Vascular Flashcards
1
Q
What are some risks of major vascular surgery?
A
- High-risk operations –> Increased risk M&M
- Always consider presence of overt or occult coronary artery disease
- <10% of vascular surgery patients have normal coronary arteries
-
>50% have severe CAD –> INDUCIBLE ISCHEMIA
- unrecognized MI and silent MI often occur in vascular surgery patient (23-28% respectively) and associated w/ long term mortality and adverse cardiac events
-
CAD: leading cause of perioperative and long-term mortality after vascular surgery
- Nearly 10% w significant myocardial injury in perioperative period
- 2% with Major adverse cardiac events (MACE) –>**new onset HF, STEMI, arrhythmias, death (depends on study for def)
- Highest risk patient are those withing 30 days after MI during which plaque an myocardial healing, remodeling occur*
- 60 days is preferred waiting period after MI for elective surgery
- MACE: Varying definitions.
- Narrowly: nonfatal stroke, nonfatal myocardial infarction, and cardiovascular death.
- Broader: CVD events, admission for HF, ischemic cardiovascular events, cardiac death
2
Q
What are the branches that come off the aortic arch?
A
- Brachiocephalic trunk (innominate)
- right common carotid artery
- right internal carotid
- right external carotid artery
- right vertebral artery
- right subclavian artery
- continues on to become right axillary artery then right brachial artery
- right common carotid artery
- left common carotid
- left internal carotid artery
- left external carotid artery
- left subclavian artery
- left vertebral artery
3
Q
Branches of abdominal aorta?
A
(from anatomy lecture)
Abomindal aorta:
- Begins at hiatus (T12), end at bifurcation (L4) of L and R common iliac artery
-
4pairs of lumbar arteries
- supply lumbar vertebrae, back muscles, posterior abdominal wall
- Inferior phrenic arteries (paired)–> suprarenal gland, diaphragm
- Suprarenal arteries (paired)–> suprarenal gland
- celiac trunk (unpaired) **
- renal arteries (paired)–> kidney
- Superior mesenteric artery (unpaired)**
- Gonadal (ovarian or testicular arteries (paired)–> ovaries or testes
- Inferior mesenteric artery (unpaired) **
- Median sacral artery–> rectum
Aorta continues on to become…
- right common iliac artery
- right internal iliac artery
- right external iliac artery
- left common iliac artery
- left internal iliac artery
- left external iliac artery
Online mneumonic for order of branches:
“In Case My Students Really Love Games I’m Monopoly”
- Inferior Phrenic
- Celiac
- Middle Suprarenal
- Superior mesenteric
- Renal
- Lumbar (x4)
- Gonadal
- Inferior mesenteric
- Median sural
4
Q
What is the pathophysiology of atherosclerosis?
A
- A generalized, progressive, chronic inflammatory disorder of the arterial tree with development of fibrous intimal plaque
- Associated endothelial dysfunction
- Medium & large arteries primarily affected; areas of branching more vulnerable
From picture
- Normal artery
- healthy endothelium
- quiescent smooth muscle in media
- early atherosclerosis
- endothelial dysfunction and activation allows macrophage adhesion
- accumulation of oxidized lipid results in fatty streaks
- plaque formation
- lipid-laden macrophages (aka foam cells) and necrotic material in lipid core
- smooth muscle cells and extracellular matrix form fibrous cap
- plaque rupture
- activated macrophages secrete matrix-degrading enzymes
- thin fibrous cap ruptures or erods
- exposure of plaque core and collagen cause PLT adhesion, thrombosis, rapid plaque expansions and/or lumen occlusion
5
Q
Progression of atherosclerosis?
A
-
Stage I : Fatty streak
- Endothelium is damaged due to hemodynamic shear stress, oxidized LDL destruction, chronic inflammatory responses, infection, and hypercoagulability resulting in thrombosis
- Lipoproteins enter the arterial intimal layer via endothelium become entrapped- promote inflammation. Lipid-laden macrophages (foam cells), smooth muscle cells & elastic/ collagen fibers
-
Stage II: Fibrous plaque
- Composed of oxidized lipid accumulation, inflammatory cells, proliferated smooth muscle cells, connective tissue fibers, and calcium deposits
- Blood flow reduction - ischemia to vital organs & extremities; thrombus risk
-
Stage III: Advanced lesion
- Plaque w/expanded lipid-rich necrotic core, calcium accumulation, endothelial dysfunction
- Physical disruption of plaque’s protective cap (rupture or ulceration) exposes blood to highly thrombogenic material promoting acute thrombus formation and vasospasm
- Complete occlusion possible (MI, stroke, limb ischemia, etc.)
-
Stable plaque causes negative remodeling and reduces lumen of blood vessel (limb ischemia, stable angina)
- Supply vs demand problem
- “Delayed” peri-op MI
- Ischemia of the coronary, cerebral, mesenteric, or peripheral circulation
-
Plaque rupture/ulceration, embolization, and thrombus formation (unstable angina, STEMI, TIA, CVA)
- Acute occlusion
- “Early” peri-op MI
- Atrophy of media with arterial wall weakening (aneurysm dilation)
- 2. Plaque erosion or rupture allows blood to come into contact with its highly thrombogenic core, leading to platelet aggregation and thrombus formation. Rapid expansion of the plaque with subsequent thrombus formation and distal microembolism results in an acute coronary syndrome or CVA.
-
Highest likelihood of V arrhythmias are within 1st 4 hours of STEMI
- For us, presenting sx of STEMI = V arrhythmias!!!!
6
Q
What is the medical management of atherosclerosis?
