UNIT 9 Fluids & Blood Flashcards
1
Q
describe the distribution of body water.
A
70kg male, water represents 60% of the total body weight. This equals 42L.
Remember: 60/40/20(15/5)
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
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/LiteR 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: 310
- 5% albumin 300
- plasmalyte: 295
- LR: 275
- 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
17
Q
what complication can result when hypertonic saline is administered too quickly?
A
central pontine myelinolysis
Disorders of sodium balance should be corrected slowly - no more than 1 - 2 mEq/L/hr.
• Treating hyponatremia too quickly causes fluid to shift from the ICF to the ECF. This can produce central pontine myelinolysis.
• Treating hypernatremia too quickly causes fluid to shift from the ECF to the ICF. This can produce cerebral edema
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
Colloid and blood you can also do 1:1:2
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)?
Review this chart:
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)
Fact: calcium is the most abundant electrolyte in the body!!!
25
describe the presentation of hypermagnesemia.
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. 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 from vWF
2. activation
3. aggregation
a platelet plug is formed in approx 5mins
38
list the 12 coagulation factors
Foolish people try climbing long slopes after Christmas, some people have fallen
```
1 = fibrinogen
2 = prothrombin
3 = tissue factor- not from the liver
4 = calcium ions- not from liver
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?
Read over:
extrinsic = 3,7
- can be purchased for 37c
- extrinsic is FAST! It can clot in 15 seconds
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 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**
**MOA Heparin binds AT III** and greatly accelerates its anticoagulant ability (1000x). The heparin-AT complex neutralizes thrombin and activated factors 10, 12, 11, and 9
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.
Fact: heparin inhibits intrinsic and final common pathway (it neutralizes it)
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
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
**It creates an ionic bond**
52
what are the side effects of protamine?
- hypotension d/t histamine release; administer >5mins
- pulmonary hypertenion due to thromboxane and serotonin release
- allergic rxn d/t previous sensitization to protamine, NPH insulin, fish allergy, or if they had a vasectomy
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 **(2, 7, 9, 10, and protein C & S)**
54
list all 4 of the antidotes for warfarin. When should each be used?
1) vitamin K in non-emergent situations or for minor surgical procedures. Requires 4-8hrs
Emergent, or high risk procedures requires:
2) reversal w/ FFP (1-2U)
3) recombinant factor 7a
4) 4 factor prothrombin complex concentrate (4PCC)
**(4PCC) contains factors 2, 7, 9 and Vitamin K**
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. Must know where to block receptor in hotspot photo
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
READ OVER
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 is von willbrand disease? what are the 3 types?
the platelet count is normal, but the platelets don't function properly.
Type I: mild reduction in the amount of vWF produced. **Give DDVAP**
Type II: vWF that is produced doesn't work well. **Give DDVAP**
Type III: SEVERE reduction in the amount of vWF produced.
- **DDVAP doesn’t work well on type 3**
- **1st line agent is Factor 8 concentrate**
- You can give cryo and Amicar for intraoperative hemorrhaging
- **Cryo is used for 3 types because it has factor 8,13, and fibrin in it**
- FFP can also be given for all 3 but it’s not really suitable to use. Cryo is preferred.
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. Helps increase endogenous vWF and factor 8
- Type 1 & 2 respond best to DDAVP
- **Type 3 don't respond to DDAVP bc they don't produce vWF** give them cryo instead
dose: 0.3-0.5 mcg/kg IV
side effect: **hypotension w/ rapid administration, and hyponatremia**
67
aside from desmopressin, list 3 other treatments that can improve the coagulopathy of von willebrand disease.
cryo: contains factors 8, 13, fibrinogen, and vWF. can be used for type 1, 2, or 3
purified 8-vWF concentrate: reduces the risk of transfusion-related infection. It is the first line agent for the patient w/ type 3 disease.
FFP: contains all of the clotting factors, so it too can be used for all disease types. Not really used. We prefer Cryo
68
describe the pathophysiology of hemophilia A.
**Sex X-linked chromosomal disorder (more common in males) that causes factor 8 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.
