Arterial (Quiz 5) Flashcards
1
Q
What is the meaning of systemic and unilateral symptoms?
A
systemic symptoms do no affect a particular side
unilateral symptoms affect the opposite side
2
Q
What are systemic symptoms of carotid artery lesions?
A
difficulty speaking (dysphasia or aphasia), dizziness/loss of balance, and sudden severe headache
3
Q
What are unilateral symptoms of carotid artery lesions?
A
focal weakness, paralysis, numbness (paresthesia), amaurosis fugax (same side as responsible carotid)
4
Q
What is amaurosis fugax?
A
eye symptom where it looks like a shade is coming down
5
Q
What is different about the unilateral symptom of carotid artery disease, amaurosis fugax?
A
this syptoms effects the same side as the responsible carotid while the other symptoms effect the opposite side
6
Q
With most unilateral symtoms, right sided symptoms equals…
A
left sided disease
7
Q
What are cerebrovascular indications?
A
asymptomatic bruit, transient ischemic attack (TIA), cerebrovascular accident (stroke), preoperative candidate, post carotid endarterectomy
8
Q
What is TIA?
A
transient ischemic attack
neurologic deficits which occur intermittently, lasting from several minutes to a few hours
(the symptoms last less than 24 hours and will self resolve)
9
Q
What is RIND?
A
reversible ischemic neurologic deficit
symptoms last from 24 hours to 3 weeks
10
Q
How long do symptoms of a cerebrovascular accident (CVA or completed stroke) last?
A
over 3 weeks
11
Q
What are symptoms of vertebrobasilar insufficiency?
A
dizziness, diplopia (double vision), and ataxia (lack of balance)
12
Q
What happens with vertebrobasilar insufficiency?
A
when the posterior circulation is compromised
13
Q
What are the mechanisms of cerebrovascular symptoms? (in other words, what can cause these symptoms)
A
emboli, high grade stenosis, arterial thrombosis, and cerebral hemorrhage
14
Q
How does an emboli cause cerebrovascular symptoms?
A
emboli from atherosclerotic plaques and ulcerated plaque gets stuck in small vessel and ischemia of a small part of the brain results causing the symtoms
15
Q
What are the most common causes of cerebrovascular symptoms?
A
emboli and cerebral hemorrhage
16
Q
How does high grade stenosis cause cerebrovascular symptoms?
A
it reduces blood flow
17
Q
Who is at a greater risk for arterial thrombosis?
A
patients with atrialfibrolation
they are also at risk for pulmonary embolism and emboli
18
Q
Who is at a greater risk of cerebral hemorrhage?
A
those on blood thinners
will also have lots of bruises
19
Q
What are risk factors for carotid artery disease?
A
alcohol abuse, cocaine use, diabetes, family history of stroke, high blood pressure, high cholesterol, increasing age, smoking (people who smoke one pack a day double their risk of a stroke)
20
Q
Explain the fact that carotids are codependent.
A
if there is disease on one side, it will effect the flow in the other
21
Q
What does intimal thickening of the carotid demonstrate?
A
predicts future disease
22
Q
What can be seen with B-mode images of the carotid?
A
demonstrate the intima and characterize plaque
23
Q
How can plaque be characterized?
A
calcified, smooth, irregular, mixed echogenicity, complex, echolucent, ulcerative (softer plaque)
24
Q
What type of plaque is more vulnerable to embolize?
A
softer plaque
25
What type of plaque are more often symptomatic?
echolucent plaque
26
How should a normal CCA waveform appear?
rapid upstroke, clear systolic window, high diastolic flow, transient low velocity flow in late systole
27
How much of the CCA supplied the ICA?