A
-
Statins
-
Statins reduce
- hepatic cholesterol synthesis,
- lower intracellular cholesterol,
- stimulate upregulation of LDL receptors,
- reduce the secretion of VLDL particles from the hepatocyte,
- and increase the uptake of non–HDL particles (small dense LDL, VLDL remnants) from the systemic circulation.(apo , apolipoprotein)
- statins help preserve renal function after aortic surgery and improve graft patency after LE bypass surgery
-
Statins reduce
- Antihypertensives
- Beta-blockers, ACE inhibitors
- Antiplatelet therapy
- Intensive glucose control
- Prevention of infection
- Cessation of smoking
- Diet modification
- Weight loss
- Exercise
7
Q
What are the 2014 ACC& AHA Preop eval guidelines?
A
-
Focus = evaluation of patient at risk for CV M&M undergoing non-cardiac surgery
- point of of preop eval is not to give medical clearance, but rather to perform an evaluation of patient’s current medical status, make recommendations concerning the evaluation, mgmt and risk for cardiac problems.
- overriding theme of preop eval is that intervention is rarely necessary to simply lower the risk associated with surgery unless such intervention is indicated, irrespective of the preop context
- Clinical History
- Clinical risk factors
- Exercise Tolerance
- Supplemental Evaluation
- ECHO and EF
- Stress test
- Perioperative Therapy
- Determine Surgical Procedure risk
- Low risk
- Intermediate risk
- High risk = >1% chance of MACE
8
Q
Recommendations for beta blocker admin perioperatively?
A
-
Beta blockers –> Bronchospasm, ↓ BP, ↓ HR
- Should be continued in all patients undergoing surgery who have been on beta blockers chronically
- in patients with intermediate or high-risk for myocardial ischemia noted in preoperative risk stratification, it may be reasonable to begin perioperative beta blockers (? Risk of stroke);
-
in patients with 3 or more RCRI risk factors (diabetes, HF, CAD, RI, CVA), it may be reasonable to begin beta blockers
- it may be better to start 2-7 days before surgery,
- beginning <1 day is at a minimum ineffective and may be harmful (should not be started day of surgery)
9
Q
DOS Beta blcoker admin recommendations?
A
- Historically: Routine admin periop BB
- Highly controversial d/t conflicting studies
- While confirming a decrease in cardiac events with aggressive preoperative beta-blockade, the POISE trial (extended-release metoprolol beginning on the day of sugery) → showed an increase in mortality and stroke risk
- Better to start 5-7 days preop
- On the other hand, DECREASE IV (fluvastatin + bisoprolol) demonstrated a cardioprotective effect of perioperative beta-blocker use without increased incidence in perioperative stroke or mortality
-
Recommendations: Indications for periop BB
-
Class I:
- BB continuation in patients who are already taking it
-
Class II/III:
- Pt w/ CAD
- multiple risk factors
- undergoing intermediate to high-risk sx (esp vascular sx) →
- *Start BB ~1 wk before sx
- *careful dose titration to avoid frank bradycardia or hypotension
- ↑ HR bad, but ↓↓HR just as bad for CAD
-
Class I:
- BB should not be used as initial/primary tx of tachycardia caused by periop events
- ex:
- hypovolemia
- anemia (demand ischemia biggest prob in CAD)
- pain
- infection
-
TREAT → underlying cause
- Tx of tachycardia caused by sympathetic stim should be considered in high-risk patients
- ex:
-
AVOID:
- Hypotension
- bradycardia
- Acute initiation of large-dose adrenergic blockade in periop period
10
Q
Recommendations for HTN perioperatively?
A
-
Autoregulatory curve shifted to right
- If BB started w/ degree of HoTN who cannot compensate for drop in BP → S/D ISSUE (increased morbidity)
- HTN Pointers:
- HTN grade 1: SBP < 180, DBP < 110 → OKAY to proceed w/ sx
- SBP > 180/DBP > 100 → cancel sx
- Avoid large BP fluctuations in chronic HTN pts
- Small doses/short acting
- Ex: NTG ready for carotids for small bolus for BP (40 mcg), have neo drip ready
11
Q
DOS recommendations for ACE/ARB?
What is the benefit for ACE/ARB admin?
A
- Controversy about the use of renin-angiotensin aldosterone system inhibitors in the perioperative period
- Admin of ACEIs and ARBs until DOS → hypotension under anesthesia
- Effects of ACEI continued in periop:
- significant vasoplegia
- inotropic support needed
- dysrhythmia
- renal dysfunction
-
mortality
- May be refractory to conventional therapy
- If stopped → make sure they are restarted as soon as feasible
- Decision to continue ACEI/ARB →
-
OPTIMIZE FLUID (hypovolemia risk → AKI)
-
Admin: alternative options
- Small doses vasopressin (1 unit/ml dilution → admin 3 units)
- methylene blue
-
Admin: alternative options
-
OPTIMIZE FLUID (hypovolemia risk → AKI)
- Effects of ACEI continued in periop:
- Most recent AHA guidelines say continuation is “reasonable” (Class II, LOE B)
- but many choose to hold due to refractory vasoplegia
- Pharm:
- Bradykinin → potent vasodilator
- ACE degrades bradykinin
- ACEI → Bradykinin no longer degraded → SE: cough & angioedema
- ARBS: fewer SE
- Not superior to ACEI
- ACEI/ARB Effects:
- Reduce degree of LV hypertrophy
- Improve mortality rates for CV insuff for actue MI, CV events, & HTN
-
Provide renal protection for DM
- DM1 & 2 nephropathy (opposite for pt w/ hypovolemia intraop)
- may improve plaque stability, endothelial function, prevent inflammation
12
Q
What are the ACC/AHA 2016 recommendations for DAPT following PCI for elective non-cardiac surgery?
A
-
ACC/AHA 2016 Update for DAPT following PCI for elective nonCV sx:
-
Drug Eluting Stents (DES):
- 2nd Generation: 6 mo
- 1st Generation: 12 mo
- Bare-Metal Stents (BMS): 30 days
-
P2Y12 inhibitors: (Clopidogrel) : 3 mo
- stopped for risk of perioperative bleeding
- BRIDGE: Continue ASA
- restart both ASAP
-
Drug Eluting Stents (DES):
- Elective nonCV sx after DES placement → 6 mo
- Urgent sx after DES placement: @ 3 mo → weight risk vs benefit of continuing or d/c DAPT
- Ex: Cancer sx
13
Q
What is some pertinent information to obtain for a vascular patient during H&P?
