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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)

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2
Q

Which populations have a greater TBW% by weight? Which have less?

A

Higher - Neonates

Lower - Obese, females, elderly

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3
Q

What are the two most important determinants of fluid transfer between capillaries and interstitial space?

A
  1. Starling forces
  2. Glycocalyx
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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)

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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)

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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

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7
Q

What disrupts the glycocalyx?

A

-Sepsis
-Ischemia
-Diabetes
-Major vascular surgery

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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

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9
Q

What happens if the lymph system fails?

A

Edema occurs

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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

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11
Q

Osmosis vs Diffusion

A
  1. Osmosis is the net movement of water across a semipermeable membrane

-Only water (solvent) can move

  1. Diffusion is the net movement of molecules from high to low

-Water (solvent) and solutes both move

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12
Q

What is osmotic pressure ?

A

Pressure pushing against a semipermeable membrane that prevents water from diffusing across.

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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

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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)

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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

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16
Q

What else can increase plasma osmolarity?

A

Hyperglycemia
Uremia

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17
Q

What is uremia?

A

High levels of waste products

Kidneys aren’t functioning well

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18
Q

What is the osmolarity of hypotonic solution?

A

255

Causes cell to swell

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19
Q

What is the osmolarity of isotonic solution?

A

285

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20
Q

What is the osmolarity of hypertonic solution?

A

315

Causes cell to shrink

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21
Q

What type of fluid is Dextran 10%

A

Hypertonic Colloid

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22
Q

What fluids are hypotonic?

A

NaCl .45%

D5W

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23
Q

What fluids are hypertonic?

A

3%

Everything with D5 except D5W

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24
Q

What can happen if hypertonic fluids are given too fast?

A

Central Pontine Myelinolysis

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25
Q

With a K level of 5.5-6.5, what ECG findings are expected?

A

Peaked T waves

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26
Q

With a K level of 6.5-7.5, what ECG findings are expected?

A

P wave flattening
PR prolongation

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27
Q

With a K level of 7-8, what ECG findings are expected?

A

QRS prolongation

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28
Q

With a K level of >8.5, what ECG findings are expected?

A

VF

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29
Q

How is hyperkalemia treated?

A

1.Give Ca to stabilize cardiac membrane

2.Shift K into cell
-Insulin+D50
-Hyperventilate
-Bicarb
-Albuterol

3.Elimation
-K wasting diuretics
-Kayexalate
-Dialysis

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30
Q

Signs of hypocalcemia?

A

-Muscle cramps
-Trousseau + Chvostek sign
-Nerve irritability
-Laryngospasm
-Long QT
-Mental changes
-Seizures

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31
Q

Signs of hypercalcemia?

A

-Nausea
-HTN
-Psychosis
-Short QT
-Seizures

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32
Q

How is hypercalcemia treated?

A

0.9%

Loop diuretic

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33
Q

How does hypermagnesemia present?

A

6-11, loss of deep tendon reflex

> 10, respiratory depression

> 10, cardiac arrest

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34
Q

How do you treat hypermagnesemia?

A

Calcium chloride or calcium gluconate

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35
Q

How does hypermagnesemia affect neuromuscular blockade?

A

Potentiates them

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36
Q

Compare and contrast acidosis and alkalosis

A
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37
Q

What does anion gap tell you? What is normal

A

Determines the cause of acidosis

Major Cations - Major anions

8-12 is normal

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38
Q

Causes of anion gap acidosis?

A

MUDPILES
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde
Isoniazid
Lactate
Ethanol
Salicylates

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39
Q

Causes of non anion gap acidosis?

A

HARDUP

Hypoaldosteronism
Acetazolamide
Renal tubular acidosis
Diarrhea
Uretersigmoid fistula
Pancreatic fistula

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40
Q

How does metabolic alkalosis occur?

A
  1. Addition of Bicarb
    -Bicarb, massive transfusion

2.Loss of acid
-Gastric fluid
-Acid in urine
-Diuretics
-ECF depletion

  1. Increased mineralocorticoid activity
    -Cushing’s
    -Hyperaldosteronism
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41
Q

Why does blood stay a liquid?

A
  1. Coagulation factors
    2.Smooth endothelium
  2. Glycocalyx repels clotting factors
    4.Continuous blood flow
    5.Undamaged endothelium does not express tissue factor or collagen
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42
Q

What are four steps of hemostasis?

A
  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
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43
Q

Where are platelets formed? Where are they metabolized?

A

Formed by megakaryocytes in the bone marrow

Cleared by macrophages in the reticuloendothelial system and the spleen

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44
Q

What is a normal Plt level? What are the critical lab values?

A

150,000-300,000

<50,000 increases surgical bleeding risk

<20,000 increases spontaneous bleeding risk

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44
Q

What are the three steps in primary hemostasis (plug formation)?

