UNIT 9 Fluids & Blood Flashcards
1
Q
describe the distribution of body water.
A
in the textbook 70kg male, water represents 60% of the total body weight. This equals 42L.
TBW is divided into:
- ICF: 40% TBW, 28L
- ECF: 20% TBW, 14L
ECF can be further divided into:
- interstitial fluid: 16% TBW, 11L
- plasma fluid: 4% TBW, 3L
remember: 60/40/20(15/5)
2
Q
which populations tend to have a greater percentage of TBW% by weight? Which have less?
A
populations w/ higher TBW% by weight: neonates
populations w/ lower TBW% by weight: females, obese, elderly
3
Q
what are the 2 more important determinantes of fluid transfer between the capillaries and interstitial space?
A
the plasma is in direct contact with the interstitial fluid by way of pores in the capillaries. The movement of fluid between the intravascular space and the interstitial space is determined by:
- starling forces
- the glycocalyx
4
Q
describe the starling forces in the context of capillary fluid transfer.
A
- forces that move fluid from the capillary to the interstitium:
- Pc: capillary hydrostatic pressure
- pi(if): interstitial oncotic pressure - forces that move fluid from the interstitium and into the capillary:
- Pif: interstitial hydrostatic pressure
- pi(c): capillary oncontic pressure
5
Q
what is the glycocalyx, and what factors disrupt it?
A
the endothelial glycocalyx forms a protective layer on the interior wall of the blood vessel. It can be viewed as the gatekeeper that determines what can pass from the vessel into the interstitial space. It also contains anticoagulant properties.
disruption of the glycocalyx contributes to capillary leak. Accumulation of fluid and debris in the interstitial space reduces tissue oxygenation. conditions that impair the integrity of the glycocalx include:
- sepsis
- ischemia
- DM
- major vascular surgery
6
Q
what is lymph, and how does the lymphatic system work?
A
lymphatic system = fluid scavenger. It removes fluid, protein, bacteria, and debris that has entered the interstitium.
It accomplishes this goal with a pumping mechanism that propels lymph through a vessel network lined w/ one way valves. This creates a net negative pressure in the interstitial space.
Edema occurs when the lymphatic system is unable to do its job.
7
Q
how is lymph returned to the systemic circulation?
A
via the thoracic duct at the juncture of the IJ and the SC vein. You can injury the thoracic duct during venous cannulation. Since the thoracic duct is larger on the L side, there is a greater risk of chylothorax (lymph in the chest) during L IJ insertion.
8
Q
What is the difference b/n osmosis and diffusioN?
A
osmosis = movement of water across a semipermeable membrane, down it’s concentration gradient.
diffusion = movement of molecules from a region of high concentration to a region of low concentration
9
Q
What is osmotic pressure, and what is its primary determinant?
A
osmotic pressure is the pressure of a solution against a semipermeable membrane that prevents water from diffusing across that membrane
- it is a function of the number of osmotically active particles in solution
- it is NOT a function of their molecular weights
10
Q
what’s the difference b/n osmolarity and osmolality?
A
both are measures of concentration: the amount of solvent within a defined space.
osmolarity = # of osmoles/L of solution
osmolality = # of osmoles/kg of solution
11
Q
what is the reference value for plasma osmolarity, and what are the 3 more important contributors?
A
280-290mOsm/L
three most important contributors: Na+, glucose, BUN
osm = 2[Na+] + glucose/18 + BUN/2.8
- -> Na+ is the most important
- -> hyperglycemia or uremia can increase plasma osm
12
Q
what is the difference b/n a hypotonic and hypertonic solution?
A
tonicity compares the osm of a solution relative to the osm of plasma.
since plasma is isotonic to cells, we can think about tonicity another way - we can use it to compare the tonicity of a solution to the tonicity of the cells.
hypotonic (i.e. 255): water enters cells & they swell
isotonic (i.e. 285): no water transfer and cells remain same size
hypertonic (i.e. 315): water exits cells and they shrink
13
Q
think of all the IV fluids you can. Which are hypo, iso, and hypertonic to plasma? Bonus points if you can list the osm of each.
A
hypotonic
- 1/2NS 154
- D5W 253
isotonic
- NS 308
- LR 273
- plasmalyte 294
- 5% albumin 300
- 6% voluven 296
- 6% hespan 309
hypertonic
- 3% NS 1026
- D5NS 560
- D51/2NS 405
- D5LR 525
- 10% dextran 350
14
Q
what is the relationship b/n the tonicity of IV solutions and increased ICP?