A
-
History: special attention to reveal concurrent undiagnosed ASCVD
- Angina
- TIA history (esp. w/in 2 wks → want to do CEA)
- Often proceeds stroke*
- Most challenging → vasomotor tone changed (BP swings)
- Peripheral ischemia
-
Co-morbid conditions → Evaluate
- DM
- pulmonary (typically smokers)
-
renal
- high risk post-op renal dysfx
- ex: w/ aortic cross-clamping
- high risk post-op renal dysfx
- Medication optimization/discuss DOS continuation/ holding
-
Physical exam
- Peripheral pulses, heart tones (gallop, murmurs- valvular issues), JVD, rales, SOB, peripheral edema, ABI
- Residual deficits from TIA or stroke
-
Labs/diagnostics
- evaluate need for additional testing if it is likely to change management
14
Q
What baseline labs and testing do you want to assess for vascular patients preoperatively?
A
- CBC
- Coagulation studies
- Metabolic panel
- Renal function
- Preoperative ECG
- Risk of periop/postop MI high → good to see changes even if one done
-
Consider:
- Cardiac bio-markers:
- Troponin
- BNP
- CRP
- ECHO- repeat (or initial) NEEDED in cases of: (elective sx)
- previously documented LV dysfunction
- worsening clinical status
- not done in previous year
- dyspnea of unknown origin
- Advanced cardiac testing
- Cardiac bio-markers:
15
Q
/
How do we determine if advanced cardiac testing is warranted preoperatively?
A
- Guidelines based approach
- ACC/AHA 2014 guidelines drive current managmenet
-
Goal = MEANINGFUL testing
- Overutilization leads to problems
- What does meaningful really mean?
- With a positive test, will we be able to reduce risk by adjusting or adding cardiac medications (e.g.,β-adrenergic blocker), direct coronary intervention (ex: PCI or coronary artery bypass grafting [CABG]),
- modifying/intensifying periop mgmt (ex: invasive hemodynamic monitoring) or
- changing preoperative plans (ex: performing endovascular aneurysm repair [EVAR] rather than open aortic repair).
- What does meaningful really mean?
- Overutilization leads to problems
-
3 Steps
- Step 1: Determine urgency of surgery
- Step 2: Evaluate for ACS or other major cardiac pathophysiology
- Acute coronary syndrome?
- Step 3: Estimate risk of major adverse cardiac events
- Based on risk index you will choose a path (see next slide)
- www.surgicalriskcalculator.com
- https://qxmd.com/calculate/calculator_195/revised-cardiac-risk-index-lee-criteria
- Note that the RCRI underestimates risk in vascular surgery
- Elevated risk of MACE is >1% calculated risk and requires further evaluation
16
Q
What is the stepwise approach to periop cardiac assessment for CAD? (Based on 2104 acc/aha guidelines)
A
-
Step 1: In patients scheduled for surgery with risk factors for or known CAD
- determine the surgery urgency
- Emergency → determine clinical risk factors that may influence perioperative management and proceed to surgery with appropriate monitoring and management strategies based on the clinical assessment.
- determine the surgery urgency
-
Step 2: If the surgery is urgent or elective
- determine if the patient has an ACS.
- If yes → refer patient for cardiology evaluation and management according to GDMT according to the UA/ NSTEMI and STEMI CPGs (18,20).
- If no → no more testing
- determine if the patient has an ACS.
-
Step 3: If the patient has risk factors for stable CAD
- Estimate the perioperative risk of MACE on the basis of the combined clinical/surgical risk.
- This estimate can use the American College of Surgeons NSQIP risk calculator (http://www.surgicalriskcalculator.com) or incorporate the RCRI (131) with an estimation of surgical risk. For example, a patient undergoing very low-risk surgery (e.g., ophthalmologic surgery), even with multiple risk factors, would have a low risk of MACE, whereas a patient undergoing major vascular surgery with few risk factors would have an elevated risk of MACE (Section 3).
- Estimate the perioperative risk of MACE on the basis of the combined clinical/surgical risk.
-
Step 4: If the patient has a low risk of MACE (<1%)
- No further testing is needed → proceed to surgery (Section 3).
-
Step 5: If the patient is at elevated risk of MACE
-
Determine functional capacity (METS) with an objective measure or scale such as the DASI (133)
- If the patient has moderate, good, or excellent functional capacity (4 METs) → proceed to surgery without further evaluation (Section 4.1).
-
Determine functional capacity (METS) with an objective measure or scale such as the DASI (133)
-
Step 6: If pt has poor (< 4 METs) or unknown functional capacity:
- Consult w/ patient and perioperative team to determine whether further testing will impact patient decision making (e.g., decision to perform original surgery or willingness to undergo CABG or PCI, depending on the results of the test) or perioperative care.
- Poor METs Yes → pharmacological stress testing is appropriate.
-
Unknown functional capacity → exercise stress testing may be reasonable to perform.
-
Abnormal stress test:
- consider coronary angiography and revascularization depending on the extent of the abnormal test.
- Pt then proceed to surgery with GDMT or consider alternative strategies (noninvasive treatment of the indication for surgery (e.g., radiation therapy for cancer) or palliation)
- Normal Stress test: proceed to surgery according to GDMT (Section 5.3).
-
Abnormal stress test:
- Consult w/ patient and perioperative team to determine whether further testing will impact patient decision making (e.g., decision to perform original surgery or willingness to undergo CABG or PCI, depending on the results of the test) or perioperative care.
- Step 7: If testing will not impact decision making or care → proceed to surgery according to GDMT or consider alternative strategies, such as noninvasive treatment of the indication for surgery (e.g., radiation therapy for cancer) or palliation. ACS indicates acute coronary syndrome
17
Q
What are the recommendations for preoperative coronary revascularization?
