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ECVECC Board Exam > Fluid/Shock/Trauma > Flashcards

Fluid/Shock/Trauma Flashcards

1
Q

Define limited fluid volume resuscitation (LFVR).

A

The goal of LFVR is to restore the perfusion with the smallest amount of fluid volume and minimize the risk of exacerbating hemorrhage.
The target blood pressure for LFVR is MAP at 70 mmHg or SAP at 90 mmHg until definitive control of hemorrhage is achieved (e.g. sx).

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2
Q

Define hypotensive resuscitation.

A

The goal is to resuscitate the patient to the MAP no greater than 60 mmHg until the definitive control of hemorrhage is achieved.

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3
Q

Define shock.

A

Inadequate cellular energy production

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4
Q

True or False: Neonates and pediatrics have higher lactate concentrations.

A

True

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5
Q

What is the equation for DO2?

A

DO2 (ml/min) = CO (ml/min) x CaO2 (ml O2/dl) = (HR x SV) x [Hb x SaO2 x 1.34 + PaO2 x 0.003]

  • 1.34 = Hufner constant for human hemoglobin oxygen binding capacity in mL/g
  • Hb (g/L)
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6
Q

What is the equation for VO2?

A

VO2 = CO x [CaO2 - CvO2]

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7
Q

According to the review paper published by Walton et al about venous oxygenation, what are the VO2 for anterior and posterior vena cava? What factors contribute this difference?

A

Anterior: 75%
Posterior: 80%

High cerebral oxygen extraction and high renal non-nutrient blood flow

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8
Q

What is the normal mixed venous oxygen saturation

A

SvO2 = 75%, PvO2 = 40mmHg

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9
Q

Define oxygen extraction ratio.

A

Oxygen extraction ratio (O2ER) = VO2/DO2

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10
Q

What cause increased O2ER?

A

Increased tissue oxygen demand
Decrease oxygen delivery

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11
Q

What is normal oxygen extraction ratio in a healthy individual? What is the critical oxygen extraction ratio?

A

Normal: 0.2 - 0.3
Critical oxygen extraction ratio: 0.79

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12
Q

What is critical oxygen extraction?

A

It is the point where the critical oxygen extraction ratio is met and the falling of DO2 fails to meet with the VO2 need. (bad bad)

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13
Q

What is the normal difference between SvO2 and ScvO2?

A

ScvO2 is usually 2-5% lower than SvO2

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14
Q

What are the four principle determinants of venous oxygen saturation?

A

Cardiac output
Hemoglobin concentration
SaO2 (arterial oxygen saturation)
Tissue oxygen consumption

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15
Q

What are the normal SvO2 and ScvO2?

A

ScvO2 65-70%
SvO2 70-75%

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16
Q

How many percentage of isotonic crystalloid will still remain in the intravascular space after fluid resuscitation?

A

25% (after 30 minutes)

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17
Q

Besides volume expansion, what are other benefits of HTS?

A

Decreased endothelial swelling
Improved cardiac contractility
Decreased intracranial pressure
Modulate inflammation (immune-modulatory effect)
Mild peripheral vasodilation

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18
Q

Draw “Tree of Life”

A
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19
Q

What are the systemic and local factors controlling the systemic vascular resistance?

A

Local: NO, CO2, Histamine, prostacyclin, endothelin, thromboxan, thrombin

Systemic: SNS (short term change), vasopressin, angiotensin II (long term change)

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20
Q

For patients experiencing acute bleeding, how many percentage of total intravascular volume needs to decrease in order for patient to be hypotensive?

A

30%

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21
Q

To respond to hypotension, the body develops what two reflexes?

A

Baroreceptor reflexes
Chemoreceptor reflexes (detect the change of arterial oxygen tension, CO2 and pH)

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22
Q

What are the two types of baroreceptors and where do they locate?

A

High-pressure arterial receptors:
- aortic arc, carotid sinuses
- when BP decreases → nerve firing is decreased → signals to the vasomotor center in medulla is decreased → increased sympathetic outflow

Low-pressure volume receptors:
- atria, ventricle, pulmonary vasculatures

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23
Q

Does angiotensin II cause release of vasopressin?

A

Yes it does

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24
Q

Which one is a strong acid, lactate or lactic acid?

