Vascular Surgery

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Vascular Surgery
2014-02-12 18:59:32
BC CRNA Vascular surgery

Greg's lecture 2/10/14
Show Answers:

  1. What is the difference between functional and organic peripheral vascular disease?
    • Functional:
    • ---No organic cause: not involving defects in vessel’s structure
    • ---May involve spasm:Raynauds dx.
    • ---Triggered by emotional stress and smoking
    • Organic:
    • ---Caused by structure changes in vessel
    • ---Inflammation (arteritis/vasculitis), tissue damage (atherosclerosis)
  2. Are women as likely to have symptoms compared to men for peripheral vascular disease?
    no, women are less likely to have symptoms
  3. TRUE or FALSE. African americans are more likely to have PAD but this does not necessarily increase their cardiovascular risk factors.
  4. Define atherosclerosis
    process in which deposits of fatty substances, cholesterol, cellular waste products, calcium, smooth muscle cells, connective tissue and other products build up in the lumen of the artery
  5. Name four causes of atherosclerosis
    • Hypercholesterolemia
    • HTN, shearing from vessel wall stress
    • Tobacco smoke
    • Diabetes
  6. How does DM become a risk factor for atherosclerosis?
    • Function of gylcation end products, they become toxic and inhibit the function of the endothelial lining and inhibit iNO.
    • Glycation end products of the blood vessels produce oxidative stress to the endothelial lining increases levels of proinflammatory cytokines.
  7. What are the controllable risk factors for atherosclerosis?
    • Cholesterol = LDL > 100 mg/dL
    • Smoking
    • HTN
    • Diabetes
    • Obesity
    • Physical inactivity
    • Hyperhomecystenemia
  8. Describe the three different types of plaque in atherosclerosis (test question!!)
    • Coronary artery plaques (unstable). Have increased macrophage content and thin caps with thick lipid core: rupture more common than occlusion
    • Carotid plaques (unstable) have similar make-up but more commonly cause problems by occlusion rather than rupture
    • Low risk plaques have thicker caps, cause more vessel lumen narrowing and produce more predictable exercise ischemic events, less likely to tear
  9. What are 4 commons sites for plaque lesions?
    • Coronary arteries
    • Carotid bifurcation
    • Abdominal aorta
    • Illiac arteries
  10. In general, the plaques tend to form at bifurcations, why is this?
    more turbulent flow
  11. What is a desirable cholesterol level? What is high risk LDL level, what's the goal level?
    • Cholesterol: desirable total cholesterol is less than 200.
    • High risk LDL is 240 and over
    • Goal LDL is less than 100.

    Youu can reverse PVD by lowering your LDL
  12. 50% have mild to no symptoms of PVD.
    BUT 30 – 50% have more severe symptoms such as...... (list the symptoms)
    • Claudication
    • Numbness or weakness of legs, calves, toes and buttocks
    • Cold legs or feet
    • Non-healing sores on lower extremities
    • Paleness of legs and feet when elevated
    • Hair loss on legs, shiny or scaly skin
    • Changes in nail beds
    • Impotence
    • Gangrene
  13. What are the 3 theories of PVD?
    • Response to injury theory: Virchow’s theory
    • Monoclonal Hypothesis
    • Clonal Senescence
  14. What is the response to injury theory for PVD?
    • Response to injury theory: Virchow’s theory 150 years ago
    • Endothelial injury caused by many physical and chemical factors
    • Leads to desquamation and exposure of the subendothelium
    • Smooth muscle proliferation caused by arterial smooth muscle migration into the intima of the vessel and platelet adherence
  15. What is the Monoclonal hypothesis for PVD?
    • Benditt and Benditt 1973
    • Each lesion is derived from a smooth muscle cell that proliferates around a focus
    • Analogous to a malignancy (cell proliferates secondary to a mutagen or virus)
  16. What is the clonal senescence theory for PVD?
    • Martin and Sprague
    • Smooth muscle proliferation is controlled by local feedback from inhibitory hormones
    • Aging decreases inhibiting feedback and increases growth of lesion producing cells
  17. Why is the aorta particularly susceptible to an aneurysm?
    due to high constant stress to vessel wall and absence of penetrating vasa vasorum in the adventitial layer
  18. What is generally the cause of an aortic aneurysm?
    Atherosclerosis and HTN is generally the cause
  19. What are the 4 contributing factors to developing an aortic aneurysm?
    • 1. Presence of genetic marker
    • 2. Deficiencies of vessel wall collagen or collagen elastin matrix
    • 3. Increase protease activity and age related non-functional elastin
    • 4. Increase turn-over of Aortic collagen
  20. Vasculitis is defined as an inflammation of blood vessels, which includes veins, arteries and capillaries. What are the symptoms of this??
