2 Peds Cardiology
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| Most common congenital heart defect | bicuspid aortic valve. Incidence of congential heart disease: 8-10/1000 (.8%), but if you take into consideration bicuspid aortic valves, the incidence is: 15/1000
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| 4 heart defects | Hypoplastic left heart syndrome, congenital aortic stenosis, Coarctation of aorta, transposition of the great heart vessels. Almost always symptomatic when born.
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| Most defects occur in | otherwise healthy, well-developed, term infants.Transition from fetal to more adult circulation unmasks the defects. Hypoplastic left and right heart is perfectly protected in utero b/c of fetal circulation.
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| Heart has finished its formation at about | 60 days post conception. 60% of spontaneous abortions occur due to lethal heart disease
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| Heart Disease associated with Down's Syndrome | AVSD (no true tricuspid or bicuspid valve, only an AV valve), TOF. (50% of all Down's Syndrome kids will have a heart disease). These kids tend to age faster: never drop pulmonary resistance to nl. Can go from birth to pulmonary vascular dz in 5 months.
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| Heart Dz associated with Turner's Syndrome | Bicuspid aortic valve, coarctation of the aorta (COA)
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| Heart Dz associated wtih DPH syndrome | PS
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| Heart Dz associated with Trisomy 13/18 | VSD, DORV
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| Heart Dz associated with Marfan's syndrome | MVP (mitral valve prolapse), MR (mitral regurgitation), AI, DAA
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| First thing to do in Down's | EKG (in nl kids, you will see a right axis deviation b/c they have a very thick R ventricle) in down's: Left axis deviation. Good marker for AVSD. Then do Echo to find extent of defect
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| First Breath | clears out all the fluid from the lung. Pulmonary vascular resistance drops but doesn't get to normal until 3-6 months of life. PO2 blood levels increase b/c you are bleeding, Pulmonary blood flow increases, pulmonary venous return to atrium goes up.
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| Increased PO2 causes | closure of the vaso vasorum around the ductus arteriosus. remnant of ductus arteriosus is the ligament arteriosum
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| Disconnecting placenta | increases vascular resistance, Left ventricle dilates. Now able to provide more output to the periphery!
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| 3 presentations of heart disease | cyanosis, CHF, murmur/abnormal physical exam
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| Early recognition is | first few days of life. late - a week out
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| Most common cause of V/Q mismatch in premies | lack of surfactant. Other causes: meconium, pneumonia, retained amniotic fluid, etc.
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| reversible form of heart failure in DM moms. | neonatal hypoglycemia (high circulating insulin levels, with no way to put out glucose fast).
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| First sign of CHF in babies | Tachypnea, then tachycardia, then hepatomegaly (not edema and rales like in adults!).
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| Cost of tachypnea | myocardial oxygen consumption
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| Sequence of evaluation | History, Physical Examination, Electrocardiogram, Chest Radiograph, Echocardiogram, Other Studies including stress test, 24-Holter, ambulatory ECG monitoring, cardiac cath, angiocardiography, nuclear imaging, cardiac MRI
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| Where is the thrill of aortic stenosis felt? | In the suprasternal notch
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| In patients with severe pulmonary htn, where is palpable pulmonary closure (P2) frequently noted? | at the upper left sternal border
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| Sx of decreased pulmonary blood flow in an infant/toddler | cyanosis, squatting, loss of consciousness
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| Sx of Increased Pulmonary blood flow in an infant/toddler | tachynpnea with activity/feeds, Diaphoresis, poor weight gain
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| Sx of Decreased pulmonary blood flow in an older child | dizziness, syncope
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| Sx of Increased Pulmonary blood flow in an older child | exercise intolerance, dyspnea on exertion, diaphoresis
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| S1 | First heart sound is teh atrioventricular (AV) valve closure. Best heard at the lower left sternal border
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| S2 | semilunar valve closure. Best heard at the upper left sternal border. Two sounds A2 and P2 (aortic and pulmonary valve closure). Normal splitting: widening w/ inspiration and narrowing with expiration. Abnl splitting of S2 may be an indication of heart dz
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| S3 | the sound of rapid filling of the left ventricle. A persistent S3 often heard in the presence of a dilated LV caused by cardiomyopathy or large L-to-R shunt
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| S4 | Associated with atrial contraction and is normally not audible. Occurs before S1. It is heard in the presence of atrial contraction into a noncompliant ventricle as in hypertrophic or restrictive cardiomyopathy or hypertrophied LV from other causes
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| ____% of children have an innocent murmur at some time during childhood | 40-45%
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| How do describe murmurs | Location and radiation, Relationship to cardiac cycle and duration (systolic, pansystolic, diastolic, and continuous), Intensity, Quality (harsh, musical, rough; high, medium, or low in pitch), Variation with position (supine, sitting, standing,squatting)
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| Murmurs heard during systolic ejection | semilunar valve stenosis (AS/PS/truncal stenosis), ASD, Coarctation
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| Causes of Pansystolic murmurs | VSD, AVVR (atrioventricular valve regurgitation)
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| Causes of diastolic murmurs | Semilunar valve regurgitation (AI/PI/truncal insufficiency), AV valve stenosis (MS/TS)
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| Causes of continuous murmurs | Runoff lesions (PDA/AVM/aortopulmonary collaterals)
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| 6 Most common Functional murmurs in childhood are: | Newborn murmur, Functional murmur of peripheral arterial pulmonary stenosis, still murmur, pulmonary ejection murmur, venous hum, innominate or carotid bruit
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| Where is a newborn murmur heard? | lower left sternal border; first few days of life, usually disappears by age 2-3 weeks.