A
hypotonic slns have a lower osm than the plasma or cells.
- this causes cells to swell & increase their volume
- this increases ICP
instead hypertonic slns are useful for treating cerebral edema (shrinks cells)
15
Q
how does dextrose affect the tonicity of IVF?
A
you may be thinking that glucose in IVF (such as D5W) should be osmotically active. Well you’re 1/2 right:
- the glucose contributes osmotically active molecules to the plasma
- the other side of the story is that this glucose is metabolized to CO2 and H2O. What’s left over? water, and water is hypotonic.
16
Q
How do isotonic IVF distribute in the patient?
A
expand the plasma volume and the ECF.
crytalloids tend to remain in the intravascular space for approx 30mins before moving to the ECF
17
Q
what complication can result when hypertonic saline is administered too quickly?
A
central pontine myelinolysis
18
Q
compare the advantages of colloids to the advantages of crystalloids.
A
colloids:
- replacement ratio = 1:1
- increases plasma volume x3-6hrs
- smaller volume needed
- less peripheral edema
- albumin has anti-inflammatory properties
- dextran 40 reduces blood viscosity (improves microcirculatory flow in vascular surgery)
crystalloids
- replacement ratio = 3:1
- expands the ECF
- restores 3rd space loss
19
Q
compare the disadvantages of colloids to the disadvantages of crystalloids
A
colloids:
- albumin binds Ca++ –> hypocalcemia
- FDA black box warning on synthetic colloids (risk of renal injury)
- coagulopathy: dextran > hetastarch > hextend; dont exceed 20mL/kg
- anaphylactic potential (dextran = highest risk)
crystalloids
- limited ability to expand plasma volume (20-30mins, then higher potential for peripheral edema)
- risk for hyperchloremic metabolic acidosis w/ NS: increased [Cl-] –> increased bicarb excretion renally
- dilutional effect on albumin (reduces capillary oncotic pressure)
- dilutional effect on coagulation factors
20
Q
how does hyperkalemia affect the EKG (list the events in order of appearance)?
A
early: long PR, peaked T, short QT
middle: flat P, wide QRS
late: QRS–> sine wave–> VF
21
Q
list all the treatment options for hyperkalemia
A
calcium (stabilizes cardiac membrane) insulin + D50 hyperventilation bicarb albuterol K+ wasting diuretics dialysis
22
Q
discuss the presentation of hypocalcemia.
A
skeletal m cramps nerve irrirability (paresthesias, tetany) Chvostek sign Trousseau sign laryngospasm MS changes --> seizures long QT interval
23
Q
discuss the presentation of hypercalcemia.
A
nausea abdominal pain hypertension psychosis MS changes --> seizures
24
Q
what is the treatment for hypercalcemia?
A
NS loop diuretics (lasix)
25
describe the presentation of hypermagnesemia.
usually caused by excessive administration (think OB and preeclampsia)
loss of deep tendon reflexes (4-6.5mEq/L or 10-12mg/dL)
resp depression (6.5-7.5mEq/L or >18mg/dL)
cardiac arrest (>10mEq/L or >25mg/dL)
26
what is the treatment for hypermagnesemia?
calcium chloride
27
how does hypermagnesemia affect NMB?
potentiates NMB (sux + NDMR)
28
compare and contrast the consequences of acid base imbalance
acidosis
- increased P50 (right = release)
- decreased contractility
- increased SNS
- increased risk of dysrhythmias
- increased CBF & ICP
- increased pulmonary vascular resistance
- hyperkalemia
alkalosis
- decreased P50 (left = love)
- decreased coronary flow
- increased risk of dysrhythmias
- decreased CBF & ICP
- decreased pulmonary vascular resistance
- hypokalemia
- decreased iCa++
29
what is the anion gap, and what does it tell you?
helps us determine the cause of acidosis.
anion gap = major cations - major anions
= [Na+]-([Cl-]+[HCO3-])
= 8-12mEq/L
accumulation of acid (AG >14) --> gap acidosis
loss of bicarbonate or ECF dilution --> nongap acidosis
30
list the possible causes of an anion gap acidosis.
```
MUDPILES
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde
Isoniazid
Lactate (decreased DO2, sepsis, cyanide poisoning)
Ethanol, ethylene glycol
Salicylates (inhibits Krebs cycle)
```
31
list the possible causes of a nongap acidosis.
