Ummeenatrbilaoiasetptiwmsaiiri

Transcription

1 atrial This This atrial CIRCULATORY CHANGES My My pressure In the foetus the left atrial is low as relatively Ummeenatrbilaoiasetptiwmsaiiri U \ \ The foramen ovale is held Antenatal circulation Postnatal circulation the 1 atrium { then 1 with the first breath ventricle resistance blood flow falls { the volume blood flowing through the lungs 1 6x causes increase in 1 pressure { 9 drop in R pressure as the placenta is excluded from the circulation causes the foramen ovqle close The ductus arteriosus artery aorta closes within the first hours or days

2 The PDA 11 left Roh CONGENITAL HEART DEFECTS CHD is the most common structural malformations in infants 8 in most common account for 801 all lesions left right shunts I breathless VSD Right Tetrqlogy shunts I blue fgllot A 51 Common mixing breathless 9 blue 6 complete 1 Outflow obstruction in a well child 7g Pulmonary 71 Aortic 51 Outflow obstruction in a sick neonate asympmatic with 9 Coa rotation the aorta 51 Causes Maternal Abnormality Rubella DDA Pulmonary HE Complete heart block anti DM overall incidence Ia Ab s Drugs Warfarin Pulmonary Alcohol VSD TOF Chromosomal Down s 11 VSD Edward s 118 complex Patau 13 complex PDA Turner 5 0 Aortic Coa rotation the aorta 911 deletion Aortic arch anomalies ToF William s Aortic Voonantlstpnll HOCM Pulmonary artery Presentation Innocent Murmurs antenatal Us abnormalities asympmatic St HF 3 syslic Shock left Sternal edge! no added sound thrills or radiation

3 trial St diuretics diaslic ACYANOTIC HEART DEFECTS! left right shunts Ventricular Detects septal most common CHD can be membranous peri adjacent tricuspid gµp % #] V or 1 muscular completely surrounded by Muscle yf small VSD vsd large Features HF asympmatic breathlessness > Faltering growth signs iouapansysioiio Feaiunrrighreasitaint at 1 Sternal Tachypnoeig edge pansyslic VSD Quiet P sound Apical mid large VSD cq uses loud Pi cardiomeggly hypertension enlarged pulm arteries ECG t vase markings oedema µ Bi hypertrophy months by age Can be observed Can be observed + HTN Closes spontaneously HF While open Prevent irreversible prevention Additional calorie damage bacterial endocarditis input f capillary septgl Defects good dental Surgery 36 months bed from HTN hygiene There are two main types secundum 80% detect in centre atrial septum involving the foramen ovqle Their anamy is quite different but present with similar sympms

4 Secundum µ Partial My z faffftptnormaiiar t with valve 3 ffiqrffjionmtemritnriyationfftf@sefjfyeantditstt g between \ Clinical atrial septum \ AV G lregurgitant valves Features asympmatic arrhythmias ejection at split widely wheeze / IR 5 sternal edge stroke 1 apical syslic pan I from due l R shunt / equal volume inspiration flow blood Y 3010 syslic fixed infections chest recurrent common in expiration G regurgitation cardiomegaly enlarged arteries markings ECG secundum R RBBB superior ors node AV deviation axis f axis displaced Ventricles superiorly conducts 3 Secundum Partial 3 Treatment infants ierm birth 5 If it years age this remains normally open CHD but due m closes after shortly month 1 after there iareaeetremtinintanttiininsptiiiteoniemeoothmaispmamisthnet from device Arteriosys Ductus Patent In occlusion correction Surgical catheterisation Cardiac prematurity is µ ff } #% \ ~

5 absent When Presentation continues in diasle as pressure if is lower than artery continuous beneath 1 clavicle the aorta throughout the pulse pressure cardiac cycle or collapsing bounding pulse asympmatic blood flow Heart failure Pulmonary HTN normal [ CG normal if large Same as VSD Closure with coil or occlusion device at lyear Surgical ligation To abolish lifelong risk bacterial endocardiiis disease Coqrctqtion the Aorta Due arterial duct tissue the encircling aorta at the point insertion the duct causing severe obstruction the left outflow the duct closes the aorta also constricts My Presentation g / Y fe* fy 1! iugdiecsgiegtiieaitiiimiinaneatiaayswnen sick baby with severe HF femoral pulses severe metabolic acidosis ECG normal cardiomegaly 1 from HFG shock I Resuscitation PGE s 3 Surgical repair

6 Four central ventricyiar cerebro M CYANOTIC HEART DISEASE Tetralogy Fallot features sub stenos is Presentation SOB R 3 VSD R overriding aorta f outflow obstruction hypertrophy atearastighniughrrj ms?rnialoueddgeieotion may My iµ syslic at f t f para clubbing sternal heave older children Hypercyqnot c Spells rapid T in poly second cythaemia hypoxia t irritability stunted growth inconsolable severe crying hypertrophy hypoxia small heart # t breathlessness boot uptilted apex shape tissue pallor t C markings acidosis [ CG normal at birth complications R 1 hypertrophy older death Surgery at 6 months VSD closing 1 relieving outflow obstruction Infants who are very shunt t cyanosed flow Hyper cyanotic spells if Is beyond mins R t prolonged sedation G pain relief self usually limiting lv propanolol } followed by a t Metabolic v fluids period sleep demand bicarbonate f muscle oxygen paralysis { artificial ventilation

7 Transposition Great Arteries the systemic circulation aorta in ooxygen the EµA rich Ymthmeonlarrgntaiiae! J parallel circuits Hitting the systemic unless there is this is mixing oxygen with life VSD incompatible poor mixed vessels PDA interventions therapeutic blood switched Y# einaittioinathnoeiamouximgoeniaite the R ventricle is connected o Clinical features Sz loud usually no SOB tachycardia parasternal heave narrow Cardiac ECG normal [ cho upper Shadow medigstinum egg on side markings maintain patency ductus arteriosus balloon atrial sepsmy allow mixing tears open PGE s the foramen Ovale arterial switch procedure first Few days life including coronary arteries