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Vascular > Arterial (Quiz 5) > Flashcards

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

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2
Q

What are systemic symptoms of carotid artery lesions?

A

difficulty speaking (dysphasia or aphasia), dizziness/loss of balance, and sudden severe headache

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3
Q

What are unilateral symptoms of carotid artery lesions?

A

focal weakness, paralysis, numbness (paresthesia), amaurosis fugax (same side as responsible carotid)

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4
Q

What is amaurosis fugax?

A

eye symptom where it looks like a shade is coming down

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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

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6
Q

With most unilateral symtoms, right sided symptoms equals…

A

left sided disease

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7
Q

What are cerebrovascular indications?

A

asymptomatic bruit, transient ischemic attack (TIA), cerebrovascular accident (stroke), preoperative candidate, post carotid endarterectomy

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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)

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9
Q

What is RIND?

A

reversible ischemic neurologic deficit

symptoms last from 24 hours to 3 weeks

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10
Q

How long do symptoms of a cerebrovascular accident (CVA or completed stroke) last?

A

over 3 weeks

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11
Q

What are symptoms of vertebrobasilar insufficiency?

A

dizziness, diplopia (double vision), and ataxia (lack of balance)

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12
Q

What happens with vertebrobasilar insufficiency?

A

when the posterior circulation is compromised

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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

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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

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15
Q

What are the most common causes of cerebrovascular symptoms?

A

emboli and cerebral hemorrhage

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16
Q

How does high grade stenosis cause cerebrovascular symptoms?

A

it reduces blood flow

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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

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18
Q

Who is at a greater risk of cerebral hemorrhage?

A

those on blood thinners

will also have lots of bruises

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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)

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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

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21
Q

What does intimal thickening of the carotid demonstrate?

A

predicts future disease

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22
Q

What can be seen with B-mode images of the carotid?

A

demonstrate the intima and characterize plaque

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23
Q

How can plaque be characterized?

A

calcified, smooth, irregular, mixed echogenicity, complex, echolucent, ulcerative (softer plaque)

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24
Q

What type of plaque is more vulnerable to embolize?

A

softer plaque

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25
Q

What type of plaque are more often symptomatic?

A

echolucent plaque

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26
Q

How should a normal CCA waveform appear?

A

rapid upstroke, clear systolic window, high diastolic flow, transient low velocity flow in late systole

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27
Q

How much of the CCA supplied the ICA?

A

70-80%

goes to brain

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28
Q

When severe stenosis is present in the ICA, the CCA waveform will resemble….

A

the ECA

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29
Q

How should a normal carotid bulb waveform appear?

A

rapid upstroke, no systolic window, boundary layer separation, complex flow with reversal

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30
Q

How should a normal ECA waveform appear?

A

rapid upstroke, clear systolic window, reversed flow in late systole, low or no end diastolic flow

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31
Q

How should a normal ICA waveform appear?

A

rapid upstroke, clear systolic window, high end diastolic flow

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32
Q

Where does atherolsclerosis usually develop within the carotid?

A

within 2 cm of bifurcation

and is rarely associated with distal ICA

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33
Q

How far is the distal ICA from carotid bulb?

A

at least 3 cm above carotid bifurcation

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34
Q

What disease may affect the distal ICA?

A

fibromuscular dysplasia

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35
Q

How do you differentiate the ICA from the ECA?

A

the ECA: no ‘e’ in brain, multiple branches, and temporal tap
the ICA: no ‘i’ in face, larger, posterior to ECA, lateral to ECA

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36
Q

How should a normal vertebral waveform appear?

A

rapid upstroke, clear systolic window, high end diastolic flow

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37
Q

What does the vertenral artery flow resemble?

A

the ICA

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38
Q

When severe stenosis is present in the ICA, the CCA waveform wil resemble ____.

A

the ECA

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39
Q

When severe stenosis is present in the ICA, what other effects are there?

A

the contralateral side will show increased diastolic flow

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40
Q

What is the progression of the waveform at stenosis?

A 
early stage: loss of systolic window
followed by
significant: elevated PSV
followed by
very significant: elevated EDV
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41
Q

What is the string sign?

A

when vessel is nearly occluded
blunted, somewhat resistive waveforms precede complete occlusion
only time when you get low velocities in a stenosis

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42
Q

Where is the string sign most commonly found?