```
HARDUP
Hypoaldosteronism
Acetazolamide
Renal tubular acidosis
Diarrhea
Ureterosigmoid fistula
Pancreatic fistula
```
large volume resuscitation w/ NS solutions can cause a nongap metabolic acidosis w/ hyperchloremia
32
discuss the etiology of metabolic alkalosis
1. addition of HCO3-
- NaHCO3 administration
- massive transfusion (liver converts preservatives to HCO3-
2. loss of nonvolatile acid
- loss of gastric fluid (vomiting, NG suction)
- loss of acid in urine
- diuretics
- ECF depletion --> increased Na+ reabsorption --> H+ & K+ excretion
3. increased mineralocorticoid activity
- cushing's syndrome
- hyperaldosteronism
33
under normal conditions, why does blood remain a liquid?
- coagulation proteins circulate in inactive form
- the endothelium is smooth and the glycocalyx repels clotting factors
- undamaged endothelium doesn't express tissue factor or collagen (prevents activation of platelets or the coag cascade)
- activated factors are removed by brisk blood flow through vessels as well as anticoagulants in circulation
34
what are the 4 steps of hemostasis?
1. vascular spasm
2. formation of the platelet plug (primary hemostasis)
3. coagulation & formation of fibrin (secondary hemostasis)
4. fibrinolysis when the clot is no longer needed.
35
where are platelets formed? where are they metabolized?
formed by megakaryocytes in the bone marrow
cleared by macrophages in the reticuloendothelial system & the spleen
36
what is the normal value for platelets? what are the critical values?
**platelet count monitors the number of platelets, not the platelet function
normal 150-300K
<50K = increased surgical bldg risk
<20 = increased spontaneous bldg risk
37
what are the 3 steps of the platelet plug formation (primary hemostasis)?
1. adhesion
2. activation
3. aggregation
a platelet plug is formed in approx 5mins
38
list the 12 coagulation factors
```
1 = fibrinogen
2 = prothrombin
3 = tissue factor
4 = calcium ions
5 = labile factor
7 = stable factor
8 = antihemophilic factor
9 = christmas factor
10 = stuart prower factor
11 = plasma thromboplastic antecedent
12 = hageman factor
13 = fibrin stabilizing factor
```
39
regarding the extrinsic pathway: what activates it? what lab tests measure it? what drug inhibits it?
extrinsic = activated by vascular injury (tissue trauma liberates TF from the subendothelium)
measured by PT & INR
inhibited by coumadin
40
regarding the intrinsic pathway: what activates it? what lab tests measure it? what drug inhibits it?
intrinsic = activated by blood injury or exposure to collagen
measured by PTT & ACT
inhibited by heparin
41
what factors are in the extrinsic pathway, intrinsic pathway, and the final common pathway?
extrinsic = 3,7
- can be purchased for 37c
intrinsic = 8, 9, 11, 12
- if you cant buy the intrinsic pathway for 12$, you can buy it for 11.98
final common = 1, 2, 5, 10, 13
- can be purchased at the 5 and dime for 1 or 2 dollars on the 13th of the month
42
describe the process of fibrinolysis
fibrinolysis = process of breaking down the clot once it's no longer needed
plasminogen = proenzyme that is synthesized in the liver. it is incorporated into the clot as it's being formed, but it lays dormant until it's activated by tPA or urokinase into plasmin
plasmin = proteolytic enzyme that degrades fibrin into fibrin degradation products
fibrin degradation products are measured by d-dimer
43
what are the three phases of the contemporary cell-based coagulation cascade?
attempts to explain how platelets, the extrinsic pathway, and the intrinsic pathway function in an interdependent manner. The idea is that coagulation takes place on the surface of a cell that expresses TF
the cascade consists of 3 phases:
1. initiation
2. amplification
3. propagation
44
understand the TEG
TEG provides a real time visual representation of disorders of coagulation and fibrinolysis
R time = time to begin forming a clot; 6-8mins
- prob: coagulation factors
- tx: FFP
K time = time until clot has achieved fixed strength; 3-7mins
- prob: fibrinogen
- tx: cryo
alpha angle = speed of fibrin accumulation; 50-60degrees
- prob: fibrinogen
- tx; cryo
maximum amplitude (MA) = measures clot strength; 50-60mm
- prob: platelets
- tx: platelets +/- DDAVP
amplitude at minutes after maximum amplitude (A60) = height of vertical amplitude 60mins after max amplitude; MA-5
- prob: excess fibrinolysis
- tx: TXA, amicar
45
be able to identify TEG abnormalities
- factor deficiency or anticoagulation (long R time)
- impaired platelet # or function (low MA)
- primary fibrinolysis (low A60)
- hypercoagulation (high MA and/or A60)
- DIC stage 1: hypercoagulable w/ secondary fibrinolysis
- DIC stage 2: hypocoagulable state.
