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What are some risks of major vascular surgery?

  • 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


What are the branches that come off the aortic arch?

  1. Brachiocephalic trunk (innominate)
    1. right common carotid artery
      1. right internal carotid
      2. right external carotid artery
    2. right vertebral artery
    3. right subclavian artery
      1. continues on to become right axillary artery then right  brachial artery
  2. left common carotid
    1. left internal carotid artery
    2. left external carotid artery
  3. left subclavian artery
    1. left vertebral artery


Branches of abdominal aorta?

(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




What are the layers in an artery and vein?

  • Tunica intimar
  • tunica media
    • artery have larger amount of smooth muscle/elastic fiber
  • tunica externa (Adventitia)
    • has collagen, elastic fibers, vasa vasorum (blood supply for arteries themselves)


artery- thicker media, relatively narrow lumen

vein- larger lumen, adventitia is thickest layer, intimar folds to form valves


What is the pathophysiology of atherosclerosis?

  • 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


Progression of atherosclerosis?

  • 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.)


What are 3 types of atherosclerosis morbidity?

  • 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!!!!


Where are the locations that have the highest percentage of atherosclerotic lesions?


aortoiliac peripheral


Risk factors for atherosclerosis?


  • DM (glucose intolerance/insulin resistance)
  • Abdominal obesity
  • Atherogenic dyslipidemia- Increased LDL and TGs, decreased HDL
  • Chronic Inflammation/ Pro-inflammatory state
  • HTN
  • Smoking
  • Renal Insufficiency – huge predictor!


What is the medical management of atherosclerosis?

  • 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
  • Antihypertensives
    • Beta-blockers, ACE inhibitors
  • Antiplatelet therapy
  • Intensive glucose control
  • Prevention of infection
  • Cessation of smoking
  • Diet modification
  • Weight loss
  • Exercise


What are the 2014 ACC& AHA Preop eval guidelines?

  • 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


What are the preop recommnedations for ASA?

  • Aspirin --> inhibits platelets -->potential bleeding and GFR
    • ASA should be continued until day of surgery, especially for carotid and peripheral cases.
    • Recent study “RECO” reported d/c of ASA for more than 5 days in patients with coronary stents increased risk of major adverse events. Regarding GFR --> monitor fluid and urine status closely.  May preclude use of regional.


Recommendations for plavix preop?

  • Plavix --> inhibits platelets --> potential bleeding
    • Held for 7-8d except CEA/severe CAD
    • Plavix general recommendation is that it should be held for 7-8 days prior to surgery, except for CEA and severe CAD, consider T&C blood products,
    •  Avoid regional anesthesia if not d/c’d more than 7 days prior to surgery.  Recent study states may be able to continue up to 2 days pre-surgery in high risk PVD cases without increasing risk of major blood loss.


Statin preop admin recommendations?

  • Statins --> liver function
    • Assess liver fxn test and continue through morning of surgery
      • statins reduce the production of free radicals and increases LDL resistance to oxidation
      • they improve plaque stability and prevent thrombus formation- it has been shown that continuing statins during hospitalization after MI or major surgery decreases M and M – less likely to die) .
    • Statins also appear to improve vascular surgery outcome – i.e. graft patency, limb salvage, lower risk of ultimate amputation.  If not on statins, should start


ACE inhibitor reocmmendations periop?

  • ACE Inhibitors--> induction hypotension, vasoplegia, coughing
    • ACE inhibitors ->>angiotensin converting enzymeà controversial. possible to continue through perioperative period vs. hold
    •  most HOLD due to potential for refractory vasoplegia and renal injury with hypovolemia, if administering, consider half dose on morning of surgery
      • they have also shown to improve plaque stabilization- keeping the fibrous cap from rupture
    • New guidelines recommend that ACE inhibitors are only restarted after patient is euvolemic to avoid renal dysfunction/damage.


Recommendations for Calcium channel blocker preop?



