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CV Perf Tech II > Management of Post-Op Bleeding-Exam 2 > Flashcards

Management of Post-Op Bleeding-Exam 2 Flashcards

1
Q

What is heparin rebound?

A

Some heparin may be protein bound and unavailable for reversal. It may become free post-CPB resulting in heparin rebound.

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2
Q

What will happen with excess protamine?

A

bleeding

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3
Q

How much of a decrease of circulating factors normally occurs on CPB due to hemodilution?

A

25-35% decrease; institution depending

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4
Q

How much does hypothermia slow enzymatic reaction times?

A

10 degree C decrease in temp, 50% decrease in enzymatic activity

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5
Q

What drives the clotting cascade?

A

Enzyme driven; enzymatic rxn times slowed during hypothermia

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6
Q

What are some sources of post-op bleeding?

A 
Reduced concentration of coag factors
Hyperfibrinolysis
Thrombocytopenia
Impaired plt aggregation
Plt Fragmentation
Loss of membrane receptors
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7
Q

What impairs coagulation and increases blood loss after CPB?

A

Increased inflammation

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8
Q

What are some extrinsic factors that can be a source of post-op bleeding?

A

Residual Heparin/Heparin Rebound
Excessive protamine
Hemodilution
Hypothermia

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9
Q

What are some ways to prevent post-op bleeding?

A 
Avoid CPB (off pump procedures)
Improved biocompatibility of foreign surfaces
Alter conduct of bypass
Hemtalogic strategies
Improved surgical technique
Make sure labs are normal pre-op
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10
Q

What are some hematologic strategies that can help prevent post-op bleeding?

A

Harvest whole blood/plasma

PRP

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11
Q

What is a major factor in use of blood products and post op bleeding?

A

Improved surgical technique

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12
Q

What drug has a mild fibrinolytic effect? Describe the effect.

A

Heparin; stimulates release of serum urokinase plasminogen activator (UPA) which induces fibrinolysis

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13
Q

CPB activates the breakdown of what?

A

Fibrinogen and other procoagulant precursors

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14
Q

Which is more potent? UPA or TPA?

A

TPA is more potent that UPA

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15
Q

What is the primary activator of fibrinolysis during heart surgery?

A

Tissue Plasminogen Activator (TPA)

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16
Q

When is there a large surge of TPA?

A

After protamine is given

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17
Q

When is the time of greatest thrombin production?

A

After protamine is given

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18
Q

If there was no fibrinolysis (left unchecked by TPA) what would happen?

A

Could result in large scale clotting or diffuse intravascular coagulation

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19
Q

When is thrombin produced?

A

Throughout CPB

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20
Q

When is there a surge of thrombin?

A

At termination of bypass

After protamine administration

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21
Q

What type of protein is thrombin?

A

Amplifier protein; activates many cell lines

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22
Q

What cell lines does thrombin activate?

A

Inflammation
Coagulation
Fibrinolysis

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23
Q

What is metabolically active in sites where heparin cannot reach it?

A

Thrombin

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24
Q

What regulates TPA?

A

Plasminogen Activator Inhibitor 1 (PAI-1)

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25
Q

What releases plasminogen activator inhibitor 1?

A

Liver and endothelial cells

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26
Q

What does PAI-1 bind to as it’s exported from endothelial cells?

A

Binds to TPA; therefore TPA must overcome circulating PAI-1 to initiate fibrinolysis

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27
Q

How is PAI-1 a buffer?

A

It’s a buffer to surges of TPA

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28
Q

When is PAI-1 released?

A

in response to inflammatory mediators

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29
Q

How does PAI-1 work as a prothrombotic?

A

Overcomes and suppresses fibrinolytic effect of TPA

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30
Q

What makes up a clot?

A

Thrombin

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31
Q

What breaks up a clot?

A

TPA

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32
Q

PAI-1 prevents what from breaking down clots?

A

TPA (hemostasis)

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33
Q

How does TPA factor into post-op bleeding?

A

TPA directly cleaves plasminogen (to make plasmin); exposes lysine binding sites, fibrinogen and fibrin bind at these lysine binding sites; proteolytic attack leads to breakdown products

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34
Q

What is needed to crosslink platelets to make a clot?

A

Fibrin

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35
Q

What does TPA do to fibrin?

A

TPA breaks down fibrin and therefore, the clot; leads to post op bleeding

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36
Q

What are antifibrinolytic agents?

A

Lysine Analogs

Aprotinin

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37
Q

What are the two lysine analogs that are commercially available?

A 
Aminocaproic Acid (ACA)/ Amicar
Tranexamic Acid (TA)
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38
Q

What is aminocaproic acid (ACA) made out of?

A

2 lysine molecules stuck together

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39
Q

What is aminocaproic acid’s mechanism of action?

A

Competitively binds to lysine sites of plasminogen/plasmin; prevents plasmin from binding to fibrinogen/fibrin

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40
Q

What is aprotinin made out of?

A 
58 amino acid polypeptide
Single lysine (high affinity for plasmin at this site)
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41
Q

What type of drug is aprotinin?

