Blood Flashcards

1
Q

Sites of Hematopoiesis

A

Intramedullary: within the bone marrow. Normal in children and adults

Extramedullary: outside the bone marrow- the spleen and liver, normal in the fetus. Abnormal in disease states

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2
Q

Hematopoiesis

A

Fetal yolk sac at 3 wks gestation develops mesenchymal blood islands

These stem cells migrate to the liver and spleen at week 6-12

Red bone marrow develops bone at the 12th week

Red marrow stops at puberty, long bones only then generate blood

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3
Q

Myeloid cell line (common myeloid progenitor)

A

Granulocytes (N E B)
Monocytes
RBC
Platelets

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4
Q

Lymphoid progenitor cell line

A

Dendritic cell
B
T
NK

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5
Q

Maturation of the RBC

A

Polychromatophilic normoblast (Blast cell) within the bone marrow have nuclei.

The reticulocyte is the blast cell without a nuclei. It still has some ribosomes and is making hemoglobin. It is released from the bone marrow and within hours it becomes RBC.

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6
Q

Erythropoietin Physiology

A

EPO is released due to hypoxic stimulation of peritubular cells in kidney via colony stimulating factor-E (erythrocyte)
Stimulates the production of RBC via progenitor line as well as release of RBC from bone marrow.

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7
Q

Normal hemoglobin content of RBC cytoplasm

A

32-36%

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8
Q

Hemoglobin Biochemistry

A

HbA is 4 globin chains each with a heme molecule. Usually is 2 alpha 2 beta.

Heme is a protophorphyrin ring with 1 atom of Fe2+ which can bind reversibly with 1 molecule of oxygen

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9
Q

Storage of Dietary iron

A

Within the liver as Ferritin Fe3+ with apoferritin

Within the liver as hemosiderin (partially degraded ferritin)

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10
Q

Storage of iron in bone marrow

A

Liver stores are transported to the bone marrow as transferrin, which is Fe3 and apotransferrin

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11
Q

Normal Forms of Hemoglobin

A

HbA2: 2 alpha2, 2 beta2 in adults.

HbF: 2 alpha 2, 2 gamma2 in infants with some A2

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12
Q

RBC senescence

A

Driven by degradation of metabolic proteins due to the lack of a nucleus over 120 days.
Once enzymes run out the cells lose membrane fluidity, and water enters cells making them spheroid, rigid, and fragile

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13
Q

Extravascular Hemolysis Physiology

A

In splenic sinusoids: the old RBCs get stuck, and are destroyed by splenic macrophages.
Also occurs in liver.
In bone marrow, unnecessary progenitors are destroyed by BM macrophages.
This causes release of unconjugated bilirubin which gets excreted in hepatic bile.

Also occurs in spleen with IgG reaction on RBC

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14
Q

Intravascular Hemolysis Physiology

A

Fibrin clots, Immune response etc causing hemoglobinemia

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15
Q

Leukocyte Maturation Times

A

Neutrophils: 12 hours
Eo; 3.5 days
Monocyte: 3 days

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16
Q

Neutrophil development

A

Proliferation within the bone marrow consists of myeloblast, promyelocyte, myelocyte, metamyelocyte.
Metamyelocytes can only mature but not proliferate.

Metamyelocytes develop to bands and then neutrophils.
The ‘band’ is the nucleus that is not segmented. Normal is 5% of neutrophils or less in peripheral smear

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17
Q

Neutrophil granule contents

A

Myeloperioxdase
Lysozyme
Alkaline phosphatase

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18
Q

Eosinophil function

A

Antigen presenting cell
Releases major basic protein (MBP) and acid phosphatase
Releases other cytokines

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19
Q

Basophil function

A

Has Surface IgE receptors that cause allergic inflammation
Releases histamine and cytokines
Similar to mast cells

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20
Q

T cell physiology

A

Proliferation in thymus. Those that do not recognize self antigens go through apoptosis.
If T cell contacts foreign antigen from lymphatic drainage then it becomes sensitized.
May become CD4 helper T cells.
May become CD8 cytotoxic t cells
May be come regulatory T cell to suppress response

