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

Lumbar Drains - Target CSF Pressure, and anatomic place to zero at

Answer 8

Allow for passive drainage of CSF to a goal pressure of 8-10 mmHg during the procedure and postoperatively (for about 48 hours) to better preserve adequate spinal cord perfusion

When draining CSF to a specific target, be sure that the zero point of the transducer is set at the patient’s mid-axillary line or external auditory meatus while the patient is in the supine position.

Question 9

What are some possible complications of spinal/lumbar drain?

Answer 9

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 10

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

Answer 10

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 11

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

Answer 11

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 12

What are the Thienopyridine’s, and how long should they be discontinued for before doing a Neuraxial procedure (such as a Lumbar Drain for CSF drainage during aortic dissection surgery, or a Thoracic Epidural pain catheter)?

Answer 12

Thienopyridines - discontinue this long before neuraxial procedures:
* clopidogrel (Plavix®) = 5-7 days
* prasugrel = 7-10 days
* ticlopidine = 10 days

Question 13

Platelet GP IIb/IIIa inhibitors + Heparin gtt - the “Bridging Therapy” when Thienopyridines (eg Plavix/Clopidogrel) are discontinued before an Aortic Dissection case

Answer 13

Platelet GP IIb/IIIa inhibitors - discontinue this long before neuraxial procedures:
* eptifibatide - UBP says 8 hours, though ASRA says like 24-48 hrs
* Abciximab (ReoPro®) - ASRA says same thing as Eptifibatide. Idk what UBP says
* Tirofiban (Aggrastat®) - ASRA actually says 4-8 hours is the time to normal plateley aggregation

First off, this UBP case is acting like this person with an urgent/emergent aortic dissection requiring surgical repair SOMEHOW had a psychic doctor who took them off their Plavix (Thienopyridine) 10 days ago (need stop for 7 days before neuraxial procedure), and 3 days ago was started on the BRIDGNING THERAPY of Eptifibate (a GP IIb/IIIa inhibitor) + heparin gtt. The pt was on the plavix because he had a coronary DES 3 months ago. now he just had the aortic dissection. The question then asks if you would still place a Lumbar Drain + Thoracic epidural for this patient, despite these blood thinner therapies? The short answer is YES, so long as the GP IIb/IIIa inhibitor (Eptifibate here) were stopped for at least 8 hours, the heparin was stopped 6 hours ago and there was a normal PTT, and there were not signs of coagulopathy.

Long C&P answer:
I would still proceed with the placement of the lumbar drain and epidural catheter because of the spinal cord protection (lumbar drain) and superior pain control (thoracic epidural catheter) provided by these catheters, respectively. However, I recognize that treatment with eptifibatide and heparin poses a risk for epidural or spinal hematoma following neuraxial instrumentation. Therefore, I would first ensure he had discontinued his eptifibatide and intravenous heparin for at least 8 hours (platelet aggregation normalizes in 4-8 hours following the discontinuation of eptifibatide), he had a normal PTT (heparin activity would prolong the PTT), and there were no signs of coagulopathy (the ASRA recommendation is to delay neuraxial placement until platelet aggregation normalizes following the discontinuation of a platelet GP IIb/IIIa inhibitor and 4-6 hours following the discontinuation of intravenous heparin).

Clinical Notes
Note: 1
Platelet GP IIb/IIIa inhibitors are sometimes used for “bridging therapy” when a patient who requires thienopyridine therapy to prevent stent thrombosis must undergo a surgical procedure where the risk of bleeding makes the continuation of a long-acting platelet inhibitor unacceptable. When the decision is made to employ bridging therapy, a typical strategy would be to:
Discontinue the thienopyridine 5-10 days prior to surgery (depending on the type of thienopyridine utilized)
Continue aspirin throughout the perioperative period
Start a short-acting platelet inhibitor, such as eptifibatide or tirofiban, 2-3 days before surgery
Consider starting a concomitant heparin infusion
Discontinue any “bridging” drugs 6 hours prior to surgery (the aspirin should be continued, if possible)
Heparin alone is insufficient to prevent stent thrombosis because the heparin-antithrombin complex’s ability to inactivate fibrin-bound thrombin and factor Xa