70-80%
| goes to brain
28
When severe stenosis is present in the ICA, the CCA waveform will resemble....
the ECA
29
How should a normal carotid bulb waveform appear?
rapid upstroke, no systolic window, boundary layer separation, complex flow with reversal
30
How should a normal ECA waveform appear?
rapid upstroke, clear systolic window, reversed flow in late systole, low or no end diastolic flow
31
How should a normal ICA waveform appear?
rapid upstroke, clear systolic window, high end diastolic flow
32
Where does atherolsclerosis usually develop within the carotid?
within 2 cm of bifurcation
| and is rarely associated with distal ICA
33
How far is the distal ICA from carotid bulb?
at least 3 cm above carotid bifurcation
34
What disease may affect the distal ICA?
fibromuscular dysplasia
35
How do you differentiate the ICA from the ECA?
the ECA: no 'e' in brain, multiple branches, and temporal tap
the ICA: no 'i' in face, larger, posterior to ECA, lateral to ECA
36
How should a normal vertebral waveform appear?
rapid upstroke, clear systolic window, high end diastolic flow
37
What does the vertenral artery flow resemble?
the ICA
38
When severe stenosis is present in the ICA, the CCA waveform wil resemble ____.
the ECA
39
When severe stenosis is present in the ICA, what other effects are there?
the contralateral side will show increased diastolic flow
40
What is the progression of the waveform at stenosis?
```
early stage: loss of systolic window
followed by
significant: elevated PSV
followed by
very significant: elevated EDV
```
41
What is the string sign?
when vessel is nearly occluded
blunted, somewhat resistive waveforms precede complete occlusion
only time when you get low velocities in a stenosis
42
Where is the string sign most commonly found?
in ICA
43
Describe the criteria for classification of disease.
normal (0%): PSV less than 125 cm/s
1-15% (diameter reduction): PSV less than 125 cm/s
16-49%: PSV less than 125 cm/s
50-79%: PSV greater than 125 cm/s and EDV less than 140 cm/s
80-99%: PSV greater or equal to 125 cm/s and EDV greater or equal to 140 cm/s
44
Why are ratios important?
because they guard against mis-diagnosis due to high or low flow states
45
What does a post stenotic waveform look like?
early stages: spectral broadening
significant: post stenotic turbulence (spikey waveform)
very significant: tardus parvus
uber significant: collateral flow
46
With collateralization, what changes may you see?
posterior to anterior: changes in vertebral
side to side: rt and lt changes
extra to intracranial: ECA taking over from ICA
47
What are the symptoms fo vessel tortuosity and kinking?
usually saymptomatic
may cause stroke or TIA symtpoms (especially when head turning)
pulsitile mass (particularly with CCA tortuosity)
48
Distal to tortuous flow, what kind of velocities will be seen?
increased velocities
49
What other pathology affects the cerebrovascular circulation?
arterial dissection, arterial thrombosis, iatrogenic injury, subclavian steal, verterbral artery stenosis, aortic valve or root stenosis, cardiac implants
(less common) fibromuscular dysplasia, carotid body tumor, carotid aneurysm, pseudoaneurysm, radiation induced arterial injury, arteritis
50
What is the direction of flow with an arterial dissection?
true lumen will have normal antegrade flow
| false lumen will have opposite (retrograde) flow direction
51
Where do dissections usually originate?
from aorta and extend into CCA
| may originate in distal ICA and extend proximally
52
What other diseases may be associated with a dissection?
marfan syndrome, ehlers-danlos syndrome
| they weaken the walls of arteries
53
Dissections can be ____ or ____.
spontaneous or traumatic
| trauma may be subtle or more obvious
54
What is spontaneous dissection associated with?
history of hypertension
55
What are duplex findings of dissection?
unusual color pattern in artery with no atherosclerosis, presence of thin white line in vessel lumen that may flutter with each pulse
antegrade flow in false lumen
56
What are the findings in a blind-ended tear?
if false lumen becomes thrombosed and encroaches on true lumen, stenotic flow profiles may be noted in true lumen
false lumen will demonstrate high resistance flow patterns unless thrombosed
reversed flow may also be noted in false lumen
57
What is subclavian steal?
where the subclavian artery steal blood from the ipsilateral vertebral
58
With subclavian steal, the vertebral artery will display what waveform contour?
hesitant - have a little backward flow in systole
| bunny sign- when flow is beginning to be reversed
59
If subclavian steal is suspected while preforming an ultrasound, what can be done?
have patient exercise their arm for a couple minutes and the waveforms may then be more exaturated and verify the syndrome
60
Where does verterbral artery stenosis commonly occur?