  • Diuretics ---> hypovolemia, electrolyte imbalance
    • Monitor fluid and urine status, continue through morning of surgery
  • Ca+ Channel blockers --> hypotension
    • Continue through perioperative period, consider holding amlodipine morning of surgery (causes most hypotension)


Recommendations for hypoglycemic drugs?

  • Hypoglycemic drugs --> hypoglycemia, lactic acidosis with metformin
    • monitor blood glucose throughout,
    • switch to insulin to manage DM perioperatively with BS goal 140-180 mg/dL
      • avoid tight management (80-110) 
      • also avoid BS >200
        • both extremes confer risk
    • PRE-OP: hold sulfonyureas; hold metformin


Recommendations for beta blocker admin perioperatively?

  • 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)


DOS Beta blcoker admin recommendations?

  • 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
  • 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
  • AVOID:
    • Hypotension
    • bradycardia
    • Acute initiation of large-dose adrenergic blockade in periop period


Recommendations for HTN perioperatively?

  • 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


DOS recommendations for ACE/ARB?

What is the benefit for ACE/ARB admin?

  • 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
  • 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 pops
        • DM1 & 2 nephropathy (opposite for pt w/ hypovolemia intraop)


What are the recommendations for DOS Anti-platelet therapy?

Anti-Platelet Therapy (APT).   (FYI DUAL APT = DAPT)

  • Multidisciplinary approach (bridge with something else?)
    • Surgical interventions may be classified as either high, medium, or low risk for bleeding complications.
    • APT used in coronary revascularization, prior cardiac valve, or in presence of CA/vascular stents and CV support devices
      • Look for possibility of bridging agent
  • Risk vs. Benefit:
    • APT benefits in reducing thrombotic risk and MACEs should be weighed against the impact on surgical bleeding
    • D/c DAPT after stent implantationstrongest predictors of stent thrombosis
      • magnitude of risk is inversely proportional to timing of noncardiac surgery after PCI


What are the ACC/AHA 2016 recommendations for DAPT following PCI for elective non-cardiac surgery?

  • 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
  • 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


DOS recommendations for alpha2 agonists?

Alpha-2 Agonists (Clonidine- BP mgmt)

  • POISE-II trail (n= >10k): increase incidence
    • significant HoTN
    • nonfatal cardiac arrest
  • most recent ACC/AHA guidelines state that α2-agonists are not recommended for prevention of MACE in patients undergoing noncardiac surgery (Class III; LOE B)
  • Exception:
    • Abrupt d/c in chronic users → consequences:
      • Rebound sympathetic surge
        • Profound HTN
        • Tachycardia
      • Diaphoresis
      • Pulm edema
  • Must weigh relative risks and benefits of continuing versus withdrawing


What is some pertinent information to obtain for a vascular patient during H&P?

  • 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
    • 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


What baseline labs and testing do you want to assess for vascular patients preoperatively?

  • 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)
      • 1. previously documented LV dysfunction
      • 2. worsening clinical status
      • 3. not done in previous year
      • 4. dyspnea of unknown origin
    • Advanced cardiac testing



How do we determine if advanced cardiac testing is warranted preoperatively?

  • 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).
  • 3 Steps


What is the stepwise approach to periop cardiac assessment for CAD? (Based on 2104 acc/aha guidelines)

  • 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.
  • 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
  • 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 ( 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).
  • 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).
  • 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).
  • 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


"Bottom line" for further cardiac testing for vascular surgeyr patients?

  • “Further cardiac testing (in the form of stress testing or cardiac catheterization) is reasonable if the results of the additional testing will change management decisions (e.g., coronary revascularization prior planned surgery or alternate plan for palliative care)” 
  • Most vascular surgery patients will fall in the elevated risk category and many will have poor to unknown functional status due to comorbid conditions → additional cardiac testing is not unreasonable prior to major vascular procedures


What are the recommendations for preoperative coronary revascularization?

  • 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.
  • MI w/ no intervention:
    • Wait > 60 days before elective noncardiac surgery
      • these patients would ideally be getting aggressive medical therapy (above) in the meantime
  • 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