Ap2 Aaa Review

Front 1

AAA involves what layers of the aorta?

Back 1

All 3 layers-however medial layer is thinner as you descend down thru the body making it prone to weakening

Front 2

Where does the Abdominal Aorta begin and end?

Back 2

Aortic hiatus in the diaphragm-T12 and ends common iliac bifurcation @ L4

Front 3

What are the main branches off the anterior aorta?

Back 3

Celiac, SMA, IMA

Front 4

What are the branches off the posterior aorta?

Back 4

Inferior phrenic, Lumbar arteries

Front 5

What are the branches off the lateral aorta?

Back 5

Suprarenal, Renal, Gonadal

Front 6

What are the main branches off the celiac artery?

Back 6

Common Hepatic, Left gastric, Splenic

Front 7

What is the #1 reason for AAA?

Back 7

Atherosclerotic Disease

Front 8

Where is the most common site for AAA?

Back 8

The aortoiliac bifurcation

Front 9

What is the risk for AAA if familial?

Back 9

25%

Front 10

Medical tx for AAA?

Back 10

Those less than 5cm (Nml-1-3cm; >50% diameter of vessel is aneurysm)
β-blocker tx
Serial ultrasounds q 6-12 mths
Avg growth rate-0.2-0.5cm/yr (any > then consider sx)

Front 11

Mortality for a ruptured AAA is?

Back 11

15-90%

Front 12

What are the most common approaches for a AAA?

Back 12

Transperitoneal - midline
Retroperitoneal -R lateral decub - Left exposure

Front 13

Which one has the least amt of EBL?

Back 13

Retroperitoneal

Front 14

Which surgical approach has less post op ileus?

Back 14

Retroperitoneal

Front 15

Which surgical approach is more painful?

Back 15

Transperitoneal

Front 16

What are the 3 types of aneurysms?

Back 16

Fusiform
Berry/Sacular
Dissecting

Front 17

What is the dosing of heparin?

Back 17

100 units/kg-given IV

Front 18

X-clamping distally is done first for what reason?

Back 18

To prevent migration of any emboli

Front 19

What are the common grafts made from?

Back 19

Dacron/Gortex/Polytetrafluorethylene- these require less dissection during sx, shorter OR times

Front 20

The main body system for concern during AAA repair is what?

Back 20

The CV system because of the increase in afterload

Front 21

What is normal size of the aorta?

Back 21

1.5-3 cm

Front 22

What is a big predictor of postoperative recovery?

Back 22

Creatinine >3

Front 23

What factors require CABG prior to AAA repair?

Back 23

LM disease\
EF<35%
TVD

Front 24

How should the pts deficit be approached?

Back 24

Euvolemia is optimal in this sx. Replace ½ of the deficit early but not entirely. Needed for optimal CO and renal function however when x-clamp is placed hypervolemic state may impair CO

Front 25

What are factors that may lead you to place a PA catheter in your pt?

Back 25

Creatinine> 3
Suprarenal clamping

Front 26

Hemodynamic parameters should remain where for this sx?

Back 26

20% of baseline as rule of thumb
HR-tachycardia causes Decreased filling and Increased MVO2-keep lower parameters

Front 27

What agents should be readily available for this sx?

Back 27

SNP/NEO/Fenoldapam
NTG
Ca++channel/β-blockers
Dopa/Dobt/
Heparin/Protamine
********Have a prepared plan ready

Front 28

Heparin may be safely given when neuraxial anesthesia is used after what time frame?

Back 28

>1hr

Front 29

What is Enoxaparin?

Back 29

LMWH

Front 30

What is considered a high dose?

Back 30

1mg/kg bid

Front 31

When can neuraxial anesthesia be used safely when LMWH is used?

Back 31

10-12 hrs after last dose or >24hrs if high dose was given

Front 32

When may the catheter be safely removed when LMWH is used?

Back 32

2hrs prior to next dose or 10-12 hrs after last dose given

Front 33

What may be the best induction agent available for AAA cases?

Back 33

Etomidate

Front 34

What should fluid status be at the time of x clamping?