at the vertebral origin
61
If the same abnormal bilateral findings, what could the problem be?
aorta or heart problem
62
With cardiac implants, what doppler waveform will be seen?
symmetrically abnormal doppler waveform
(double peak waveform with intra-aortic balloon pump)
(contiuous flow with LVAD)
63
What is fibromuscular dysplasia?
abnormal growth of smooth muscle cells and fibrous tissue in arterial walls
can cause stenosis; media involvement most common
64
Describe the 'string of beads' appearance with fibromuscular dysplasia.
slight aneurysmal dilation may be noted in between stenotic sections
this causes a string of beads appearance of artery on arteriography
65
What is the incidence of fibromuscular dysplasia?
young caucasian females
66
What is the most common location of fibromuscular dysplasia?
renal arteries resulting in hypertension
67
What is the second most commonly involved vessel with fibromuscular dysplasia?
ICA
68
What are the symptoms of fibromuscular dysplasia?
often does not cause symptom
cervical bruit
embolization may occur and cause TIAs
69
With fibromuscular disease, what vessels are effected?
mid to distal ICA are the most frequently involved segments
bilateral disease is typical
string of beads sign may be difficult to visually appreciate on B-Mode
70
What are the most common findings with fibromuscular dysplasia?
spectral turbulence and elevated velocities
71
What is a carotid body tumor?
a 1 to 1.5mm structure in the adventitia of the carotid birfurcation
72
What role does a carotid body tumor play?
plays a role in control of blood pressure, arterial pH, and blood gases
73
What are carotid body tumors classified as?
paragangliomas
| usually benign
74
What is the clinical presentation of a carotid body tumor?
usually asymptomatic; patient may notice small lump in anterior neck; may result in slight discomfort; rarely can cause dysphagia, headaches, or change in voice
75
What is the sonographic appearance of a carotid body tumor?
well defined mass between ICA and ECA at bifurcation; causes splaying of the two vessels; highly vascular tumor, low resistive flow
76
What is considered a true aneurysm?
aneurysm involves all three arterial walls
| very rare
77
Where do carotid aneurysms commonly occur?
in the CCA, near the bifurcation
78
What causes a carotid aneurysm?
atherosclerosis appears to be the major cause
| may be a result of infection (mycotic aneurysm)
79
What is the clinical presentation of a carotid aneurysm?
nontender, pulsatile mass in the neck; asymptomatic; TIA or stroke symptoms; rupture is rare but can cause cranial nerve dysfunction
80
Some reports of CCA aneurysm with diameter..
double ICA or 1.5x CCA
81
What is a pseudoaneurysm?
perferation in arterial wall allowing blood to extravasate into surrounding tissue
aka false aneurysm
uncommon in carotid arteries
82
What causes a pseudoaneurysm?
pseudoaneurysm is usually the result of penetrating trauma or iatrogenic injury
83
Where may a pseudoaneurysm form?
at endarterectomy site or at anastomotic site of carotid bypass graft
84
What is the clinical presentation of pseudoaneurysm?
palpable, pulsatile neck mass; associated with neck trauma; presence of carotid bypass graft with pulsatile mass; TIA and stroke symptoms are rare but possible as is rupture
85
What may the sonographic appearance of pseudoaneurysm look like?
blood flow outside arterial wall creates mass in surrounding tissue; mass is connected to artery by 'neck'; blood flow in neck has to-and-fro appearance; swirling flow may be noted within mass
86
What is the classic pseudoaneurysm appearance?
pulsatile mass with yin-yang color filling
87
With pseudoaneurysms, what is important to demonstrate?
to-and-fro flow in neck mass; swirling flow in mass; extent of thrombus; defect in arterial wall
88
What does radiation do to blood vessels?
it preferentially injures cancers cells but can cause damage to endothelial cells in blood vessels
it can cause fibrosis due injury to the vaso vasorum (blood vessels that feed arterial wall) in the medial layer of vessel
89
What vessels are affected with radiation?
capillaries, arterioles, and venules are primarily affected
| but large arteries may be damaged in some patients
90
What may radiation caused fibrosis do to vessels?