A

Non-specific serine protease inhibitor; but has other actions

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42
Q

What is aprotinin’s mechanism of action?

A

Catalyzes multiple reactions of inflammation, coagulation, and other cellular attack mechanisms

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43
Q

How long have lysine analogs been clinically available?

A

40+ years

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44
Q

How long do the prophylactic use in cardiac surgery of lysine analogs date back to?

A

1960’s

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45
Q

When are lysine analogs primarily thought to use?

A

After CPB

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46
Q

What study showed lysine analogs are effective in decreasing blood loss?

A

1989- Del Rossie, et al.
Large placebo controlled group (350 pts)
Pre-CPB administration of ACA decreased post operative chest tube drainage and transfusion without inducting thrombotic complications

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47
Q

What type of administration do lysine analogs use?

A

IV

48
Q

What type of uptake do lysine analogs have?

A

Uptake is immediate

49
Q

What type of molecules are lysine analogs?

A

Small, water-soluble molecules

50
Q

How are lysine analogs distributed?

A

Distributed readily into extravascular water spaced before being taken up into various cells and tissues

51
Q

What lysine analog is weak protein-bound and crosses BBB and Placenta?

A

TA

52
Q

How are lysine analogs eliminated?

A

Renal excretion

53
Q

What is the half-life of lysine analogs?

A

1-2 hours with IV administration

54
Q

Describe the loading dose for lysine analogs pre CPB.

A

Loading dose pre-CPB over 1-15 min followed by a continuous IV infusion; sometimes a pump dose

55
Q

What is the loading dose of ACA?

A

75-150 mg/kg (5-10 gm in adults)

56
Q

What is the IV infusion dose for ACA?

A

10-15 mg/kg/hr; continues until the end of CPB or until protamine is given

57
Q

What is the pump dose for ACA?

A

2-2.5 g/ L; some add/some don’t; makes sense to add b/c of added plasma volume on pump

58
Q

What is the “10-10-10” protocol for ACA dosing?

A

Daily et. al protocol
10g given as slow bolus (5-10 min) pre CPB
10g in CPB prime
10g after CPB

59
Q

What type of loading dose of ACA is used in patients with kidney disease?

A

Normal/reduced

60
Q

What type of infusion rate of ACA is used in patients with kidney disease?

A

Reduced continuous infusion rate

ACA: 5mg/kg/hr

61
Q

What is the infusion rate of TA used in patients with kidney disease?

A

0.5 mg/kg/hr

62
Q

When should you dose lysine analogs?

A

As early as induction and incision; reports of clot formation on PA catheter and EKG ST-segment changes

Await full anticoagulation with heparin prior to administration

63
Q

What study showed that ACA is acceptable to give prior to CPB but after heparin?

A

Kluger et al.
90 primary CABG pts
Given ACA pre-incision, after heparin and placebo; both ACA protocols decreased chest tube drainage and there was no difference between groups

64
Q

How does TA dosing compare to ACA dosing?

A

TA dosing is 1/7 to 1/10th of ACA

65
Q

What are the doses for TA?

A

Loading dose: 10-15 mg/kg over 10-15 minutes
Infusion: 1-1.5 mg/kg/hr
Pump: 2-2.5 mg/L

66
Q

What are the side effects of lysine analogs in DIC patients?

A

Intravascular clots

67
Q

What are the thromboembolic complications that can occur with lysine analogs?

A 
Reduced graft patency
DVT
PE
Stroke
MI
*All theoretically possible after heparin neutralization but no association has been found
68
Q

Why are anti-fibrinolytics something to consider when thinking about transfusions?

A

Patients at low risk for transfusion (despite CPB) may not benefit from prophylactic anti-fibrinolytics. But it maye help tip the scales between transfusion or not if they are on the fence

69
Q

Where is aprotinin found?

A

Found in all mammalian lung tissue

Isolated from bovine lung

70
Q

Describe the activated sites on aprotinin.

A

Contains single lysine; binding site for most serine proteases it inhibits

71
Q

What is the name of the most common regimen of aprotinin?

A

Full Hammersmith Regimen

72
Q

What is the Full Hammersmith Regimen of Aprotinin?

A

2 million KIU in pump
2 million KIU to pt over 30-60 min
500,000 KIU/hr infusion for pump run

73
Q

What’s the 1/2 life and excretion method of aprotinin with the full hammersmith region?

A

5 hours; renal excretion

74
Q

What’s a major advantage of the full hammersmith regimen?

A

Blood loss and transfusion required are lowest

75
Q

Aprotinin has a similar size to what?

A

Protamine

76
Q

What can cause an allergic rxn to aprotinin?

A

Foreign protein from bovine source (1st time exposure reaction rate)

77
Q

Describe the test dose of aprotinin.

A

1 mL given prior to loading dose

Wait 10 min after test dose before starting loading dose

78
Q

When are aprotinin reactions in kids less?

A

Kids with less than 6 months between exposures; FDA revised advisory to put 12 months between exposures

79
Q

What dose aprotinin affect?

