General Pediatric Board Review: Pediatric Cardiology

General Pediatric Board Review: Pediatric Cardiology
Daniela Rafii, M.D. Associate Director, Pediatric Cardiology Maimonides Infants and Children’s Hospital of Brooklyn

Innocent Heart Murmurs
Over 50% of children have an innocent heart murmur  no intervention, require reassurance Most common innocent heart murmurs: Still’s murmur AKA function heart: Musical/twangy/vibratory systolic ejection murmur Louder while supine Usually located over the LLSB Venous hum: Continuous murmur Softer/resolve while supine or w/ pressure to jugular vein or w/ turning the head Usually RUSB or LUSB Plan the appropriate eval of an innocent heart murmur and manage appropriately

Pathologic Murmurs AS  PS  PDA  continuous machinery murmur
Harsh crescendo-decrescendo SEM RUSB Radiates to the neck PS  LUSB Radiates to the back PDA  continuous machinery murmur Diastolic murmurs are never innocent

Reassure the parents about the benign prognosis
Upon routine 3 year physical, a 3 yo female who is new to the practice is noted to have a continuous grade 2/6 continuous murmur at the RUSB while sitting. When supint, she is noted to have a 3/6 vibratory systolic ejection murmur at the LLSB only. The remainder of the PE is norma. Of the following, the MOST appropriate next step is: Reassure the parents about the benign prognosis Request a cardiology consult Order a chest X ray Request a transthoracic echocardiogram Request an EKG

Acyanotic Congenital Heart Disease (CHD)
Acyanotic (pink) CHD  ASD (left to right shunt) VSD (left to right shunt) PDA (left to right shunt) AS PS Coarc

Atrial Septal Defect (ASD)

ASD Acyanotic CHD 3 types Asymptomatic in childhood
Primum Secundum (most common) Sinus Venosus Asymptomatic in childhood SEM loudest at LUSB  relative PS murmur w/ fixed widely split S2

ASD EKG w/ right ventricular conduction delay

ASD Dx  echo Treatment  surgical vs percutaneous closure
Natural history in the 3rd-4th decade of life: Arrhythmias Pulmonary HTN Paradoxical emboli

Ventricular Septal Defect (VSD)

VSD Acyanotic CHD Most common CHD 4 main types of VSD
Perimembranous Muscular Inlet Outlet Small VSDs  no sx only loud harsh 3/6 holosystolic murmur loudest at LLSB Large VSDs  congestive heart failure (CHF)

VSD & CHF CHF x typically start at 6-8 weeks old from a VSD
Babies present with: Some degree of resp distress: tachypnea, retractions, abd breathing, etc Irritability Hepatomegaly Cardiomegaly NO peripheral edema NO cyanosis Poor po intake, easy fatiguing w/ feeds, prolonged feeding times Poor weight gain: weight drops off before height Excessive sweating Sinus tachycardia Loud harsh holosystolic murmur loudest at the LLSB

CXR Cardiomegaly Inc lung markings Pulm edema

VSD EKG: Normal Sinus tachy LVH Echo: diagnostic

VSD Treatment If CHF treat with:
Digoxin 5mcg/kg/dose bid Lasix 1mg/kg/dose bid Enalapril  afterload reduction Increase caloric intake  24kcal/oz formula Surgical closure of large VSDs ~ 6 mo old  sooner if FTT despite medical trt CHF

VSD Natural History Small VSDs: Large VSDs:
80% close within the 1st year of life Large VSDs: CHF  40% of babies will die w/o treatment in 1st year of life Unrepaired large VSDs past 1yo  develop Eisenmenger’s syndrome in teen years Progressive pulmonary HTN w/ progressive cyanosis Right to left shunt Mean survival mid-20’s

Atrioventricular Canal
AKA: AV Canal endocardial cushion defect AV septal defect

AV Canal ~50% of children w/ T21 have CHD
~40% of those with T21 and CHD have AVC EKG: often has left superior axis Echo: diagnostic Treatment: Medically manage CHF (same as w/ large VSD) Surgical repair 4-6 months old

