Shunting physiology


A shunting lesion is one in which blood flows from one circulation to the other (most commonly the systemic to pulmonary arterial circulation) in the atrium, ventricle, arterial or venous circulation. The physiology depends upon the location of shunting. Atrial level shunting

  • Atrial level shunting occurs in the setting of an atrial level defect, including atrial septal defects as well as anomalies involving the systemic or pulmonary veins (e.g. sinus venosus defect).
  • Most atrial defects result in left to right shunting (since the RV is more compliant than the LV). This means that a portion of the blood (called the shunt fraction) that was meant to cross the mitral valve is instead diverted to the right atrium. Because the shunting in this case is above the ventricular level (pre-tricuspid), shunted blood is pumped by the right ventricle. Said another way, the hemodynamic effect of atrial level shunting is right ventricular volume loading. In many cases, this is tolerated well into childhood since the load on the pulmonary circulation is purely one of volume, rather than of pressure and volume. If unrepaired, though, this volume load eventually leads to right ventricular dilation and dysfunction, as well as reactive pulmonary hypertension and pulmonary edema.
  • In some cases, ASDs (or atrial level fenestrations) shunt right to left (RA to LA). In most cases, this is a favorable phenomenon that preserves LV preload in circumstances in which it could otherwise be compromised. For example, a patient with TOF or PA/IVS with restrictive RV physiology may be able to pump 90% of cardiac output through the pulmonary circulation without trouble; the presence of a fenestrated ASD allows shunting of the remaining 10% into the LA. It may also occur in a patient with a fenestrated Fontan, in which right (Fontan pathway) to left (common atrium) shunting preserves cardiac output in cases of elevated pulmonary resistance. This decreases pulmonary blood flow (i.e. Qp/Qs ratio <1) and causes a (usually) mild and well-tolerated hypoxemia. Recall that breathing hyperoxic gas (FiO2>21%) increases dissolved oxygen fraction in pulmonary veins that can oxygenate deoxygenated shunted blood; for this reason, a patient who would have a saturation of 92% on room air due to atrial shunting will have a saturation of 100% while on 100% oxygen. Ventricular level shunting
  • Ventricular level shunting occurs in the ventricles between the AV valves and the semilunar valves. This occurs in the setting of a ventricular septal defect.
  • When the VSD approximates or exceeds the size of the aortic valve, the defect is generally unrestrictive. Multiple small VSDs can also create the same physiology. Conversely, a large VSD can sometimes become obstructed by tricuspid valve tissue or RV trabeculations.
  • Physiologically unrestrictive VSDs are those that do not permit a gradient to exist between the LV and RV, so that LVP=RVP. In the absence of aortic or pulmonary valve stenosis, then, aortic = pulmonary artery systolic pressure. This creates a combined pressure and volume load on the pulmonary circulation that usually causes clinical heart failure earlier in life than an isolated atrial level shunt.
  • In patients who have an unrestrictive VSD, RV pressure is by definition systemic. In these cases, RVP cannot be used to assess the resistance of the pulmonary circulation. Instead, the direction of ventricular level shunting is used to understand resistance in the pulmonary circulation (including the RVOT, pulmonary valve, main and branch PAs, and fPVR) and the systemic circulation (including the subaortic region, aortic valve, supra-aortic region, and systemic circulation). If the patient is desaturated, this may represent right to left ventricular shunting (if intrapulmonary and atrial shunting is not present).
  • In VSDs which flow left to right in systole (i.e. LV–>RV–>PA), the RV serves as a conduit, and the stroke work for the shunt fraction is performed by the LV. In order to pump 1 cardiac output through the aortic valve, the LV must pump the shunt fraction + the cardiac output. The RV only pumps what returns from the systemic circulation through the TV. Over time, therefore, VSDs lead to LVVO, LV dilation, and cardiomegaly. RVVO can additionally occur over time due to LV–>RV diastolic shunting.
  • VSDs which flow right to left in systole generally do not create a ventricular volume load since no stroke work is wasted in order to provide a single cardiac output to the body. Instead, pulmonary blood flow is diminished, causing hypoxemia.

Arterial level shunting

  • Arterial-level shunting can occur through any anatomic connection between the aorta and PA, such as a PDA, AP window, BT shunt, ALCAPA, hemitruncus, or truncus arteriosus. Similar to VSD, arterial level shunts create a volume load on the systemic ventricle, which must pump 1 cardiac output (to the tissues) + the shunt fraction.
  • As with VSD, such shunts can be restrictive or unrestrictive (in which case PA=Ao pressure, and therefore RV=LV systolic pressure). Ao to PA flow can occur throughout the cardiac cycle and unrestrictive defects typically cause increased pulmonary blood flow and PA pressure. During ventricular diastole, pulmonary>systemic arterial elastance which promotes PBF, further exacerbating pulmonary overcirculation.
  • Aorta-pulmonary shunts can compromise systemic blood flow by run-off into the pulmonary circulation. This can compromise the coronary, cerebral, mesenteric, renal and other circulations and cause related ischemic complications. Ligation of large shunts (when possible) typically causes significant increases in blood pressure, perfusion, and hemodynamic stability.
  • Aortic or pulmonary regurgitation similarly causes volume loading of their ventricle receiving regurgitant volume and may similarly compromise cardiac output.
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