Cerebral Blood Flow

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296 PEDIATRICS Vol. 71 No. 2 February 1983 Uncharitable Pediatricians

To the

Editor.-The image of the pediatrician as a compassionate

per-son, aware of and deeply concerned about community

affairs, has been eroded oflate. It is important to find out why public confidence is slipping away. A recent incident

in one state (which shall be nameless since there is no

reason to suspect that the behavior to be described is

regional) may provide a clue.

A well-established voluntary agency that has provided

services for blind adults for the better part of a century, launched a children’s program in 1980 to deal with unmet

needs of a growing number of blind children in the region. After 1 year it was found that the need for parent

coun-seling, nonvisual aids, teacher training, etc was very much

larger than had been predicted. In order to keep the

fledgling program afloat, the agency mounted a campaign for funds. It was reasoned that pediatricians, more than

others in the community, would understand the

impor-tance of the new children’s program since they were well

aware of evidence indicating an increase in the incidence

of blindness among children. Thus, a letter appealing for

a generous contribution to keep the operation going was

sent by the president of the Board of Directors to each of the 826 Fellows of the American Academy of Pediatrics

in the area. Not a single contribution was received.

Incredulous, the agency sent a letter to the Regional

Chairman asking for help in the form of an appeal to the

Fellows in his next communication to support the

agency’s plea for funds. No reply was received from the

Chairman.

The Academy’s catch slogan, “Speak Up for Children”

has a very hollow ring to the disifiusioned agency for the blind. And, if this experience is in any way representative,

the future for improved community:pediatric relations

looks very dark indeed.

Cerebral Blood Flow

DISAPPOINTED FELLOW

To the

Editor.-Doppler ultrasound assessment of flow velocity in

cere-bral vessels in neonates has generated intense interest

since the technique was originally applied to the preterm

infant by Bada et al.’ The value and indication both as a

research tool and useful clinical tool have yet to be

defmed. We have been using a range-gated, pulsed

Dop-pler instrument with a specially designed transducer for

the past 18 months and would like to add some comments

to those of Bejar et al2 and Volpe et a!3 concerning

Doppler ultrasound, pulsatility index, patent ductus

ar-teriosus effects on cerebral flow, and autoregulation.

With the general acceptance of Doppler ultrasonic

velocimeters, there should be discussion concerning the

usefulness of the currently popular continuous wave

Dop-pler instruments and the new generation pulsed Doppler

devices. Of particular interest, is the use of these

instru-ments for the study of arterial blood velocities in the

neonate whose carotid artery is approximately 3 to 4 mm

in diameter and whose cerebral arteries are about 100 to

250 jm in diameter (reference 4, and personal communi-cation Dr Takei).

The transmission frequency determines the maximum

depth at which both types of instruments can make

meaningful measurements; specifically, the attenuation

of the signal is proportional to the fourth power of the

transmission frequency.

The main difference between the two types of

instru-ments is the size of the sample volumes measured and

how they are obtained. Continuous wave instruments

have a transducer with two crystals mounted adjacent to

and at an angle to one another. One crystal continuously

transmits the carrier frequency and the other

continu-ously receives the reflected and shifted frequencies. The region of insonification is dependent upon the dimensions

of the crystals and the fixed angle between them. The

greater the angle the longer the sample volume. This

length can range from 1 to 3 cm depending on the man-ufacturer. Every moving reflector within this sample

vol-ume contributes to the shifted Doppler frequency, hence

the velocity and direction recorded. Consequently,

mul-tiple vessels within the sample volume will contribute to

the received signal. Although with experience, it is pos-sible to distinguish arterial forward pulsations from return venous flow, it is impossible to determine velocity for an

isolated vessel. For example, the venous return could

mask the reversal occuiring during diastole in an artery if the two vessels were contained in the sample volume.

On the other hand the transducer of a pulsed Doppler

instrument has only one crystal that both transmits and

receives. The size of its sample volume is variable,

de-pendent upon the dimensions ofthe crystal and the length of time the crystal is allowed to receive the reflected

signal. The length of its sample volume, called the gate,

can be varied from approximately 0.5 to 5.0 mm. In

addition, the depth at which this sample volume is taken

also can be varied from 0 mm to the maximum depth

allowed by the transmission frequency, and the maximum

range velocity “constraint” associated with its pulse rep-etition frequency.5

It can be seen that the advantage of the pulsed Doppler instrument is its ability to isolate specific vesseLs without

interference from neighboring vessels. Its disadvantage is

the ease of locating this vessel and the increased

com-plexity of the additional controls of gate and depth. It is our belief that the advantage of isolating a specific vessel

with a pulsed Doppler instrument outweighs the

addi-tional complexity when measuring velocity in cerebral vessels.