A

in ICA

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43
Q

Describe the criteria for classification of disease.

A

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

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44
Q

Why are ratios important?

A

because they guard against mis-diagnosis due to high or low flow states

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45
Q

What does a post stenotic waveform look like?

A

early stages: spectral broadening
significant: post stenotic turbulence (spikey waveform)
very significant: tardus parvus
uber significant: collateral flow

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46
Q

With collateralization, what changes may you see?

A

posterior to anterior: changes in vertebral
side to side: rt and lt changes
extra to intracranial: ECA taking over from ICA

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47
Q

What are the symptoms fo vessel tortuosity and kinking?

A

usually saymptomatic
may cause stroke or TIA symtpoms (especially when head turning)
pulsitile mass (particularly with CCA tortuosity)

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48
Q

Distal to tortuous flow, what kind of velocities will be seen?

A

increased velocities

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49
Q

What other pathology affects the cerebrovascular circulation?

A

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

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50
Q

What is the direction of flow with an arterial dissection?

A

true lumen will have normal antegrade flow

false lumen will have opposite (retrograde) flow direction

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51
Q

Where do dissections usually originate?

A

from aorta and extend into CCA

may originate in distal ICA and extend proximally

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52
Q

What other diseases may be associated with a dissection?

A

marfan syndrome, ehlers-danlos syndrome

they weaken the walls of arteries

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53
Q

Dissections can be ____ or ____.

A

spontaneous or traumatic

trauma may be subtle or more obvious

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54
Q

What is spontaneous dissection associated with?

A

history of hypertension

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55
Q

What are duplex findings of dissection?

A

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

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56
Q

What are the findings in a blind-ended tear?

A

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

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57
Q

What is subclavian steal?

A

where the subclavian artery steal blood from the ipsilateral vertebral

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58
Q

With subclavian steal, the vertebral artery will display what waveform contour?

A

hesitant - have a little backward flow in systole

bunny sign- when flow is beginning to be reversed

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59
Q

If subclavian steal is suspected while preforming an ultrasound, what can be done?

A

have patient exercise their arm for a couple minutes and the waveforms may then be more exaturated and verify the syndrome

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60
Q

Where does verterbral artery stenosis commonly occur?

A

at the vertebral origin

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61
Q

If the same abnormal bilateral findings, what could the problem be?

A

aorta or heart problem

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62
Q

With cardiac implants, what doppler waveform will be seen?

A

symmetrically abnormal doppler waveform
(double peak waveform with intra-aortic balloon pump)
(contiuous flow with LVAD)

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63
Q

What is fibromuscular dysplasia?

A

abnormal growth of smooth muscle cells and fibrous tissue in arterial walls
can cause stenosis; media involvement most common

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64
Q

Describe the ‘string of beads’ appearance with fibromuscular dysplasia.

A

slight aneurysmal dilation may be noted in between stenotic sections
this causes a string of beads appearance of artery on arteriography

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65
Q

What is the incidence of fibromuscular dysplasia?

A

young caucasian females

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66
Q

What is the most common location of fibromuscular dysplasia?

A

renal arteries resulting in hypertension

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67
Q

What is the second most commonly involved vessel with fibromuscular dysplasia?

A

ICA

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68
Q

What are the symptoms of fibromuscular dysplasia?

A

often does not cause symptom
cervical bruit
embolization may occur and cause TIAs

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69
Q

With fibromuscular disease, what vessels are effected?

A

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

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70
Q

What are the most common findings with fibromuscular dysplasia?

A

spectral turbulence and elevated velocities

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71
Q

What is a carotid body tumor?

A

a 1 to 1.5mm structure in the adventitia of the carotid birfurcation

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72
Q

What role does a carotid body tumor play?

A

plays a role in control of blood pressure, arterial pH, and blood gases

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73
Q

What are carotid body tumors classified as?

A

paragangliomas

usually benign

74
Q

What is the clinical presentation of a carotid body tumor?

A

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
Q

What is the sonographic appearance of a carotid body tumor?

A

well defined mass between ICA and ECA at bifurcation; causes splaying of the two vessels; highly vascular tumor, low resistive flow

76
Q

What is considered a true aneurysm?

A

aneurysm involves all three arterial walls

very rare

77
Q

Where do carotid aneurysms commonly occur?

