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N934 Adv Principles Fa 21 > Anesthesia for Vascular Surgery Part 2: Aneurysms > Flashcards

Anesthesia for Vascular Surgery Part 2: Aneurysms Flashcards

1
Q

describe an aortic aneurysm

A

dilation of all 3 layers of artery. occasionally produce symptoms of compression on surrounding areas including possibly pain

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2
Q

describe an aortic dissection

A

occurs when blood enters the medial layer
initiation occurs with a tear in the intima
can occur over minutes to hours
severe sharp pain described in the posterior chest or back

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3
Q

risk factors for abdominal aortic aneurysm (AAA)

A

elderly, male
smoking
family history
atherosclerotic disease

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4
Q

what degradation occurs to create an AAA

A

adventitial elastin degradation (genetic, biochemical, metabolic, infectious, mechanic, and hemodynamic factors may contribute)

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5
Q

how do AAA’s present

A

asymptomatic pulsatile abdominal masses

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6
Q

how do AAA’s present

A

asymptomatic pulsatile abdominal masses

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7
Q

when to repair AAA

A

all patients with AAA 6cm or larger or when small aneurysms become symptomatic/expand >.5cm in 6mo period

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8
Q

aneurysms less than ___cm in diameter are thought to be relatively benign in terms of rupture or expansion

A

4cm

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9
Q

law of laplace in relation to aneurysm

A

increasing diameter is associated with increased wall tension, even when arterial pressure is constant
frequent incidence of associated systemic HTN enhances aneurysm enlargement

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10
Q

law of laplace in relation to aneurysm

A

increasing diameter is associated with increased wall tension, even when arterial pressure is constant
frequent incidence of associated systemic HTN enhances aneurysm enlargement

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11
Q

classic triad of sx for a ruptured AAA

A

HoTN, back pain, pulsatile abdominal mass

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12
Q

what types of aortic diseases is EVAR approach used for

A 
traumatic injuries
ruptures
dissections
TAA and AAA
(all types)
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13
Q

positive aspects of the EVAR approach to aortic aneurysms

A

less invasive
reduced M&M
shorter hospital stay
most common technique for repair

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14
Q

how are femoral arteries accessed during EVAR

A

cutdowns or percutaneous procedures

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15
Q

what are the anesthesia techniques for EVARs

A

MAC with local/regional versus GA
consider patients functional status (can they lay flat), co morbidities, aneurysm complexity, surgery urgency (full stomach)

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16
Q

anesthesia for EVAR’s, steering guiding sheaths may require what?

A

left arm arterial cut down

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17
Q

what is the artery that remains at most risk on spinal cord during EVAR

A

single anterior spinal cord artery that usually originates off descending aorta between T9-12

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18
Q

what are some anesthesia considerations intraoperatively for EVAR procedures

A 
hemodynamic management 
preservation of organ perfusion
blood loss and intravascular volume 
temperature
risk of conversion to open
radiation safety
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19
Q

what are the two most important factors that contribute to contrast induced nephropathy (a possible complication from EVAR)

A

contrast load and preexisting kidney disease

limit the load and adequately hydrate

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20
Q

early EVAR complications (5)

A

paraplegia, stroke, ARI, aneurysm rupture, pelvic hematoma

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21
Q

late EVAR complications (5)

A

endoleaks, aneurysm rupture, device migration, limb occlusion, graft infection

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22
Q

how are endoleaks usually treated

A

by balloon angioplasty of proximal attachment site so that the desired seal is obtained through remodeling of the stent graft
open surgical treatment remains an option if endovascular treatment of endoleaks fails or is not possible

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23
Q

how are type 2 endoleaks treated

A

transarterial embolization through the iliac arteries or retrograde embolization through the superior mesenteric or inferior mesenteric arteries

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24
Q

describe open abdominal aortic reconstruction considerations and procedure

A

large incision, extensive dissection, clamping and unclamping of aorta or its major branches
varying duration of organ ischemia-reperfusion
significant fluid shifts
temperature fluctuations
activation of neurohumoral and inflammatory responses
think about help and rapid infuser (esp if TAA)

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25
Q

most common sites of chronic atherosclerosis contributing to arotoiliac occlusive disease (2)

A

infrarenal aorta and iliac arteries

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26
Q

when do patients undergo surgery for aortoiliac occlusive disease?