Recently there has been considerable emphasis in the

use of a pulsatility index (P1), usually derived from

non-invasive continuous wave Doppler measurements of

blood velocity and defined by the relation P1 = (S - D)/

5, where S is the peak systolic velocity and D is either

the minimum velocity during diastole or is zero,

which-ever is greater. One of the motivations for employing such

an expression is that the usually unknown Doppler angle

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LETTERS TO THE EDITOR 297

right-hand side of the equation, and hence the P1 is

independent of this angle. Another reason for obtaining the P1 is the apparent belief that the “P1 value denotes

the degree of resistance to cerebral blood flow,”6 and as

such may provide data on increased resistance, for

ex-ample, associated with intraventricular hemorrhage

(IVH).’ However, such direct interpretations of P1 may

be quite misleading. From the fluid dynamics viewpoint,

the concept of resistance is best suited for describing steady, rather than pulsatile flows. It is defined by the

relation R = P/Q, where P is the mean pressure drop

across a vascular bed or segment and

Q

is the mean flow

rate. Impedance is the variable employed for the

descrip-tion of pulsatile flow and is defined by Z = P/Q, where P

and

Q

represent instantaneous pressure drop and flow

rate. Even assuming a steady-state condition, it can be

seen that determination of resistance requires both a

pressure and a flow measurement. Consequently, it is

impossible to relate resistance directly to the P1, which is

derived solely from blood flow velocity measurements.

For example one may consider the data reported by

Penman and Volpe7 on P1 measurements in the anterior

cerebral arteries of infants with patent ductus arteriosus.

In table 2 of that report, the increase in P1 observed

during patent ductus arteriosus was strongly correlated with a decrease in diastolic blood pressure. This is con-sistent with the concept that changes in the P1 reflected changes in the pressure gradient, not necessarily a result

of cerebral resistance variation. In other words, the

de-termination of P1 gives very little information on

hemo-dynamics unless other parameters-such as pressure waveform, collateral circulation, and recording site-are

measured or controlled in the study. Consequently,

re-porting P1 as a measure of cerebral resistance should be avoided.

We have looked at the value of Doppler-calculated P1

in patients with patent ductus arteriosus or at risk for

developing patent ductus arteriosus. We have collected

carotid and anterior cerebral velocity data on 21 infants. We have seen decreased diastolic velocities (increased P1)

in the anterior cerebral artery, after surgical ligation of

the ductus, and therefore do not view this “abnormality”

as being very specific for ductus. However, a

character-istic pattern of diastolic velocity reversal is observed in

the carotid artery before or simultaneously with any

clinical or M-mode echocardiographic evidence of ductus.

This pattern may be transmitted to the anterior cerebral artery as a decreased diastolic velocity when the ductus

has progressed and there is a large reversed velocity to

forward velocity ratio in the carotid artery. The pattern seen in the carotid is very sensitive and specific both in

diagnosing ductus and following its evolution. Our data

indicate that it is a more sensitive indicator of ductus than careful clinical examination, M-mode echocardiog-raphy, or calculation of a cerebral P1.8

Do Doppler studies of the carotid and anterior cerebral

vessels have a role in assessing the preterm infant’s con-trol of cerebral circulation? We have studied 29 infants

using our pulsed Doppler system to determine whether cerebral blood flow is pressure passive and whether it is

related to the genesis of subependymal (SE/IVH).

Stud-ies were performed serially with each infant serving as

his/her own control.9 Anterior cerebral flow velocities for

a given infant were compared at different mean arterial

pressures when the variables of pH, Po2, and Pco2 were

similar. An infant was assessed as pressure passive if

anterior cerebral flow velocity increased or decreased

concomitant with an increase or decrease in the mean

pressure. We have found that some infants are pressure

passive and others are not. Our results indicate that SE!

IVH occurs much more frequently in infants who are

pressure passive; however, SE/IVH also occurs in infants who are not pressure passive. This suggests that the lack

of control of the cerebral arterial flow is not the sole

factor in the genesis of SE/P/H.

