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Peds, cardiovascular

Peds, Cardiovascular & Hematologic problems by Lucy

QuestionAnswer
Fetal Circulation Gas exchange. Placenta. anatomic structures: foramen ovale, ductus venosus, ductus arteriosus
Neonatal Circulation Gas exchange transfers from placenta to lungs. fetal shunts close in response to pressure changes.increase in O2, decrease in PVR, Increase in pulmonary blood flow, increase in systemic arterial pressure. Time frame:may take several days for closure.
Pediatric Cardiac Assessment: History Family history (SIDS), prenatal care (maternal), birth history, neonatal hx; feeding, poor weight gain, tachypnea, respiratory infection, fatigue, color changes in the skin.
Pediatric Cardiac Assessment: Inspection Color: skin, mucous membranes, nail beds, conjunctiva. Activity level: exercise tolerance, comfort, chest (PMI point of maximal impulse/apical pulse). Respiratory: signs of distress.
Pediatric Cardiac Assessment: Auscultation Heart sounds: S1, S2, S3, S4. Rhythm Murmurs: location, intensity, pitch, duration.
Cardiac Heart Sounds S1- "Lub" AV closure/systole S2- "Dub" semilunar closure S3- "Ventricular Gallop" CHF? "kentucky". S4- "Atrial Gallop" Ventricular hypertrophy? "Tennessee"
Pediatric Cardiac Assessment: Diagnostics Palpation:Temperature, pulses, BP, Cap. refill, abdomen. Percussion. EKG:Holter monitor. Chest X-ray. Echocardiography. MRI. Pulse oximetry. Cardiac catherization.
Heart Disease in Children: Congenital One or more structural abnormalities that develop before birth.
Heart Disease in children: Acquired Develop after birth. Rheumatic Fever, Kawasaki Disease, and Endorcarditis.
Chromosome Aberrations in CHD Trisomy 21 (Down Syndrome ~50%. Turner's Syndrome (only a singe X, females). DiGeorge Syndrome (velocardiofacial syndrome). Klinefelter's Syndrome ( Boys with extra X). Marfan.
Shunting in CHD Abnormal openings or connection between cardiac chambers. Pressure higher on one side of the heart compared to the other. Oxygen saturation- increased or decreased in normally desaturated or fully saturated blood.
Left-to-Right Sunting Lesions: Patent Ductus Arteriosus (PDA) Etiology: failure to close after birth. Hemodynamics: Increased workload, L side; increased pulmonary blood flow. Clinical manifestation: Depends on size of defect. Continuous murmur. Widened pulse pressure. Bounding pulses.
Clinical Manifestations of PDA X-rays. Heart enlargement. Increased pulmonary vascular markings.
Physical Symptoms of PDA Tachypnea, poor feeding and weight gain, fatigue. Frequent URI, diaphoresis. Preemies often have CHF, respiratory distress.
Treatment for PDA Infants with CHF, diuretics, Digoxin, high calories formula, rest. positioning, prevent exposure to URI. Medical closure (Indomethacin-Indocin) Interventional cardiology: PDA coil. Surgical closure. Risks for uncorrected PDA: CHF, endocarditis, Aneurysm.
Left-to-Right Lesions: Atrial Septal Defect (ASD) Abnormal opening between atria. Three types: Ostium Secundium, Ostium Primum, Sinus Venosus. Hemodynamics: Lover RV compliace, RA, RV enlargement, Increased pulmonary blood flow.
ASD: Manifestations Asymptomatic: Changes over time. Symptoms: Fatigue, dyspnea, palpitations, atrial dysrhythmias, URI, Murmurs, Rare: CHF, stroke, paradoxical embolism.
ASD: Therapeutic Management Monitoring(spontaneous closure). Medical: assymptomatic, symptomatic- CHF protocal, antidysrhythmics if needed. Interventional cardiology: transcatheter closure. Open heart surgery: pericardial or prosthetic patch.
Left-to-Right Shunting Lesions: Ventricular Septal Defect (VSD) Type; Based on location, conoventricular, AV canal type, muscular. Hemodynamics: Degree of shunting depends on size of defect, PVR. Pulmonary hypertension can result w/large defects. Manifestations:S&Sx vary with size of defect, presence of other defects.
VSD: Manifestations Small defects: usually assymptomatic. Larger defects: Symptomatic in 1st. few weeks. Murmur (loud harsh) palpable thrill. Diastolic with Lg defects. Gallop. Potential for CHF. Poor feeding and failure to thrive.
