Fluids Flashcards
1
Q
How much water is in the human body? How is it divided?
A
42L
28L - Intracellular
14L - Extracellular
(11L interstitial, 3L plasma)
2
Q
Which populations have a greater TBW% by weight? Which have less?
A
Higher - Neonates
Lower - Obese, females, elderly
3
Q
What are the two most important determinants of fluid transfer between capillaries and interstitial space?
A
- Starling forces
- Glycocalyx
4
Q
What forces move fluid from the capillary to the interstitium?
A
Capillary hydrostatic pressure (pushes fluid out)
Interstitial oncotic pressure (pulls fluid in)
5
Q
What forces move fluid from the interstitium into the capillary?
A
Interstitial hydrostatic pressure (pushes fluid out of capillary)
Capillary oncotic pressure (pulls fluid into capillary)
6
Q
What is the glycocalyx?
A
Endothelial wall that acts as a gate keeper. Determines what can pass from vessel into the interstitial space
7
Q
What disrupts the glycocalyx?
A
-Sepsis
-Ischemia
-Diabetes
-Major vascular surgery
8
Q
What is lymph? How does the lymphatic system work?
A
Fluid scavenger that removes fluid, protein, bacteria, and debris that enters the interstitum
9
Q
What happens if the lymph system fails?
A
Edema occurs
10
Q
How is lymph returned to the systemic circulation ?
A
Through the thoracic duct at the juncture of the internal jugular and subclavian vein
Left thoracic duct is larger so there is a greater risk of a chylothorax
11
Q
Osmosis vs Diffusion
A
- Osmosis is the net movement of water across a semipermeable membrane
-Only water (solvent) can move
- Diffusion is the net movement of molecules from high to low
-Water (solvent) and solutes both move
12
Q
What is osmotic pressure ?
A
Pressure pushing against a semipermeable membrane that prevents water from diffusing across.
13
Q
What is the primary determinant of osmotic pressure?
A
A function of the number of osmotically active particles
NOT A FUNCTION OF THEIR MOLECULAR WEIGHTS
14
Q
What is the difference between osmolarity and osmolality ?
A
Osmolarity measures the number of osmoles per LITER (One L for Liter)
Osmolality (measures the number of osmoles per Kg of solvent)
15
Q
What is the reference value of plasma osmolarity? What are the three contributors?
A
Think double your Sodium, 280-290
Na
Glucose
BUN
16
Q
What else can increase plasma osmolarity?
A
Hyperglycemia
Uremia
17
Q
What is uremia?
A
High levels of waste products
Kidneys aren’t functioning well
18
Q
What is the osmolarity of hypotonic solution?
A
255
Causes cell to swell
19
Q
What is the osmolarity of isotonic solution?
A
285
20
Q
What is the osmolarity of hypertonic solution?
A
315
Causes cell to shrink
21
Q
What type of fluid is Dextran 10%
A
Hypertonic Colloid
22
Q
What fluids are hypotonic?
A
NaCl .45%
D5W
23
Q
What fluids are hypertonic?
A
3%
Everything with D5 except D5W
24
Q
What can happen if hypertonic fluids are given too fast?
A
Central Pontine Myelinolysis
25
With a K level of 5.5-6.5, what ECG findings are expected?
Peaked T waves
26
With a K level of 6.5-7.5, what ECG findings are expected?
P wave flattening
PR prolongation
27
With a K level of 7-8, what ECG findings are expected?
QRS prolongation
28
With a K level of >8.5, what ECG findings are expected?
VF
29
How is hyperkalemia treated?
1.Give Ca to stabilize cardiac membrane
2.Shift K into cell
-Insulin+D50
-Hyperventilate
-Bicarb
-Albuterol
3.Elimation
-K wasting diuretics
-Kayexalate
-Dialysis
30
Signs of hypocalcemia?
-Muscle cramps
-Trousseau + Chvostek sign
-Nerve irritability
-Laryngospasm
-Long QT
-Mental changes
-Seizures
31
Signs of hypercalcemia?
-Nausea
-HTN
-Psychosis
-Short QT
-Seizures
32
How is hypercalcemia treated?
0.9%
Loop diuretic
33
How does hypermagnesemia present?
6-11, loss of deep tendon reflex
>10, respiratory depression
>10, cardiac arrest
34
How do you treat hypermagnesemia?
Calcium chloride or calcium gluconate
35
How does hypermagnesemia affect neuromuscular blockade?