AVC EKG

Patent Ductus Arteriosus (PDA)

PDA All babies are born with a PDA
Usually closes within 1st 2 wks of life in full term babies Persists longer in preterm babies Small PDAs  no symptoms Large PDAs  CHF sx similar to large VSDs In preemies  resp distress can be seen in the 1st few days of life

PDA Classic murmur  continuous machinery murmur secondary to continuous shunt in systole and diastole loudest under L clavicle Murmur is not heard in newborns secondary to elevated pulm vascular resistance (PVR) Murmur develops only after PVR srops

PDA Treatment If significant sx in preterm babies 
Indomethacin May try CHF rx Surgical PDA ligation If CHF sx in term babies  Medically treat CHF If babies can reach 10kg  percutaneous PDA closure If cannot gain weight  surgical PDA ligation

A 3 month old female with T21 presents with 1 month history of poor weight gain and tachypnea. She has an active precordium and soft systolic murmur on exam. Chest X-ray demonstrates cardiomegaly and increased lung markings. EKG demonstrates a left superior axis. Of the following, the MOST likely diagnosis is: Coarctation of the aorta Atrioventricular canal defect Patent ductus arteriosus Large ventricular septal defect Secundum atrial septal defect

Patient is a 5 day old infant born at 31 weeks gestation on ventilatory support in the NICU. He has a hyperdynamic precordium, bounding peripheral pulses, and a continuous heart murmur. His Hgb, electrolytes, and creatinine are all normal. Of the following, the most appropriate INITIAL management is to: Administer furosemide intravenously Administer indomethacin intravenously Perform an echocardiogram Defer interventions since spontaneous closure is likely Obtain a surgical consult for PDA ligation

Cervical spine radiography Echocardiogram Head ultrasound
You are called to evaluate a 6 hour old female. Labor and delivery were uncomplicated, however amniocentesis at 20 weeks revealed T21. The infant is sleeping, has facial features consistent with T21, he is well perfused, heart rate is 140 bpm, and there are no audible murmurs. Of the following, the MOST appropriate diagnostic study to perform is: Barium swallow Cervical spine radiography Echocardiogram Head ultrasound Radiography of the abdomen

Coarctation of the Aorta

Coarctation More common in males Almost always juxtaductal [A]
Preductal [B]  present earlier Postductal [C]  present later 85% of children with coarc have a BAV Frequently seen in Turners syndrome {45, XO} 10% have severe coarc 30% have bicuspid aortic valve (BAV)

Coarc Variable presentation  Infant with cardiogenic shock
Child or adolescent with systemic hypertension Child with a heart murmur

Neonatal Coarctation Severe coarc in a neonate 
Often present before 2 weeks old Cardiogenic shock: resp distress/failure, poor perfusion, altered metal status Multisystem organ failure: NEC, renal failure, intracranial bleed **Diminished lower extremity pulses Moderate coarc in a neonate  CHF: resp distress, poor feeding, poor growth Mild coarc in a neonate  No symptoms +/- murmur

Older Children with Coarc
Older children and adolescents do NOT present with heart failure sx Can have upper extremity hypertension refractory to antihypertensive rx Can have diminished lower extremity pulses Can have claudication Can just have a murmur

Coarc EKG: CXR: often nonspecific findings, normal or: Often normal
Can have LVH with strain pattern (ST elevation +/- T wave inversion in precordial leads) CXR: often nonspecific findings, normal or: Cardiomegaly Increase pulm vascular markings Rib notching (not seen in infants, uncommon prior to 5 years old)

Coarc Echo: diagnostic Treatment:
Infant in shock  immediate PGE + aggressively trt shock Surgical repair for children or for complex coarc Percutaneous stent placement in adult sized patients

Hypoplastic Left Heart Syndrome (HLHS)

