Fluids and blood Flashcards
Describe the distribution of body water
In the textbook 70 kg male, water represents 60% of the total body weight. This equals 42 L
TBW can be divided into:
* Intracellular volume = 40% of total body weight (28L)
* Extracellular volume= 20% of total body weight or (14L)
ECV can be further divided into:
* Interstitial fluid = 16% of total body weight (11L)
* Plasma fluid = 4% of total body weight or (3L)
Remember 60/40/20 (15/5) or (16/4)- either will work
Which populations tend to have a greater percentage of TBW% by weight? which have less?
Populations with higher TBW% by weight: Neonates
Populations with lower TBW% by weight: Females, obese, and elderly
what are the 2 most important determinants 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:
(c= capillary, if= interstitial fluid)
* Pc= capillary hydrostatic pressure (pushes fluid out of the capillary)
* (pie symbol) if = interstitial oncotic pressure (pulls fluid out of capillary) - Forces that move fluid from the interstitium into the capillary:
* Pif= Interstitial hydrostatic pressure (pushes fluid into capillary)
* (Pie symbol) c= capillary oncotic pressure (pulls fluid into capillary)
net filtration pressure= (Pc- Pif) - (pie c- pie if)
NFP >0= filtration (fluid exits capillary)
NFP <0= Reabsorption (fluid is pulled into capillary)
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 glycocalyx include:
- Sepsis
- Ischemia
- Diabetes mellitus
- Major Vascular surgery
what is lymph and how does the lymphatic system work?
You can think of the lymphatic system as a 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 line with 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?
Lymph is returned to the venous circulation by way of the thoracic duct at the juncture of the internal jugular and subclavian vein.
You can injure the thoracic duct during venous cannulation. Since the thoracic duct is larger on the left side, there is a greater risk of chylothorax (lymph in the chest) during left-sided IJ insertion.
What is the difference between osmosis and diffusion?
Osmosis is the net MOVEMENT of WATER across a semipermeable membrane, where the direction of water movement is driven by the difference in solute concentration on either side of the membrane (only the solvent moves)
Diffusion is the net Movement of MOLECULES from a region of high concentration to a region of low concentration (solvent AND solute move)
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
- osmotic pressure is a function of the number of osmotically active particles in a solution
- It is NOT a function of their molecular weights
what’s the difference between osmolarity and osmolality?
Both are measures of concentration- the amount of solvent within a defined space
* Osmolarity measures the number of osmoles per liter of solution
* osmolality measures the number of osmoles per kilogram of solvent
what is the reference value for plasma osmolarity, and what are the 3 most important contributors?
Plasma osmolarity is normally 280-290 mOsm/L
The 3 most important determinants are: sodium, glucose, and BUN
Plasma osmolarity= 2(Na) + Glucose/18 + BUN/2.8
from this equation, you can see that sodium is the most important determinant of plasma osmolarity
* you should also notice that hyperglycemia or uremia can increase plasma osmolarity
What is the difference between hypotonic and hypertonic solution?
Tonicity compares the osmolarity of a solution relative to the osmolarity of the plasma. Remember that plasma is the reference point we use to make the comparison.
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
Isotonic: 285 mOsm/L
Hypotonic: 255 mOsm/L - cells swell
Hypertonic: 315 mOsm/L- cells shrink
Think of all the IV fluids you can. Which are hypo-, iso-, and hypertonic to plasma? Bonus points if you can list osmolarity of each
Hypotonic solutions
NaCl 0.45% - 154 mOsm/L
D5W- 253
isotonic
NaCl 0.9%- 308
LR- 273
Plasmalyte A- 294
Albumin 5%- 300
Hespan 6%- 309
Hypertonic:
NaCl 3%- 1026
D5 NaCl 0.9%- 560
D5 NaCl 0.45%- 405
D5 LR- 525
Dextran 10%- 350
What is the relationship between the hypotonicity and hypertonicity of IV solutions and increased ICP?
Hypotonic solutions have a lower osmolarity than the plasma (or cells). These fluids are the same as giving free water, and this free water distributes throughout all of the body compartments.
This is why hypotonic solutions are poor expanders of intravascular volume and why you should never give hypotonic solution to a pt with increased ICP. It will cause these cells to swell, increase their volume, and increase ICP.
Instead, hypertonic saline is useful for treating cerebral edema (it pulls water out of cells, causing them to shrink)
how does dextrose affect the tonicity of IV fluids?
you may be thinkin that glucose in IVF (such as D5W) should be osmotically active. Well…you’re half right…
* you’re right because the glucose contributes osmotically active molecules to the plasma
* the other side of the story is that this glucose is metabolized to carbon dioxide and water. What’s left over? Water, and this water is, you guessed it… hypotonic.
how do isotonic IV fluids distribute in the patient?
