Principles of Intracardiac Shunts
Significant hypoxemia can result from right-to-left intracardiac shunting through a patent foramen ovale, an atrial septal defect or a ventricular septal defect. Pulmonary embolus, congenital heart disease and pericardial tamponade are well-recognized causes of right-to-left shunting.
With the continued presence of a congenital defect of the cardiac septum or great vessels in which there is a communication between the left and right cardiac structures, blood flow is diverted from the area of greater resistance to the chamber or vessel of least resistance. As a result, a percentage of blood which characteristically flows from the right side of the cardiac structure through the pulmonary system, may be shunted back to the venous side of the heart in deference to greater left heart pressures. This condition is referred to as a left-to-right shunt and is most commonly associated with the presence of a congenital lesion such as an atrial septal defect (ASD) or ventricular septal defect (VSD). If left unresolved this condition will result in right atrial enlargement as a compensatory mechanism for increased volume and workload associated with the shunt.
Pathological changes will be witnessed in the pulmonary system due to this increase in blood flow and will eventually be reflected as an extension of the muscle layer into peripheral vessels resulting in medial hypertrophy of the lung. The subsequent development of pulmonary hypertension ultimately results in right ventricular hypertrophy which in time will elevate right cardiac pressures to a point where the shunt is reversed to right-to-left. When outflow tract resistance exceeds systemic vascular resistance the result is reduced pulmonary blood flow. This condition is commonly referred to as Eisenmenger’s syndrome.
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