A
-
CABG or PCI
- Not recommended prior to even high risk surgery, unless revascularization is independently indicated according to current practice guidelines
- EXCEPTION: unprotected left main disease → benefit from pre-op revascularization (no collaterals)
- Aggressive medical therapy in advanced of surgery is beneficial (BBs, ASA, statins) in high risk patients
- Considerations:
- DEMAND ischemia → predominant cause of periop MI
- Stable plaques w/ periods of low BP, tachycardia → demand ischemia
- Perioperative strategies aimed at reducing potential triggers of coronary plaque destabilization and rupture may be more appropriate than those leading to coronary revascularization.
- DEMAND ischemia → predominant cause of periop MI
-
MI w/ no intervention:
- Wait > 60 days before elective noncardiac surgery
- these patients would ideally be getting aggressive medical therapy (above) in the meantime
- Wait > 60 days before elective noncardiac surgery
- MI with no intervention: wait at least 60 days before elective noncardiac surgery; these patients would ideally be getting aggressive medical therapy (above) in the meantime
- A revascularization procedure is rarely needed solely for the purpose of getting a patient through the perioperative period.
- Extensive cardiac evaluation before vascular operations can result in morbidity, delays, and patient refusal to undergo vascular surgery.
- Clearly, issues are involved that go beyond critical coronary lesions; perhaps the current understanding of the pathophysiology of perioperative MI is incomplete. For example, perioperative MI may be caused by culprit lesions (i.e., vulnerable plaques with high likelihood of thrombotic complications) often located in coronary vessels without critical stenosis.29
- For this type of MI (atherothrombotic), perioperative strategies aimed at reducing potential triggers of coronary plaque destabilization and rupture may be more appropriate than those leading to coronary revascularization.
Demand ischemia is likely the predominant cause of perioperative MI, which has been confirmed by** **a recent angiographic study.30
18
Q
When might additional pulmonary workup be necessary preop?
A
Patient population risk:
- Smokers/COPD pts typical
- Baseline hypercapnia (> 45 mmHg) → increases morbidity
-
Tx:
- STERIODS (short preop course)
- Epidurals (LE revascularization sx)
- may improve postop deep breathing/spirometry
- minimize resp dep d/t opioids
- Complications w/ sx: atelectasis, pneumonia, respiratory failure, and exacerbation of underlying chronic disease
-
Risk factors for morbidity:
- *Open aortic procedures (highest pulmonary morbidity)
- Baseline hypercapnia (> 45)
- Assessment:
- Severe pulm compromise → obtain PFTs
- Optimize pulm fx preop?
- Severe pulm compromise → obtain PFTs
19
Q
Renal workup around surgery for vascular patients?
A
- Chronic renal disease is common in vascular patients
- a/w increased risk for death
- LABS: Assess renal function periop
- Serum creatinine: > 2 mg/dL
-
Creatinine clearance: < 60 mL/min
- → HIGH risk postop complications
- Medications to decrease death risk in these patients:
- BB
- Statins
- CONTINUE meds
- Risk of renal ischemia with cross clamping
- Risk of emboli when clamps released
20
Q
What monitors are utilized during vascular surgery?
A
- Should we use every monitor available?
- A-line (preinduction?)
- Minimum invasive
- EKG (multi-lead analysis a MUST)*
- Know baseline ST segment*
- Lead II & V → Dx 90% intraop ischemia
- TEE
- CVP
- PA Catheter
- Brain monitoring (EEG, SSEP, MEP, cerebral oximetry)
- I-stat (BG), bedside coags
- Foley (UO)
- ASA monitors
- A-line (preinduction?)
21
Q
What are the general guidelines for MI prevention?
A
- Minimize interruptions in chronic pharmacotherapies
- Ex: Don’t stop BB, R vs. B ACEI, length of time for DAPT/ASA, continue statins, check BG
-
Management:
- BP w/in ~20% baseline
- Keep 10% higher than baseline while clamped
- Anemia
- Tx: Hgb < 10 w/ severe vascular dx
- Pain (multimodal/epidural anesthesia)
- Generous narcotics
- BP w/in ~20% baseline
-
Avoid:
- Tachycardia (HR < 85 bpm)
- Tachy → shortens diastole (diastole perfuses coronaries)
- Hypothermia (keep warm)
- Shivering → increase metabolic rate/increase MI risk
- Tachycardia (HR < 85 bpm)
-
Wait appropriate time after CV intervention:
- DES: 6 mos
- 3 mo if urgent sx
- BMS: 30 days
- CABG: no specific recommendation but must weigh urgency of procedure and optimization of patient
- DES: 6 mos
22
Q
Risk with carotid artery disease/stenosis?
A
- Strong association w/ ischemic stroke
- Ischemic stroke:
- 4th leading cause of death
- 87% = ischemic
- 13% = hemorrhagic
- Major cause of disability
- 4th leading cause of death
- Reduce risk:
- Control HTN, smoking cessation, and DAPT have reduced mortality
- Ischemic stroke:
- Peri-op Ischemic Stroke Risk:
- General population: 0.1%
- Carotid bruit (symptom free): 1.0%
- > 50% carotid stenosis: 3.6%
-
TIA:
- Any focalized neurologic deficit lasting < 24 hrs w/ no evidence of permanent infarction
- ~15% strokes are heralded by TIA 1st
- Recent TIA → most important risk factor for future stroke *
- Any focalized neurologic deficit lasting < 24 hrs w/ no evidence of permanent infarction
Note the frequent incidence at the branching of the CC into the IC and EC
→ at bifurcation where freq vessel occlusion occurs
23
Q
Anatomy review for cere bral vasculature
Where do the common carotids originate?
Where do the common carotids divide? branches?
Purpose of circle of willis?
