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.
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