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What is a pro/con to direct reconstruction (anatomic reconstruction)?

What is a pro/con to extra-anatomic reconstruction?

  • Aorta-iliac bypass
  • Normal anatomy (left)
  • Percutaneous revascularization (top right)
  • Surgical revascularization (bottom right)
    • Direct reconstruction
      • Higher morbidity (more complications)
      • Better long-term patency
      • Aorto-Fem; Fem-Pop; Fem-Tib; etc
    • Extra-anatomic reconstruction (reconstruction does not mimic normal anatomy?)
      • Reduced morbidity
      • Long term patency inferior to direct reconstruction
      • Fem-Fem; Ax-Fem

Extra-anatomic bypass is typically reserved for patients deemed particularly high risk for direct surgical reconstruction such as previous graft or stent complication, infection, or previous intra-abdominal surgery with resultant abdominal adhesions. Open revascularization of infrainguinal disease depends on the level of the lesion(s), and may involve the femoral, popliteal, or infrapopliteal vessels.


Risk factors for PAD?

Indications for surgery?

first symptom PAD?

Lower Extremity PAD

  • The same risk factors that lead to PAD also cause:
    • CAD (50% concurrence)
    • CVD
    • Aortic vascular disease
  • Indications for surgery for PAD
    • gangrene, ischemic ulceration, & intermittent claudication/ischemic rest pain
  • PAD patients are at high risk for adverse CV events
    • Previous graft/stent complications, abdominal adhesions
  • Intermittent claudication often first symptom
    • Slow, progressive decline in function

Risk factors for PAD

  • Nonwhite
  • Male
  • Age > 50 yo
  • Smoking
  • DM
  • HTN
  • HLD
  • Chronic renal insufficiency
  • Hyperviscous/hypercoaguable states
  • Hyperhomocysteinemia
  • Elevated inflammatory markers
    • Vulnerable to stoke, MI, death
      • Tx: Antiplt, anticoagulation medications → when stopped, high risk for periop event


Outcomes of patients with PAD?

  •  Individuals with atherosclerotic lower extremity PAD may be
    • asymptomatic (without identified ischemic leg symptoms, albeit with a functional impairment)
    •  OR have leg symptoms (classic claudication or typical leg symptoms) 
    • OR present with critical limb ischemia (  CLI  ). 
  • All individuals with PAD face a risk for
    • progressive limb ischemic symptoms
    • high short-term cardiovascular ischemic event rate 
    • increased mortality.
  • These events rates are most clearly defined for individuals with claudication or CLI and less well-defined for individuals with asymptomatic PAD. 


FROM PIC- doubtful we need to know specifics. overall takeaway is these are sick patients with very high moribidty/mortality


What are indications for peripheral revascularization for acute ischemia?

  • Acute ischemia patho:
    • emboli
    • thrombus
    • pseudoaneurysm postop from femoral arterial line
  • Irreversible ischemic damage:
    • occurs 4-6 hours
    • Urgent thrombolytic therapy and or angioplasty
    • Arteriography → assess flow
    • Surgical intervention (emergency case → with full stomach?)


What are indications for peripheral revascularization with chronic ischemia?

  • Chronic limb ischemia: demand > supply
    • s/s: Rest pain, ulceration, gangrene
    • Often present with multi-segmental occlusion
    • Patho:
      • atherosclerotic plaques progressively narrowing vessel → claudication w/ eventual thrombosis of vessel
  • Surgery indicated when:
    • severe disabling claudication
      • unable to establish METs → will need CV testing (cant walk w/o severe pain)
    • critical limb ischemia (limb salvage)
    • ankle-brachial index (ABI) is clinical standard for documenting severity of PVD
  • Semi-elective sx (time to optimize)


What is the ankle brahcial index?

  • ABI <0.9= PAD diagnosis
  • Performed by taking systolic pressure in arms and in legs. Patient should rest supine in warm from for 10 minutes prior to testing
    • highest average ankle pressure/highest average arm pressure
    • each side done separately


What is the traditional surgical approach for peripheral occlusions?

  • Unobstructed blood flow source (donor) artery exposed. Ex:
    • common femoral
    • superficial femoral
    • deep femoral
  • Target distal artery (recipient) is exposed at or below the knee.  Ex:
    • dorsalis pedis artery
    • posterior tibial artery
  • If saphenous vein used →
    • vein dissected all branches ligated → divided and excised (reversed - permits blood flow in direction of valves).
  • Proximal anastomosis first with clamping, then can unclamp and move distal
  • Bypass area with graft that has reduced flow


Summary of Fem-Pop bypasS?

