents before liver congestion)
5. liver congestion (long term complication)
6. If high enough pressure in RA, can cause FO to stay open


CXR and EKG findings for pulmonary stenosis

-normal or RVH

-normal or RAD


tx of pulmonary stenosis

balloon angioplasty


Sx/PE of PDA

1. murmur- 2nd ICS, across diastole and systole/continous, machine-like
2. tachypnea
3. cough
4. increased fluid in lungs
5. LAE and LVH
6. widen pulse pressure


CXR and EKG findings of PDA

-increased pulmonary vascular markings
-normal or LVH



tx of PDA

1. indomethacin (NSAID)
2. ligature procedure to ligate off before 1 y/o--> reduces risk for Eisenmeger syndrome


what is tetrology of fallot

1. pulmonary stenosis
2. VSD
3. RVH
4. over-riding aorta (PA is shifted ofter and pushes against the aorta)

*cyanotic heart lesion


presentation of tetrology of fallot

1. murmur- 4th ICS and 2-4th ICS that radiates to BACK
2. RVH


CXR and EKG findings of tetrology of fallot

-widen mediastinum
-"boot-shaped heart"



tx of tetrology of fallot

1. relieve pulmonary artery valve via surgery (decreases risk of CHF)
2. meds
3. full VSD surgery closure by age 1


what causes a Tet spell

*from crying or feeding= increased pulmonary shift, increase PVR (rapid)

-PVR increases rapidly so deoxygenated blood is shunted through VSD from RV to LV


What do tet spells cause

1. rapid cyanosis
2. acidotic w/ cyanosis
3. rapid increased PVR (from crying or feeding typically)

*in kids w/ tetrology of fallot


Tx of tet spells

1. shift pressure L--> R by increase SVR: knee to chest mechanism
2. oxygen
3. morphine decreases RR (vasodilator and decreases preload)
4. NaHCO3


what is transposition of the great artery/vessel (TGA/TGV)

-aorta comes off LV and feeds into lungs
-Pulm. artery comes off RV and goes to aorta


PE/Sx of transposition of the great artery/vessel (TGA/TGV)

1. RVH
2. tachypnea
3. male
4. large babies
5. no murmur

"large blue baby boy"


CXR and EKG findings of transposition of the great artery/vessel (TGA/TGV)

-narrowing mediastinum-- "egg of a string"



tx of transposition of the great artery/vessel (TGA/TGV)

surgery 1st week of life
-anastomosis and reposition vessels


what is total anomalous venous return (TAVR)

-PV inserts in odd places like superior vena cava


when does total anomalous venous return (TAVR) typically present

4-6 weeks of life


Sx/PE of total anomalous venous return (TAVR)

1. cyanotic 1st 2 days of life when PDA starts to close
2. RVH and RAE
3. presents 4-6 weeks of life
4. increased fluid in lungs
5. tachypnea
6. CHF
7. coughing
8. poor weight gain/feeding


CXR and EKG findings of total anomalous venous return (TAVR)

-RVH and RAH--> cardiomegaly
-"Snowman shaped heart"



tx of total anomalous venous return (TAVR)



what heart defects cause RAD on EKG?

1. coarctation of aorta of newborn (late presentation has LAD)
2. hypoplastic L heart syndrome
3. ASD
4. pulmonary stenosis
5. tetrology of fallot
6. transposition of great artery/vessels (TGA/TSV)
7. total anomalous venous return (TAVR)


what heart defects cause LAD on EKG?

1. coarctation of aorta late presentation (newborn has RAD)
2. VSD
3. PDA


5 T's of cyanotic heart lesions

1. Tetrology of Fallot
2. Transposition of the Great Vessels (TGA)
3. Tricupsid Atresia
4. Truncus Arteriosus
5. Total Anomalous Pulmonary Venous Connection (TAPVC)
6. pulmonary atresia
7. hypoplastic L heart syndrome

*caused by decreased pulmonary blood flow and R--> L shungs where blood is mixing


Acyanotic heart lesions

1. PDA
2. VSD
3. critical aortic stenosis
4. Coarctation of the aorta
5. hypoplastic L heart syndrome
6. ASD


ductal dependent heart lesions

1. Coarctation of the aorta of the newborn
2. hypoplastic L heart syndrome
3. critical aortic stenosis

4. pulmonary atresia
5. severe tetralogy of Fallot
6. tricuspid atresia


Infants with heart failure exhibit poor growth, with __ being more significantly affected than __ and __

with weight being more significantly affected than height and head circumference


Sx of CHF

1. fatigue
2. diaphoresis with feeds
3. fussiness.
4. Tachypnea without significant dyspnea may be present.

