Fluid, Blood, Coagulation Flashcards
Describe the distribution of body water
60% of TBW = 42 L
60/40/20 (15/5)
40% = intracellular
20% = extracellular
15% = interstitial
5% = plasma
What populations tend to have a greater percentage of TBW by weight?
neonates have the most
women, elderly, obese have the least
What are the 2 most important determinants of fluid transfer between capillaries and interstitial space?
starling forces
glycocalyx
Net filtration pressure
(Pc - Pif) - (iic - iiif)
<0 = reabsorption
> 0 = filtration
What is the glycocalyx - what disrupts it?
forms a protective layer on the interior wall of the blood vessel. it has anticoagulant properties. it is the gatekeeper.
DM, sepsis, ischemia, vascular surgery all disrupt it
how is lymph returned to the systemic circulation?
via thoracic duct at the juncture of the IJ and subclavian vein
what is osmotic pressure and what is its primary determinant
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 a solution. not a function of their molecular weights!
osmolarity vs osmolality
osmolarity = osmoles per liter
osmolality = osmoles per kg
reference for plasma osmolarity? and what are the 3 most important contributors
it is 280 - 290 mOsm/L
most important determinatns: sodium, glucose, BUN
Nax2 + Glucose/18 + BUN/2.8
NaCl 0.45%
hypotonic @ 154
D5W
hypotonic @253
NaCl 0.9%
isotonic @ 308
LR
isotonic @ 273
plasmalyte
294
albumin 5%
300
nacl 3%
1026
d5 nacl 0.9% (0.45%)
560, 405
D5 LR
525
How do isotonic IV fluids distribute to the patient?
they expand plasma volume and ECF
remain intravascularly (crystalloids) for30 minutes before moving to the ECF
what is the fda black box for on synthetic colloids
risk of renal injury
coagulopathy risks with colloids
dextran > hetastarch > hextend
dont exceed 20 mL/kg
not a problem with voluven
colloid anaphylactic potential
dextran
albumin leads to what electrolyte abnormality
hypocalcemia
how does hyperkalemia affect the EKG?
5.5 - 6.5 = peaked T wave
6.5 - 7.5 = p wave flattening, PR prolong
7 - 8 = QRS prolonged
> 8.5 = sine wave, VF
discuss hypocalcemia s/s
nerve irritability - tetany
change in LOC = sz
long QT
hypercalcemia s/s
nausea, abdominal pain
HTN
psychosis, sz
short QT
treatment for hypercalcemia
0.9% NaCl
diuretic
Hypermagnesemia
DTR loss = 5.8 - 10 mEq/ 7 - 12 mg/dL
Resp. Depression = > 10 or > 12
Cardiac arrest > 10 or > 12
What is the treatment for hypermagnesemia
CaCl
Ca gluconate
Acidosis
hyperkalemia, increased ICP, increased SNS tone
Alkalosis
decreased coronary blood flow, decreased calcium and potassium
Anion gap
Na - Cl + HCO3
Normal = 8-12
Accumulation of acid = gap acidosis (>12)
Loss of bicarbonate or ECF dilution = non-gap acidosis
Possible causes of anion gap
MUDPILES
M-methanol
U-uremia
D- DKA
p- paraldehyde
I- isoniazid
L- lactate
E- ethanol
S- salicylates
Nongap acidosis
HARDUP
H-hypoaldosteronism
A-acetazolamide
R- renal tubular acidosis
D- diaarrhea
U-uretrosigmoid fistula
P-pancreatic fistula
LARGE VOLUME NACL CAN CAUSE THIS TOO
Etiology of metabolic alkalosis
-Sodium bicarb administration
-Massive transfusion (liver converts preservatives to HCO3)
-Loss of gastric fluid (NG, vomiting)
-Diuretics
-ECF depletion –> sodium reabsorption –> H+ and K+ excretion to maintain electroneutrality
-Cushings or hyperaldosteronism
What is the most common electrolyte d/o found
HYPOKALEMIA
Major intracellulaar ions
Potassium, magnesium, and phosphate
what are the 4 steps of hemostasis
- vascular spasm
- platelet adhesion (primary hemostasis)
- coagulation and formation of fibrin (secondary hemostasis)
- fibrinolysis
where are platelets formed?
by megakaryocytes in the bone marrow. they are cleared by macrophages in the reticuloendothelial system and the spleen
platelet valuess
< 50 k = increased surgical bleeding risk
< 20 k = increased spontaneous bleeding risk
what are the 3 steps of plt plug formation?