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21
Q

B cell physiology

A

lymphoid progenitor in bone marrow develops to naive B cells, which migrate to germinal centres of lymph tissue.
When exposed to antigens they transform to plasma/memory cells which produce antibodies

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22
Q

NK cell physiology

A

matures directly from common lymphocyte progenitor and has non specific immunity capable of killing tumour cells or virus infected cells without prior exposure

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23
Q

Control of thrombopoiesis

A

Thrombopoietin is produced by the kidney, liver and smooth muscle
It binds to receptors on platelets and is destroyed. The lower the number of platelets the more the hormone circulates.

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24
Q

Platelet plasma membrane structure

A

Contains negative glycocalyx carbohydrates making it very negative and repelling other platelets
Has proteins for binding collagen directly
Has proteins for binding vWF

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25
Q

FVIII

A

Cofactor that circulates bound to vWF, produced in liver
Binds with FIX
Extremely unstable unless bound to vWF.

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26
Q

FV

A

Cofactor produced by megakaryocytes, stored in alpha granules, 20% circulates in platelets
Binds to FX

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27
Q

vWF Functions

A

Carries FVIII
Binds to collagen
Binds to GpIb on platelets especially in high shear stress environments
Has a heparin binding site

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28
Q

ADAMTS-13

A

Breaks down vWF multimers
Deficiency causes familial TTP
Can be inhibited by inflammation causing immune-mediated TTP

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29
Q

vWF Disease, Inherited

A

Autosomal dominant resulting in decreased vWF and mucocutaneous bleeding. Made in endothelium and megakaryocytes
Type 1: asymptomatic, heterozygous
Type 2: Qualitative, mild symptoms that generate multimers
Type 3: Homozygous, hemorrhage

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30
Q

vWf Disease, acquired

A

Autoantibody generation against vWF, associated with aortic stenosis and VAD

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31
Q

Functions of thrombin

A

-Fibrinogen to fibrin monomers
-Activates FV,FVIII, IX
-Cross links with FXIII
-Activates platelets, thromboxane
-Endothelial stim: tPA, NO, prostacyclin
-Activates protein C, thrombomodulin
Thrombin is the final serine protease in the cascade

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32
Q

Platelet Granule contents

A
  • ADP causes aggregation
  • Epinephrine
  • Calcium
  • Thromboxane: aggregation and vasoconstriction
  • FV
  • vWF
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33
Q

Thombomodulin function

A

Constititutively expressed on endothelial cell surface
Acts as cofactor to the activation of protein C by thrombin
In combination with protein S, proteolytically clears FVIII and FV

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34
Q

Antithrombin III

A

Inhibits thrombin, and F 9-12 as a serine protease
Produced in the liver
Increased allosteric function of anti FIXa and FXa via minimal heparin pentasaccharide sequence

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35
Q

Extrinsic Clotting pathway

A
  • Exposed TF activates FVII(Serine protease) on endothelial surface
  • Happens on negative endothelial surface, with presence of positive Ca ions
  • FVIIa acts on X
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36
Q

Intrinsic Clotting pathway

A

Prekallikrein, HMWK and XII activate in the presence of tissue injury (polyanions, -). Also activated via thrombin
Activates XI, IX.
This complexes with FVIIIa on platelet surface to create tenase complex (IXa+VIIIa), which cleaves X and creates common pathway

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37
Q

Common clotting pathway

A

Xa+ Va on platelet surface causes thrombin generation

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38
Q

Rosenthal correction factor for pH and temperature

A

Water increases 0.017 pH unit for every degree decrease in blood

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39
Q

Collection bags of Canadian blood

A

Buffy coat collection set: whole blood cooled then centrifuged, separating plasma, Buffy coat, and RBC. RBC then LR. Allows for pooled platelet product creation.
Whole blood collection set: cooled, LR (WBC and PLT removed) and then RBC/plasma extracted