Older children with heart failure may have:
1. easy fatigability
2. shortness of breath on exertion
3. sometimes orthopnea.
4. decreased exercise intolerance


Respiratory rate may be increased when there is a ___ shunt or ___


pulmonary venous congestion


Comparing pulse oximetry between the___ and ___ may allow diagnosis of a ___ lesion in which desaturated blood flows right to left across a PDA to perfuse the lower body

right arm

lower extremity

ductal dependent lesion


R--> L shunts

1. tetraology of fallot
2. transposition of great vessels
3. tricuspid atresia

**Cyanotic lesions


L--> R shunts

1. PDA
2. VSD
3. ASD

**Acyanotic lesions
-results in increased pulmonary blood flow


mixing heart lesions

1. truncus
3. Hypoplastic L heart syndrome


stenotic heart lesions

1. aortic stenosis
2. pulmonary stenosis
3. coarctation of the aorta


what is the most common congenital heart defect?



-Cyanosis with respiratory distress



-cyanosis w.o resp. distress

-RH obstruction

ex. tricuspid atresia
pulm. stenosis


sx hypoperfusion

LH obstruction
-Aortic stenosis


___is the most common cyanotic congenital heart defect, representing about __% of all congenital heart defects

Tetralogy of Fallot



most common cyanotic lesion to present in the newborn period



most common cause of death from cardiac defects in the first month of life

hypoplastic left heart syndrome


failure of development of the mitral or aortic valve or the aortic arch.

hypoplastic left heart syndrome


3 types of cardiomyopathy

1. dilated (most common)
2. hypertrophic
3. restrictive


what cardiomyopathy:
often idiopathic, but may be due to infection (echovirus or Coxsackie B virus) or be postinfectious, familial, or secondary to systemic disease or to cardiotoxic drugs.



what cardiomyopathy:
usually familial with autosomal dominant inheritance, but may occur sporadically



what cardiomyopathy:
rare; they may be idiopathic or associated with systemic disease



What murmur?
-Heard between apex and LSB on the anterior chest
-Vibratory/musical, higher pitched sound (bass guitar string vibrating)

Still's murmur


What murmur?
-Best heard in axilla bilaterally
-Radiates to back
-Will not hear anything or very low sound when auscultating the anterior chest

Peripheral pulmonary stenosis


What murmur?
-Heard best in left and right infraclavicular areas
-Diminishes by turning the patient’s head

Venous Hum


What murmur?
-Sound generated along the pulmonary valves (valves themselves though are not abnormal)
-LUSB anteriorly
-Systolic ejection murmur

Pulmonary Ejection murmur

*Sometimes cannot differentiate well from Still’s murmur, just be able to differentiate if it is innocent murmur vs a pathologic cause


What murmur?
-Heard best at 2nd ICS
-Widely fixed splitting S2
-no radiation



What murmur?
-Heard best at 4th ICS
-no radiation


*only one heard at 4th ICS


What murmur?
-Heard best at 2nd ICS
-radiates to whole back

pulmonary stenosis


What murmur?
-Heard best at 2nd ICS
-Continuous during systole and diastole- machine like



What murmur?
-Holosystolic murmur 2 and 4 ICS
-radiates to chest and back

Tetrology of fallot
- Depends on which is the major defect


What murmur?
-Heard best at 2nd ICS
-radiates to left axilla

Coarc- early presentation and late presentation


What CHD do not have a murmur associated w/ them



Explain the management approach of pediatric patients with cardiac murmurs in the primary care setting

1. All children with a 3/6 or greater murmur, or holosystolic murmur, need pediatric cardiology referral
2. If history/exam is + in less than 2 m/o, get pediatric cardiology consult ASAP
3. If older and stable, can screen with EKG, and refer if abnormal

*PCP do not interpret EKG