A
- Common Carotid : Originate in thorax
- Right CC: originates at bifurcation of brachiocephalic trunk
- Left CC: originates from aortic arch
- Travel w/in carotid sheath
- At level of thyroid cartilage → each CC bifurcates into internal/external carotid arteries
- External CA branches:
- Superior thyroid
- Lingual
- Fascial
- Ascending pharyngeal
- Occipital
- Posterior auricular
- Internal CA
- Passes through neck w/o branching to enter the middle cranial fossa
- Enters middle cranial fossa through carotid canal of temporal bone
- Supplies:
- Major portion of supratentorial region of brain
- hypophysis cerebri
- orbit.
- Circle of willis provides collateral circulation to the brain
- **Many autopsies revealed anomalies in CoW
- Hypoplasia → most frequently noted anomaly (24%)
-
Incomplete circle d/t complete absence of a vessel (6%)
- Even anatomically intact COW → may not provide adequate cerebral blood if collateral perfusion compromised *
- Ex:
- contralateral carotid occlusive dx
- vertebral artery occlusive dx
- hypotensive pt compared to baseline.
- Ex:
- Even anatomically intact COW → may not provide adequate cerebral blood if collateral perfusion compromised *
Cross-clamping acutely disrupts blood flow to the ipsilateral hemisphere, even if flow was markedly diminished by severe stenosis. In this case, blood supply to the brain will depend entirely on collateral flow from an intact circle of Willis
24
Q
Review of barareceptor vs chemoreceptor function?
A
- Frequent incidence of clotting at high branches of CC into the IC and EC
- Likely to have stenosis
- Atherosclerotic regions can obstruct chemo/baroreceptor fx → make pt less sensitive to baroreceptors
- Manipulation/removal of plaque → causing variable reactions
- Baroreceptor Function
- Sense pressure changes by responding to change in tension of arterial wall (increase or decrease)
- Located in carotid sinus and in aortic arch
- Chemoreceptor function
- Sensitive to changes in arterial CO2, O2, and pH.
25
Q
When is a CEA indicated?
Preop issues? ASA PLAVIX continuation?
When do we want to perform a CEA?
What is the most common etiology behind neurological deficits after a CEA?
A
Most common major vascular surgery in U.S.
- Intervention for BOTH symptomatic & asymptomatic carotid stenosis
- Pooled analysis= no benefit to tx lesions < 50% stenosis
- Most benefit = >70% stenosis (need > 50% stenosis to see benefit)
- URGENT surgery
- Pooled analysis= no benefit to tx lesions < 50% stenosis
Pre-op issues
- CAD major source of M & M
- Treat all CEAs as if they HAVE CAD
- 0-4% incidence of MI
-
Medications:
- Do not D/C ASA
- Consider withholding Plavix for shorter period of time peri-op
- Operative risk increased if performed early after a neurological event
-
HOWEVER- Many CEA’s done shortly after neuro events since risk of acute stroke is high following TIA or stroke where deficits are mild/ resolving
- “index event” = stroke, TIA
-
HOWEVER- Many CEA’s done shortly after neuro events since risk of acute stroke is high following TIA or stroke where deficits are mild/ resolving
- “Most recent recommendations favor definitive intervention w/in 2 weeks of index event
- URGENT SURGERY —> TONS of BP swings, vasomotor off
- Extensive CV workup may not be feasible d/t urgency
- URGENT SURGERY —> TONS of BP swings, vasomotor off
-
Considerations:
- 65-95% neurological deficits during CEA from thromboembolic events (not HoTN)
- Bits of plaques become dislodged and go to brain → neuro event (wake extubation w/ good neuro assessment before)
- 65-95% neurological deficits during CEA from thromboembolic events (not HoTN)
- Treat all CEAs as if they HAVE CAD
Indications for surgery:
- TIAs with angiographic evidence of stenosis
- Reversible ischemic neurologic deficits w/ > 70% vessel wall stenosis or ulcered plaque (w/ or w/o stenosis)
- An unstable neurologic status that persists despite anticoagulation
26
Q
What is perfusion like to atherosclerotic regions?
A
- Autoregulation assumed to be lost in underperfused areas of brain.
- Vascular regions w/ chronic hypoperfusion and relative ischemia →
- Regions become:
- maximally vasodilated
- unresponsive to factors that induce vasoconstriction in normally reactive vascular beds.
- Regions become:
- Consequences: BF completely dependent on BP!
- D/t BF dependent on BP → avoid HoTN in period before BF is restored
- Vascular regions w/ chronic hypoperfusion and relative ischemia →
- Key point:
-
MAXIMALLY DILATED
- Cannot alter diameter of BV that we normally can (already maximally dilated)
-
PERFUSION IS BLOOD PRESSURE DEPENDENT
- Maintain BP w/in 10% baseline until reperfusion
-
MAXIMALLY DILATED
27
Q
CEA preop/monitoring anesthetic considerations?
A
- Preoperative
- Continue all long-term cardiac meds, aspirin, statins
- Other anti-platelet therapy (R vs B)
- Stop smoking
-
Continue:
- Aspirin
- Antihypertensives
- Statins
- Other anti-platelet therapy/when to stop
- If active cardiac conditions, esp. unstable CAD, consider need for workup
- CABG vs. CEA vs. combined procedure???
- Continue all long-term cardiac meds, aspirin, statins
- Anesthesia monitoring techniques:
- A-line w/ noninvasive BP in contralateral arm
- Consider awake A-line especially if severe ASCVD
- 5-lead EKG
- Leads II, V5
- ST analysis on (proper ischemia monitoring)
- multi-lead analysis
- (2) 18G IV catheters
- secured & running well as both arms are tucked (one for maintenance the other for vasoactive drugs)
- Brain monitoring- EEG, SSEP, MEP, NIRS/Cerebral oximetry
- Good to know if surgeon routinely shunts or not
- Foley Catheter
- Positioning:
- Arms tucked
- head in horseshoe
- Evaluate ability to tolerate turning (nonop side) and extension of neck pre-op
- may have bilateral disease
- Evaluate ability to tolerate turning (nonop side) and extension of neck pre-op
- A-line w/ noninvasive BP in contralateral arm
28
Q
What is the purpose of shunting in CEA?