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40
Q

Average CBS RBC unit

A

293 mL containing 56 grams of Hgb, Hct 0.68. One unit typically increases [Hgb] by 10 g/L in adults.
American= 300-400 mL, hot 55-65%, increases hct by 3%

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41
Q

Conditions in which blood products may be returned to inventory

A

Bag intact, pass visual inspection, maintained an acceptable temperature or the RBC have not been outside of fridge for more than 60 min

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42
Q

CBS RBC shelf life

A

-42 days from the time of collection
-24 hours if entered without use of sterile connection device, if stored at 1-6C or 4 hours if stored above 6C
-unit irradiated at CBS within 14 days and may be stored for another 14 days
-

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43
Q

CBS RBC unit transportation

A

1-6 C in temp controlled storage with alarm, fan and continuous monitoring.
1-10C if transport is less than 24h
Must have documentation to allow tracing of each portion of transport.

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44
Q

Manufacture method of CBS pooled platelets

A

From whole blood via Buffy coat collection method using CPD anticoagulant. Plasma top layer and RBC bottom layers removed, leaving Buffy coat containing PLT and WBC.
4 donations of same ABO group with plasma from one of the same 4 donations (usually male) are pooled then LR.
Pool is Rh neg if all donor units are Rh neg.
Produced within 28 hours of collection, stored for 7 days

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45
Q

Average CBS pooled platelet unit

A

342 mL with 300 x10^9

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46
Q

Manufacture method of CBS Apheresis platelets, average aperheresis platelets

A

Flow cytometer separates RBC/WBC from platelets and plasma. Contains 242 mL with 370 X10^9

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47
Q

Use of Apheresis platelets vs pooled Buffy coat platelets

A

Aperesis is single donor. Can be used for HLA typing when recipient has demonstrated anti-HLA antibodies for platelet refractoriness

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48
Q

Storage of platelets

A

20-24C under continuous agitation for 7 days since collection
Expires 4 hours after opening unless opened under sterile conditions for aliquot preparation, in which case the aliquots can be stored for 7 days

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49
Q

CBS Frozen plasma manufacture

A

Whole blood collection in CPD, red cell reduced by centrifugation, either Buffy coat removed via centrifugation or through filtration. CPD FP frozen within 24 hours of collection.
Not considered LR because processing removes cells but remaining plasma has variable WBC

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50
Q

CBS fresh frozen plasma manufacture

A

Apheresis generation removes plasma, collected and frozen within 8 hours and labelled as apheresis fresh frozen plasma

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51
Q

Difference in use between FP and FFP

A

AFFP contains 87% of FVIII and 0.7 IU/mL FVIII
FP contains 70-75% of the FVIII and 0.52 IU/mL
Other factors are similar. Therefore AFFP should be used with isolated FVIII or VWF deficiency if recombinant products are unavailable.
FV also reduced in FP.
1 apheresis donation=2 whole blood donations by volume

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52
Q

General indications for plasma transfusion

A

Bleeding, severe liver disease, DIC, massive transfusion, invasive procedure on warfarin before vit K can work and PCC is not available, rare protein deficiencies, TTP/HUS by plasma exchange, other indications for plasma exchange

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53
Q

Indications for cryosupernatant plasma transfusion

A

Treatment of TTP and HUS by plasma exchange, or multiple plasma deficiency especially where fibrinogen replacement is not required (eg. warfarin replacement that does not require fibrinogen)

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54
Q

Contraindications of plasma transfusion

A
  • Volume replacement use alone
  • single factor deficiency with available recombinant product/virally inactivated product available
  • reversal of therapy with INR below 1.8
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55
Q

Contraindications of cryosupernantant plasma transfusion

A
  • conditions that require fibrinogen replacement

- FVIII or VWF replacement

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56
Q

General adult dosing for FP/FFP transfusion

A

10-15 mL/kg will achieve 30% of plasma clotting factor activity. (US recommends 10-20 mL/kg)
-5-8 mL/kg will usually reverse warfarin
-should be aided by serial coagulation testing
Generally, small adult= 3 units, large=4 units

