Thoracic Aortic Dissection

Question 1

Debakey Classification of Aortic Dissection

Answer 1

Debakey and Stanford Classification of aortic DISSECTIONS are different from the CRAWFORD Classification (Types I-V) of Thoracoabdominal ANEURYSMS

Debakey Type I Dissection: Ascending aorta –> descending aorta (thoracic and/or abdominal aorta)

Debakey Type II Dissection: Ascending aorta ONLY (so from aortic valve to start of innominate [brachiocephalic] artery, and does NOT involve the arch)

Debakey Type III Dissection: originate beyond the aortic arch (ie, beyond the left subclavian artery) and extend distally to the diaphragm (type IIIa) or the aorto-iliac bifurcation (type IIIb)

Question 2

Stanford Classification of Aortic Dissection

Answer 2

Stanford Type A Dissection: Any involvement of the ascending aorta, +/- involvement of the arch and descending aorta. Includes Debakey Types I and II dissection

Stanford Type B Dissection: all cases in which the ascending aorta is NOT involved. Useful cuz you know it’s probably NOT a surgical emergency. Includes Debakey Type IIIa and IIIb

Question 3

If aortic dissection went back to the aortic valve and caused Aortic Insufficiency, 1) where might you auscultate the murmur and 2) what are the hemodynamic consequences of acute AI?

Answer 3

You’ll auscultate a DIASTOLIC murmur along the LEFT sternal border

Consequences of Acute AI:
- volume overload of LV
- reduced forward SV
- Pulmonary edema 2/2 increased LVEDP’s
- increased myocardial O2 demand
- reduced myocardial blood supply 2/2 reduced diastolic pressures in AORTA and/or increased LVEDP’s
All of this can lead to myocardial ischemia even in the absence of CAD.

Avoid bradycardia so regurgitant volume remains low by decreasing diastolic filling time

Question 4

A thoracic aortic dissection patient is on CHRONIC Beta blocker therapy. Should you give ADDITIONAL Beta-blockers for Thoracic Aortic Dissection? What about if they also have acute aortic insufficiency?

Answer 4

Without AI, it’s an easier “yes” if necessary. Beta blockers reduce intramural pressures anda aortic shear forces that could propagate or rupture the dissection - decreasing BP and the force of ventricular contractions reduces aortic wall stress by reducing shear pressure or dP/dT (dP/dT = the change in blood pressure / change in time).

Even though BB’s would decrease HR which could worsen AI, the reduced afterload offered by BB’s could reduce regurgitant volumes.

Also, BB’s in general are associated with reduced perioperative and long-term cardiac morbidity/mortality when undergoing high-risk vascular surgery (different than the also good Class I recommendation to continue BB therapy in patients undergoing NONcardiac surgery who are currently taking BB’s for tx of indicated conditions, as the discontinuation of BB therapy is associated with an increased risk of myocardial ischemia and chest pain).

HOWEVER, bradycardia from BB’s increases regurgitant volume in AI. An infusion of esmolol, a SHORT acting BB, would be best in this situation so it could be discontinued if the

Question 5

Would you initiate Beta blocker therapy in a thoracic aortic dissection patient who was NOT already taking a BB?

Answer 5

I would NOT, unless absolutely necessary. This is tricky, because I think the purely MEDICAL treatment of ABDOMINAL aortic aneurysms is to start a Beta Blocker, but for THORACIC aortic aneurysms it mostly falls under the general NON-CARDIAC SURGERY guideline to NOT start beta blockers on the day of surgery! This is despite the true statement that BB therapy could reduce risk of aneurysm rupture, aneurysm propagation, and reduce the pt’s CARDIOVASCULAR morbidity and mortality. So you’d say the standard answer that you WOULD start BB therapy if you had the opportunity to start it 2-7 days prior to surgery, and you’d carefully titrate to HR 60-80 while avoiding significant bradycardia and hypotension

Question 6

Detail the NON-CARDIAC surgery guidelines for beta blockers in patients NOT on chronic BB therapy

Answer 6

in pt’s undergoing NON-cardiac surgery who are NOT currently taking BB’s, routine administration of high-dose, un-titrated perioperative BB is NOT recommended (Class III recommendation).