Back 34

Euvolemic or mild hypovolemia

Front 35

What is Mesenteric Traction Syndrome?

Back 35

A metabolite of prostacyclin and thromboxane B2 that causes:
Flushing
decrease SVR/MAP
Tachycardia
Pronounced increase CI
***Will not be seen with the retroperitoneal approach

Front 36

How is MTS tx’d?

Back 36

Cycoloxygenase inhibitors however may be contraindicated in sx so tell surgeon to release traction-use phenylephrine and/or β blockers, not fluids

Front 37

What metabolite of prostacyclin and thromboxane B2 affects MTS?

Back 37

6-Ketoprostaglandin F1

Front 38

What is the affect of x-clamping the aorta?

Back 38

Myocardial stress increases due to increased afterload-the amount of stress is r/t the height of the clamp. Hypervolemia at the time of x-clamping will accentuate the afterload and stress. This is why it is good to have a PA/CVP in place

Front 39

What should be done prior to x-clamping?

Back 39

Assess renal function-U/O and myocardial function

Front 40

What actions may be taken prior to x-clamping for the kidneys?

Back 40

Mannitol/Lasix/Fenoldopam
Blood flow will decrease as much as 40%

Front 41

What is Fenoldapam?

Back 41

DA1 agonist that produces renal artery dilation

Front 42

What should be done immediately after x clamping?

Back 42

Check myocardial function/EKG

Front 43

Evidence of ischemia or LV failure post clamp should include what interventions?

Back 43

Inform surgeon Full or partial removal of clamp Vasoactive drugs

Front 44

What effects should be anticipated post removal of clamp?

Back 44

HOTN
Metabolite washout/Vasoactive agents-causes Pulm HTN
increase ETCO2
Hypovolemia
Initial increase in CO then decrease in CO

Front 45

Important documentation of this surgery includes?

Back 45

Keeping the x clamp time

Front 46

Prior to removal x clamp one should consider?

Back 46

Decrease SNP and/or lightening the anesthesia

Front 47

Where should Hct be kept?

Back 47

Around 30

Front 48

Where should PCWP be?

Back 48

12-18-careful not to overdilate the myocardium.

Front 49

HOTN > 4 minutes after x clamp release may be due to what problems?

Back 49

Excessive anesthesia
Vasodilators still on
Myocardial dysfunction
Bleeding

Front 50

What is the #1 morbidity in the post op period r/t?

Back 50

Myocardial dysfunction

Front 51

Spinal cord perfusion comes from what areas?

Back 51

Superior: Upper thoracic/Cervical
Subclavian/Vertebral
Mid Thoracic-T2-T8
Intercostals
Thoracolumbar: T8-Conus (L1-2)
Artery of Adamkiewicz
75% T8-12
15% L1-2

Front 52

What is the latest solution to traditional AAA repair?

Back 52

Endovascular grafting

Front 53

Selection of patients may include what characteristics for endovascular grafting?

Back 53

Infrarenal aneurysms-cant do for suprarenal or long aneurysms
Abnormal mesenteric circulation
Tortuous or angled iliac or aorta

Front 54

Decreased BP may be desired in the endovascular graft for what reasons?

Back 54

To prevent forward flow of the graft

Front 55

The reason for higher circulating levels of epi in the open procedure vs. the closed procedure is?

Back 55

The NE response is activated much more

Front 56

Goals of the anesthetic management of ruptured AAA include?

Back 56

Immediate attempt to control proximal aorta –may require cutting prior to induction
Blood loss control
Attain BP
Preserve myocardial function
Induction/cut

Front 57

How should induction occur with a ruptured AAA?

Back 57

Awake-Etomidate and MR
Unconscious- MR and Scopolamine

Front 58

Management of ruptured AAA?