46
what is the mechanism of action of heparin?
inhibits the intrinsic and final common pathways
antithrombin III is a naturally occurring anticoagulant that circulates in the plasma. heparin binds AT III and greatly accelerates its anticoagulant ability (1000x). The heparin-AT complex neutralizes thrombin and activated factors X, XII, XI, and IX
47
how do you treat a patient w/ antithrombin III deficiency?
AT III concentrate
FFP
ATIII deficiency = common cause for failure to achieve anticoagulation despite an adequate dose of heparin prior to CPB
48
can a pregnant patient receive IV heparin?
yes; it doesn't cross the placenta.
49
what is the normal ACT? What value should be achieved prior to CPB?
90-120sec = normal
ACT >400 prior to CPB
ACT is measured before heparin administration, 3mins after administration, and every 30mins thereafter
50
what are the doses for heparin (for CPB) and protamine?
300-400U/kg heparin (cardiac surgery dose)
1mg protamine/100U of heparin predicted to be in circulation
51
how does protamine reverse heparin?
heparin is a large, negatively charged, water soluble compound
protamine is a highly alkaline compound w/ strong positive charge.
the + and - charge create a neutralization reaction and stop heparin's anticoagulation activity
52
what are the side effects of protamine?
hypotension d/t histamine release; administer >5mins
pHTN d/t TxA2 and serotonin release
allergic rxn d/t previous sensitization to protamine, NPH, or fish allergy
53
what is the mechanism of action of warfarin?
inhibits the enzyme vitamin K epoxide reductase complex 1 (VKOR c1), which is responsible for converting inactive vitamin K to active vitamin K
it indirectly blocks the manufacturing of vitK dependent factors (II, VII, IX, X, and protein C & S)
54
list all of the antidotes for warfarin. When should each be used?
vitamin K (10-20mg PO, IM, or IV) in non-emergent situations or for minor surgical procedures. Requires 4-8hrs
emergent, or high risk procedures requires reversal w/ FFP (1-2U), recombinant factor VIIa, or PT complex concentrate
55
what conditions can cause vitK deficiency?
vitK is a fat soluble vitamin that requires the presence of fat and bile for absorption. It's also manufactured by bacteria in the gut.
malabsorptive diseases, impaired GI flora, and decreased bile production can impair fat absorption adn therefore create vitK deficiency.
- this can lead to coagulopathy
56
what is the risk associated w/ IV phytonadione?
life-threatening anaphylaxis.
| thus IV administration is best avoided, but if it's necessary, then administration shouldn't exceed 1mg/min
57
why do neonates receive vitamin K after birth?
healthy intestinal flora is required for the gut to synthesize vitK.
Neonates don't have the intestinal flora that synthesize it, so 0.5-1mg IM after delivery is common.
58
List 4 examples of ADP receptor inhibitors, and state how long each must be discontinued prior to surgery.
ADP receptor inhibitors prevent platelet aggregation and thrombus formation.
clopidogrel 7 days
ticlopidine 14 days
prasugrel 2-3 days
ticagrelor 1-2 days
59
list 3 examples of GIIb/IIIa receptor antagonists, and state how long each must be discontinued prior to surgery.
inhibit platelet aggregation and thrombus formation
abciximab 3 days
eptifibatide 1 day
tirofiban 1 day
60
what drugs can be used to provide anticoagulation in a patient who is unable to receive heparin? How long must each be stopped prior to surgery?
thrombin inhibitors can be used instead of heparin
bivalrudin 2-3hrs
argatroban 4-6hrs
hirudin 8hrs
(heparin should be stopped 6hrs prior to surgery)
61
what is the mechanism of action of COX inhibitors? Which agents provide irreversible COX inhibition?
prevent platelet aggregation by blocking COX-1 (cyclooxygenase). This stops the conversion of arachidonic acid to prostaglandins and ultimately thromboxane A2.
aspirin is irreversible (lasts for the lifetime of the platelet)
NSAIDs are reversible (DOA is shorter than the lifetime of the platelet.
