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APEX Study Guide > Unit 9: Fluids & Blood > Flashcards

Unit 9: Fluids & Blood Flashcards

1
Q

What is the distribution of body water?

A

Water represents 60% of the total body weight (42L in 70kg male)

Intracellular Volume = 40% of total body weight (28L)

Extracellular Volume = 20% of total body weight (14L)
-interstitial fluid = 16% (11L)
-plasma fluid = 4% (2L)

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2
Q

Which populations tend to have a greater percentage of TBW% by weight? Which have less?

A
  • Higher TBW% = Neonates
  • Lower TBW% = Females, Obese, and Elderly
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3
Q

What are the 2 most important determinants of fluid transfer between the capillaries and interstitial space?

A

Movement of fluid between intravascular space and the interstitial space is determined by:

-Starling Forces
-The Glycocalyx

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4
Q

What are the Starling forces in the context of capillary fluid transfer?

A

Forces that move fluid from the capillary to the interstitium:

  • Pc = capillary hydrostatic pressure (pushes fluid out of capillary)
  • πif = interstitial oncotic pressure (pulls fluid out of capillary)

Forces that move fluid from interstitium into the capillary:

  • Pif = interstitial hydrostatic pressure (pushes fluid into capillary)
  • πc = capillary oncotic pressure (pulls fluid into capillary)

*net filtration pressure > 0 = filtration (fluid exits capillary)
*net filtration pressure < 0 = reabsorption (fluid is pulled into capillary

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5
Q

What is the glycocalyx? What factors disrupt it?

A

Endothelial glycocalyx = protective layer on the interior wall of blood vessels
-determines what can pass from the vessel into the interstitial space

Disruption = Capillary Leak – accumulation of fluid and debris in the interstitial space reduces tissue oxygenation
-Conditions that impair the integrity = sepsis, ischemia, DM, major vascular surgery

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6
Q

What is lymph, and how does the lymphatic system work?

A

Lymphatic system removes fluid, protein, bacteria, and debris that has entered the interstitium

Accomplishes this with a pumping mechanism that propels lymph through a vessel network lined with one-way valves
-creates a net negative pressure in the interstitial space

*edema occurs when lymphatic system is unable to do its job

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7
Q

How is lymph returned to the systemic circulation?

A

Returned to the venous circulation by way of the thoracic duct at the juncture of the IJ and subclavian vein

*thoracic duct can be injured during venous cannulation – greater risk of chylothorax during left sided IJ insertion

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8
Q

What is the difference between osmosis and diffusion?

A

Osmosis = net movement of WATER across a semipermeable membrane (direction of water movement is driven by the difference in solute concentration on either side of the membrane)

Diffusion = net movement of MOLECULES from a region of high concentration to a region of low concentration (solvent and solute move)

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9
Q

What is osmotic pressure, and what is its primary determinant?

A

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

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10
Q

What is the difference between osmolarity and osmolality?

A

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

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11
Q

What is the normal plasma osmolarity? What are the 3 most important contributors?

What is the equation to determine plasma osmolarity?

A

Plasma Osmolarity = 280 - 290 mOsm/L

Important Determinants:
-Sodium, Glucose, BUN

= 2 [Na] + Glucose/18 + BUN/2.8

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12
Q

What is the difference between a hypotonic and hypertonic solution relative to plasma osmolarity?

A

Hypotonic (255 mOsm/L) = solution osmolarity is less than plasma osmolarity – water enters and cell swells

Hypertonic (315 mOsm/L) = solution osmolarity is more than plasma osmolarity – water exits and cell shrinks

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13
Q

What IV fluids are hypotonic, isotonic, and hypertonic?

A

Hypotonic:
-NaCl 0.45% (154 mOsm/L)
-D5W (253 mOsm/L)

Isotonic:
-LR (273 mOsm/L)
-Plasmalyte A (294 mOsm/L)
-Albumin 5% (300 mOsm/L)
-NaCl 0.9% (308 mOsm/L)

Hypertonic:
-D5 NaCl 0.45% (405 mOsm/L)
-D5 LR (525 mOsm/L)
-D5 NaCl 0.9% (560 mOsm/L)
-NaCl 3% (1026 mOsm/L)

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14
Q

How does dextrose affect the tonicity of IV fluids?

A

Glucose contributes osmotically active molecules to the plasma

Glucose is metabolized to CO2 and water –> water = hypotonic

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15
Q

How do isotonic IV fluids distribute in the patient?