fibrosis and overgrowth of endothelium can cause lumen narrowing
91
What is the clinical presentation of radiation induced arterial injury?
history of radiation (often several years prior); lack of typical risk factors for atherosclerosis; atypical location of atherosclerotic plaque (single, unusually located plaque); TIA and stroke symptoms may occur
92
What is the sonographic appearance of radiation induced arterial injury?
significantly longer than most typical atherosclerotic lesions; maximum stenosis tends to be located at the distal end of stenosis region; do not typically contain calcifications and may have hypoechoic foci
93
What may arteritis result from?
results in breakdown of parts of wall structure
may result in occlusion and distal ischemia
diagnosed through blood tests and clinical presentations
94
What are the two forms of arteritis often encountered?
takayasu disease and temporal arteries (giant cell arteries)
95
What vessels does takayasu arteritis affect?
affects aortic arch and great vessels (brachiocephalic, carotid, subclavian)
96
What vessels does giant cell arteritis affect?
affects medium and larger sized arteries; may include aortic arch and carotid
vascular lab often asked to evaluate superficial temporal artery
97
What are the symptoms for takayasu arteritis?
claudication of arms, no radial pulses, TIA and stroke symptoms, multiple bruits
98
What are the symptoms for giant cell arteritis?
headaches, low grade fever, jaw claudication, tenderness in temporal region, visual problems/blindness
99
What are the symptoms for arteritis?
wide variety of clinical presentations
no know etiology
autoimmune deficiencies are suspended
100
What is the incidence of arteritis?
women are affected more commonly than men
101
What is the incidence of takayasu arteritis?
younger individuals
102
What is the incidence of giant cell arteritis?
elderly
103
What is the sonographic appearance of takayasu arteritis?
lesions tend to appear as long, smooth, homogeneous narrowing (general wall thickening)
104
What exam techniques should be remembered for giant cell arteritis?
may affect branches of ECA; superficial temporal artery may have halo appearance surrounding the artery; inflammation may include stenosis or occlusion
105
What is TCI and TCD?
transcranial imaging - ultrasound duplex
| transcranial doppler - continuous wave
106
What are the branches of the ICA?
ophthalmic artery and posterior communicating artery
107
What is part of the anterior circulation?
cavernous internal carotid artery (carotid siphon), ICA branches, MCA, ACA (crosses center of brain)
108
What is part of the posterior circulation?
vertebral arteries, basilar arteries, PCA (1and2)
109
What are the different PCAs?
P1: pre-communicating (red antegrade flow)
P2: post-communicating (blue retrograde flow)
110
Describe the TCD (non-imaging) equipment.
1-2 MHz pulsed wave transducer; spectral analysis; may have M-mode capabilities; should allow measurements of PSV, EDV, TAP-V (time average peak velocity), PI (pulsitality index)
111
Describe the TCI (duplex US) equipment.
broadband pahsed array transducers (2-3 MHz doppler frequencies; 4MHz imaging frequencies)
similar computational packages as dedicated TCD unit
112
List the five primary criteria used to identify vessels for TCD.
approach (cranial window/where you are on the head); sample volume depth; direction of blood flow relative to US transducer; spatial relationship of one artery to another; flow velocity
113
What is the flow velocity of cranial vessels? (from highest to least)
MCA > ACA > PCA = BA = VA
114
What are the advantages of TCI?
accurate vessel identification
| decreased learning curve time
115
What are the disadvantages of TCI?
larger transducer footprint (limited access)
| inability to monitor (only continuous - only snapshot of what is going on right then)
116
What are the anatomical approaches? (windows)
transtemporal, transorbital, transoccipital, submandibular, atlas loop
117
What is the most common anatomical approach?
temporal
118
Where is the transtemproal approach located?
over the temporal bone, superior to the zygomatic arch
119
The transtemporal approach is subdivided as:
posterior, middle, anterior, frontal
120
Where is the transorbital approach located?
