Anesthesia for vascular surgery Flashcards

1
Q

What are the risk factors of peripheral vascular disease?

A

-Advanced age
-smoking
-HTN
-Diabetes
-insulin resistance
-obesity
-family history/genetics
-physical inactivity
-male>female
-elevated c-reactive protein
-elevated lipoprotein
-elevated triglycerides
-hyperlipidemia

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2
Q

What is homocysteine?

A

protein in the blood; can make blood clot more easily than it should; comes from eating meat; may also be elevated if you do not have enough folate

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3
Q

In peripheral vascular disease and peripheral artery disease what may need to be elevated to perfuse their organs?

A

May rely on increased MAP to perfuse vital organs

-Increased range of coronary and cerebral autoregulation

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4
Q

Even short periods of what can lead to ischemia in these pts with PVD and PAD?

A

hypotension
-invasive BP monitoring is recommended for these cases

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5
Q

What are the major risk factors for an abdominal aortic aneurysm?

A

-Smoking** most highly correlated with AAA
-older age
-gender

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6
Q

what are some other risk factors for a AAA?

A

-Family Hx
-CAD- single most significant risk factor influencing long term survival
-Cholesterol
-COPD
-HTN

-2-6 times more common in men
-2-3 times more common in while males vs black males
(MIs are responsible for 40-70% of all fatalities that occur in aneurysm reconstruction)

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7
Q

How is AAA diagnosed?

A

Pulsatile abdominal mass- often missed in a routine physical exam

-CTA: imaging best of choice for AAA

CT, ultrasound and MRI are useful for determining size.

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8
Q

When is the risk of rupture low for AAA?

A

Less than 4cm in diameter

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9
Q

When is surgical intervention recommended for a AAA?

A

-5.5cm or greater

-4-5 cm with greater than 0.5cm enlargement in the last 6 months

-(growth more than 0.6-0.8 cm per year)

-Ruptured AAA

-pts who are symptomatic

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10
Q

How much do AAA approximately expand per year?

A

4 mm per year

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11
Q

Which law do the vessel dimensions correlate to?

A

Law of LaPlace

T= Px r

T= wall tension
p= transmural pressure
r= vessel radius

as the radius increases, the wall tension increases!
the larger the aneurysm, the higher the likelihood of spontaneous rupture.

Wall tension is directly proportional to: vessel radius and intraluminal pressure

Wall tension is inversely proportional to wall thickness

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11
Q

Which law do the vessel dimensions correlate to?

A

Law of LaPlace

T= Px r

T= wall tension
p= transmural pressure
r= vessel radius

as the radius increases, the wall tension increases!
the larger the aneurysm, the higher the likelihood of spontaneous rupture.

Wall tension is directly proportional to: vessel radius and intraluminal pressure

Wall tension is inversely proportional to wall thickness

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12
Q

What are the contraindications to an elective AAA repair?

A

-Intractible angina pectoris
-Recent MI
-Severe pulmonary dysfunction
-Chronic renal insufficiency

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13
Q

What is the most frequent site for an AAA?

A

Infrarenal

least risk of AKI bc its below renal arteries

-approx 5-15% involve the suprarenal area

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14
Q

Identify the statement that BEST describes perioperative considerations in the pt with an abdominal aortic aneurysm (select 2)

a.) surgical intervention is recommended when the diameter is >5.5cm

b.) risk of aneurysmal rupture is best described by poiseuille’s law

c.) it is more common in females

d.) back pain and hypotension suggest rupture

A

a.) surgical intervention is recommended when the diameter is >5.5cm

d.) back pain and hypotension suggest rupture

The law of LaPlace states that increased diameter increases wall tension. The greater the wall tension, the greater the risk of rupture. Surgery is indicated when aneurysmal diameter exceeds 5.5

Independent risk factors for AAA include cigarette smoking, gender (male>female), and advanced age. Acute onset of back pain and hypotension suggest rupture

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15
Q

What are the mechanisms for the development of AAA?

A

-Destruction of elastin and collagen (primary)
-inflammation
-endothelial dysfunction
-platelet activation
-atherosclerosis

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16
Q

What is the classic triad of symptoms for a AAA rupture?

A

-Hypotension
-Back pain
-pulsatile abdominal mass

(this triad is only present in 50% of pts)

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17
Q

what is the most common cause of post-op death?

A

MI

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18
Q

Why don’t all pts with an aortic aneurysm rupture exsanguinate immediately?

A

Most aneurysms rupture in the left retroperitoneum allowing for tamponade and clot formation

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19
Q

List the different AAA sites from most involved to least involved

A

Suprarenal AAA
Pararenal AAA
Juxtarenal AAA
Infrarenal AAA

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20
Q

How should you optimize a patient for adominal aortic reconstruction?

