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Evaluation And Treatment Of Common But Non-Complex Congenital Heart Defects/Problems John E. Pliska, M.D. Chief of Pediatric Cardiology McLane Children’s Hospital Scott & White Texas A&M College of Medicine Temple, Texas Discussion Topics Atrial Septal Defects Ventricular Septal Defects Patent Ductus Arteriosus Premature Atrial Contractions (Complexes) Premature Ventricular Contractions Normal Cardiac Physiology Cardiac shunts: Left-to-right Examples Patent Ductus Arteriosus Atrial Septal Defect Ventricular Septal Defect ASD case 3 week old male infant with heart murmur Echo-Moderate size secundum atrial septal defect with right atrial enlargement, normal biventricular fxn ECG with sinus rhythm and RVH Feeding well, no resp distress, +wt gain (BW 3kg, Wt: 3.35kg) ASD continued Discharged home with plans for outpatient follow-up with pediatric cardiology Atrial Septal Defects Types Clinical Presentation Treatment Follow-up and Consideration for Closure (cath vs surgical) Anatomic types of ASDs ASDs Basic Echo Diagram Sinus Venosus ASD Secundum ASD Primum ASD ASD Basic Types Secundum atrial septal defect Primum atrial septal defect Sinus venosus defect BUT THAT’S NOT THE WHOLE PICTURE…….. ASD Types Patent foramen ovale Ostium secundum atrial septal defect Superior vena caval atrial septal defect Inferior vena caval atrial septal defect ASD in the septum intermedium Coronary sinus atrial septal defect Ostium primum atrial septal defect The Atrial Septum http://www.med.uc.edu/embryology/ch apter7/animations/contents.htm Patent Foramen Ovale Between the superior rim of the septum secundum on the right atrial side and septum primum on the left atrial side Normally closes due to overlapping of the septum secundum and the septum primum Abnormally high atrial pressures can cause the two septa to pull apart Patency 25% at autopsy Ostium secundum ASD The floor of the fossa ovalis is thin ostium primum, bounded by the limbic septum Defects in the septum ovale or septum primum are called “ostium secundum ASD” and make up 69% of ASDs Defects may be multiple (fenestrated) Results from developmental failure of the septum primum or secondary fenestrations in the septum primum Ostium secundum ASD - Echo Superior vena caval ASD / “Sinus venosus ASD” Coronary sinus ASD Rare Appears as large ostium of the coronary sinus A defect in the “roof” of the coronary sinus Invariably a persistent left SVC to LA is present Noted due to the relatively frequent isolated finding of persistent left superior vena cava draining through an enlarged coronary sinus which does not have an associated ASD or intracardiac shunt, and is benign clinically Persistent Left SVC draining via enlarged coronary sinus Ostium Primum ASD 15% of ASDs (30% if includes AV Septal Defects) Is a defect in the atrioventricular septum Therefore most often has an endocardial cushion type inlet VSD as part of the defect Cleft mitral valve present Ostium Primum ASD Partial atrioventricular septal defect “Atrial Septal Aneurysm” Echocardiographic definition is somewhat arbitrary Hanley, et al: Dilatation protruding at least 1.5 cm beyond the plane of the atrial septum or if septal phasic excursion during cardiorespiratory cycle exceeded 1.5 cm and if the base of the protrusion was at least 1.5 cm in diameter Stroke associated with R-L shunting and thrombus formation in some types of ASA ASD Hemodynamics Primarily a left-to-right shunt lesion Therefore enlarged RA and RV May shunt right-to-left with elevated right atrial and/or elevated right ventricular pressure and elevated pulmonary vascular resistance, especially if tricuspid regurgitation present Right-to-left shunt risk increased during pregnancy Atrial Septal Defects – When To Be Concerned If associated with other congenital cardiac anomalies Generally tolerated well during infancy and childhood with closure indicated at 2-4 years of life If patient