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a Chapter 5 Venous Hemodynamics 59<br />

that the velocity pulsation of the Doppler recording<br />

incompletely describes the pulse wave, excluding such<br />

information as variation in volume or cross section,<br />

pressure, pulse velocity and direction.<br />

Cardiac Function and Waveform<br />

Fig. 5.4. Estimated spatial velocity distribution at the umbilical<br />

vein±ductus venosus junction based on a computer<br />

model. The velocity increases before the blood has reached<br />

the narrow entrance of the ductus venosus. The high axial<br />

velocity is maintained for a longer distance compared with<br />

the peripheral velocities that are reduced with the growing<br />

cross section along the vessel (see also Figs. 5.2, 5.3). (From<br />

[32])<br />

Fig. 5.5. Blood velocity recorded at the isthmus of the<br />

ductus venosus at 12 weeks of gestation (left). During atrial<br />

contraction the velocity shows a deflection below the zero<br />

line (a), but at the same time retaining some antegrade velocity<br />

(arrow). The reason could be that the velocity profile<br />

across the vessel cross section at this moment is transformed<br />

and contains both antegrade and retrograde velocities<br />

(right)<br />

traced and what is actually defined as the minimum<br />

velocity during atrial contraction.<br />

Pulsation in Veins<br />

Venous pulsation observed during ultrasound Doppler<br />

recording is commonly used for diagnostic purposes.<br />

It is a regularly repeated velocity increment or<br />

inflection; however, it is worthwhile to keep in mind<br />

The waveform of the venous pulse is determined by<br />

the function of the heart. Usually there is a systolic<br />

peak (during ventricular systole), a diastolic peak<br />

(during passive filling of the ventricles) and a diastolic<br />

nadir (reflecting the atrial contraction; Fig. 5.6).<br />

The more energy put into the pulse, the further out<br />

in the system it will reach. That is particularly obvious<br />

during atrial contraction. The Frank-Starling<br />

mechanism causes an augmented contraction in a<br />

distended atrium during fetal bradycardia, and the<br />

wave propagating along the veins reflects that. A particularly<br />

strong atrial wave is seen in cases of arrhythmia<br />

when atria and ventricles happen to beat<br />

simultaneously. An augmented atrial wave is also seen<br />

in cases with increased afterload and adrenergic drive<br />

during hypoxemia [18±23]. Although the atrial contraction<br />

wave is the most commonly used sign for<br />

cardiac function, there is additional information hidden<br />

in the waveform [24, 25].<br />

The smooth systolic peak of the wave of a precordial<br />

vein also reflects a normal compliance of the<br />

heart. External constricting processes (e.g. high-pressure<br />

pleural effusion; Fig. 5.6), particularly a stiffer<br />

and less compliant myocardium (e.g. hypoxia, acidosis,<br />

cardiomyopathy), gives a quick rise in pressure<br />

during systolic filling of the atrium, and a corresponding<br />

steep downstroke of velocity resulting in<br />

the more pointed systolic peak velocity (Fig. 5.6) [26,<br />

27]. A quick rise in atrial pressure is sometimes<br />

caused by a significant tricuspid regurgitation leading<br />

to a similar but less acute downstroke during systole.<br />

Reduced compliance of the myocardium is not<br />

only reflected in the acute downstroke of the systolic<br />

peak but also in the dissociation of the systolic and<br />

diastolic peak (Fig. 5.6). The dissociation between the<br />

systolic and diastolic peak seems to be a late and<br />

ominous sign of myocardial compromise [27, 28].<br />

Transmission Lines<br />

The pulse generated in the heart is not transmitted<br />

equally well in all tissues. It travels better along<br />

transmission lines, and arteries and veins connected<br />

to the heart constitute such transmission lines.<br />

A discontinuation of the transmission line affects<br />

the pulse propagation and deprives the venous waveform<br />

of its usual details [27, 29]. If the pulmonary vein<br />

is not connected to the left atrium but to the portal system,<br />

the pulse recorded in the vein no longer reflects

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