A

Lactic acid

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25
Q

True or False: The metabolic acidosis associated by lactate production is due to excessive lactate accumulation.

A

False

The metabolic acidosis is due to ATP depletion (and decreased H+ consumption) instead of lactate accumulation.

  • When the ATP made by glycolysis is utilized, H+ is released into the cytosol. This proton would usually enter the mitochondrion and be used to maintain the proton gradient required for the electron transport chain and oxidative phosphorylation. When oxygen supplies are insufficient this cannot happen and H+ ions accumulate and are then transported out of the cell.
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26
Q

Under normal condition, which organs are the major lactate production organs?

A

Skeletal muscles (40-50%)
Erythrocytes
Skin
Brain

  • Red blood cells, leukocytes (predominantly neutrophils), and platelets are responsible for 80, 13, and 7% of lactate production in blood, respectively. (From lactate review paper)
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27
Q

Under normal condition, which organs are the major lactate consumption organs?

A

Renal cortex
Liver
Myocardium

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28
Q

Normally can we detect lactate in the urine? Where is it absorbed in the nephrons?

A

No
Proximal renal tubule (threshold: 6 to 10 mmol/L)

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29
Q

What is the half-life for lactate?

A

30-60 min

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30
Q

What are the definitions of type A and type B hyperlactatemia?

A

Type A: evidence of tissue oxygen deficiency (absolute or relative)

Type B: no evidence of tissue oxygen deficiency
- B1: associated with underlying diseases
- B2: associated with drugs or toxins
- B3: congenital errors in metabolism

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31
Q

How is propylene glycol caused hyperlactatemia?

A

Propylene glycol is metabolized into L-lactate, R-lactate and pyruvate.

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32
Q

True or False: An animal with hyperlactatemia will also has metabolic acidosis.

A

False

If the mitochondria function is normal and H+ can be metabolized, patient may not have metabolic acidosis.

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33
Q

True or False: The POC lactate meter can measure both L-lactate and D-lactate.

A

False

Only L-lactate

  • In healthy animal, D-lactate is only 1-5% of L-lactate
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34
Q

What are the characteristic of 5% dextrose solution (isotonic vs hypotonic; isoosmotic vs hypoosmotic)?

A

Isoosmotic (250 mOsm/L), hypotonic (dextrose is metabolized in the vessels)

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35
Q

What are the three main natural colloid particles? Which one is the main contributor to COP?

A

Albumin (main; 80%), globulin, fibrinogen

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36
Q

What is the minimal degree of dehydration that can be detected on PE?

A

5%

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37
Q

When we assess patient’s hydration status by checking the skin tent and MM moisture, what are we actually checking?
A) Interstitial hydration status
B) Intravascular hydration status
C) Intracellular hydration status

A

A) Interstitial hydration status

  • Intracellular hydration status cannot be detected by PE
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38
Q

Why shouldn’t we give HTS at a fast rate (> 1ml/kg/min)?

A

It can cause hypotension by central vasomotor center inhibition or peripheral vasomotor effect (due to hyperosmolality)

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39
Q

How much intravascular volume will 4 ml/kg of 7.5% HTS expand?

A

12-16 ml/kg

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40
Q

Where are lactate, acetate and gluconate metabolized?

A

Lactate - liver
Acetate - skeletal muscle
Gluconate - most cells in the body

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41
Q

What are normal COP in dogs and cats?

A

Dogs: 15-26 mmHg
Cats: 18-33 mmHg

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42
Q

What characteristics of a colloid solution are associated with longer half-life?

A

Higher molecular weight
Higher degree of substitutions
Higher C2 : C6 ratio

** These characteristics also confers to more significant coagulopathic effect

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43
Q

On the package of VetStarch, you will see 130/0.4. What does that mean?

A

130 means average molecular weight is 130K Da
0.4 means 4 hydroxyethyl group substitutions per 10 glucose molecules

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44
Q

How are the synthetic colloids metabolized/eliminated?

A
  • Reticuloendothelial system (e.g. liver, spleen, lymphatic system)
  • Amylase in the blood can also metabolized hydroxyethyl starch
  • Excreted via the kidneys
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45
Q

What is the body fluid composition?

A
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46
Q

What are the most abundant cation and anion in ICF? What about ECF?

