Vascular Anesthesia Pt.1 (Exam I)

Question 1

What comorbidities are typical of “vasculopaths”?

Answer 1

• DM
• HTN
• CRI
• COPD

>50% have CAD.

Question 2

Heparin is a naturally occurring anticoagulant produced by ______ and ___ ____.

Answer 2

basophils & mast cells

Question 3

What does heparin directly bind to?

Answer 3

Antithrombin III

Question 4

What is the consequence of heparin binding to antithrombin?

Answer 4

Enhances antithrombin by 1000x to inactivate factors 9, 10, 11, & 12.

Question 5

What are the the three mechanism of actions of heparin?

Answer 5

• Binds to Antithrombin
• Inhibits thrombin
• Inhibits platelet function

Question 6

What occurs when heparin inhibits thrombin?

Answer 6

Thrombin won’t active factors 5 & 7

Question 7

Is heparin technically a direct anticoagulant?

Answer 7

No. Binds to Antithrombin which is a direct anticoagulant.

Question 8

Heparin is _______ lipid soluble.

Answer 8

poorly

Question 9

Does heparin cross the placenta?

Answer 9

no

Question 10

How is heparin absorbed in the GI tract?

Answer 10

poorly

No PO formulation.

Question 11

What conditions/factors will potentiate heparin’s anticoagulant activity?

Answer 11

• Hypothermia
• Liver dysfunction
• Kidney dysfunction

Question 12

What will occur with heparin administration if circulating plasma protein concentrations are low?

Answer 12

Heparin won’t be bound and will be more active

Question 13

What occurs with the vasculature when heparin is administered?

Answer 13

Vascular smooth muscle dilates

↓ MAP, PAP, SVR.

Question 14

What is the most common, serious complication that occurs with heparin usage?

Answer 14

Hemorrhage

Especially higher if patient is already on ASA.

Question 15

A platelet count of < 100k with concomitant heparin administration might be indicative of….

Answer 15

Mild HIT (Heparin-induced Thrombocytopenia)

Question 16

What are the characteristics of severe HIT (Heparin-induced Thrombocytopenia)?

Answer 16

• PLT <50k
• IgG antibody formation

Question 17

Severe HIT occurs _____ days after heparin initiation typically.

Answer 17

5 - 10 days

Question 18

Mild HIT typically occurs ________ after initiation of therapy.

Answer 18

Within hours to 15 days

Question 19

How do IgG antibodies neutralize toxins, viruses & bacteria?

Answer 19

IgG antibodies opsonize (bind) to foreign pathogens & make them targets for phagocytosis.

Question 20

Where does IgG bind to on platelets?

Answer 20

FC receptor on platelet surface

Question 21

What are the results of IgG binding to platelets?

Answer 21

• PLT activation
• PLT release of pro-thrombotic substances (like thrombin)
• Activation of more PLTs

Question 22

What is the typical dose of heparin for vascular cases?

Answer 22

1mg/kg = 100u/kg

Question 23

What is a normal aPTT?

Answer 23

30 - 35s

Question 24

What is target aPTT for vascular cases?

Answer 24

~ 60 seconds

Goal is 1.5 - 2.5x normal.

Question 25

What is normal ACT?

Answer 25

90 - 120seconds

Question 26

What is protamine derived from?

Answer 26

Salmon sperm *how about that*

Question 27

What is the mechanism of action of protamine?

Answer 27

Protamine = (+) charged alkaline Heparin = (-) charged acidic **neutralize each other**.

Question 28

What is the typical vascular surgery dosage of protamine?

Answer 28

1mg Protamine per 1mg of Heparin given

Question 29

What clears protamine?

Answer 29

Reticular endothelial system

Question 30

Protamine is cleared _____ than heparin.

Answer 30

faster

Question 31

Which patient groups are more susceptible to protamine allergies?

Answer 31

- Patients with protamine insulins (NPH insulin) - Vasectomy hx - Fish allergy hx

Question 32

What drug would be given for heparin reversal in a patient who is allergic to protamine?

Answer 32

PLT Factor IV

Question 33

What is a rare pulmonary adverse effect associated with protamine administration?

Answer 33

Pulmonary Hypertension

Question 34

Protamine induced pulmonary hypertension is mediated by the release of ______ and ______.

