Vascular Anesthesia Flashcards
coexisting diseases
- DM
- HTN
- renal impairment
- pulmonary disease
- systemic atherosclerosis
- coronary artery disease
coronary artery disease (CAD)
- leading cause of perioperative mortality at the time of vascular surgery
- less than 10% of vascular patients who undergo surgery have normal coronaries
- unrecognized silent MIs occur in 23-28% of patients
- long term the prevalance of MI and death is 8.9 and 11.2% in patients undergoing vascular surgery
pathology of atherosclerosis
- generalized, progressive, chronic inflammatory disorder of the arterial tree with development of fibrous intimal plaque associated with endothelial dysfunction
- potentially compromises blood flow to all the organs and extremities leads to MI, stroke, gangrene
- combo of lipid disorder and inflammatory process
stage I of atherosclerosis
- fatty streak
- endothelium damaged –> chronic inflammatory response and hypercoagulable state
- lipoproteins enter intimal layer
- can start in childhood
stage II of atherosclerosis
- fibrous plaque
- made of oxidized lipids, inflammatory cells, calcium deposits, etc.
- blood flow reduction occurs here
- ischemia to vital organs and extremities
stage III of atherosclerosis
- advanced lesion
- plaque with necrotic core, calcium accumulation, and endothelial dysfunction
- physical disruption of plaques protective cap exposes blood to highly thrombogenic material which promotes acute thrombus formation and vasospasm
- complete occlusion possible at this level
three types of atherosclerotic morbidity
- enlarged plaque reduces lumen of blood vessel (limb ischemia, stable angina)
- plaque rupture/ulceration, embolization, and thrombus formation
- atrophy of media with arterial wall weakening (aneurysm dilation)
most common sites for atherosclerotic lesions
- aortoiliac peripheral
- coronary
- aortic arch branches
- combined
- mesenteric renal
CAD ACC and AHA pre-op evaluation guidelines
- focus = evaluation of patient at risk for CV M&M undergoing non-cardiac surgery
- goal = best possible quality of care and outcome for the patient
- goal = information obtained should be used for both peri-op period and to inform the long term treatment plan
components of pre-op guidelines for vascular patients
- clinical history - clinical risk factors, exercise tolerance
- supplemental evaluation
- perioperative therapy
- surgical procedure - low, intermediate or high risk
aspirin
- inhibits platelets
- potential for increased bleeding and decreased GFR
plavix
- inhibits plts
- potential for increased bleeding
statins
-can effect liver function
ACE inhibitors
- induction hypotension
- coughing
Diuretics
- hypovolemia
- electrolyte imbalance
ca+ channel blockers
-hypotension
hypoglycemic drugs
- hypoglycemia
- lactic acidosis with metformin
beta blockers
- bronchospasm
- decreased BP
- decreased HR
other medical management for CAD
- smoking cessation
- weight loss
- exercise
- all the meds
bare metal stent minimum DAPT
1-3 months
drug eluting stent minimum DAPT
- 6 months
- so cant do some types of surgery for 6 months post coronary stenting if you have drug eluting stent
causes of periop MIs
- culprit lesions - vulnerable plaques with high likelihood of thrombotic complications; often located in coronary vessels without critical stenosis
- demand ischemia - predominant cause of periop MI
preop assessment of cardiac function
- advanced cardiac testing used to determine if coronary intervention is needed prior to vascular surgery OR to determine if aggressive intraop and post op management
- exercise/pharm stress test
- ECHO
- assessment of myocardial ischemia, MI, valve dysfunction, heart failure
- duplex imaging of carotid arteries or angiography
preop assessment of pulmonary function
- the most important pulmonary complications are atelectasis, pneumonia, resp failure, and exacerbation of underlying chronic disease
- high prevalence of cigarette smoking in this population and COPD common