We feel that pulsed Doppler ultrasonic velocity

mea-surements have a role in assessing cerebral flow, although

further development, refmement, and study are

neces-say. The major value of this technique is that it is

noninvasive and can be repeated many times on a sick

infant without stress. We would anticipate that study of

flow in vessels by pulsed Doppler ultrasound will have

increasing application in the newborn,supplying “on line”

information to the neonatologist, cardiologist, and

neu-rologist on the status of carotid flow for ductus diagnosis and intervention, and on cerebral blood flow in a variety of clinical settings.

REFERENCES

PETER A. AHMANN, MD FRANCINE D. DYKES, MD ANTHONY LAZZARA, MD W. DEAN WILCOX, MD TIMOTHY CARRIGAN, MA

Department of Pediatrics

Emory University School of Medicine

Thomas K. Glenn Memorial Building

Atlanta, GA 30303

DON P. GIDDENS, PHD Georgia Institute of Technology School of Aerospace Engineering

1. Bada H, Haffai W, Chua C: Noninvasive diagnosis of neo-natal asphyxia and intraventricular hemorrhage by Doppler ultrasound. J Pediatr 1979;95:775

2. Bejar R, Merritt TA, Coen RW, et al: Pulsatiity index, patent ductus arteriosus, and brain damage. Pediatrics

1982;69:818

3. Volpe J, Penman J, Hill A, et al: Cerebral blood flow velocity

in the human newborn: The value of its determination.

Pediatrics 1982;70:147

4. Haruda F, Blanc W: Structure of intracerebral arteries in premature infants and autoregulation of cerebral blood flow, abstracted. Ann Neurol 1981;10:303

5. Webster J: Medical Instrumentation: Application and De-sign. Boston, Houghton Muffin Co, 1978, pp 409-414

6. Lipman B, Serwer GA, Brazy JE: Abnormal cerebral he-modynamics in preterm infants with patent ductus

arterio-sus. Pediatrics 1982;69:778

7. Perlman J, Volpe J: Cerebral blood flow velocity in relation to intraventricular hemorrhage in the premature newborn infant. J Pediatr 1982;100:956

8. Wilcox WD, Carrigan T, Dooley KJ, et al: Range gated pulse

Doppler ultrasonographic evaluation of carotid

anterior-cerebral blood flow in small preterm infants with patent ductus arteriosus, abstracted. Presented at the Annual Meet-ing of the Americdn Academy of Pediatrics, New York, October 1982

9. Ahmann P, Dykes F, Lazzara A, et al: The relationship of

at Viet Nam:AAP Sponsored on September 7, 2020

www.aappublications.org/news

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298 PEDIATRICS Vol. 71 No. 2 February 1983

pressure passivity to the genesis of

subependymal/intraven-tricular hemorrhage, abstracted. Presented at the 11th An-nual Child Neurology Society Meeting, Salt Lake City,

Oc-tober 1982

Doppler-Pulsatility Index

To the

Editor.-The determination of cerebral blood velocity in the

newborn infant using transfontanel Doppler ultrasound

has been discussed in detail in two recent 1,2

Whereas the use of the Doppler effect to determine blood velocity is well accepted, it is apparent that considerable controversy exists regarding the ability of this technique

to measure cerebral blood flow in the neonate.”2 In

par-ticular, the hemodynamic significance of the pulsatiity index (P1) remains unclear.

It has been suggested that the P1 reflects cerebral

vascular resistance based on the assumption that, as

resistance is altered, primarily diastolic, and not systolic,

blood velocity will change. A study by Pourcelot1 has

been quoted widely as justification for this assumption.

Pourcelot studied extracranial carotid artery blood flow

in adult patients with peripheral vascular disease. The

hemodynamics in this situation cannot be assumed to be

comparable to intracerebrai hemodynamics in premature

infants. A study by Grossman and Wood4 has also been

quoted5 as providing evidence that the P1 correlates with vascular resistance. These workers also studied the extra-cranial carotid artery blood flow in adults; no data that

permit the calculation of the P1 were provided. In fact,

there are no published studies that demonstrate a

rela-tionship between P1 and any measure of cerebral vascular resistance.

