and Structural Heart Disease
|In a normal heart, one
without any septal defects, the output from the right and left
ventricles are identical. Whatever leaves the right ventricle will
circulate through the lungs, then return to the left heart to be ejected
to the body. In this event, the systemic blood flow (Qs) is equal
to the pulmonary blood flow (Qp). Therefore, the Qp:Qs ratio is
|When there is a septal defect, a
communication between the right and left heart is created.
Blood can travel through this communication.
Blood goes where resistance is least.
Therefore, the direction of blood flow depends upon the resistance of
the pulmonary vascular system (pulmonary vascular resistance, or PVR)
and that of the systemic circulation (systemic vascular resistance, or
Normally, the PVR (about 3 Wood units) is much lower than the systemic
vascular resistance (about 25 Wood units).
Therefore, with any communication between the left and right sides of
the heart, blood will shunt from the high resistance to low resistance
sides, i.e. from left to right.
This will cause increase pulmonary blood flow (PBF).
ASD defect with low PVR results in high PBF. The
pulmonary arteries are engorged and the lungs become edematous.
ratio is NOT a static phenomenon
Over time, the increase blood flow through the pulmonary vasculature
will cause damage to the muscular walls of the pulmonary arterioles,
causing them to hypertrophy. This will eventually cause an
increase in the resistance of these blood vessels, leading to elevation
of the PVR.
As the PVR elevates, an increase in the resistance to pulmonary blood
flow and left to right shunting at the septal defect will result,
leading to reduction of PBF. The patient will actually feel better
as congestive heart failure (CHF) is improving. However, the
pulmonary vascular pathology is worsening.
ASD defect with increasing PVR results in reduction of
high PBF. The pulmonary arteries' walls become thicker leading to
less PBF and improvement of pulmonary edema.
|Cyanosis in ASD
indicates high PVR
Eventually, the pulmonary vascular pathology worsens leading to a PVR
higher than the systemic vascular resistance (SVR). Since blood
will go were resistance is least, shunting at the atrial level becomes
right to left. This will actually cause a PBF that is less than
normal as well as cyanosis. The pulmonary vascular pathology is
ASD defect with high PVR results in right to left
shunting at the ASD manifesting as cyanosis. The PBF is
actually less than normal and the lungs are no longer edematous.
The animation below summarizes
the progress of ASD and PVR over time, the changes in this
animation usually occur over 4-5 decades
oxygen saturation a good thing in cyanotic congenital heart disease?
|An infant with truncus arteriosus awaiting
surgical repair is noted to have increasing oxygen saturation. Is
this a good thing? NO!
An increase in oxygen saturation indicates that the PBF is
excessive. Remember, high PBF results in a large volume of highly
oxygenated blood returning to the left atrium, this will in turn dilute
the de-oxygenated blood returning from the body, thus making the mixed
blood going to the truncus and eventually to the aorta and pulmonary
arteries better saturated. Better oxygen saturated blood may be a
good thing, but not when it is at the expense of very high PBF.
High PBF causes CHF and pulmonary edema, which may be so severe that it
would compromise respiration. Significantly edematous lungs poses
risks, particularly if surgery and placement of patient on heart-lung
|Small pulmonary artery from the truncus
offers resistance to PBF, resulting in small Qp and low oxygen
||Mild narrowing of pulmonary artery from the
truncus offers mild resistance to PBF, resulting in equal Qp & Qs
with acceptable oxygen saturation.
||Normal size pulmonary artery from the
truncus offers no resistance to PBF, resulting in high Qp:Qs and high
oxygen saturation. Pulmonary edema and CHF will be present.