    • Fever
    • Fatigue
    • Weight Loss
    • Muscle and joint pain
    • Loss of appetite
  21. Is vascultitis common or rare? What age group does it effect?
    Effects people of all ages. RARE in occurrence.
  22. What is the CAD risk in those w/PVD?
    < 10% of patients having vascular surgery have normal coronaries

    Protecting the heart is important
  23. A patient w/PVD is high risk if they have more than 3 of the following...
    • Advanced age
    • CHF
    • Previous MI
    • Limited ETT
    • CRI
    • Diabetes
  24. How do we do intraoperative risk reduction for the patient w/PVD?
    • Beta Blockers
    • Forced air warming
    • ICU Monitoring
  25. What kind of pre-op exam would you want to do for a patient w/PVD?
    • Auscultation of the neck and abdomen.
    • Listen and look for evidence of left ventricular dysfunction.
    • Assess distal extremities for evidence of ischemia.
    • Palpate radial pulses.
    • Cuff blood pressure assessment in both arms.
    • Baseline ECG and preoperative laboratory studies.
    • Preoperative chest radiograph for patients with chronic obstructive pulmonary disease, active pulmonary symptoms, or procedures involving the abdomen or thorax.
  26. Describe MAJOR predictors of increased perioperative CV risk
    • Unstable coronary syndromes (acute or recent MI, unstable severe angina)
    • Decompensated HF
    • Significant arrhythmia
    • Severe Valve disease
  27. What are the INTERMEDIATE predictors of increased perioperative CV risk?
    • Mild angina
    • Previous MI by history or Qwave
    • Compensated or prior HF
    • DM
    • Renal insufficiency
  28. What are the MINOR predictors of increased perioperative CV risk?
    • Advanced age
    • Abnormal EKG
    • Rhythm other than sinus
    • Low functional capacity
    • History of stroke
    • Uncontrolled systemic HTN
  29. What are HIGH risk surgery (cardiac risk are high)
    • Emergent major operations
    • Aortic or major vascular surgery
    • Peripheral vascular surgery
    • Anticipated long procedures w/fluid shifts
  30. What are INTERMEDIATE risk surgeries (cardiac risk)
    • Carotid endarterectomy
    • Head and Neck surgery
    • Intraperitoneal and intrathoracic surgery
    • Orthopedic surgery
    • Prostate surgery
  31. What are the LOW risk surgeries (cardiac risk)
    • Endoscopic procedures
    • Superficial procedures
    • Cataract surgery
    • Breast surgery
  32. What is the most common cause of perioperative death??
    Myocardial ischemia, usually occurs POST-OP
  33. Why is a TEE useful in detecting ischemia?
    • detects segmental wall motion abnormalities that occur earlier than EKG changes at the onset of ischemia.
    • You may see decreased ventricular wall thickening during systole
  34. Do we initially try medications or surgery to treat PVD???
    • Medication initially.
    • Peripheral vascular surgery is reserved for severe ischemia secondary to limited durability of bypass graft
  35. Arterial insufficiency: acute or chronic limb ischemia. Describe the difference in acute and chronic
    • Acute: embolism, thrombus or pseudoaneurysm. Irreversible tissue injury within 4-6 hours
    • Chronic: atherosclerotic plaque; claudication
  36. What is the ankle/arm index?
    • evaluates severity of arterial insufficiency Ankle SBP/brachial SBP
    • > 1 normal
    • < 0.6 claudication
    • < 0.25 pain at rest
  37. What are the 4 common procedures for peripheral vascular surgery?
    • Axillofemoral bypass
    • Femorofemoral bypass
    • Aortofemoral bypass
    • Femoral Popliteal bypass*most common*
  38. What are some pre-operative considerations for peripheral vascular surgery?
    • Regional vs. General
    • Avoid tachycardia and hemodynamic extremes
    • Control of blood pressure and heart rate (NTG, Esmolol)