62
name 2 antifibrinolytics and 4 fibrinolytics.
antifibrinolytics: stop the conversion of plasminogen to plasmin; they promote clot formation (reduces bleeding in cardiac and orthopedic surgery):
- TXA
- amicar
fibrinolytics: facilitate the conversion of plasminogen to plasmin. They break down clots (useful for MI or CVA)
- tPA
- urokinase
- reteplase
- alteplase
63
where is vWF synthesized and what is it's function?
synthesized by the vascular endothelium and megakaryocytes. It serves two key functions:
- anchors the platelet to the vessel wall at the site of vascular injury (platelet adhesion)
- carried inactivated factor VIII in the plasma
64
what are the 3 types of von willebrand disease?
most common inherited disorder of platelet function. As a qualitative platelet disorder, the platelet count is normal, but the platelets don't function properly.
Type I: mild-moderate reduction in the amount of vWF produced
Type II: vWF that is produced doesn't work well
Type III: severe reduction in the amount of vWF produced.
65
what lab results are consistent w/ von willebrand disease (PT/INR, PTT, platelet count, bleeding time, fibrinogen)?
PT/INR, platelets, fibrinogen = no change
PTT, bleeding time = increased
66
what is the mechanism of action of desmopressin? What is the dose?
DDAVP is a synthetic analogue of ADH. It stimulates the release of endogenous vWF and increases factor VIII activity.
- pts w/ Type I respond best to DDAVP
- pts w/ Type III don't respond to DDAVP bc they don't produce vWF
dose: 0.3-0.5 mcg/kg IV
side effect: hypotension w/ rapid administration
67
aside from desmopressin, list 3 other treatments that can improve the coagulopathy of von willebrand disease.
cryo: contains factors VIII, XIII, fibrinogen, and vWF. can be used for type 1, 2, or 3
FFP: contains all of the clotting factors, so it too can be used for all disease types
purified VIII-vWF concentrate: reduces the risk of transfusion-related infection. It is the first line agent for the patient w/ type 3 disease.
68
describe the pathophysiology of hemophilia A.
X-linked chromosomal disorder (more common in males) that causes factor VIII deficiency.
severe disease (factor VIII activity <1%) is associated w/ spontaneous bleeding into the joints, muscle, and vital organs. These patients often require orthopedic surgery.
69
What lab results are consistent w/ hemophilia A (PT/INR, PTT, platelet count, bleeding time, fibrinogen)?
factor VIII is part of the intrinsic pathway. Therefore, the PTT will be greatly prolonged w/ severe disease and only slightly prolonged in mild disease.
all other lab values are unchanged.
70
What is the treatment for hemophilia A?
- factor VIII concentrate prior to surgery
- FFP & cryo can also be used to replace factor VIII, but increase in transfusion related disease transmission
- antifibrinolytics (TXA, amicar) can be used to minimize bleeding during dental procedures
- T&C is required for any surgical procedure
71
how is hemophilia B different from hemophilia A?
hemophilia B is factor 9 deficiency. (vs factor 8 deficiency w/ A)
labs and anesthetic management are similar w/ one exception: instead of factor 8 replacement, factor 9 concentrate may be used instead.
72
What is the role of recombinant factor 7 in the management of hemophilia A & B?
sometimes these pts develop inhibitors that prevent exogenous factor 8 or 9 from achieving their therapeutic goals.
For a clot to form, the missing coagulation factor must be replaced or bypassed. Recombinant factor 7 is a bypass agent bc it skips over factor 8 or 9 in those w/ inhibitors.
dose 90-120mcg/kg
increased risk of arterial thrombosis (MI, CVA) as well as venous thrombosis (PE< DVT)
73
describe the pathophysiology of disseminated intravascular coagulation.
characterized by disorganized clotting and fibrinolysis that leads to the simultaneous occurrence of hemorrhage and systemic thrombosis.
generalized thrombin formation creates microvascular clots that impair tissue perfusion, resulting in tissue hypoxia and acidosis. The body attempts to break down these clots by activating it's anticoagulation system, however this leads to widespread consumption of its coagulation factors, fibrinogen, and platelets.