- adhesion (d/t collagen exposure, vwf and tf release)
- activation
- aggregation
MADE IN 5 MINUTES
list the 12 coagulation factors
1 - fibrinogen
2 - prothrombin
3 - tissue factor
4 - calcium
5 - cofactor (labile)
7 - stable factor
8 - cofactor (antihemophilic)
9 - christmas factor
10 - stuart-prower
11 - plasma thromboplastin
12 - hageman’s factor
13 - fibrin stabilizing
what activates the extrinsic pathway?
vascular injury (tissue trauma liberates TF from subendothelium)
measured by PT, INR
inhibited by warfarin
What activates the intrinsic pathway
blood injury or collagen exposure
PTT, ACT
inhibited by hepaarin
what factors are in the extrinsic pathway
3, 7 (EXTRINSIC)
13, 10, 5, 2, 1 (COMMON)
12, 11, 9, 8 (INTRINSIC)
…can be purchased for 37 cents
….. if you can’t buy it from $12, you can buy it for $11.98
describe the process of fibrinolysis
since the clot is a temporary fix - we need a process to break down the clot once the body has healed itself.
plasminogen is a proenzyme that is synthesized in the liver. it is incorporated into the clot but it lays dormant until it is activated. plasmin degreades fibrin into FDP
what two enzymes are needed for the converison of plasminogen to plasmin
tpa
urokinase
what is R time
the time it takes for the clot to start forming
normal = 6 - 8 minutes
measures clotting factors
replace with FFP
what is K time
time it takes for the clot to reach a certain strength
normal = 5 - 7 minutes
measures fibrinogen
replace with cryo
what is alpha angle
the rate of fibrin deposition. obviously measures fibrinogen then.
normal = 50 - 60 degrees
treat with cryo
what is maximum amplitude
the strength of the clot
normal = 50 - 60 mm
if it is low, treat with ddavp or platelets
what is A60
height of vertical amplitude 60 minutes after MA
normal = MA5
if it is abnormal, it is due to excess fibrinolysis. treat with txa
MOA of heparin
it inhibits the intrinsic and final common pathway.
antithrombin III is a naturally occurring anticoagulant that circulates in the plasma. heparin binds to AT and accelerates its anticoagulant activity 1000x
heparin AT complex neutralizes 9, 10, 11,12
what drugs can you give to someone who can’t have heparin but need CPB
bivalirudin - 2 - 3 hours
argatroban - 4 - 6 hours
MOA for COXi
prevent platelet aggregation by blocking COX1. this stops conversion of arachidonic acid to PG and ultimately txA2
name 2 antifibrinolytics and 4 fibrinolytics
antifibrinolytic - txa, amicar
*block conversion of plasminogen to plasmin, promote clot formation
fibrinolytic - tPa, urokinase, streptokinase, reteplase, alteplase
*facilitate conversion of plasminogen to plasmin. they break DOWN clots!! (MI, stroke)
what are the 3 types of vwd
1- mild, moderate reduction
2 - vWF that is produced doesn’t work well
3 - severe reduction in the amount of vwf produced
lab values with vwdx
prolonged PTT and bleeding time
MOA of desmopressin … dose?
synthetic analogue of ADH. it facilitates the release of vwf and f8
dose = 0.3 mcg/kg
type 1 > type 2
type 3 it doesn’t work at all
causes hotn with administration
other than desmopressin .. what are 3 other treatments for vwdx
factor 8
ffp
cryo - 8. 13. fibrinogen. vwf.
describe pathophysiology of hemophilia a
x-linked recessive d/o.
factor 8 deficiency
lab values associated
PTT prolonged only
hemophilia A treatment
factor 8 before surgery and continued for 2 - 6 weeks after
half life = 8 - 12 hours
T&C prior to surgery
antifibrinolytics
hemophilia b
factor 9 deficiency
factor 9 is the concentrate to treat it. otherwise, same as hemophilia a.