The preoperative initiation of BB therapy (notice this is NOT INTRA-operative) BB therapy in the absence of titration may REDUCE CARDIOVASCULAR M&M (ie, ischemia, afib, requirement for coronary interventions). HOWEVER, it also INCREASES the OVERALL M&M, 2/2 to increased HYPOTENSION, BRADYCARDIA, STROKE, and DEATH

BB therapy should NOT be started day of surgery (Class III: harm)

In general BB should be started well in advance of a planned procedure (2-7 days atleast) and carefully titrated perioperatively to achieve adequate HR control (goal 60-80 bpm)

Question 7

Lumbar drains. Should you place for Thoracic Aortic Dissections?

Answer 7

Basically, yes, assuming there are no contraindications. Monitoring and manipulating spinal cord perfusion pressure with the use of a spinal drain is a class I (level of evidence: B) recommendation in the 2010 US Guidelines for Spinal Cord Protection During Thoracic Aortic Repair as established by the ACC and AHA Task Force on Practice Guidelines.

A Lumbar Drain (spinal drain) allows for passive drainage of CSF to a pressures of 8-10 mmHg during the procedure and postoperatively (for about 48 hours) to better preserve adequate spinal cord perfusion. Spinal Cord Perfusion Pressure = mean diastolic aortic pressure minus CVP or CSF (whichever is highest). SC blood flow is controlled by autoregulation (from 50-125 mmhg), however there is potential for IMPAIRED autoregulation in thoracic dissection and repair. The AORTIC CROSS-CLAMP increases CSF pressure (hyperemia above the clamp increases CSF pressure, causing redistribution of CSF into the intrathecal space and increase in CSF pressure by 10-15 mmHg, which then impairs SC perfusion per the equation). Drainage of CSF lowers the CSF pressure, which improves SC perfusion.

Some CONTRAINDICATIONS to a lumbar drain would be anticoagulation (say ACS patients with stents!) so you don’t get spinal/epidural hematoma.

Question 8

What are some possible complications of spinal/lumbar drain?

Answer 8

headache, intracranial bleeding, meningitis, and chronic CSF leak.

Also need to avoid rapid removal of CSF through the drain, as it can result in tearing of cerebral bridging veins with subsequent intracranial bleeding.

Question 9

Can you have BOTH a lumbar drain (for improved spinal cord perfusion) and an epidural (for pain control) at the same time?

Answer 9

YES, you can. They aren’t even in the same space (intrathecal vs epidural), and the epidural is probably thoracic and the lumbar drain in lumbar spine, so wouldn’t run into each other.

Question 10

Gotta memorize all the fucking timelines for discontinuation of anticoagulants for being able to do neuraxial anesthesia.

Answer 10

They’ll scare you out of doing a neuraxial procedure by saying they’re on anticoagulants, but the correct answer is to YES still place the neuraxial catheter as long as they’ve been off the anticoagulants for just long enough.

Question 11

If you were going to do left-heart bypass with a pump, oxygenator, and heat exchanger during the thoracic aortic dissection repair, would you still place a lumbar drain??

Answer 11

YES, outrageously you would. You would for the purpose of improving SC perfuison in the perioperative period, even though left heart bypass requires HEPERINIZATION.

So you’d discuss the plan with everyone, ensure Pre-operative anticoagulants were discontinued for a sufficient amount of time, rule out any OTHER coagulopathy, delay systemic heparinization for 60 min following lumbar drain placement, use the smallest amount of heparin necessary to achieve therapeutic objectives (partial bypass usually requires 100 U/kg), monitor pt for S/S spinal/epidural hematoma, and ensure adequate coagulation at the time of catheter removal!

Question 12

Plavix (Clopidogrel, or Thienopyridine therapy, or “long-acting” platelet inhibitor) is what ACS pts with fresh coronary stents are on. It prevents stent thrombosis. How do you “bridge” these pts to high risk bleeding surgeries so they’re covered with adequate anti-coagulation as long as possible after stopping the thienopyridine?

Answer 12

Platelet GP IIb/IIIa inhibitors are sometimes used for “bridging therapy” to prevent plavix pts from getting stent thrombosis after they stop the plavix before a surgery where the risk of bleeding makes continuation of long-acting platelet inhibitors (plavix) is unacceptable.