Back 58

***Primary concern is to gain control of bleeding
Monitors after induction
MR/Vasoactive drugs
Type specific non-crossed blood or O-
NO Heparin

Front 59

List the branches of the aorta from superior to inferior:

Back 59

Inferior phrenic- posterolateral
Celiac trunk - anterior T12
SMA - anterior L1
Suprarenal - lateral, paired L1
Renal - lateral, paired L2
Gonadal - lateral, paired L2
IMA - anterior L3
Lumbar - posterolateral
"I Can Smell Supper Real Good I'm Lucky"

Front 60

Criteria for high risk in AAA repair include:
a) serum creatinine level > 3 mmg/dl
b) PaO2 50-85 mmHg
c) Age > 85 yrs
d) LVEF<30%
e) Male gender

Back 60

a,c,d
PaO2 should be < 40 mmHg, gender isn't a criteria for high risk repair

Front 61

Classify the following hemodynamic changes to aortic cross clamping/declamping as: increase,decrease or no change:
1.MAP with aortic clamping
2. CO with declamping
3. SVR with declamping
4. Pulmonary artery occlusion pressure with declamping
5. CO with clamping
6. Afterload with clamping

Back 61

1. Increase
2. no change or increase
3. decrease
4. decrease
5. no change or decrease
6. increase

Front 62

Place the following branches from the abdominal aorta in order from diaphragm to iliac bifurcation:
a) inferior phrenic arteries
b) renal arteries
c) inferior mesenteric artery
d) celiac trunk
e) superior mesenteric artery

Back 62

a,d,e,b,c

Front 63

Which of the following actions are appropriate when preparing for the cross clamp to come off in a AAA repair?
a) start Nipride infusion
b) add PEEP
c) restore circulating blood volume
d) have bicarb readily available
e) increase IA

Back 63

c,d
SNP, PEEP and increasing agent are not appropriate actions to take when the cross clamp is coming off as these actions would decrease SVR and venous return. Declamping causes hypotension and decreased CO.

Front 64

Renal failure post op can be linked to:
a) cross clamp time> 45 min
b) infrarenal cross-clamp
c) suprarenal cross-clamp
d) complete cross clamp removal vs. staged removal

Back 64

c
there is an 80% decrease in RBF with a 13% occurrence of post -op failure with suprarenal clamping

Front 65

Pt status just prior to pre-clamp should include:
a) hypervolemia to euvolemia to maintain adequate perfusion and blood pressure.
b) Use of mannitol and low dose Epi for optimal renal protection
c) dosage of Heparin at 200 units/kg IV
d) vasodilator dose of Nitroglycerin at 0.25 mcg/kg/min

Back 65

d
Some of the initial hemodynamic changes of cross clamping can be attenuated by vasodilators given immediately before clamp placement -Nipride 0.3-0.7 mcg/kg IV over 10 min/NTG at 0.25 mcg/kg/min

Front 66

There are many physiologic changes with the clamping of the aorta. Choose the best answer to manage these changes:
a) Afterload reduction (diastolic wall tension) with Nipride
b) Preload reduction (systolic wall tension) with Nipride
c) Renal protection with mannitol, fluid restriction, Lasix
d) Afterload reduction (systolic wall tension) with inhalation agents

Back 66

d
Afterload reduction is a decrease in systolic wall tension and includes interventions such as Nipride, IA, amrinone, shunts and aorta-to-femoral bypass.

Front 67

Physiologic changes and therapeutic management with aortic unclamping include:
a) decreased myocardial contractility, decreased pulmonary artery pressure that can be managed by decrease in IA, increase in fluid admin
b) decreased venous return, decreased cardiac output, increased myocardial contractility, managed by a decrease in vasodilators, increase in vasoconstrictors, increase in fluid admin.
c) decreased venous return, ecreased cardiac output, increased pulmonary artery pressure, managed by a decrease in inhalational anesthetics, decrease in vasodilators

Back 67

c
Hemodynamic changes: decreased myocardial contractility/ arterial BP/ CVP/ venous return/ CO, increased PAP
Metabolic changes: increased total body O2 consumption/lactate/prostaglandins, activated complement and myocardial depressant factors, decreased mixed venous O2 sat/temp, metabolic acidosis
Therapeutic interventions:
decrease IA/ vasodilators, increase fluid admin/vasoconstrictors, reapply cross clamp for severe hypotension, consider mannitol and sodium bicarb