A 
Trypsin
Chymotrypsin
Plasmin
Kallikrein
Bradykinin
TPA
Urokinase Plasminogen Activator 
Complement
80
Q

How long has aprotinin been used?

A

1960’s

81
Q

When was aprotinin used in cardiac surgeries and by which surgeons?

A

1980’s by Ben Bidstrup and Kenneth Taylor and an anesthesiologst, David Royston.

82
Q

What hospital was aprotinin first used in open heart surgeries?

A

Hammersmith Hospital, London

83
Q

1st 20 patients tested with aprotinin had what kind of effect?

A

No effect on pulmonary gas exchange and post op lung dysfunction, BUT the surgical field was dramatically dry

84
Q

What is the main advantage of aprotinin which is the reason its widely used in open heart surgeries?

A

Transfusion-sparing and decrease chest tube drainage associated

85
Q

What is an example of blood loss data with aprotinin?

A

Aprotinin patients: 245 mL

Placebo patinets: 1979 mL

86
Q

How does aprotinin affect kallikrein?

A 
Decreases Kallikrein
Decreases inflammation (doesn't affect bleeding)
87
Q

What cascade does aprotinin activate?

A

Intrinsic cascade; activation of coagulation precursor proteins; activates pro-inflammatory WBCs; inhibits platelet-WBC interactions

88
Q

What does inflammatory down regulation of aprotinin do?

A

Protects platelets; GPIb and IIb/iiia receptors are better preserved

89
Q

Describe aprotinin efficacy.

A

Decreased chest tube output in re-operation cases, complex CABG, CABG with ASA/Plt inhibits on board

90
Q

Aprotinin results in what percent reduction in chest tube output?

A

40-80% reduction in chest tube output compared in placebo

91
Q

Why was aprotinin called into question?

A

Called to question graft patency with its use

92
Q

Describe the Bidstrup that looked at aprotinin issues with graft patency.

A

Bidstrup: via MRI at 7 and 12 days post op
90 primary CABG
No difference in vein graft patency
All arterial grafts patent at 12 days

93
Q

Describe the Lemmer study that looked at aprotinin’s effect on MI rates.

A

Lemmer et al. CT scans
151 primary CABG, 65 reop CABG
7 and 30 days post-op
Randomized, placebo controlled; no significant difference in graft patency; trend toward lower patency rates in aprotinin groups; no difference and no trend in MI rates

94
Q

What study looks at aprotinin affect on neurologic function?

A

Levy et al.

Aprotinin may have neurologic protective effects

95
Q

How does aprotinin affect risk of stroke?

A

No strokes in any patient who received mid/high dose of aprotinin

96
Q

Describe aprotinin’s affect on renal function

A

Pts with worse renal function before bypass have greatest risk for further renal impairment/failure requiring dialysis with or without aprotinin

97
Q

What is risk for dialysis with normal GFR

A

low risk

98
Q

What is risk for dialysis with 50% normal GFR

A

> 20% risk for dialysis

99
Q

What is risk for dialysis with <20% normal GFR

A

85% risk for dialysis

100
Q

What does aprotinin compete with?

A

Competes with creatinine in the ascending loop of henle; expect the rise in creatinine with aprotinin not necessarily indicator of renal damage

101
Q

Describe the creatinine rise with aprotinin.

A

Higher 3-7 days post op
Statistical significance at day 7
By day 14-30 post op, return to identical levels in both groups

102
Q

Cost of ACA (generic)

A

$1.50 - $10 per 5gm vial

Case: $5-$30

103
Q

Cost of TA (generic)

A

Case: $20-$300

104
Q

Cost of aprotinin

A

Off patent, but costly to extract
$300-$400 per bottle
per case: $1000-$1500

105
Q

Cost of recombinant factor VIIa

A

$5000-$9000/ dose

may require multiple doses

106
Q

RBC cost

A

$300-$500

107
Q

Platelets cost

A

$850

108
Q

FFP cost

A

$100

109
Q

When did the FDA revise labeling of aprotinin?

A

December 2006

110
Q

How did the FDA revise labeling of aprotinin?

A

Don’t give w/in 12 mo of prior exposure; only for patients hwo are at increased risk for blood loss and blood transfusion associated with CPB in the course of a CABG

111
Q

Are TA and ACA approved for prophylactic use in cardiac surgery?

A

no

112
Q

Aprotinin Downfall: 2007

A

Temporarily withdrawn form the market worldwide

113
Q

Aprotinin Downfall: 2005/8

A

permanently withdrawn from the market; use is limited to very select research

114
Q

What complications are seen with both lysine analogs and aprotinin?

A

Intravascular thrombis

aprotinin increases serum creatinine transiently

115
Q

Retrospective studies associate aprotinin with:

A

renal failure
stroke
mi
increase mortality (not seen with lysine analogs)

116
Q

How to avoid post op bleeding?

A 
Rewarm the patient thoroughly
Reverse protamine
Get all the surgical bleeders
be aware of hemodilution
consider use of antifibrinolysis lysine analog

CV Perf Tech II (17 decks)

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