A

-optimize myocardial o2 supply and demand

-pre-op beta blockers and statins

-pre-op fluid loading (Large bore IV is a must)

-Type and cross pt- blood available in room

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21
Q

What monitors should be on the pt for AAA repair?

A

EKG:
- lead 2 for arrhythmia evaluation
-Lead V5 for detection of ischemic ST-segment changes
-a-line
-intra-op TEE (can guide fluid management, wall abnormalities, detect PE)

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22
Q

What monitors should be on the pt for AAA repair?

A

EKG:
- lead 2 for arrhythmia evaluation
-Lead V5 for detection of ischemic ST-segment changes
-a-line
-intra-op TEE (can guide fluid management, wall abnormalities, detect PE)

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23
Q

What hemodynamic changes are increased during cross clamping?

A

-Increase arterial BP above the clamp

-increased afterload which can lead to left ventricular myocardial wall tension and o2 demand

-increased MAP

-Increased SVR

  • increased wall motion abnormalities and left ventricular wall tension
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24
Q

What will be decreased during cross clamping?

A

decreased arterial blood pressure below the clamp

metabolic changes: decreased total body carbon dioxide production

clamping starves distal tissues of o2, so these cells convert to anaerobic metabolism. The metabolic byproducts are washed into systemic circulation when clamp is released.

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25
Q

What is the most common site for cross-clamping?

A

Infra-renal

(most aneurysms appear below the level of the renal arteries)

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26
Q

What drug is good to give if the pts pressure is too high?

A

Nitro (d/t short half-life)

can also give:
- SNP
-Inhalation anesthetics
-milrinone

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27
Q

What are the metabolic alterations during aortic cross clamping?

A

-Hypoxic and ischemic environment distal to the clamp

-release of cytokines, prostaglanidns, nitric oxide, arachidonic acid

-anaerobic metabolism: build up of serum lactate

-acceleration of throboxane A-2 synthesis: leads to decrease in myocardial contractility/decrease CO

-Traction on mesentary- done for exposure to the aorta (may cause decrease in BP, SVR, tachycardia, increased CO, and facial flushing)

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28
Q

What is thought to be a main factor in cardiac instability and myocardial depression during cross-clamping?

A

Arachidonic acid

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29
Q

What does thromboxane A2 do?

A

produced by platelets during hemostasis Prothrombotic properties - stimulates activation of new platelets as well as increased platelet aggregation

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29
Q

What does thromboxane A2 do?

A

produced by platelets during hemostasis Prothrombotic properties - stimulates activation of new platelets as well as increased platelet aggregation

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30
Q

Which clamping positions are associated with a higher risk for kidney injury?

A

Suprarenal and juxtarenal –> reduce renal blood flow by as much as 80%

intrarenal reduces renal blood flow by 40%

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31
Q

if the suprarenal cross clamp time is longer than 30 mins what does it increase the risk for?

A

Post-op renal failure

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32
Q

if the suprarenal cross clamp time is longer than 30 mins what does it increase the risk for?

A

Post-op renal failure

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33
Q

What nephrotoxic meds should be avoided when managing an AKI post-cross clamp?

A

NSAIDs
aminoglycosides antibiotics (gentamicin, neomycin)

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34
Q

are warm or cold crystalloids thought to have a renal protective effect?

A

cold fluids!

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35
Q

What provides 20% if the spinal cord blood flow?

A

two posterior and two posterolateral arteries

-supply dorsal (sensory) portion of the spinal cord.

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36
Q

What provides 80% of spinal cord blood flow?

A

one anterior spinal artery–> 80% of spinal cord blood flow

(supply anterior (motor) portion of spinal cord)

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37
Q

What controls the transverse blood flow to the spinal cord?

A

Greater radicular artery
AKA: artery of Adamkiewicz

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38
Q

What can cause paraplegia?

A

Interruption of blood flow to the greater radicular artery (artery of Adamkiewicz) in the absence of collateral blood flow.

Bowel and bladder dysfunction, flaccid extremities - motor affected if injured

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39
Q

Where does the artery of Adamkiewicz originate?

A

between spinal segments T8-T12 but can originate as low as L2

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40
Q

Incidence of neurologic complications increases as:

A

the cross clamp is positioned higher and more proximal to the heart

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41
Q

Methods to decrease the risk of spinal cord ischemia

A

-Cerebrospinal fluid drainage
-mild hypothermia
-maintenance of normotension (SBP >120) through second post-op day.

Risk is highest for motor spinal dysfunction

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42
Q

What is another type of injury that can occur with abdominal aortic resections?

A

Ischemic colon injury

-Attributed to the manipulation of the inferior mesenteric artery which supplies the main blood supply to the left colon. This vessel is often sacrificed during surgery. Blood flow to the descending and sigmoid colon rely on collateral vessels.

