P. Rao 's Atrial Septal Defect PDF

By P. Rao

ISBN-10: 9535105310

ISBN-13: 9789535105312

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Scand Cardiovasc J. 36:73-79. Botto LD, Lin AE, Riehle-Colarusso T, Malik S, Correa A, and the National Birth Defects Prevention Study. (2007). Seeking Causes: Classifying and Evaluating Congenital Heart Defects in Etiologic Studies. Birth Defects Research (Part A): Clinical and Molecular Teratology 79:714-728. Cedergren MI and Kallen BAJ (2003). Maternal obesity and Infant Heart Defects. Obesity Research 11:1065-1071 Correa A, Cragan JD, Kucik ME, et al. (2007). Reporting birth defects surveillance data 19682003.

In second stage of labor, cardiac output increases significantly due to vigorous expulsive effort. (Ueland & Metcalfe 1975). After delivery, removal of placenta leads to increase in systemic vascular resistance. Blood loss during labor is a stress on the heart. Equally important is the fact that several hormonal stimuli that occur during pregnancy are receding during postpartum, leading to return of blood volume, hematocrit and cardiac output to pre-conception levels. 3. Effect of pregnancy on ASD Hemodynamic changes outlined above will affect the hemodynamics of ASD.

Since placenta offers very low vascular resistance, maternal systemic vascular resistance decreases. A reduction in left ventricular afterload occurs (Metcalfe & Ueland 1974). A corresponding increase in cardiac output occurs during the same period, keeping blood pressure stable in spite of the reduction in afterload. Overall, circulatory changes can be summarized as follows: Increase in stroke volume by 1825% with heart rate increase by 20%. Net effect of this is a 30-50% increase in cardiac output.

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Atrial Septal Defect by P. Rao


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