A

ICF: potassium, phosphate
ECF: sodium, chloride and bicarb

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47
Q

Fill out the blank.

A
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48
Q

What is the Na concentration in 0.9% NaCl, LRS and Normosol-R, respectively?

A

0.9% NaCl: 154 mEq/L
LRS: 130 mEq/L
Normosol-R: 140 mEq/L

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49
Q

What is the buffer in 0.9% NaCl, LRS and Normosol-R, respectively?

A

0.9% NaCl: none
LRS: lactate
Normosol-R: acetate, gluconate

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50
Q

What is the K concentration in LRS and Normosol-R, respectively?

A

LRS: 4 mEq/L
Normosol-R: 5 mEq/L

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51
Q

What is the Cl concentration in 0.9% NaCl, LRS and Normosol-R, respectively?

A

0.9% NaCl: 154 mEq/L
LRS: 109 mEq/L
Normosol-R: 98 mEq/L

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52
Q

Which fluid contains Ca and which contains Mg?

A

LRS contains Ca 3mEq/L
Normosol-R contains Mg 3 mEq/L

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53
Q

What is the osmolality of 0.45% NaCl + 2.5% Dextrose?

A

280 mOsm/L

  • 0.9% NaCl: 308 mOsm/L
  • D5W: 250 mOsm/L
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54
Q

What is the equation for free water deficit?

A

Free water deficit (L) = [(Measured Na - Normal Na)/Normal Na] x body weight x 0.6

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55
Q

Is VetStarch made up of tetrastarch or hetastarch?

A

6% Tetrastarch (hydroxyethyl starch)

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56
Q

What is recommended CRI for VetStarch? What is the daily dose limit?

A

0.5 - 2 ml/kg/hr
20 - 40 ml/kg/day

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57
Q

What are the recommend “shock” dose for synthetic colloid in dogs and cats?

A

Dogs: 10-20 ml/kg
Cats: 5-10 ml/kg

*usually start with 2-5 ml/kg IV over 10-20 min

58
Q

What is “turbostarch”?

A

Mix 23.4% HTS with 6% hetastarch at 1:2 ratio and give 3-5 ml/kg

59
Q

Define Osmolarity.

A

The number of solute particles per 1L of solvent.

60
Q

Define Tonicity.

A

The ability of a solution to move water across the cell membrane and change the volume of the compartment. It is usually determined by the effective particles number, which are those solute particles that do not freely permeate most of the cell membrane.

61
Q

What are the examples of effective osmoles and ineffective osmoles?

A

Effective osmoles: Na+, K+, glucose, mannitol

Ineffective osmoles: BUN

*Mannitol is NOT a colloid

62
Q

What is the starling principle? What is the equation and the definition of each parameter?

A

Starling’s principle: the movement of the water between the capillary and tissue is determined by the net force of capillary and interstitial hydrostatic pressure difference as well as the oncotic pressure difference.

Jv = K [(Pc - Pi) - σ (𝛑c - 𝛑i)]

Jv = net fluid flux across the capillary wall
K = capillary filtration coefficient (membrane permeability to water)
Pc = capillary hydrostatic pressure
Pi = interstitial hydrostatic pressure
σ = reflection coefficient (membrane impermeability to proteins)
𝛑c = capillary oncotic pressure
𝛑i = interstitial oncotic pressure

63
Q

Define revised Starling principle.

A

Jv = K [(Pc - Pi) - σ (𝛑c - 𝛑g)]

𝛑g = subglycocalyx oncotic pressure

In the revised Starling principle, the recognization of endothelial glycocalyx and subglycocalyx place redefines the fluid movement across the capillary. The force of interstitial oncotic pressure is replaced by the subglycocalyx oncotic pressure. There is no resorption of water from the interstitial space as the capillary hydrostatic pressure decreases. The water that move out of the capillary will return to the systemic circulation via the lymphatic system.

64
Q

Describe Gibbs-Donnan Effect.

A

The transmembrane potential difference exists due to the presence of impermeable charged particles (e.g. protein) which affect the equilibrium of the charged ions across the membrane.

65
Q

What are the four types of catheters?

A

Winged
Over-the-needle
Through-the-needle
Multilumen

66
Q

Describe venous cutdown technique.