Recombinant factor 7 is a bypass agent bc it skips over factor 8 or 9 in those w/ inhibitors. **Last emergency treatment for hemophilia A and B**
increased risk of arterial thrombosis (MI, CVA) as well as venous thrombosis (PE< DVT)
73
describe the pathophysiology of disseminated intravascular coagulation.
disorganized clotting and fibrinolysis = 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 its anticoagulation system, however this leads to widespread consumption of 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 ( #1 highest risk = gram- bacilli)**
2. obstetric complications **(preeclampsia, placenta previa, placental abruption, and Amniotic fluid embolism)**
3. malignancy (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
Type I and type II heparin induced thrombocytopenia:
Type 1
- **heparin induced platelet aggregation**
- 1-4 days post administration
- **occurs after large heparin dose**
- **platelet count <100K**
- **tx: resolves spontaneously**
Type 2
- **IgG attack factor 4** immune complexes --> platelet aggregation; pt is resistant to heparin anticoagulation
- **occurs after any heparin dose more like an allergy**
- **5-14 days post administration**
- **platelet count <50K**
- **hypercoagulable state = high risk of amputation & death**
- **stop heparin and switch to direct thrombin inhibitor**
78
describe the patho and treatment of protein C and S deficiency
- protein C and S = inhibits factor 5a and 8a
- Protein C and S deficiency in either can produce a hypercoaguable state = **thrombosis risk**
tx:
- **thromboembolism is treated w/ heparin that is transitioned to warfarin**
79
describe the patho and treatment of factor V leiden mutation.
causes a resistance to the anticoagulant effect of protein C = **increased clotting**
tx:
- only those w/ thromboembolism require anticoagulation
- lifelong tx is unwarranted
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.
- 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
Common manifestation of Sickle cell disease?
What’s the deadliest?
What is a common co-morbidity associated with sickle cell disease?
**Vaso-occlusive crisis**
- tx: analgesics (oral or IV) and hydration
- hydroxyurea reduces the incidence and severity of vaso-occlusive crisis
**The deadliest result of SCD is Acute chest syndrome**
**Most common CO-MORBIDITY is Asthma**
83
discuss the relationship b/n blood type, erythrocyte antigens, and plasma antibodies.
blood type is determined byglycoproteins present on the erythrocyte cell membrane. These glycoproteins have an antigenic potential, so administering blood of the wrong type has catastrophic consequences!
- **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 (plasma)? How about the universal acceptor?
universal FFP donor = AB+
universal FFP acceptor = O-
**It’s opposite of blood**
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, think of it like a vaccin
- **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:
- screening for 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 no time to wait for crossmatched blood. What is the next best option for this patient?
1) 1st best option : type specific, **partially crossmatched blood**
2) 2nd option : type specific, uncrossmatched blood
3) Last 3rd 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
• Women who might have children someday: If they’re Rh-negative and we give them Rh-positive blood, it can cause problems in future pregnancies by attacking the baby’s blood. So, we give them Rh-negative blood to avoid this.
• People who need lots of blood later: If someone is Rh-negative and we give them Rh-positive blood now, their immune system might react badly to it in the future. Using Rh-negative blood avoids that risk.
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?
Factor 1 (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 and Hct by 2-3%
- FFP 10mL/kg
- warfarin reversal 5 mL/kg
- coagulopathy 10 mL/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 mL/kg
neonate: fullterm: 90mL/kg
infant: 80mL/kg
adult male: 75mL/kg
Adult female 65 mL/kg
97
what is the formula for maximum allowable blood loss?
ABL = EBV*(Hgb initial -target Hgb)/Hgb initial
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/ banked blood
- **decreased 2,3 DPG: L shift of oxyHgb dissociation curve**
- **decreased ATP: shift to anaerobic metabolism**
- **decreased pH: increased lactic acid** acidosis!!!
- **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
**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.
**good for sick children, NOT adults**
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
Bacterial contamination is more common in platelets, 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?