HLHS Varying degrees of left heart hypoplasia
Babies present in cardiogenic shock when PDA closes Immediate treatment with PGE IV infusion

HLHS Surgical treatment: Norwood palliation  1st week of life
Bidirectional Glenn  4-6 months old Fontan palliation  2-4 years old

A 7 month old female has undergone the second stage of surgical palliation (Glenn) for hypoplastic left heart syndrome. She was discharged from the hospital 1 week ago. Her mother brings her to the office because of irritability that began in the morning. On physical exam, she is awake and irritable, heart rate 150 bpm and respiratory rate of 50 bpm. She has cyanosis of the face and mucosal surfaces and welling of the arms and head. Of the following, the BEST explanation for this patient’s clinical presentation is: Polycythemia Postpericardiotomy syndrome Protein-losing enteropathy Superior vena cava syndrome Thoracic duct injury

Pulmonary Stenosis (PS) and Aortic Stenosis (AS)

PS AS Stenosis may be valvular, subvalvar, or supravalvar
Mild-mod PS  no sx Severe or critical PS  cyanosis Murmur  harsh SEM at LUSB Echo –> diagnostic Treatment: ballooning or surgical Stenosis may valvular, subvalvar, or supravalvar More common in males More significant lesion compared to PS, no cyanosis, (+) heart failure/cardiogenic shock Valvar AS is often associated w/ BAV Murmur  harsh SEM at RUSB Echo –> diagnostic Treatment: ballooning or surgical

Hypertrophic Cardiomyopathy (HCM)
Mild to severe usually asymmetric thickening of the myocardium Often autosomal dominant Incidence 1:500 Symptoms: Sudden death (on exertion) Arrhythmias Syncope Chest pain

Critical aortic stenosis Erythroblastosis fetalis
A 3 day old infant is found unconscious in her crib and brought to the ED. Findings include: tachypnea, tachycardia, pallor, poor cap refill, hepatomegaly, cardiomegaly with increased pulmonary vascular markings, hgb 17 gm/dl, hematocrit 51%. Of the following, the cardiogenic shock in the girl is most likely due to : Critical aortic stenosis Erythroblastosis fetalis Patent ducts arteriosus Severe hypovolemia Ventricular septal defect

A 6 hour old infant has increasing pallor, tachypnea and resp distress
A 6 hour old infant has increasing pallor, tachypnea and resp distress. Pysical exam reveals an enlarged liver, gallop, poor pulses in the upper extremities and absent pulses in the lower extremities. In addition to treating the infant for sepsis, the most appropriate INITIAL management is to administer: Dopamine infusion Loading dose of digoxin 25% glucose and water solution Furosemide Prostaglandin E1

Cyanotic CHD Cyanotic (blue) CHD  Often have cyanosis with NO resp distress Need some sort of L to Right shunt to have cyanosis TOF (right to left shunt) TGA Tricuspid atresia (right to left shunt) Truncus arteriosus TAPVR Ebstein’s Anomaly (right to left shunt) Single Ventricles

Tetralogy of Fallot (TOF)

TOF PS VSD Overriding aorta Right ventricular hypertrophy (RVH)

TOF Most common cyanotic heart lesion Signs/symptoms: Cyanosis
Loud harsh SEM at the LUSB (PS murmur) Squatting in older kids Tet spells  cyanosis often worsened or caused by crying Lose PS murmur b/c less blood across pulm valve Increase right to left shunt across VSD Trt  calm kid down, knees to chest, morphine, oxygen, general anesthesia

Transposition of the Great Arteries (TGA)

TGA Aorta arises from the RV and the pulmonary artery arises from the LV Mixing of blood occurs at the PFO/ASD, PDA, +/-VSD Sx: Cyanosis +/- murmur May have higher sats in the lower extremities vs the upper extremities Echo: diagnostic

Tricuspid Atresia (TA)

TA TA  left superior axis on EKG (like AVC)