A

Isotonic solutions are very close to plasma –> these solutions expand the plasma volume and the ECV

-crystalloids tend to remain in the intravascular space for ~30 min before moving to the ECF

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16
Q

What complication can result when hypertonic saline is administered too quickly?

A

Central Pontine Myelinolysis

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17
Q

What are the advantages and disadvantages of colloids?

A

Advantages:

  • Replacement ratio = 1:1
  • Increases plasma volume (3-6 hrs)
  • Smaller volume needed
  • Less peripheral edema
  • Albumin has anti-inflammatory properties
  • Dextran 40 reduces blood viscosity (improves microcirculatory flow in vascular surgery)

Disadvantages:

  • Albumin – binds Ca (hypocalcemia)
  • FDA black box warning on synthetic colloids (risk of renal injury)
  • Coagulopathy (Dextran > Hetastarch > Hextend)
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18
Q

What are the advantages and disadvantages of crystalloids?

A

Advantages:
-Replacement ratio = 3:1
-Expands the ECF
-Restores 3rd space loss

Disadvantages:
-limited ability to expand plasma volume – increases plasma volume 20-30 min (higher potential for peripheral edema)
-large volume of NaCl –> hyperchloremic metabolic acidosis
-dilutional effect on albumin (reduces capillary oncotic pressure)
-dilutional effect on coagulation factors

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19
Q

How does hyperkalemia affect the EKG? (list in order of appearance)

A

K+ 5.5 - 6.5 = Peaked T waves

K+ 6.5 - 7.5 = P wave flattening / PR prolongation

K+ 7.5 - 8.0 = QRS prolongation

K+ >8.5 = QRS –> sine wave –> VF

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20
Q

How do you treat hyperkalemia?

A

Cardiac membrane stabilization –> Calcium

Redistribution (shift K+ intracellularly –> Insulin/D50, Hyperventilation, Bicarbonate, Albuterol

Elimination –> Potassium wasting diuretics, Kayexalate, Dialysis

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21
Q

What are the signs/symptoms of hypocalcemia?

A

-Skeletal muscle cramps
-Neve irritability –> paresthesia and tetany
-Chvostek sign
-Trousseau sign
-Laryngospasm
-Mental status changes –> seizures
-Long QT interval

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22
Q

What are the signs/symptoms of hypercalcemia?

A

-Nausea
-Abdominal pain
-Hypertension
-Psychosis
-Mental status change –> seizures
-Short QT interval

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23
Q

How do you treat hypercalcemia?

A

0.9% NaCl

Loop Diuretic (Furosemide)

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24
Q

What are the signs/symptoms of hypermagnesemia?

A

5.8 - 10 mEq/L or 7 - 12 mg/dL = Loss deep tendon reflex

> 10 mEq/L or >12 mg/dL = Respiratory depression and Cardiac arrest

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25
Q

What is the treatment for hypermagnesemia?

A

Calcium chloride or Calcium gluconate

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26
Q

How does hypermagnesemia affect neuromuscular blockade?

A

Potentiates neuromuscular blockade

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27
Q

What are the cardiac, CNS, pulmonary, and electrolyte effects of acidosis?

A

Cardiac:

  • increases P50 (right = release)
  • increases SNS tone
  • increases risk of dysrhythmias
  • decrease contractility

CNS:

  • increases cerebral blood flow and ICP

Pulmonary:

  • increases pulmonary vascular resistance

Electrolyte:

  • hyperkalemia
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28
Q

What are the cardiac, CNS, pulmonary, and electrolyte effects of alkalosis?

A

Cardiac:

  • decreases P50 (left = love)
  • decreases coronary blood flow
  • increases risk of dysrhythmias

CNS:

  • decreases cerebral blood flow and ICP

Pulmonary:

  • decreases pulmonary vascular resistance

Electrolyte:

  • hypokalemia
  • decreased ionized calcium
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29
Q

What is the anion gap? What does it tell you?

A

Anion gap helps determine the cause of acidosis

Anion Gap = [Na+] - ([Cl-] + [HCO3-])
-normal = 8-12 mEq/L

-Accumulation of acid (AG >12) = gap acidosis
-Loss of bicarb or ECF dilution = non-gap acidosis

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30
Q

What are the possible causes of an anion gap acidosis?

(MUDPILES)

A

-Methanol
-Uremia
-Diabetic Ketoacidosis
-Paraldehyde
-Isoniazid
-Lactate (decreased DO2, sepsis, cyanide poisoning)
-Ethanol, ethylene glycol
-Salicylates (inhibits Krebs cycle)

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31
Q

What are the possible causes of a non-gap acidosis?

