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Anesthesia Pharm I > anticoagulation/reversal > Flashcards

anticoagulation/reversal Flashcards

1
Q

describe basic hemostasis

A
  • adhesion of platelets to damaged vessel wall
  • activation of platelets
  • aggregation of platelets: fibrinogen links platelets together, but clot still water soluble and fragile
  • production of fibrin (secondary hemostasis): extrinsic, intrinsic, and final common pathways
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2
Q

what is the MOA of Heparin?

A
  • binds to antithrombin (naturally occurring anticoagulant)
  • increases antithrombin ability 1000x
  • inactivates thrombin (IIa), factors X, XII, XI, IX
  • inhibits platelet function (not main effect)
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3
Q

describe heparin

A
  • poorly lipid soluble (cant cross lipid barriers)
  • given IV or SubQ (IM causes hematoma)
  • binds to plasma proteins, only 1/3 binds to antithrombin
  • duration increases as dose increases
  • elimination not completely understood, some in the urine
  • endogenous in basophils, mast cells, and liver (“HEP”)
  • one unit = vol. of solution that will prevent 1 ml of sheep blood from clotting for 1 hr after 0.2 ml CaCl added
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4
Q

what is the ACT? and describe proper procedure

A

activated coagulation time

  • monitors the heparin effect
  • get a baseline measurement prior to giving heparin (control is usually 90-120 seconds)
  • measurement 3 minutes after admin. (for CPB want ACT > 300 seconds)
  • measure every 30 minutes
  • mix blood with an activation substance which initiates the clotting cascade; measure the onset of clot formation
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5
Q

what affects the ACT?

A
  • hypothermia, hemodilution prolong ACT (two major factors in bypass)
  • thrombocytopenia (heparin may induce)
  • presence of contact activation inhibitors (aprotinin)
  • preexisting coagulation deficiencies (hemophilia, etc; do a baseline)
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6
Q

what should be given if ACT is not increasing?

A

FFP

-heparin can not work without antithrombin to activate so may need to be given antithrombin

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7
Q

what are clinical uses of heparin?

A
  • venous thrombosis, PE
  • prevention of mural thrombosis after MI
  • unstable angina, acute MI
  • prevention of coronary artery rethrombosis after thrombolysis
  • prevention of thrombosis formation during CPB
  • treat fetal growth retardation in pregnancy (prevent thrombosis of placental arteries)
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8
Q

what are side effects of heparin?

A
  • hemorrhage (most serious): greater risk if pt. on aspirin; avoid with intraocular or intracranial surgery (a little bleeding and cause serious damage); avoid epidural or spinal, axillary block (chance of hematoma on spinal cord or deep plexus block can cause nerve damage)
  • thrombocytopenia: mild- platelet
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9
Q

what are CV effects of heparin?

A
  • decreased MAP, PAP
  • decrease in SVR d/t relaxant effect on smooth muscle of vessels
  • drop in BP seen especially with large doses given before bypass
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10
Q

what is protamine?

A

reversal of heparin

-positively charged protein (salmon sperm)

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11
Q

what is MOA of protamine?

A
  • combines with negatively charged heparin
  • resulting complex has no anticoagulation effect
  • removed by reticuloendothelial system
  • if given and there is no heparin to bind to, acts as an anticoagulant
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12
Q

what is the dose of protamine?

A

1 mg per every 100 U of heparin circulating

*calculated off of ACT if doing bypass

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13
Q

what are CV effects of protamine?

A
  • hypotension: histamine release, tachycardia (pt. with decreased LV function may not be able to compensate)
  • to minimize hypotension give over 5 minutes and give peripherally to dilute the complex that causes histamine release in the lungs
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14
Q

what are respiratory effects of protamine?

A

-pulmonary hypertension: thromboxane release causing pulmonary vasoconstriction, pulmonary HTN, and bronchoconstriction

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15
Q

what is another possible effect of protamine?

A

allergic reaction

  • protamine-containing insulin (NPH)
  • fish, shellfish
  • pre treat with H1 and H2 blockers and steroid
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16
Q

how do platelets normally function?

A
  • thrombin activates the platelet
  • phospholipase converts a membrane phospholipid to arachidonic acid
  • cyclooxygenase converts arachidonic acid to prostaglandin G2
  • PGG2 is metabolized to PGH2
  • PGH2 is converted to multiple prostaglandins and thromboxane A2
  • thromboxane A2 uncovers fibrinogen receptors allowing attachment of fibrinogen to link platelets together
17
Q

what is the MOA of aspirin?

A

interfere with the activity of cyclooxygenase (COX) and with the release of ADP, which interrupts the synthesis of thromboxane A2, thus causing impaired platelet aggregation
*doesn’t affect platelet count, just function; no need to check labs if on ASA

18
Q

what is the duration of action of aspirin?

A

irreversible effect for the life of the platelet (8-12 days)

*recommended to stop 7 days prior to surgery if at low risk for cardiac events

19
Q

describe MOA of clopidogrel (Plavix) and ticlopidine (Ticlid)

A

block ADP receptors (irreversibly) on the platelets which inhibits the platelet activation, aggregation for the life of the platelet

  • used in combination with aspirin to maintain patency of coronary stents
  • Prilosec decreases Plavix function
20
Q

when should Plavix and Ticlid be stopped?

A

Plavix: 7 days prior to surgery
Ticlid: 14 days prior to surgery
*both must be stopped

21
Q

what normally happens to fibrin after the clot is formed and bleeding has stopped?

A
  • clot needs to be broken down
  • plasminogen is produced in the liver and stored in the clot
  • tissue-type plasminogen activator (tPA) and urokinase convert plasminogen to plasmin
  • plasmin breaks down fibrin
22
Q

what is the MOA of the anti fibrinolytic agent aprotinin (Trasylol)?

A
  • naturally occurring plasma kinin
  • inhibits plasmin
  • a more stable clot is formed b/c fibrin breaks down slowly and bleeding is decreased
  • may protect platelets
  • inhibits inflammatory response to CPB by preventing the movement of leukocytes through vascular lining
  • not seen often, risks thrombus formation
23
Q

what are some uses of aprotinin?

A
  • “redo” cardiac operations
  • prevention and treatment of hemorrhage during surgery (decreases blood loss and transfusion requirements by 40-80% in cardiac surgery pt. with aspirin and “redo”s
  • contraindication: shouldn’t be given if a known or suspected exposure within past 12 months
24
Q

describe aminocaproic acid (Amicar)

A
  • synthetic anti-fibrinolytic
  • forms a reversible complex with plasminogen which prevents fibrinolysis
  • used to decrease postop bleeding and transfusions needed (CPB, scoliosis, orthotopic liver transplant, lower urinary tract surgery
  • avoid with renal or ureteral bleeding (may lead to obstruction of the ureter d/t clotting)
25
Q

describe tranexamic acid

A
  • synthetic anti-fibrinolytic
  • prevents the interaction b/w plasminogen and fibrin
  • studies show similar effects as aprotinin

Anesthesia Pharm I (28 decks)

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