at risk for stroke: eg, pulmonary hypertension, thrombi/hypercoagulable state present, intractable atrial dysrhythmia Atrial Septal Defect Closure Cath lab interventional procedure – device closure Surgical repair – primary closure vs patch closure Timing – 2+ to Five years Heart size and hemodynamics normalize shortly after closure Increased risk of atrial arrhythmia if late closure ASD Closure Device closure in cath lab, or surgical CHF and pulmonary hypertension (35% by age 40 yrs) may develop if not closed Atrial arrhythmias may occur in adults (30% by age 50 yrs) Cerebrovascular accident (CVA) results from paradoxical embolization through ASD Indications for closure: L-R shunt > 1.5:1, ASD > 5mm with RV enlargement ASD Repair – Cath Lab Appropriate size and location of the Secundum ASD may be closed in cath lab Smaller children (< 3 yrs) may not be candidates because of the size of the vascular catheters ASD Repair - Surgical Usually 2 to 5 yrs of age – suture or pericardial patch Performed to avoid RV dilatation and scarring, PA HTN? Can be done at any size ? Need for long term follow-up ASD Surgical Closure (patch) VSD Case Near full term infant male delivered by NSVD. Birth weight 2.9 kilograms. Normal APGAR scores. DOL 1 a grade 2-3/6 harsh systolic murmur heard on exam. Stable VS without cyanosis or feeding difficulty. Murmur still present 8 hours later and clinically stable. Echocardiogram: small, mid-muscular ventricular septal defect. Baby discharged home with plans for outpatient f/u. Anterior muscular VSDs Ventricular Septal Defects Types Clinical presentation scenarios Treatment Intervention (surgical vs cath)/timing Ventricular Septal Defects Types Looking from right ventricle. Size and Location of VSD affect amount of shunt. Right Atrium Pulmonary Valve Ventricular septal defect Produce left-to-right shunt which increases as the infants pulmonary artery pressure and pulmonary vascular resistance decrease with normal maturing of the lungs after birth Early surgical intervention (1 month) if significant VSD or significant heart failure Some moderate to large “muscular” ventricular septal defects are more successfully “closed” in the cath lab VSD Closure Surgery Cath Lab Case: Patent Ductus Arteriosus Init eval: 6 day old baby boy delivered at 35 weeks EGA with birth weight of 2.4 kg. Mild tachypnea and continuous murmur. Cardiomegaly. Echo: moderate PDA with L-R shunt, LA and LV enlargement. Rx with indomethacin: 4 days later: Continuous murmur still present, heart size improved. Feeds OK. + wt gain. Echo: Small to mod PDA L-R shunt. Normal LA & LV size with nl biV function. Laxis given every other day and baby improved and discharged home. F/U 3 months later: Continuous murmur present, feeding well, pos weight gain. Echo: Small to mod PDA L-R, no cardiac enlargement. F/U 9 months of age: Cont murmur, nl growth. Echo: sm to mod PDA L-R, mild left atrial enlargement, Borderline enlarged LV. Referral for PDA closure: performed successfully in cath lab 1 year of age PDA Chest X-Ray Pre-closure Post-closure Patent Ductus Arteriosus Isolated vs Associated with other CHD Ductal Dependent CHD Clinical Presentation Scenarios Treatment Closure of PDA (surgical vs cath)/timing Ductal Dependent Congenital Heart Disease; Examples Transposition of the Great Arteries Severe Pulmonary Stenosis or Pulmonary Atresia (with VSD/without VSD) Tricuspid Atresia with restrictive VSD Critical Aortic Stenosis “Interrupted Aortic Arch-Coarctation Ao Patent Ductus Arteriosus Ductus arteriosus present at birth, constricts and “closes” by 3 days after birth Oxygen constricts the ductus arteriosus; PGE1 relaxes the ductus arteriosus Persistent PDA shunts right-to-left with pulmonary hypertension and elevated pulmonary vascular resistance – “Wait for shunt to change to L-R before considering closure” Patent Ductus Arteriosus Shunt becomes left to right as lungs “mature” (decreased PA pressure and decreased