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43
Q

Which factors increase following cross-clamp removal during abdominal aortic aneurysm repair? (select 2)

a.) pulmonary vascular resistance
b.) venous return
c.) total body oxygen consumption
d.) coronary blood flow

A

a.) pulmonary vascular resistance

c.) total body oxygen consumption

When the aortic cross-clamp is released, ischemic tissue releases acid and vasoactive substances into the systemic circulation. This increases pulmonary vascular resistance and pulmonary artery pressure.

removal of the cross-clamp increases the size of the vascular tank and so venous return falls. hypotension reduces coronary blood flow.

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44
Q

What causes the transient vasodilation after cross clamp release?

A

-Tissue hypoxia
-release of adenine
-Leads to decreased preload and afterload

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45
Q

What is decreased during cross clamp release?

A

SVR
Venous return

Can give ca2+
restoration of circulating blood volume is paramount in providing circulatory stability before the release of the cross clamp.

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46
Q

What is decreased during cross clamp release?

A

SVR
Venous return

Can give ca2+
restoration of circulating blood volume is paramount in providing circulatory stability before the release of the cross clamp.

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47
Q

what influences the magnitude of circulatory instability during clamp release?

A

site and duration of clamping

-partial release of aortic clamp over time can decrease hypotensive response.

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48
Q

what influences the magnitude of circulatory instability during clamp release?

A

site and duration of clamping

-partial release of aortic clamp over time can decrease hypotensive response.

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49
Q

What is an EVAR? What are the benefits?

A

A minimally invasive approach of correcting an abdominal aortic aneurysm.

shorter operative times, lower rates of transfusion, shorter length of stay, reduced morbidity.

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50
Q

When does an endoleak occur?

A

when the original graft fails to prevent blood from entering the aortic sac. Sometimes endoleaks resolve spontaneously while others may require placement of a second graft or an open repair.

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51
Q

When does an endoleak occur?

A

when the original graft fails to prevent blood from entering the aortic sac. Sometimes endoleaks resolve spontaneously while others may require placement of a second graft or an open repair.

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52
Q

The pt’s physiologic response ot the aortic cross-clamp is related to what 3 factors?

A

1.) location of clamp placement (infrarenal most common)

2.) intravascular volume status

3.) cardiac reserve

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53
Q

Applying the aortic cross-clamp creates central hypervolemia by:

A

-reducing venous capacity

-shifting a greater proportion of the blood volume proximal to the clamp

-increasing venous return

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54
Q

removing the aortic cross-clamp creates central hypovolemia by:

A
  • restoring venous capacity

-shifting a greater proportion of the blood to the lower body

-decreasing venous return

-creating a capillary leak that contributes to the loss of intravascular volume

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55
Q

Advantages of epidural anesthesia for open AAA repair:

A

-decreases preload and afterload
-preserves myocardial oxygenation
-decreases stress response
-decreases pulmonary complications
-post-op pain relief

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56
Q

Disadvantages of epidural anesthesia for open AAA repair:

A

-anticoagulation/possibility of epidural hematoma
-severe hypotension w blood loss or cross-clamp removal

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57
Q

What are the 3rd space losses for open AAA repair?

A

10ml/kg/hr

replace basal and 3rd space loses at 3:1 ratio

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58
Q

What do you want to keep UPO around?

A

1ml/kg/hr

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59
Q

Where is the Juxtarenal aneurysm located?

A

at level of renal arteries. Do spare the renal artery orifice

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60
Q

Where is a suprarenal aneurysm located?

A

more proximal, includes at lease one of the renal arteries, and may include visceral vessels

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61
Q

Where is a suprarenal aneurysm located?

A

more proximal, includes at lease one of the renal arteries, and may include visceral vessels

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62
Q

what are you more at risk for with a juxtarenal or suprarenal aneurysm?

A

spinal cord ischemia

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63
Q

what is the triad of symptoms for a ruptured aortic aneurysm?

A

-severe abdominal/back pain
-altered LOC from HoTN
-pulsatile abdominal mass

other symptoms: syncope, groin/flank pain, hematuria, groin hernia

surgical emergency: need art-line, central line, blood in room and likely infused from start and vasopressor infusions

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64
Q

what factors are associates with the poorest prognosis after AAA rupture?

A

-Cardiac disease
-HoTN

-increased age
-women
-non-white race
-insurance status
-comorbid conditions
-CHF
-renal failure
-Valvular heart disease

65
Q

What are the signs and symptoms of a thoracic aortic aneurysm?

A

-pain
-stridor
-cough (aneurysm can impinge left RLN)

66
Q

Fusiform classification of thoracic aortic aneurysm:

A

spindle shape and result in the dilation of the aorta

67
Q

Saccular classification of thoracic aortic aneurysm:

A

spherical dilation; generally limited to one segment of the vessel wall.

68
Q

what’s the most common cause of thoracic aneurysm?

A

Artherosclerosis

69
Q

What is a “true aneurysm”?

