Peds cardiac

mlinnie's version from 2018-11-09 22:40


Question Answer
• Increased Pulmonary Blood Flow DefectsAbnormal connection between the two sides of the heart that allows for increased blood volume on right side of heart. Thus, increased pulmonary blood flow. L to R shunts
• Increased Pulmonary Blood Flow Defects Presentationtachypnea, poor feeding, poor weight gain and FTT
• Increased Pulmonary Blood Flow Defects associated with which heart conditionsAtrial septal defect, Ventricular septal defect and Patent ductus arteriosus. L to R shunt
• Atrial septal defectopening between atria so blood flows from left → right atria and puts increased blood flow to lungs. L to R shunt
• Ventricular septal defectabnormal opening between L and R ventricles. Blood Flows L → R, sometimes one common ventricle if severe. L to R shunt
• Ductus arteriosusartery connecting aorta and pulmonary artery
• Patent ductus arteriosusductus arteriosus doesn’t close for some reason. Blood flows from high pressure atria → low pressure pulmonary artery. L to R shunt.
• Obstructive DefectsStructural abnormality on the left side of the heart causing decreased systemic blood flow
• Obstructive Defects Presentationdecreased pulses, unequal limb blood pressures, to extremely ill presentations
• Obstructive Defects assossiated with which heart conditions?Coarctation of the aorta, Aortic stenosis, Mitral stenosis
• Stenosis=narrowing
• Regurgitation=leaking in the wrong direction
• Coarctation of the aortastenosis in aorta near ductus arteriosus past arteries going to head and neck. Increased pressure proximal to defect (head and upper body) and decreased pressure distal to defect (lower body). So upper limbs have bounding pulses and high BP and lower have low bp and weak pulses + cold
• Aortic stenosisnarrowing of the aortic value (can be valvular, supra or super) which leads to resistance of blood flow in the L ventricle, decreased cardiac output, L VENTRICLE HYPERTROPHY, and pulmonary vascular congestions. Commonly caused by misshapen value (bicuspid instead of tri). Interferes with coronary artery perfusion → MI
• Decreased Pulmonary Blood Flow DefectsStructural abnormality causing too little pulmonary blood flow. Abnormality on the right side of the heart. Causes unsaturated blood to shunt to the left side of the heart, into the systemic circulation (via VSD, ASD). Pulmonary blood flow is obstructed + have defect of ASD or VSD.>>Blood backs up in R side of heart. Causes desaturated blood to shunt to the left, and into systemic circulation.
• Decreased Pulmonary Blood Flow DefectsPresentation usually hypoxemic and cyanotic
• Tetralogy of Fallot4 components= 1. Pulmonary stenosis. 2. Overriding aorta. 3. Ventricular septal defect 4. Right ventricular hypertrophy. Hemodynamics vary widely; depends on extent of pulmonic valve stenosis & size of VSD. IF VSD is large pressures are = in R and L ventricles. Blood is shunted in the direction of the least resistance (pulm or systemic vascular resistance.
• Tetralogy of Fallot Clinical manifestations Vary with types of defect. “TET SPELLS” or “blue spells” with acute episodes of cyanosis and hypoxia. May be anoxic after feeding or w/ crying. RISK of emboli, LOC, Sudden death , Seizures.
• Tetralogy of Fallot REPAIRSusually indicated when tet spells and hypercyanotic spells increase.
• Tetralogy of Fallot REPAIRS Stage 1Blalock or Modified Blalock shunt>>blood to pulm arteries from L or R subclavian artery
• Tetralogy of Fallot REPAIRS Complete repair Usually in 1st yr of life. Repair of VSD, resect stenosed area, and patch R ventricular outflow.
• Tricuspid atresia no tricuspid valve (connects RA + RV), blood flows through atrial septal defect (ASD) or patent foramen ovale to LA then to LV then either to body or RV through hole and to the lungs, blood is mixed
• Pulmonary stenosisnarrowing of pulmonary artery which decreases blood flow to lungs
• Mixed DefectsBlood is mixed from pulmonary and systemic circulations within the heart chambers. >>Relative desaturation of blood in systemic blood flow. Cardiac Output decreases because of volume load on ventricle. Signs of desats, cyanosis, and CHF, but variable depending on anatomy.
• Mixed Defects typesTransposition of great vessels, Total anomalous pulmonary venous connection, Hypoplastic left heart syndrome
• Mixed Defects Presentationvaries greatly depending on anatomy and amount of “mixing”
• Transposition of Great Vessels (TGA)The great vessels (arteries), aorta and pulmonary artery, arise from the wrong ventricle. The great vessels are “transposed” from their normal position. Aorta comes off of RV. Pulmonary artery comes off of LV. Must have ASD, VSD, or PDA to allow “mixing” of blue and red blood. If this happens at birth they will give them prostaglandin very quickly to try and keep the duct open to allow mixing. This kid will die soon after birth if not caught once the ductus arterious closes you will start to see signs of problems. Procedure done to switch them back
• Hypoplastic Left Heart SyndromeGroup of cardiac anomalies involving the left sided structures of the heart. One of the most complex of CHD. One of the most challenging to manage. Ductal dependent lesion (PGE1 infusion). Repaired in 3 stages. Norwood, glenn and fontan