Risks of shutting?
A
-
Maintains cerebral perfusion in absence of adequate collateral circulation
- Bypasses arteriotomy site
- enables partial antegrade blood flow from CCA → ICA → brain
- Variation among surgeons
- Some shunt everyone
- Some base decision on EEG after clamping
- Ipsilateral attenuation on EEG → will want shunting (or increase BP if not shunting)
- Some never shunt
- Found to be unnecessary in up to 85% of patients
-
Risks of shunting:
- Air/plaque embolization
- Carotid dissection/artery damage
- Nerve injury
- Hematoma
- Infection
- Increased risk of long-term restenosis
- TO Shunt or NOT TO Shunt???
- Surgeon preference
- EEG changes noted after CCA and ICA clamped to dissect plaque
29
Q
Main goals for anestheisa in CEA?
Intraop BP considerations?
CO2 considerations?
What do we want to avoid in CEA?
A
Goals:
- Prevent ischemia
- control hemodynamics
- minimize pain/stress responses
Preop:
-
Avoid BZD
- if needed, very small doses midaz à want FULL WAKE UP for neuro assessment
Intraop:
-
High-normal BP (20% of baseline)
- watch for baroreceptor reflex
- (HoTN and bradycardia à get anti-cholinergics), if use local at site à will help
- Communicate preinduction BP to surgeon → calculate tolerated 20% baseline
- watch for baroreceptor reflex
-
Normocapnia –> don’t want cerebral steal with hypocapnia (divert blood flow away from diseased areas)
-
Hypocapnia/hyperventilation → causes cerebral vasoconstriction
- Decrease cerebral BF w/ maximally dilated vessels that cant further respond → other vessels constrict, dx vessels cant constrict–> minimizing blood flow to brain= bad
- Barash:
- *Normocapnia should be maintained during CEA. Hyperventilation (hypOcapnia) may lead to cerebral vasoconstriction and decrease cerebral blood flow during critical periods of carotid cross-clamping.
- Hypercapnia/Hypoventilation may be equally detrimental if it leads to dilation of the cerebral vasculature in normal areas of the brain, whereas vessels in ischemic areas are already maximally dilated and are unable to further respond. The net effect is a “steal” phenomenon with diversion of blood flow from hypoperfused to normal areas of the brain.
-
Hypocapnia/hyperventilation → causes cerebral vasoconstriction
Avoid
- hyperglycemia < 200 mg/dL
-
Stress on heart
- Ex: avoid BP extremes, lg. vasopressor doses - especially large/prolonged phenylephrine infusions
-
Fluid overload
- no dextrose-containing solutions
- not big EBL
- give 1L total
Medication techniques:
-
Esmolol
- blunt noxious/sympathetic stimuli (short acting!)
-
NTG or other short-acting agents
- Tx: HTN
- Nicardipine (Cardene) → causes tachycardia
- Start w/ labetolol then add Hydralazine (BB then use vasodilator)
- Tx: HTN
- Phenylephrine (small doses)
- Heparin → 10,000 units
30
Q
GA vs Regional with CEA?
A
GA
- General approach: minimize hemodynamic swings
- BP w/in 20% of baseline (shift in autoregulatory curve → Right shift)
- Short acting agents only
Regional anesthesia
- Must evaluate candidacy if considering awake (regional)
- No claustrophobia; must be able to speak/ communicate; no orthopnea (SOB when flat); ability to lay flat for an extended period (consider those with chronic pain/ arthritis/ back pain potentially poor candidates)
- Must be prepared for urgent conversion to general
- Conversion rate to GA → < 5%
- Decision based on pt, anesthesia, and surgeon preference because there is no clear outcome advantage
-
Considerations:
- TIVA techniques:
- More rapid wakeup w/ remi & propofol
- Less emetogenic (N/V) over VA
- TIVA techniques:
31
Q
Induciton considerations with GA for CEA?
A
- Pre-induction: avoid BZD or dose conservatively
- Standard monitors
- A-line precedes induction for sicker pt’s
- 1 good IV; second can be placed following induction
- Both vasoactive and anti-hypertensive infusions prepared (short acting)
- Smooth induction
- LTA
- Propofol or etomidate (both decrease CMRO2); selection based on co-existing disease
- +/- Esmolol → blunt sympathetic response to DL
- NMB (check on neuromonitoring)
- Short acting opioids only and in small doses (do not want to delay emergence)
- NMB helpful because you will run these patients in a lighter plane to avoid interference with neuromonitoring (cannot usually use with MEP beyond induction)
- ETT
- LMA possible (not common) → less stimulating/hemodynamic changes during induction
- Local anesthetic infiltration at site
- good opioid sparing strategy
- helps with hemodynamic swings (per surgeon)
- BP response during intubation:
- Unpredictable
- Prepare for immediate tx
- HoTN: Phenylephrine 50-100 mcg
- HTN: Na nitroprusside 5-25 mcg or clevidipine 100-250 mcg
- Poorly controlled HTN (DBP > 100) typically intravascularly depleted → severe HoTN during induction
- Preinduction fluid bolus
32
Q
GA Maintenance considerations for CEA?
A
-
Maintenance:
- watch ABP closely- especially once clamped
- avoid BP swings (has to be up!! Since using collateral circ)
- Balanced anesthetic technique (VA & TIVA)
- TIVA preferred with EP monitoring
- Your choice of VA but consider need for rapid emergence and do not exceed 1 MAC
- Neuromonitoring:
- ½ MAC volatile with IV supplementation is okay
- DO NOT allow hypotension while clamped- esp with contralateral dz
- Use shortest acting agents to treat labile BPs
- watch ABP closely- especially once clamped
- Volatile HD 2° proximity to carotid sinus baroreceptors
-
Carotid sinus manipulation → Rapid, severe, transient bradycardia
- inform surgeon
- atropine/ glycopyrrolate available
-
Patho:
- Normal: baroreceptors and carotid sinus involved in BP and HR regulation.