74
What lab results are consistent w/ DIC (PT, PTT, D-dimer, platelets, fibrinogen)?
increased: PT, PTT, D-dimer
decreased: platelets, fibrinogen
75
name 3 conditions that are associated with a high risk of developing DIC.
1. sepsis (highest risk = gram- bacilli)
2. obstetric complications (highest risk = preeclampsia, placental abruption, and AFE)
3. malignancy (highest risk = adenocarcinoma, leukemia, and lympthoma)
76
describe the management for the patient with DIC
DIC is not a disease in itself, but rather a manifestation of some other underlying problem. The definitive tx is reversing the underlying cause. Otherwise, treatment is supportive:
- hypovolemia: IVF
- coagulopathy: replace consumed blood products w/ FFP, platelets, cryo (it's ok to feed the beast)
- severe microvascular thrombosis: IV heparin or LMWH
77
compare and contrast type I and type II heparin induced thrombocytopenia.
causes clot formation throughout the body.
HIT occurs when the body mounts an immune response against heparin after it binds to platelet factor 4 (PF4). IgG antibodies activate platelets, which ultimately results in uncontrolled clot formation. The platelet count falls bc platelets are consumed faster than they are produced.
Type 1
- heparin induced platelet aggregation
- occurs after large heparin dose
- 1-4 days post administration
- platelet count <100K
- minimal morbidity
- tx: resolves spontaneously
Type 2
- IgG attack factor 4 immune complexes --> platelet aggregation; pt is resistant to heparin anticoagulation
- occurs after any heparin dose
- 5-14 days post administration
- platelet count <50K
- hypercoagulable state = high risk of amputation & death
- heparin must be discontinued, anticoagulate w/ direct thrombin inhibitor
78
describe the patho and treatment of protein C and S deficiency
protein C produces an anticoagulant effect by inhibiting facotrs Va and VIIIa, creating a feedback mechanism that prevents unnecessary clot formation
- protein S is a cofactor of protein C (helps it do it's job)
- deficiency in either can produce a hypercoaguable state --> thrombosis risk.
tx:
- thromboembolism is treated w/ heparin that is transitioned to warfarin
- this may or may not be lifelong
79
describe the patho and treatment of factor V leiden mutation.
causes a resistance to the anticoagulant effect of protein C
tx:
- only those w/ thromboembolism require anticoagulation
- lifelong tx is unwarranted unless the pt experiences recurrent thrombotic events.
80
describe the patho of sickle cell anemia.
inherited disorder that affects erythrocytes. amino acid substitution (valine for glutamic acid) on the beta globulin chain alters RBC geometry. This affects RBC function in several ways:
- deoxygenation of HgbS --> sickling
- in severe cases, sickling causes the RBCs to clump together, which causes mechanical obstruction of the microvasculature in the vital organs and joints --> impaired tissue perfusion + intense pain
- sickled cells are more prone to hemolysis and removal by the spleen (lifespan = 12-17 days vs. normal RBC 120 days)
81
list the triggers that cause sickling of HgbS
```
pain
hypothermia
hypoxemia
acidosis
dehydration
```
anesthetic managment focuses on avoiding these triggers.
82
what is the treatment of vaso-occlusive crisis?
sickled cells --> impaired tissue perfusion --> ischemic injury
this is the most common manifestation of sickle cell disease
tx: analgesics (oral or IV) and hydration
hydroxyurea reduces the incidence and severity of vaso-occlusive crisis
83
discuss the relationship b/n blood type, erythrocyte antigens, and plasma antibodies.
blood type is determined by specific glycoproteins present on the erythrocyte cell membrane. These glycoproteins have an antigenic potential, so administering blood of the wrong type has catastrophic consequences. The most clinically important antigens are the ABO and Rh systemics
- if an antigen is expressed on the erythrocyte, then there will NOT be an antibody against that specific antigen in the plasma
- if an antigen is NOT expressed on the erythrocyte, then there WILL be an antibody against that specific agent in the plasma.
84
what blood type is the universal donor for erythrocytes? How about the universal acceptor?
universal donor = O-
| universal acceptor = AB-
85
what blood type is the universal donor for FPP? How about the universal acceptor?
universal FFP donor = AB+
| universal FFP acceptor = O-
86
what is the concern about an Rh- mother and pregnancy?
a person who is Rh- can be sensitized by exposure to Rh+ blood during transfusion or pregnancy.
