Anesthesia for Vascular Surgery Part 2: Aneurysms Flashcards
describe an aortic aneurysm
dilation of all 3 layers of artery. occasionally produce symptoms of compression on surrounding areas including possibly pain
describe an aortic dissection
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
risk factors for abdominal aortic aneurysm (AAA)
elderly, male
smoking
family history
atherosclerotic disease
what degradation occurs to create an AAA
adventitial elastin degradation (genetic, biochemical, metabolic, infectious, mechanic, and hemodynamic factors may contribute)
how do AAA’s present
asymptomatic pulsatile abdominal masses
how do AAA’s present
asymptomatic pulsatile abdominal masses
when to repair AAA
all patients with AAA 6cm or larger or when small aneurysms become symptomatic/expand >.5cm in 6mo period
aneurysms less than ___cm in diameter are thought to be relatively benign in terms of rupture or expansion
4cm
law of laplace in relation to aneurysm
increasing diameter is associated with increased wall tension, even when arterial pressure is constant
frequent incidence of associated systemic HTN enhances aneurysm enlargement
law of laplace in relation to aneurysm
increasing diameter is associated with increased wall tension, even when arterial pressure is constant
frequent incidence of associated systemic HTN enhances aneurysm enlargement
classic triad of sx for a ruptured AAA
HoTN, back pain, pulsatile abdominal mass
what types of aortic diseases is EVAR approach used for
traumatic injuries ruptures dissections TAA and AAA (all types)
positive aspects of the EVAR approach to aortic aneurysms
less invasive
reduced M&M
shorter hospital stay
most common technique for repair
how are femoral arteries accessed during EVAR
cutdowns or percutaneous procedures
what are the anesthesia techniques for EVARs
MAC with local/regional versus GA
consider patients functional status (can they lay flat), co morbidities, aneurysm complexity, surgery urgency (full stomach)
anesthesia for EVAR’s, steering guiding sheaths may require what?
left arm arterial cut down
what is the artery that remains at most risk on spinal cord during EVAR
single anterior spinal cord artery that usually originates off descending aorta between T9-12
what are some anesthesia considerations intraoperatively for EVAR procedures
hemodynamic management preservation of organ perfusion blood loss and intravascular volume temperature risk of conversion to open radiation safety
what are the two most important factors that contribute to contrast induced nephropathy (a possible complication from EVAR)
contrast load and preexisting kidney disease
limit the load and adequately hydrate
early EVAR complications (5)
paraplegia, stroke, ARI, aneurysm rupture, pelvic hematoma
late EVAR complications (5)
endoleaks, aneurysm rupture, device migration, limb occlusion, graft infection
how are endoleaks usually treated
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
how are type 2 endoleaks treated
transarterial embolization through the iliac arteries or retrograde embolization through the superior mesenteric or inferior mesenteric arteries
describe open abdominal aortic reconstruction considerations and procedure
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)
most common sites of chronic atherosclerosis contributing to arotoiliac occlusive disease (2)
infrarenal aorta and iliac arteries
when do patients undergo surgery for aortoiliac occlusive disease?
only if they are symptomatic which includes claudication and limb threatening ischemia
surgical management of aortoiliac occlusive disease includes (3)
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.
what does the pathophysiology of aortic cross clamping depend on (6)
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)
complications of aortic cross clamp r/t BP management
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
aortic cross clamp complications: common ischemic complications
renal failure (esp if clamped suprarenal) hepatic ischemia coagulopathy bowel infarction paraplegia
thoracic aortic cross clamp: what to expect with vital signs
increase in MAP, CVP, pulmonary arterial pressure, pulmonary wedge pressure
decrease in CI and EF
no change in HR
how the aortic cross clamp effects the left ventricle: normal intact heart
can withstand large increases in volume without significant ventricular distention or dysfunction
how the aortic cross clamp effects the left ventricle: impaired heart
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
aortic cross clamp: baroreceptor activation
results from increased aortic pressure and should depress the HR, contractility, and vascular tone
aortic cross clamp: metabolic effects. cross clamping of thoracic aorta decreases total body O2 consumption by
50%
aortic cross clamp: blood flow through tissues and organs below the level of aortic occlusion is dependent on _____ and independent of _____
dependent on perfusion pressure and
independent of CO
hemodynamic changes associated with aortic cross clamping
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)
metabolic changes associated with aortic cross clamping includes
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
significance of impact on perfusion to vital organs in order from most to least detrimental
thoracic>supraceliac>infrarenal
management of aortic cross clamp: pharmacologic intervention
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
renal effects of cross clamping
while there is a dramatic reduction in RBF when clamped above renal arteries, there is still a reduction in RBF below renal arteries
renal failure after repair of aneurysm results from
preexisting renal dysfunction, ischemia during cross clamping, thrombotic or embolic interruption of RBF, hypovolemia and HoTN
how does renal sympathetic blockade with epidural anesthesia to a T6 level effect renal perfusion and function
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
strongest predictor of postoperative renal function
preoperative renal insufficiency
how to facilitate renal protection during aortic repair
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
patients with which two preexisting cardiac conditions/dysfunctions are most vulnerable to stress imposed on CV system by aortic cross clamping?