A

involves all 3 layers
-tunica adventitia
-tunica media
-tunica intima

70
Q

What is a “false aneurysm”?

A

involves just the adventitia

71
Q

Crawford classification

A

Normal

72
Q

Crawford classification

A

class 1
distal to the left subclavian artery to the renal arteries

73
Q

Crawford classification

A

class 2- can affect the kidneys the most - there is no blood flow to the renal arteries

distal to the left subclavian artery below the renal arteries

74
Q

Crawford classification

A

class 3
from the 6th intercostal space to the renal arteries

75
Q

Crawford classification

A

class 4
from the 13th intercostal space to the iliac bifurcation (entire abdominal aorta )

76
Q

Crawford classification

A

class 5
below the 6th intercostal space to the renal arteries

77
Q

What is the preferred side for an a-line is the thoracic region or distal aortic arch is involved

A

right radial artery

-left subclavian artery blood flow may be compromised during surgery

78
Q

How is spinal cord perfusion pressure calculated?

A

MAP- CSF pressure

79
Q

What is the goal CSF pressure?

A

less than 10 mmhg

80
Q

What is an aortic dissection?

A

spontaneous tear of the vessel wall= passage of blood along a false lumen

81
Q

what is the most common factor that contributes to the progression of a dissection?

A

Hypertension

82
Q

Which type of aortic aneurysm has the highest incidence of rupture (A or B)

A

type A

83
Q

what are the anesthetic considerations for a dissection?

A

Keep HR slow, Keep BP low, Keep them warm, avoid anemia (keep Hct >25-30)

84
Q

Debakey Classification of acute aortic dissection

A

Type 1: originates in the ascending aorta and extends at least to the aortic arch and often in the descending aorta

85
Q

Debakey Classification of acute aortic dissection

A

Type 2: originates in the ascending aorta; confined to this segment

86
Q

Debakey Classification of acute aortic dissection

A

Type 3a and b: originates in the descending aorta, usually just distal to the left subclavian artery, and extends distally

87
Q

Stanford classification of acute aortic dissection

A

Type A: dissections that involve the ascending aorta (with or without extension into the descending aorta)

88
Q

Stanford classification of acute aortic dissection

A

Type B: dissections that do not involve the ascending aorta

89
Q
A

Normal

90
Q

EVAR procedure

A

Bilateral femoral arteries are cannulated –>guidewire is threaded throughiliac artery to the level of the aneurysm –>sheath placed over wire and linedup in appropriate site via fluoroscopy –> stent is deployedoff ofthe sheath

91
Q

What is the # 1 complication of an EVAR?

A

Endoleak

92
Q

Endoleak: attachment site leaks

A

type 1 (device related)

93
Q

Endoleak: branch leaks (ex: lumbar artery, renal artery, internal iliac artery, inferior mesenteric artery)

A

type 2: caused by collateral retrograde perfusion (majority of leaks)

94
Q

Endoleak: graft defect (fabric tear, modular disconnection)

A

Type 3: device related

95
Q

Endoleak: graft wall fabric porosity/suture holes

A

type 4

96
Q

endotension:

A

systemic pressure on aneurysm sac despite no evidence of endoleaks

-70% close spontaneously within first month after implantation

97
Q

what kind of strokes are responsible for 80% of first time strokes?

A

ischemic

98
Q

When is a carotid endarterectomy performed? (CEA)

A

pts with greater than 70% carotid artery stenosis

99
Q

what are the signs and symptoms of carotid artery stenosis?

A

-TIA/stroke
-carotid bruit
-monocular blindness d/t microthrombi occlusions of optic nerve via ophthalmic artery

100
Q

How is carotid artery stenosis diagnosed?

A

CTA
carotid ultrasound

101
Q

What causes a TIA?

A

Plaque may rupture and release fibrin, calcium, cholesterol, and inflammatory cells, which can lead to abrupt occlusion distal the carotid artery –> abrupt decrease in cerebral blood flow –> TIA
More than half of all strokes are preceded by TIAs

102
Q

What are the risk factors for morbidity during a CEA?

A

-Hx of stroke
-Hyperglycemia
-multiple comorbidities
-age
- contralateral carotid artery disease
-ulcerative lesion
-intra-op hemodynamic instability
-operative timing

103
Q

What are the risk factors for morbidity during a CEA?

A

-Hx of stroke
-Hyperglycemia
-multiple comorbidities
-age
- contralateral carotid artery disease
-ulcerative lesion
-intra-op hemodynamic instability
-operative timing

104
Q

Pts with carotid stenosis are at higher risk of:

A

TIA or stroke

104
Q

Pts with carotid stenosis are at higher risk of:

A

TIA or stroke

105
Q

What is Amaurosis Fugax?