Isotonic solutions have an osmolarity that is very close to the plasma (or cells). These solutions expand the plasma volume and the ECV.
Crystalloids tend to remain in the intravascular space for around 30 min, before moving the 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
Crystalloids:
Replacement ration= 3:1
Expands the ECF
Restores 3rd space loss
* existence of the 3rd space is debatable
Colloids
Replacement ration= 1:1
Increases plasma volume (3-6hrs)
Smaller volume needed
less peripheral edema
Albumin has anti-inflammatory properties
Dextran 40 reduces blood viscosity
* improves microcirculatory in vascular surgery
Compare the disadvantages of colloids to the disadvantages of crystalloids.
Crystalloids:
Limited ability to expand plasma volume
* increases plasma volume (20-30 min)
* higher potential for peripheral edema
Large volume of NaCl-> hyperchloremic metabolic acidosis
* Increase Cl -> HCO3 excretion by the kidney
Dilutional effect on albumin
* reduces capillary oncotic pressure
Dilutional effect on coagulation factors
Colloids:
Natural colloids:
Albumin
* binds Ca -> hypocalcemia
synthetic colloids:
FDA black box on synthetic colloids
* risk of renal injury
coagulopathy
* Dextran > hetastarch > hextend
* Don’t exceed 20mL/kg
* not a problem with voluven
Anaphylactic potential
* Highest risk = Dextran
How does Hyperkalemia affect the EKG? (list the events in order of appearance)
Potassium= 5.5-6.5:
* Peaked T waves
Potassium= 6.5-7.5
* P wave flattening
* PR prolongation
Potassium 7-8:
* QRS prolongation
Potassium >8.5:
* QRS -> sine wave-> VF
How do you treat Hyperkalemia?
Cardiac membrane stabilization:
Calcium
Redistribution (shift K intracellularly):
* Insulin +D50
* Hyperventilation
* Bicarbonate
* Albuterol
Elimination
* Potassium wasting diuretics
* Kayexalate
* Dialysis
Discuss the presentation of hypocalcemia
Skeletal muscle cramps
Nerve irritability -> paresthesia and tetany
Chvostek sign
trousseau sign
Laryngospasm
Mental status changes -> seizures
Long QT interval and short PR
discuss the presentation of hypercalcemia
Nausea
Abdominal pain
HTN
Psychosis
Mental status changes -> seizures
Short QT interval and prolonged PR
What is the treatment of hypercalcemia
0.9% NaCl
Loop diuretic
Describe the presentation of hypermagnesemia
Hypermagnesemia complication is usually caused by excessive administration (Think OB and preeclampsia)
* Loss deep tendon reflex = 5.8-10 mEq/L or 7-12 mg/dL
* Respiratory depression = >10 mEq/L or >12 mg/dL
* cardiac arrest = >10 mEq/L or >12 mg/dL
What is the tx for hypermagnesemia
Calcium chloride or calcium gluconate -> directly antagonizes neuromuscular and cardiovascular effects of magnesium
how does hypermagnesemia affect neuromuscular blockade?
potentiates neuromuscular blockade (succ’s and nondepolarizers)
Compare and contrast the consequences of acidosis and alkalosis
what is the anion gap, and what does it tell you?
The anion gap helps us determine the cause of the acidosis
anion ion gap= Major cations - Major anions
or
Na- Cl +HCO3= 8- 12 mEq/L is considered normal
- accumulation of acid (AG>12) -> gap acidosis
- loss of bicarbonate or ECF dilution -> non-gap acidosis
list the possible causes of anion gap acidosis
Mnemonic: MUDPILES
- Methanol
- Uremia
- diabetic ketoacidosis
- Paraldehyde
- Isoniazid
- Lactate ( decreased DO2, sepsis, cyanide toxicity)
- Ethanol, ethylene glycol
- Salicylates (inhibits Krebs cycle)
List the possible causes of a non-gap acidosis
Mnemonic: HARDUP
* Hypoaldosteronism
* Acetazolamide
* Renal tubular acidosis
* Diarrhea
* Ureterosigmoid fistula
* Pancreatic fistula
Large volume resuscitation with NaCl solutions can cause a non-gap metabolic acidosis with hyperchloremia (think trauma)
Discuss the etiology of metabolic alkalosis
under normal conditions, why does blood remain a liquid?
blood exists as a viscous liquid. When there is no injury, blood remains a liquid because:
* coagulation proteins circulate in an inactive form
* the endothelium is smooth, and the glycocalyx repels clotting factors
* undamaged endothelium does not express tissue factor or collagen. This prevents the activation of platelets and the coagulation cascade
* Activated factors are removed by brisk blood flow through the vessels as well as anticoagulants in circulation
When there is a vascular injury, the blood plugs the damaged vessel by forming a clot (it solidifies). Over the next several days, the vessel repairs itself, ad the clot is reabsorbed
what are the 4 steps of hemostasis?