Potentiates them
36
Compare and contrast acidosis and alkalosis
37
What does anion gap tell you? What is normal
Determines the cause of acidosis
Major Cations - Major anions
8-12 is normal
38
Causes of anion gap acidosis?
MUDPILES
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde
Isoniazid
Lactate
Ethanol
Salicylates
39
Causes of non anion gap acidosis?
HARDUP
Hypoaldosteronism
Acetazolamide
Renal tubular acidosis
Diarrhea
Uretersigmoid fistula
Pancreatic fistula
40
How does metabolic alkalosis occur?
1. Addition of Bicarb
-Bicarb, massive transfusion
2.Loss of acid
-Gastric fluid
-Acid in urine
-Diuretics
-ECF depletion
3. Increased mineralocorticoid activity
-Cushing's
-Hyperaldosteronism
41
Why does blood stay a liquid?
1. Coagulation factors
2.Smooth endothelium
3. Glycocalyx repels clotting factors
4.Continuous blood flow
5.Undamaged endothelium does not express tissue factor or collagen
42
What are four steps of hemostasis?
1. Vascular spasm
2. Formation of platelet plug (primary hemostasis)
3. Coagulation and the formation of fibrin (secondary hemostasis)
4. Fibrinolysis when the clot is not needed
43
Where are platelets formed? Where are they metabolized?
Formed by megakaryocytes in the bone marrow
Cleared by macrophages in the reticuloendothelial system and the spleen
44
What is a normal Plt level? What are the critical lab values?
150,000-300,000
<50,000 increases surgical bleeding risk
<20,000 increases spontaneous bleeding risk
44
What are the three steps in primary hemostasis (plug formation)?
1. Adhesion
2. Activation
3. Aggregation
45
List the 12 coagulation factors?
1- Fibrinogen
2- Prothrombin
3 - Tissue factor
4 - Calcium
5- Labile factor
7 - Stabile factor
8- Antihemophilic factor
9 - Christmas
10- Stuart Prowar factor
11- Plasma thromboplastin antecedent
12- Hageman factor
13- Fibrin stabilizing factor
46
Where are all but two coagulation factors synthesized?
Liver
47
What two factors are not synthesized in the liver?
Tissue factor - vascular wall
Calcium - Diet
48
What activates the extrinsic pathway? How is it measured? How is it inhibited?
Activated by vascular injury
Measured with PT and INR (Shorter pathway, shorter letters)
Inhibited by warfarin
49
What activates the intrinsic pathway? How is it measured? How is it inhibited?
Activated by blood injury or exposure to collagen
Measured by PTT and ACT (Long pathway, longer letters)
Inhibited by heparin
50
What is the final common pathway?
1, 2, 5, 10, 13
Can be purchased at the 5 and dime (10) store for 1 or 2 dollars on the 13th month
51
What is the extrinsic pathway?
3,7
Can be purchased for 37 cents
52
What is the intrinsic pathway?
8, 9, 10, 11
If you can't by the intrinsic for 12m you can buy it for 11.98
53
Describe fibrinolysis
1. Plasminogen is converted to Plasmin through tPa and urokinase
2.Plasmin degrades Fibrin and turns this into degradation products
D-Dimer measures how many fibrin degradation products there are
54
What are the 3 contemporary cell-based coagulation cascade?
1. initiation
2. Amplification
3. propagation
Explains how the three pathways work independently from one another
55
TEG 1
56
TEG 2
57
TEG 3
58
What is the MOA of heparin?
inhibits intrinsic and final common pathways
Heparin binds to antithrombin (AT) and greatly accelerates its anticoagulant ability 1000-fold
59
How do you treat a patient with ATIII deficiency?
AT concentrate or FFP
60
Can pregnant patient receive heparin?
YES
Does not cross placenta
61
What is a normal ACT? What level is acceptable for bypass?
Normal is 90-120
Needs to be greater than 400 seconds
Recheck in 3 minutes then every 30 minutes after
62
Heparin and Protamine doses for bypass?
heparin 400 U/KG
Protamine 1 mg for every 100 units of heparin
63
How does protamine reverse heparin?
Heparin is a large negatively charged water soluble compound
Protamine is highly alkaline with strong positive charge
negative charge plus positive charge = neutralization
64
Side effects of protamine?
1. hypotension through histamine release, give over 5 minutes
2. pulmonary htn through TxA2 and serotonin release
3. Allergic reaction - careful with fish allergy, vasectomy, multiple drug allergies, sensitization to NPH insulin
65
MOA of warfarin ?
