UBP Book 3 Flashcards
Perioperative concerns for thoracoabdominal aortic aneurysm
Aneurysm rupture
Dissection propagation
Myocardial ischemia
Post-operative respiratory complications (one-lung ventilation, surgical manipulation diaphragm/lungs)
Paraplegia (disruption of radicular arteries supplying anterior spinal cord)
Post-op AKI
Visceral/mesenteric injury
Stroke
Difficult airway (aneurysm may compress airway)
Hemorrhage
CHF
DeBakey classification of aortic dissection
Type I: originate in ascending aorta and extend distally to descending aorta
Type II: originate in ascending aorta and do not extend beyond brachiocephalic artery (first branch)
Type III: originate beyond L SCA and extend distally to diaphragm (IIIA) or aorto-iliac bifurcation (IIIB)
Type I and II = Type A (surgical emergency)
Type III = Type B (medical mgmt, surgical tx if e/o end organ ischemia, significant dilation, risk of rupture)
Acute aortic regurgitation concerns
LV volume overload
Reduced effective forward stroke volume
Rapid increase in LVEDP = pulm edema
Increased myocardial O2 demand
Reduced myocardial blood supply (reduced DBP and increased LVEDP)
Aortic dissection hemodynamic goals
Reduce intramural pressure
Reduce aortic shear force/force of ventricular contraction
This is accomplished by decreasing BP and force of ventricular contraction to reduce dP/dT (anti-impulse therapy)
Current guidelines recommend goal-directed therapy to achieve HR<60 and SBP 100-120.
Crawford classification of TAA
Type I: originates below L SCA, extends to abdominal aorta
Type II: originates below l SCA, extends to infrarenal abdominal aorta
Type III: originates below 6th rib, involves remaining aorta
Type IV: originates at diaphragm, involves abd aorta only
Type V: originates below 6th rib, extends to renal arteries
How does aortic cross clamping affect CSF pressure?
Cross clamp leads to hyperemia above clamp –> increased ICP –> redistribution of CSF to intrathecal space –> increase in CSF pressure by 10-15
Goal CSF pressure 8-10 to preserve spinal cord perfusion
Complications of lumbar drain placement
Epidural/spinal hematoma
HA
Intracranial bleeding (tearing subdural veins w/ rapid CSF removal)
Meningitis
Chronic CSF leak
How long to hold antiplatelet and anticoagulant agents prior to neuraxial instrumentation
Heparin gtt: 6 hours
Heparin SQ: 24 hrs (check aPTT for normalization)
Enoxaparin: 12 hrs (ppx dose) or 24 hrs (therapeutic dose)
Eptifibatide: 8 hours
Clopidogrel: 7 days (if high risk for thrombus, 5 days + platelet function test)
Apixaban: 3 days
Prasugrel: 7-10 days
Ticagrelor: 5 days
Warfarin: 5 days (check INR for normalization)
Protamine reaction
Type I: Hypotension (histamine release)
Type II: True anaphylaxis (IgE) vs anaphylactoid
Type III: catastrophic pulmonary vasoconstriction
Management of traumatic lumbar drain placement
Delay surgery for 24 hrs if heparinization will be used
If emergent case and unable to delay: delay systemic heparinzation for 60 mins, minimize heparin dosing, neurologic exam q1h, avoid local anesthetic through epidural if using to allow for motor exams
Why use an epidural for thoracoabdominal aorta surgery?
- Excellent post-op pain control
- Improve resipratory function (decreased atelectasis, pulm infxn, respiratory failure)
- Improve graft patency (reduced coagulation response)
- Reduce postop myocardial ischemia (attenuate stress response)
What is acute normovolemic hemodilution? What are the pros/cons?
ANH: autologous blood collected at beginning of case, then re-infused (need initial Hcg >33/Hgb >11). Collect 1-2 units blood and administer warmed crystalloid to maintain normovolemia.
Pros: reduce exposure to allogenic blood
Cons: only save up to 1-2 units pRBC, reduction in oxygen carrying capacity may not be tolerated by some patients
Contraindications:
- anemia (Hcg <33, Hgb <11)
- impaired renal function (since giving extra crystalloid)
- pt cannot tolerate increased cardiac output from decreased blood viscosity (e.g. AS)
- significant pulm disease (decreased oxygen content of blood)
- pre-existing coagulopathy
Blood pressure goals during aortic cross-clamp for TAA repair
Above cross clamp: MAP ~100
Below cross clamp: MAP>50
How to manage decrease in SSEP signal after aortic cross clamp placement
- optimize hemodynamics
- check ABG
- ask perfusionist to increase distal pump flows and correct hypo/hypercarbia and acisosis
- if needed, ask surgeon to reposition clamp (may be blocking critical intercostal artery)
- ensure adequate hypothermia (30-34 C)
- withdraw 10-20cc CSF from lumbar drain (target ICP 8-10)
- consider pharmacologic intervention (corticosteroids, Mg, CCB, mannitol, etc.)
Causes of hypotension following aortic cross-clamp release
Central hypovolemia and decreased cardiac preload
There is tissue ischemia and vasoactive mediator release distal to cross-clamp, leading to decreased SVR, increased venous capacitance, and increased capillary permeability. Acid metabolites and vasoactive mediators released into bloodstream lead to decreased myocardial contractility and increased PVR.