Answer 34

thromboxane & serotonin

Question 35

How can protamine induced pulmonary hypertension be pre-treated?

Answer 35

COX inhibitors (indomethacin, aspirin, etc.)

Question 36

Renal disease is usually noted when GFR drops below....

Answer 36

25 mL/min

Question 37

Patients become dialysis dependent when GFR drops to _____ mL/min.

Answer 37

10 mL/min

Question 38

What metabolic abnormalities (mentioned in lecture) are typically of kidney patients?

Answer 38

- ↑ K⁺ - ↑ Mg⁺⁺ - ↓ Ca⁺⁺ - ↓ Albumin - H₂O & Na⁺ retention - Metabolic acidosis

Question 39

What Hgb might be typical for a renal patient?

Answer 39

6 - 8 g/dL

Question 40

How does V̇_T change in renal patients?

Answer 40

Minute ventilation will increase to offset metabolic acidosis

Question 41

What adverse cardiac changes occur in renal patients?

Answer 41

- ↑CO - HTN - CHF - Dysrhythmias

Question 42

What GI issues with renal patients are of special consideration with anesthesia?

Answer 42

- Hypersecretion of gastric acid - Delayed gastric emptying *Consider RSI*.

Question 43

What are the "pros" of native vessel AV fistulas?

Answer 43

- Long-term patency - Low infection rate

Question 44

What are the "cons" of a native vessel AV fistula?

Answer 44

- Maturation time (6 weeks) - May require multiple operations

Question 45

What are the "pros" of AV grafts?

Answer 45

- Shorter maturation time - Typically only one operation

Question 46

What are the "cons" of AV grafts?

Answer 46

- Doesn't last - Prone to infections - Clotting is common

Question 47

Why is LR often avoided in renal patients?

Answer 47

Contains K⁺

Question 48

When would NS be avoided with a renal patient?

Answer 48

If the renal patient is already: - Hypochloremic - Acidotic NS will worsen both of these things

Question 49

Which anesthetic drugs will have an increased effect due to decreased serum protein binding in renal patients?

Answer 49

- Etomidate - Barbiturates - Benzo's

Question 50

What are clinical indications for **elective** revascularization surgery?

Answer 50

- Claudication - Ischemic pain (at rest) - Gangrene (possibly emergent if bad enough)

Question 51

What causes claudication?

Answer 51

Ischemic pain due to muscle metabolic requirements from movement. *Pain when active, relief at rest*.

Question 52

What is an ankle/brachial index study?

Answer 52

Comparison of systolic pressure in the arm vs the ankle. Ankle systolic ÷ Arm systolic = ABI

Question 53

What is a normal ankle/brachial index?

Answer 53

1.0 - 1.4

Question 54

At what ankle/brachial index is pain at rest likely to occur?

Answer 54

0.4

Question 55

At what ankle/brachial index is gangrene likely to occur?

Answer 55

0.25

Question 56

What ABI (Ankle-Brachial Index) values are indicative of moderate disease & severe arterial disease?

Answer 56

Moderate = 0.5 - 0.8 Severe = < 0.5

Question 57

What are the five mainstays of PAD treatment?

Answer 57

- Stop smoking - Maintain normoglycemia - Maintain normotension - Antiplatelet therapy (ASA or ASA/Plavix) - Revascularization Therapy (stents, surgery,etc)

Question 58

What drug class is protective for atherosclerotic patients at risk for cardiac disease?

Answer 58

Βeta blockers

Question 59

Is success more often seen in Iliac artery stenting or in Femoral/Popliteal artery stenting?

Answer 59

- Iliac artery stenting is more successful - Thrombosis/restenosis is common in femoral/popliteal arteries.

Question 60

When are synthetic grafts indicated over insitu (saphenous vein) grafts?

Answer 60

Large vessel revascularization (aorta-femoral, femoral-femoral, etc.)

Question 61

Which coagulation factors are part of the intrinsic pathway?

Answer 61

8, 9, 11, and 12

Question 62

Which coagulation factors are a part of the extrinsic pathway?

Answer 62

3 and 7

Question 63

Which coagulation factors are a part of the common pathway of the coagulation cascade?

Answer 63

1, 2, 5, 10, and 13