(HARDUP)

A

-Hypoaldosteronism
-Acetazolamide
-Renal Tubular Acidosis
-Diarrhea
-Ureterosigmoid Fistula
-Pancreatic Fistula

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32
Q

What is the etiology of metabolic alkalosis?

A

Addition of HCO3:
-sodium bicarb administration
-massive transfusion (liver converts preservatives to HCO3)

Loss of Nonvolatile Acid:
-loss of gastric fluid (most common)
-loss of acid in urine
-diuretics
-ECF depletion (increased Na reabsorption –> H and K excretion)

Increased Mineralocorticoid Activity:
-Cushing’s syndrome
-hyperaldosteronism

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33
Q

What are the 4 steps of hemostasis?

A
  1. Vascular Spasm
  2. Formation of the platelet plug (primary hemostasis)
  3. Coagulation and Formation of Fibrin (secondary hemostasis)
  4. Fibrinolysis when the clot is no longer needed
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34
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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35
Q

What is the normal value for platelets? What are the critical values?

A

Normal = 150,000 - 300,000

<50,000 = increases surgical bleeding risk

<20,000 = increases spontaneous bleeding risk

*monitors number of platelets, not the function

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36
Q

What are the 3 steps of platelet plug formation (Primary Hemostasis)?

A
  1. Adhesion
  2. Activation
  3. Aggregation

*platelet plug is formed in ~5 minutes

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37
Q

What are the 12 coagulation factors?

A

1 - Fibrinogen
2 - Prothrombin
3 - Tissue Factor
4 - Calcium Ions
5 - Labile Factor
7 - Stable Factor
8 - Antihemophilic Factor
9 - Christmas Factor
10 - Stuart-Power Factor
11 - Plasma Thromboplastin
12 - Hageman Factor
13 - Fibrin Stabilizing Factor

*all except factor 3 and 4 are synthesized in the liver

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38
Q

What activates the extrinsic coagulation pathway? What lab test measures it? What drug inhibits it?

A

Activated by vascular injury (tissue trauma liberates tissue factor from the subendothelium)

-measured by the PT and INR
-inhibited by warfarin

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39
Q

What activates the intrinsic coagulation pathway? What lab test measures it? What drug inhibits it?

A

Activated by blood injury or exposure to collagen

-measured by the PTT and ACT
-inhibited by heparin

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40
Q

What factors are in the extrinsic pathway, intrinsic pathway, and final common pathway of the coagulation cascade?

A

Extrinsic Pathway: Factors 3 and 7
-“…can be purchased for 3 cents”

Intrinsic Pathway: Factors 8, 9, 11, and 12
-“if you can’t buy the intrinsic pathway for $12, you can buy it for $11.98”

Final Common Pathway: Factors 1, 2, 5, 10, and 13
-“…can be purchased at the5 and dime (10) for 1 or 2 dollars on the 13th of the month

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41
Q

What is fibrinolysis? What enzyme causes it?

A

The breakdown of a clot once it is no longer needed

-Plasminogen is a proenzyme that is synthesized in the liver –> it is incorporated into the clot as it is being formed, but lays dormant until it is activated
-Plasmin is a proteolytic enzyme that degrades fibrin into fibrin degradation products

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42
Q

What are the 3 phases of the contemporary cell-based coagulation cascade?

A

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

Three Phases:
1. Initiation
2. Amplification
3. Propagation

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43
Q

What are the components of the TEG? What products are used to treat each component?

A

R Time: time to begin forming clot – 6-8 min – issue w/ coagulation factors – treat w/ FFP
K Time: time until clot has achieved fixed strength – 3-7 min – issue w/ fibrinogen – treat w/ Cryo
Alpha Angle: speed of fibrin accumulation – 50-60 degrees – issue w/ fibrinogen – treat w/ Cryo
Max Amplitude: highest vertical amplitude on the TEG (measures clot strength) – 50-60 mm – issue w/ platelets – treat w/ platelets +/- DDAVP
Amplitude at min after max amplitude (A60): height of vertical amplitude 60 min after the max amplitude – MA-5 – issue w/ excess fibrinolysis – treat w/ TXA, Aminocaproic acid

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44
Q

Identify the cause of the following TEGs

A
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45
Q

What is the mechanism of action of heparin?

A

Inhibits the intrinsic and final common pathways

-antithrombin III is a naturally occurring anticoagulant that circulates in the plasma – heparin binds to antithrombin and greatly accelerates its anticoagulant ability 1000-fold
-Heparin-AT complex neutralized thrombin and activated factors 9, 10, 11, and 12

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46
Q

How do you treat a patient with ATIII deficiency?