A
  1. Identify the vein (e.g. cephalic vein)
  2. clip the hair and surgically prepare the skin
  3. Inject some local anesthetic (e.g. lidocaine) if the animal is awake or not on any pain medication
  4. Put on sterile gloves and make a full thickness skin incision parallel to the vein (about 1-2 cm).
  5. Use hemostats to bluntly dissect and isolate the vein from the surrounding connective tissue
  6. Place an encircling suture (absorbable) at the proximal and distal site of the vein. The segment in between the two sutures is the venotomy site.
  7. Insert the catheter into the vein. Use the encircling suture to facilitate catheter insertion.
  8. Tie the proximal suture to secure the catheter. Remove the distal suture.
  9. Close the skin with simple interrupted or cruciate suture pattern (absorbable). Bandage the catheter.
67
Q

When you get blood sample from IO catheter. What values may not be very accurate and require careful interpretation?

A

Potassium
Glucose

68
Q

What are the contraindication for IO catheter placement?

A

Fractured bone
Bones with osteomyelitis or skin infection at the insertion
Bones where catheterization has been attempted

69
Q

What are the common IO catheter sites in dogs and cats?

A
  • Flat medial surface of proximal tibia (1-2 cm distal to the tibial tuberosity) or tibial tuberosity
  • Trochanteric fossa of the femur
  • Ilium wing
  • Greater tubercle of the humerus
70
Q

What are the possible complications for IO catheter?

A

Osteomyelitis
Fluid extravasation
Growth plate injury (tibia)
Sciatic nerve injury (femur)
Compartment syndrome
Fat embolism

71
Q

Describe Seldinger technique for CVC placement

A

1) Place the patient in lateral recumbency (or dorsal recumbency). Put a rolled towel under the neck to help with the positioning
2) Clip and aseptically prepare the jugular vein CVC insertion site
3) Inject lidocaine subcutaneously at the CVC insertion site
4) Put on sterile gloves. Make a small skin incision at the CVC insertion site.
5) Identify the jugular vein and insert an over-the-needle catheter. When the blood is observed in the hub, gently advance both the catheter and the stylet for about 1mm. Insert the catheter and remove the stylet.
6) Pre-measure the length from the catheter insertion site to 3-4 intercostal space (this is how deep the guide-wire should be or shouldn’t pass beyond). Insert the guide-wire into the catheter.
7) Remove the catheter while keep the guide-wire at the same place.
8) Insert the dilator over the guide-wire into the jugular vein and keep it there for several seconds. Remove the dilator.
9) Insert the CVC over the guide-wire into the jugular vein until the pre-measured length is achieved. Make sure the guide-wire end is coming out of the CVC port and is grasped and secured before advancing the CVC. Remove the guide-wire after the CVC is in place.
10) Aspirate from all the ports of the CVC. Blood should be flowing very smoothly. Flush the catheter and port with heparinized saline and put on caps.
11) Secure the CVC with suture and place a bandage on the insertion site.

72
Q

Where are the common site for arterial catheter placement

A

Dorsal pedal artery
Coccygeal artery
Femoral artery
Auricular artery
Radial artery
Sublingual artery (not ideal)

73
Q

What is the landmark for jugular catheter placement?

A

Keep the head in neutral position. Draw a line between the angle of mandible and the thoracic inlet. The jugular catheter should lie along there.

74
Q

Describe three syringe technique.

A

It is often used to draw blood sample from an arterial catheter.

1) Prepare three 3ml syringe. One contains 0.5ml heparinized saline. One is empty. One contains 2-3ml heparinized saline.
2) Use the 0.5ml heparinized saline syringe to flush the arterial catheter, then pull 3 ml of blood with the same saline. Keep it aseptically.
3) Use the empty syringe to pull the amount of blood sample needed.
4) Flush 2-3ml of heparinized saline into the arterial catheter with the third syringe. Return the blood mixed with heparinized saline in the first syringe back to the patient through a peripheral IV catheter.

75
Q

How does D-lactate formed?

A

1) glyoxalase pathway
2) produced by commensal bacteria in mammalian GI tract

76
Q

Which step of glycolysis is the rate-limiting step?

A

Conversion from Fructose 6-Phosphate to Fructose 1,6-biphosphate by Phosphofructokinase

77
Q

How many ATP does each glucose produce under aerobic metabolism?