describe the role of rf7 in the management of hemophilia A and B
BYPASSSSSSS factor 8 or 9.
dose = 90 - 120 mcg/kg
SE: thrombosis arterial and venous.
last ditch effort treatment for idiopathic bleeding (20 - 40 mcg/kg) off-label
Lab Results for DIC
increased PT, PTT, D-dimer
Decreased plt, fibrinogen
Name 3 conditions that are at risk for DIC
sepsis - gram negative
pregnant - pre-e, abruption, AFE
malignancy - adenocarcinoma, leukemia, lymphoma
DIC management
coagulopathy - FFP - feed the beast (plt, cryo ok)
severe thrombosis - IV heparin or LMWH
hypovolemia - give fluids
HIT vs HIT 2 pathophys.
HIT is heparin induced platelet aggregation after a large dose of heparin
HIT 2 - antiplatelet abs (IGG) attack factor 4 immune complexes –> platelet aggregation. They are resistant to heparin anticoag. occurs after any dose of heparin
onset of HIT 1 & 2
1 - 1-4 days
2- 5 - 14 days
Plt count of HIT 1 vs 2
1 - <100
2 - < 50
treatment for HIT 1 vs 2
no treatment for HIT 1
HIT 2 - d/c heparin. anticoagulate with direct thrombin inhibitor (bivalirudin, hiruidin, argatroban)
Protein C/S deficiency
hypercoagulable
*heparin –> warfarin
*may or may not need lifelong anticoagulation
factor 5 Leiden
causes a resistance to the anticoagulant effect of protein C
-only pt w/thromboembolism require anticoagulation
Pathophys sickle cell
Amino acid substitution (valine for glutamic acid) on beta globulin chain
spleen removes sickled cells at 12 - 17days, compared to 120days
Treatment for vaso-occlusive crisis
hydroxyurea
analgesics
hydration
discuss blood type, antigens, plasma antibodies
Blood type = specific glycoproteins present on the erythrocyte cell membrane. They have an antigenic potential.
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 antigen in the plasma
Universal donor vs universal acceptor of FFP
Donor = AB +
Acceptor = O -
(opposite of RBC stuff)
Type only
tests for ABO and Rh-D antigens.
5 minutes
recipient blood is mixed with anti-A, anti-B, anti-Rh D antibodies. 0.2% chance of incompatibility after this test
Type & Screen
Tests for most clinically significant antibodies
45 minutes
recipient blood mixed with COMMERCIALLY prepared O RBCs that contain known antigens. 0.06% incompatibility rxn after this test
Type & Crossmatch
tests for compatibility btw recipient plasma and the actual blood unit to be transfused.
45 minutes
simulates transfusion in a test tube. 0.05% chance of incompatibility reaction after this.
specific units are assigned to the patient after this!
what are the indications for FFp
PT x 1.5
warfarin reversal
antithrombin deficiency
massive tx
DIC
c1 esterase deficiency
cutoff for plt tx
< 100 for eye or neurosurgery
< 50 for neuraxial, invasive procedures, most surgeries
what is in cryo
factor 8, 13
vwf
fibrinogen
cryo indications
fibrinogen < 80
vwb dx
hemophilia
FFP dosing
warfarin reversal 5 - 8 mL/kg
coagulop. = 10 - 20 mL/kg
Plt dosing
1 pack per 10 kg body weight
cryo dosing
5 bag pool increases fibrinogen by 50 mg/dL
What is leukoreduction
Removes WBCs from RBCs and platelets
Leukocytes are responsible for HLA alloimmunization, febrile rxn, CMV tx
What is washing and why is it used
removes any remaining plasma and antigens in the donor blood
prevents anaphylaxis in IgA deficient patients
What is irradiation
Exposes units to gamma radiation, disrupting WBC DNA, destroying donor leukocytes. This prevents GVHost dx in immunocompromised pt.
leukemia, lymphoma, digeorge pt, stem cell pt
Most common infection complication of RBC
CMV
leukoreduction reduces this risk
List 4 most common complications of RBC
CMV > Hep B > Hep C > HIV