- tests - PFTs, ABGs, CXRs
- consider - incentive spirometry, steroids, regional, abx, and cpap
preop assessment of renal function
- chronic renal disease strongly predicts long term mortality in patients with symptomatic lower extremity arterial occlusive disease
- tests - serum cr, cr clearance
- consider - contrast dye use, beta-blockers, statins, volume status, perfusion pressures
lower extremity peripheral artery disease
defined as insufficiency in lower extremities presenting with acute or chronic limb ischemia with occlusions distal to the inguinal ligament
lower extremity revascularization
- PAD or atheroslcerotic occlusive disease of lower extremities
- risk for amputation, MI, stroke, death
- probable atherosclerosis in other beds
- DM at extra high risk
- often on antiplt and anticoags, makes challenging in preop perioid
indications for peripheral revascularization
- acute ischemia due to emboli, thrombus or pseudoaneurysm
- irreversible ischemic damage occurs 4-6 hours (urgent thrombolytic therapy, arteriography, surgical intervention
- chronic ischemia due to - athersclerotic plaque progressively narrowing vessel, claudication with eventual thrombosis of vessel
- surgery indicated when severe disabling claudication, critical limb ischemia
peripheral occlusions traditional surgical approach
- unobstructed blood flow source (donor) artery exposed (usually common femoral, superficial femoral, or deep femoral)
- target distal artery (recipient) exposed at or below the knee (usually dorsalis pedis or posterior tibial)
- after donor and recipient arteries exposed, a tunnel is created and graft is passed
- graft may be saphenous vein or prosthesis
- IV heparin given
- anastomosis are constructed
- arteriogram to confirm adequate flow
- heparin in not likely to be reversed
what if saphenous vein is used?
-if saphenous vein used, the vein is dissected all branches are ligated, divided and excised; saphenous vein is reversed to permit blood flow in direction of valves
anesthetic management for peripheral revascularization
- preop beta blockers and or other chronic med
- intraop - arterial line
- continuous EKG monitoring + ST analysis (leads II and V)
- monitor intravascular volume by foley (+/- CVP or PA cath)
- minimal blood loss and 3rd space
what do you need for emergency revascularization surgery
- carefully watch K+ levels
- myoglobinemia
- fasciotomy may be required
- coag studies
- ECG ischemia
regional vs general for peripheral revascularization
- assess for coagulopathy or anticoagulation therapy
- spinal may be best to avoid hematoma
- most studies have shown no difference between RA and GA in terms of cardiopulmonary complications
- significant difference 5x in complication rate in terms of graft occlusion with regional being superior
- studies regarding efficacy of post op pain management with epidural vs opioids are poorly designed
why is graft occlusion significant with GA in postop period?
- hypercoagulable state with GA as opposed to RA
- fibrinolysis decreased after GA, therefore fibrinogen not broken down and clots form
- epi, norepi, and cortisol release increased after GA compared to RA
- patency of graft maintained with RA secondary to increased blood flow with sympathectomy
what is the appropriate regional anesthesia for peripheral reperfusion
- L1-L4 dermatomes
- T10 level usually adequate
- epidural dosing usually 9-12 mL including test dose
- ELDERLY require decreased dosing
post op management for peripheral revascularization
- control pain and anxiety (high risk for MI in this period)
- avoid anemia (need Hgb greater than 9-10)
- control HR and BP
- frequent checks of peripheral pulses
- continuous EKG monitoring and ST analysis
lower extremity endovascular treatment anesthetic management
- GA, neuraxial, MAC
- percutaneous procedures so often MAC
- open access needed, consider GA instead
what is the principal cause of carotid artery disease?