57
Q

Thawing of FP, FFP, CSP

A

Thawed in circulating water bath of 30-37C for 30-60 min or in dry system for 12-30 min depending on volume and equipment.
Thawed product stored at 1-6C for 5 days

58
Q

Administration/storage of thawed FP, FFP, CSP products

A

Transfuse FFP immediately or store at 1-6C for 5 days with ACD-A.
Apheresis thawed samples in sodium citrate are stored for 24 hours.
Once thawed, products cannot be refrozen

59
Q

Return of plasma products

A

If thawed plasma needs to be returned it can be done so it should be kept in refrigerator or transport device and only if passes visual inspection and bag is intact. Must not be out of freezer for 30 min

60
Q

Frozen plasma product storage

A

-18C or colder in a controlled monitored freezer for 1 year

61
Q

Usual CBS cryoprecipitate unit

A

10 mL containing 285 mg of fibrinogen.

10 units usually contains 4 grams fibrinogen

62
Q

Indications for cryoprecipitate transfusion

A

Fibrinogen replacement for acquired hypofibrinogenemia, massive transfusion.
Typically fibrinogen less than 1.0 g/L in DIC and less than 1.5 in massive transfusion and leukaemia.
No longer recommended as FVIII replacement.
Fibrinogen deficiency should be documented.

63
Q

Contraindications for cryoprecipitate transfusion

A

Any use other than fibrinogen replacement with 1.0 or less or in massive transfusion with coagulopathy.
Should not be used to make fibrin glue, hemophilia treatment or VWD.

64
Q

Calculation of fibrinogen dose

A

Estimated blood volume x (1-hct)= plasma volume
Desired fibrinogen-actual fibrinogen x plasma volume= Amount needed.
Amount needed/285 mg fibrinogen per unit= # units needed
Usual adult dose is 1-2 units per 10 kg body weight
10 units increases fibrinogen by 0.7-1 gram/L

65
Q

Storage of cryoprecipitate

A

-18C or colder for a max of 12 months, must not be out of the freezer for longer than 30 min.
-Once thawed, transfuse within 4 hours
If cryoprecipitate is pooled with NS, all units will need to be used within 4 hours of opening. If not used immediately the product should be returned to the storage device and returned

66
Q

Human serum albumin size

A

67 kDa

67
Q

Oncotic activity of albumin

A

1 gram of albumin attracts 18 mL water. 25 g expands volume by 450 mL.
5% is iso osmotic, 25% is hyperoncotic and therefore expansionists plasma by 4-5x volume infused

68
Q

Serum albumin loss in hemorrhage

A

12 grams per 500 mL of blood lost via hemorrhage

69
Q

usual sodium concentration of albumin

A

130-160 mEq/L

70
Q

Administration of albumin

A

max 5 mL/min for 5%, 1-2 ml/min for 25%. Don’t mix with hypotonic solutions like SWFI because it can lead to hemolysis. Infuse within 4 hours once opened.

71
Q

Disadvantages to albumin infusion

A

Cost compared to crystalloid
Dilution of hemoglobin
circulatory overload
dilution of plasma proteins and coagulopathy

72
Q

List of most common causes of transfusion associated mortality

A
  1. Transfusion-related acute lung injury (TRALI)
  2. TACO
  3. Hemolytic transfusion reactions (non ABO more common than ABO)
  4. microbial contamination
  5. allergic reaction
73
Q

Diagnostic criteria for TRALI

A
  • clinical diagnosis

- hypoxemia and pulmonary edema within 6 hours of transfusion

74
Q

Mechanism of TRALI

A

HLA incompatibility between donor WBC and host immune system.