Inhibits Vit K epoxide reductase complex 1 which is responsible for converting inactive vit k to active vit k
66
What are the vitamin k dependent factors?
2, 7, 9, 10 and protein C+S
67
What reverses Warfarin
1. Vitamin K, 10-20mg but takes 4 to 8 hours to work
2. For emergency
FFP 1-2 units, recombinant factor VIIa, or prothrombin complex concentrate
68
What conditions can cause Vit K deficiency?
Needs fat and bile to be absorbed, also manufactured by bacteria in the guy
Malabsorptive disease, impaired GI flora, and decreased bile production
69
What risk is associated with IV phytonadione?
Anaphylaxis - avoid if possible
Do not exceed 1mg/min
70
Why do neonates need Vit K at birth?
Do not have the gut flora needed to synthesize Vit k
71
Examples of ADP receptor inhibitors?
When do they need to be stopped?
Prevent platelet aggregation and thrombus formation
1. Prasugrel - 3 days
2. Ticagrelor - 5 days
3. Clopidogrel- 7 days
4.Ticlopidine- 14 days
72
Examples of GIIb/IIa receptor antagonists
When do they need to be stopped?
Inhibit platelet aggregation and thrombus formation
1. Tirofiban - 1 day
2. Eptifibatide - 1 day
3. Abciximab - 3 days
73
What drugs can be given in replace of heparin? When do they need to be stopped?
1. Bivalirudin -2 hours
2. Argatroban - 4 hours
74
MOA of COX inhibitors?
Block COX 1 which stops the conversion of arachidonic acid to prostaglandins and ultimately thromboxane A2
Aspirin - irreversible
NSAIDS - reversible
75
2 Antifibrinolytics? What do they do?
TXA, Aminocaproic acid
Stop conversion of plasminogen to plasmin which promotes clot formation thus reducing bleeding
76
Examples of Fibrinolytics?
They facilitate the conversion of plasminogen to plasmin (break down clots)
1. tPa
2. Urokinase
3. Streptokinase
4. Reteplase
5. Alteplase
77
Where is vWF synthesized? What is its function?
Made in the endothelium and megakaryocytes
Anchors platelet to the vessel wall (adhesion)
Carries inactivated factor 8 in the plasma
78
What are the three types of Von Willebrand disease?
Normal platelet number but platelets are dysfunctional
1. Type 1 - mild to moderate reduction in the amount of vWF produced
2. Type 2 - vWF is produced but doesn't work
3. Type 3 - severe reduction in the amount of vWF produced
79
What will be seen in PT/INR with vWF disease?
No change
80
What will be seen in PTT with vWF disease?
Increase in time
81
What will be seen in PLT count with vWF disease?
No change
82
What will be seen in bleeding time with vWF disease?
Increase
83
What will be seen in Fibrinogen with vWF disease?
No change
84
MOA of desmopressin? Dose?
Synthetic of antidiuretic hormone
Stimulates the release of endogenous vWF and increases factor 8
Dose - 0.3-0.5 mcg/kg IV
85
Which patients respond to desmopressin? Side effects?
Type 1 respond the best
Type 3 will not respond because they do not produce vWF
Side effects - hypotension with rapid administration
86
List 4 treatments for vWF
1. Desmopressin
2. Cyro
3. FFP
4. Purified 8-vWF concentrate
87
What is the first line of treatment for vWF type 3?
Purified 8-vWF concentrate
88
What two treatments are used in all 3 types of vWF?
Cryo and FFP
89
Describe pathophysiology of hemophilia A
X-Linked chromosome disorder that causes factor 8 deficiency
90
What is severe Hemophilia A?
Factor 8 activity <1%
Severe spontaneous bleeding into the joints, muscle, and vital organs. Require orthopedic surgery
91
What ONE lab value is increased with Hemophilia A?
Increased PTT
92
What is the treatment for Hemophilia A?
-Factor 8 concentrate
-FFP and cryo but may see increase in reaction
-Antifibrinolytics to minimize bleeding during dental procedure (TXA or aminocaproic acid)
**NEED TYPE AND CROSSMATCH BEFORE ANY PROCEDURE
93
What is the difference between hemophilia A and B?
B - is a factor 9 deficiency so the treatment is to give factor 9 concentrate
94
What is recombinant factor 7 used for?
"bypass" agent to help factor 8 or 9 in the treatment of hemophilia A+B
Last ditch treatment for unexplained bleeding
Many side effects like MI and stroke
95
Lab values in DIC?