atherosclerosis
where do carotid plaques commonly occur
- common carotid artery
- internal and external carotid arteries
S/S of carotid artery disease
- fatal or debilitating stroke
- TIA
- amaurosis fugax (transient attack of mononuclear blindness)
- asymptomatic bruit
strokes
- 5th leading cause of death in US
- varies by race/ethnicity
- 795,000 new strokes each year in US
- risk factors = HTN, smoking, obesity, DM
- 87% are ischemic
- extracranial atherosclerotic disease accounts for up to 20% of all ischemic strokes
Carotid endarterectomy (CEA)
- has been around for 50 years
- most common peripheral vascular surgical procedure performed in US
- 130,000 performed annually in US
- definitive results for symptomatic patients with high-grade carotid stenosis (70-99%)
preop assessment for CEA
- recent symptoms - surgical intervention timing
- optimize medical management - beta blockers, statins, antiplt therapy, HTN control, restore intravascular volume, reset cerebral autoregulation, DM control
- CAD is common
- bad signs = UA, decompensated CHF, significant valve disease
anesthesia for CEA
- awake vs GA/ETT
- continue ASA throughout periop period
- continue cardiac meds
- EKG monitoring should include continuous leads II and V for detection of rhythm disturbances and ST changes
- a line
- PIV x2, large bore, arms tucked
lead II measures what?
inferior
lead V5 measures what?
lateral
CEA case setup
- type and screen
- a line
- ACT machine, fluid warmer, lower body bair hugger
- phenyl and remi in line
- clevidipine and NTG available
- beta blockers and ephedrine available
- heparin and protamine
CEA case monitoring
- routine with V5 lead and ST segment analysis plus a line
- consider cerebral oximetry
- occasionally surgeons want to measure stump pressures (so need extra pressure line tubing and blue male to male adapter to connect to a line transducer)
CEA and GA
- sedative pre med
- fentanyl for awake aline placement
- induction - prop, etomidate, roc
- consider esmolol during DL
- immediate treatment of hyper of hypo tension
- inhalation agent
- cerebral oximetry
- adjuncts - prop, remi, precedex
arterial blood pressure monitoring during CEA
- abp should be maintained in the high-normal range throughout the procedure particularly during the period of carotid clamping to increase collateral flow and prevent cerebral ischemia
- induced HTN to approximately 10-20% above baseline
- careful with increased BP, HR, and myocardial demand
- MAKE SURE to note preinduction MAP
what happens with surgical manipulation of carotid sinus?
- baroreceptor reflex
- HR will decreased
- BP will decrease
- cessation of surgical stim promptly restores hemodynamics
- infiltration of carotid bifurcation with 1% lido usually prevents further episodes
emergence for CEA
- neuro deficits on emergence require immediate discussion with the surgeon about the need for angiography, reoperation, or both
- emergence may be associated with marked hypertension and tachy –> need aggressive pharmacologic intervention
regional anesthesia for CEA
- blocking C2-C4 dermatomes by use of superficial, intermediate, deep or combined cervical plexus block
- regional and local anesthesia allow continuous neuro assessment
- reduces need for shunt
- greater hemodynamic stability
- reduced cost
- requires patient cooperation
- conversion to GA 2-6%
superficial cervical plexus block
- midpoint of posterior border of SCM muscle
- injection along posterior border of medial surface of the muscle
- may block accessory nerve causing trapezius muscle paralysis
cerebral autoregulation
- hypocapnia - decrease CBF (vasoconstrict)
- hypercapnia - increase CBF (vasodilate)
- if there is poor collateralization and resultant cerebral hypoperfusion, cerebral resistance vessels in hypo-perfused territories will dilate to maintain cerebral blood flow
carotid artery stump pressure
- internal carotid artery stump pressure represents the back-pressure resulting from collateral flow through the circle of Willis via the contralateral carotid artery and vertebrobasilar system
- ideally above 45-50 mmHg
- may or may not be done
cerebral NIRS
- non-invasive technique that allows continuous monitoring of regional cerebral oxygen sat through scalp and skull
- based on absorption characteristics of oxygenated vs deoxygenated blood
- measure O2 sat of Hgb in entire tissue bed (brain, arterial, and venous)
- predominantly venous so therefore approximates VENOUS blood O2 sat
CEA post op complications
- HTN - surgical denervation of carotid sinus baroreceptors
