UNIT 9 Fluids & Blood Flashcards
describe the distribution of body water.
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)
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/L 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 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
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?
expand the plasma volume and the ECF.
crytalloids tend to remain in the intravascular space for approx 30mins before moving to the ECF
what complication can result when hypertonic saline is administered too quickly?
central pontine myelinolysis
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
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)?
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)
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)
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
- formation of the 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
- activation
- aggregation
a platelet plug is formed in approx 5mins
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
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?
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
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 idea is that coagulation takes place on the surface of a cell that expresses TF
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
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