    • A Line-you will need it even if it’s difficult to put in
    • Maintain normal volemia
    • Avoid postoperative tachycardia, hypothermia, hypervolemia and pain
  39. What are the pros and cons of general anesthesia for peripheral vascular surgery?
    • PROS: Patient may remain on IV anticoagulation therapy without interruption
    • Able to graft upper extremities
    • CONS: Hypercoagulable state (GA causes this)Increased postop catecholamines
    • May pose ventilatory challenges postop-May increase ICU stay because of it, intubated or not it can do this
  40. Where would you place the epidural for vascular surgery?
    T12 but may need T10 for Fem/Fem Sub q tunneling of graft. T8 if exposing the pelvis
  41. What are the pros and cons of regional anesthesia for peripheral vascular surgery?
    • CONS: IV anticoagulation must be stopped prior to regional, Limited duration,Thoracic epidurals pose challenge, & Risk of high sypathectomy
    • PROS: Stable hemodynamics with incremental dosing & Evidence of improved graft patency
  42. What drugs should we avoid for patients at risk for delirium
    • Avoid intra-op atropine, benzodiazepines, scopolamine.
    • Judicious drug dosing, CHF depressant, H2 antagonists, anticholinergics.
  43. What are the goals of anesthetic management in carotid endarterectomy?
    • Optimize cerebral perfusion in patients with high probability of CAD
    • Minimize CVA risk
  44. When is cartoid endarterectomy more effective than medical management?
    More effective than medical treatment for patients with ICA narrowing 60% to 90%
  45. What are the symptoms of someone w/carotid occlusion or narrowing?
    • Symptoms include TIA, CVA, upper or lower extremity numbness or weakness, unilateral monocular blindness (vision loss in one eye)
    • Often hemispheric neurologic symptoms
  46. For carotid endarterectomy, Neurologic deficits often occur ____ hours postop in patient with poorly controlled hypertension preop
  47. Where does carotid atherosclerosis develop?
    • Commonly at carotid bifurcation
    • Origin of ICA
  48. Cerebral injury usually occurs from embolic or stenotic lesions?
    Embolic vs. stenotic (90% embolic)
  49. For carotid atherosclerosis, Degree of cerebral injury depends on:
    • Integrity of circle of Willis
    • Plaque morphology
    • Collateral flow
  50. What type of CAD is common in patients w/carotid stenosis?
    L. main CAD
  51. What nerves are we concerned about for carotid endarterectomy?
    • Vagus nerve (CN X) near the carotid sinus.
    • Carotid bodies are innervated by the glossopharyngeal nerve and hypoglossal nerve
  52. For carotid endarterectomy, increased risk in poor neurologic outcome seen in patients with: (What 7 things)
    • Poor collaterals
    • Contralateral carotid occlusion
    • Renal insufficiency (Cr above 2)
    • Poorly controlled HTN
    • CAD requiring bypass
    • Decreased consciousness preop (key!)
    • Active neurologic process prior to surgery
  53. What type of receptors are at the carotid sinus vs carotid bodies?
    • Carotid sinus: baroreceptors
    • Carotid bodies: chemo receptors
  54. Why is it very important to know if the glossopharyngeal nerve was injuried?
    If you injure glossopharyneal nerve, and patient is insensitive to hypoxia.
  55. Is Etomidate recommended as a cerebral protectant for carotid endarterectomy?
    Etomidate: short duration of action can worsen ischemic injury. Not recommended as a cerebral protectant
  56. Can we use a thiopental gtt for a carotid endarterectomy?
    • Evidence does not support use of barbiturates as a cerebral protectant for permanent focal ischemia. It is supported for transient focal ischemia.
    • No evidence that says a thiopental gtt is good.
    • Methohexital can have significant cardiac depression and delay awakening.