Increased PT/PTT
Increased D dimer
Decreased Platelets
Decreased fibrinogen
96
What is DIC?
Blood and Clot at the same time
97
Three conditions that may lead to DIC?
1. Sepsis (highest risk if gram negative bacilli)
2. OB (highest risk is preeclampsia, placental abruption, and amniotic fluid embolism)
3. Malignancy (highest risk is adenocarcinoma, leukemia, lymphoma)
98
How is DIC treated?
TREAT THE UNDERLYING CAUSE
1. Treat with fluids
2. Give FFP, PLT, and CYRO
3. IV heparin or LMWH
99
Type 1 vs 2 HIT
100
What does protein S do?
It is a co factor of Protein C (Helps protein C do its job)
101
What does protein C do?
Produces anticoagulant effect by inhibiting 5a and 8a.
A deficiency in Protein C or S may lead to a hypercoagulable state
102
How is a deficiency in protein C or S treated?
Need to use heparin or warfarin for lifelong treatment
103
Describe factor 5 Leiden mutation
Factor 5 Leiden causes a resistance to the anticoagulant effect of protein C
Only patient with thromboembolism need anticoagulation
104
What is sickle cell anemia?
Inherited disorder= valine is substituted for glutamic acid and alters the shape of the blood cell
105
Three ways sickle cell disease affects RBC function?
1. Deoxygenation of HgbS leads to sickling (Change in shape)
2. In severe cases it causes to the RBCs to clump together which causes obstruction in the microvasculature (causes tons of pain and impairs tissue perfusion)
3. Sickled cells are more prone to hemolysis and removal by the spleen
106
Normal lifespan of RBC vs Sickled RBC?
Sickled - 12 days
Normal - 120 days
107
What triggers sickle cell? What is the goal of anesthesia?
Pain
Hypothermia
Hypoxemia
Acidosis
Dehydration
Goal is to prevent these
108
What is the treatment of vaso-occlusive crisis?
*most common manifestation of sickle cell disease
-treat with fluids and pain meds
-Hydroxyurea reduces incidence and occurrence
109
Which electrolyte abnormalities are caused by hyperventilation?
Hypocalcemia
Hypokalemia
Produces acute metabolic alkalosis. The body buffers acid-base disturbances by redistributing K into the cells and pumping hydrogen out
110
Which electrolyte disturbance is seen with administration of albumin?
Hypocalcemia - binds to it
111
What does it mean if an antigen is present on an RBC?
Then there will not be an antibody for that antigen
112
What does it mean if an antigen is not present on an RBC?
Then there will be antibody which means a reaction will occur
113
What is the universal donor for RBC? Acceptor?
Donor - O negative
Acceptor - AB positive
114
What is the universal donor for Plasma? Acceptor?
Donor - AB positive
Acceptor - O negative
(Reversed)
115
What will the mother receive to prevent sensitization?
Rhogam
116
What is a Type? What does it test for? How long?
ABO and Rh-D antigens
Blood is mixed with other blood
5 minutes
117
What is a Screen ? What does it test for? How long?
Most clinically significant antibodies
Looking for other antibodies that are not as common
Recipient plasma is mixed with prepared O RBC's that contain known antigens
45 minutes
118
What is a crossmatch ? What does it test for? How long?
Compatibility between recipient and potential donor
Simulates transfusion in a test tube
45 minutes
119
A patient is suffering from a acute hemorrhage and there is not time to wait for crossmatched blood, What are the next best options?
1. Type-specific partially crossmatched blood
2. Type-specific uncrossmatched blood
3. Type O negative uncrossmatched blood
120
If you don't have time for a type and crossmatch, can O positive blood be used?
Yes because 85% of the population is Rh-D positive
DO NOT USE IN WOMAN OF CHILDBEARING AGE AND HAS NOT RECEIVED A PREVIOUS TRANSFUSION
-Not okay for young women
-Not okay if received previous transfusion
121
What is the goal for RBCs? When are they indicated?
To increase CaO2
HGB <6 often required
Guided by patient status
122
What is the goal for FFP? When are they indicated?
1. Coagulopathy (PT or PTT >1.5x)
2. Acute Warfarin reversal
3. Antithrombin deficiency
4. Massive transfusion
5.DIC
6. C1 esterase deviancy
123
What is the goal for platelets? When are they indicated?
Defective platelets
Thrombocytopenia < 50,000 for invasive procedures, neuraxial blockade, most surgeries
Thrombocytopenia <100,000 for eye and neurosurgery
124
What is included in cyro?