- HoTN - baroreceptor hypersensitivity or reactivation
- cerebral hyper-perfusion syndrome - abrupt increase in blood flow with loss of autoregulation
- cranial and cervical nerve dysfunction (RLN, SLN, hypoglossal, mandibular)
- carotid body denervation
- wound hematoma
s/s cerebral hyperperfusion syndrome
- HA
- seizure
- focal neurologic signs
- brain edema
- intracerebral hemorrhage
bilateral RLN dmage
- results in bilateral vocal cord paralysis
- life threatening upper airway obstruction
s/s carotid body denervation
- impaired ventilatory response to mild hypoxemia
- central chemoreceptors impaired
- worsened with opioid admin
aortic aneurysm
- dilation of all 3 layers of an artery
- occasionally produce symptoms of compression on surrounding areas
- s/s - may be asymptomatic or present with pain mostly due to compression of adjacent structures or vessels
aortic dissection
- surgical emergency
- mortality up to 58%
- occurs when blood enters the medial layer
- initiation occurs with a tear in the intimal layer
- can occur over minute to hours
- s/s - severe sharp pain in the posterior chest or back pain
three layers of aorta
- intima (inner most)
- media
- adventitia (outermost)
abdominal aortic aneursym risk factors
- elderly, male
- smoking
- family history of AAA
- athersclerotic disease and HTN
contributing factors to adventitial elastin degradation
- genetic
- biochemical
- metabolic
- infectious
- mechanical
- hemodynamic
AAA
- asymptomatic pulsatile abdominal mass
- concomitant aortoiliac occlusive disease is present in approximately 20-25% of patients
- rare causes include trauma, myocotic infection, syphilis, marfan
elective AAA repair… WHEN?
- done 6cm or larger
- controversial if it is 5.5-5.9 cm
- aneurysms less than 4.0 cm in diameter are thought to be relatively benign in terms of rupture and expansion
- surgery may be considered for smaller aneurysms if they become symptomatic
law of LaPlace
- increasing diameter is associated with increased wall tension, even when arterial pressure is constant
- the frequent incidence of associated systemic HTN enhances aneurysm enlargent
ruptured AAA
- periop mortality for ruptured AAA is around 50%
- death before reaching hospital is >90%
classic triad of ruptured AAA
- hypotension
- back pain
- pulsatile abdominal mass
EVAR technique
- used for all types of aortic diseases (trauma, rupture, dissection)
- less invasive
- reduced M&M
- shorter hospital stay
- now most common technique for AAA repair
- femoral arteries are accessed either by cutdown or percutaneous punctures
anesthesia for EVAR
- MAC with local/regional vs GA
- consider patient’s functional status
- steering guiding sheaths that may require L arm arterial cutdown
- spinal cord - extensive collateral network
- hemodynamic management
- preservation of organ perfusion
- blood loss and intravascular volume
- temperature
- risk of conversion to open
- radiation safety
two most important factors that contribute to CIN
- contrast load
- preexisting kidney disease
how to prevent CIN
- limit contrast load
- adequate hydration to decrease viscosity of idodine based dyes
EVAR early complications
- paraplegia
- stroke
- ARI
- aneurysm rupture
- pelvic hematoma
EVAR late complications
- endoleaks
- aneurysm rupture
- device migration
- limb occlusion
- graft infection
endoleak
- normally tx with balloon angioplasty of proximal attachment site so that the desired seal is obtained through remodeling of stent-graft
- type II endoleak - treated with transarterial embolization through iliac arteries or retrograde embolization through superior mesenteric or inferior mesenteric arteries
- open surgical treatment also an option
open abdominal aortic reconstruction
- large incisions and extensive dissection
- clamping and unclamping of aortic or its major branches
- varying duration of organ ischemia reperfusion
- significant fluid shifts
- temperature fluctuations
- activation of neurohumoral and inflammatory responses
aortoiliac occlusive disease
- infrarenal aorta and iliac arteries are two of the most common sites of chronic atherosclerosis
- diffuse and progressive plaque enlargement may reduce blood flow to the lower extremities below a critical level and result in symptoms of ischemia
- patients have surgery only if symptomatic (claducation and ischemia)
management of aortoiliac occlusive disease
- direct reconstruction (gold standard)
- extra-anatomic or indirect bypass graft
- catheter based endoluminal techniques (for local disease)
patho of aortic cross clamping depends on what?