A

only if they are symptomatic which includes claudication and limb threatening ischemia

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27
Q

surgical management of aortoiliac occlusive disease includes (3)

A 
direct reconstruction (aortobifemoral bypass, gold standard)
extra anatomic orr indirect bypass grafts (ex axillofemoral bypass. for infection or with previous reconstruction)
catheter based end-luminal techniques like percutaneous transluminal angioplasty (PTA) with or without tent insertion. relatively local disease.
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28
Q

what does the pathophysiology of aortic cross clamping depend on (6)

A 
level of cross clamp
status of left ventricle
degree of periarotic collateralization
intravascular blood volume and distribution, activation of SNS
anesthetic drugs and techniques
heparinization (monitor ACT's)
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29
Q

complications of aortic cross clamp r/t BP management

A

arterial HTN above cross clamp is common (increase in MAP, CVP, SVR but decrease in EF and CI)
arterial HoTN below the clamp will occur

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30
Q

aortic cross clamp complications: common ischemic complications

A 
renal failure (esp if clamped suprarenal)
hepatic ischemia
coagulopathy
bowel infarction
paraplegia
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31
Q

thoracic aortic cross clamp: what to expect with vital signs

A

increase in MAP, CVP, pulmonary arterial pressure, pulmonary wedge pressure
decrease in CI and EF
no change in HR

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32
Q

how the aortic cross clamp effects the left ventricle: normal intact heart

A

can withstand large increases in volume without significant ventricular distention or dysfunction

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33
Q

how the aortic cross clamp effects the left ventricle: impaired heart

A

a heart with reduced contractility and coronary reserve may respond to such increases in volume conditions with marked ventricular distention as a result of acute LV dysfunction and myocardial ischemia

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34
Q

aortic cross clamp: baroreceptor activation

A

results from increased aortic pressure and should depress the HR, contractility, and vascular tone

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35
Q

aortic cross clamp: metabolic effects. cross clamping of thoracic aorta decreases total body O2 consumption by

A

50%

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36
Q

aortic cross clamp: blood flow through tissues and organs below the level of aortic occlusion is dependent on _____ and independent of _____

A

dependent on perfusion pressure and

independent of CO

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37
Q

hemodynamic changes associated with aortic cross clamping

A

increased arterial blood pressure above clamp
decreased arterial BP below clamp
increased segmental wall motion abnormalities
decreased EF, CO, RBF
increased pulmonary occlusion pressure
increased CVP
increased coronary BF (maybe)

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38
Q

metabolic changes associated with aortic cross clamping includes

A 
decreased total body O2 consumption
decreased total body CO2 production
increased MVO2
decreased total body oxygen extraction
increased epi and NE
respiratory alkalosis
metabolic acidosis
39
Q

significance of impact on perfusion to vital organs in order from most to least detrimental

A

thoracic>supraceliac>infrarenal

40
Q

management of aortic cross clamp: pharmacologic intervention

A

use vasodilators to decrease after load, wall stress on LV and myocardial O2 demand
ex) nitroprusside, NTG, nicardipine, clevedipine (run these when theyre getting ready to clamp)
avoid long acting medications

41
Q

renal effects of cross clamping

A

while there is a dramatic reduction in RBF when clamped above renal arteries, there is still a reduction in RBF below renal arteries

42
Q

renal failure after repair of aneurysm results from

A

preexisting renal dysfunction, ischemia during cross clamping, thrombotic or embolic interruption of RBF, hypovolemia and HoTN

43
Q

how does renal sympathetic blockade with epidural anesthesia to a T6 level effect renal perfusion and function

A

it does not prevent or modify the impairment of perfusion/function
plus youre stuck with the vasodilation after unclamping if you’ve been infusing through the epidural

44
Q

strongest predictor of postoperative renal function

A

preoperative renal insufficiency

45
Q

how to facilitate renal protection during aortic repair

A

mannitol 12.5g/70kg (reduces ischemia induced renal vascular endothelial cell edema and vascular congestion, scavenger of free radicals)
low dose dopamine 1-3mcg/kg/min
loop diuretics
methylprednisolone

46
Q

patients with which two preexisting cardiac conditions/dysfunctions are most vulnerable to stress imposed on CV system by aortic cross clamping?