Fibrinogen
Factor 8
Factor 13
vWF
125
When is cyro given ?
Fibrinogen deficiency <80-100
vWB disease
Hemophilia
126
When giving PRBC, how much should Hgb go up?
1 unit increases Hgb by 1g/dl
127
Dose for Plt?
1 pack per 10kg/body weight
128
FFP dosing?
Warfarin reversal = 5-8ml/kg
Coagulopathy = 10-20 ml/kg (increases factor concentration by 20%)
129
Cyro dosing?
5 bag pool increases fibrinogen by 50mg/dl
130
Estimated blood volume?
1. Premature Neonate - 100mL/kg
2. Full term Neonate - 90ml/kg
3. Infant - 80ml/kg
4. Adult - 70ml/kg
131
Formula for max allowable blood loss?
132
What is used to extend shelf life of RBC's?
Citrate - anticoagulant that inhibits calcium
Phosphate - buffer to combat acidosis
Dextrose - primary substrate for glycolysis
Adenine - Substrate that helps RBCs re-synthesis ATP (allows for 35 day storage)
133
How does RBC storage affect 2,3 DPG?
Shifts it to the left so it holds onto the O2 (Decreased Release)
134
How does RBC storage affect ATP?
Decreased - shifts to anaerobic metabolism
135
How does RBC storage affect pH?
Decreases - leads to lactic acid
136
How does RBC storage affect Potassium?
Increases it (caution in renal failure and neonates
137
How does RBC storage affect its ability to change shape?
Impairs it (this is vital for capillary flow)
138
How does RBC storage hemolysis and proinflammatory mediators?
increases hemolysis (breakdown of RBC)
Increased mediators
139
What is leukoreduction?
Removes WBC from RBC which decreased risk of transfusion reactions and CMV transmission
140
What is washing?
Blood products are washed with saline which removes any remaining plasma and antigens
RBC antigens are NOT removed
Prevents anaphylaxis in IgA deficient patients
141
What is irradiation?
Uses gamma radiation and destroys donor leukocytes which helps prevent graft-vs-host
Useful in cancer patients
142
What is the most common infection with RBC transfusion?
CMV (cytomegalovirus)
Leukoreduction greatly reduces the risk
Anyone that is immunocompromised should receive this
143
What are the 4 most common complications with RBC administration?
1. CMV
2. Hep B
3. Hep C
4. HIV
144
Why is bacterial infection more common in platelets?
They are stored at room temperature
145
Signs and symptoms of a transfusion reaction seen under anesthesia?
1. Hemoglobinuria
2. Hypotension
3. Bleeding
146
Signs and symptoms of a transfusion reaction MASKED under anesthesia?
Fever
Chills
Chest pain
Dyspnea
Nausea
Flushing
147
Complications from an acute hemolytic reaction
1. Renal failure - acute tubular necrosis
2. DIC
3. Hemodynamic instability
148
Steps for treating a transfusion reaction?
1. Stop it
2. Maintain urine output > 75mL/hr
3. Bicarb to alkalinize the urine
4. Send urine and plasma Hgb to blood bank
5. Check Plt, PT, Fibrinogen
6. Send unused blood back
7. Support hemodynamics
149
Patho of a TRALI?
Caused by human leukocyte antigens and neutrophil in the plasma
FFP and Plt have greatest concentration of antibodies
150
How does the source of the blood affect TRALI?
Donor groups that impart the highest risk
1. Multiparous women
2. History of blood transfusion
3. History of organ transplant
151
Diagnostic criteria for TRALI?
1. Onset < 6 hours
2. Bilateral infiltrates on a frontal CXR
3. PaO2/FiO2 < 300 mmHg or SpO2 < 90% on RA
4. Normal pulmonary occlusion pressure
152
What physiologic disturbances are seen from massive transfusion
Alkalosis
Hypothermia
Hyperglycemia
Hypocalcemia
Hyperkalemia (from older blood)
153
What is the lethal triad of trauma?
1. Acidosis
2. Hypothermia
3. Coagulopathy
154
What is salvaged blood syndrome?
Happens with cell saver because it does not return Plt or Coag factors
155
How does cell saver differ from PRBCs?
Cell saver has higher concentrations of 2,3 DPG and ATP so CaO2 is greater and the cells are able to maintain their shape
156
When should cell saver not be used?
1. Sickle Cell
2. Thalassemia
3. Topical drugs (betadine, chlorhexidine, and topical antibiotics)
4. Infected site
5. Cancer
Okay to use in Tx
Controversial in C sections