A typical strategy for “bridging therapy” after stopping plavix is the following:
- Discontinue thienopyridine 5-10 days prior to the surgery
- Continue ASA throughout
- Start short-actting platelet inhibitor, suhc as eptifibatide or tirofiban, 2-3 days before surgery
- Consider starting concomitant heparin infusion
- Discontinue any “bridging” drugs (so the eptifibatide and heparin gtt) 6 hours prior to surgery (but continue the ASA)

fyi, heparing alone is insufficient to prevent stent thrombosis because the heparin-antithrombin complex’s ability to inactivate fibrin-bound thrombin and factor Xa

Question 13

What happens is you have a traumatic lumbar drain placement (large amount of blood back through the catheter)?

Answer 13

• Delay surgery 24 hours if possible to reduce risk of spinal/epidural hematoma, though there’s no evidence to support this practice; ASRA recs delay when utilizing full heparinization, but dos NOT make a recommendation when planning low dose systemic heparinization such as 100 U/kg.
• However probably can’t delay the urgent/emergent thoracic aortic dissection. So, I’d ensure normal coagulation prior to removal of the lumbar drain and order neuro exams q1hr to detect the first signs of spinal cord compression 2/2 hematoma formation. If an epidural catheter were in place for post-op pain control, I would utilize narcotics alone or in combo w/low concentration local anesthetics in order to preserve the patient’s lower extremity motor fxn and allow for adequate neuro monitoring

Question 14

Should you still place an epidural if you’re planning to neuromonitor with SSEP’s or MEP’s?

Answer 14

YES you should STILL place one. If you neuraxial local anesthetics throughout the case, it WOULD interfere with the neuromonitoring, so I’d only use neuraxial OPIOID intraoperatively. Then use neuraxial LA + opioid POST-OP.

Question 15

What are some benefits of epidural anesthesia for this case

Answer 15

Epidural analgesia has NOT been definitively proven to reduce the incidence of cardiovascular, pulmonary, or renal complications.

1) improved respiratory fxn (decreased atelectasis, pulm infxns, resp failure, and prolong mechanical ventilation)
2) improved GI motility
3) improved graft patency (reduced coagulation response)
4) reduced postop myocardial ischemia (2/2 attenuation of the stress response, and when it’s a thoracic epidural, coronary artery dilation).

Question 16

What are the complications associated with neuraxial catheter placement

Answer 16

1) epidural/spinal hematoma
2) sympatholysis-induced hypotension
3) epidural abscess
4) headache
5) meningitis

Question 17

What lines and other things should you have in the room for potential massive blood loss

Answer 17

1) Large bore central access (MAC Cordis)
2) Two large bore PIV’s
3) Rapid transfusion devices, warming devices
4) 1 FFP for every 1-2 pRBC’s in the room: so 5 FFP and 10-15 pRBC’s
5) Additional everything ready in the blood bank
6) Use cell-salvage
7) Discuss with surgeon additional blood conservation strategies such as acute normovolemic hemodilution and/or antifibrinolytic usage (ACA, TXA)

Question 18

What is ANH (acute normovolemic hemodilution)?

Answer 18

It’s a blood conservation strategy. Autologous blood is collected at the beginning of the case prior to intentional hemodilution by IVF (so it has a higher hematocrit), and then re-infused when significant bleeding has been controlled).

The procedure is you collect 1-2 units of blood while simultaneously (I thought it was afterward??) adminstering warmed crystalloid or colloids to maintain normovolemia. Use the EABL (estimated allowable blood loss) to calculate the approximate amount of blood to withdraw

After the CESSATION of significant blood loss in the case (or EARLIER if indicated), re-infuse the autologous blood in REVERSE ORDER of the collection, recognizing that the first unit collected contains the highest concentration of coagulation factors and plateles

Question 19

What are the Contraindications to ANH

Answer 19

Contraindications to ANH:
- Anemia defined as Hgb/HCT < 11 g/dL or 33%
- Significant pulmonary disease - already challenged O2 delivery to tissues becomes inadequate with decreased O2 content of blood in ANH
- Impaired renal function - may be unable to handle the fluid load from the normovolemic hemodilution part
- cardiac disease (end-organ ischemia would be bad) is bad, but not necessarily a contraindication. Don’t let HCT fall < 27% (I think Hgb 9-10) in CAD

Question 20

What is the rationale for ANH?

Answer 20

The rationale for ANH is that blood loss is minimized by reducing the HCT of blood likely to be shed during the procedure. However, it’s only been shown to have a moderate benefit, saving ~ 1-2 Units of pRBCs even when initial HCT is very high and intraoperative blood loss is substantial (> 70% of pt’s blood volume).