A

38 ATPs

78
Q

Describe the aerobic metabolism and lactate formation.

A
79
Q

How is lactate transported across cell membrane?

A

Via proton-linked or sodium-coupled monocarboxylate transporters (MCTs)

80
Q

How does catecholamine cause hyperlactatemia?

A

Catecholamine activates 𝜷2 adrenergic receptor → increase cAMP production → increase glycogenolysis, glycolysis, lipolysis and stimulate Na-K ATPase pump

  • Na-K ATPase can increase lactate production (by generating ADP and stimulate PFK)
81
Q

How dose cyanide cause mitochondrial dysfunction?

A

Cyanide inhibits aerobic metabolism by noncompetitively inhibiting ferric iron in cytochrome c oxidase (complex IV), the final step in the electron transport chain

82
Q

How does glucocorticoid cause hyperlactatemia?

A

1) potentiates catecholamine’s effect
2) increase protein metabolism and produce more pyruvate
3) inhibit pyruvate dehydrogenase
4) alter carbohydrate metabolism

83
Q

How does Ethylene glycol cause hyperlactatemia

A

Increase NADH/NAD+ ratio and inhibit pyruvate metabolism

84
Q

What are the dynamic and static variables when we evaluate fluid responsiveness?

A

Static:
- MAP
- Inferior caudal vena cava diameter
- CVP
- Left ventricle end-diastolic area (LVEDA)
- Shock index
- HR

Dynamic:
- Pulse Pressure Variability
- Stroke Volume Variability
- Plethysmographic Variability Index
- Caudal Vena Cava Collapsibility Index

85
Q

What are the four patterns of shock in the “2014 Consensus on circulatory shock and hemodynamic
monitoring. Task force of the European Society of Intensive Care Medicine” ?

A

Hypovolemic
Cardiogenic
Obstructive
Distributive

86
Q

True or False: In the “2014 Consensus on circulatory shock and hemodynamic
monitoring. Task force of the European Society of Intensive Care Medicine,” arterial hypotension (SAP < 90mmHg, MAP < 65mmHg) is one of the diagnostic criteria for shock.

A

False

Statement:
We recommend that the presence of arterial hypotension (defined as systolic blood pressure of <90 mmHg, or MAP of <65 mmHg, or decrease of ≥40 mmHg from baseline), while commonly present, should not be required to define shock

87
Q

What is the bloody viscous cycle mentioned in the review about hemorrhagic shock published by Cannon JW in 2018 NEJM?

A

Acidosis
Hypothermia
Coagulopathy

88
Q

What are the principles of damage-control resuscitation in the Hemorrhagic Shock review paper in 2018 NEJM?

A
  1. Avoid or correct hypothermia
  2. Stop the bleeding by applying direct pressure, tourniquets or hemostatic dressings
  3. Delay fluid administration in certain patients until complete hemostasis is achieved (e.g. those with penetrating trauma to the torso and short prehospital transport times)
  4. Limit crystalloid administration (< 3L in 6 hours)
  5. Use a massive-transfusion protocol
  6. Avoid delays in definitive surgical, endoscopic, or angiographic hemostasis
  7. Try to keep a balance between pRBC, plasma and platelet transfusion to optimize hemostasis
  8. Do coagulation tests to guide the transfusion therapy
  9. Consider using some medications to reverse anticoagulant or treat coagulopathy

basically still around avoid hypothermia, acidosis (from fluid), and coagulopathy!

89
Q

Explain three-stage reduction of oxygen, Fenton/Haber-Weiss reaction, myeloperoxidase reaction and reactive nitrogen species formation.

A
90
Q

What is Fe2+ and Fe3+ called, respectively?

A

Fe2+ : ferrous
Fe3+ : ferric

91
Q

What type of lipid molecules are the major target to oxidative injury?

A

Polyunsaturated fatty acid is main target for lipid peroxidation

92
Q

Which two amino acids are most susceptible to oxidative injury?

A

Cysteine
Methionine

93
Q

What are the common reactive oxygen species and reactive nitrogen species?

A

Superoxide anion (O-2)
Hydrogen peroxide (H2O2)
Hydroxyl anion (-OH)
Hydroxyl free radical (OH)
Hypochlorous acid (HOCl)
Peroxynitrite (ONO2-)

94
Q

Which system is heavily involved in the ischemic-reperfusion injury?