Truncus Arteriosus

Total Anomalous Pulmonary Venous Return (TAPVR)

TAPVR Sx occur when pulm veins are obstructed
Can occur soon after birth Babies present with severe cyanosis (unresponsive to O2) and resp distress No murmur Treatment  emergent surgery

Ebstein Anomaly

Ebstein Anomaly Apical displacement of the tricuspid valve
Can present with: Severe TR R to L shunting  neonatal cyanosis 25% can have SVT or WPW Neonatal treatment  decrease PVR iNO Oxygen CXR  severe cardiomegaly

Coarctation of the aorta Myocarditis Tetralogy of Fallot
The mother of a 5 month old reports that following a feeding, the child began to breath deeply, became increasingly blue and then lost consciousness. After being held briefly, the infant regained her usual color and became alert. Physical examination reveals a harsh murmur. Of the following the MOST likely diagnosis is: Aortic stenosis Coarctation of the aorta Myocarditis Tetralogy of Fallot Ventricular septal defect

You are called at 3am from the nursery about a 36 hour old BB Bleu who was noted to be cyanotic . The nurse reported that he had been feeding well and appeared well prior to the episode. Apgars were 9/9. Until this evening the baby appeared pink. They report no significant tachypnea. You order a chest X-ray and pulse oximetry to be done while you rush to the hospital. On arrival the pulse oximetry indicates a saturation of 55% and the X-ray shows no increase pulmonary vascular marking or infiltrate. The next MOST appropriate intervention is to: Obtain a stat EKG to evaluate for SVT Intubate the infant and place on 100% O2 Start IV PGE infusion at mcg/kg/min Start iNO at 40ppm inspired to reduce PVR Arrange for transfer to a facility capable of ECMO

Following an uncomplicated delivery, a 3
Following an uncomplicated delivery, a 3.7kg term infant develops cyanosis in the first hour of life. Physical exam reveals: HR 140 bpm, RR 56 bpm, no heart murmur, on room air the right arm saturation is 70% and the right leg saturation in 75%, on 100% O2 the right had saturation increased to 75 and the right foot increases to 90%. Chest X-Ray is normal. These findings are MOST consistent with: Primary pulmonary hypertension of the newborn Pulmonary valve atresia Transient tachypnea of the newborn Transposition of the great arteries Truncus arteriosus

Hypoplastic left heart syndrome Neonatal sepsis
At 1 hour old at full term 3.5kg infant appears cyanotic but otherwise well. Oxygen saturation in the upper and lower extremities is 79%, there is a soft systolic murmur heard across the precordium. The remainder of the physical exam is within normal limits. After placing the baby on O2,there is no change in saturations. Of the following, the MOST likely cause of this child’s findings is: Anemia Hypoplastic left heart syndrome Neonatal sepsis Retained fetal lung liquid syndrome Tracheoesophageal fistula

Arrhythmias

Supraventricular Tachycardia (SVT)
Most common arrhythmia in childhood Babies present with poor feeding, pallor, irritability Older kids present w/ palp, dizziness, fatigue EKG diagnostic  narrow complex regular tachy >220bpm Can be associated with WPW If patient hemodynamically stable  vagal maneuvers: Ice to face Valsalva If doesn’t work  adenosine If patient hemodynamically unstable  synchronized cardioversion

Valsalva Maneuvers Ice to face “Bearing down”
Blowing against and occluded straw Gag Cough

Atrial Flutter/Fib Atrial flutter: saw tooth p waves
Atrial fib: irregularly irregular Adenosine is diagnostic not therapeutic Treat both with synchronized cardioversion

Heart Block 1st degree HB: prolonged PR interval 2nd degree HB:
Rheumatic fever, myocarditis, KD, congenital 2nd degree HB: Type I: Wenkebach, progressive prolongation of PR interval then dropped beat  high vagal tone, benign Type II: dropped (nonconducted beats)  can progress to CHB  pacemaker 3rd degree: complete HB Postop, lyme disease, myocarditis Congenital CHB  maternal SLE

