Internal Carotid Artery Velocity Research Articles

Internal carotid artery stenosis: accuracy and reproducibility of color-Doppler-assisted duplex imaging.

The accuracy, rapidity, and reproducibility of color-Doppler-assisted duplex sonography in the diagnosis of significant internal carotid artery stenosis were prospectively evaluated. Only the point of maximal color shift on the color map was used for spectral analysis. When compared with angiography in 60 carotid bifurcations, a measured peak systolic velocity above 1.25 m/sec was 87% accurate in the detection of significant internal carotid artery stenoses greater than 50%. Determination of maximal internal carotid artery velocity was 40% faster with color-Doppler-assisted duplex sonography than with nonassisted duplex ultrasound. The correlation coefficient for interobserver agreement was .90. It increased to .97 when cases of extensive (greater than 1 cm) acoustic shadowing (7% of bifurcations) were excluded. The authors conclude that the color flow map is an accurate and reproducible means of depicting the point of maximal stenosis within the internal carotid artery.

Cerebral vasospasm diagnosis by means of angiography and blood velocity measurements.

We investigated 76 patients with known subarachnoid haemorrhage (SAH) in order to compare the results of angiography and non-invasive Doppler recordings of cerebral artery blood velocity in the diagnosis of cerebral vasospasm. One radiologist and one neurovascular surgeon assessed angiographic spasm visually on a four-level scale. The radiologist's ratings were the term of reference for the study. When there was angiographic spasm of the middle cerebral artery (MCA), the MCA blood velocity was higher and the blood velocity in the distal extracranical internal carotid artery (ICA) was lower than when MCA spasm was scored as absent. Analysis by Kappa statistics, a measure for the agreement between two independent judges with correction for random coincidence, revealed moderate agreement between angiographic spasm and the absolute MCA blood velocity (Kappa = 0.47). However, there was substantial agreement (Kappa = 0.64) between angiographic spasm and the index calculated from dividing the blood velocity in the MCA (VMCA) by the blood velocity in the ipsilateral ICA (VICA). The results indicate that this VMCA/VICA index gives more appropriate information on MCA spasm. Congenitally asymmetric circles of Willis with one wide dominant ACA showed normal blood velocities. In asymmetry induced by vasospasm, the diameter of the major ACA was normal or even reduced, and the blood velocity was significantly elevated. Hence, the agreement between blood velocity recordings and angiographic findings was substantial (Kappa = 0.64) when considering together the findings from both sides of the anterior circle of Willis.(ABSTRACT TRUNCATED AT 250 WORDS)

Usual clinical dose of acetazolamide does not alter cerebral blood flow velocity

Prior reports indicate that acetazolamide, an inhibitor of carbonic anhydrase, in moderate doses reduces symptoms of acute mountain sickness, and in large dose increases cerebral blood flow. The effect on flow is not known for a moderate dose, but were flow to increase, then increased cerebral cortex oxygen delivery would be one mechanism of benefit from acetazolamide at high altitude. We utilized Doppler ultrasound in 8 volunteers to determine whether a usual acetazolamide dose (250 mg three times daily) would increase flow velocities in internal carotid and vertebral arteries. Acetazolamide during normoxia decreased pHa, Pa CO 2 , and P ET CO 2 , but baseline flow velocity remained unchanged. In 2 subjects without acetazolamide, voluntary hyperventilation decreased both P ET CO 2 and flow velocity. Both hypoxia and hypercapnia caused increases in arterial velocities. The increases were not altered by acetazolamide administration. In one sybject, 1 g acetazolamide by acute i.v. injection induced an increase in flow velocity (40%) concomitant with a 5 mm decrease in P ET CO 2 confirming prior reports using similar intravenous dose. In doses employed for prevention of acute mountain sickness, acetazolamide induced metabolic acidosis and may have prevented the fall in velocity usually associated with hypocapnia, but it neither increased baseline cerebral blood flow velocity nor velocity responses to hypoxia and hypercapnia. Benefit of acetazolamide at high altitude may related to mechanisms other than increased cerebral blood flow.

Failure of autoregulation of cerebral blood flow in neonates studied by pulsed Doppler ultrasound of the internal carotid artery.

To reveal the influence of therapeutically induced changes of arterial blood pressure on cerebral circulation, pulsed Doppler measurements of blood velocity in the right internal carotid artery were performed in 23 neonates. A positive correlation between mean arterial blood pressure and time-averaged maximum blood velocity (change more than 0.5%/torr) could be noticed in 16 infants. These infants were supposed to have loss of autoregulation. The main characteristics in this non-autoregulating group were: gestational age less than 31 weeks, birth weight less than 1501 g and mean carotid blood velocity less than 20 cm/s. In accordance with animal experiments we assume that autoregulation does not work below a definite lower limit of brain perfusion, which is reflected by carotid blood velocity in our study. Patients below/equal 1500 g or 30 gestational weeks very often do not exceed this limit and thus do not reach the "range of autoregulation".

CEREBRAL BLOOD VELOCITIES AND THEIR VARIABILITY IN DIFFERENT SLEEP STATES IN THE NEWBORN INFANT

This study was planned to determine the variability of cerebral arterial blood velocities in normal newborn infants. Velocities were measured in intracranial arteries and the internal carotid artery using pulsed bidirectional doppler ultrasound in 15 fullterm infants, 4-5days old, in both active (REM) and quiet (NREM) sleep continuously for periods of 1 to 6 mins. without movements. The doppler signals were analysed by computer and the time averaged mean velocity calculated per consecutive heartbeat. Internal carotid artery velocities always varied more in REM than NREM sleep (mean c.v. 8.4% v 6.3%) but this difference was less marked in the intracranial arteries (mean c.v. 8.5% v 7.5%). In both states sudden spontaneous increases and decreases in velocities occurred (most often in REM) and also regular cyclical variations (most often in NREM) at 2-5c/s and 35-45c/s. The latter was clearly related to respiratory rate. Heartrate also varied considerably, sometimes in phase with, sometimes independently of the velocity variations such that it was not possible to conclude that velocity variations were always secondary to heartrate fluctuations. Cyclical velocity variations were most marked in periods of quiet regular or periodic breathing and may be the results of interactions between the central and peripheral control of respiration, blood pressure and temperature.