VSD: Medical Management Infants who develop CHF. Digoxin, diuretics, afterload reduction (ACE), nutritional supplements, sometimes G-tube, Avoid URI.
VSD: Interventional Cardiology Management umbrella closure devices (new)
VSD: Surgical Intervention Management Open heart, patch closure, location of VSD, symptoms. usually in 1st year of life.
Complications With VSD management Residual VSDs, pulmonary hypertension, heart block, dysrhythmias.
Atrioventricular Septal Defect Inappropriate development of endocardial cushion tissue. Abnormalities in atrial, ventricular septum. Abnormalities in AV valves (tricuspid, mitral).
Types of Atrioventricular Septal Defect Partial incomplete (ASD, 2 AV valves, cleft in mitral). Intermediate or transitional (aV valve malformation, ASD, no significant VSD). Complete (single AV valve orifice, ASD, VSD).
Atrioventricular Septal Defect: Therapeutic Management Medical: CHF, nutrition (increase calories,NGT) Surgical: partial defects, asymptomatic. Elective, later infancy or early childhood. Open heart Patch for closure device: complete defects done @3-4 months if symptomatic. mortality 10%.
Obstructive or Stenotic Lesions Pulmonary stenosis, Aortic stenosis, and Coarctation of the Aorta.
Pulmonary Stenosis: Lesions and Valve Lesions: Narrowing at the entrance to pulmonary artery, may be valvular, subvalvular, supravalvular. Valve: either normal (bicuspid, tricuspid) or dysplastic.
Pulmonary Stenosis: Hemodynamics Resistance at RV or valve leads to RVH. Elevated RV pressures.
Pulmonary Stenosis: Manifestations Assymptomatic- murmur with thrill, enlarged heart. Symptomatic- exercise intolerance, possible RV failure, CHF, cyanosis (mild to severe).
Pulmonary Stenosis: Medical Management Asymptomatic- Cardiac follow-up, antibiotic prophylaxis. Intervention- gradient across valve. Symptomatic: Balloon dilation, surgical valvotomy, Prostaglandin E1 infusion (maintain ductus arteriosus)
Pulmonary Stenosis: Interventional Cardiology Management Balloon valvuloplasty (isolated pulomary stenosis, valve is dilated; reintervention due to continued stenosis) Surgical: Surgical valvotomy.
Aortic Stenosis (AS) Hemodynamics: Pressure gradient across aortic valve (stneosis) LVH, decrease in cardiac output and myocardial blood supply (severe AS).
Aortic Stenosis: Classifications Mild, moderate, severe. Pressure gradient, degree of stenosis.
Aortic Stenosis: Diagnosis Echocardiogram, cardiac catheterization.
Aortic Stenosis: Mild to Moderate Manifestations Mild-moderate AS: asymptomatic. Normal growth&development.EKG abnormalities w/exercise, systolic murmur.
Aortic Stenosis: Severe Manifestations Severe AS:infants have decreased CO, faint peripheral pulses, poor peripheral perfusion, CHF, poor feeding. Older children: may have chest pain,dizziness, syncope on exertion, sudden death
Aortic Stenosis: Medical Management On going f/u cardiology. Prophylactic antibiotics. Activity limitations (moderate to severe AS).
Aortic Stenosis: Intervention Cardiology Management Aortic balloon valvuloplasty.
Aortic Stenosis: Surgical Management Surgical valvotomy. Valve replacement (recurrent stenosis, progressive insufficiency) Restenosis possible (after surgical or balloon).
Coarctation of the Aorta Hemodynamics:Aortic narrowing impedes systemic blood flow.CHF decreased CO, LV failure. Pulmonary congestion or edema, LV pressure.High aortic pressure proximal to constriction.Less severe cases collateral circulation, blood flow past the constricted area
Coarctation of the Aorta Severe Manifestation Severe coarctation symptoms after PDA closes: poor lower body perfusion. Metabolic acidosis. CHF. Shock.
Coarctation of the Aorta Mold to Moderate Manifestation Asymptomatic. Systolic hypertension (upper extremities). Disparity in pulses. Weakness, tingling in legs. Muscle cramps on exertion. Systolic murmur, ejection click or thrill.
Coarctation of the Aorta: Medical Management Newborn or infant. CHF management. PGE1 infusion to keep PDA open.
Coarctation of the Aorta: Older Child Management BP management. Corrective interventions.
Coarctation of the Aorta: Interventional cardiology Management Balloon dilation, possible stent.
Coarctation of the Aorta: Surgical Management Newborns: open heart. Elective: left thoracotomy. Patch, end-to-end anastamosis (to rejoin), subclavin flap. Potential renal failure.