US is transmitted through the thin orbital plane of frontal bone
power intensity must be reduced to limit direct exposure to the eye
121
Where is the transoccipital approach located?
foramen magnum approach
takes advantage of the natural opening in the skull which the spinal cord passes
transducer is placed at base of skull and aimed toward the nose
122
Where is the submandibular approach located?
transducer is placed at the angle of the jaw and beam is directed cephalad
allows interrogation of the very distal extracranial ICA
123
Where is the atlas loop approach located?
used to evaluate extracranial vertebral artery
| transducer is placed below the mastoid process, behind the sternocleidomastoid muscle
124
What arteries are identified with the temporal approach?
MCA, ACA, TICA (terminal ICA), PCA, PCoA, ACoA
125
What direction of flow is the MCA?
toward the transducer
| bidirectional flow is noted at the ICA bifurcation
126
What direction of flow is the ACA?
away from transducer
127
What are the velocities like with the TICA? Flow direction?
low due to poor angle of insonation
both toward and away from transducer
should be 's' shaped
128
What direction of flow is P1 and P2?
P1: toward transducer
P2: away transducer
129
With the orbital approach, what arteries are identified?
ophthalmic and cavernous carotid (siphon)
130
What direction of flow is the ophthalmic artery?
toward transducer
131
What direction of flow is the siphon?
directed toward, away, or bidirectional depending on vessel segment
132
What arteries are identified via the occipital approach?
vertebrals and basiliar arteries
133
What direction of flow are the vertebral arteries?
away from transducer
| may be tortuous
134
With TCI, what brain structures should be identified via the temporal approach?
contralateral skull, falx cerebri, midbrain
135
When doing a TCI, where should the notch of the transducer face?
always face towards the eye
136
What direction of flow is the ACA?
away from transducer
| and courses to the left
137
What structure does the PCA surround?
butterfly shaped midbrain (thalamus)
138
What should be considered when doing an orbital approach?
should not be done sooner than 6 weeks postoperative for recent eye surgery
139
What is the normal course of the OA?
course from lateral to medial across the optic nerve
| waveform will have low velocity with high resistance
140
What direction of flow is the carotid siphon?
toward, away, or both
141
Why is the submandibular approach used?
retromandibular ICA obtained in patients that require calcifications of the lindegaard ratio; also useful for determining distal arterial narrowing
142
What is the lindegaard ratio?
mean velocity in the MCA / mean velocity in ipsilateral extracranial internal carotid artery. high velocities in the MCA (>120cm/s) may be due to hyperaemia or vasospasm. the Lindegaard Ratio helps distinguish these conditions.
143
What direction of flow is the ICA?
away from transducer
| moving from right to left
144
What size should the sample volume be with spectral imaging?
large
| this will result in spectral broadening
145
With spectral doppler, what velocites are measured?
TAP-V
| time averaging peak velocites
146
What is the typical appearance of the transcranial waveforms?
all vessels except OA are low resistance with high diastolic flow
147
What are technical considerations when performing a TCI?
hyperpstosis (thick skull): no or limited temporal bone window
anatomical variations in circle of willis: differences in origin, size, course of vessel
148
What are technical considerations when performing a TCI?
hyperpstosis (thick skull): no or limited temporal bone window
anatomical variations in circle of willis: differences in origin, size, course of vessel
149
What are the pitfalls of transcranial imaging?
TCD accuracy is operator dependent; velocity calculation depends on angle of insonation; patient cooperation is required; aliasing often present in the setting of severe stenosis, vasospasm, collateral flow, and hyperemia
150
List conditions that can be diagnosed with TCD.
intracranial stenosis/occlusion, embolism/stroke, vasospasm, collateral flow, emboli monitoring, cardiac shunts, brain death, sickle cell disease
151
What is used for diagnosis?
spectral waveforms are primarily used for diagnosis
primary diagnostic features include alteration in velocity, deviations from laminar flow, changes in pulsatility, changes in direction of flow
152
Spectral waveform parameters include:
time averaged mean velocity, gosling's pulsitality index, disturbed or turbulent flow, systolic upstroke, lindegaard ratio (DICA/MCA), sviri ratio (BA/VA)
153
What is the criteria dependent upon reason for exam?
intracranial stenosis, recanalization post-thrombolytics, vasospasm, identification of collateral flow, monitoring of embolic events, detection of cardiac shunts, sickle cell disease, and brain death
154
What is useful for detection of stenosis/occlusion?