pulmonary vascular resistance) With increasing left to right shunt, cardiomegaly, poor lung function and congestive heart failure ensue Patent Ductus Arteriosus Left to right ductal shunt (1) Increased pulmonary blood flow If significant – enlarged left atrium and LV PDA Patent ductus arteriosus: Early Intervention Treatment: Oxygen, Indomethacin, Ibuprofen, Diuretic, Surgical Closure If fails medical treatment for ductal closure and has clinical signs and symptoms of CHF (tachypnea, inability to wean from vent, cardiomegaly, poor weight gain), or other heart defects contributing to left to right shunt, surgery for ductal ligation should be considered early PDA Options for closure in infant Medical: O2, Indomethacin, Ibuprofen Surgical: Ligation (metal clip) Interventional: If baby several months old may be considered for catheter interventional procedure in which a “feathered” coil or ductal closure device is placed to occlude the ductus arteriosus PDA closure in the catheterization laboratory “Feathered” coil may be deployed to close small patent ductus arteriosus Amplatzer ductal occluder used for larger PDAs PDA closed with “coil” in the catheterization laboratory PACs - Case Fetal bradycardia Delivered; frequent PACs (no SVT) Resolve with time (days) Premature Atrial Contractions PACs Premature Atrial Contractions Premature Atrial Complexes How common Clinical presentation scenarios (Irreg heart beats-pauses with bradycardia) Treatment Concerns (red flag abnormalities on ECG) Follow-up Premature Atrial Contractions (PACs) PACs or atrial premature beats (APCs) Early electrical activation of left or right atrium May be conducted or non-conducted to ventricles PACs with “aberrancy” may look like PVCs Early beats with pause or non-conducted both lead to irregular heart rate Common in otherwise structurally and functionally normal hearts; rarely occur with underlying cardiomyopathy or atrial tumor PACs may be caused mechanically by central venous lines in the atria Premature Atrial Contractions - PACs PACs Occur in 14% of infants (all with fewer than 12 PACs/hour) (up to 21% in older children) Infants generally remain asymptomatic PACs may be noted during fetal monitoring (may have fetal ventricular bradycardia if atrial bigeminy present) PACs benign in most all cases: rare that PACs are trigger for SVT or Atrial Flutter PACs – When To Be Concerned If runs of tachycardia (SVT) present If evidence of cardiac dysfunction If persisting after interventions to move central line or correct metabolic abnormality Premature Atrial Contractions What to Do? Electrocardiogram ordered if irregular heart beats noted If no evidence of runs of tachycardia on monitoring no treatment needed Echocardiogram if concern for congenital heart disease No additional follow-up needed; most resolve or diminish significantly in the first weeks of life PVCs - Case Irregular heart beat in newborn, Frequent PVCs Check lytes, Mg++, Ca++ Runs of tachy, bradycardia? Premature Ventricular Contractions - PVCs Incessant V-tachycardia in an infant Premature Ventricular Contractions PVCs How common Concerns Treatment Follow-up Premature Ventricular Contractions Less common than PACs Almost always benign Usually resolve Usually never need treatment Frequent PVCs may warrant echo PVCs – When To Be Concerned If runs of tachycardia present (> 3 beats) Evidence of ventricular dysfunction (echo) If prolonged QTc present (ECG) Usually improve/resolve if metabolic abnormalities corrected (Ca++, Mg++) Bradycardia / Heart Block Bradycardia in infants usually related to increased vagal tone or “blocked” PACs Premature atrial contractions (PACs) generally benign Not benign if associated with SVT Complete heart block often associated with maternal lupus erythmatosis or Sjogren’s disease Adequate heart rate > 60 BPM Lower heart rates may cause cardiomegaly, cardiac dysfunction, or congestive heart failure Early pacemaker placement may be needed