A

Treat with AT concentrate of FFP

-antithrombin deficiency is a common cause for failure to achieve anticoagulation despite an adequate heparin dose prior to cardiopulmonary bypass

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47
Q

Can a pregnant patient receive IV heparin?

A

Heparin does not cross the placenta and is safe in pregnancy

48
Q

What is the normal ACT? What value should be achieved prior to transitioning to cardiopulmonary bypass?

A

Normal ACT = 90-120 seconds

ACT should be >400 seconds before going on cardiopulmonary bypass

ACT is measured before heparin administration, 3 min after it’s given, and every 30 min thereafter

49
Q

What are the doses for heparin (for CPB) and protamine?

A

Heparin Dose = 300-400 U/kg (cardiac surgery dose)

Protamine Dose = 1 mg for every 100 U of heparin predicted to be in the circulation

50
Q

How does protamine reverse heparin?

A

Heparin is a large, negatively charge, water-soluble compound

Protamine is a highly alkaline compound with a strong positive charge

Positive charge of protamine and negative charge of heparin create a neutralization reaction and stop heparin’s anticoagulant activity

51
Q

What are the side effects of protamine?

A

-Hypotension (from histamine release – administer >5min)
-Pulmonary Hypertension (from TxA2 and serotonin release)
-Allergic Reaction (from previous sensitization to NPH insulin, fish allergy, vasectomy, multiple drug allergies)

52
Q

What is the mechanism of action of warfarin?

A

Inhibits the enzyme Vitamin K epoxide reductase complex 1 (VKOR c1) – which is responsible for converting inactive Vit K to active Vit K

-indirectly blocks the manufacturing of the Vit K dependent factors (2, 7, 9, and 10 and protein C and S)

53
Q

What are the antidotes for warfarin? When should each be used?

A

Vitamin K (10-20 mg PO, IM, or IV) – used to reverse for non-emergent, minor surgical procedures
-requires 4-8 hours to restore the concentration of Vit K dependent clotting factors in the blood

FFP (1-2 units), Recombinant Factor VIIa, or Prothrombin Complex Concentrate – emergent or high-risk procedures, such as intracranial procedures

54
Q

What conditions can cause vitamin K deficiency?

A

Vit K is a fat-soluble vitamin that requires the presence of fat and bile for absorption – also manufactured by bacteria in the gut

Following impair fat absorption thus create Vit K deficiency:
-malabsorptive diseases
-impaired G flora
-decreased bile production

*deficiency of Vit K leads to coagulopathy

55
Q

What is the risk associated with IV phytonadione?

A

IV admin is associated with life-threatening anaphylaxis

-best to avoid IV administration but if given by this route – rate should not exceed 1mg/min

56
Q

Why do neonates receive vitamin K after birth?

A

Healthy intestinal flora is required for the gut to synthesize vitamin K

Neonates don’t have the intestinal flora that synthesizes vitamin K, so 0.5-1 mg IM after delivery is common

57
Q

What are ADP receptor inhibitors? Give 4 examples.
How long must each be discontinued prior to surgery?

A

ADP receptor inhibitors prevent platelet aggregation and thrombus formation

-Ticagrelor: 1-2 days
-Prasugrel: 2-3 days
-Clopidogrel: 7 days
-Ticlopidine: 14 days

58
Q

What are GIIb/IIIa receptor antagonists?

Give 3 examples. How long must each be discontinued prior to surgery?

A

Inhibit platelet aggregation and thrombus formation

-Abciximab: 3 days
-Eptifibatide: 1 day
-Tirofiban: 1 day

59
Q

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?

A

Thrombin inhibitors

-Bivalirudin: 2-3 hours
-Argatroban: 4-6 hours

*hepartin should be stopped 6 hours prior to surgery

60
Q

What is the mechanism of action for COX inhibitors? Which agents provide irreversible COX inhibition?

A

COX inhibitors prevent platelet aggregation by blocking cyclooxygenase 1 (COX-1) –> stops conversion of arachidonic acid to prostaglandins and ultimately thromboxane A2

-Aspirin is irreversible (lasts for the life of the platelet
-NSAIDs are reversible (duration is shorter than the life of the platelet)

61
Q

What are antifibrinolytics? Give 2 examples

A

Antifibrinolytics stop the conversion of plasminogen to plasmin – Promote clot formation (reduces bleeding in cardiac and orthopedic surgery)

-Tranexamic Acid (TXA)
-Aminocaproic Acid

62
Q

What are fibrinolytics? Give 5 examples

A

Facilitate the conversion of plasminogen to plasmin – breakdown clots (useful for myocardial infarction or embolic stroke)

-tPA
-Urokinase
-Streptokinase
-Reteplase
-Alteplase

63
Q

Where is vWF synthesized? What is its function?