  57. Why are young people more likely to have serious injury from an embolic event?
    No time for collaterals to develop
  58. What are some intraoperative goals and considerations for carotid endarterectomy?
    • Hemodynamic control, prevention of ischemia and minimize stress response
    • Ventilation: normocarbia-not hyper--don't want steal
    • Glycemic Control: avoid hyperglycemia
    • Temperature
    • Monitoring
    • Short Acting Agents: Smooth wake up but want to do neuro exam ASAP
    • Hemodynamic Control
    • Fluid Management
    • Carotid Sinus: euvolemia
  59. What are our goals of intraoperative monitoring for carotid endarterectomy?
    • Prevent intraoperative stroke
    • Prevent neurologic deficit due to impaired CP
    • Identify patients in need of shunting
    • Identify patients who may benefit from BP augmentation
  60. At what cerebral blood flow are tracings of EEG abolished?
    CBF of less than 12 (Normal CBF is 45-50ml/100g of brain tissue)

    But the EEG can detect tracings when the flow is lower than 40
  61. What type of Regional/local anesthesia can you give for a carotid endarterectomy?
    • Requires cervical plexus block and subsequent local infiltration with 1% lidocaine
    • CPB blocks innervation of the anterolateral neck through anterior primary rami of C2-C4
  62. What are the advantages and disadvantages of the cervical plexus block for carotid endarterectomy?
    • Advantages: Allows continual neurological assessment of awake pt Limits need for expensive monitors. Prompt wake up. Hemodynamic stability. Less hospital cost
    • Disadvantages: Necessitates constant cooperation. Limits sedation and amnesia. Risk of poor patient satisfaction. No difference in postop stroke incidence (3%). No airway access. Phrenic nerve paralysis (d/t block)
  63. What are the contraindications for the cervical plexus block?
    • High carotid lesions
    • Language barrier
    • Claustrophobia
    • Patient prefers to be asleep
  64. What are the advantages and disadvantages of general anesthesia for the cervical plexus block?
    • Advantages: Ability to manipulate hemodynamics. Reduce O2 demand and catecholamine level. Reliable amnesia. Airway security. Larger potential population
    • Disadvantages: Expense, monitoring. Slower wake up. Potential for postop increase in catecholamine level. Potential for ventilatory challenges
  65. Name 4 post-op considerations for carotid endarterectomy
    • Recurrent laryngeal nerve palsy, unilateral vs. bilateral (7%-8% incidence.)Effects muscles that move vocal cords.Hoarse voice if unilateral.
    • Hyperperfusion syndrome:  HA, seizures, focal seizures, vision changes (transient, can occur some days after sug until autoregulation returns)
    • Stroke
    • Carotid body denervation: Unilateral usually tolerated & Bilateral yields poor ventilatory response
  66. Who is a candidate for carotid stenting?
    • Cath lab procedure
    • Generally MAC Anesthesia
    • High risk patients
    • Patients that have narrowing after CEA, trying to expand exisiting graft
  67. What is the risk of rupture of a AAA directly related to???
    • Risk of rupture directly related to diameter of aneurysm
    • Risk of rupture increases with diameter > 4.5 to 5 cm
  68. When is surgery indicated for a AAA?
    • Elective repair with diameter 6 cm or greater
    • Surgery indicated if larger than 0.5 cm increase in 6 months or symptomatic
  69. What are risk factors for AAA?
    • Increased age
    • smoking > 40 years
    • HTN
    • Increased LDL
    • low platelet count
    • history of atherosclerosis
  70. What is the law of Laplace?
    T = PR/2h
  71. What are the causes of AAA? (common and uncommon)
    • Causes (common)
    • --Age
    • --Atherosclerosis (greater than 90%)
    • --Genetics
    • --Mechanical factors
    • --Hemodynamics
    • Causes (uncommon)
    • --Trauma
    • --Mycotic infections
    • --Marfan syndrome
    • --Rheumatoid arthritis
    • --Syphilis
  72. Describe the cardiovascular changes with Aortic cross clamping
    • MAP ↑ SVR ↑ 50%
    • CO ↓ initially 5-10%
    • ↓O2 consumption below clamp
    • Preload may ↑ in myocardial dysfunction (LV dysfunction)
    • Myocardial ischemia
    • Infrarenal vs. Suprarenal
  73. Where are most AAA located?
  74. What are some therapeutic interventions we can do for cross clamping
    • Sodium nitroprusside, Fenoldopam, inhalations anesthetics, NTG.
    • Beta blockers
  75. What physiologic change would you see with cross clamping?
    • ↑ Arterial blood pressure above the clamp
    • ↓ Arterial blood pressure below the clamp
    • ↑ Segmental wall motion abnormalities
    • ↑ Left Ventricular wall tension
    • ↓ Ejection Fraction
    • ↓ Cardiac Output
    • ↓ Renal Blood Flow
    • ↑ Pulmonary Occlusive Pressure
    • ↑ CVP ↑ Coronary Blood Flow
  76. What metabolic changes would you see with cross clamping?
    • ↓ Total body Oxygen Consumption
    • ↓Total Body Carbon dioxide production
    • ↑Mixed Venous Oxygen Saturation
    • ↓ Total body Oxygen extraction
    • ↑ Epinephrine and Norepinephrine
    • Respiratory Alkalosis
    • Metabolic Acidosis.