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| Systolic ejetion murmur heard with equal intensity at the upper left sternal border, at the back and in both axillae; usually disappears before age 2 | Functional murmur of peripheral arterial stenosis; results from the normal branching of the pulmonary artery
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| Most common innocent murmur of early childhood | still murmur. Usually heard between ages 2-7 years. Musical, vibratory, short, high-pitched, systolic.
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| Most common innocent murmur in older children | Pulmonary ejection murmur. Heard from age 3 years onward. Usually a soft systolic murmur, well localized to the upper left sternal border
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| This functional murmur is continous and is produced by turbulence at the confluence of the subclavian and jugular veins | venous hum
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| long harsh systolic murmur that is heard in the right supraclavicular area. Functional | Innominate or carotid bruit
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| Bounding pulses are characteristic of | run-off lesions, including patent ductus arteriosus (PDA), aortic regurgitation, arteriovenous malformation (AVM), or any condition with low diastolic pressure (fever, anemia, or septic shock)
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| Extracardiac Examination | Arterial Pulse, Quality and amplitude of pulse, arterial BP (UE & LE), Extremities (cyanosis, clubbing, edema), Abdomen
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| Cardinal sign of right heart failure | hepatomegaly. Hepatomegaly can also be seen in a child with pulmonary edema from lesions causing L-R shunting or left heart failure. Splenomegaly may be present in pts with longstanding CHF & is characteristic of infective endocarditis
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| heart size in relation to chest in child older than 1 yr | heart size should be less than 50% of the chest diameter
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| Components to check on CXR | 1. position of cardiac apex, 2.Position of abdominal viscera, 3. Cardiac Size, 4. Cardiac configuration, 5. Character of the pulmonary vasculature
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| Dextrocardia | heart on the right side of the chest. Levocardia - on the left, mesocardia-in the middle
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| This imaging technique is useful in assessing fixed and reversible areas of ischemia | Nuclear imaging. Valuable in evaluating myocardial perfusion in patients with Kawasaki dz, etc.
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| What causes the closure of the ductus arteriosus? | Pulmonary vascular resistance falls below that of the systemic circuit, resulting in a change in blood flow across the ductus arteriosus from left to right which closes the flap. Usually closes between 7-14 days
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| The one-way valve in fetal life that shunts blood from the inferior vena cava to through the right atrium to the left atrium | foramen ovale. At birth, pulmonary and systemic vascular resistance increase; left atrial pressure rises above that of the right atrium.This functionally closes the flap preventing flow across the septum. 10-15% of adults have a probe patent foramen ovale
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| Persistent pulmonary htn is a clinical syndrome that occurs in | full-term infants
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| In the nl newborn, pulmonary vascular resistance and the pulmonary arterial pressure (Decrease/increase) | Decrease; this phenomenon results from demusclularization of the pulmonary arterioles
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| HF | condition in which the heart fails to meet the circulatory and metabolic needs of the body. Usually occurs in infants before 6 months. Common causes in infancy: VSD, PDA, COA, AVSD, Large AVMs, and chronic atrial tachyarrhythmias
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| Children with HF may present with | irritability, diaphoresis with feeds, fatigue, exercise intolerance, or evdienceof pulmonary congestion, tachypnea
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| In CHF, when ventricular systolic dysfunction presents, what neurohormone is activated? | catecholamines from the adrenal glands are released and results in tachycardia, diaphoresis, and indirectly through activation of the renin-angiotensin system, peripheral vasoconstriction, and salt and water retention
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| Acyanotic heart disorders | ASD & VSD, PDA, Coarctation of the Aorta, Aortic stenosis, MVP
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| ASD: Rarely presents as CHF. Peripheral pulses nl and equal. | RV heave felt best at the mid to lower left sternal border. Ejection-type systolic murmur heard best at left sternal border at 2nd intercostal space. Murmur caused by increased flow across pulmonic valve
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| Most common congenital heart malformation | Simple VSD, accounting for about 30% of all cases of congenital heart dz. 80-85% are small and close spontaneously.
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| Consequence of Large VSD | CHF. Large: 6-10mm in diameter
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| VSD presentation | small to moderate: no CV sx. Large: ill early in infancy. Frequent upper and lower respiratory infxns. Gain weight slowly. Dyspnea, diaphoresis, exercise intol and fatigue common.
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| AVSD | Common in Down's kids.CHF develops in infancy, recurrent bouts of pneumonia common. Heart is significantly enlarged. Echo is the diagnostic test of choice.
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| PDA |
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