A

Blindness in one eye= sign of impending stroke

Emboli travel from the internal carotid artery to the ophthalmic artery. This impairs perfusion of the optic nerve and causes retinal dysfunction.

It occurs in 25% of pts w high-grade carotid stenosis

106
Q

How do you calculate cerebral perfusion pressure?

A

MAP-CVP (or ICP- whichever is higher)

ICP is typically not elevated in CEA, so MAP plays the major role in determining cerebral perfusion

107
Q

When does cerebral auto-regulation occur?

A

When MAP is maintained between 60-160 mmHg

108
Q

Chronic HTN shift’s a pts cerebral regulation curve to the:

A

RIGHT= a higher MAP is needed to maintain adequate perfusion

109
Q

During a CEA, after the carotid artery is clamped, ipsilateral cerebral perfusion relies on collateral flow from:

A

the circle of Willis (from the contralateral carotid and vertebral vessels)

110
Q

anesthetic agents _____ (increase/decrease) CBF

A

Increase d/t cerebral vascular dilation

111
Q

Anesthetic agents with the exception of ______, decrease cerebral metabolic rate of oxygen consumption (CMRO2)

A

ketamine

112
Q

What is the normal cerebral blood flow (CBF)?

A

50mL/100g per min

113
Q

During CEA the primary goal is to ensure:

A

adequate CBF by maintaining/augmenting MAP

114
Q

When does cerebral steal occur?

A

During hypercarbia= leads to cerebral vascular dilation in cerebral vessels and increases the risk of ischemia

115
Q

what are the different kinds of cerebral monitoring?

A

EEG- gold standard
SSEP
carotid stump pressure monitoring
transcranial doppler
cerebral oximetry

EEG = gold standard in identifying neurologic deficits related to carotid artery cross-clamping. Limitations: effects of BP, temp, and anesthetic agents on monitoring & only detects superficial layers of brain and not deep cortical structures

116
Q

What are some interventions for cerebral protection?

A

avoid:
- hyperglycemia
-hemodilution
-maintain normocarbia
-keep tight control of arterial BP

117
Q

What does a decrease in cerebral oximetry values of greater than 20% indicate?

A

regional and global ischemia during CEA

118
Q

carotid stump pressure:

A

Assessing collateral flow –> After carotid cross-clamp is placed, blood flow from the nonoperative carotid artery and basilar artery provides blood flow to the circle of Willis. A catheter is placed on the operative side (above the clamp), and pressure can be monitored. Carotid stump pressure is a gross measurement of the pressure inside the circle of Willis. Stump pressure > 40-50 mmHg reflects neurologic hypoperfusion = criteria for shunt placement

119
Q

SSEP

A

SSEP –> somatosensory evoked potential, reflects sensory integrity of spinal cord and brain = dorsal column. Assesses sensory-evoked potential (motor deficits can occur despite normal SSEP (MEP – anterior column)

119
Q

SSEP

A

SSEP –> somatosensory evoked potential, reflects sensory integrity of spinal cord and brain = dorsal column. Assesses sensory-evoked potential (motor deficits can occur despite normal SSEP (MEP – anterior column)

120
Q

transcranial doppler

A

noninvasive and measures cerebrovascular dynamics through CBF velocity

121
Q

Anesthetics EXCEPT ________ have cerebral protection properties

A

ETOMIDATE

Propofol decrease CMRO2 to 40% below normal values
Precedex decreases CBF and CMRO2
Inhalation agents decrease CBF in a dose-dependent fashion

N2O should be AVOIDED – potential for pneumocephalus from microbubble expansion

Ketamine will INCREASE CBF

122
Q

Anesthetics EXCEPT ________ have cerebral protection properties

A

ETOMIDATE

Propofol decrease CMRO2 to 40% below normal values
Precedex decreases CBF and CMRO2
Inhalation agents decrease CBF in a dose-dependent fashion

N2O should be AVOIDED – potential for pneumocephalus from microbubble expansion

Ketamine will INCREASE CBF

123
Q

During carotid cross-clamping how much higher should the MAP be from the pt’s preoperative MAP?

A

20% GREATER

Goal is SBP 160 mmhg or greater

Use a phenylephrine infusion during this portion of procedure
Watch for carotid sinus baroreceptor manipulation: may see hypotension and bradycardia

124
Q

goal blood pressure following CEA and for cross-clamp removal is:

A

SBP < 140 mmhg

Use a nitroglycerin or nicardipine infusion for this portion to maintain goal range SBP– continue postoperatively

Induction, incision, dissection, emergence are all times of increased stress = increased BP – use short-acting beta blockers

125
Q

What block can be used as a regional technique for CEA?

A

Deep and superficial cervical plexus block

Anesthetizes cranial nerves C2-C4
May have to place local at the angle of the mandible to cover that area innervated by the trigeminal nerve

126
Q

What is anesthetic preconditioning?

