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41 Cards in this Set
- Front
- Back
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Define pediatric cardiology
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Pediatric subspecialty dedicated to the study of congenital and acquired heart problems in the fetus, infants, children, and adolescents
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Explain major milestones in cardiac embryology
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-CV system comes from mesoderm
-2 endocardial tubes fuse along embryonic midline to form cardiac tube -Heart beats at day 22 but no circulation until days 27/29 -heart tube bends ventrally, caudally and slightly to the right (d-looping) |
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Locate major structures during cardiac embryology and identify what parts of the developed heart they become
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Paired atria form a common chamber and move into the pericardial sac
Septum primum grows from the roof of the common atrium into the lumen Septum secundum is a fold into the atria and is not a complete partition Opening left by septum secundum is called the foramen ovale |
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Contrast fetal and adult circulation
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Right and left ventricles are in parallel
Lungs do not provide gas exchange Vessels in the pulmonary circulation are vasoconstricted 3 unique cardiovascular features Ductus venosus, Foramen ovale, Ductus arteriosus -Oxygenated blood flows through unbilical vein -50% bypasses liver via ductus venosus -Enters RA and crosses to LA via foramen ovale and ejected via LV -Major portion of blood (~90%) ejected from RV passes through ductus arteriosus (R to L shunt) |
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Diagram the changes that occur to the circulatory pathway when a baby is born
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At birth, expansion of lungs and increase in arterial PO2 results in rapid decrease in pulmonary vascular resistance (lower than systemic resistance)
This causes ductus arteriosus to reverse to a L to R shunt High arterial PO2 constricts ductus arteriosus until it closes Remnants are called ligamentum arteriosum |
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Identify major structures in fetal circulation and what they are termed after their closure
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ductus arteriosus (L-R shunt) becomes ligamentum arteriosum.
ductus venosus (bypass liver) becomes ligamentum venosum. |
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Demonstrate how to perform a pediatric cardiologic history including composing relevant questions to ask patients and families
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Detail the perinatal period: Cyanosis, Respiratory distress, Prematurity
Maternal complications of pregnancy: Gestational diabetes, Medications, Diseases (systemic lupus erythematosis) Feeding difficulties: Infants with heart failure take less volume during feeds and often dyspneic or diaphoretic while feeding Respiratory distress: Rapid breathing, Nasal flaring, True cyanosis, Intercostal retractions, Exercise intolerance Family history of: Early CAD or STROKE, Familial hypercholesterolemia, Generalized muscle disease, Muscular dystrophy, Dermatomyositis, Familial or metabolic cardiomyopathy, Relatives with congenital heart disease |
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Demonstrate how to perform a pediatric cardiologic physical examination
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Vital signs, check for resp. distress, growth curve, inspect for cyanosis, palpations, auscultation. Abdominal exam, face and extremities.
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Second Heart Sound (S2)
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Best evaluated at left and right upper sternal borders
Caused by closure of the semilunar valves (aortic and pulmonary) Splitting of S2 is normal when -Occurs during inspiration and -Followed by a single sound on expiration Fixed splitting is a sign of a cardiac defect |
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s1 heart sounds
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best heard at the apex.
closed by closure of the AV valves. splitting can be normal finding. |
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S3
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Low frequency sound related to filling of the ventricle
Best heard using bell at the apex in mid-diastole May be normal in an adolescent with a slow heart rate May be heard as a gallop rhythm in patients with heart failure and tachycardia |
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S4
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rare in children. pathologic finding related to poor compliance.
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grading murmurs
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1 is less, 2 is the same, 3 is louder no thrill, 4 is louder with thrill, 5 is very loud with thrill heard with stethoscope barely on chest, 6 is heard with steth barely on chest and visible thrill.
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What are ejection clicks?
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heard best in L and R upper sternal borders. Heard in early systole (dilatation of the aorta or pulomnary a or semilunar valve stenosis). Seen in aortic/pulmonary stenosis, dilated great arteries in systemic pulm. HTN, tetralogy of Fallot.
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Fixed splitting... what is it, and what is it a sign of?
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breath in there's 2 sounds, breath out there's a single sound. it's not normal if it's all the time (fixed splitting). This is a sign of an atrial-septal defect in S2.
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Midsystolic Click is...
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best heard at the apex.
most often precedes a late systolic murmur and is suggestive of MITRAL VALVE PROLAPSE. |
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What are murmurs?
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a physical finding... not a diagnosis. they are graded on intensity (1-6).
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What are functional heart murmurs?
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innocent, not an ass'd with hemodynamic abnormality, 30% kids will have it at some point, localized in left sternal border, occur in systole.
