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436 A.A. Baschat<br />

Clinical Applications in Fetuses<br />

with Normal Cardiac Anatomy<br />

In fetuses with normal cardiac anatomy disorders are<br />

frequently only apparent through alterations in cardiovascular<br />

status. Under these circumstances coronary<br />

blood flow dynamics may be altered to accommodate<br />

changes in myocardial oxygen requirements. Since<br />

spectral Doppler of the coronary sinus is rarely<br />

achieved, clinical observations revolve primarily<br />

around color- and pulsed-wave Doppler characteristics<br />

in coronary arterial vessels.<br />

The ªHeart-Sparing Effectº<br />

in Fetal Growth Restriction<br />

Severe fetal growth restriction (IUGR) can progress<br />

to decompensation of cardiovascular status. Such deterioration<br />

can be documented through progressive<br />

deterioration of arterial and venous Doppler studies<br />

[50]. This progression often accompanies the deterioration<br />

of acid±base status from chronic hypoxemia<br />

to acidemia [51±54]. Under these circumstances the<br />

combination of elevated central venous pressure, elevated<br />

afterload, and worsening oxygenation places<br />

unique demands on myocardial oxygen balance. Elevated<br />

afterload increases myocardial oxygen demand<br />

because of an increase in cardiac work. Elevated central<br />

venous pressure and aortic pressures decrease the<br />

pressure difference across the coronary vascular bed<br />

and therefore diminish the driving force for coronary<br />

perfusion. The summation of these factors has detrimental<br />

effects on coronary perfusion at a time when<br />

myocardial oxygen balance and fetal metabolic state<br />

are critical. Consequently, adaptive mechanisms need<br />

to be evoked in order to maintain myocardial oxygen<br />

balance. The necessary augmentation of coronary<br />

blood flow can be achieved in two principal ways.<br />

One way is to increase the proportion of oxygenated<br />

left ventricular output available for myocardial delivery.<br />

The second way is through autoregulationmediated<br />

coronary vasodilatation.<br />

Several mechanisms operate in IUGR fetuses that<br />

increase the potential delivery of oxygenated blood to<br />

the myocardium. Under conditions of elevated placental<br />

resistance the relative proportion of left ventricular<br />

output increases [55±57]. Decreases in oxygen<br />

tension may further increase the proportion of oxygenated<br />

umbilical venous blood that is delivered<br />

through the ductus venosus to the left side of the<br />

heart [58, 59]. Prolonged chronic myocardial hypoxemia<br />

allows for angiogenesis and increases in vascular<br />

cross-sectional area and therefore myocardial flow<br />

reserve. These responses constitute chronic heart<br />

sparing in IUGR. When acute worsening of cardiovascular<br />

status and/or oxygenation is superimposed<br />

the only mechanism to significantly augment myocardial<br />

blood flow is marked coronary vasodilatation<br />

with massive recruitment of coronary vascular reserve.<br />

This vascular response is more acute, often occurring<br />

over the course of 24 h, and is most consistently<br />

associated with severe elevation of precordial<br />

venous Doppler indices [60, 61].<br />

The chronic initial phase of heart sparing can be<br />

implied by demonstrating certain Doppler abnormalities<br />

in the arterial and venous circulations. These include<br />

absent or reversed umbilical artery end-diastolic<br />

velocity and/or end-diastolic blood flow reversal in<br />

the aortic isthmus [62]. In the second trimester the<br />

magnitude of coronary blood flow may still be below<br />

the visualization threshold of ultrasound equipment;<br />

therefore, augmentation of coronary blood flow cannot<br />

be documented by spectral Doppler measurement<br />

of coronary arteries. With acute worsening of fetal<br />

cardiovascular and respiratory status color- and<br />

pulsed-wave Doppler measurement of coronary artery<br />

blood flow is readily achieved as a reflection of maximal<br />

augmentation of coronary blood flow ± now exceeding<br />

the visualization threshold [40]. In IUGR<br />

both diastolic and systolic coronary artery peak<br />

blood flow velocities are significantly higher than in<br />

appropriately grown fetuses providing additional evidence<br />

of blood flow augmentation. There are no associated<br />

changes in the coronary sinus diameter as evidence<br />

of increased coronary venous return [63]. Since<br />

coronary artery blood flow may be visualized in normal<br />

and IUGR fetuses at overlapping gestational ages,<br />

concurrent examination of the arterial and venous<br />

circulations is mandatory to assess fetal status. Clinical<br />

management cannot be based on the evaluation of<br />

coronary vascular dynamics alone. In IUGR fetuses<br />

with abnormal arterial and venous Doppler, heartsparing<br />

prognosis is poor with a high perinatal mortality<br />

and a high risk for acidemia and neonatal circulatory<br />

insufficiency requiring the highest level of<br />

neonatal care.<br />

Fetal Anemia<br />

Severe fetal anemia can result in reduction of oxygencarrying<br />

capacity and subsequently impaired myocardial<br />

oxygenation. Fetal hydrops with tricuspid insufficiency<br />

and abnormal precordial venous flow is associated<br />

with elevated right-heart pressures and a decline<br />

in coronary perfusion pressure. Under these circumstances<br />

short-term augmentation of myocardial<br />

blood flow of four to five times basal flow can be<br />

achieved through autoregulation. Color- and spectral<br />

Doppler measurement of coronary artery blood flow<br />

velocities has been successful in circumstances of<br />

acute fetomaternal hemorrhage, non-immune hy-

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