- Rh- other can be sensitized by her Rh+ fetus. transfer occurs across the placenta, usually several days after delivery
- the mother receives Rhogam to prevent sensitization
- if the mother becomes sensitized and develops antibodies, a subsequent pregnancy with an Rh+ fetus may result in erythroblastosis fetalis.
87
Compare and contrast type, screen, and crossmatch in terms of what each tests for and how long each takes.
type:
- ABO & Rh-D antigens
- 5mins
- recipient blood is mixed w/ antibodies, 0.2% of incompatibility reaction after this test.
screen:
- tests for most clinically significant antibodies
- 45mins
- recipient blood is mixed w/ known antigens, 0.06% chance of incompatibility rxn after this test.
crossmatch:
- tests for compatability b/n recipient plasma and the actual blood unit to be transfused.
- 45mins
- simulates transfusion in a test tube, 0.05% chance of incompatibility rxn after this test.
88
a pt is suffering from acute hemorrhage and there is not time to wait for crossmatched blood. What is the next best option for this patient?
2nd best option: type specific, partially crossmatched blood
3rd best option: type specific, uncrossmatched blood
4th best option: type O negative uncrossmatched blood (universal donor)
89
if type O uncrossmatched blood is administered, most people may safely receive Rh+. Name two populations where Rh- blood is best.
women of child bearing age
patient who has not received a previous transfusion
90
what is the indication to transfuse PRBCs?
to increase CaO2
Hgb >10: transfusion rarely required
Hgb <6: transfusion often required
decision to transfuse is guided by patient factors.
91
what are the indications for FFP transfusion?
```
coagulopathy (PT or PTT > 1.5x control)
warfarin reversal (acute need)
antithrombin III deficiency
massive transfusion
DIC
C1 esterase deficiency (hereditary angioedema)
```
conditions that can be treated with factor concentrates often carry less infectious risk
92
what are the indications for platelet transfusion?
thrombocytopenia <50K): invasive procedures, neuraxial blockade, or most surgeries
thrombocytopenia <100K: eye and neurosurgery
qualitative platelet defect.
93
What is in cryoprecipitate?
fibrinogen
factor 8
factor 13
vWF
94
what are the indications for cryoprecipitate transfusion?
fibrinogen deficiency (<80-100)
vWB disease
hemophilia
95
what is the dose for PRBC, FFP, platelets, and cryo?
RBC: 1 U increases Hgb by 1g/dL
FFP
- warfarin reversal 5-8mL/kg
- coagulopathy 10-20mL/kg
platelets: 1 pack/10kg TBW
cryo: 5 bag pool increases fibrinogen by 50mg/dL
96
what is the estimated blood volume in preterm neonates, full term neonates, infants, and adults?
neonate: preterm: 90-100mL/kg
neonate: fullterm: 80-90mL/kg
infant: 80mL/kg
adult: 70mL/kg
97
what is the formula for maximum allowable blood loss?
ABL = EBV*(Hgb-target Hgb)/Hgb
98
Name 4 substances that extend the shelf-life of RBCs. What is the function of each?
citrate: anticoagulant that inhibits calcium (factor IV). After transfusion of multiple units, the citrate load can cause hypocalcemia.
phosphate: buffer that combats acidosis
dextrose: primary substrate for glycolysis
adenine: substrate that helps RBCs re-synthesize ATP. It extends storage time from 21-35 days
newer preservatives extend storage time to 42 days.
99
discuss the RBC storage lesion.
although the CDPA preservative extends the life of banked blood, there are several important physiochemical changes that occur during storage. This is known as the RBC storage lesion
- decreased 2,3 DPG: L shift of oxyHgb dissociation curve
- decreased ATP: shift to anaerobic metabolism
- decreased pH: increased lactic acid
- increased K+
- impaired ability to change shape
- hemolysis
- increased production of proinflammatory mediator
100
What is leukoreduction, why is it used, and who does it benefit?
removes WBCs from RBCs and plasma
since leukocytes are responsible for HLA alloimmunization, febrile nonhemolytic transfusion reactions, and CMV transmission, it makes sense that removing leukocytes reduces these risks
101
What is washing, why is it used, and who does it benefit?
washing the blood products with saline removes any remaining plasma (and antigens) in the donor RBCs (RBC antigens aren't removed)
this prevents anaphylaxis in IgA deficient patients.