1) **hemoglobinuria (usually presenting sign)**
2) hypotension
3) bleeding
4) fever
other s/s (masked by anesthesia):
- fever
- chills
- chest pain
- dyspnea
- nausea
- flushing
107
discuss the complications of an acute hemolytic reaction
- Recipient’s blood activates complement, and their plasma antibodies attack the antigens present on the donor blood
- **ABO incompatibility is the most lethal = Renal failure, DIC, and hypotension (complications of intravascular hemolysis)**
- renal failure: ATN: occurs 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) =hypotension**
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
- name the products with highest risk
- state patient risk factors
**TRALI is caused by human leukocyte antigens and neutrophil antibodies 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 = highest risk of TRALI**
**Pt risk factors: multipareous, lots of transfusions, organ transplant**
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**. They still need blood products and all you’re giving them in volume
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")
Contraindications: SCD, thalaessemia, infected site, oncologic procedures, topical drugs like betadine
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.
117
1 unit of PRBC has how much hemocrit %?
70 %
118
Sickle cell hemoglobin
polymerizes and precipitates in the RBC
It also has decreased solubility compared to hemoglobin A
(Got this from core concepts QOD)
119
Labs for vWF?
Only PTT and bleeding time are increased
120
Which symptom below is most common in a Non-hemolytic reaction?
- Hypotension
- Fever
- Increased PAOP
- Hypocalcemia
Fever
121
TACO transfusion associated circulatory overload
Non-immune mediated reaction, given too much volume, increased **PAOP = pulmonary edema**
Left ventricular dysfunction, MR, increased brain natriuretic peptic
122
Albumin is ANTI- inflammatory not Pro-inflammatory
123
Presentation for hyponatremia and hypernatremia
124
125
What does the hormone calcitonin do?
It lowers calcium
126
127
128
What is the typical volume administered to assess the patient's position on the Starling curve in goal-directed fluid therapy?
200-250ml
129
ERAS
Avoid premedication, ok to drink clear soda 2 hours before sx
130
Which electrolyte disturbance is associated with 5% albumin administration?
Hypocalcemia
Explanation:
Serum calcium binds to albumin, so changes in albumin concentration can affect the ionized calcium concentration. Resuscitation with albumin can reduce ionized calcium because it binds with the newly introduced protein in the bloodstream. This is something to think about if you're giving more than a few bottles of albumin.
131
A patient has a blood pH of 7.4. If his blood pH decreases to 7.32, then his PaCO, has:
A) increased by 10 mmHg.
B) decreased by 10 mmHg.
C) decreased by 5 mmHg.
D) increased by 5 mmHg.
Increased by 10 mmHg
Explanation:
You should be able to predict how a change in PaCO, affects pH.
**For every 10 mmHg increase in PaCO2, the pH will decrease by approximately 0.08.**
Think about this when you give an opioid to a spontaneously ventilating patient.
In response to chronic respiratory acidosis, the pH will decrease by only 0.03 due to renal-mediated bicarbonate retention.
132
During a laparoscopic low anterior resection, the patient has the following blood gas:
pH =7.28, PaCO2 = 55 mmHg, Pa02 = 108 mmg, and HCO3 = 24 mEq/L. What are the
MOST likely explanations for these findings? (Select 2.)
A) Exhausted soda lime
B) Diabetic ketoacidosis
C) Malignant hyperthermia
D) Continuous nasogastric suction
Exhausted soda lime and malignant hyperthermia
This patient's ABG reveals respiratory acidosis without compensation.
Diabetic ketoacidosis is an example of a gap metabolic acidosis (addition of acid), while continuous nasogastric suction can lead to metabolic alkalosis (chloride loss). In both circumstances, the patient will attempt to normalize pH by increasing minute ventilation to reduce PaCO2
133
Which intravenous fluid is MOST likely to exacerbate cerebral edema in the patient with intracranial hypertension?
Dextran 10%
Sodium chloride 0.45%
Lactated Ringer's
Albumin 5%
Sodium chloride 0.45%
Hypotonic solutions (e.g., sodium chloride 0.45%) have a lower osmolarity than the plasma (or cells).
This explains why hypotonic solutions are poor expanders of intravascular volume and why you should never give a hypotonic solution to a patient with increased ICP (risk of cerebral edema).