Anatomic Bypass: ex. Fem-Pop

  • After donor and recipient arteries are exposed a tunnel is created and graft is passed
  • Graft may be saphenous vein or prosthesis
  • Femoral cross clamping is required
    • Fewer hemodynamic changes than with AoX
  • Heparin IV given
  • Anastomosis constructed
  • Arteriogram to confirm adequate flow
  • Heparin not likely to be reversed


Summary of aorto-fem bpyass?

Anatomic Bypass: Aorto-Fem

  • Aortic cross-clamping (Aox) and uncross-clamping is required
    • better tolerated than for aneurysmal disease
      • more distal clamp location (why its more tolerated)
      • likelihood of extensive collateralization related to chronic atherosclerotic disease → tolerate crossclamp better w/ collaterals
        • Note: with aneurysms this collateral flow is not present


What type of patient is more likely to undergo an extra-anatomic bypass (ie ax-fem/fem-fem bypass)?

Considerations for the procedure?

Do  they need to cross clamp during the procedure?

Extra-Anatomic Bypass:

Ax-Fem/ Fem-Fem

  • Reserved for high risk patients → examples:
    • previous graft or stent complication
    • infection
    • adhesions from previous abdominal surgery
  • No need for Aox and uncross-clamping
  • Frequent site:
    • axillary artery to ipsilateral femoral artery
    • with +/- fem-fem
  • Considerations:
    • Less durable → 5 year patency
    • Art-line must be on opposite side of Ax-fem site
      • → Axillary artery clamping
    • Tunneling (mid-axillary)
      • *key point in the surgery à MOST STIMULATING PART
        • Deepen anesthetic!


Preop management of LE Revascularization procedures?

  • Preop – beta-blockers and/or other chronic medication
  • A-line*
    • (plan for very difficult insertion- US recommended)
  • Adequate vascular access -->min EBL though
  • Continuous EKG monitoring + ST analysis
  • Monitor volume status
    • Foley catheter
    •  +/- CVP or PA catheter/ TEE (more likely needed for Aorto-fem with Aox
    • Non-invasive/ minimally invasive hemodynamic monitoring
  • I stat/ Hemochron to follow labs (coag status)
  • For emergency surgery: carefully watch →
    • K+ levels
    • acidosis
    • Myoglobinemia
    • Coagulation status
    • ECG ischemia
    • fasciotomy may be required (compartment syndrome)


Regional vs general for LE revascularization procedures?

Regional vs. General

  • 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
    • Perfusion to limbs (Regional > GA)
    • Studies regarding efficacy of post-op pain mgt. w/ epidural vs. opioids are poorly designed


What is graft occlusion higher with GA versus RA?

Hypercoagulable state with GA as opposed to RA


  • With GA →
    • Decreased Fibrinolysis → fibrinogen not broken down and clots form
    • Increased Epi, NE, and cortisol release (compared to RA)
  • Patency of graft maintained with RA secondary to increased blood flow with sympathectomy


Anesthetic maintenance with LE revascularization?

  • AVOID Vasopressors
  • Keep warm
  • GA --> balanced anesthetic with opioids, inhalation agent, nitrous oxide, neuromuscular blocker
    • Minimal opioids to facilitate extubation
      • Do have postop pain
    • Deepen anesthetic level during the tunneling phase
      • Example: 3-5 mcg/kg fentanyl
    • Avoid hemodynamic extremes – short acting β blockers intraop often necessary
  • RA --> L1-L4 dermatomes (T10 level adequate)
    • Epidural dosing usually - 9-12 ml including test dose
      • Remember elderly patients require decreased dosing!


Postop managmeent for LE revascularization procedures?

  • Control Pain and anxiety
    • High risk for MI in this period - stress reduction essential!
    • Epidural catheter is beneficial for postop pain control but must consider use of anticoagulants
  • Avoid Anemia
  • Control HR and BP
  • Frequent checks of peripheral pulses (doppler)
  • Continuous EKG monitoring + ST analysis


Review of abdominal aorta branches?

What is critical during abdominal aorta surgery?

*Higher clamp → more complications pt will have*

Review and be prepared to discuss branches and levels.