Long QT Syndrome QTc >0.45 sec
Genetic  often family hx sudden death Arrhythmia  torsades de pointes (type of VT) Be suspicious if: Family hx SCD Hx seizure d/o Congenital deafness Syncope following loud noises, being startled Acute treatment: magnesium Long term treatment: beta blockers

Torsades de Pointes

Commotio Cordis Sudden, blunt, non-penetrating trauma to the chest  V fib  sudden death Typical story: healthy kid gets hit with a baseball to the chest and drops Treatment  stat defib

Syncope Benign causes of syncope:
Vasovagal: during blood draws, site of blood Orthostatic hypotension: standing up quickly, standing up for too long, especially if hot Hyperventilation Breath holding spells: 6-18mo, associated w crying, +/- cyanosis Concerning, potentially life-threatening syncope: Associated w/ exertion (VT, LQTS, HCM, other cardiomyopathy) Associated w/ excitement/startle (LQTS) Family hx sudden death

Sudden Death in Young Athletes

Carditis Carditis refers to inflammation of any of the 3 layers of the heart, occur in isolation or conjunction with one another Endocarditis  inflammation of the cardiac valves  valvar dysfunction Myocarditis  inflammation of the muscular walls of the heart  myocardial dysfunction, conduction abnormalities (heart block, arrhythmias) Pericarditis  inflammation of the pericardium  pericardial effusion

Infective Endocarditis (IE)
Diagnosis  Modified Duke Criteria 2 major 1 major + 3 minor 5 minor Treatment  IV abx, type and length of treatment vary Natural hx of infective endocarditis Pathogens commonly associated with IE Recog clinical findings of IE and initial management Diagnostic eval IE IE ppx

Major Criteria Positive Bcx w/ typical IE microorganism:
Typical microorganism consistent w/ IE from 2 separate Bcx: Viridans-grp strep, or Strept bovis including nutritional variant strains, or HACEK group (Haemophilus spp, Actinobacillus, Cardiobacteriom hominis, Eikenella spp, Kingella), or Staph aureus, or Community-acquired Enterococci, in the absence of a primary focus Microorganisms consistent w/ IE from persistently (+) Bcx: 2 positive Bcx drawn >12 hours apart, or All of 3 or a majority of 4 or more separate Bcx (w/ first and last sample drawn at least 1 hour apart) Coxiella burnetii on at least 1 (+) Bcx or antiphase I IgG antibody titer >1:800 Evidence of endocardial involvement w/ (+) echo: Oscillating intracardiac mass on valve or supporting structure, or in the path of regurgitant jet, or on implanted material, or Abscess, or New partial dehiscence of prosthetic valve or new valve regurgitation

Minor Criteria Predisposing factor: CHD, recreational IV drug use
Fever >38°C Evidence of embolism: arterial emboli, pulmonary infarct, Janeway lesions, conjunctival hemorrhage, mycotic aneurysm, intracarnial hemorrhage Immunological problems: glomerulonephritis, Osler’s nodes, Roth spots, rheumatoid factor Positive Bcx (that doesn't meet a major criterion) or serologic evidence of infection w/ organism consistent with IE but not satisfying major criterion

Minor Criterea Janeway lesions: small, erythematous, non-tender, macular or nodular lesion on soles/palms  septic emboli  microbscesses Osler’s nodes: painful, red, raised lesions on hands/feet  immune complex deposition Roth spots: retinal hemorrhages w/ white or pale centers composed of coagulated fibrin  immune complex mediated vasculitis

Subacute Bacterial Endocarditis Prophylaxis
2007 AHA guidelines: Prosthetic valves Previous IE Unrepaired cyanotic heart disease Repaired CHD <6 months after surgery Repaired CHD >6mo if residual lesion near prosthetic material Cardiac transplant with valvulopathy