-
Patho: Plaque formation on intimal layer of carotid bifurcation → receptors have decreased contact w/ BF → gradually decrease sensitivity to stimuli
- During dissection → Carotid sinus manipulation feels intense d/t barorecptors not normally stimulated → elicit heme instability, rhythm changes (significant bradycardia)
- Bradycardia → decrease CO, compromise organ perfusion
- Tx: Let surgeon know, have atropine/glyco
- During dissection → Carotid sinus manipulation feels intense d/t barorecptors not normally stimulated → elicit heme instability, rhythm changes (significant bradycardia)
-
Carotid sinus manipulation → Rapid, severe, transient bradycardia
- Minimal EBL; no large fluid requirement
- Heparinize before cross-clamp applied
- ACT 200-250 seconds
- Cross-clamping is a critical portion of the case & BP must be maintained
35
Q
EEG monitoring basics?
A
- Normal CBF: 50 ml/min/100g brain tissue
- Most common finding during ischemia: ipsilateral slowing or attenuation
- Bilateral changes = anesthestic (too deep)
- Ipsilateral changes* = more likely ischemia/surgery
- Sensitivity of EEG is poor- up to 40% of ischemia may go unrecognized with EEG
- high false-negative
- Deep brain structures are not being measured with EEG
- cortical structures only
- Prone to erroneous interpretation with changes in anesthetic depth- especially with propofol
- Ask EEG tech if slowing is ipsilateral or bilateral; more likely to be the anesthetic if bilateral changes noted.
50
Q
Open abdominal aortic aneurysam repair overview of procedure
A
- Challenging Intraoperative Management
- Aortic cross clamping
- hemodynamic changes/metabolic changes
- renal impairment
- spinal cord damage
- bowel ischemia
- Unclamping
- hemodynamic changes/metabolic changes
- effect anesthesia management
- Aortic cross clamping
Pic:
- left top and bottom
- clamps are placed across aorta and common iliac arteries
- anerysm is opened
- clot is removed
- inimtal lining is repaired
- right top and bottom
- a graft is sutured between upper and lower ends of aorta
- preserved wall is wrapped around the graft
- the clamps are removed to allow blood flow
51
Q
What determines the effect of aortic cross clamp?
What are some effects of cross clamping?
A
Pathophysiology depends on:
- 1. Level & duration of clamp
-
2. Volume status of patient
- 2 most important predictors of outcomes while clamping*
- extent of CAD
- myocardial function
- degree of arterial collateralization (chronic pts w/ collateral flow → do better!)
- anesthetic agents used
- vasodilators used
- body temperature
- neuroendocrine activation
Clamping effects
- Little to no effect on HR
- Effects:
- Catecholamine surge
- ↑ SVR and MAP as a result of the sudden impedance to aortic flow
- Extent depends on cross clamp level applied
- Ex:
- infrarenal cross-clamping → ↑ BP 2%-10%
- Supraceliac clamp → ↑ MAP up to 50%
- Ex:
- ↑ or ↓ in cardiac preload, central filling pressures, and CO → depends on where clamp located
- Catecholamine surge
- BV redistribution occurs proximal to clamp placement
- Lower clamping →
- BV shift into compliant splanchnic vasculature –> all redistributes to gut (wont really see change)
- like a reservoir for majority of autotransfusion
- splanchnic organs hold 25% total BV
- > 800 ml can be autotx to systemic circ in seconds
- like a reservoir for majority of autotransfusion
- Increases in plasma epinephrine & norepinephrine = venoconstriction of splanchnic capacitance vessels – translocates blood to central circulation. Infraceliac cross-clamping is relatively well tolerated compared with supraceliac crossclamping.
- BV shift into compliant splanchnic vasculature –> all redistributes to gut (wont really see change)
-
Supraceliac cross-clamp → don’t have ability to shift BV to splanchnic vasculature (not going to compliant gut) →
- ↑ VR
- ↑ central filling pressures
-
↑ CO
- ↑ myocardial workload – large 90% develop new LV wall motion abnormalities d/t acute ↑ in BV –> HARD on already sick heart (especially those with CAD or decreased EF)
- Lower clamping →
Supraceliac has most significant impact on MAP, PAP and EF
53
Q
What si the systemic hemodynamic response to aortic crossclamping?
A
- Passive recoil distal to clamp → ↑ preload
-
↑ Catecholamines (and other vasoconstrictor) →
- Active venoconstriction proximal and distal to clamp →
- leading to ↑ preload
- Active venoconstriction proximal and distal to clamp →
-
↑ Ao flow impedance
-
→ ↑ afterload
-
Overall:
- ↑ Preload
- ↑ Coronary flow
- ↑ Afterload
-
↑ contractility → ↑ CO
- But if no ↑ in coronary flow or contractility → ↓ CO
-
Overall:
-
→ ↑ afterload
- Systemic hemodynamic response to aortic crossclamping (AoX).
- Preload does not necessarily increase.
- Most dramatic and consistent effect →
- ↑ SVR and MAP (result of sudden aortic flow).
54
Q
What is the blood volume redistribution following aortic cross clamp placement?
A
- Passive venous recoil distal the aortic cross-clamp →
- Result: shift BV from distal to aortic occlusion to proximal to the occlusion.
- 1. Aorta occluded above celiac axis level → splanchnic reserve redistributed to organs and tissues proximal to the clamp.
-
2. Infraceliac cross-clamp placed →
- BV shift into splanchnic system
- Shift into other organs proximal to clamp
- The ability to shift into or out of the splanchnic vasculature accounts for variability in preload augmentation.
- Result: shift BV from distal to aortic occlusion to proximal to the occlusion.
56
Q
What determines pathophys during aortic unclamping?
Hemodynamic changes during unclamping?
Metabolic changes during unclamping?