  • abdominal branches
    • inferior phrenic
    • middle suprarenal
    • celiac 
    • first lumbar
    • Superior mesenteric artery
    • renal
    • gonadal
    • second lumbar
    • inferior mesenteric artery
    • third lumbar
    • fourth lumbar

Ex: higher clamping in thoracic or abdominal aorta → anticipate more complications

Surgical Procedures Overview

  • Surgeon-anesthesia communication critical
    • All open procedures have a degree of ischemia-reperfusion
  • Reconstruction for aneurysmal
  • Reconstruction for aortic dissection
  • Endovascular aortic surgery
    • ~60-70% of patients requiring infrarenal repair
    • Trials ongoing for juxtarenal, suprarenal and thoracoabdominal repair


What is an aneurysm?

Most frequent location of aneurysms?


  • > 50% dilation of normal expected arterial diameter
    • abdominal aortic diameter > 3.0 cm
  • Abdominal aorta: most frequent location of arterial aneurysm
    • 9x more common than thoracic
  • Statistics:
    • Thoracic:
      • ascending (40%)
      • descending (35%)
      • aortic arch (15%)
  • AAAs: classified as:
    • Infrarenal (85%)
    • Juxtarenal
    • Suprarenal
  • Must know level of aneurysm: location of Aox is critical


What is the pathophysiology behind an aneurysma?

  • Distinct patho from atherosclerotic disease
  • Degenerative process
    • degradation of aortic wall connective tissue
    • primarily, the medial and adventitial layers (muscular layer)
    • Turbulent BF causes →
      • inflammation and immune responses
      • biomechanical wall stress
  • Size of aneurysm = single most important predictor of subsequent rupture and mortality


What is a anuerysm rupture vs dissection?

AAA Rupture

  • Catastrophic
    • Many don’t even make it to the OR
      • 50% mortality for repair of ruptured AAA
      • 85%-90% mortality rate
  • Goal: balance risk of surgery with risk of rupture
  • Current recommendations:
    • serial monitoring of known aneurysms
    • Elective Surgical repair indication: (decrease risk of rupture)
      • AAAs = > 5.5 cm
      • Descending thoracic aortic aneurysm = > 6.5 cm

Aortic Dissection

  • Tear in the intimal layer of the arterial wall that creates a false lumen
    • propagated by pulsatile blood flow
      • Acute = < 14 days
      • Chronic = >2 weeks symptom duration
  • Approximately ½ of aortic dissections originate from the ascending aorta
  • Ascending Aorta Dissection
    • Surgical emergency
    • Leads to:
      • acute aortic regurgitation
      • pericardial tamponad
      • myocardial ischemia
  • Acute descending aortic dissection:
    • → end-organ compromise due to malperfusion of the visceral vessels → death


Open abdominal aortic aneurysam repair overview of procedure

  • 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


  • 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


What determines the effect of aortic cross clamp?

What are some effects of cross clamping?

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%
      • ↑ or ↓ in cardiac preload, central filling pressures, and CO → depends on where clamp located
  • 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
      • 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.
    • 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)

​Supraceliac has most significant impact on MAP, PAP and EF


What si the systemic hemodynamic response to aortic crossclamping?

  • Passive recoil distal to clamppreload
  • ↑ Catecholamines (and other vasoconstrictor) →
    • Active venoconstriction proximal and distal to clamp →
      • leading to preload
  • ↑ Ao flow impedance
    • → ↑ afterload
      • Overall:
        • ↑ Preload
        • ↑ Coronary flow
        • ↑ Afterload
        • ↑ contractility → ↑ CO
          • But if no ↑ in coronary flow or contractility →  ↓ CO
  • 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).


What is the blood volume redistribution following aortic cross clamp placement?

  • 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.



What is the goal during aortic clamping?

Therapeutic interventions?

  • Goal:
    • Offset ↑ afterload & myocardial work          
      • Tx: systemic vasodilation
    • HR 60-65 (balance S/D)
      • Tx: Esmolol
  • 1. Afterload reduction                                 
    • Sodium nitroprusside (0.3-0.7 mcg/kg prior to clamp)
    • Inhaled anesthetics
    • Milrinone (50 mcg/kg)
    • Nicardipine (200-600mcg)
    • Shunts /aorta-to-femoral bypass                   
  • 2. Preload normalized                                 
    • Nitroglycerin
    • Thoracic epidural
    • Atrial-to-femoral bypass  
  • 3. Maintain CO
    • Avoid myocardial depressant anesthetics
    • Inotropes (rarely needed)

Recognize attempts to normalize SVR above level of clamp can even further compromise blood flow distal to the clamp.