A

Synthesized by the vascular endothelium and megakaryocytes

Serves Two Functions:
-anchors the platelet to the vessel wall at the site of vascular injury (platelet adhesion) – binds to GP Ib receptor
-carries inactivated factor 8 in the plasma

64
Q

What is Von Willebrand disease? What are the 3 types?

A

Most common inherited disorder of platelet function – platelet count is normal but do not function properly

Type 1: mild-moderate reduction in the amount of vWF produced
Type 2: vWF that is produced doesn’t work well
Type 3: severe reduction in the amount of vWF produced

65
Q

How are the following lab results affected with Von Willebrand disease (PT/INR, PTT, platelet count, bleeding time, fibrinogen)?

A

PT/INR – no change
PTT – increased
Platelet Count – no change
Bleeding Time – increased
Fibrinogen – no change

66
Q

What is the mechanism of action of desmopressin? What is the dose?

A

Synthetic analogue of antidiuretic hormone – stimulates the release of endogenous vWF and increases factor 8 activity

Patients with Type 1 disease respond best to desmopressin
Patients with Type 3 disease don’t respond to desmopressin because they do not produce vWF

Dose = 0.3 - 0.5 mcg/kg IV
Side Effect = hypotension w/ rapid admin

67
Q

What are three other treatments (besides desmopressin) that can improve the coagulopathy of Von Willebrand disease?

A

-Cryoprecipitate: contains factors 8, 13, fibrinogen, and vWF (can be used for all types of disease)
-FFP: contains all clotting factors (can be used for all types of disease)
-Purified 8-vWF Concentrate: reduces risk of transfusion related infection (first line agent for the pt w/ type 3)

68
Q

What is the pathophysiology of hemophilia A?

A

X-linked chromosomal disorder (more common in males) that causes factor 8 deficiency

-severe disease (factor 8 activity <1%) is associated with spontaneous bleeding into the joints, muscles, and vital organs
-patients often require orthopedic surgery

69
Q

How are the following lab results affected in Hemophilia A (PT/INR, PTT, platelet count, bleeding time, fibrinogen)?

A

PT/INR – no change
PTT – increased
Platelet Count – no change
Bleeding Time – no change
Fibrinogen – no change

70
Q

What is the treatment for hemophilia A?

A

-Factor 8 concentrate prior to surgery
-FFP and Cryo can also be used to replace factor 8 (increases risk of transfusion related disease transmission)
-Antifibrinolytics (TXA or Aminocaproic Acid) can be used to minimize bleeding during dental procedures
-A type and crossmatch is required for any surgical procedure

71
Q

How is hemophilia B different from hemophilia A?

A

Hemophilia B is factor 9 deficiency

-labs and anesthetic management are similar to hemophilia A, but instead of factor 8 replacement, factor 9 concentrate is indicated

72
Q

What is the role of recombinant factor 7 in the management of hemophilia A and B?

A

Sometimes pts w/ hemophilia A or B develop inhibitors that prevent exogenous factor 8 or 9 from achieving their therapeutic goals – Recombinant factor 7 is a “bypass” agent

-it skips over factor 8 or 9 in patients with inhibitors allowing the patient to form a clot
-Dose: 90-120 mcg/kg

*can increase risk of arterial thrombosis (MI and embolic stroke) as well as venous thrombosis (DVT or PE) –> risk/benefit ratio must be considered

73
Q

What is the pathophysiology of disseminated intravascular coagulation (DIC)?

A

Characterized by disorganized clotting and fibrinolysis that lead to simultaneous occurrence of hemorrhage and systemic thrombosis

-generalized thrombin formation creates microvascular clots that impair tissue perfusion – results in tissue hypoxia and acidosis
-body attempts to break down these clots by activating its anticoagulant system – leads to widespread consumption of coagulation factors, fibrinogen, and platelets

74
Q

What lab values are consistent with DIC? (PT/PTT, D-dimer, Platelets, Fibrinogen)

A

Increased PT/PTT

Increased D-dimer

Decreased Platelets

Decreased Fibrinogen

75
Q

What 3 conditions are associated with a high risk of developing DIC?

A
  1. Sepsis (highest risk = gram-negative bacilli)
  2. Obstetric Complications (highest risk = preeclampsia placental abruption, and amniotic fluid embolism)
  3. Malignancy (highest risk = adenocarcinoma, leukemia, and lymphoma)
76
Q

How do you manage a patient with DIC?