A

in the CCA, near the bifurcation

78
Q

What causes a carotid aneurysm?

A

atherosclerosis appears to be the major cause

may be a result of infection (mycotic aneurysm)

79
Q

What is the clinical presentation of a carotid aneurysm?

A

nontender, pulsatile mass in the neck; asymptomatic; TIA or stroke symptoms; rupture is rare but can cause cranial nerve dysfunction

80
Q

Some reports of CCA aneurysm with diameter..

A

double ICA or 1.5x CCA

81
Q

What is a pseudoaneurysm?

A

perferation in arterial wall allowing blood to extravasate into surrounding tissue
aka false aneurysm
uncommon in carotid arteries

82
Q

What causes a pseudoaneurysm?

A

pseudoaneurysm is usually the result of penetrating trauma or iatrogenic injury

83
Q

Where may a pseudoaneurysm form?

A

at endarterectomy site or at anastomotic site of carotid bypass graft

84
Q

What is the clinical presentation of pseudoaneurysm?

A

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
Q

What may the sonographic appearance of pseudoaneurysm look like?

A

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
Q

What is the classic pseudoaneurysm appearance?

A

pulsatile mass with yin-yang color filling

87
Q

With pseudoaneurysms, what is important to demonstrate?

A

to-and-fro flow in neck mass; swirling flow in mass; extent of thrombus; defect in arterial wall

88
Q

What does radiation do to blood vessels?

A

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
Q

What vessels are affected with radiation?

A

capillaries, arterioles, and venules are primarily affected

but large arteries may be damaged in some patients

90
Q

What may radiation caused fibrosis do to vessels?

A

fibrosis and overgrowth of endothelium can cause lumen narrowing

91
Q

What is the clinical presentation of radiation induced arterial injury?

A

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
Q

What is the sonographic appearance of radiation induced arterial injury?

A

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
Q

What may arteritis result from?

A

results in breakdown of parts of wall structure
may result in occlusion and distal ischemia
diagnosed through blood tests and clinical presentations

94
Q

What are the two forms of arteritis often encountered?

A

takayasu disease and temporal arteries (giant cell arteries)

95
Q

What vessels does takayasu arteritis affect?

A

affects aortic arch and great vessels (brachiocephalic, carotid, subclavian)

96
Q

What vessels does giant cell arteritis affect?

A

affects medium and larger sized arteries; may include aortic arch and carotid
vascular lab often asked to evaluate superficial temporal artery

97
Q

What are the symptoms for takayasu arteritis?

A

claudication of arms, no radial pulses, TIA and stroke symptoms, multiple bruits

98
Q

What are the symptoms for giant cell arteritis?

A

headaches, low grade fever, jaw claudication, tenderness in temporal region, visual problems/blindness

99
Q

What are the symptoms for arteritis?

A

wide variety of clinical presentations
no know etiology
autoimmune deficiencies are suspended

100
Q

What is the incidence of arteritis?

A

women are affected more commonly than men

101
Q

What is the incidence of takayasu arteritis?

A

younger individuals

102
Q

What is the incidence of giant cell arteritis?

A

elderly

103
Q

What is the sonographic appearance of takayasu arteritis?

A

lesions tend to appear as long, smooth, homogeneous narrowing (general wall thickening)

104
Q

What exam techniques should be remembered for giant cell arteritis?

A

may affect branches of ECA; superficial temporal artery may have halo appearance surrounding the artery; inflammation may include stenosis or occlusion

105
Q

What is TCI and TCD?

A

transcranial imaging - ultrasound duplex

transcranial doppler - continuous wave

106
Q

What are the branches of the ICA?

A

ophthalmic artery and posterior communicating artery

107
Q

What is part of the anterior circulation?

A

cavernous internal carotid artery (carotid siphon), ICA branches, MCA, ACA (crosses center of brain)

108
Q

What is part of the posterior circulation?

A

vertebral arteries, basilar arteries, PCA (1and2)

109
Q

What are the different PCAs?

A

P1: pre-communicating (red antegrade flow)
P2: post-communicating (blue retrograde flow)

110
Q

Describe the TCD (non-imaging) equipment.

A

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
Q

Describe the TCI (duplex US) equipment.