Avoiding exposure to allgoeneic blood transfusion (ie, other ppl’s blood) reduces the risk of infection, transfusion rxns, nad red cell alloimmunization.

Question 21

L/D/A and Monitors for Thoracic Aortic Dissection

Answer 21

1) Standard ASA monitors
2) 5-lead EKG - high incidence intraop myocardial ischemia and infarction
3) Upper (RIGHT arm) AND lower extremity arterial lines - monitor the hemodynamic stability with expected HTN, blood loss, XC
4) large bore central line - RVEDP TREND guides fluid replacement and can estimate left heart pressures if compliance is normal.
5) PA cath - can also do transvenous pacing. See a few questions down for more details on why to place PA catheter.
6) TEE - confirm extent of aortic disease, ID cardiac ischemia (TEE is most sensitive modality for detecting heart ischemia - WMA on TEE appears earlier than ST segment or pACwaveform changes
7) Core (bladder, nasopharynx, tympanic membrane, PA cath, or distal esophagus) AND Peripheral (axilla or rectum) temp monitors
8) SSEP and MEP to monitor SC ischemia - loss of signal lasting 15-30 min is associated with neurologic injury. MEPs in particular (not SSEPs - their response to ischemia is too slow) can IDENTIFY critical intercostal arteries supplying the cord, and successful REIMPLANTATION of those same arteries. SSEP’s are ablated with the conduction blockade that epidural or spinal anesthesia causes
9) Foley - UOP, fluid status, renal perfusion

Question 22

Why should the upper extremity arterial line be in the RIGHT arm for thoracic aortic aneurysm/dissection repair, and then what does the lower extremity arterial line provide?

Answer 22

RIGHT upper extremity avoids surgical interference of CROSS-CLAMPING, as sometimes the XC is placed even proximal to the left subclavian artery (common for surgery involving proximal descending aorta), so a LUE A-line may have errant readings.

During XC, the PROXIMAL arterial line (RUE) provides accurate info for Cerebral and Cardiac perfusion pressures, as well as cardiac afterload. The DISTAL (lower extremity) A-line monitors distal perfusion to the kidneys, spinal cord, and mesenteric circulation.

Question 23

Would you place a pulmonary artery catheter (PAC)? Why?

Answer 23

Yes, because it would help INTRAOP ith:
- Fluid mgmt
- assessment of cardiac fxn
- Timely identification of cardiac ischemia intraoperatively.

Along with TEE, the PAC helps ID cardiac ischemia, fluid status, and valvular disease.

ALSO, since TEE is usually NOT continued POSTOP, the PAC can be left in place to help detect myocardial ischemia and cardiac failure, which these patients are at great risk for.

Question 24

What are the signs of Myocardial ischemia on the PAC?

Answer 24

• Prominent A-waves - result when the atrium contracts into the stiff LV
• Prominent V-waves - result when ischemic affects on the papillary muscles, chordae tendineae, and/or myocardium cause functional mitral regurgitation
• Increased pulmonary artery occlusion pressures (Wedge Pressure) and Increased pulmonary artery diastolic pressure - 2/2 to ischemia-induced increased (so this is all “increased FILLING PRESSURES,” I think)

Question 25

What are some key things to do for INDUCTION a person with a bad heart for Thoracic Aortic Dissection Surgery?

Answer 25

1) Double Lumen Tube - Don’t forget this! ONE LUNG VENTILATION for this case. It’s an obvious thing. Will have to get into the chest
2) Expanding aortic aneurysm/dissection could compress the airway
3) this one is in contrast to a question above, but this question says to “ensure adequate beta-blockade to reduce the risk fo myocardial ischemia and/or aortic rupture/propagation
4) Get a baseline set of vitals for EVERYTHING - NIBP cuff, SPO2, 5-lead EKG, both A-lines, CVP, PAC pressures, and evoked potential monitoring
5) Perform a carefully titrated, high-narcotic IV induction with goals of maintaining complete hemodynamic stability - BP not too high or low, and no tachycardia (dissection propagation i think) and no bradycardia (worsens aortic regurgitation if you have it)

Question 26

What are some key things to do for anesthesia MAINTENANCE a person with a bad heart for Thoracic Aortic Dissection Surgery?