A

Definitive treatment is reversing the underlying cause

Supportive treatment includes:
-hypovolemia –> treat with IV fluids
-coagulopathy –> replace consumed blood components with FFP, platelets, and Cryo
-severe microvascular thrombosis –> IV heparin or LMWH

77
Q

Compare and contrast type 1 and type 2 heparin-induced thrombocytopenia

A

HIT Type 1: Heparin induced platelet aggregation

  • occurs after large heparin dose
  • onset 1-4 days after heparin admin
  • platelet count <100,000
  • minimal morbidity
  • treatment = resolves spontaneously even if heparin is continued

HIT Type 2: Antiplatelet antibodies (IgG) attack factor 4 immune complexes –> platelet aggregation

  • occurs after any heparin dose
  • onset 5-14 days after heparin admin
  • platelet count <50,000
  • hypercoagulable state causes high risk of amputation and death
  • treatment = heparin must be discontinued – anticoagulate with direct thrombin inhibitor (Bivalirudin, Hirudin, Argatroban)
78
Q

What is the pathophysiology and treatment of protein C and S deficiency?

A

Protein C produces an anticoagulant effect by inhibiting factor Va and VIIIa – creates feedback mechanism that prevents unnecessary clot formation (Protein S helps protein C do its job)

Deficiency can produce a hypercoagulable state, increasing risk of thrombosis

Treatment:
-thromboembolism is treated with heparin that is transitioned to warfarin
-pts may or may not require life-long anticoagulation w/ warfarin

79
Q

What is the pathophysiology and treatment of factor 5 Leiden mutation?

A

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

Treatment:
-only pts with thromboembolism require anticoagulation
-lifelong anticoagulation is unwarranted unless the pt experiences recurrent thrombotic events

80
Q

What is the pathophysiology of sickle cell anemia?

A

Inherited disorder that affects erythrocytes – Amino acid substitution on the beta globulin chain alters RBC geometry

Affects RBC function:
-Deoxygenation of HgbS leads to sickling (conformational change that alters the erythrocyte geometry)
-in severe cases, sickling causes RBCs to clump together – causes mechanical obstruction of microvasculature in vital organs and joints (impairs tissue perfusion and causes intense pain)
-sickled cells are more prone to hemolysis and removal by the spleen (lifespan = 12-17 days)

81
Q

What are the triggers that cause sickling of HgbS?

A

-Pain
-Hypothermia
-Hypoxemia
-Acidosis
-Dehydration

*anesthetic management focuses on avoiding there triggers

82
Q

What is vaso-occlusive crisis?

A

Sickled cells –> impair tissue perfusion–> ischemic injury

  • most common manifestation of sickle cell disease

Treatment: analgesics (oral or IV) and hydration

  • hydroxyurea reduces the incidence and severity of vaso-occlusive crisis
83
Q

What is the relationship between blood type, erythrocyte antigens, and plasma antibodies?

A

-Blood type is determined by specific glycoproteins present on the erythrocyte cell membrane
-These glycoproteins have an antigenic potential (wrong type has catastrophic consequences)
-Most clinically important antigens are the ABO and Rh systems

-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 antigen in the plasma

84
Q

What blood type is the universal donor for erythrocytes? How about the universal acceptor?

A

Universal RBC Donor = O negative

Universal RBC Acceptor = AB positive

85
Q

What blood type is the universal donor for FFP? How about the universal acceptor?

A

Universal FFP Donor = AB positive

Universal FFP Acceptor = O negative

86
Q

What is the concern about an Rh-negative mother and pregnancy?

A

A person who is Rh-negative can be sensitized by exposure to Rh-positive blood during transfusion or pregnancy

-Rh-negative mother can be sensitized by her Rh-positive fetus –> transfer across the placenta
-mother receives Rhogam to prevent sensitization
-if the mother becomes sensitized and develops antibodies, a subsequent pregnancy with an Rh-positive fetus may result in erythroblastosis fetalis

87
Q

What do each of the following blood tests test an how long does each test take?

Type
Screen
Crossmatch

A

Type:

  • ABO and Rh-D antigens
  • takes 5 min
  • recipient blood is mixed with anti-A, anti-B, and anti Rh-D antibodies (0.2% chance of incompatibility reaction after this test - specific units not assigned to pt)

Screen:

  • most clinically significant antibodies
  • takes 45 min
  • recipient plasma is mixed with commercially prepared O RBCs that contain known antigens (0.06% chance of incompatibility reaction after this test - specific units not assigned)

Crossmatch:

  • compatibility between recipient plasma and the actual blood unit to be transfused
  • takes 45 min
  • simulates transfusion in a test tube (0.05% chance of incompatibility reaction after this test - specific units are assigned)
88
Q

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

A
  1. Type-specific partially crossmatched blood
  2. Type-specific uncrossmatched blood
  3. Type O negative uncrossmatched blood (universal donor)

*listed most to least favorable options

89
Q

Can type O positive blood ever be used for emergency transfusion?