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Still's Murmur
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Common between ages 2 and 8 years of age
Grade I – III Musical, vibratory, or twangy Increases in supine position Louder with exercise and fever Caused by vibrations in ventricle |
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Pulmonic Flow Murmur
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Common from 6 years of age to adolescence
Grade I – III Blowing, high-pitched murmur Increases when supine, exercising, fever, or excitement Caused by turbulent flow where main pulmonary artery connects to RV |
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Venous Hum
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Common from 3 to 7 years of age
Continuous murmur located in low, anterior part of neck or right upper chest Disappears in supine position Gets louder by turning head away from side of murmur Caused by turbulent flow in jugular venous / SVC systems |
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Peripheral Pulmonic Stenosis (PPS)
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Common in infants up to 2 months old
Especially premies Mumur radiates into axillae Resolves in 3-6 months Caused by turbulent flow in relatively hypoplastic branched pulmonary arteries and by their angle of take-off |
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Different Types of Diagnostic Tools for Cardiac Structure
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echocardiogram (ultrasound), cardiac catheter, MRI, EKG
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indications for obtaining a fetal echocardiogram
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Previous child or 1st degree relative with previous congenital heart disease
High risk of having child with heart disease Insulin dependent diabetes Exposure to teratogens during pregnancy Maternal systemic lupus erythematosus Any fetus a chromosomal abnormality is suspected |
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What's the magic number for the hyperoxia test?
(after given 100% o2 for 15 minutes) |
150mmHg. if it's less than 150, this usually means that the intracardiac shunt is present, the lung oxygenation is working well, the mixing of arterial and venous blood keeps the PaO2 from rising much. so it's a heart problem. If it's greater than 150, this means the intracardiac shunt is most likely not present. most likely not a heart problem, and it's a brain problem.
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What are the congenital heart lesions presenting as neonatal cyanosis?
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1.Tetralogy of Fallot
2. Tricuspid Atresia 3. Transposition of the Great Arteries (TGA) 4. Truncus Arteriosus 5. Total Anomalous Pulmonary Venous Return (TAPVR) Five Terrible T's that show up for neonatal cyanosis. |
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Tetralogy of Fallot
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1. pulmonary stenosis
2. overriding aorta 3. ventricular septal defect 4. right ventricular hypertrophy |
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Transposition of the Great Arteries (TGA)
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Egg shaped or egg on a string appearance
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Tetralogy of Fallot
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Boot-shaped heart
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Total Anomalous Pulmonary Venous Return (TAPVR)
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Snowman
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What would an EKG do?
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Help determine ventricular hypertrophy
-Right axis deviation suggests right ventricular hypertrophy -Likewise for left ventricular hypertrophy -Superior axis deviation can be associated with atrioventricular canal defects or tricuspid atresia Discover conduction defects |
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What are ductal dependent lesions?
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lesion requiring a patent ductus arteriosus (PDA) to maintain life. needed for adequate pulmonary blood flow, and systemic blood flow.
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Can we do anything to keep a PDA open after birth?
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Prostaglandin E1
-continuous drip, that keeps the baby alive until surgery. causes vasodilation of the ductus. |
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What are the signs of a patent ductus arteriosus (PDA)?
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A continuous (systolic and diastolic) machinery-like murmur
Bounding pulses (in the absence of other anomalies) -always there, sounds like a machine |
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How can we close a PDA if the baby is not dependent on it?
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NSAIDS or surgery. Drugs to use are ibuprofin (expensive) and indomethacin (cheap, bad side effects)
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Eisenmenger Syndrome
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Patient has a left to right shunt (VSD, ASD, atrioventricular septal defect, PDA, etc.)
Increased volume of blood on right side causes pulmonary vascular disease (medial hypertrophy and/or intimal hyperplasia) These changes cause pulmonary hypertension Pressure on right side increases so much the shunt reverses to become right to left Usually occurs in 2nd or 3rd decade of life |
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What can uncorrected tetrology of fallot cause in the first 2 years of life?
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"tet" spells. pt becomes hyperpneic, restless, increased cyanosis, gasping respirations, syncope. due to a reduction in pulmonary blood flow. give o2 and/or morphine. knee to chest squatting helps too.
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Williams Syndrome
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Caused by deletion of genes from chromosome 7
Elfin facies Hypercalcemia “Cocktail” personality- very talkative. Mild mental retardation Supravalvular aortic stenosis** Renal artery stenosis |
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Turner Syndrome
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(45, XO)
Webbed neck Puffy hands and feet “Shield” shaped chest Short stature Delayed puberty **Coarctation of the aorta (rib notching!) **Horseshoe shaped kidneys |
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DiGeorge Syndrome
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Remember CATCH-22
22q11 chromosome deletion syndrome Cardiac anomalies - (conotruncal with tetralogy of Fallot being most common followed by an interrupted aortic arch and then truncus arteriosus) Abnormal facies (hypertelorism) Thymic aplasia Cleft palate Hypocalcemia |
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Marfan Syndrome
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Connective tissue disorder
Mitral Valve Prolaspe Aortic root dilation Aortic dissection |