102
What is irradiation, why is it used, and who does it benefit?
irradiation exposes PRBCs to gamma radiation, which disrupts WBC DNA in the donor erythrocytes. This process is useful in preventing graft vs. host disease in immunocompromised patients who require transfusion.
populations who benefit from irradiated cells include: leukemia, lymphoma, hematopoietic stem cells transplants, and DiGeorge syndrome.
103
What is the most common infectious complication of RBC transfusion? How can this risk be reduced?
CMV (cytomegalovirus) is the most common infection complication.
leukoreduction greatly reduces the risk, so immunocompromised patients should receive leukoreduced blood
104
List the 4 most common infectious complications of RBC transfusion from most to least common.
CMV (1-3% of all transfusions)
Hep B (1:366,500)
Hep C (1:1,657,000)
HIV (1:1,860,000)
105
Why is bacterial contamination more common with platelets than w/ RBCs or FFP?
platelets are stored at room temperature, which explains why bacterial contamination is more common
bacterial contamination can progress to sepsis.
106
what are the s/s of an acute hemolytic transfusion reaction?
hemoglobinuria (usually presenting sign)
hypotension
bleeding
other s/s (masked by anesthesia):
- fever
- chills
- chest pain
- dyspnea
- nausea
- flushing
107
discuss the complications of an acute hemolytic reaction
complement is activated in the recipient's blood, and plasma antibodies attack the antigens present on the donor blood cell membranes. ABO incompatibility is the most lethal. Renal failure, DIC, and hypotension are the most catastrophic complications of intravascular hemolysis.
renal failure: ATN: precipitation occurs w/in the renal tubules --> mechanical obstruction
DIC: erythrocyin released from the RBC, activates the intrinsic clotting cascade --> uncontrolled fibrin formation & factor consumption
hemodynamic instability: free Hgb activates the kallikrein system --> bradykinin production (potent vasodilator)
108
what is the treatment plan for an acute hemolytic reaction?
1. stop the transfusion
2. maintain UOP >75-100mL/hr w/ IVF, mannitol, lasix
3. alkalinize the urine w/ NaHCO3
4. send urine & plasma Hgb samples to blood bank
5. check platelets, PT, and fibrinogen
6. send unused blood back to blood bank to double check cross match
7. support hemodynamics w/ IVF and pressors as needed
109
Discuss the patho of transfusion related acute lung injury
TRALI is probably caused by HLA and neutrophil antibodies present in the donor plasma.
donor antibodies --> neutrophil activation in the lungs --> endothelial injury --> capillary leak --> pulmonary edema --> impaired gas exchange --> hypoxemia --> acidosis --> death
FFP and platelets contain the highest concentration of these antibodies
110
How does the source of blood products affect the risk of TRALI?
Where the blood produces come from also affects the risk of TRALI. These donor groups impart the highest risk:
- multiparous women (highest risk)
- hx of blood transfusion
- hx of organ transplant
111
what are the diagnostic criteria for TRALI?
onset <6hrs post transfusion
b/t infiltrates on CXR
PaO2 <300 or SpO2 <90 on RA
normal PAOP (no LA HTN or volume overload)
112
What physiologic disturbances result from massive transfusion?
associated with:
- alkalosis from citrate metabolism to bicarb in the liver
- hypothermia d/t cold blood
- hyperglycemia from dextrose additive in stored blood
- hypocalcemia from binding of calcium by citrate
- hyperkalemia from administration of older blood
113
what is the lethal triad of trauma?
acidosis
hypothermia
coagulopathy
the problem begins w/ hemorrhage and hypoperfusion, and this ultimately impairs coagulation and acid-base balance
114
what is salvaged blood syndrome?
cell saver blood doesn't return platelets and coagulation factors to the patient.
if a large volume of salvaged blood is returned to the patient, you should consider the possibility of dilutional coagulopathy. (this is also called "salvaged blood syndrome")
115
How is cell saver blood different from PRBCs?
contains higher concentrations of 2,3 DPG and ATP, so CaO2 is greater and the cells are better able to maintain their biconcave shape (less sludging in the microcirculation)
116
List the contraindications and controversial uses for intraoperative blood salvage
contraindications:
- sickle cell disease
- thalassemia
- topical drugs in sterile field (betadine, chlorhexidine, topical antibiotics)
- infected surgical site
- oncologic procedures
controversial uses:
- c/s d/t theoretical risk of anaphylactoid syndrome of pregnancy (AFE)
intraoperative blood salvage is considered safe for transplant surgery.
