UNIT 9 Fluids & Blood Flashcards
describe the distribution of body water.
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
which populations tend to have a greater percentage of TBW% by weight? Which have less?
populations w/ higher TBW% by weight: neonates
populations w/ lower TBW% by weight: females, obese, elderly
what are the 2 more important determinantes of fluid transfer between the capillaries and interstitial space?
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
describe the starling forces in the context of capillary fluid transfer.
- 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
what is the glycocalyx, and what factors disrupt it?
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
what is lymph, and how does the lymphatic system work?
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.
how is lymph returned to the systemic circulation?
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
What is the difference b/n osmosis and diffusioN?
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
What is osmotic pressure, and what is its primary determinant?
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
what’s the difference b/n osmolarity and osmolality?
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
what is the reference value for plasma osmolarity, and what are the 3 more important contributors?
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
what is the difference b/n a hypotonic and hypertonic solution?
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
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.
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
what is the relationship b/n the tonicity of IV solutions and increased ICP?
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)
how does dextrose affect the tonicity of IVF?
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.
How do isotonic IVF distribute in the patient?
what complication can result when hypertonic saline is administered too quickly?
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
compare the advantages of colloids to the advantages of crystalloids.
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
compare the disadvantages of colloids to the disadvantages of crystalloids
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
how does hyperkalemia affect the EKG (list the events in order of appearance)?
Review this chart:
early: long PR, peaked T, short QT
middle: flat P, wide QRS
late: QRS–> sine wave–> VF
list all the treatment options for hyperkalemia
calcium (stabilizes cardiac membrane) insulin + D50 hyperventilation bicarb albuterol K+ wasting diuretics dialysis
discuss the presentation of hypocalcemia.
skeletal m cramps nerve irrirability (paresthesias, tetany) Chvostek sign Trousseau sign laryngospasm MS changes --> seizures long QT interval
discuss the presentation of hypercalcemia.
nausea
abdominal pain
hypertension
psychosis
MS changes –> seizures
what is the treatment for hypercalcemia?
NS loop diuretics (lasix)
Fact: calcium is the most abundant electrolyte in the body!!!
describe the presentation of hypermagnesemia.
what is the treatment for hypermagnesemia?
calcium chloride
how does hypermagnesemia affect NMB?
potentiates NMB (sux + NDMR)
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++
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
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)
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
discuss the etiology of metabolic alkalosis
- addition of HCO3-
- NaHCO3 administration
- massive transfusion (liver converts preservatives to HCO3- - 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 - increased mineralocorticoid activity
- Cushing’s syndrome
- hyperaldosteronism
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
what are the 4 steps of hemostasis?
- vascular spasm
- platelet plug (primary hemostasis)
- coagulation & formation of fibrin (secondary hemostasis)
- fibrinolysis when the clot is no longer needed.
where are platelets formed? where are they metabolized?
formed by megakaryocytes in the bone marrow
cleared by macrophages in the reticuloendothelial system & the spleen
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
what are the 3 steps of the platelet plug formation (primary hemostasis)?
- adhesion from vWF
- activation
- aggregation
a platelet plug is formed in approx 5mins
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
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
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
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
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
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:
- initiation
- amplification
- propagation
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
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.
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
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
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)
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
what are the doses for heparin (for CPB) and protamine?
300-400U/kg heparin (cardiac surgery dose)
1mg protamine: 100U of heparin
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
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
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)
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
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
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
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.
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
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
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)
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.
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.
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
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.
What lab results are consistent w/ DIC (PT, PTT, D-dimer, platelets, fibrinogen)?
increased: PT, PTT, D-dimer
decreased: platelets, fibrinogen
name 3 conditions that are associated with a high risk of developing DIC.
- sepsis ( #1 highest risk = gram- bacilli)
- obstetric complications (preeclampsia, placenta previa, placental abruption, and Amniotic fluid embolism)
- malignancy (adenocarcinoma, leukemia, and lympthoma)
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
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
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
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
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)
list the triggers that cause sickling of HgbS
pain hypothermia hypoxemia acidosis dehydration
anesthetic managment focuses on avoiding these triggers.
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
what blood type is the universal donor for erythrocytes? How about the universal acceptor?
universal donor = O-
universal acceptor = AB+
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
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.
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)
What is in cryoprecipitate?
Factor 1 (fibrinogen)
factor 8
factor 13
vWF
Albumin is ANTI- inflammatory not Pro-inflammatory
Presentation for hyponatremia and hypernatremia
What is the typical volume administered to assess the patient’s position on the Starling curve in goal-directed fluid therapy?
200-250ml
ERAS
Avoid premedication, ok to drink clear soda 2 hours before sx
Coagulation values
Just read over
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.