  77. What can we do for afterload reduction during cross clamping?
    • Sodium Nitroprusside
    • Inhaled Anesthetics
    • Amrinone
    • Shunts and Aorto to femoral Bypass.
  78. What can we do for preload reduction during cross clamping?
    • Nitroglycerin
    • Phlebotomy.
    • Atrial to femoral bypass
  79. What can we do for renal protection during cross clamping?
    • Fluid administration
    • Distal aortic perfusion techniques
    • Mannitol
    • Drugs to Augment renal perfusion.
  80. What other things can we during cross clamping (think metabolic and acid/base)
    • Hypothermia
    • ↓ Minute Ventilation
    • Sodium Bicarbonate
  81. When the aortic clamp is released, what cerebrovascular and metabolic changes do you see?
    • Reactive Hyperemia and Central Hypovolemia
    • Decreased BP
    • CVP decrease
    • CO and Cardiac contractility decreases (because of humoral factors)
    • pH decreases, lactate increases
    • CO2 increases
  82. What therapeutic interventions can you do during the release of the aortic clamp?
    • Volume, phenylephrine
    • Calcium, ephedrine, epinephrine
    • Sodium bicarbonate
    • ↑Minute ventilation
  83. In aortic cross clamping, blood is redistributed away from hypoxia prone renal medulla, with a cross clamp an increase in renal vascular resistance may persist for ______________ after clamp is released.
  84. How are the renal HD affected by the aortic cross clamp?
    • ARF approaches 5% with infrarenal clamping; 13% with suprarenal clamp
    • Mortality is 5 times higher with postop dialysis
    • RBP ↓ 80% with suprarenal clamp
    • Renal vascular resistance Increases 70%.
  85. What are Barash goals of treatment for cross-clamping?
    • Wedge at 5-15mmHg, keep HR less than 80.
    • Use narcotics prior to cross clamping.
    • Keep patient somewhat hypovolemic or increase volatile. (just keep euvolemic).
    • Try to avoid neosynephrine, Neo has been associated with wall motion abnormalities.
    • Keep Hct 30% during clamp time.
    • Let BP increase gradually and let the clamp up slowly.
  86. What can we do for renal protection during cross clamping??
    • Mannitol– 12.5 to 25 mg/70 kg
    • Lasix-- .5 to 1 mg/kg
    • Dopamine– 1 to 3 µg/kg/min
    • Fenoldopam--.05 to 0.1µg/kg/min
    • Mucomyst-600 mg PO bid
  87. What two things are the best predictors of post-op renal function??
    Pre-op renal function and volume status
  88. Describe humoral and coagulation changes with aortic cross clamping.
    • Humoral mediators released from underperfused areas
    • May result in pulmonary hypertension and pulmonary edema
    • Increased clotting factor consumption after clamping
    • Increased clotting activity with clamping
    • May require cryoprecipitate, 1:1 PRBC with FFP, Amicar, desmopresin, ↑ room temperature
  89. Describe the visceral and mesenteric ischemia that happens with cross clamping
    • Bowel ischemia
    • Gut permeability and bacterial translocation
    • Inflammatory mediators from gut ischemia may be factors in renal failure and respiratory failure
  90. What happens to the cerebral vasculature during unclamping?
    • Cerebral vasoconstriction caused from chemical mediators
    • Cerebral vasodilation after unclamping followed by profound vasoconstriction
  91. Spinal cord ischemia is more likely to occur the more proximal the repair is.  Which artery is very important in perfusing the spinal cord and where does it enter ?
    Artery of Adamkiewicz – 75% joins anterior spinal artery between T8 and T12; 10% L1 to L2
  92. Name the 8 methods of CNS protection during AAA surgery
    • Fast surgery/clamp time less than 30 minutes
    • Intraoperative regulation of hemodynamics (normohemodynamics)
    • Maintain or increase perfusion pressure
    • May need bypass if longer clamp times
    • Hypothermia 30 to 32 degrees Celsius
    • CSF drainage
    • Barbiturates
    • Calcium channel blockers
  93. What is the single best anesthetic technique for AAA? (regional vs general)
    • Trick question, there isn't a single best! Balanced approach is probably best!