75
Q

American Red Cross RBC transfusion recommendations

A

<6 g/dL in young healthy patient
<7g/dL in critically ill patient
<7-8 in patients with cardiovascular disease

76
Q

STS recommendations for transfusion trigger on CPB

A

<6 g/Dl for patients on CPB with moderate hypothermia, but high risk patients need higher hemoglobin levels

77
Q

Evidence based practice on RBC transfusion

A

liberal transfusion triggers of 9-10 have no difference in primary outcome compared to restrictive 7.5-8 transfusion trigger

78
Q

Minimum FDA standard for stored RBC’s

A

75% remain in circulation 24 hours post transfusion. (Longer the storage time the less RBC survival due to storage lesion)

  • less than 1% hemolysis
  • no consideration of function of the cells themselves
79
Q

RBC storage lesion

A
  • Degredation of structure: membrane rigidity, aggrebility
  • chemical: lactate, K, free hemoglobin increase.
  • 2,3DPG decrease by 95% after 21 days
  • depletion of NO from microvasculature from free hemoglobin constriction
80
Q

RBC size

A

Approx 7 microns

81
Q

Mechanism of free hemoglobin injury

A

Free hemoglobin (hemolysis, transfusion storage lesion) causes vasoconstriction in microvasculature, causing depletion of nitric oxide. Leads to insufficient NO bioavailability

82
Q

Evidence for new vs old blood

A

No difference between stored blood for shorter and longer storage blood, but few patients receive very old blood. Very fresh blood and medium blood have similar outcomes

83
Q

Usual recipe for massive transfusion, empiric

A

1 RBC: 1FFP: 1Plt theoretically prevents dilutional coagulopathy

84
Q

General Red Cross recommendation for platelet therapy, dose of adult platelets

A

Give for less than 50 k/microL. Standard dose is 1 unit/10 kg body weight. 6 units from whole blood (apheresis) increases put by 30

85
Q

Most common/highest cost transfusion reaction

A

Platelet bacterial contamination. 1 in 3000 bags are contaminated.
TRALI is most often associated with platelet transfusion, due to women not being excluded from being platelet donors and high female rates of HLA antibodies

86
Q

Fibrinogen content of FP

A

4 units of CBS FP contain 2.5 grams fibrinogen

87
Q

INR and FP/FFP transfusion

A

FFP fails to improve INR that is less than 1.6

INR designed to follow anticoagulant dosing with Vit K antagonists and TEG may be normal when INR less than 2

88
Q

Blood administration set filter size

A

170-260 micron

89
Q

Hensley rapid transfusion definition

A

1 entire blood volume replaced in 24 hours

90
Q

Disadvantage to erythropoietin administration

A

Thrombotic events and promotion of tumour growth

91
Q

Hensley definition of ANH

A

Blood withdrawn from the patient prior to heparinization and then read ministered after CPB

92
Q

Benefit of ANH

A
  • Reduced allogenic transfusion, especially with greater than 800 mL phlebotomy.
  • low volume ANH is shown to decrease intraoperative RBC transfusion, but no outcome change
93
Q

Evidence for cell salvage in cardiac surgery

A

Use decreases risk of transfusion by 34% and saves 1 unit PRBC transfusion per patient on average

94
Q

Functions of Thrombin

A

Fibrinogen to Fibrin
FXI, FXIII positive feedback loop activation
Cofactor V VIII activation
Protein C pathway inhibitin V VIII
Platelet aggregation
Stimulates tPA release from endothelial cells

95
Q

Platelet granule contents

A

Fibrinogen, vWF, Factor V, Calcium, Serotonin, Plasminogen, Platelet factor 4

96
Q

FVIII Physiology

A

Produced primarily in hepatocytes
Extremenly unstable except when bound to vWF
Binds with FIX and vWF in coagulation complex

97
Q

Activation of Intrinsic pathway (Contact activation)

A

FXII binds to negatively charged surface (polyanion either from surface or platelet secretion).
FXIIa activates prekallikrein to stimulate fibrinolysis and inflammation, and FXI to intrinsic pathway.

