INCREASED PULMONARY BLOOD FLOW
Overview
Increased pulmonary blood flow may result in leakage of fluids into the interstitial space with subsequent pulmonary edema because of increased pulmonary pressures and congestion (Capozzi & Santoro, 2011). In patients with acyanotic congenital heart disease, this increase in pulmonary blood flow occurs in heart defects with left to right shunts. Cardiac shunting occurs when there is a diversion of normal blood flow. The type and location of the shunt, as well as the pathophysiology of the defect, determine the risk of potential complications from increased pulmonary blood blow. These complications include pulmonary bleeding, pulmonary hypertension, and eventually irreversible parenchymal lung disease. The most common congenital cardiac lesions related to increased pulmonary blood flow are patent ductus arteriosus (PDA), atrial septal defect (ASD), ventricular septal defect (VSD), and atrioventricular canal (AVC) defect also known as endocardial cushion defect.
Background
The PDA accounts for approximately 10% of newborns with cardiac defects, and is a normal part of fetal circulation (Park, 2016). In utero, oxygenated blood from the placental circulation bypasses the nonaerated fetal lungs and is delivered directly to the fetus’s lower body organs (Capozzi & Santoro, 2011). The PDA is a vascular communication between the main pulmonary artery and the descending aorta. The degree of left to right shunting is determined by the size of the PDA, which includes measurement of the diameter, length, and level of pulmonary vascular resistance (Park, 2016). The PDA functionally closes within 48 hours after birth and by 2 weeks of age closes anatomically (Delaney, Baker, Bastardi, & O’Brien, 2015).
Isolated ASD accounts for 5% to 10% of all congenital heart defects and is most common in females (Park, 2016). ASDs are openings in the atrial septum that allow blood flow to shunt from the left side of the heart to the right side, leading to right atrial dilatation, right ventricular volume overload, and increased pulmonary blood flow (Jone, Darst, Collins, & Miyamoto, 2016).
There are four types of ASDs that can be distinguished by their location within the atrial septum: ostium secundum, sinus venosus, ostium primum, and coronary sinus. The type and location of the defect and/or enlargement of the right heart chambers determine what intervention is needed.
VSDs are the most common forms of congenital heart disease, accounting for 15% to 20% of all pediatric heart surgeries (Park, 2016). VSDs are openings in the ventricular septum that allow for blood flow to shunt from the left side of the 180heart to the right side, leading to left atrial dilation, left ventricular volume overload, and increased pulmonary blood flow. If left to right shunting is significant at the ventricular level, there will be excessive pulmonary blood flow leading to pulmonary edema and tachypnea (Nelson et al., 2015). The effects of increased pulmonary blood flow depend on the size and number of defects and resistance to flow through the lungs.
There are three types of VSDs that can be distinguished by their location within the ventricular septum: perimembraneous, infundibular, and muscular defects. Infants with small VSDs usually do not require surgery. Infants with a large VSD are usually repaired by 1 year of age.
AVC defects account for 2% of all congenital heart diseases and 30% of these defects occur in children with Trisomy 21 (Park, 2016). AVC defects consist of three components: ostium primum ASD, an inlet VSD, and clefts in the mitral valve leaflet and the septal leaflet of the tricuspid valve (Park, 2016). AVC defects can be delineated into two categories: complete or partial. A complete AVC consists of an ASD, large VSD, and single atrioventricular valve; infants may have ventricular asymmetry which is categorized as an unbalanced AVC (Nelson et al., 2015). A partial AVC consists of an ASD with a cleft in the anterior leaflet of the left atrioventricular valve, no VSD, and two atrioventricular valves present (Nelson et al., 2015
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