A
  1. Adhesion
  2. Activation
  3. Aggregation
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45
Q

List the 12 coagulation factors?

A

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

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46
Q

Where are all but two coagulation factors synthesized?

A

Liver

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47
Q

What two factors are not synthesized in the liver?

A

Tissue factor - vascular wall

Calcium - Diet

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48
Q

What activates the extrinsic pathway? How is it measured? How is it inhibited?

A

Activated by vascular injury

Measured with PT and INR (Shorter pathway, shorter letters)

Inhibited by warfarin

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49
Q

What activates the intrinsic pathway? How is it measured? How is it inhibited?

A

Activated by blood injury or exposure to collagen

Measured by PTT and ACT (Long pathway, longer letters)

Inhibited by heparin

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50
Q

What is the final common pathway?

A

1, 2, 5, 10, 13

Can be purchased at the 5 and dime (10) store for 1 or 2 dollars on the 13th month

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51
Q

What is the extrinsic pathway?

A

3,7

Can be purchased for 37 cents

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52
Q

What is the intrinsic pathway?

A

8, 9, 10, 11

If you can’t by the intrinsic for 12m you can buy it for 11.98

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53
Q

Describe fibrinolysis

A
  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

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54
Q

What are the 3 contemporary cell-based coagulation cascade?

A
  1. initiation
  2. Amplification
  3. propagation

Explains how the three pathways work independently from one another

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55
Q

TEG 1

A
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56
Q

TEG 2

A
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57
Q

TEG 3

A
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58
Q

What is the MOA of heparin?

A

inhibits intrinsic and final common pathways

Heparin binds to antithrombin (AT) and greatly accelerates its anticoagulant ability 1000-fold

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59
Q

How do you treat a patient with ATIII deficiency?

A

AT concentrate or FFP

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60
Q

Can pregnant patient receive heparin?

A

YES

Does not cross placenta

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61
Q

What is a normal ACT? What level is acceptable for bypass?

A

Normal is 90-120

Needs to be greater than 400 seconds

Recheck in 3 minutes then every 30 minutes after

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62
Q

Heparin and Protamine doses for bypass?

A

heparin 400 U/KG

Protamine 1 mg for every 100 units of heparin

63
Q

How does protamine reverse heparin?

A

Heparin is a large negatively charged water soluble compound

Protamine is highly alkaline with strong positive charge

negative charge plus positive charge = neutralization

64
Q

Side effects of protamine?

A
  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
Q

MOA of warfarin ?

A

Inhibits Vit K epoxide reductase complex 1 which is responsible for converting inactive vit k to active vit k

66
Q

What are the vitamin k dependent factors?

A

2, 7, 9, 10 and protein C+S

67
Q

What reverses Warfarin

A
  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
Q

What conditions can cause Vit K deficiency?

A

Needs fat and bile to be absorbed, also manufactured by bacteria in the guy

Malabsorptive disease, impaired GI flora, and decreased bile production

69
Q

What risk is associated with IV phytonadione?

A

Anaphylaxis - avoid if possible

Do not exceed 1mg/min

70
Q

Why do neonates need Vit K at birth?

A

Do not have the gut flora needed to synthesize Vit k

71
Q

Examples of ADP receptor inhibitors?

When do they need to be stopped?

A

Prevent platelet aggregation and thrombus formation

  1. Prasugrel - 3 days
  2. Ticagrelor - 5 days
  3. Clopidogrel- 7 days
    4.Ticlopidine- 14 days
72
Q

Examples of GIIb/IIa receptor antagonists

When do they need to be stopped?

A

Inhibit platelet aggregation and thrombus formation

  1. Tirofiban - 1 day
  2. Eptifibatide - 1 day
  3. Abciximab - 3 days
73
Q

What drugs can be given in replace of heparin? When do they need to be stopped?

A
  1. Bivalirudin -2 hours
  2. Argatroban - 4 hours
74
Q

MOA of COX inhibitors?

A

Block COX 1 which stops the conversion of arachidonic acid to prostaglandins and ultimately thromboxane A2

Aspirin - irreversible
NSAIDS - reversible

75
Q

2 Antifibrinolytics? What do they do?

A

TXA, Aminocaproic acid

Stop conversion of plasminogen to plasmin which promotes clot formation thus reducing bleeding

76
Q

Examples of Fibrinolytics?

A

They facilitate the conversion of plasminogen to plasmin (break down clots)

  1. tPa
  2. Urokinase
  3. Streptokinase
  4. Reteplase
  5. Alteplase
77
Q

Where is vWF synthesized? What is its function?

A

Made in the endothelium and megakaryocytes

Anchors platelet to the vessel wall (adhesion)

Carries inactivated factor 8 in the plasma

78
Q

What are the three types of Von Willebrand disease?