98
Q

Activation of extrinsic coagulation pathway

A

TF in sub endothelial system activates is presented via injury to its ligand FVII

99
Q

3 Major coagulation cascade complexes

A
  1. TF +FVIIa
  2. IXa +FVIII (Tenase)
  3. Xa+ Va (Prothrombinase)
    All complexes require Ca, anionic phospholipid surface,, cofactors
100
Q

Action of heparin

A

UFH binds to ATIII AND THROMBIN and forms a complex: the complex inactivates thrombin, 9,10,11,12
Short heparin binds to ATIII ONLY but the complex mainly inactivates FXa.
LMWH binds less to proteins so is more predicable.

101
Q

1 USP unit of heparin

A

keeps 1 mL citrated re-calcified sheep blood liquid for 1 hour

102
Q

Heparin pharmacokinetics

A

Half life:30 min at small doses, 2-3 hours at large doses. Half life is dose dependent.
Onset 1 minute.
Renal elimination or by endothelial cells

103
Q

Heparin chemistry

A

glycosaminoglycan, negatively charged, very acidic

104
Q

Hensley Heparin prime content

A

CPB prime should contain heparin at the same concentration as that of the patient (3-4 units/mL) to account for the expanded plasma blood volume

105
Q

ACT and temperature

A

At temperatures below 25, act is so prolonged that alternative tests should be considered

106
Q

Hensley ACT minimum recommendation

A

400 s

107
Q

Aprotinin and ACT

A

Aprotinin prolongs the ACT in cases where celite activators are used, therefore consider titrating heparin to ACT of 750 with celite. Kaolin is not affected by aprotinin

108
Q

Clinical use of heparin concentration testing

A

In hypothermia under 25C
To maintain heparin concentrations of 3-4 u/mL which may suppress thrombin more effectively.
Can be used in context of aprotinin
Must be used with ACT as variable sensitivity to heparin between patients is known
Can determine protamine dose, only if blood volume is constant

109
Q

Initial Loading Dose of Heparin

A

300-400 units/kg, usually to a max of 35-40 thousand units as patient weight tends to max at lean body mass, with maximum lean body mass usually 90-110 kg

110
Q

Usual acceptable ACT/heparin dose for off pump revascularization procedures

A

200-300 seconds with dose of 100-300 units/kg

111
Q

Use of heparin concentration monitoring on CPB

A

whole blood concentration targeted for 3-4 u/mL are sufficient.
Use of [Heparin] substantially increases the amount of heparin given but suppresses thrombin formation, at the expense of heparin rebound and platelet activation
Patient sensitivity to heparin varies, therefore another clotting test (simultaneous ACT) is recommended

112
Q

LMWH vs UFH for CPB

A

LMWH does not bind to thrombin as well (primarily anti Xa activity) compared to long chain UFH. Thrombin inactivation is pivotal for CPB
LMWH has a long half life
LMWH poorly neutralized by protamine

113
Q

Factors decreasing the response to heparin

A
  • ATIII Deficiency (familial or acquired)
  • Hypercoaguable states (Sepsis, arteriosclerosis, pregnancy, HIT, thrombocytosis)
  • Nitroglycerine
  • Drug protein binding (acid glycoproteins, immunoglobulin)
  • Extremes of age
114
Q

Use of ATIII supplementation

A

For suspected heparin resistance, if more than 600 units/kg given.
2 units of FFP=500 units of ATIII

115
Q

Clinical approach to heparin resistance

A
  1. Add more heparin, though usually >4u/kg does not tend to improve anticoagulation
  2. Add 2 units or 500 mL FFP
  3. Add ATIII concentrate
  4. Accept the ACT due to the wide acceptability of range for safe bypass
116
Q

Serum vs plasma

A

Serum is obtained after the sample is clotted. Contains no fibrinogen. Contains no cells.
Plasma has clotting factors (including fibrinogen.) Used for testing coagulation

117
Q

Polychromasia

A

Increased reticulocyte count; reticulocytes released indicate early release of immature RBC

118
Q

Hypochromasia

A

Less Hgb inside the cell, usually due to insufficient hemoglobin production.