A

broadband pahsed array transducers (2-3 MHz doppler frequencies; 4MHz imaging frequencies)
similar computational packages as dedicated TCD unit

112
Q

List the five primary criteria used to identify vessels for TCD.

A

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
Q

What is the flow velocity of cranial vessels? (from highest to least)

A

MCA > ACA > PCA = BA = VA

114
Q

What are the advantages of TCI?

A

accurate vessel identification

decreased learning curve time

115
Q

What are the disadvantages of TCI?

A

larger transducer footprint (limited access)

inability to monitor (only continuous - only snapshot of what is going on right then)

116
Q

What are the anatomical approaches? (windows)

A

transtemporal, transorbital, transoccipital, submandibular, atlas loop

117
Q

What is the most common anatomical approach?

A

temporal

118
Q

Where is the transtemproal approach located?

A

over the temporal bone, superior to the zygomatic arch

119
Q

The transtemporal approach is subdivided as:

A

posterior, middle, anterior, frontal

120
Q

Where is the transorbital approach located?

A

US is transmitted through the thin orbital plane of frontal bone
power intensity must be reduced to limit direct exposure to the eye

121
Q

Where is the transoccipital approach located?

A

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
Q

Where is the submandibular approach located?

A

transducer is placed at the angle of the jaw and beam is directed cephalad
allows interrogation of the very distal extracranial ICA

123
Q

Where is the atlas loop approach located?

A

used to evaluate extracranial vertebral artery

transducer is placed below the mastoid process, behind the sternocleidomastoid muscle

124
Q

What arteries are identified with the temporal approach?

A

MCA, ACA, TICA (terminal ICA), PCA, PCoA, ACoA

125
Q

What direction of flow is the MCA?

A

toward the transducer

bidirectional flow is noted at the ICA bifurcation

126
Q

What direction of flow is the ACA?

A

away from transducer

127
Q

What are the velocities like with the TICA? Flow direction?

A

low due to poor angle of insonation
both toward and away from transducer
should be ‘s’ shaped

128
Q

What direction of flow is P1 and P2?

A

P1: toward transducer
P2: away transducer

129
Q

With the orbital approach, what arteries are identified?

A

ophthalmic and cavernous carotid (siphon)

130
Q

What direction of flow is the ophthalmic artery?

A

toward transducer

131
Q

What direction of flow is the siphon?

A

directed toward, away, or bidirectional depending on vessel segment

132
Q

What arteries are identified via the occipital approach?

A

vertebrals and basiliar arteries

133
Q

What direction of flow are the vertebral arteries?

A

away from transducer

may be tortuous

134
Q

With TCI, what brain structures should be identified via the temporal approach?

A

contralateral skull, falx cerebri, midbrain

135
Q

When doing a TCI, where should the notch of the transducer face?

A

always face towards the eye

136
Q

What direction of flow is the ACA?

A

away from transducer

and courses to the left

137
Q

What structure does the PCA surround?

A

butterfly shaped midbrain (thalamus)

138
Q

What should be considered when doing an orbital approach?

A

should not be done sooner than 6 weeks postoperative for recent eye surgery

139
Q

What is the normal course of the OA?

A

course from lateral to medial across the optic nerve

waveform will have low velocity with high resistance

140
Q

What direction of flow is the carotid siphon?

A

toward, away, or both

141
Q

Why is the submandibular approach used?

A

retromandibular ICA obtained in patients that require calcifications of the lindegaard ratio; also useful for determining distal arterial narrowing

142
Q

What is the lindegaard ratio?

A

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
Q

What direction of flow is the ICA?

A

away from transducer

moving from right to left

144
Q

What size should the sample volume be with spectral imaging?

A

large

this will result in spectral broadening

145
Q

With spectral doppler, what velocites are measured?

A

TAP-V

time averaging peak velocites

146
Q

What is the typical appearance of the transcranial waveforms?

A

all vessels except OA are low resistance with high diastolic flow

147
Q

What are technical considerations when performing a TCI?

A

hyperpstosis (thick skull): no or limited temporal bone window
anatomical variations in circle of willis: differences in origin, size, course of vessel

148
Q

What are technical considerations when performing a TCI?

A

hyperpstosis (thick skull): no or limited temporal bone window
anatomical variations in circle of willis: differences in origin, size, course of vessel

149
Q

What are the pitfalls of transcranial imaging?