We have examined the effect of alterations in cerebral vascular resistance on the P1 in the newborn puppy using

a transfontanel approach.6 The dogs were paralyzed and

placed in a stereotaxic frame while the Doppler probe

remained in a fixed position throughout the experiment.

Cerebral vascular resistance was altered by changing

Paco2 and changes in regional cerebral blood flow were

determined by autoradiography. We were able to confirm

a good relationship between the Doppler determinations of blood velocity and cerebral blood flow. Contrary to the published data, however, we found the P1 to be indirectly and not directly related to cerebral vascular resistance.

This relationship occurred because systolic as well as

diastolic blood velocity fluctuated with changes in

resist-ance. Although these animal data may not be directly

applicable to the human infant, no other experimental

information is available and, until further studies are

done, it seems inappropriate to assume that the P1 is a

direct index of cerebral vascular resistance.

From the basic Doppler principles’ it is clear that

consistency of the probe angle is crucial for reliable, serial

determinations of blood velocity. For this reason, the

calculated P1 has been used in clinical studies to minimize

the effect of variation in the probe angle.2 Volpe et a12

state that “it is obvious from consideration of the formula,

P1 = (S - D)/S, that individual changes in systolic or

diastolic flow velocity alter the value of P1 in opposite

directions. Thus, it is crucial when utilizing the P1 for serial comparisons of blood flow velocity, to indicate

whether changes in D or 5, or both, account for the

changes in P1.” But individual blood velocities cannot be analyzed when the angle of the probe is not fixed. For example, a recording that suggests a change in diastolic

velocity does not demonstrate that the velocity has, in

fact, changed unless the probe angle has remained

con-stant. For the same reason, lack of (graphic) change is

not evidence that no change has occurred. Thus, unless

the probe angle is consistent, no conclusions can be drawn

as to whether a change in the systolic or diastolic velocity

is responsible for a change in the P1. Based on the

principles of Doppler ultrasound and the current

knowl-edge of the calculated P1, the only conclusion that can be drawn concerning a change in the P1 is that the difference

between the systolic and diastolic blood velocity (S - D)

has changed. As currently measured under clinical

con-ditions, the P1 remains a calculation that cannot be used

to explain hemodynamic changes.

Finally, all the clinical studies done with this technique

appear to have been performed by examiners who are,

presumably, familiar with the purpose of the study as

well as the clinical condition of the infant. We agree with Bejar et a!’ that, under these circumstances, considerable examiner bias can be introduced. If possible, examiners

blinded to the purpose of the study should be used to

make the Doppler measurements.

Many investigators have become interested in Doppler

evaluation of cerebral hemodynamics in the newborn, but

it is a technique whose validity has not been verified.

Until this is done under properly controlled experimental conditions, the interpretation of the P1 in the human

newborn remains speculative. We suggest future clinical

studies should determine blood velocity rather than the

P1, and should be performed with a technique that assures a consistent probe angle during sequential measurements.

DANIEL G. BATFON, MD

JONATHAN HELLMANN, MB, BCH M. JEFFREY MAISELS, MB, BCH Division of Newborn Medicine Department of Pediatrics

The Milton S. Hershey Medical Center

The Pennsylvania State University

Hershey, PA 17033

REFERENCES

1. Bejar R, Merritt TA, Coen RW, et al: Pulsatiity index,

patent ductus arteriosus, and brain damage. Pediatrics

1982;69:818

2. Volpe JJ, Penman JM, Hill A, et al: Cerebral blood flow

velocity in the human newborn: The value of its

determi-nation. Pediatrics 1982;70:147

3. Pourcelot L: Applications cliniques de l’exumen Doppler

transcutane, in Peronneun P (ed): Velocimetre Ultrasonore

Doppler. Paris, Institut National de la Sante et de la

Re-cherche M#{233}dicale(INSERM), 1975, p 213

4. Grossman BL, Wood EH: Doppler ultrasonic evaluation of extracranial cerebrovascular disease, in Tarases JM, Fisch-gold H, Dilenge D (eds): Recent Advances in the Study of

Cerebral Circulation. Springfield, IL, Charles C Thomas,

1970, p 175

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1983;71;296

Pediatrics

WILCOX, TIMOTHY CARRIGAN and DON P. GIDDENS

PETER A. AHMANN, FRANCINE D. DYKES, ANTHONY LAZZARA, W. DEAN