A

Xanthine oxidoreductase sytem

95
Q

Where have high number of xanthine oxidase and are highly susceptible to IRI?

A

GI system
Endothelium

96
Q

Explain IRI including how xanthine oxidoreductase system participates in the pathogenesis of it.

A

When the body experiences ischemia injury, the ATP will be degraded to ADP, adenosine, inosine and then hypoxanthine. There will also be increased lactate and hydrogen ion intracellularly. The Na-K ATPase is dysfuncitonal, which leads to inflow of Na, Cl and Ca, which cause cell swelling and death. High intracellular Ca will activate calpain and convert xanthine dehydrogenase to xanthine oxidase.
When the oxygen is reintroduced to the tissue. The accumulated xanthine oxidase is activated and hypoxanthine will be transformed to urine acid with NADH and production of ROS (e.g. syperoxide anion, H2O2…etc). The reperfusion injury usually happens 10-30 sec after O2 is introduced.

97
Q

What is “no flow” phenomenon?

A

During ischemic phase, NO depletion can cause vasoconstriction and decreased tissue perfusion. When the ischemic phase is resolve and the occlusion being resolved, there can still be decreased blood flow and perfusion due to leukocyte adhesion, platelet-leukocyte aggregration and microvascular thrombosis, and decreased endothelium-dependent vasorelaxation.

98
Q

What is the formula for lactate clearance?

A

Lactate clearance = (Lactate T0 - Lactate T1)/Lactate T0 x 100

99
Q

What are the three categories of antioxidant and what are the examples?

A

1) Endogenous enzymatic antioxidant: superoxide dismutase (SOD), glutathione peroxidase, catalase

2) Endogenous non-enzymatic antioxidant: glutathione, albumin, ferritin, transferrin, haptoglobin, bilirubin, uric acid, coenzyme Q, vitamin C, vitamin E, selenium, melatonin

3) Exogenous antioxidant: vitamin E, vitamin C, selenium, phenolics, zinc, acetylcysteine

100
Q

What is pulse pressure?

A

Pulse pressure = SAP - DAP

101
Q

What is the formula for pulse pressure variation? What is the cutoff for fluid responsive?

A

PPV = [(PPMax - PPmin)/(PPMax+PPmin)/2] x 100%

> 10-15% is considered fluid responsive

  • Patient needs to be on mechanical ventilation
  • Inspiration → PPMax
  • Expiration → PPmin
102
Q

What is the formula for caudal vena cava collapsibility index? What is the cutoff for fluid responsive?

A

(CVCMax - CVCmin)/CVCMax x 100%

> 30% is considered fluid responsive

103
Q

How much percentage of PCV can splenic contraction provide in hemorrhagic shock canine model?

A

about 20%

104
Q

What is the definition of massive hemorrhage?

A

Loss of more than one total body blood volume within 24 hours

Lost of more than 50% of total body blood volume within 3 hours

105
Q

What are the windows to measure caudal vena cava diameters?

A

Hepatic view: the transducer was placed parallel to the ribs (transverse to the CVC and aorta) at the 10th-12th right intercostal space approximately just below the epaxial muscles in the upper third of the thorax.

Subxiphoid view
Paralumbar view

106
Q

Write down SOFA score. What is the total score number? Is the higher score better or worse?

A

Total score: 6 organ systems x 4 (max) = 24
The higher score the worse

107
Q

Write down Modified Glasgow Coma Score. What are the three main categories? What is the total score number? Is the higher score better or worse?

A

Three categories: motor activities, brainstem reflexes, level of consciousness

Total score number: 3 categories x 6 (max) = 18

The higher score the better

108
Q

What are the maximal score number for dogs and cats Acute Patient Physiologic and Laboratory Evaluation (APPLE) score? What about APPLE fast score?

A

80

50

109
Q

Is the higher APPLE score better or worse

A

The higher score the worse

110
Q

What are the five components for APPLE fast score for dogs? What about cats?

A

Dog: glucose, lactate, albumin, platelet count, mentation

Cat: mentation, temperature, MAP, lactate, PCV

111
Q

Describe Animal Trauma Triage (ATT) Score.