Myocarditis Myocarditis  inflammation of the muscular walls of the heart  myocardial dysfunction/failure, heart block, arrhythmias Presentation in babies  irritability, poor feeding, pallor, shock, cardiomegaly, hepatomegaly, pulm edema Presentation in older kids  fatigue, dyspnea, chest pain, palpitations, pallor, hypotension, cardiomegaly, hepatomegaly, pulm edema

Myocarditis Infectious vs noninfectious vs idiopathic
Viral  most common cause in US: coxsackie, adenovirus, parvovirus B19, enterovirus, EBV, CMV, HSV 6 Other infectious  Lyme dz and other spirochetes, fungal, bacterial Toxic/hypersenstivity reactions  chemotherapeutic agents, abx, amphetamines Systemic dz  Giant-cell myocarditis, sarcoidosis, KD, Crohn’s, UC, SLE, thyrotoxicosis Clinical findings Commonly associated pathogens Diagnostic eval

Myocarditis No single clinical or imaging test to confirm dx
Dx made by: Clinical sx Serologic: CKMB, troponin, BNP, CRP Noninvasive: EKG, echo, MRI Invasive: myocardial biopsy Treatment: depends on severity of sx, mostly supportive: ionotropic support, mechanical vent, ECMO, trt CHF, antiarrhythmics, temporary pacing, IVIG or steroids Long term: fully recover (50%), chronic heart failure, need for transplant

Pericarditis Viral pericarditis most common Preceded by a viral URI
Sx: sharp chest pain, improves with leaning forward PE: friction rub, pulses paradoxus (exaggeration of normal finding of dec in systolic BP w/ inspiration) EKG diagnostic: diffuse ST segment elevation Echo: pericardial effusion Risk  cardiac tamponade Treatment  NSAID, pericardiocentesis if severe

Diminished feeding volume Pretibial edema
In addition to irritability, sweating and difficulty breathing with feeding, the symptom that is MOST indicative of congestive heart failure is a 3 week old infant is: Ascites Cough Cyanosis Diminished feeding volume Pretibial edema

2 days 2 weeks 2 months 6 months 12 months
A term infant was born with a large ventricular septal defect. At what age is the infant MOST likely to first demonstrate clinical findings of congestive heart failure? 2 days 2 weeks 2 months 6 months 12 months

Rheumatic Fever ARF results from a complex interaction btw GAS and a susceptible host Abnormal immune response leads to acute inflammation of joints, brain, heart, and or skin All organ systems recover w/o sequelae except the heart ARF can lead to chronic RHD Diagnosis  modified Jones Criteria

Rheumatic Fever 2 major or 1 major + 2 minor
And evidence of a preceding streptococcal infection Except w/ presence of chorea or indolent carditis Major criteria: Polyarthritis Carditis Sydenham’s chorea Erythema marginatum Subcutaneous nodules—extensor surf Minor criteria Fever Polyarthralgia Elevated acute phase reactants (ESR, CRP) Prolonged PR interval

RF Cardiac Involvement
Initial cardiac involvement is a pancarditis Most prominent feature is valve involvement #1 mitral (MR) #2 mitral + aortic (MR + AI) #3 aortic (AI) Treatment: Primary ppx: Treat strep infection High dose aspirin or NSAIDs or steroids (4-6 weeks) Secondary ppx: monthly IM PCN Long term RHD: MR + AI  MR/MS + AI/AS

Kawasaki Disease Arteritis of medium size arteries
AKA mucocutaneous lymph node syndrome Diagnosis  5 days of fever + 4/5 of the following: B/l nonexudative conjunctivitis Erythema of the lips or oral mucosa Changes in the extremities: swelling, erythema Rash Cervical LAN, >1.5cm

Typical Kawasaki Disease
Supplemental laboratory criteria: Albumin </=3.0 g/dL Anemia for age Elevation of ALT Plt after 7d >/=450 WBC >/= 15 Urine 10 WBC/high-power field Newburger, J. W. et al. Circulation 2004;110:

