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Fall25 AdvPrin C > Vascular Anesthesia Pt.1 (Exam I) > Flashcards

Vascular Anesthesia Pt.1 (Exam I) Flashcards

1
Q

What comorbidities are typical of “vasculopaths”?

A
  • DM
  • HTN
  • CRI
  • COPD

>50% have CAD.

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2
Q

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

A

basophils & mast cells

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3
Q

What does heparin directly bind to?

A

Antithrombin III

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4
Q

What is the consequence of heparin binding to antithrombin?

A

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

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5
Q

What are the the three mechanism of actions of heparin?

A
  • Binds to Antithrombin
  • Inhibits thrombin
  • Inhibits platelet function
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6
Q

What occurs when heparin inhibits thrombin?

A

Thrombin won’t active factors 5 & 7

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7
Q

Is heparin technically a direct anticoagulant?

A

No. Binds to Antithrombin which is a direct anticoagulant.

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8
Q

Heparin is _______ lipid soluble.

A

poorly

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9
Q

Does heparin cross the placenta?

A

no

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10
Q

How is heparin absorbed in the GI tract?

A

poorly

No PO formulation.

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11
Q

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

A
  • Hypothermia
  • Liver dysfunction
  • Kidney dysfunction
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12
Q

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

A

Heparin won’t be bound and will be more active

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13
Q

What occurs with the vasculature when heparin is administered?

A

Vascular smooth muscle dilates

↓ MAP, PAP, SVR.

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14
Q

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

A

Hemorrhage

Especially higher if patient is already on ASA.

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15
Q

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

A

Mild HIT (Heparin-induced Thrombocytopenia)

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16
Q

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

A
  • PLT <50k
  • IgG antibody formation
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17
Q

Severe HIT occurs _____ days after heparin initiation typically.

A

5 - 10 days

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18
Q

Mild HIT typically occurs ________ after initiation of therapy.

A

Within hours to 15 days

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19
Q

How do IgG antibodies neutralize toxins, viruses & bacteria?

A

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

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20
Q

Where does IgG bind to on platelets?

A

FC receptor on platelet surface

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21
Q

What are the results of IgG binding to platelets?

A
  • PLT activation
  • PLT release of pro-thrombotic substances (like thrombin)
  • Activation of more PLTs
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22
Q

What is the typical dose of heparin for vascular cases?

A

1mg/kg = 100u/kg

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23
Q

What is a normal aPTT?

A

30 - 35s

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24
Q

What is target aPTT for vascular cases?

A

~ 60 seconds

Goal is 1.5 - 2.5x normal.

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25
Q

What is normal ACT?

A

90 - 120seconds

26
Q

What is protamine derived from?

A

Salmon sperm

how about that

27
Q

What is the mechanism of action of protamine?

A

Protamine = (+) charged alkaline

Heparin = (-) charged acidic

neutralize each other.

28
Q

What is the typical vascular surgery dosage of protamine?

A

1mg Protamine per 1mg of Heparin given

29
Q

What clears protamine?

A

Reticular endothelial system

30
Q

Protamine is cleared _____ than heparin.

A

faster

31
Q

Which patient groups are more susceptible to protamine allergies?

A
  • Patients with protamine insulins (NPH insulin)
  • Vasectomy hx
  • Fish allergy hx
32
Q

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

A

PLT Factor IV

33
Q

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

A

Pulmonary Hypertension

34
Q

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

A

thromboxane & serotonin

35
Q

How can protamine induced pulmonary hypertension be pre-treated?

A

COX inhibitors (indomethacin, aspirin, etc.)

36
Q

Renal disease is usually noted when GFR drops below….

A

25 mL/min

37
Q

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

A

10 mL/min

38
Q

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

A
  • ↑ K⁺
  • ↑ Mg⁺⁺
  • ↓ Ca⁺⁺
  • ↓ Albumin
  • H₂O & Na⁺ retention
  • Metabolic acidosis
39
Q

What Hgb might be typical for a renal patient?

A

6 - 8 g/dL

40
Q

How does V̇T change in renal patients?

A

Minute ventilation will increase to offset metabolic acidosis

41
Q

What adverse cardiac changes occur in renal patients?

A
  • ↑CO
  • HTN
  • CHF
  • Dysrhythmias
42
Q

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

A
  • Hypersecretion of gastric acid
  • Delayed gastric emptying

Consider RSI.

43
Q

What are the “pros” of native vessel AV fistulas?

A
  • Long-term patency
  • Low infection rate
44
Q

What are the “cons” of a native vessel AV fistula?

A
  • Maturation time (6 weeks)
  • May require multiple operations
45
Q

What are the “pros” of AV grafts?

A
  • Shorter maturation time
  • Typically only one operation
46
Q

What are the “cons” of AV grafts?

A
  • Doesn’t last
  • Prone to infections
  • Clotting is common
47
Q

Why is LR often avoided in renal patients?

A

Contains K⁺

48
Q

When would NS be avoided with a renal patient?

A

If the renal patient is already:

  • Hypochloremic
  • Acidotic

NS will worsen both of these things

49
Q

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

A
  • Etomidate
  • Barbiturates
  • Benzo’s
50
Q

What are clinical indications for elective revascularization surgery?

A
  • Claudication
  • Ischemic pain (at rest)
  • Gangrene (possibly emergent if bad enough)
51
Q

What causes claudication?

A

Ischemic pain due to muscle metabolic requirements from movement.

Pain when active, relief at rest.

52
Q

What is an ankle/brachial index study?

A

Comparison of systolic pressure in the arm vs the ankle.

Ankle systolic ÷ Arm systolic = ABI

53
Q

What is a normal ankle/brachial index?

A

1.0 - 1.4

54
Q

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

A

0.4

55
Q

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

A

0.25

56
Q

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

A

Moderate = 0.5 - 0.8
Severe = < 0.5

57
Q

What are the five mainstays of PAD treatment?

A
  • Stop smoking
  • Maintain normoglycemia
  • Maintain normotension
  • Antiplatelet therapy (ASA or ASA/Plavix)
  • Revascularization Therapy (stents, surgery,etc)
58
Q

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

A

Βeta blockers

59
Q

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

A
  • Iliac artery stenting is more successful
  • Thrombosis/restenosis is common in femoral/popliteal arteries.
60
Q

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

A

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

Fall25 AdvPrin C (11 decks)

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