A

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
Q

What will be seen in PT/INR with vWF disease?

A

No change

80
Q

What will be seen in PTT with vWF disease?

A

Increase in time

81
Q

What will be seen in PLT count with vWF disease?

A

No change

82
Q

What will be seen in bleeding time with vWF disease?

A

Increase

83
Q

What will be seen in Fibrinogen with vWF disease?

A

No change

84
Q

MOA of desmopressin? Dose?

A

Synthetic of antidiuretic hormone

Stimulates the release of endogenous vWF and increases factor 8

Dose - 0.3-0.5 mcg/kg IV

85
Q

Which patients respond to desmopressin? Side effects?

A

Type 1 respond the best

Type 3 will not respond because they do not produce vWF

Side effects - hypotension with rapid administration

86
Q

List 4 treatments for vWF

A
  1. Desmopressin
  2. Cyro
  3. FFP
  4. Purified 8-vWF concentrate
87
Q

What is the first line of treatment for vWF type 3?

A

Purified 8-vWF concentrate

88
Q

What two treatments are used in all 3 types of vWF?

A

Cryo and FFP

89
Q

Describe pathophysiology of hemophilia A

A

X-Linked chromosome disorder that causes factor 8 deficiency

90
Q

What is severe Hemophilia A?

A

Factor 8 activity <1%

Severe spontaneous bleeding into the joints, muscle, and vital organs. Require orthopedic surgery

91
Q

What ONE lab value is increased with Hemophilia A?

A

Increased PTT

92
Q

What is the treatment for Hemophilia A?

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
Q

What is the difference between hemophilia A and B?

A

B - is a factor 9 deficiency so the treatment is to give factor 9 concentrate

94
Q

What is recombinant factor 7 used for?

A

“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
Q

Lab values in DIC?

A

Increased PT/PTT
Increased D dimer
Decreased Platelets
Decreased fibrinogen

96
Q

What is DIC?

A

Blood and Clot at the same time

97
Q

Three conditions that may lead to DIC?

A
  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
Q

How is DIC treated?

A

TREAT THE UNDERLYING CAUSE

  1. Treat with fluids
  2. Give FFP, PLT, and CYRO
  3. IV heparin or LMWH
99
Q

Type 1 vs 2 HIT

A
100
Q

What does protein S do?

A

It is a co factor of Protein C (Helps protein C do its job)

101
Q

What does protein C do?

A

Produces anticoagulant effect by inhibiting 5a and 8a.

A deficiency in Protein C or S may lead to a hypercoagulable state

102
Q

How is a deficiency in protein C or S treated?

A

Need to use heparin or warfarin for lifelong treatment

103
Q

Describe factor 5 Leiden mutation

A

Factor 5 Leiden causes a resistance to the anticoagulant effect of protein C

Only patient with thromboembolism need anticoagulation

104
Q

What is sickle cell anemia?

A

Inherited disorder= valine is substituted for glutamic acid and alters the shape of the blood cell

105
Q

Three ways sickle cell disease affects RBC function?

A
  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
Q

Normal lifespan of RBC vs Sickled RBC?

A

Sickled - 12 days
Normal - 120 days

107
Q

What triggers sickle cell? What is the goal of anesthesia?

A

Pain
Hypothermia
Hypoxemia
Acidosis
Dehydration

Goal is to prevent these

108
Q

What is the treatment of vaso-occlusive crisis?

A

*most common manifestation of sickle cell disease

-treat with fluids and pain meds

-Hydroxyurea reduces incidence and occurrence

109
Q

Which electrolyte abnormalities are caused by hyperventilation?

A

Hypocalcemia
Hypokalemia

Produces acute metabolic alkalosis. The body buffers acid-base disturbances by redistributing K into the cells and pumping hydrogen out

110
Q

Which electrolyte disturbance is seen with administration of albumin?

A

Hypocalcemia - binds to it

111
Q

What does it mean if an antigen is present on an RBC?

A

Then there will not be an antibody for that antigen

112
Q

What does it mean if an antigen is not present on an RBC?

A

Then there will be antibody which means a reaction will occur

113
Q

What is the universal donor for RBC? Acceptor?

A

Donor - O negative
Acceptor - AB positive

114
Q

What is the universal donor for Plasma? Acceptor?

A

Donor - AB positive
Acceptor - O negative

(Reversed)

115
Q

What will the mother receive to prevent sensitization?

A

Rhogam

116
Q

What is a Type? What does it test for? How long?

A

ABO and Rh-D antigens

Blood is mixed with other blood

5 minutes

117
Q

What is a Screen ? What does it test for? How long?

A

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
Q

What is a crossmatch ? What does it test for? How long?

A

Compatibility between recipient and potential donor

Simulates transfusion in a test tube

45 minutes

119
Q

A patient is suffering from a acute hemorrhage and there is not time to wait for crossmatched blood, What are the next best options?