Cyanotic Lesions with Decreased Pulmonary Blood Flow Unoxygenated blood enters systemic circulation. Tetralogy of Fallot. Tricuspid Atresia. Pulmonary Atresia- Intact ventricular septum.
Tetralogy of Fallot Malalignment of ventricular septum during fetal development.Four characteristics: VSD, pulmonary stenosis, overriding of the aorta into RV instead over LV, RVH (right ventricular hypertrophy).
Tetralogy of Fallot: Hemodynamics Degree of pulmonary stenosis. VSD usually large. Pressures equal in both ventricles. Blood flow. Desaturated blood enters systemic circulation.
Tetralogy of Fallot: Manifestations Cyanosis. "Tet"Spells. Fatigue. Difficulty feeding. Poor weight gain. Harsh murmur with palpable thrill. Heart of boot shaped on CXR.
Tetralogy of Fallot: Symptomatic newborns Management PGE1 infusion. Palliative or surgical intervention in first days of life.
Tetralogy of Fallot: Medical Management Monitoring for hypoxemia. At risk for for dehydration when ill. Monitor H&H for anemia.
Tetralogy of Fallot: Surgical Management Palliative (Blalock-Taussig). Increase pulmonary blood flow. Intracardiac repair. Post op complications. Mortality rate 2% - 5%.
Tricuspid Atresia Tricuspid valve does not develop. ASD or patent foramen ovale for survival RV hypoplastic underdeveloped. VSD present,varied size. Pulmonary artery may be transposed w/aorta.Pulmonary Stenosis varying degrees. Ductus arteriosus for pulmonary blood flow.
Tricuspid Atresia: Hemodynamics Blood: desaturated, shunted from R - L: ASD/foramen ovale into LA, through VSD to RV to lungs. Mixing of oxygenated and unoxygenated blood.
Tricuspid Atresia: manifestations Profound cyanosis in neonate. Less cyanosis with increased pulmonary blood flow, CHF. Auscultation: single first heart sound (no closure of absent tricuspid valve for second sound). Systolic murmur of VSD.
Tricuspid Atresia: Medical Management PGE1 for infants who depend on PDA. Stabilize for surgery.
Tricuspid Atresia: Interventional Cardiology Management Balloon atrial septostomy (effective for newborns). Catheter blade septostomy.
Tricuspid Atresia: Surgical Management Palliative (Blalock0Taussig). 3 Procedures to correct (Staged Approach). Infancy- establishment or limitation of pulmonary flow. infancy- SVC to PA anastomosis. early childhood- IVC to PA.
Pulmonary Atresia with Intact Ventricular Septum Failure of pulmonary valve to develop. Hypoplastic pulmonary artery and RV. Tricuspid valve may be underdeveloped. RV pressures high. Coronary arteries may be abnormal.
Pulmonary Atresia with Intact Ventricular Septum: Hemodynamics blood enters RV can not flow to the pulm arteries directly, propelled back through tricuspid valve into RA,shunted R-L through foramen ovale to LA. Saturated & desaturated blood mix in LA, flows into LV, pumped to aorta, body & brain.
Pulmonary Artresia with Intact Ventricular Septum: manifestations Cyanosis- survival depends on PDA. Single heart sound (S1). Patent ductus murmur, or continuous murmur.
Pulmonary Atresia with Intact Ventricular Septum: Medical Management PGE1 for ductal patency.
Pulmonary Atresia with Intact Ventricular Septum: Interventional Cardiology Management Alternative to surgery. Wire and radiofrequency-assisted valvulotomy. Decreased risk for mortality (5%). Balloon dilation of valve following valvulotomy.
Pulmonary Atresia with Intact Ventricular Septum: Surgical Management Early intervention. Pulmonary valvotomy and/or systemic-to-pulmonary shunt. Later closure of ASD.
Cynatoic lesions with Increased Pulmonary Blood Flow Truncus Arteriosus. Hypoplastic left heart syndrome. Transposition of the Great arteries.
Truncus Arteriosus Inadequate division of the common great vessel into separate aorta and pulmonary artery. Manifestations: Cyanosis,systolic click, VSD murmur, CSR-enlarged heart, CHF, Bounding arterial pulses, widened pulse pressures.
Truncus Arteriosus: Medical Management CHF control. Antibiotic prophylaxis.
Truncus Arteriosus: Surgical Management Palliative pulmonary banding: Infants with increased pulmonary blood flow. CHF unresponsive to medical management. Corrective surgery: Closure of VSD. Placement of RV Conduit to pulmonary artery. Valvuloplasty of truncal valve.