  • Admin Na Nitroprusside → decrease aortic pressure distal to cross clamp level
    • This decrease was unresponsive to increases in preload via volume challenge or CO
  • Critical to maintain perfusion pressure below level of cross clamp that will not potentiate visceral or SC ischemia


What are some metabolic changes with aortic cross clamp?

  • ↓ Total-body oxygen consumption
  • ↓ Total-body CO2 production
  • ↑ Mixed venous oxygen saturation
  • ↓ Total-body oxygen extraction
  • ↑ Epinephrine and norepinephrine
  • Respiratory alkalosis if vent settings not adjusted
  • Metabolic acidosis


What determines pathophys during aortic unclamping?

Hemodynamic changes during unclamping?

Metabolic changes during unclamping?

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.


What are some therapeutic interventions during aortic unclamping?

  • Communication & Awareness of procedure
  • Volume
    • Volume loading while clamped
    • Fluid bolus before unclamping
  • Vasodilators → D/c or
  • VA → ↓
  • Vasopressors
    • Phenylephrine 100-200 ug
    • Norepinephrine 8 mcg
      • Avoid HTN → Anastomoses damage
      • Small doses/short acting*
  • Inotropes
    • CaCl 500 mg &/or
    • 10 mcg Epinephrine doses / NE
  • Other management techniques:
    • Slow/ gradual clamp release with reapplication for hypotension
    • Sequential reperfusion to each leg if iliacs are clamped
  • Caution: watch carefully!!!
    • Bleeding at anastomosis= reclamping


Intraop monitoring for AAA repair?

Lines needed?

  • Intraop monitoring
    • Open repair – standard monitors +  CVP & A-line (proximal to clamp)
      • Abdominal versus retroperitoneal approach
    • PA cath – LV failure (EF < 30%), cor pulmonale, CRF, and those having suprarenal repair
    • TEE intraop to assess ventricular function, guide fluid therapy, monitor for myocardial ischemia
  • 8.5 Fr IJ + 1-2 large bore PIVs
  • T & C
    • 4-6 units PRBC minimum
  • Cell saver, normovolemic hemodilution, autologous pre-donation


Anesthetic technique for AAA?

Induciton/maintenance considerations

  • Most common: lumbar or low thoracic epidural with light GA
    • 6-8 ml LA bolus
    • 4-6 ml hr
  • Induction should be controlled → no wide swings (avoid tachycardia/HTN)
    • Ex: Thiopental, Etomidate or propofol with fentanyl 3-8mcg/kg and VA
    • HTN:
      • Esmolol 10-25 mg
      • nitroprusside 5-25mcg
      • nitroglycerine 50-100mcg
    • HoTN:
      • phenylephrine 50-100mcg (small doses)
    • need blood in room with large bore peripheral IV prior to induction. aline prior to induction may be appropriate to better titrate induction agents
  • Maintenance:
    • fentanyl or sufentanil
    • low inhalation agent
    • with 50% nitrous oxide

From notes below ppt: Prior to cross clamp

  • patient kept slightly hypovolemic (Assessed by CVP, PAOP, or echo) to limit hypertensive extremes with aortic occlusions
  • at time of x-clamp, vasodilating infusions may b erequired
    • can deepen VA or inject epidural catheter with LA to increase vasodilation
    • if concerned about spinal cord perfusion, may b prudent to allow permissive HTN above the level of the clamp to provide higher distal perfusion pressure and avoid distal ischemia
      • this may come at the expense of myocardial well being
  • prudent to volume load during cross clamping to prepare for vasoplegic washout and reactive hyperemia (period of increased blood flow following period of ischemia) that will occur with removal of cross clamp
    • keep cvp/paop 2-3 points higher than baseline
  • d/c vasodilator prior to removal of cross clamp
    • refractory hypotension can be treated by reapplication of cross clamp
    • short acting vasoactive agents utilized
    • may see temporary increase in CVP/PAOP despite hypotension d/t washout of lactic acid and inflammatory mediators which can result in pulmonary vasoconstriction and cardiac stunning


Emergence for AAA repair?

  • Emergence – must be normal hemodynamics and temperature for extubation
    • utilize epidural for pain mgmt/hemodynamic control
  • Avoid post-operative hypothermia
  • ICU intubated if:
    • Supraceliac clamp time >30 min
    • Pulmonary disease- preexisting
    • Large blood loss