- level of cross clamp
- status of LV
- degree of periaortic collateralization
- intravascular blood volume and distribution
- activation of SNS
- anesthetic drugs and techniques
- heparinization
- monitor ACTs
Aortic cross clamp above the clamp
arterial hypertension
aortic cross clamp below the clamp
arterial hypotension
common ischemic complications with aortic cross clamp
- renal failure
- hepatic ischemia
- coagulopathy
- bowel infarction
- paraplegia
thoracic aortic cross clamp effects
- increased MAP
- increased CVP
- increased mean pulmonary arterial
- increased pulmonary wedge
- decreased cardiac index
- decreased EF
- no change in HR
aortic cross clamp metabolic effects
- decreases total body O2 consumption by 50%
- blood flow through tissues and organs below the level of aortic occlusion is DEPENDENT ON PERFUSION PRESSURE and is independent of cardiac output
management during aortic cross clamp
- acute increase in SVR and decreased CO
- the higher the clamp the more significant the impact on perfusion to vital organs
- use vasodilators to decrease afterload, wall stress, and myocardial oxygen demand
- avoid long acting meds
- perfusion to distal organs is dependent on collaterals which originate proximal to the clamp or shunts
renal effects of aortic cross clamp
- clamp above renal arteries decrease renal blood flow up to 80-90%
- epidural anesthesia does not reduce/prevent impairment of renal perfusion
- preop renal insufficiency is STRONGEST predictor of post op renal dysufnction
renal protection during aortic cross clamp
- controversial
- mannitol (12.5 g/70kg)
- loop diuretics
- methylprednisolone
- dopamine (1-3 mcg/kg/min)
mannitol renal protective effects
- improves renal cortical blood flow
- scavenges free radicals
- decreases renin secretion
- increases renal prostaglandin synthesis
what cardiac dysfunctions are most vulnerable to stress of aortic cross clamp
- preexisting impaired ventricular function
- reduced coronary reserve
goals during cross clamp for those with pre-existing cardiac dysfunction
- reduce afterload (nitroprusside, clevidipine)
- maintain normal preload (IVF)
- maintain CO (inotropes, MAP goals)
aortic unclamping
- massive hemodynamic response
- hypotension
- reactive hyperemia
- washout of vasoactive and cardio-depressant mediators
- pulmonary hypervolemia (flash pulm edema picture)
how severe the hemodynamic response to unclamping is depends on what?