preexisting impaired ventricular funciton
reduced coronary reserve
goals during cross clamp for CV patients include
reducing after load (nitroprusside or clevidipine) maintain normal preload (IV fluid) maintain CO (inotropes, MAP goals)
what does the hemodynamic response to unclamping depend on
level of aortic occlusion, total occlusion time, use of diverting support, intravascular volume
if HoTN persists for more than a few minutes after removal of cross clamp, consider
unrecognized bleeding or inadequate volume replacement
aortic unclamping: expect these symptoms (4)
HoTN, reactive hyperemia, washout of vasoactive and cardio depressant mediators, pulmonary hypervolemia
therapeutic interventions to consider during aortic cross clamping
decrease inhaled anesthetics decrease vasodilators increase fluid administration administer vasoconstriction reapplication of cross clamp for severe refractory HoTN consider mannitol consider sodium HCO3-
anesthetic technique for open AAA
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
anesthetic managment for open AAA: lines
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
anesthetic management for open AAA and temperature control
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
hemodynamic management of open AAA (3 main considerations)
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
postoperative considerations for open AAA
aggressively control HTN and tachycardia
hemodynamic, metabolic, and temperature homeostasis should be achieved before extubations
LOS is variable
can do epidural versus CVA
where is CSF pressure maintained for aortic aneurysm repair (especially TAA)
less than 10cmH2O and in the days immediately after surgery
postoperative complications from open AA repair
MI, PNA, sepsis, renal failure, decreased tissue perfusion, hypothermia
TAA’s are associated with these genetic syndromes
marfans, Ehlers-danlos syndrome, bicuspid aortic valve, non syndromic familial aortic dissection
repair approach for TAA: descending aorta
left posterolateral thoracotomy, OLV using left tube (depending on where TAA is)
partial versus full bypass
repair approach for TAA: ascending aorta
supine, median sternotomy
partial versus full bypass
s/sx of TAA
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
hoarseness as sx of TAA is result of
stretching of RLN
stridor or dysphagia sx of TAA is result of
tracheal compression
esophageal compression
edema as sx of TAA results from
compression of SVC
crawford classification of TAA: type 1
aneurysm involving descending thoracic and upper abdominal aorta
crawford classification of TAA: type 2
descending thoracic and most of abdominal aorta (difficult to repair)
crawford classification of TAA: type 3
lower thoracic aorta and most abdominal aorta (difficult to repair)
renal ischemia worst for this one
crawford classification of TAA: type 4
most or all of abdominal aorta
debakey classification of dissecting aortic aneurysms aka “how they dissect” type 1
ascending aortic tear with dissection down entire aorta
debakey classification of dissecting aortic aneurysms aka “how they dissect” type 2
tear in ascending aorta with dissection limited to ascending aorta
debakey classification of dissecting aortic aneurysms aka “how they dissect” type 3
tear in proximal descending thoracic aorta with dissection from thoracic aorta to abdominal aorta
the artery that supplies blood to the lower 2/3 of the spinal cord
artery of adamkiewics or great radicular artery
located between T9-12
increased risks of paraplegia after aortic surgery includes
duration of cross clamp and anatomic location
not a problem if <30 minutes
anterior spinal artery syndrome
flaccid paralysis of lower extremities and bowel and bladder dysfunction
sensation and proprioception are spared
how to promote spinal cord protection
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
how much does ICP increase with cross clamping
10-15mmHg
SSEP monitoring: what it monitors and considerations
posterior/lateral cord, sensory
cant run increased inhalation, maybe keep under a MAC
MEP monitoring: what it monitors and considerations
anterior cord, motor
cannot use NMB, do TIVA
reduction in amplitude >25%=SCI induction
MEP’s and inhalationals
inhalational anesthetics depress synaptic condition and significantly decrease amplitude of myogenic MEP’s
how do fentanyl and ketamine effect MEP’s
they have little effect
TAA preop considerations
know extent of aneurysm, technique of repair, plans for distal aortic reperfusion
have 15U PRBC 15U FFP and platelets in room in a cooler
TAA invasive lines to have include
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
what does right femoral artery monitor during TAA
perfusion to kidneys, SC, and mesenteric circulation
how to minimize risk of paraplegia in TAA case (3)
epidural cooling
regional hypothermia
in line mesenteric shunting
contributing factors to coagulopathy during AA surgery (3)
residual heparin, liver ischemia, persistent hypothermia
how to treat persistent coagulopathy after AA surgery
FFP, PLT’s, cryo
PT/PTT, fibrinogen, PLT count, TEG/ROTEM
TCA, amicar, desmopressin
normothermia
emergent ruptured aneurysm considerations
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
various induction dosages in vascular anesthesia (fent, sufent, etomidate, esmolol, NGT, SNP, lidocaine, rocuronium, scopolamine)
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
various medication doses for maintenance of vascular anesthesia (GA and regional)
O2/narcotic/benzo low dose volatile des epidural with morphine 2-4mg or hydromorphone .5-.8mg. avoid LA remifent .05-.2mcg/kg/min
medication dosages of mannitol, lasix, and heparin pre cross clamp in vascular anesthesia
mannitol (.25-.5g/kg)
furosemide (20-40mg IV)
heparin 100-300 units/kg IV
medication dosages of SNP, NTG, esmolol during cross clamp in vascular anesthesia
SNP .5-2mcg/kg/min
NGT .5-2mcg/kg/min
esmolol 50-300mcg/kg/min
bolus NTG is 100mcg
medication dosages during uncross clamping in vascular anesthesia
giving volume!