A

When inhalation agents provide a degree of protection against ischemia

127
Q

Post-op complications of CEA

A

Most common: HTN

Systolic BP greater than 180 mmhg is associated with increased incidence of TIA, stroke or MB

  • BP goal is 140/80 or less

(managed with NTG, or nicardipine infusion)
esmolol on emergence

128
Q

What is cerebral hyperperfusion syndrome?

A

caused by increased blood flow to the brain d/t loss of cerebral autoregulation = severe headache, visual disturbances, LOC, seizures

129
Q

What are the signs and symptoms of an intracranial hemorrhage following CEA?

A

Initial manifestations may be upper airway obstruction (may make reintubation difficult d/t tracheal deviation

requires immediate surgical intervention for hematoma evacuation

Recurrent laryngeal nerve damage can occur–> manifests as inspiratory stridor

130
Q

What are the signs and symptoms of an intracranial hemorrhage following CEA?

A

Initial manifestations may be upper airway obstruction (may make reintubation difficult d/t tracheal deviation

requires immediate surgical intervention for hematoma evacuation

Recurrent laryngeal nerve damage can occur–> manifests as inspiratory stridor

131
Q

Post-op complications of carotid endarterectomy:

A

-hemodynamic instability
-myocardial ischemia/infarction
-cerebral hyperperfusion syndrome
-stroke
-respiratory insufficiency
-recurrent/superior laryngeal nerve damage
-hematoma
-carotid body dysfunction
-tension pneumothorax
-acute carotid occlusion

132
Q

Complications of carotid stenting

A

Most common: stroke caused by thromboembolism
-MI
-Bradycardia
-HoTN
-Horner syndrome
-cerebral hyperperfusion syndrome
-carotid artery dissection or rupture
-hemorrhage from anticoagulation

Stroke: neurologic deficits are significantly reversible if CBF is restored within 2 hrs.

CAS pts get duplex scans prior to discharge, @ 6 wks, 6 months, 1 year, then yearly.

Will be on ASA for rest of life

133
Q

The most common cause of death following abdominal aortic aneurysm repair is

A. aortic dissection
B. cerebrovascular accident
C. myocardial infarction
D. pulmonary embolism

A

C. myocardial infarction

134
Q

What nerves are most at risk for damage or temporary dysfunction from a carotid endarterectomy? (select three)

A. Median
B. Superior laryngeal
C. Trochlear
D. Trigeminal
E. Spinal accessory
F. Hypoglossal
G. Recurrent laryngeal
H. Abducens

A

B. Superior laryngeal
F. Hypoglossal
G. Recurrent laryngeal

135
Q

Which structure is most likely to be injured during a nasal intubation?
A. superior nasal concha
B. medial nasal concha
C. inferior nasal concha
D. ethmoid sinus

A

C. inferior nasal concha

136
Q

You are performing anesthesia for a 70 kg patient undergoing a carotid artery stent procedure. What dose of heparin would you expect to administer as an intravenous bolus during the case?

A. 1500 units
B. 3500 units
C. 10000 units
D. 15000 units
A

B. 3500 units

Heparin in the range of 50 to 100 units per kilogram is typically administered as a bolus for a carotid artery stent procedure.

137
Q

What is the perioperative mortality rate for a carotid endarterectomy?

A. 20-25 percent
B. 10-15 percent
C. 3-5 percent
D. 0.5-2.5 percent
A

D. 0.5-2.5 percent

138
Q

Which location would be least appropriate for placement of an arterial line in a patient undergoing surgery on the distal aortic arch?

A. Right wrist
B. Left wrist
C. Left femoral
D. Right dorsalis pedis

A

B. Left wrist

Because the left subclavian artery may be manipulated during the operation, which would disrupt monitoring in the left radial artery, monitoring pressures via another site would be preferred. The right radial is often used.

139
Q

Which location would be least appropriate for placement of an arterial line in a patient undergoing surgery on the distal aortic arch?

A. Right wrist
B. Left wrist
C. Left femoral
D. Right dorsalis pedis

A

B. Left wrist

Because the left subclavian artery may be manipulated during the operation, which would disrupt monitoring in the left radial artery, monitoring pressures via another site would be preferred. The right radial is often used.

140
Q

What is the most common causative factor in the mortality of patients undergoing surgery for vaso-occlusive disease?

A. Atherosclerotic disease
B. Renal impairment
C. Hemorrhagic stroke
D. Respiratory failure

A

A. Atherosclerotic disease

Events related to atherosclerotic cardiovascular disease are responsible for more than half of the perioperative deaths in patients undergoing surgery for vaso-occlusive disease.

141
Q

You are assessing a patient in the PACU area following a carotid endarterectomy. Which of the following deficits could indicate damage to branches of the vagus nerve?