Question 14

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 14

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 15

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 15

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 16

S/S of Coagulopathy

Answer 16

There’s not always a test to see if pt has proper coagulation happening after the discontinuation of blood thinners. Part of the decision to proceed with a neuraxial procedure after the proper discontinuation timelineo of blood thinners is to assess for the S/S of coagulopathy. Some S/S of coagulopathy:
* Epistaxis. Similarly, heavy menstruation
* easy bruising
* hematuria, or blood in stool
* Petechia
* fatigue, headache, shortness of breath (ie, anemia)

Question 17

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

Answer 17

• 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 18

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

Answer 18

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 19

What are some benefits of epidural anesthesia for this case

Answer 19

Epidural analgesia has NOT been definitively proven to reduce the incidence of cardiovascular, pulmonary, or renal complications. my note: this is kind of fucked, because the question literally lists the benefits (below) in the same question, and those benefits are well known; but whatever.

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 20

What are the complications associated with neuraxial catheter placement

Answer 20

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

Question 21

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

Answer 21

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 22

What is ANH (acute normovolemic hemodilution)?

Answer 22

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 23

What are the Contraindications to ANH

Answer 23

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. UBP suggests that for CAD pts, using the MABL equation to take no more blood than what would give the pt a HCT 27% (Hgb 9 mg/dL)

Question 24

What is the rationale for ANH?

Answer 24

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 25

Explain how you actually do ANH

Answer 25

collect 1-2 units of his blood *while simultaneously* by administering warmed crystalloids or colloids to maintain normovolemia. Keep HCT above 27% (Hgb 9) for CAD patients like this one (use MABL equation). Then, following the cessation of significant blood loss (or earlier if clinically indicated), I would re-infuse the autologous blood in reverse order of collection, recognizing that the first unit collected contains the highest concentration of coagulation factors and platelets (re-infusion in reverse order of collection is only advantageous if all the blood collected is to be returned to the patient). * note: UBP says to simultaneously take out blood and put in crystalloid or colloid, then use the reverse order thing for re-infusing. Other sources say to take out the blood FIRST, then IMMEDIATELY infuse the crystalloid/colloid once done draining blood. Clinical Notes Note: 1 The reduction in RBC concentration associated with ANH **decreases blood viscosity, leading to decreased peripheral vascular resistance and increased cardiac output**. This **compensatory increase in cardiac output helps to maintain adequate oxygen delivery to the tissues despite a decreased hematocrit**.

Question 26

L/D/A and Monitors for Thoracic Aortic Dissection

Answer 26

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 27

Good notes on CVP Monitoring

Answer 27

Central Venous Pressure Monitoring * In the setting of normal right ventricular function, the central venous pressure may give an indirect estimation of right ventricular end-diastolic volume and right ventricular preload. This information may then be used to guide fluid replacement and, where ventricular compliance is normal, to allow estimation of left heart pressures. * Isolated CVP measurements are difficult to interpret and should be assessed rather as a trend analysis, keeping in mind the patient’s hemodynamic variables and overall condition. * The CVP is informative only when the pressure is very low or very high because of the relatively increased compliance of the right side of the heart as compared to the left. also, SSEP's are ablated with conduction blockade (such as happens when infusing Local anesthesia in a thoracic epidural), and MEP's are ablated with paralysis obvi

Question 28

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 28

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 29

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

Answer 29

Increased pulmonary artery occlusion pressure and increased pulmonary artery diastolic pressure occur secondary to ischemia-induced increases in LVEDP (ie, increased filling pressures). Yes, because it would help INTRAOP with: - 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 30

What are the signs of Myocardial ischemia on the PAC?

