list the mechanism behind:
- acute hemolytic reaction
- delayed transfusion rxn
- febrile transfusion rxn
- graft vs host dz
- acute hemolytic reaction: ABO
- delayed transfusion rxn: antigens on donor RBC which recipient has been exposed to –> lysis of those RBC
- febrile transfusion rxn: cytokines and antibodies to leukocyte antigens
- graft vs host dz: donor lymphocytes reacting against the recipient
TRALI most often occurs after transfusion with which products?
FFP Platelets non-cardiogenic pulmonary edema onset within 6hrs transfusion hypoxemia
patient’s with IgA deficiency are at increased risk for what during transfusions?
they have antibodies against IgA so unless the blood has been washed or from an IgA deficient donor, they can have an ALLERGIC RXN to antigens in donor blood
what’s the leading cause of death from transfusions?
1) TRALI 55%
2) Hemolytic transfusion Rxns non- ABO > ABO 22%
3) infection and transfusion-associated sepsis
What is in cryoprecipitate?
vWF fibrinogen (200mg/unit) fibronectin factor 8 factor 13
when should you give cryo?
- microvascular bleeding w/ low fibrinogen
- bleeding 2/2 uremia not responsive to DDAVP (causes vWF release)
- vWD
- factor 13 def
- hemophemia A (def in factor 8)
- Dysfibrinogenemia (fibrinogen abnormal)
how much fibrinogen is in cryo?
fibrinogen 200mg/unit
10 units will raise 70kg patient’s fibrinogen by 70mg/dL
how much FFP should you give?
dose FFP at 10-15mL/kg
FFP has 250cc / unit
mL FFP needed = (desired % - present %) * kg
what is maximum allowable blood loss equation?
EBV* (starting Hct - target Hct) / starting Hct
adult female 60-65 cc/kg
adult male 65- 70 cc/kg
TRALI diagnosis
- sudden hypoxia within 6hrs: PaO2/FiO2 usually 200-300
- bilateral fluffy infiltrates
- no change in cardiac filling or LA pressures (not cardiogenic)
- r/o all other etiologies
PRBC storage: what changes happen to pH, 2,3 DPG, and K
pH decreases
DPG decreases
K increases
what are the least stable factors in FFP
- factor 8; released by vascular endothelium and liver sinusoidal cells. vWF is a carrier molecule for factor 8.
- factor 5
what happens with acute normovolemic hemodiultion
- used in high blood loss cases
- give lots of fluid to intentionally dilute blood/ Hct
- idea is to remove blood and save for later
- decreased blood viscosity –> less peripheral vascular resistance –> increased CO –> increased blood flow but NO increase in oxygen carrying capacity
what do you give if TEG abnormal
- R
- K
- MA
- teardrop
- R –> FFP
- K –> cryo
- MA –> platelets
- teardrop –> anti-fibrinolytics
how does ABG change if it’s heated from 30deg to 37deg
higher temp –> decreased solubility = more of the gas comes out = higher partial pressure = higher PaO2 and PaCO2
higher temp –> think of it as the PaCO2 going up so higher acidity, pH goes down
how does hypocalemia relate to ventilation?
hyperventilation –> hypocalcemia –> loss of calcium ions binding to proteins
hetastarch and platelets
hetastarch can inhibit GP2b3a availability –> can’t aggregate
List MOA for: enoxaparin, rivaroxaban, dabigatran
- enoxaparin: LMWH –> binds to antithrombin –> irreversibly shuts off factor Xa –> longer PTT
- rivaroxaban: direct factor Xa inhibitor –> longer PTT
- dabigatran: direct thrombin inhibitor, linear prolonged PT and PTT but doesn’t correlate with therapeutic levels of the drug
List anti-platelet drugs that work by:
1) ADP receptor antagonist
2) GP 2b/3a inhibibior
2) Direct thrombin inhibitor
3) PDE inhibitor
- ADP receptor antagonist: ticlopidine, clopidogrel, prasugrel (lasts 1-2wks, CAD, in-stent thrombosis)
- GP2b/3a: eptifibatide, abciximab, tirofiban (acute coronary syndrome, renally excreted, 1/2life 2.5hrs, abciximab has 1/2life 12hrs)
- direct thrombin inhibitor: dabigitran (renal excretion)
- PDE inhibitor: dipyridamole (stroke PPX, CVA)