Kawasaki Disease Treatment for typical and atypical KD is the same
IVIG w/i 10 days of fever, may repeat if still febrile High dose aspirin W/o treatment  20% of children will develop coronary artery aneurysms W/ treatment w/ IVIG and ASA5% of pts will develop aneurysms Aneurysms develop usually w/i 2 weeks Can have an associated mild myocarditis

Syndromes T21: CHD incidence 50%, think AV canal defects
Turner’s: 10% coarc, 30% BAV Pompe’s: Hypertrophic cardiomyopathy (HCM) Alagille : Peripheral pulmonic stenosis (PPS) Williams’s: Supravalvar aortic stenosis, PPS Noonan: PPS and (HCM) Marfan’s: Aortic root dilatation, MVP DiGeorge (22q11 del): TOF, truncus arteriosus, interrupted Ao arch, right aortic arch Kartagener: dextrocardia, situs inversus totalis, immotile cilia Holt-Oram: Limb abnormalities, ASD Ellis-van Creveld: ASD

Teratogens Lithium: Ebstein’s anomaly
Ethanol: ASD,VSD (fetal alcohol syndrome) Anticonvulsants: PS, AS, TOF Retinoic Acid: TGA Rubella: PDA, PPS Coxsachie B: Neonatal myocarditis Maternal Diabetes: HCM, TGA Maternal Lupus: Complete heart block PKU: VSD, ASD, complex CHD

A 5 year old girl is very excited following a ride on a ferris wheel
A 5 year old girl is very excited following a ride on a ferris wheel. In the midst of her excitement she suddenly loses consciousness and falls to the ground. Paramedics on the scene document a ventricular tachycardia. Family history reveals a maternal uncle who died suddenly at 16 years old. Following treatment of her ventricular tachycardia, an EKG is most likely to demonstrate: Corrected QT interval of 0.52 sec P wave axis of -30 degrees PR interval of 0.81 sec QRS axis of -15 degrees QRS interval of 0.12 sec

Julie, an otherwise healthy 9 year old comes to the ED because she “passed out”. After asking questions and examining the patient, all but one of the following reassures you that she has vasovagal syncope, a relatively benign cause of syncope in children: She was standing in line waiting to see “The Hunger Games: Mockingjay part 2” when she passed out She fainted once before when she had a blood test After falling to the ground she came to quickly and remembered feeling warm and dizzy She was lying on the sofa watching TV when a door slammed and she suddenly became unresponsive S1 and S2 were normal and no murmurs were noted

A 13 year old boy wishes to participate in competitive sports
A 13 year old boy wishes to participate in competitive sports. His father died suddenly at age 28 years, and hypertrophic cardiomyopathy was found on autopsy. Of the following , the MOST helpful test for assessing the boy’s risk is: Echocardiography Electrocardiography Exercise myocardial perfusion scintigraphy Genetic testing for myosin chain mutations Genetic testing for troponin mutations

Infective endocarditis Myocarditis Paroxysmal atrial tachycardia
Two weeks after a nonspecific upper respiratory infection, a previously healthy , 3 year-old boy is noted to have a resp. rate of 40 breaths/min, a HR of 140 beats/min, hepatomegaly and a gallop rhythm. No heart murmurs are detected. Of the following, the MOST likely diagnosis is: Acute rheumatic fever Infective endocarditis Myocarditis Paroxysmal atrial tachycardia Pericarditis

Acute rheumatic fever Arrhythmia Costochondritis Myocardial ischemia
A 14 year old boy complains of dull chest pain over the precordium. It began 4 days ago and occurs intermittently. It is not associated with activity, but it does increase when he is in a supine position and decreases when he is leaning forward. The frequency, duration, and the intensity of the pain has been increasing. Among the following, the MOST likely explanation for these findings is: Acute rheumatic fever Arrhythmia Costochondritis Myocardial ischemia Pericarditis

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General Pediatric Board Review: Pediatric Cardiology

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