    • Opioids, Nondepolarizers, Benzodiazepines, & Epidural catheter
  94. What are some important things to remember about epidural catheters for AAA repair?
    • Intraop or postop dosing
    • Blood tap = cancelled case or delay case?Monitor coags
    • May use IV heparin after catheter is placed
    • May improve graft function
    • Watch for hemodynamic changes
  95. When would you want a PA catheter during AAA repair?
    PA catheter for LV dysfunction, cr > 2.0, EF < 30%, CHF, and suprarenal clamp
  96. Describe type A and type B of aortic dissection
    • Type A: Ascending aorta to aortic arch
    • Type B: Proximal descending aorta and ends distally
  97. What are some s/s of aortic dissection?
    • “Tearing” pain unrelieved with position change
    • Radiating pain in 20% of patients
    • Dissection of ascending aorta yields anterior chest pain with radiation to neck
    • Dissection of descending aorta yields interscapular back pain, lower back pain with radiation to abdomen
    • Less common signs and symptoms include syncope and CHF
  98. Where do we want the BP in an aortic dissection??? (TEST question)
    Surgical goal is to decrease SBP 90-120 mmHg to reduce wall tension.
  99. What is the CRAWFORD classification of aortic dissection? (TEST question)
    • Type I: begins distal to subclavian artery
    • Type II: involves most of descending aorta & most or all of abdominal aorta
    • Type III: distal descending thoracic aorta & abdominal aorta
    • Type IV: involves most or all of abdominal aorta
  100. What is the Debakey classification of aortic dissection? (TEST question)
    • Type I: begin in the ascending aorta and extend throughout the entire aorta.
    • Type II: confined to the ascending aorta
    • Type III: begin just distal to the left subclavian artery and extend either to the diaphragm or to the aortoiliac bifurcation
    • Type III B: a subclass of type III involving both the thoracic and the abdominal aorta
  101. What kind of anesthesia would you do for an Endovascular AAA repair?
    • Typical technique is lumbar epidural and radial A Line
    • T10 Level preferred, T12 Level required
    • Single shot spinal vs. epidural?
    • Combined general with regional
    • General if regional is contraindicated
    • May convert to general if extensive groin exploration is used or if vasculature will not permit endo repair
    • Likely more endo repair with thoracic aneurysms and patients with extensive aortic disease
  102. Keep systolic BP less than ___ for
    descending thoracic aorta endo repair
  103. Is a fever normal after endo AAA repair?
    YES, 24 – 48 hours patient may occasionally have low grade fever and leukocytosis secondary to reaction to graft material
  104. What would a vascular injury appear as in an endo AAA repair?
    • Vascular injuries may present as hypotension, tachycardia and low HCT
    • *Retroperitoneal bleed may not be appreciated*
  105. What are the major complications of an endo AAA repair?
    Endoleaks graft migration kink or occlusion, aneurysm rupture
  106. How often is follow up for an endo AAA repair?
    Follow up CT scans 1, 6, 12 months
  107. What are the 4 types of Endo leaks? (TEST question!)
    • Type I: When there is an inadequate seal between the endograft and the aortic wall at the proximal or distal attachment sites
    • Type II: Occurs when there is retrograde filling of the aneurysms sac from patent lumbar, intercostal, or inferior mesenteric arteries
    • Type III: Caused by structural failure of the endograft that allows blood flow directly into the aneurysm sac
    • Type IV: Related directly to the porosity of the graft material and is usually self-limiting
  108. Type ___ and Type __ endoleaks are associated with an increased risk of rupture and are treated aggressively
    I and III
  109. Type ___ endoleaks are often associated with aneurysm enlargement, but usually do not required urgent treatment
  110. For endo AAA repair, Stent graph device requires and infrarenal neck of at least ____ to avoid occluding one or both renal arteries
  111. Angiographic balloon sometimes used for placement during endo AAA repair. What should we know about this??
    • Heparin 100 units/kg given prior to deployment of balloon
    • Induced hypotension, adenosine induced asystole, and induced V-Fib are used to prevent graft migration during stent deployment (4)
  112. What post-op tests should we get for AAA repair?
    • Renal function
    • H and H, coags
    • Telemetry monitoring
    • Chest X-ray
    • ABGs (respiratory management)
  113. What are some common complications of AAA surgery?
    • Coagulopathy
    • Myocardial ischemia
    • Hypovolemia
    • Renal failure
    • Graft occlusion
    • Illeus-bowel ischemia
    • Paraplegia