- level of aortic occlusion
- total occlusion time
- use of diverting support
- intravascular volume
therapeutic interventions to unclamping
- decrease inhaled agents
- decrease vasodilators
- increase IVF
- increase vasoconstrictor drugs
- reapply cross clamp for SEVERE hypotension
- consider mannitol
- consider sodium bicarb
anesthetic management for open AAA
- rapid blood loss possible - LARGE PIVs, a line, central line, cross-matched blood, cell salvage
- TEE
- cerebral oximetry
- techniques = GA/ETT, regional, combined, low volatile
- esmolol, nitroprusside, nitroglycerin, clevidpine, phenyl READY TO GO
- heparin + protamine
- monitor ACT
- temperature control - do not warm below the clamp, this could increase ischemic injury by increasing metabolic demand
heparin dose
100-300 units/kg
hemodynamic management for AAA
- HTN avoided bc acute stress on aneurysm can cause rupture
- HR maintained at or below baseline
- euvolemic resuscitation may be deferred until aortic rupture surgically controlled in OR
post op management for AAA
- tight control of HTN and tachycardia
- homeostasis of hemodynamics, metabolic, and temp prior to extubation
- LOS is variable
- pain - epidural vs PCA
complications in post op period for AAA
- MI
- pneumonia
- sepsis
- renal failure
- decreased tissue perfusion
- hypothermia
thoracic aortic aneurysm
-associated with genetic syndromes - marfan, ehlers-danlos, bicuspid aortic valve, non-syndromaic familial aortic dissection
repair approach for thoracic aortic aneurysm
- descending aorta - left posterolateral thoracotomy (w OLV)
- ascending aorta - supine, median sternotomy
- full or partial CPB
S/S thoracic aortic aneurysms
- s/s result of impingement of surrounding structures
- hoarseness results form stretching of L RLN
- stridor due to compression of trachea
- dysphagia due to compression of esophagus
- dyspnea due to compression of lungs
- edema from compression of SVC
thoracic aortic dissection symptoms
- acute, severe sharp pain in anterior chest, neck, or between shoulder blades
- dimunition or absence of peripheral pulses
Crawford type I for TAA
aneurysm involving descending thoracic aorta and upper abdominal aorta
Crawford type II for TAA
descending thoracic and most abdominal aorta
Crawford type III for TAA
lower thoracic aorta and most abdominal aorta
Crawford type IV for TAA
most or all abdominal aorta
most difficult crawford TAA types to repair
types II and III
DeBakey Classification of Dissecting AA Type I
ascending aortic tear with dissection down entire aorta
DeBakey Classification of Dissecting AA Type II
tear in ascending aorta with dissection limited to ascending aorta
DeBakey Classification of Dissecting AA Type III
tear in proximal descending thoracic aorta with dissection from thoracic aorta to abdominal aorta
spinal cord perfusion
- two posterior arteries (25% blood flow)
- one anterior artery (75% blood flow)
- largest radicular artery = artery of Adamkiewicz (AKA)
artery of adamkiewicz (AKA)
- major blood supply to lower 2/3 of spinal cord
- segmental supplier of AKA is usually located between T9-T12 75% of the time
- can be T5-L5 (VARIABLE)
anterior spinal artery syndrome
- flaccid paralysis of lower extremities
- bowel and bladder dysfunction
- sensation + proprioception are SPARED!!!
spinal cord protection
- limit x-clamp time < 30 min
- distal aortic perfusion (ECMO)
- CSF drainage - to decrease pressure in spinal cord and increase perfusion)
- intrathecal papaverine (help increase BF to area)
- mild hypothermia to reduce O2 requirements
- barbiturates
- corticosteroids
- avoid hyperglycemia
SSEPs
posterior lateral cord, sensory
MEPs
anterior cord, motor
what is indication of SCI
reduction in MEP amplitude to less than 25% of baseline
may require corrective measures
what things in anesthesia effect MEPs (i.e. things we cannot use)
- muscle relaxation
- inhaled agents
TAA preop prep + monitoring
- know extent of aneurysm TALK TO SURGICAL TEAM
- PRBCs, FFP, plts
- invasive lines - aline, PA cath, CSF Pressure, LARGE BORE IV
- TEE common
- R fem artery cath to monitor BP distal to clamp
- Double lumen ETT or bronchial blocker for OLV
- position = thoracoabdominal incision + retroperitoneal dissection
- SSEPs + MEPs
- body temp
where do you put the a line in TAA surgery
R radial because cross clamp may be placed proximal to L subclavian artery which occludes flow to LUE
TAA anesthetic technique
- induction slow and controlled to avoid aneurysm rupture
- usually a balanced anesthetic
- opioid, low dose volatile, benzo, NDMR
- TIVA if MEP
- consider combined epidural/GA
- +/- thoracic epidural for post op pain
- Extubate in ICU
TAA post op care
- may consider extubation in OR
- normally not tho and done in ICU
- admit to ICU DUH