A. Asymmetrical smile
B. Inability to shrug the shoulders
C. Inability to stick the tongue out
D. Hoarseness
A

D. Hoarseness

Hoarseness or an inability to say ‘EEE’ may indicate damage to the superior laryngeal or recurrent laryngeal branches of the vagus nerve. An asymmetrical smile could indicate damage to the facial nerve. An inability to shrug the shoulders could indicate damage to the spinal accessory nerve. An inability to stick the tongue out could indicate damage to the hypoglossal nerve.

142
Q

You are assessing a patient in the PACU area following a carotid endarterectomy. Which of the following deficits could indicate damage to branches of the vagus nerve?

A. Asymmetrical smile
B. Inability to shrug the shoulders
C. Inability to stick the tongue out
D. Hoarseness
A

D. Hoarseness

Hoarseness or an inability to say ‘EEE’ may indicate damage to the superior laryngeal or recurrent laryngeal branches of the vagus nerve. An asymmetrical smile could indicate damage to the facial nerve. An inability to shrug the shoulders could indicate damage to the spinal accessory nerve. An inability to stick the tongue out could indicate damage to the hypoglossal nerve.

143
Q

What pharmacologic agent has been shown to decrease the morbidity rate 10-fold in patients undergoing surgery for aortic aneurysm repair?

A. Beta-blocker
B. Calcium channel blocker
C. Angiotensin receptor blocker
D. Mannitol
A

A. Beta-blocker

Because these patients have a high incidence for coronary artery disease, the ability of beta-blockers to improve the balance between supply and demand in the myocardium has been shown to reduce the perioperative morbidity of patients undergoing aortic aneurysm repair ten-fold.

144
Q

What is the most common cause of perioperative mortality following an abdominal aortic aneurysm repair?

A. postoperative hemorrhage
B. cerebrovascular accident
C. respiratory failure
D. myocardial infarction
A

D. myocardial infarction

145
Q

What is the most common cause of perioperative mortality following an abdominal aortic aneurysm repair?

A. postoperative hemorrhage
B. cerebrovascular accident
C. respiratory failure
D. myocardial infarction
A

D. myocardial infarction

146
Q

You are performing a general anesthetic for a patient undergoing a carotid endarterectomy. Which statement below best illustrates an understanding of how to manage the mean arterial blood pressure for this procedure?

A. For severe hypotension, labetolol is the agent of choice

B. The mean arterial pressure should be maintained at about 80 percent of the preoperative pressure

C. For hypotension, ephedrine is preferred for its indirect, sympathomimetic activity

D. A pure-alpha agonist such as phenylephrine is preferred for the treatment of hypotension

A

D. A pure-alpha agonist such as phenylephrine is preferred for the treatment of hypotension

During a carotid endarterectomy, it is advised to maintain the patient’s MAP slightly above their highest recorded preoperative pressure. For severe hypertension, labetolol may be used, but nitroglycerin is preferred for its swift onset and short duration of action as labetolol could result in postoperative hypotension due to its long duration of action. For hypotension, a pure alpha-agonist such as phenylephrine is preferred because it has minimal dysrhythmogenic potential.

147
Q

A patient presenting for carotid endarterectomy has amaurosis fugax. You know that this is

A. hemiparesis of the extremities
B. facial nerve paralysis
C. memory loss due to chronic cerebral microemboli
D. monocular blindness
A

D. monocular blindness

Amaurosis fugax is monocular blindness that occurs in 25% of all patients with high-grade carotid stenosis. It is believed to be caused by emboli that migrate from the carotid lesion to the opthalmic artery.

148
Q

Carotid surgery can be performed under regional anesthesia by blocking the nerves originating from which spinal levels?

A. C1-C3
B. C2-C4
C. C4-C7
D. C3-T2

A

B. C2-C4

Carotid surgery can be performed under local anesthesia by performing a blockade of the superficial and deep cervical plexus which derive innervation from the C2-C4 nerve roots.

149
Q

What is the most sensitive indicator of cardiac ischemia during thoracic surgery when the aorta is cross-clamped?

A. Transesophageal echocardiography
B. Systolic blood pressure
C. Pulmonary artery occlusive pressure
D. Heart rate
A

A. Transesophageal echocardiography

Although TEE and 12-lead ECG have little advantage over preoperative clinical data and two-lead ECG monitoring in non-cardiac surgery, the advantage of TEE during cardiac or thoracic surgery is evident. PA catheter data has a low sensitivity and specificity for ischemia in these patients and the TEE will display wall motion abnormalities before the ECG demonstrates changes

150
Q

Which of the following occurs in response to aortic cross-clamping?

A. Hypotension proximal to the clamp
B. Hypertension distal to the clamp
C. Hypertension proximal to the clamp
D. No change in MAP distal to the clamp

A

C. Hypertension proximal to the clamp

Aortic cross-clamping is associated with hypertension proximal to the clamp and hypotension (and hypoperfusion) distal to the clamp.

