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Complete Cardiac Diagnosis Congenital Heart Disease – Atrial Septal Defect; cardiomegaly with multi-chamber enlargement, RVH, dilated RA and main PA, MVP-anterior mitral valve leaflet, PR; sinus rhythm, pulmonary HPN, incomplete right bundle branch block; Functional Class III C AUSCULTATORY FINDINGS OF THE PATIENT DIFFERENTIAL DIAGNOSIS Hx Patient ASD VSD PDA RHD “heart disease” in childhood Prolonged symptom-free period most children with small defects remain asymptoma-tic frequent URTI Palpitations premature birth, perinatal distress, or perinatal hypoxia may be present (+) upper respiratory tract infection Mitral stenosis easy fatigability occasional chest pain Fatigue Dyspnea on exertion Orthopnea Frequent respiratory infections Symptoms of right ventricular failure In patients with Eisenmenger syndrome, symptoms in adult life consist of exertional dyspnea, syncope and hemoptysis R-L shunt leads to cyanosis, clubbing, and erythorocytosis -dyspnea and cough on exertion -orthopnea and PND -hemoptysis Mitral regurgitation -dyspnea and cough on exertion -orthopnea and PND -ankle edema P.E. Patient ASD VSD PDA RHD Hyposthenic, narrow AP chest diameter Prominent RV impulse loud, harsh, or blowing holosystolic murmur is heard best over the lower LSB in the 3rd or 4th ICS precordial activity is increased Mitral stenosis diastolic thrill at the apex S1 and P2 are accentuated S2 is split or fixed OS of the mitral valve on expiration (+) carvallo's sign Normal JVP and CAP Left lower sternal lift Normal S1 ff. by gr. 3/6 crescendodecrescendo murmur S2 wide with fixed splitting Multiple clicks at apex S1 normal or split, with accentuation of TV closure sound Wide & fixed splitting of the S2 Systolic ejection murmur (heard in pulmonic area) Diastolic rumble across the tricuspid valve Neck vein distention Ascites Edema displaced cardiac apex with a similar holosystolic murmur apical impulse is laterally displaced S1 normal, S2 typically obscured by murmur Continuous machinery-like apical diastolic murmur rumble and third heart Bounding sound (S3) peripheral pulses Mitral regurgitation (+) systolic thrill at the apex holosystolic murmur -(+) S4 ECG Patient ASD VSD PDA RHD Normal sinus rhythm Ostium secundum defects – incomplete right bundle block & right axis deviation May be normal LVH with a larger PDA LVH RVH Incomplete RBBB Diffuse ST-T changes Ostium primum defects – left anterior hemiblock & left axis deviation With larger defects there are various degrees of right axis deviation associated with right ventricular Enlargement CXR Patient ASD Cardiomegaly with multichamber enlargement and pulmonary congestion Shunt vascularity Right (inc. pulm. Ventricular vascular markings) enlargement LAE Right ventricular enlargement PAE Enlargement of the pulmonary artery segment in P-A view VSD Increased pulmonary vascular markings PDA LVE PVE RHD Mitral stenosis -(+) kerley B lines -concentric hypertrophy of left atrium -cephalization -prominent main pulmonary artery and branches -constriction of arteries in the middle and peripheral lung zones Mitral regurgitation -eccentric hypertrophy of the left atrium -LA and LV enlargement -equalization, cephalization -mitral annulus calcification Echo Patient ASD ASD, ostium secundum type Enlargement of RV color flow can Negative-contrast show the image at the site shunting of of defect (saline blood from injection) the left ventricle to Doppler – the right abnormal pressure of left-to-right VSD's can blood flow across result in a the septum shunt from below the tricuspid valve to below the pulmonary valve. Markedly dilated right ventricle with adequate wall motion and contractility with evidence of RV pressure and volume overload Dilated RA w/o thrombus Dilated MPA Severe TR PR Mod. Pul. HPN Reverse E/A across mitral valve VSD PDA RHD LAE Mitral stenosis -mitral orifice <4cm -concentric hypertrophy of left atrium -annular calcifications Continuous flow from the aorta into the main pulmonary artery Mitral regurgitation -eccentric hypertrophy of the left atrium -LA enlargement -hyperdynamic LV -annular calcifications/ LV dyskinesis -ruptured chordae tendineae CHEST X-RAY FINDING IN A LEFT TO RIGHT SHUNT DIFFERENTIATE PULMONARY ARTERIAL HYPERTENSION FROM PULMONARY VENOUS CONGESTION Pulmonary Arterial Hypertension • Causes – Primary/ Idiopathic • Genetic – Secondary • • 1. 2. 3. Cardiac Pulmonary hypoxic vasoconstriction decreased area of the pulmonary vascular bed volume/pressure overload Secondary Pulmonary Arterial Hypertension • Hypoxic Vasoconstriction – COPD and obstructive sleep apnea – Due to down regulation of endothelial nitric oxide synthetase • Decreased Area of Pulmonary Bed – Occurs when loss of vessels exceed 60% of the total pulmonary vasculature – Occurs in patients with collagen vascular disease like CREST and scleroderma. And those with chronic emboli • Volume/ Pressure Overload – Seen in patients with left to right intracardiac shunts – May passively occur in patients with left atrial hypertension and left ventricular dysfunction, mitral valve disease and hose with aortic stenosis Pulmonary Arterial Hypertension • Chest radiograph - Classic finding is enlargement of central of pulmonary arteries, attenuation of peripheral vessels and oligemic lung fields - Findings of RV and RA dilatation are possible Pulmonary Venous Hypertension • Secondary to increased resistance to pulmonary venous drainage • Associated with diastolic dysfunction of the LV and valvular dysfunction • Features – Capillary congestion – Focal alveolar edema – Dilatation of interstitial lymphatics •mild cardiomegaly •normal pulmonary arterial markings •pulmonary venous congestion •fluid within the horizontal fissure •prominent Kerley B lines (indicative of lymphatic engorgement) Lateral chest film show marked venous congestion with fluid visible in both the horizontal and oblique fissures Pulmonary Arterial Congestion Pulmonary Venous Congestion “active congestion” – increased in flow Passive congestion – obstructed of blood venous outflow, swollen capillary beds Physiologic Systemic: Pathologic Localized • Increase blood flow into skeletal muscle (e.g. exercise) • Systemic: generalized hypoxia, metabolic activity • Localized acute inflammation • due to RHF • diminution of CO and tissue perfusion • Hypoxia – decreased Hemoglobin • Cyanosis • Raised LA pressure secondary to LV failure & MS • Thrombotic occlusion of femoral vein MANAGEMENT