119
Q

MCV size interpretation

A

Large cells: insufficient cell division usually caused by vitamin deficiency. Target cells have large cell membranes caused by liver failure.
Small cells: cell division is normal but don’t contain enough Hgb, usually thalassemia or iron deficiency

120
Q

Prothrombin time testing method

A
Adds thromboplastin (tissue factor and phospholipid) and calcium. Simulates extrinsic pathway via FVII activation and common pathway activation. 
Most affected by Coumadin, as FVII gets affected first  by VitK block. Done with centrifuged, platelet poor plasma
121
Q

activated partial thromboplastin time testing method

A

2 reagents are added separately: thromboplastin (TF and phospholipid), calcium, and negatively charged activator like kaolin. Done with centrifuged, platelet poor plasma

122
Q

Beta Thalassemia pathophysiology and management

A
  • reduced/absent production of beta chain in hemoglobin, leading to excess alpha chain production and precipitation. This causes extracellular hemolysis in spleen, and increased compensatory iron
  • Tx: transfusion, iron chelation and splenectomy
123
Q

Heparin Induced Thrombocytopenia Pathophysiology.

A

Most often occurs 5 days following continuous heparin, average is 9 days. Antibodies are created between heparin and PF4 complex, causing aggregation of platelets and thrombocytopenia.

124
Q

Safe time for heparin administration following HIT

A

Antibodies usually disappear 50-85 days following the most recent exposure to heparin

125
Q

Bivalirudin use

A

For CPB is 1 mg/kg bolus then 2.5 mg/kg/hr for CPB. While it has a shorter half life than heparin, at 24 min, there is no reversal. Direct thrombin inhibitor

126
Q

Usual protamine dosing

A

1 mg of protamine neutralizes 100 IU of heparin. Most clinicians give 0.6 mg/100 IU to 1:1 protamine.

127
Q

ACT post protamine

A

Should be no more than 10% above the value before heparin administration

128
Q

Protamine administration speed

A

Greater than 3 minutes at 3 mg/kg. Faster than that causes dropping of SVR and PVR which can then be partially resolved with addition of volume. 10 minutes recommended.

129
Q

Protamine PVR hypertension reaction cause

A

Pulmonary vasoconstriction thought to be due to heparin-protamine complexes stimulating pulmonary macrophages to produce thromboxane

130
Q

Treatment of adverse protamine reactions

A
  • Usually low BP within 10 min of protamine is because of protamine, but consider LV failure or hypovolemia.
  • If hypotension and normal/low SVR, treat as anaphylactoid. Give fluid and epi, consider steroids
  • if low BP and high PAP consider isoproterenol and milronone. Occasionally, additional heparin will resolve the reaction
131
Q

Blood shear stress equation, definition

A

Force applied to an area of liquid confined between 2 plates that is sufficient to set the liquid in motion.
Stress= viscosity x shear rate
Where; shear rate is the velocity relative to the plates

132
Q

Blood viscosity relationship

A

Poiseuille: flow is related to r^4 and inversely related to viscosity. As diameter decreases the shear rate decreases.
Flow is lowest and viscosity highest in postcapillary venules

133
Q

Hematocrit and viscocity

A

Is a linear relationship

134
Q

Blood temperature and viscocity

A

Not linear. Temp decrease of 10C increases viscocity. 20-25%. Highest viscocity is seen at temperatures below 25C

135
Q

Perfusion pressure and blood flow relationship

A

Per Poseuille, perfusion pressure cannot be an adequate marker of flow because pressure depends on flow and viscocity, and viscocity depends on temperature.

136
Q

Optimum hematocrit for o2 delivery (Gravlee)

A

30%. Lower amounts have too little hemoglobin, too high causes an increase in SVR due to increased viscocity

137
Q

Recommended max cell saver suction

A

Less than 150 mmHg

138
Q

Ratio of blood to anticoagulation in cell saver

A

1-5 to 1:10 with a target of 15 mL/100 mL blood with heparin or 70