151
Q

For what procedure can cervical plexus blocks provide adequate anesthesia?

A. Carotid endarterectomy
B. Shoulder arthroscopy
C. LeFort osteotomy
D. Dilation and curettage
A

A. Carotid endarterectomy

Cervical plexus blocks can provide adequate anesthesia for anything in the C2-C4 distribution including carotid endarterectomy. Bilateral cervical plexus blocks are also useful for tracheostomy and thyroidectomy.

152
Q

Which of the following parameters would you expect to increase upon release of an aortic cross-clamp ?

A. Pulmonary artery pressure
B. Cardiac output
C. Mean arterial pressure
D. Systemic vascular resistance

A

A. Pulmonary artery pressure

Upon release of an aortic cross-clamp, the pulmonary artery pressure will typically increase. The cardiac output decreases slightly. The mean arterial pressure and systemic vascular resistance also decrease.

153
Q

The risk of ischemic damage to the spinal cord caused by cross-clamping the thoracic aorta during aortic aneurysm repair can be reduced by

A. coronary artery bypass
B. the use of nitroprusside to vasodilate the arteries supplying the spinal cord
C. placing a lumbar cerebrospinal fluid drain
D. increasing the core temperature of the patient
A

C. placing a lumbar cerebrospinal fluid drain

Measures that can reduce the risk of spinal cord ischemia during aortic cross-clamping include a short cross-clamp time, maintaining normal cardiac function, higher perfusion pressures, hypothermia, and drainage of cerebrospinal fluid.

154
Q

A patient undergoing carotid endarterectomy exhibits profound bradycardia (23 bpm) which is successfully treated with atropine. To prevent a recurrence of this event, you should

A. administer atropine 0.4 mg IV q10 minutes prophylactically

B. ask the surgeon to infiltrate the carotid sinus area with lidocaine

C. administer lidocaine 100 mg IV

D. begin a phenylephrine infusion

A

B. ask the surgeon to infiltrate the carotid sinus area with lidocaine

Bradycardia may be caused by manipulation of the baroreceptors in the carotid sinus. To lessen the likelihood that this will occur again, the surgeon can infiltrate the area around the carotid sinus with lidocaine and the administration of an anticholinergic may be required. Atropine 0.4 mg every 10 minutes, however, would be an inappropriately large amount.

155
Q

What are the major contributing factors to the development of peripheral vascular disease? (select two)

A. Renal failure
B. Diabetes mellitus
C. Raynaud's phenomenon
D. Smoking
A

B. Diabetes mellitus

D. Smoking

Diabetes mellitus, smoking, and elevated proinflammatory mediators are the major contributing factors to the development of peripheral vascular disease.

156
Q

Which of the following statements is not true of a cervical plexus blockade?

A. It produces adequate blockade of the carotid sinus reflex

B. The sensory and motor fibers of the cervical plexus can be blocked separately

C. The main risk of this procedure is vertebral artery injection

D. Subarachnoid anesthesia is a potential risk of this procedure

A

A. It produces adequate blockade of the carotid sinus reflex

The sensory and motor fibers of the cervical plexus originate from the cervical 2, 3, and 4 nerve roots and are unique in that the sensory fibers separate from the motor fibers early and can be blocked separately. The main potential risk of this procedure is vertebral artery injection, but if the needle is advanced too far medially into the vertebral foramen, epidural or even subarachnoid anesthesia is a potential risk as well, particularly because the dural sleeves of the cervical nerves are longer on these branches. A cervical plexus block does not protect against the carotid sinus reflex and local injection of the carotid sinus at the point where the carotid artery bifurcates is often necessary.

157
Q

Following a carotid endarterectomy, a patient exhibits inspiratory stridor. What would be the most likely cause?

A. Congestive heart failure induced by fluid overload
B. Recurrent laryngeal nerve damage
C. Asthma
D. Glossopharyngeal nerve impairment

A

B. Recurrent laryngeal nerve damage

The recurrent laryngeal nerve is at risk for damage during a carotid endarterectomy. Damage to the nerve could manifest as inspiratory stridor following emergence.

158
Q

Hemodynamic changes during cross-clamping

A

-Increased MAP
-Increased SVR (d/t activation of circulation catecholamines)
-Increased BP above clamp
-decreased BP below clamp
-increased wall motion abnormalities
-left ventricular wall tension
-Decreased EF
-decreased CO
-Decreased renal blood flow

-Increased PAOP
-increased CVP
-Increased coronary blood flow

159
Q

Hemodynamic changed during unclamping:

A

-Decreased arterial BP
-Decreased myocardial contractility
-decreased SVR
-decreased CVP
-decreased preload
-decreased CO
- increased pulmonary artery pressure
-metabolic acidosis

160
Q

Normal cerebral blood flow:

A

50ml/100g per min