Answer 30

- 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)

Question 31

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

Answer 31

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 sort of 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 32

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

Answer 32

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** or a "**low-normal SBP**" in my words 5) Goal **MAP ~ 100 above** the clamp, **~ 50 or greater below** the clamp  Goal CI 2-2.5 L/min/m2 6) **Paralysis**

Question 33

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 33

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 34

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

Answer 34

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 35

What is the equation for Spinal Cord Perfusion?

Answer 35

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

Question 36

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

Answer 36

CSF pressures may increase 10-15 mmHg

Question 37

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

Answer 37

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 38

List the complications associated with CSF drainage

Answer 38

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

Question 39

Describe the blood supply to the spinal cord

Answer 39

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** and/or posterior inferior cerebellar arteries (**PICA**), and receive some [posterior] intercostal **radicular artery contributions** 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 40

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

Answer 40

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). My note: REwarming is different than just MAINTAINING WARMTH with a bair hugger, which we do all the time with lower body bair huggers. 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 41

BP tanks after release of aortic XC. Why?

Answer 41

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 42

How do you deal with BP tanking after XC release?

Answer 42

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 43

Would you extubate after a Thoracic aortic dissection repair?

Answer 43

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 44

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

Answer 44

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)

Question 45

Pt with both a thoracic epidural catheter and a lumbar drain (after the open thoracic aortic rupture repair) wakes up with Paralyzed legs. What's your DDx for leg weakness?

Answer 45

1. epidural/spinal hematoma with cord compression (secondary to lumbar drain and/or epidural catheter placement) 2. neurologic injury secondary to intra-operative spinal cord ischemia, or the 3. infusion of local anesthetics through an epidural catheter inadvertently placed in the intrathecal space.

Question 46

What do you do to address the leg paralysis?

Answer 46

1. Perform a neurologic examination 2. Increase the mean arterial pressure to > 80 mmHg to optimize spinal cord perfusion 3. Discontinue the epidural infusion (the motor weakness associated with neuraxial local anesthetics may confuse the clinical picture) 4. Aspirate the epidural catheter for CSF to identify intrathecal placement 5. Decrease the CSF pressure to 5-10 mmHg to maximize spinal cord perfusion 6. Give consideration to a CT/MRI and neurological consult.

Question 47

Aortic Cross Clamps: How does surgical dissection and aortic cross clamping increase the risk of spinal cord ischemia?

Answer 47

The risk of spinal cord ischemia is increased because surgical ligation of significant radicular arteries and the application of the aortic cross-clamp can lead to hypoperfusion of the spinal cord. The anterior spinal cord is particularly vulnerable due to its reliance on a single anterior spinal artery for blood supply, the largest and most important of these being the artery of Adamkiewicz. Moreover, spinal cord perfusion may be further compromised by the increase in CSF pressure associated with aortic cross-clamp application (application of the cross-clamp leads to cerebral hyperemia with subsequent shifting of CSF into the spinal compartment). This increase in CSF pressure in combination with decreased distal aortic pressures can lead to decreased spinal cord perfusion and ischemia. The risk of spinal cord ischemia can be reduced by: (1) avoiding hypotension (the maintenance of proximal hypertension should be considered – especially when planning a “clamp and sew” technique without distal bypass), (2) minimizing aortic cross-clamp time, (3) reattaching critical segmental arteries, (4) achieving an appropriate level of hypothermia, (5) lowering CSF pressure via passive drainage and maintaining lower pressures postoperatively, (6) monitoring spinal cord function using SSEPs and MEPs, (7) utilizing a shunt or bypass to increase distal perfusion, (8) ensuring a normal hematocrit and PaO2, and (9) considering the administration of one or more of the various pharmacologic agents utilized for spinal cord protections, such as corticosteroids (e.g. dexamethasone or methylprednisolone), magnesium, barbiturates, calcium channel blockers, dextrorphan, papaverine, mannitol, and naloxone.