Thoracic Aortic Dissection Flashcards
(38 cards)
Debakey Classification of Aortic Dissection
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)
Stanford Classification of Aortic Dissection
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
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?
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
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?
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
Would you initiate Beta blocker therapy in a thoracic aortic dissection patient who was NOT already taking a BB?
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
Detail the NON-CARDIAC surgery guidelines for beta blockers in patients NOT on chronic BB therapy
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)
Lumbar drains. Should you place for Thoracic Aortic Dissections?
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.
What are some possible complications of spinal/lumbar drain?
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.
Can you have BOTH a lumbar drain (for improved spinal cord perfusion) and an epidural (for pain control) at the same time?
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.
Gotta memorize all the fucking timelines for discontinuation of anticoagulants for being able to do neuraxial anesthesia.
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.
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??
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!
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?
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
What happens is you have a traumatic lumbar drain placement (large amount of blood back through the catheter)?
- 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
Should you still place an epidural if you’re planning to neuromonitor with SSEP’s or MEP’s?
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.
What are some benefits of epidural anesthesia for this case
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).
What are the complications associated with neuraxial catheter placement
1) epidural/spinal hematoma
2) sympatholysis-induced hypotension
3) epidural abscess
4) headache
5) meningitis
What lines and other things should you have in the room for potential massive blood loss
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)
What is ANH (acute normovolemic hemodilution)?
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
What are the Contraindications to ANH
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
What is the rationale for ANH?
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.
L/D/A and Monitors for Thoracic Aortic Dissection
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
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?
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.
Would you place a pulmonary artery catheter (PAC)? Why?
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.
What are the signs of Myocardial ischemia on the PAC?
- 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)