A
Aortic Unclamping
- Pathophysiology depends on:
- Level of clamp
- Duration of clamp time
- Use of diverting support
- Intravascular volume
Aortic Unclamping: Hemodynamic Changes
- Drop in SVR up to 80% *
- ↓ Myocardial contractility
- ↓ CO
- ↑ PAP
- Release of inflammatory mediators →
- increase pulmonary vascular resistance
- Pulmonary edema
- ↓ Arterial blood pressure
- ↓ Central venous pressure
- ↓ Venous return
- ↓ LV pressure
- Relative central hypovolemia develops as blood pools in tissues distal to crossclamp
Aortic Unclamping: Metabolic Changes
- ↑ Total-body oxygen consumption
- ↑ Lactate
- ↓ Mixed venous oxygen saturation
- ↑ Prostaglandins
- ↑ Activated complement
- ↑ Myocardial depressant factor(s)
- ↓ Temperature
- Metabolic acidosis**
PIC: A complex cascade of events, including release of inflammatory mediators, distal vasodilation, increased vascular permeability, and decreased myocardial contractility results in a relative central hypovolemia, decreased cardiac output/VR, and systemic hypotension.
63
Q
Describe the perfusion to the spinal cord and the role of radicular artery distrubiton in maintaining spinal cord perfusion.
A
- The spinal cord is supplied primarily by the single anterior and paired posterior spinal arteries, arising from the posterior circulation.
- Posterior spinal arteries supply approximately 25% of spinal cord blood flow and supply the sensory tracts of the posterior columns.
-
Anterior spinal artery supplies anterolateral cord
-
Includes: motor tracts
- supplies 75% of SC flow.
-
Includes: motor tracts
-
Anterior spinal artery is fed by a series of radicular arteries
- arising from the aorta, although collateralization is variable.
- This leaves areas of the spinal cord vulnerable to watershed ischemia, particularly with aortic occlusion or prolonged hypotension.
- Most important radicular artery supplying the thoracolumbar cord is derived from the artery of Adamkiewicz.
- The artery of Adamkiewicz originates between T8 and T12 in 75% of cases and at the level of L1 or L2 in an additional 10% of cases.
Artery of Adamkiewicz- presence at T11-12
Radicular arteries present throughout thoracic and abdominal aorta
64
Q
What can we do to prevent spinal cord damage during aortic cross clamp?
A
- *Short cross clamp time & total surgical time
- Optimization of cardiac function
-
CSF lumbar drainage (most common in thoracic repairs)
- Goal = CSF pressure < 12 mmHg
- Rationale: SC pp can be augmented by →
- Increasing forward driving pressure (MAP)
- w/ Aneurysmal dx & vascular reconstruction→ best not augment MAP
-
Relieving any obstructing pressure (CSF)
- Autoregulatory mech w/ AoX → increase CSF (lowers SC pp)
- → CSF drainage improves SC perfusion
- Autoregulatory mech w/ AoX → increase CSF (lowers SC pp)
- Increasing forward driving pressure (MAP)
- Rationale: SC pp can be augmented by →
- Goal = CSF pressure < 12 mmHg
- Hypothermia: prolongs the safe ischemic time for the SC
PIC: Relationship between spinal cord injury and length of aortic occlusion
67
Q
What is the crawford classification of TAA?
A
- Type I - Aneurysm involving descending thoracic and upper abdominal aorta
-
Type II –
-
Descending thoracic and most abdominal aorta
-
Greatest risk:
- Paraplegia
-
Renal failure
- d/t ischemia during crossclamp even w/ extracorporal circulatory support
-
Greatest risk:
-
Descending thoracic and most abdominal aorta
-
Type III –
-
Lower thoracic aorta and most abdominal aorta
-
Type II & III → most difficult to repair
- à involves the thoracic and abdominal segments of the aorta
-
Type II & III → most difficult to repair
-
Lower thoracic aorta and most abdominal aorta
- Type IV - most or all abdominal aorta
68
Q
What ist he DeBakey classification of dissecting aortic aneurysms?
A
- Type I - ascending aortic tear with dissection down entire aorta
- Type II - tear in ascending aorta with dissection limited to ascending aorta
- Type III - tear in proximal descending thoracic aorta with dissection from thoracic aorta to abdominal aorta
71
Q
What is the effect of aortic cross clamping during thoracic repairs?
A
- AoX (Thoracic) → BV shift to brain → increase ICP
- → decrease SC pp and flow
- Ao distal pressure decrease
- Ao proximal pressure increase
- Spinal cord blood flow and perfusion pressure during thoracic aortic occlusion, with or without sodium nitroprusside (SNP) infusion.
- The changes (arrows) represent the response to aortic cross-clamping per se.
- SNP+ - SNP aggravates the effect of cross-clamping;
- SNP- = SNP counteracts the effect of cross-clamping
- AoX - aortic cross-clamping; Ao = aortic; ICP = intracranial pressure; [arrow up] and [arrow down] increase and decrease, respectively.
78
Q
What is the technique for endovascular stent grafting?
A
- Pre-op aortic anatomy studied extensively via radiological exam
- high IV contrast load – may need diuretics, mannitol
- Bilateral groin incisions
- used for access to femoral or iliac arteries
- Occasional extensive retroperitoneal surgical incisions required for vascular access with unusual anatomy- small femoral and iliac arteries, etc.
- Supine position – arterial sheaths introduced 16-27F
- Expandable stent is deployed
80
Q
What are the different classifications of endo leaks?
A
- Type I- high flow leak adjacent to a stent that is not sealing the sac from the systemic circulation (requires immediate intervention).
- Type II—low flow leak due to arterial branches that have been excluded by the stent (can be treated with embolization).
- Type III—failure with the stent itself or at its junction with another stent (requires immediate recognition and treatment).
- Type IV—porosity in the stent (often resolves with reversal of anticoagulation).
- Type V (endotension)—persistent or recurrent pressurization of the aneurysm sac despite no detectable endoleak.