A
  1. Type-specific partially crossmatched blood
  2. Type-specific uncrossmatched blood
  3. Type O negative uncrossmatched blood
120
Q

If you don’t have time for a type and crossmatch, can O positive blood be used?

A

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
Q

What is the goal for RBCs? When are they indicated?

A

To increase CaO2

HGB <6 often required

Guided by patient status

122
Q

What is the goal for FFP? When are they indicated?

A
  1. Coagulopathy (PT or PTT >1.5x)
  2. Acute Warfarin reversal
  3. Antithrombin deficiency
  4. Massive transfusion
    5.DIC
  5. C1 esterase deviancy
123
Q

What is the goal for platelets? When are they indicated?

A

Defective platelets

Thrombocytopenia < 50,000 for invasive procedures, neuraxial blockade, most surgeries

Thrombocytopenia <100,000 for eye and neurosurgery

124
Q

What is included in cyro?

A

Fibrinogen
Factor 8
Factor 13
vWF

125
Q

When is cyro given ?

A

Fibrinogen deficiency <80-100

vWB disease

Hemophilia

126
Q

When giving PRBC, how much should Hgb go up?

A

1 unit increases Hgb by 1g/dl

127
Q

Dose for Plt?

A

1 pack per 10kg/body weight

128
Q

FFP dosing?

A

Warfarin reversal = 5-8ml/kg

Coagulopathy = 10-20 ml/kg (increases factor concentration by 20%)

129
Q

Cyro dosing?

A

5 bag pool increases fibrinogen by 50mg/dl

130
Q

Estimated blood volume?

A
  1. Premature Neonate - 100mL/kg
  2. Full term Neonate - 90ml/kg
  3. Infant - 80ml/kg
  4. Adult - 70ml/kg
131
Q

Formula for max allowable blood loss?

A
132
Q

What is used to extend shelf life of RBC’s?

A

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
Q

How does RBC storage affect 2,3 DPG?

A

Shifts it to the left so it holds onto the O2 (Decreased Release)

134
Q

How does RBC storage affect ATP?

A

Decreased - shifts to anaerobic metabolism

135
Q

How does RBC storage affect pH?

A

Decreases - leads to lactic acid

136
Q

How does RBC storage affect Potassium?

A

Increases it (caution in renal failure and neonates

137
Q

How does RBC storage affect its ability to change shape?

A

Impairs it (this is vital for capillary flow)

138
Q

How does RBC storage hemolysis and proinflammatory mediators?

A

increases hemolysis (breakdown of RBC)

Increased mediators

139
Q

What is leukoreduction?

A

Removes WBC from RBC which decreased risk of transfusion reactions and CMV transmission

140
Q

What is washing?

A

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
Q

What is irradiation?

A

Uses gamma radiation and destroys donor leukocytes which helps prevent graft-vs-host

Useful in cancer patients

142
Q

What is the most common infection with RBC transfusion?

A

CMV (cytomegalovirus)

Leukoreduction greatly reduces the risk

Anyone that is immunocompromised should receive this

143
Q

What are the 4 most common complications with RBC administration?

A
  1. CMV
  2. Hep B
  3. Hep C
  4. HIV
144
Q

Why is bacterial infection more common in platelets?

A

They are stored at room temperature

145
Q

Signs and symptoms of a transfusion reaction seen under anesthesia?

A
  1. Hemoglobinuria
  2. Hypotension
  3. Bleeding
146
Q

Signs and symptoms of a transfusion reaction MASKED under anesthesia?

A

Fever
Chills
Chest pain
Dyspnea
Nausea
Flushing

147
Q

Complications from an acute hemolytic reaction

A
  1. Renal failure - acute tubular necrosis
  2. DIC
  3. Hemodynamic instability
148
Q

Steps for treating a transfusion reaction?

A
  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
Q

Patho of a TRALI?

A

Caused by human leukocyte antigens and neutrophil in the plasma

FFP and Plt have greatest concentration of antibodies

150
Q

How does the source of the blood affect TRALI?

A

Donor groups that impart the highest risk

  1. Multiparous women
  2. History of blood transfusion
  3. History of organ transplant
151
Q

Diagnostic criteria for TRALI?

A
  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
Q

What physiologic disturbances are seen from massive transfusion

A

Alkalosis
Hypothermia
Hyperglycemia
Hypocalcemia
Hyperkalemia (from older blood)

153
Q

What is the lethal triad of trauma?

A
  1. Acidosis
  2. Hypothermia
  3. Coagulopathy
154
Q

What is salvaged blood syndrome?

A

Happens with cell saver because it does not return Plt or Coag factors

155
Q

How does cell saver differ from PRBCs?

A

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
Q

When should cell saver not be used?

A
  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

Fluids (5 decks)

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