Answer 26

1) TIVA if doing SSEP/MEP Monitoring
2) Various short-acting vasoactive agents available to ensure hemodynamic stability, especially during XC placement and removal (NTG, Nicardine or better yet Clevidipine, esmolol, nitroprusside)
3) Goal HR 60-80
4) Goal SBP 105-115
5) Goal MAP ~ 100 above the clamp, ~ 50 or greater below the clamp
Goal CI 2-2.5 L/min/m2
6) Paralysis

Question 27

You’re monitoring SSEP’s and there is a decreased amplitude and latency immediately after aortic XC is placed. What defines a significant change in SSEP and what do you do (The real question is how do you IMPROVE SPINAL CORD PERFUSION)?

Answer 27

SSEP significant change: 50% decreased amplitude and/or 10% increased latency.

MEP significant change: 50% decreased amplitude (some say only 75-80% is significant)

Assuming the anesthetic is stable and that you ARE doing partial bypass, Here’s how to increase SCP (spinal cord perfusion) to improve evoked potential signals:
1) Optimize hemodynamics - eg, increase MAP
2) Correct any metabolic disturbances - so send labs, correct hypo/hypercarbia, and acidosis
3) Ask perfusionist to increased pump flows distal to the aortic clamp
4) Ask surgeon to release or reposition the aortic clamp, which may renew flow through a critical intercostal artery
5) Hypothermia, which you should already be doing: 30-34 deg C (Class IIa rec)
6) Drain 10-20 cc of CSF from lumbar drain for a target ICP 8-10 mmHg (Class I rec for pts at significant risk of neurologic injury during thoracic aneurysm repair)
7) consider pharmacologic intervention to reduce spinal cord ischemia:
- Corticosteroids (methylpred or decadron)
- naloxone
- dextrorphan
- Magnesium
- Intrathecal papavarine
- CCB’s (but NOT if have BB on board, I think)
-

Question 28

Explain Hypothermia for spinal cord protection in thoracic aortic aneurysm/dissection repair

Answer 28

Hypothermia reduces O2 requirements by 5-7% for each deg C decrease in temp

for the very proximal aorta (aortic ARCH or ASCENDING aorta surgery), DEEP hypothermic cardiac arrest is required at 15 deg C (as compared to the 30-34 deg C for more distal thoracic aortic dissection surgery)

both systemic AND regional cooling is beneficial:
- Systemic hypothermia - achieved with ACTIVE cooling (full CPB or partial bypass) or by PASSIVE cooling (allowing patient to cool PASSIVELY to drift down to 30-34 deg C)
- Regional Cooling - achieved with EPIDURAL infusion of 4 deg C

Question 29

What is the equation for Spinal Cord Perfusion?

Answer 29

SCP = DISTAL MAP (so leg arterial line) - CSF pressure of CVP (whichever is higher)

Question 30

How much can CSF pressures increase with aortic XC of the DESCENDING aorta?

Answer 30

CSF pressures may increase 10-15 mmHg

Question 31

What is the target ICP / SCP (Spinal Cord Pressure):
- Intra-op
- after 48 hours postop
- after confirmation of preserved motor fxn after that

Answer 31

Goal SCP:
- Intra-op = 8-10 mmHg. Drain 10-20cc of CSF from the lumbar drain to achieve this
- after 48 hours postop = 10-12 mmHg
- After motor fxn confirmed = 10-15 (so basically normal ICP = 7-15mmHg)

Question 32

List the complications associated with CSF drainage

Answer 32

headache
spinal/epidural hematoma
intracranial bleeding 2/2 tearing of cerebral bridging vessels
meningitis
persistent CSF leak

Question 33

Describe the blood supply to the spinal cord

Answer 33

Fyi, autoregulation of the SC is relatively constant b/w 50-125 mmHg, but may be ablated in teh setting of hypoxia or hypercarbia.

Two posterior spinal arteries supply the posterior 1/3rd of SC (sensory). The posterior spinal arteries arise from the vertebral artery.

A single anterior spinal artery (ASA) arises from the basilar and vertebral arteries. The ASA supplies the anterior 2/3 of the SC (motor). The ASA receives contributions from 6-8 [transverse] radicular arteries (which originate from intercostal arteries that come directly off of the aorta at variable locations), and the most important of these radicular arteries is the Artery of Adamkiewicz.

The artery of Adamkiewicz serves the major supply to the anterior, lower 2/3rd of the SC. It is usually located on the left side, originating anywhere from T5-L5 (T9-T12 60% of the time). The variable origin of this artery may explain why paraplegia may even occur with infrarenal aortic aneurysm repair! When the Aortic XC is applied distal to this essential radicular artery, the risk of spinal cord ischemia is extremely low.