A

preexisting impaired ventricular funciton

reduced coronary reserve

47
Q

goals during cross clamp for CV patients include

A 
reducing after load (nitroprusside or clevidipine)
maintain normal preload (IV fluid)
maintain CO (inotropes, MAP goals)
48
Q

what does the hemodynamic response to unclamping depend on

A

level of aortic occlusion, total occlusion time, use of diverting support, intravascular volume

49
Q

if HoTN persists for more than a few minutes after removal of cross clamp, consider

A

unrecognized bleeding or inadequate volume replacement

50
Q

aortic unclamping: expect these symptoms (4)

A

HoTN, reactive hyperemia, washout of vasoactive and cardio depressant mediators, pulmonary hypervolemia

51
Q

therapeutic interventions to consider during aortic cross clamping

A 
decrease inhaled anesthetics
decrease vasodilators
increase fluid administration
administer vasoconstriction
reapplication of cross clamp for severe refractory HoTN
consider mannitol
consider sodium HCO3-
52
Q

anesthetic technique for open AAA

A

GETA most common. regional, combined, low volatile all options but dont do intraop epidural infusion or something. can have it for postop pain
N2O okay
propofol v thiopental v etomidate
fentanyl or sufenta
esmolol, nitroprusside, nitroglycerin, clevidipine, phenylephrine boluses ready
heparin IV 100-300 units/kg: monitor ACT and have protamine

53
Q

anesthetic managment for open AAA: lines

A

potential for rapid blood loss so get CVC (more for volume versus monitoring if you think it will be bloody)
PIV’s
aline
cell salvage and cross matched blood

54
Q

anesthetic management for open AAA and temperature control

A

forced warming for upper body, fluid warmers
lower part of body should not be warmed during the cross clamp period because doing so can increase injury to ischemic tissue distal to the cross clamp by increasing metabolic demands

55
Q

hemodynamic management of open AAA (3 main considerations)

A

HTN avoided because acute stress can cause rupture
HR should be maintained at or below baseline r/t ischemia risk
euvolemic resuscitation deferred until aortic rupture surgically controlled

56
Q

postoperative considerations for open AAA

A

aggressively control HTN and tachycardia
hemodynamic, metabolic, and temperature homeostasis should be achieved before extubations
LOS is variable
can do epidural versus CVA

57
Q

where is CSF pressure maintained for aortic aneurysm repair (especially TAA)

A

less than 10cmH2O and in the days immediately after surgery

58
Q

postoperative complications from open AA repair

A

MI, PNA, sepsis, renal failure, decreased tissue perfusion, hypothermia

59
Q

TAA’s are associated with these genetic syndromes

A

marfans, Ehlers-danlos syndrome, bicuspid aortic valve, non syndromic familial aortic dissection

60
Q

repair approach for TAA: descending aorta

A

left posterolateral thoracotomy, OLV using left tube (depending on where TAA is)
partial versus full bypass

61
Q

repair approach for TAA: ascending aorta

A

supine, median sternotomy

partial versus full bypass

62
Q

s/sx of TAA

A

typically reflect impingement of aneurysms on adjacent structures
acute, severe, sharp pain in anterior chest, neck, or between shoulder blades with diminution or absence of peripheral pulses is how this usually represents

63
Q

hoarseness as sx of TAA is result of

A

stretching of RLN

64
Q

stridor or dysphagia sx of TAA is result of

A

tracheal compression

esophageal compression

65
Q

edema as sx of TAA results from

A

compression of SVC

66
Q

crawford classification of TAA: type 1

A

aneurysm involving descending thoracic and upper abdominal aorta

67
Q

crawford classification of TAA: type 2

A

descending thoracic and most of abdominal aorta (difficult to repair)

68
Q

crawford classification of TAA: type 3

A

lower thoracic aorta and most abdominal aorta (difficult to repair)
renal ischemia worst for this one

69
Q

crawford classification of TAA: type 4

A

most or all of abdominal aorta

70
Q

debakey classification of dissecting aortic aneurysms aka “how they dissect” type 1

A

ascending aortic tear with dissection down entire aorta

71
Q

debakey classification of dissecting aortic aneurysms aka “how they dissect” type 2

A

tear in ascending aorta with dissection limited to ascending aorta

72
Q

debakey classification of dissecting aortic aneurysms aka “how they dissect” type 3