Hypoplastic Left Heart Syndrome Inadequate of development of left heart (one effective ventricle). Additional defects often present (CNS dysfunction: Aortic valve atresia. Hypoplasia of LV. Atresia or hypoplasia of ascending aorta. Mitral stenosis or atresia.
Hypoplastic Left Heart Syndrome: Hemodynamics Blood flow from left atrium across foramen ovale, L-R shunting. Mixes with desaturated blood.
Hypoplastic Left Heart Syndrome: Manifestations Progressive cyanosis, pallor, mottling, grayish/blue. Tachycardia, tachypnea, dyspnea, hypoxemia. CXR- heart enlargement, pulmonary venous congestion. Hypoperfusion (systemic), shock, hypotension, CHF.
Hypoplastic Left Heart Syndrome: Medical Management emergency Tx: Acid-base and electrolyte corrections, PGE1 (continous); if family decides against surgical/transplant interventions: Stop PEG1, provide supportive care.
Hypoplastic Left Heart Syndrome: Surgical Management Cardiac transplant (successful, esp early; neonatal donors tissues, retransplant). Three stage palliative repair (Norwood procedure): single ventricle at the completion, 4yr survival: 50%, survivors have normal growth & development, few limitations.
Transposition of the Great Arteries: Pathophysiology Improper septation and rotation of the common truncal vessel in utero.
Transportation of the Great Arteries: Hemodynamics Aorta receives unoxygenated blood, returns it to systemic circuit. Two separate parallel circulations (pulmonary or systemic). Survival depends on mixing through fetal structures.
Transportation of the Great Arteries: Manifestations Cuanosis. Hypoxemia, min response to oxygen administration. Progressive desaturation. CHF development. Acidosis. CXR: enlarged heart, narrow base (egg shaped).
Transportation of the Great Arteries: Therapeutic Management Medical: correction of acidosis, oxygen PGE1. Interventional cardiology: Balloon atrial septostomy. Surgical correction: arterial switch.
Acquired Cardiovascular Problems Cardiac conditions not present at birth: Infective Endocarditis. Rheumatic Fever. Kawasaki Disease.
Infective Endocarditis (IE) Definition:Inflammation resulting form infection of cardiac valves and endocardium by bacteria, fungi,virus.Infection can result from dental work,invasive surgery, respiratory tract,poor oral hygiene.Etiology:G+ organisms: Strep,Staph.Long term use CVC.
Infective Endocarditis: S & Sx Can be subtle, nonspecific. Fatigue, weight loss, anorexia, intermittent fever. Weakness, malaise. Arthralgias. Chest pain. Heart failure. Possible septic emboli (stroke, brain, abscess) IE: mimics other diseases.
Infective Endocarditis: Diagnosis Blood cultures (multiple). echocardiography (vegetation visual).
Infective endocarditis: Treatment Prevention. Antibiotics, surgery only if necessary.
Rheumatic Fever:Definition Diffuse inflammatory condition, autoimmune orgin; resulting from earlier group A beta-hemolytic strep infection. Self-limiting except for cardiac effects, permanent valve damage possible.
Rheumatic Fever: S & Sx Fever, arthritis (classic swollen joints, joint pain). Carditis in 40%-50% 1st attack (new murmur, possible CHF, arrhythmias). Chorea (CNS, involuntary jerky muscle movements) erythema marginatum (red skin lesions). Subcutaneous nodules.
Rheumatic Fever: Dianosis Throat culture. Antisterptolysin O titer. Hx: Scarlet fever. ECG- rhythm abnormalities.
Rheumatic Fever: Treatment Antibiotics (Penicillin) 10 days. Anti-inflammatory agents. Prophylactic antibiotics. Sequelae: Susceptability to recurrent attacks. Possible valve damage usu mitral & aortic.
Kawasaki Disease Generalized, acute, self-limited immune mediated vasculitis of unknown etiology. Triggers: acute infection, bacterial toxin. Most common in Japanese, Asian, Pacific children.
Kawasaki Disease: Manifestations 3Phases: Acute-days 10-14 fever non-responsive to antibiotic Tx. Conjunctivitis changes in mucous membranes, extremities, rash on trunk, cracking of the lips, strawberry tongue. Subacute-Day 15-25. Final or convalescent Day 26 until sed rate is normal.
Kawasaki Disease: Diagnosis & Management Fever X5 days, 4 of primary acute symptoms. Management: prevent or reduce coronary artery damage: IVIG (1 gm/kg over 12 hr IV), ASA (80-100 mg/lg per day)
Created by: tiniekittie12