Page 214 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

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3. As a result, there is physiological reversal of tion the left ventricle ejection volume is in-
the shunt through the foramen ovale (FO) creased (Frank–Starling mechanism; possibly
and ductus arteriosus (DA), from right-to- ventricular hypertrophy), and there will be a
left to left-to-right (left atrium to right atri- lasting increased volume load on the left ventri-
um and aorta to pulmonary artery). cle (→ E, left), especially when the pulmonary
4. These shunts normally close at or soon after vascular resistance is very low postnatally
birth, so that systemic and pulmonary cir- (e.g., in preterm infants). As the ability of the
culations are now in series. neonate’s heart to hypertrophy is limited, the
Abnormal shunts can be caused by patency of high volume load can often lead to left ventric-
the duct (patent or persisting DA [PDA]; → E) ular failure in the first month of life.
or of the FO (PFO), by defects in the atrial or If, on the other hand, the pulmonary vascu-
ventricular septum (ASD or VSD), or by arterio- lar resistance (R pulm ) remains relatively high
venous fistulae, etc. Size and direction of the postnatally (→ E, right), and therefore the
shunt volume through the ductus is relatively
shunt in principle depend on: 1) the cross-sec-
Heart and Circulation pressure difference between the connected ves- moderately increased left ventricular load can
small despite a large cross-sectional area, a
tional area of the shunt opening; and 2) the
be compensated for a long time. However, in
sels or chambers (→ D). If the opening is rela-
tively small, 1) and 2) are the principal deter-
these circumstances the level of pulmonary ar-
tery pressure will become similar to that of the
mining factors (→ D1). However, if the shunt
aorta. Pulmonary (arterial) hypertension occurs
between functionally similar vascular spaces
lead to damage and hypertrophy of the pulmo-
atrium, ventricle and ventricle) is across a
large cross-sectional area, pressures in the
nary vessel walls and thus to a further rise in
7 (e.g., aorta and pulmonary artery; atrium and (→ E, right and p. 214). This, if prolonged, will
two vessels or chambers become (nearly) pressure and resistance. Ultimately, a shunt re-
equalized. In this case the direction and vol- versal may occur with a right-to-left shunt
ume of the shunt is determined by 3) outflow through the ductus (→ E, bottom left). Aortic
resistance from the shunt-connected vessels blood distal to the PDA will now contain an ad-
or chambers (→ D2; e.g., PDA), as well as 4) mixture of pulmonary arterial (i.e., hypoxic)
their compliance (= volume distensibility; e.g., blood (cyanosis of the lower half of the body;
of the ventricular walls in VSD; → D3). clubbed toes but not fingers). The pressure
The ductus arteriosus (DA) normally closes load on the right heart will after a period of
within hours, at most two weeks, of birth due compensating right ventricular hypertrophy
to the lowered concentration of the vasodilat- ultimately lead to right ventricular failure. If
ing prostaglandins. If it remains patent (PDA), functional pulmonary valve regurgitation oc-
the fetal right-to-left shunt turns into a left- curs (caused by the pulmonary hypertension),
to-right shunt (→ E, top), because the resis- it may accelerate this development because of
tances in the systemic and pulmonary circuits the additional right ventricular volume load.
have changed in opposite directions. At aus- Early closure of the PDA, whether by pharma-
cultation a characteristic flow murmur can be cological inhibition of prostaglandin synthesis,
heard, louder in systole than diastole (“ma- by surgical ligation or by transcatheter closure,
chinery murmur”). If the cross-sectional area will prevent pulmonary hypertension. How-
of the shunt connection is small, the aortic ever, closure of the ductus after shunt reversal
pressure is and remains much higher than will aggravate the hypertension.
that in the pulmonary artery (→ D1, ∆P), the A large atrial septal defect initially causes a
shunt volume will be small and the pulmonary left-to-right shunt, because the right ventricle
artery pressure nearly normal. If the cross-sec- being more distensible than the left ventricle
tional area of the shunt connection is large, the offers less resistance to filling during diastole
shunt volume will also be large and be added and can thus accommodate a larger volume
to the normal ejection volume of the right ven- than the left ventricle. However, when this vol-
tricle, with the result that pulmonary blood ume load causes hypertrophy of the right ven-
204 flow and inflow into the left heart chambers tricle its compliance is decreased, right atrial
are much increased (→ E, left). In compensa- pressure rises and shunt reversal may occur.
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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