Question Answer
• Open heart surgery(heart-lung bypass)
• Closed heart procedures(no heart-lung bypass)
• Palliative versus Curative (staged surgeries vs one repair)
• Post-pericardiotomy Syndrome Symptomsfever, malaise or irritability, nausea/vomiting pericardial friction rub
• Post-pericardiotomy SyndromeOccurs in first few days or weeks after surgery. Anytime you open up pericardium it starts to swell and will become irritated. Ibuprophen decreases swelling and lasix flushes out the water.
• Post-pericardiotomy Syndrome Caused byan increasing pericardial effusion
• Post-pericardiotomy Syndrome Treatment includesconfirm dx with echo, anti-inflammatory drugs (steroid, NSAID), diuretics, may need drainage of fluid


Question Answer
• Acquired Heart DiseasesCongestive heart failure, Infectious heart disease and Inflammatory heart disease
• Congestive Heart FailurePathophysiologic state in which the heart is unable to pump blood at a rate that meets the body’s metabolic needs
• Congestive Heart Failure the most common cause in children Volume overload
• CHF Causesmetabolic abnormalities, myocarditis, CHD, cardiomyopathies, etc
• CHF Systemic venous congestionright-sided failure, edema, weight gain, hepatomegaly, ascites
• CHF Pulmonary congestionleft-sided failure. Tachypnea, retraction, nasal flaring, poor feeding, exercise intolerance
• CHF ManagementOxygen, Rest, Sodium/fluid restriction, Drug therapy: inotropes, afterload reduction, Correction on underlying CHD or precipitating cause


Question Answer
• EndocarditisBacteria start eating heart valves. If there is a mixing disorder you are more prone to this.
• Endocarditis Predisposing FactorsStructural abnormalities: all CHD with the exception of secundum ASD, Bacteremia- any localized infection can seed organisms into the circulation, dental procedures, diseased teeth/gums, drug abuse
• Endocarditis Clinical ManifestationsHx of CHD, recent dental procedure, Insidious onset: fever, fatigue, weight loss, Murmur 100%, Fever 80-90% , Splenomegaly 70%, Laboratory findings: +BC, anemia, increased sed rate, Echo may indicate vegetations
• Endocarditis Management3-5 blood cultures drawn in 24-48 hrs. Initial empiric therapy should be started before BC results available. Anti-staphylococcal penicillin (naficillin, oxacillin) and aminoglycocide (gentamicin). 4-6 weeks of tx


Question Answer
• Rheumatic FeverImmunologic disease sequela of Group A streptococcal pharyngitis. Infrequently seen in U.S.; big problem in Third World . Inflammatory lesion found in many parts of the body (heart, brain, joints, and skin). Dx with 2 major, or 1 major and 2 minor criteria…
• Rheumatic Heart DiseaseMost common complication of rheumatic fever, Damage to valves as a result of rheumatic fever, Valvar lesions most frequently involve the mitral and less commonly the aortic valve
• Rheumatic Heart Disease Major ManifestationsPolyarthritis (70%), Carditis (50%) – tachycardia, murmur, cardiomegaly, Chorea (15%) – “St. Vitus Dance’=neuropsychiatric disorder, Erythema Marginatus (<10%) – rashes most on trunk, Subcutaneous nodules (2-10%) – hard, painless, freely mobile over bony prominences, scalp
• Treatment of Rheumatic FeverTreatment of streptococcal pharyngitis, Penicillin V is the drug of choice, PO, Penicillin G, IM, Erythromycin if PCN allergic, ASA and bed rest, if mild-mod carditis, Prednisone and bed rest if mod-severe carditis


Question Answer
• Kawasaki DiseaseVasculitis of unknown etiology characterized by a multisystem involvement and inflammation of small to medium-sized arteries with resulting aneurysm formation
• Kawasaki Disease Acute Phase (1-2 weeks)Fever > 5 days, Erythema and edema of hands, Polymorphous rash, Conjunctivitis, “Strawberry tongue”, Cervical lymphadenopathy
• Kawasaki DiseaseSubacute Phase (up to 30 days), Resolution of fever, Peeling of fingers and toes, Increased platelet count, Onset of coronary aneurysms, Often diagnosed in this phase
• Kawasaki Disease TreatmentAimed at reduction of inflammation within the coronary anatomy and prevention of thrombus by inhibition of platelet aggregation, IVIG and ASA


Question Answer
• HypertensionBlood pressure > 95% for age/gender/height
• Hypertension PrimaryNo known cause
• Hypertension SecondaryIdentifiable cause
• Hypertension In pediatrics, HTN generally secondary tostructural abnormality or underlying pathology- Renal disease (glomerular nephritis), CV disease (COA), Endocrine or neurologic disorders (hyperthyroidism, primary aldosteronism)
• HypercholesterolemiaChildren with LDL levels at least 130/mg/100 ml should be identified and evaluated. Primary (most likely familial) and Secondary (obesity, oral contraceptive, anabolic steroid, or Accutane use)
• Hypercholesterolemia Treatmentdepends on type/cause
• Hypercholesterolemia Only medication recommended – bile acid sequesterants- colestipol (Colestid) and cholestyramine (Questran). Increase excretion of bile acids in stool and increase LDL receptor activity