Transcranial Doppler ch.23 Flashcards
What vessels does the transtemporal window for a TCD evaluate?
MCA, ACA, Terminal ICA, PCA
What vessels does the suboccipital/ transforamenal window for a TCD evaluate?
VA, BA
What vessels does the transorbital window for a TCD evaluate?
ICA and ophthalmic
carotid siphon
vessel: MCA
window, depth, direction, velocity, and angle
transtemporal, 30-60 mm, antegrade, 55 +/- 12, anterior and superior
vessel: terminal ICA
window, depth, direction, velocity, angle
transtemporal, 55-65 mm, bidirectional, 55 +/- 12, anterior and superior
vessel: ACA
window, depth, direction, velocity, angle
transtemporal, 60-80mm, retrograde, 50 +/- 11, anterior and superior
vessel: PCA
window, depth, direction, velocity, angle
transtemporal, 60-70mm, antegrade, 39 +/- 10, posterior
vessel: ICA
window, depth, direction, velocity, angle
transorbital, 60-80mm, parasellar: antegrade supraclinoid: retrograde genu: both, 47 +/- 14, varies
vessel: ophthalmic
window, depth, direction, velocity, angle
transorbital, 40-60mm, antegrade, 21 +/- 5, medial
vessel: VA
window, depth, direction, velocity, angle
transforamenal/ suboccipital, 60-90mm, retrograde, 38 +/- 10, right and left of midline
vessel: BA
window, depth, direction, velocity, angle
transformenal/ suboccipital, 80-120mm, retrograde, 41 +/- 10, midline
crossover collateralization
antegrade flow in the ipsilateral anterior cerebral artery, flow comes from the contralateral ACA via the AcomA
ipsilateral MCA flow diminishes with contralateral compression of the CCA and respond positively to contralateral oscillation maneuvers of the CCA
external to internal collateralization
retrograde flow in the ipsilateral OA, flow comes from the ECA branches, flow reduction, obliteration, or reversal of flow occurs in the OA with compression of the ipsilateral ECA branches
posterior to anterior collateralization
when flow velocities in the ipsilateral PCA exceed those in the ipsilateral MCA >125%
increased flow velocities in the PCA may occur with compression of the ipsilateral CCA confirms the patency of the PcomA
General considerations for TCD
accessibility of the ultrasonic windows within the skull that can be penetrated with the ultrasonic beam are often limited
arteries at the base of the skull vary greatly in size, course, development, and site of access
the power measured behind the skull is rarely >35% of the transmitted power, the bone of the skull absorbs the major portion of the power
To achieve acceptable signal to noise ratio systems utilize dopplers with
lower bandwidth
larger and less defined sample volume
TCD systems use….
2MHz pulsed-wave doppler
TCCS systems use
transcranial color-coded duplex sonography
1.8-3.6 MHz phased array sector transducer
instrument requirements
transmitting powers between 10 and 100mW/cm2
adjustable doppler gate width
PRF up to 20kHz
focusing of the ultrasound beam at a depth of 40-60mm
online display of: TAMV and peak systolic velocity
what is the submandibular approach useful for?
ICA dissection
chronic ICA occlusion
velocities for calculating the Lindegaard ratio
Hyperemia
globally elevated mean velocities, intra- and extracranially
Lindegaard ratio <3 TAMV of MCA/ TAMV of ICA
vasospasm and stenosis due to atherosclerosis
focal velocity elevation
distal turbulence
patients with SAH and suspected vasospasm
initial baseline study should demonstrate relatively normal mean velocities
vasospasm due to SAH generally occur by the 5th day
most often there will be a gradual increase in mean velocity measurements, with changes noted over time
treatment of vasospasm
percutaneous transluminal angioplasty
pharmacologic infusion- generally papaverine (vasodilator)
HITS aka MES
high intensity transient signals aka microembolic signals
HITS or MES commonly occur during what?
operative procedures: CEA or cardiopulmonary bypass
HITS aka MES criteria
short in duration, <300ms
increased intensity, at least 3dB above background signal
unidirectional within doppler spectrum
sound chirp or snap
Why and how do you do a vasomotor reactivity testing?
to identify patients at higher risk of stroke
testing is done using various stimuli, such as increasing or decreasing CO2 and monitoring the response.
Normal vasomotor reactivity test
increased carbon dioxide: decrease in blood pH, vasodilatation of resistance vessels of the brain, increase in cerebral blood flow
decreased carbon dioxide; increase in blood pH, vasoconstriction of resistance vessels of the brain, decrease in cerebral blood flow
vasomotor reactivity test abnormal
occlusive disease of extracranial internal carotid arteries and intracranial cerebral arteries-
maximal dilatation of the resistance vessels of the brain, autoregulation functions of the distal vessels are diminished, carbon dioxide testing.
Abnormal MCA velocity waveform
decreased amplitude and pulsatility, increased acceleration time due to proximal occlusive disease
moyamoya disease
Most common cause of subarachnoid hemorrhage
ruptured cerebrovascular aneurysm: occurs in approx. 28,000 people in north america annually with the mortality rate exceeding 50%
other causes of SAH
trauma, tumor, AVM, spontaneous bleed
What can result from a SAH?
possible vasospasm (delayed, sustained contraction of the cerebral arteries)
vasospasm vs. hyperemia, lindegaard ratio
normal ?
mean velocity: 30-80 cm/s
vasospasm vs. hyperemia,
degree of vasospasm: hyperemia
< 3.0
vasospasm vs. hyperemia,
degree of vasospasm: moderate
3-6
vasospasm vs. hyperemia
degree of vasospasm: severe
> 6
triple H therapy
hemodilution, hypertension, hypervolemia