A

If you don’t have time to obtain a type and crossmatch, type O negative is best for emergency transfusion, but…

Because 85% of the population is Rh-D positive, O positive can be used for emergency transfusion if the patient is NOT a woman of childbearing age and has NOT received a previous transfusion

90
Q

What is the indication to transfuse packed RBCs?

A

RBCs are transfused to increase CaO2:

-hgb >10 (transfusion rarely required)
-hgb <6 (transfusion often required)

*decision to transfuse is guided by pt factors

91
Q

What are the indications for FFP transfusion?

A

-Coagulopathy (PT or PTT >1.5x control)
-Warfarin reversal (acute need)
-Antithrombin deficiency
-Massive transfusion
-DIC
-C1 esterase deficiency (heredity angioedema)

*conditions that can be treated with factor concentrates often carry less infectious risk

92
Q

What are the indications for platelet transfusion?

A

Thrombocytopenia (<50,000): invasive procedures, neuraxial blockade, or most surgeries

Thrombocytopenia (<100,000): eye and neurosurgery

Qualitative platelet defect

93
Q

What is in cryoprecipitate? (4)

A

-Fibrinogen
-Factor 8
-Factor 13
-vWF

94
Q

What are the indications for Cryo transfusion?

A

-Fibrinogen deficiency (<80-100 mg/dL)
-vWB disease
-Hemophilia

95
Q

What is the dose for PRBC, FFP, Platelets, and Cryo?

A

-PRBCs = 1 unit increases Hgb by 1g/dL
-FFP = 5-8 mL/kg for warfarin reversal or 10-20 mL/kg for coagulopathy (increases factor concentration by 20-30%)
-Platelets = 1 pack per 10 kg/body weight
-Cryo = 5 bag pool increases fibrinogen by 50 mg/dL

96
Q

What is the estimated blood volume in preterm neonates, full term neonates, infants, and adults?

A

Preterm Neonate: 90-100 mL/kg

Full Term Neonate: 80 -90 mL/kg

Infant: 80 mL/kg

Adult: 70 mL/kg

97
Q

What is the formula for maximum allowable blood loss?

A

EBV x [(Startin Hbg - Target Hbg) / Starting Hbg)]

98
Q

What four substances extend the shelf life of PRBCs? What is the function of each?

A

Citrate: anticoagulant that inhibits calcium (factor 4) - after transfusion of multiple units, citrate load can cause hypocalcemia

Phosphate: buffer that combats acidosis

Dextrose: primary substrate for glycolysis

Adenine: substrate that helps RBCs re-synthesize ATP – storage time to 35 days

*newer preservatives (adsol, nutricel, and optisol) extend storage time to 42 days

99
Q

What does RBC storage lesion lead to?

A

-Decreased 2,3 DPG –> shifts oxyhemoglobin dissociation curve to the left (left=love) –> decreased O2 release
-Decreased ATP –> shift to anaerobic metabolism
-Decreased pH (increased lactic acid)
-Increased potassium (caution in neonates and renal failure)
-Impaired ability to change shape (important for capillary flow)
-Hemolysis
-Increased production of proinflammatory mediators

100
Q

What is leukoreduction of blood? Why is it used and who does it benefit?

A

Leukoreduction removes WBCs from RBCs and platelets

-leukocytes are responsible for HLA alloimmunization, febrile nonhemolytic transfusion reactions, and CMV transmission – removing them reduces these risks

101
Q

What is washing of blood? Why is it used and who does it benefit?

A

Washing the blood products with saline removes any remaining plasma (and antigens) in the donor RBCs – does not remove RBC antigens

Prevents anaphylaxis in IgA deficient patients

102
Q

What is irradiation of blood? Why is it used and who does it benefit?

A

Irradiation exposes units to gamma radiation – disrupts WBC DNA in the donor leukocytes

Prevents graft-vs-host disease in immunocompromised patients

Populations who benefit include: leukemia, lymphoma, hematopoietic stem cell transplant, and DiGeorge syndrome

103
Q

What is the most common infectious complication of RBC transfusion? How can this risk be reduced?