While distal aortic perfusion (eg, left-heart-bypass) helps maintain spinal cord perfusion below the artery of Adamkiewicz during aortic XC, it does little to maintain perfusion above this radicular artery (specifically, above the artery, but still below the aortic clamp), because resistance to flow moving up the ASA (proximal to the artery of Adamkiewicz) is 51x greater than that going down the artery.

Question 34

How would you REWARM the patient prior to releasing the XC as surgeon gets close to releasing it

Answer 34

do NOT use forced-air rewarm for the lower extremities because warming ischemic tissues increases metabolic requirements, acidosis, and ischemic injury (forced-air warming is contraindicated for the lower body).

However, i understand that actively warming the patient is often required. Therefore, I would siuggest warming the patient via the left-heart bypass circuit, which is a more effective method of warming than forced-air warming. If it were decided to utilize forced-air warming in conjunction with the bypass circuit (which contains a heat exchanger), I would ensure it was ONLY applied to the patient’s UPPER body.

Question 35

BP tanks after release of aortic XC. Why?

Answer 35

CENTRAL HYPOVOLEMIA ==> decreased PRELOAD is the primary cause of HoTN after XC release. During XC, there is distal tissue ischemia ==> release of vasoactive mediators that drop systemic vascular resistance, cause increased venous capacitance distal to the clamp, and increased capillary permeability overall (third spacing). This all leads to a distal shift of blood volume and loss of intravascular volume, causing central hypovolemia. Surgical blood loss doesn’t help either.

When XC is released, those acidic metabolites and vasoactive mediators from distal to clamp go to heart and caused the following:
- Decreased myocardial contractility (which is further compromised 2/2 reduced preload from central hypovolemia)
- Increased pulmonary vascular resistance
- Increased capillary permeability

Question 36

How do you deal with BP tanking after XC release?

Answer 36

1) fluid bolus, and better yet, VOLUME LOAD (with the vasodilators + volume) PRIOR to releasing XC
2) Trendelenberg
3) vasopressors
4) ID any other contributing factors to HoTN: hemorrhage (low filling pressures, observation of bleeding), arrhythmias, cardiovascular depression from anesthetic, TEE (WMA’s), EKG changes, PAC (elevated filling pressures), Tension PTX, acid-base disturbances (labs), citrate-induced hypocalcemia, hypothermia.

5) reapply aortic XC, and next time GRADUALLY release XC to allow for physiologic compensation
6) correct any abnormalities ID’d in #4
7) decrease anesthetic depth

Question 37

Would you extubate after a Thoracic aortic dissection repair?

Answer 37

Note the person will likely have cardiac and pulmonary problems at baseline.

Probably NOT extubate. OLV is quite bad on pulmonary function - OLV, surgical manipulation of diaphragm, phrenic nerve and RLN injury

Other factors that make extubation a bad idea:
- Potential for airway and pulmonary edema 2/2 thoracic aortic repair (due to significant fluid administration and increased capillary permeability associated with aortic XC)

So the better idea than extubating would be to:
- to ICU intubated
- allow hemodynamic stabilization
- complete NMB reversal
- Confirm adequate respiratory function:
- Vital capacity >/= 10 mL/kg, Vt > 6 mL/kg, NIF > 20 cm H2O, PaO2 > 60 with FiO2 < 50%, PaCO2 < 50 mmHg, and RR < 30 breaths/min
- verify normothermia and adequate pain control
perform cuff leak test (auscultate for breath sounds with cuff deflated in pt breathing spontaneously
- extubate in ICU when awake and cooperative with intact gag reflex

Question 38

Why does surgical dissection and placement of an aortic XC increase the risk of spinal cord ischemia?

Answer 38

This has been answered pretty well with different cards. I just want to hammer home that the anterior spinal cord (motor fxn) is vulnerable because of a few big reasons:
1) reliance on single ASA
2) Artery of Adamkiewicz is the most import and can be disrupted with XC
3) CSF pressure increases with aortic XC since it leads to cerebral hyperemia, with subsequent shifting of CSF into the spinal compartment
4) there is DECREASED DISTAL Aortic pressures, and SCPP = MAP - CSFP (analogous to CPP = MAP - ICP)