What are the common intracardiac left-to-right shunting lesions?
The ASD is located in the area of the fossa ovalis and shunting occurs between two low-pressure circulations. Despite a large volume of shunting resulting in a marked increase in pulmonary blood flow, pulmonary artery pressure remains low over many years. These patients are generally asymptomatic throughout childhood and adolescence but may develop mild pulmonary hypertension in the third and fourth decades of life. In this lesion, the right ventricle is volume-overloaded. Treatment consists of elective closure of the defect during later childhood either surgically or with an intracardiac device. The main anesthetic concern in asymp-tomatic patients is prevention of systemic embolization from injection of air or debris from IV lines. Endocarditis prophylaxis is necessary only if it is within 6 months of repair or after 6 months if there is a residual lesion present.
Small VSDs restrict the amount of left-to-right shunting and thereby limit the hemodynamic consequences. With a large defect (approximating the size of the normal age-appropriate aortic orifice or larger), there is no restriction to flow and shunting depends largely on the relative ratio of the PVR to systemic vascular resistance (SVR). In the early neonatal period, the PVR is high and the patient may have no signs or symptoms related to the VSD. As PVR declines during the second to third weeks of life, the left-to-right shunting increases and may result in congestive heart failure due to the volume overload on the left ventri-cle. In this lesion, the pulmonary vascular bed is exposed to increased blood flow and systemic blood pressure.
An estimated 25–50% of small to moderate-sized VSDs close spontaneously, generally during the first year of life. Many become smaller throughout life and remain benign. Probably less than 5% of large VSDs undergo spontaneous closure. Surgery is indicated for primary closure of the defect during the first year of life in infants with congestive heart failure and failure to thrive despite medical therapy. Failure to close a large VSD will lead to progressive pulmonary vascular obstructive disease, particularly after the second year of life.
Before the development of pulmonary vascular disease, the volume of the shunt may be manipulated by changing PVR and/or SVR. High oxygen concentrations, hyperven-tilation, and alkalosis lead to pulmonary vasodilation and may cause massive increases in left-to-right shunting. With the limited cardiac output of the small infant, this can lead to severe systemic underperfusion and cardiovascular collapse. Increased afterload will lead to an increase in left-to-right shunting as long as PVR is less than SVR. Most patients with large shunts are, therefore, on anticongestive medications (digoxin and lasix) and an afterload-reducing agent (angiotensin converting enzyme inhibitor) prior to cardiac surgery or if only medically managed.
Large PDAs present clinically in a similar way to large VSDs and are managed surgically or with a device closure to protect the pulmonary vascular bed.