134
Vitamin K dependent factors?
2, 7, 9, 10
135
Identify the BEST predictor of bleeding during surgery.
A) PT/INR
B) History and physical
C) Thromboelastogram
D) Bleeding time
B) History and physical
136
Coagulation values
Just read over
137
D antigen is referred to as to Rh positive or negative?
- **A patient who has the D antigen is referred to as Rh positive**
If the D antigen is absent, they are called Rh negative.
**The first exposure of an Rh negative patient usually produces no reaction. Over the next 2-4 weeks, however, the patient develops enough antibodies to produce agglutination of the previously transfused cells still circulating. This is referred to as a delayed transfusion reaction.**
138
What is the recommended dose of fresh frozen plasma to reverse the effects of warfarin?
5ml/kg for warfarin
For all other purposes, the dose should be 10-20 mL/kg.
(Got this from prodigy)
139
What is the major ion in the intracellular compartment?
What is the major ion in the extracellular compartment?
What is the major cation in the intracellular compartment? Potassium
What is the major cation in the extracellular compartment? Sodium
140
What are the primary risks of administration of Dextran? (select two)
A. Pulmonary edema
B. Hypomagnesemia
C. Anticoagulation
D. Anaphylaxis
C. Anticoagulation
D. Anaphylaxis
141
What is acute normovolemic hemodilution?
is an alternative to transfusion in which whole blood is removed from the patient prior to surgery with replacement of the lost volume in the form of crystalloids or colloids.
By diluting the vascular bed, any blood lost during surgery will have a lower hematocrit.
The previously removed blood is then reinfused back to the patient when intraoperative blood loss has ceased.
142
What issue is this?
- impaired fibrinolysis
- depletion of coagulation factors
DIC!!!
143
Which of the following is a potential side effect of DDAVP administration in the treatment of von Willebrand disease?
Hypotension if given too rapidly
144
During a preoperative interview, a patient informs you that his vWF levels are low. Which of the following is the first step you should take?
A. Order a platelet count
B. Order a PT/PTT
C. Order a bleeding time
D. Obtain an accurate bleeding history
D. Obtain an accurate bleeding history
The number of patients with a low vWF level is markedly higher than the number who have clinical significant bleeding. Therefore, it is imperative to obtain an accurate bleeding history.
145
What are the 4 factors that are inactivated by antithrombin?
9, 10, 11, 12
Antithrombin deficiency leads to thromboembolism!
146
Protein C inactivates what 2 factors?
5a and 8a
147
148
A deficiency in which mediators favor hypercoagulability? (Select 2.)
A) Alpha-antiplasmin
B) Fibronectin
C) Protein S
D) Antithrombin
C) Protein S
D) Antithrombin
Naturally occurring anticoagulants include antithrombin, protein C, protein S, and tissue pathway factor inhibitor.
A deficiency in any of these can lead to = hypercoagulation.
149
Which lab test measures fibrin break down?
D-dimer
150
Best treatment for prolonged R on TEG?
FFP
A prolonged R time reflects a problem with coagulation factors, and the best treatment is fresh frozen plasma (factor replacement).
151
Patient’s deficient in protein C are at risk for:
A) vasoocclusive crisis
B) thrombosis
C) acute chest syndrome
D) spontaneous hemorrhage
B) thrombosis
Protein C and S are naturally occurring anticoagulants.
**Protein C degrades factors 5a and 8a, and protein S is a cofactor for protein C.**
A deficiency in either of these proteins increases the risk = thrombosis.
152
Severe liver failure will reduce the synthesis of which coagulation factors? (Select 2.)
A) 1
B) 8
C) 4
D) 3
1 & 8
Remember 3 Tissue factor and 4 calcium are NOT produced in the liver
153
Which clotting factor has the shortest half time?
A) 2
B) 7
C) 9
D) 10
B) 7
Remember extrinsic pathway 3 and 7 are FAST!
Factor 7 has the shortest half-life of all the coagulation factors
It's going to be the first factor to become deficient in patients with liver failure, vitamin K deficiency, and those on warfarin.
154
Which fluid should be used for a burn patient?
LR!!!!