A

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
Q

List conditions that can be diagnosed with TCD.

A

intracranial stenosis/occlusion, embolism/stroke, vasospasm, collateral flow, emboli monitoring, cardiac shunts, brain death, sickle cell disease

151
Q

What is used for diagnosis?

A

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
Q

Spectral waveform parameters include:

A

time averaged mean velocity, gosling’s pulsitality index, disturbed or turbulent flow, systolic upstroke, lindegaard ratio (DICA/MCA), sviri ratio (BA/VA)

153
Q

What is the criteria dependent upon reason for exam?

A

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
Q

What is useful for detection of stenosis/occlusion?

A

TCD is useful for detection of >50% intracranial stenoses and occlusions

155
Q

Name conditions that produce stenosis.

A

atherosclerosis, dissection, fibromuscular dysplasia, radiation-induced vasculopathy, moyamoya disease, inflammatory vasculopathies

156
Q

What is the most common cause of intracranial stenosis?

A

atherosclerosis
affects cavernous ICA, MCA, ACA, VA, BA, and PCA
may cause microemboli or significant stenosis or occlusion

157
Q

What is the diagnosis of stenosis primarily based on?

A

focal velocity increases, velocity differences from side to side, and downstream hemodynamic effects

158
Q

What is the most common cause of occlusion beyond the circle of willis?

A

embolism

159
Q

What is a major cause of embolism?

A

cardiac disease as is extracranial atherosclerosis

160
Q

What is the preffered treatment of stenosis/occlusion?

A

thrombolysis

TCD plays important role in determining effectiveness

161
Q

What is the main indicator of a vasospasm?

A

elevated velocities

162
Q

What are the symptoms of vasospasm?

A

complaint of severe headaches and dilusional

163
Q

When does a vasospasm begin after a subarachnoid hemorrhage?

A

within 3-4 days
peaks around 6-8 days
resolves within 2-4 weeks

164
Q

Why are TCDs done following a subarachnoid hemorrhage?

A

used to detect elevated blood velocities indicative of vasospasm and to identify patients at risk of delayed ischemic neurologic defecits

165
Q

What is the treatment to stop aneurysmal bleeding?

A

surgery (tie off aneurysm and stitch it closed)

coiling (less invasive)

166
Q

Patients are monitored daily for what vasospasm events?

A

onset, location, degree, resolution

MCA is most commonly monitored

167
Q

Why may the interpretation of a TCD be complicated?

A

due to intracranial pressure, blood pressure, hematocrit, arterial CO2, collateral flow, autoregulation, responses to therapeutic interventions

168
Q

What patients would sonographers perform a TCD on?

A

stenosis, vasospasm, collateral flow, emboli monitoring, sickle cell disease

169
Q

When does collateral flow occur?

A

with hemodynamically significant extracranial carotid artery stenosis, the brain will compensate with collateral flow and autoregulation

170
Q

What may TCD identify with collateral flow?

A

help identify and assess presence and adequacy of collateral circulation
can also help predict hemodynamic consequences of cross-clamping during carotid endarterectomy

171
Q

You can tell there is collateral flow from the ECA to ICA how?

A

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
Q

Crossover collateral through the ACA can be seen as:

A

retrograde flow in the ACA
increased flow velocities in the contralateral ACA
usually very high velocities detected at midline in the small ACoA

173
Q

Posterior to anterior collateral via posterior communicating artery may be seen as:

A

increased flow velocities in the ipsilateral PCA

velocities in PCoA are usually quite high

174
Q

TCD can be used to monitor for emboli during procedures such as:

A

carotid endarterectomy, carotid stenting, cardiomulmonary bypass surgery, neurologic procedures

175
Q

How is the MCA typically monitored with emboli monitoring?

A

using headband to secure transducer
microemboli have a unique doppler signal (HITS)
information used to modify surgical technique to reduce stroke risk

176
Q

How is a cardiac shunt detected?

A

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
Q

Along with clinical findings, TCD can be used to confirm what?

A

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
Q

Sickle cell patients are prone to stoke involving what vessels?

A

MCA and ACA

179
Q

With sickle cell patients, what successfully reduces rate of first stroke?

A

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
Q

How often do children with sickle cell disease undergo TCD screening?

A

routine annual

Vascular (6 decks)

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