Atrial septal defect evaluation of shunt flow: Difference between revisions
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Shunt flow
Many factors influence the potential for a high rate of shunt flow. These include:
Defect size
The larger the size of an atrial septal defect the greater the hemodynamic burden on the right ventricle. Patients should be measured for the pulmonary-to-systemic flow ratio, defined as Qp/Qs. Qp/Qs is estimated through imaging scans such as a Doppler ultrasound. Qp/Qs is calculated as Qp/Qs = [PA diameter(2) x VTI-PA] ÷ [LVOT diameter(2) x VTI-LVOT] where PA = pulmonary artery, VTI-PA = velocity time of the Doppler flow signal, LVOT = left ventricular outflow tract, and VIT-LVOT = maximum Doppler flow velocity apical to the aortic valve. Surgical therapy of an atrial septal defect is often recommended when the value of Qp/Qs is greater than 1:1. No exact threshold value exists for repair. The American Heart Association recommends a threshold Qp/Qs ≥1.5:1, for patients 21 years of age or older. The Canadian Cardiac Society recommends a threshold Qp/Qs >2:1, or >1.5:1 in the presence of reversible pulmonary hypertension. Patients who do not initally meet the Qp/Qs criteria for defect closure may do so at a later time as defect size and shunt flow can increase over time. Follow-up for Qp/Qs criteria is usually done every two to three years to ensure to track for this.
If the pulmonary arterial pressure is more than 2/3 the systemic systolic pressure, there should be a net left-to-right shunt of at least 1.5:1 or evidence of reversibility of the shunt when given pulmonary artery vasodilators prior to surgery. If Eisenmenger's physiology has developed, it must be demonstrated that the right-to-left shunt is reversible with pulmonary artery vasodilators prior to surgery.
Pulmonary hypertension
Patients with pulmonary hypertensive conditions face additional challenges with atrial septal defect treatment. For this reason, prior to medical and surgical therapy, Severe fixed pulmonary hypertension, where pulmonary vascular resistance is greater than 15 Wood units, experience prohibitive morbidity regardless of treatment therapy method. In these atrial septal defects, the interatrial communication provided by the hole in the septum decompresses the pressure in the right ventricle and is surprisingly advantageous. Treatment therapies in this population often have a poor outcome. Research has found that surgical, medical, and natural disease progression had similar high mortality rates. Patients with less severe forms of pulmonary hypertension have more favorable outcomes to medical and surgical therapy.
If there is a suspicion that pulmonary hypertension is present, the evaluation may include a right heart catheterization. This involves placing a catheter in the venous system of the heart and measuring pressures and oxygen saturations in the SVC, IVC, right atrium, right ventricle, pulmonary artery, and in the wedge position. Individuals with a pulmonary vascular resistance (PVR) of less than 7 wood units show regression of symptoms (including NYHA functional class). On the other hand, individuals with a PVR of greater than 15 wood units have increased mortality associated with closure of the ASD.
Surgical mortality due to closure of an ASD is lowest when the procedure is performed prior to the development of significant pulmonary hypertension. The lowest mortality rates are achieved in individuals with a pulmonary artery systolic pressure of less than 40 mm Hg.
Eisenmenger syndrome considerations
Eisenmenger syndrome occurs when there is a right-to-left shunting of blood flow. When combined with pulmonary hypertension, it presents a number of potential clinical concerns such as thrombosis, bleeding, consideration for organ transplant (lung or heart-lung), and increased risk of maternal mortality during pregnancy.
If Eisenmenger's syndrome has occurred, there is significant risk of mortality regardless of the method of closure of the ASD. In individuals who have developed Eisenmenger's syndrome, the pressure in the right ventricle has raised high enough to reverse the shunt in the atria. If the ASD is then closed, the afterload that the right ventricle has to act against has suddenly increased. This may cause immediate right ventricular failure, since it may not be able to pump the blood against the pulmonary hypertension.