A

tear in proximal descending thoracic aorta with dissection from thoracic aorta to abdominal aorta

73
Q

the artery that supplies blood to the lower 2/3 of the spinal cord

A

artery of adamkiewics or great radicular artery

located between T9-12

74
Q

increased risks of paraplegia after aortic surgery includes

A

duration of cross clamp and anatomic location

not a problem if <30 minutes

75
Q

anterior spinal artery syndrome

A

flaccid paralysis of lower extremities and bowel and bladder dysfunction
sensation and proprioception are spared

76
Q

how to promote spinal cord protection

A

limit cross clamp to less than 30 minutes
distal aortic perfusion via CPB
CSF drainage to maintain normal ICP
intrathecal papaverine to increase BF to area
mild hypothermia
barbs, corticosteroids
avoid hyperglycemia

77
Q

how much does ICP increase with cross clamping

A

10-15mmHg

78
Q

SSEP monitoring: what it monitors and considerations

A

posterior/lateral cord, sensory

cant run increased inhalation, maybe keep under a MAC

79
Q

MEP monitoring: what it monitors and considerations

A

anterior cord, motor
cannot use NMB, do TIVA
reduction in amplitude >25%=SCI induction

80
Q

MEP’s and inhalationals

A

inhalational anesthetics depress synaptic condition and significantly decrease amplitude of myogenic MEP’s

81
Q

how do fentanyl and ketamine effect MEP’s

A

they have little effect

82
Q

TAA preop considerations

A

know extent of aneurysm, technique of repair, plans for distal aortic reperfusion
have 15U PRBC 15U FFP and platelets in room in a cooler

83
Q

TAA invasive lines to have include

A

aline (right radial), ability to draw off CSF/measure pressures, IV access, TEE is routine
right femoral artery cath placed to monitor BP distal to clamp
double limen ETT or bronchial blocker

84
Q

what does right femoral artery monitor during TAA

A

perfusion to kidneys, SC, and mesenteric circulation

85
Q

how to minimize risk of paraplegia in TAA case (3)

A

epidural cooling
regional hypothermia
in line mesenteric shunting

86
Q

contributing factors to coagulopathy during AA surgery (3)

A

residual heparin, liver ischemia, persistent hypothermia

87
Q

how to treat persistent coagulopathy after AA surgery

A

FFP, PLT’s, cryo
PT/PTT, fibrinogen, PLT count, TEG/ROTEM
TCA, amicar, desmopressin
normothermia

88
Q

emergent ruptured aneurysm considerations

A

can be repaired open or EVAR
awake intubation v RSI .1mg/kg etomidate
if open, surgeon will be prepping to clamp aorta at same time as induction
PRBC’s, normothermia if possible
dopa, epi, NE, vasopressin if needed
after aorta is clamped and hemodynamics restored, then worry about placing lines
TEE recommended for assessment of ventricular function, filling pressure, etc

89
Q

various induction dosages in vascular anesthesia (fent, sufent, etomidate, esmolol, NGT, SNP, lidocaine, rocuronium, scopolamine)

A 
fentanyl 10-15mcg/kg
sufentanil 1-2mcg/kg
etomidate .1-.3mg/kg
esmolol 100-500mcg/kg bolus or
SNP 25-50mcg bolus or
NTG .5-3mcg/kg bolus
lidocaine 1.5mg/kg
rocuronium 1.2mg/kg
if hemodynamically unstable, scopolamine 400mcg provides amnesia
90
Q

various medication doses for maintenance of vascular anesthesia (GA and regional)

A 
O2/narcotic/benzo
low dose volatile
des
epidural with morphine 2-4mg or hydromorphone .5-.8mg. avoid LA
remifent .05-.2mcg/kg/min
91
Q

medication dosages of mannitol, lasix, and heparin pre cross clamp in vascular anesthesia

A

mannitol (.25-.5g/kg)
furosemide (20-40mg IV)
heparin 100-300 units/kg IV

92
Q

medication dosages of SNP, NTG, esmolol during cross clamp in vascular anesthesia

A

SNP .5-2mcg/kg/min
NGT .5-2mcg/kg/min
esmolol 50-300mcg/kg/min
bolus NTG is 100mcg

93
Q

medication dosages during uncross clamping in vascular anesthesia

A

giving volume!

N934 Adv Principles Fa 21 (23 decks)

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