This document summarizes various congenital heart diseases including their anatomy, hemodynamics, symptoms, and clinical findings. Atrial septal defects (ASDs) allow blood to shunt from the left atrium to the right, enlarging the left atrium over time. Patent ductus arteriosus (PDA) causes a continuous shunt between the aorta and pulmonary artery. Ventricular septal defects (VSDs) allow blood to pass between the left and right ventricles during systole. Tetralogy of Fallot consists of four anatomical abnormalities that cause cyanosis. Clinical exams can detect murmurs and thrills associated with the direction and timing of shunts in each condition.
This document summarizes various congenital heart diseases including their anatomy, hemodynamics, symptoms, and clinical findings. Atrial septal defects (ASDs) allow blood to shunt from the left atrium to the right, enlarging the left atrium over time. Patent ductus arteriosus (PDA) causes a continuous shunt between the aorta and pulmonary artery. Ventricular septal defects (VSDs) allow blood to pass between the left and right ventricles during systole. Tetralogy of Fallot consists of four anatomical abnormalities that cause cyanosis. Clinical exams can detect murmurs and thrills associated with the direction and timing of shunts in each condition.
This document summarizes various congenital heart diseases including their anatomy, hemodynamics, symptoms, and clinical findings. Atrial septal defects (ASDs) allow blood to shunt from the left atrium to the right, enlarging the left atrium over time. Patent ductus arteriosus (PDA) causes a continuous shunt between the aorta and pulmonary artery. Ventricular septal defects (VSDs) allow blood to pass between the left and right ventricles during systole. Tetralogy of Fallot consists of four anatomical abnormalities that cause cyanosis. Clinical exams can detect murmurs and thrills associated with the direction and timing of shunts in each condition.
This document summarizes various congenital heart diseases including their anatomy, hemodynamics, symptoms, and clinical findings. Atrial septal defects (ASDs) allow blood to shunt from the left atrium to the right, enlarging the left atrium over time. Patent ductus arteriosus (PDA) causes a continuous shunt between the aorta and pulmonary artery. Ventricular septal defects (VSDs) allow blood to pass between the left and right ventricles during systole. Tetralogy of Fallot consists of four anatomical abnormalities that cause cyanosis. Clinical exams can detect murmurs and thrills associated with the direction and timing of shunts in each condition.
CVS PGMEE notes MV Flow murmur: DDM at mitral area
Congenital heart disease: Loud S-1
Lt side of heart has higher pressure than Rt side Symptomps (CHF: S3) at 6-10 weeks of age All L-R shunt have enlarged LA (L-R shunt 80% small : Spontneous closure PAlungPul vein LA) except ASD as it has Max risk of IE extra exit for blood in LA inform of ASD CXR : Normal heart (small VSD) , cardiomegaly (Large VSD) Girls ASD,VSD,PDA,PS Boys TGA, Left obst(AS,CoA) PDA: Physiological closure (muscular contraction by bradykinin/low oxygen/low PGF2) : immediately after ASD: few hrs of birth anatomical closure (intimal osteum secundum (at/sup/post to fossa ovalis) > proliferation) at 10-21 days obliterate to form osteum primum (endocardial cushion defect-inf to ligamentum arteriosum fossa ovalis :asso cleft in ant MV leaflet ± septal TV MC site : just distal/below subclavian a. cleft) Hemodynamics : associated Ds: Aorta o holt oram synd PDA Shunt thoughout cardiac cycle (systole + diastole) : o down synd Continuous machinery murmur & thrill : after S1 -peak at S2-part of diastole : Lt ICS & lt Clavicle o ellis van crevald synd Pul a Also from Rt heart o rubinstein taybi synd Lung Pul Plethora pulHT o thrombocytopenia absent radius (TAR) synd Pul v o pierre robbin synd LA LAH o ehler danlos synd MV Flow murmur : DDM & loud S1 o fetal alcohol synd LV LVH o lutembacher syndrome : ASD +MS AV High flow causes delayed closure : late A2 hemodynamics : narrow/Paradoxical Spliting of S2 (P2-A2) LA Aortic Ejection click ASD Low pr diff : no shunt murmur Aortic ESM (masked by cont murumur) RA RAH Dilated ascending aorta TV DDM at lower sternal border D/D : Aortopul window defect (large : shunt only in loud S-1(T1) systole / small mimic PDA) RV RVH parasternal heave CHF(S3 at apex) at 6-8 weeks of age PV Pulmonary ESM : systolic thrill at Lt 2nd ICS MC cause of death in PDA : CHF >IE delayed loud P2 widely split fixed S2 Preterm infant PDA (no structural abnormality but d/t PA oxygen unresponsiveness) : spontaneous closure may Lungs Pul plethora Pul HT occur if not Indomethacin > ibuprofen usually works Asymptomatic > ex intolerance , chest infection in 90% CHF & IE is rare : no S3 Term infant PDA (structural abnormality) : cannot ECG : RAD in osteum secundum > LAD in osteum spontaneously close – give Indomethacin > ibuprofen primum (d/t asso lack of ant-sup LBB) fail usually Sx ligation
VSD: Duct dependent condition :
MC cong heart ds keep it open by PGE1 (Alprostadil ,rioprostil , misoprost) Memb > muscular > multiple For Pul flow TA , critical PS + intact septum , TOF Hemodynamics : For syst flow AS , CoA , HLHS , Interrupted aortic arch LV For oxygen TGV VSD Shunt murmur : PSM – systolic thrill at 3-4-5lt ICS Ductal independent But require immediate Sx : masking S-1 &S-2 TAPVR , PTA , ALCAPA Low blood flow thro aorta (early A2) RV Normal size (shunting occurs during systole only) TOF: PV Pul ESM (masked by PSM) in pul area MC cyanotic Cong Heart ds : cyanosis NOT at Birth Delayed loud P2 (&Early A2) : widely split S2 4 components (usually masked by PSM except at pul area at upper 1. VSD lt sterna border) 2. RVH PA 3. RV out flow obst (Infundibular stenosis > both > PS Lungs Pul plethora pul HT >PA) Pul v 4. Overriding of aorta LA LAH Hemodynamics : Mild : no RVOT Mimic VSD (no cyanosis) Severe : with RVOT (PS) Pul ESM Delayed soft P2 = only A2 = single S2 R-L shunt (low pr : no shunt murmur) Low PBF : soft P2 MC symp : dyspnea on exertion & Exercise intolerance