- Vascular spasm
- formation of the platelet plug (primary hemostasis)
- Coagulation and the formation of fibrin (secondary hemostasis)
- Fibrinolysis when the clot is no longer needed
Where are platelets formed? Where are they metabolized?
Platelets are:
* Formed by megakaryocytes in the bone marrow
* Cleared by macrophages in the reticuloendothelial system and the spleen
What is the normal value for platelets? what are the critical values?
Platelet count monitors the number of platelets, but not how well the platelets function. A normal count does not signify normal function.
* normal is 150,000- 300,000 mm^3
* <50,000mm^3 increases surgical bleeding risk
* <20,000mm^3 increases spontaneous bleeding risk
What are the 3 steps of platelet plug formation (primary homeostasis)?
After vascular injury occurs, platelets evolve into a platelet plug via a 3 step process:
1. Adhesion
2. Activation
3. Aggregation
The platelet plug is formed in about 5 minutes
list the 12 coagulation factors
there is no factor 6
Regarding the extrinsic pathway: what activates it? what lab tests measure it? what drug inhibits it?
The extrinsic pathway is activated by vascular injury (tissue trauma liberates tissue factor from the subendothelium).
* it’s measured by the PT and INR
* It’s inhibited by warfarin
Regarding the intrinsic pathway: What activates it? what lab tests measure it? what drug inhibits it?
The intrinsic pathway is activated by blood injury or exposure to collagen
* It’s measured by the PTT and ACT
* It’s inhibited by heparin
What factors are in the extrinsic pathway, intrinsic pathway, and final common pathway?
Extrinsic pathway: 3,7
* “…can be purchased for 37 cents”
Intrinsic pathway: 8, 9, 11, 12
* “ If you can’t buy the intrinsic pathway for $11.98, you can buy it for $12
Final common pathway: 1, 2, 5, 10, 13
* “…can be purchased at the 5 and dime (10) for 1 or 2 dollars on the 13th month”
Describe the process of fibrinolysis.
Since the clot is only a temporary fix while the vessel repairs itself, the body must have a way to break down the clot after it is no longer needed. This process is called fibrinolysis.
- Plasminogen is a proenzyme that is synthesized in the liver. It is incorporated into the clot as it’s being formed, but it lays dormant until it is activated.
- Plasmin is a proteolytic enzyme that degrades fibrin into fibrin degradation products
What are the 3 phases of the contemporary cell-based coagulation cascade?
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 tissue factor.
the cascade consists of 3 phases:
1. initiation
2. Amplification
3. propagation
What are the components of the TEG?
The TEG provides a “real time” visual representation of disorders of coagulation and fibrinolysis.
Be able to identify TEG abnormalities
What is the mechanism of action of heparin?
Heparin inhibits the intrinsic and final common pathways.
Antithrombin III is a naturally occurring anticoagulant that circulates in the plasma. Heparin binds to antithrombin (AT) and greatly accelerates its anticoagulant ability 1000-fold. The heparin-AT complex neutralizes thrombin and activated factors 9, 10, 11, 12
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)
* tranexamic acid
* Aminocaproic acid
Fibrinolytics facilitate the conversion of plasminogen to plasmin. They break down clots (useful for myocardial infarction or embolic stroke)
* tPA
* Urokinase
* Streptokinase
* Reteplase
* Alteplase
where is vWF synthesized, and what is its function?
vWF is synthesized by the vascular endothelium and megakaryocytes. It serves two key functions:
- it anchors the platelet to the vessel wall at the site of vascular injury (platelet adhesion)
- It carries inactivated factor 8 in the plasma
What lab results are consistent with Von Willebrand disease (PT/INR, PTT, platelet count, bleeding time, fibrinogen)?
Describe the pathophysiology of disseminated intravascular coagulation.
DIC is characterized by disorganized clotting and fibrinolysis that lead 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 clots by activating its anticoagulant system. However this leads to widespread consumption of its coagulation factors, fibrinogen, and platelets
Compare ad contrast type 1 and type 2 heparin-induced thrombocytopenia.
Heparin-induced thrombocytopenia causes clot formation throughout the body! the platelet count falls because platelets are consumed faster than they are produced
Compare and contrast type, screen, and crossmatch in terms of what each tests for and how long each takes.
What is the estimated blood volume in preterm neonates, full term neonates, infants, and adults?