A

Cytomegalovirus (CMV)

-leukoreduction greatly reduces this risk (immunocompromised pts should receive leukoreduced blood)

104
Q

What are the four most common infectious complications of RBC transfusion from most to least common?

A

-CMV (cytomegalovirus) – 1-3% of all transfusions
-Hepatitis B – 1 in 366,500
-Hepatitis C – 1 in 1,657,000
-HIV – 1 in 1,860,000

105
Q

Why is bacterial contamination more common with platelets than with RBCs or FFP?

A

Platelets are stored at room temperature

*bacterial contamination can progress to sepsis

106
Q

What are the signs and symptoms (observed under anesthesia and masked by anesthesia) of an acute hemolytic transfusion reaction?

A

Observed Under Anesthesia:

  • hemoglobinuria (usually presenting sign)
  • hypotension
  • bleeding

Masked By Anesthesia:

  • fever
  • chills
  • chest pain
  • dyspnea
  • nausea
  • flushing
107
Q

What is an acute hemolytic reaction? What are the complications?

A

Complement is activated in the recipient’s blood and plasma antibodies attack the antigens present on the donor blood cell

Complications:
-renal failure (acute tubular necrosis): free hgb in the form of acid hematin precipitates inside the renal tubules leading to mechanical obstruction
-DIC: erythrocyin is released from the RBC and it activates the intrinsic clotting cascade
-hemodynamic instability: free hemoglobin activates the kallikrein system – final product of this pathway is bradykinin (potent vasodilator)

*ABO incompatibility is most lethal

108
Q

What is the treatment plan for an acute hemolytic reaction?

A
  1. Stop the transfusion
  2. Maintain urine output >75-100 mL/hr (IV fluids, mannitol 12.5-25g, or furosemide 20-40mg)
  3. Alkalinize the urine with Sodium Bicarb
  4. Send urine and plasma hemoglobin samples to blood bank
  5. Check platelets, PT, and fibrinogen
  6. Send unused blood to the blood bank to double-check cross match
  7. Support hemodynamics with IVF and pressors as needed
109
Q

What is the pathophysiology of transfusion-related acute lung injury (TRALI)?

A

Caused by human leukocyte antigens (HLA) and neutrophil antibodies present in the donor plasma

Donor Antibodies –> Neutrophil activation in the lungs –> Endothelial injury –> Capillary leak –> Pulmonary edema –> Impaired gas exchange –> Hypoxemia –> Acidosis –> Death

*FFP and platelets contain the highest concentration of these antibodies

110
Q

How does the source (donor group) of blood products affect the risk of TRALI?

A

The following donor groups impact the highest risk:

-multiparous women (highest risk)
-history of blood transfusion
-history of organ transplant

111
Q

What are the diagnostic criteria for TRALI?

A

-Onset < 6 hours following transfusion
-Bilateral infiltrates on frontal CXR
-PaO2/FiO2 <300 mmHg or SpO2 <90% of RA
-Normal pulmonary artery occlusion pressure (no left atrial HTN or volume overload)

112
Q

What physiologic disturbances result from massive transfusion?

A

-Alkalosis from citrate metabolism to bicarb in the liver
-Hypothermia from transfusion of cold blood
-Hyperglycemia from dextrose additive to stored blood
-Hypocalcemia from binding of calcium by citrate
-Hyperkalemia from admin of older blood

113
Q

What is the lethal triad of trauma?

A
  1. Acidosis
  2. Hypothermia
  3. Coagulopathy

*problem begins with hemorrhage and hypoperfusion – ultimately impacts coagulation and acid-base balance

114
Q

What is salvaged blood syndrome?

A

“Salvaged Blood Syndrome” = dilutional coagulopathy

-cell saver blood doesn’t return platelets and coagulation factors to the patient – large volume of salvaged blood returned to the patient has the possibility of dilutional coagulopathy

115
Q

How is cell saver blood different from PRBCs?

A

Cell saver blood contains higher concentrations of 2,3-DPG and ATP, so CaO2 is greater and the cells are better able to maintain their biconcave shape (less sludging in the microcirculation)

116
Q

What are the contraindications and controversial uses for intraop blood salvage?

A

Contraindications:

  • sickle cell disease
  • thalassemia
  • topical drugs in a sterile field such as betadine, chlorhexidine, and topical antibiotics
  • infected surgical site
  • oncologic procedures

Controversial Uses:

  • c-section due to the theoretical risk of anaphylactoid syndrome of pregnancy (amniotic fluid embolism)

*it is considered safe for transplant surgery

APEX Study Guide (13 decks)

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