TCD is useful for detection of >50% intracranial stenoses and occlusions
155
Name conditions that produce stenosis.
atherosclerosis, dissection, fibromuscular dysplasia, radiation-induced vasculopathy, moyamoya disease, inflammatory vasculopathies
156
What is the most common cause of intracranial stenosis?
atherosclerosis
affects cavernous ICA, MCA, ACA, VA, BA, and PCA
may cause microemboli or significant stenosis or occlusion
157
What is the diagnosis of stenosis primarily based on?
focal velocity increases, velocity differences from side to side, and downstream hemodynamic effects
158
What is the most common cause of occlusion beyond the circle of willis?
embolism
159
What is a major cause of embolism?
cardiac disease as is extracranial atherosclerosis
160
What is the preffered treatment of stenosis/occlusion?
thrombolysis
| TCD plays important role in determining effectiveness
161
What is the main indicator of a vasospasm?
elevated velocities
162
What are the symptoms of vasospasm?
complaint of severe headaches and dilusional
163
When does a vasospasm begin after a subarachnoid hemorrhage?
within 3-4 days
peaks around 6-8 days
resolves within 2-4 weeks
164
Why are TCDs done following a subarachnoid hemorrhage?
used to detect elevated blood velocities indicative of vasospasm and to identify patients at risk of delayed ischemic neurologic defecits
165
What is the treatment to stop aneurysmal bleeding?
surgery (tie off aneurysm and stitch it closed)
| coiling (less invasive)
166
Patients are monitored daily for what vasospasm events?
onset, location, degree, resolution
| MCA is most commonly monitored
167
Why may the interpretation of a TCD be complicated?
due to intracranial pressure, blood pressure, hematocrit, arterial CO2, collateral flow, autoregulation, responses to therapeutic interventions
168
What patients would sonographers perform a TCD on?
stenosis, vasospasm, collateral flow, emboli monitoring, sickle cell disease
169
When does collateral flow occur?
with hemodynamically significant extracranial carotid artery stenosis, the brain will compensate with collateral flow and autoregulation
170
What may TCD identify with collateral flow?
help identify and assess presence and adequacy of collateral circulation
can also help predict hemodynamic consequences of cross-clamping during carotid endarterectomy
171
You can tell there is collateral flow from the ECA to ICA how?
through reversed opthalmic artery:
retrograde flow in OA
decreased pulsitality and increased velocity in OA
obliteration, decrease, ir reversal of flow in OA with compresssion of the branches of the ECA
172
Crossover collateral through the ACA can be seen as:
retrograde flow in the ACA
increased flow velocities in the contralateral ACA
usually very high velocities detected at midline in the small ACoA
173
Posterior to anterior collateral via posterior communicating artery may be seen as:
increased flow velocities in the ipsilateral PCA
| velocities in PCoA are usually quite high
174
TCD can be used to monitor for emboli during procedures such as:
carotid endarterectomy, carotid stenting, cardiomulmonary bypass surgery, neurologic procedures
175
How is the MCA typically monitored with emboli monitoring?
using headband to secure transducer
microemboli have a unique doppler signal (HITS)
information used to modify surgical technique to reduce stroke risk
176
How is a cardiac shunt detected?
confirmed when there are HITS detected while monitoring the MCA
more HITS=more severe the shunt
study uses 'bubbles' (intravenous agitated saline mixed with air)
177
Along with clinical findings, TCD can be used to confirm what?
brain death
cerebral circulatory arrest produces classic to and fro TCD waveform (short systolic spike followed by either a small retrograde deflection in diastole or no flow in diastole
178
Sickle cell patients are prone to stoke involving what vessels?
MCA and ACA
179
With sickle cell patients, what successfully reduces rate of first stroke?
early detection of MCA velocities by TCD with subsequent intitiation of blood transfusion
<170 cm/s = normal
170-200 cm/s = borderline
>200 cm/s = abnormal
180
How often do children with sickle cell disease undergo TCD screening?
routine annual