A

Total score: 6 organ systems x 3 = 18
The higher the score the worse

Each point increase in the ATT score resulted in a 2.3–2.6 times decreased likelihood of survival

112
Q

What are the three principle mechanisms of syncope?

A

1) Primary cardiac disease
- arrhythmias, structural hear disease

2) Reflex-mediated bradycardia & hypotension
- Vasovagal reflex, PH?

3) Decreased venous return due to blood loss or redistribution of blood (i.e. Orthostatic hypotension)
- Drug induced vasodilation, hypovolemia

113
Q

Describe Bezold–Jarisch reflex (BJR).

A

An initial drop in blood pressure due to a “perceived” hypovolemia (exacerbated in dehydrated patients) is sensed in the carotid sinus baroreceptors, resulting in augmented activity of efferent sympathetic fibers which leads to increased heart rate, contractility, and vasoconstriction. The strong contraction of the “underfilled” ven- tricle stimulates mechanoreceptors in the wall, sending impulses via afferent C-fibers to the medulla oblongata, resulting in a sudden withdrawal of sympathetic tone and simultaneous increased vagal tone. This triggers a paradoxical bradycardia and decreased contractility, resulting in a relatively sudden decrease in arterial blood pressure and syncope.

Clinically: bradycardia, hypotension

114
Q

As HES solution generations develop, does the average molecular weight decrease or increase?

A

Decrease

115
Q

What is the normal renal threshold for HES?

A

45-60 kDa

116
Q

True or False: HES with higher molar substitution has longer half-life.

A

True

117
Q

What is COP for VetStarch?

A

36 mmHg

118
Q

Of all the characteristics in HES, which two determine the pharmacokinetics of HES?

A

Molar substitution (the higher, the longer half-life)
C2/C6 ratio (the higher, the slower the breakdown)

119
Q

What is the typical HES dose for dogs and cats?

A

Dogs: 5-20 ml/kg
Cats: 2-10 ml/kg

Daily dose: 20-30 ml/kg/d

120
Q

In a VetCOT registry study published in 2021 about the development of veterinary trauma score (VetCOT) in canine trauma patient, what are the 4 variables included in the final model. What was its correlation with ATT score?

A

Plasma lactate and ionized calcium within 6 h of admission
Presence of head trauma
Presence of spinal trauma

Good and comparable performance when compared to ATT score (AUROC = 0.87)

Cutoff at 0.5 → Sensitivity 28.97%, Specificity 97.95%

121
Q

List Kirby’s Rule of 20

A

1) Fluid balance
2) Oxygen & ventilation
3) Blood pressure
4) Heart rate, contractility, rhythm
5) Glucose
6) Body temperature
7) Albumin
8) Electrolytes
9) Mentation
10) RBC & hemoglobins
11) GI motility and integrity
12) Nutrition
13) Renal function
14) Coagulation
15) Immune status, antibiotics
16) Drug dosage & metabolism
17) Wound care & Bandage
18) Pain control
19) Nursing care
20) Tender, love, care

122
Q

Name the 5 views of TFAST.

A

Chest tube views bilaterally (7-9 intercostal spaces)
Pericardial views bilaterally (5-6 interconstal spaces)
Subxiphoid view

123
Q

On POCUS, what is A line?

A

A-lines are a result of reverberation artifact as the ultrasound waves reflect off the soft tissue–air interface at the level of the pleural line (which causes the pleural line to be replicated in the sonographic far field)

124
Q

True or False: A lines are absent in patients with pneumothorax.

A

False

A-lines may be seen in patients with and without pneumothorax

125
Q

In POCUS, what is lung point?

A

The point at which the glide sign returns. It is used to evaluate the size of pneumothorax.

126
Q

What is the optimal hematocrit value for oxygen transport?

A

27 - 33%

127
Q

What are the contents in LRS, Normosol-R and 0.9% NaCl?

A
128
Q

How does thiamine affect lactate production?

A

Thiamine is an important coenzyme for pyruvate dehydrogenase. Thiamine deficiency limits the function of pyruvate dehydrogenase, and pyruvate will be diverted toward lactate production.

129
Q

What is normal lactate:pyruvate ratio?

A

10:1

130
Q

Normally, the critical oxygen extraction ratio is ____. During sepsis, the critical oxygen extraction ratio can __________ (increase vs reduce).

A

70%

Reduce (to 50%)

131
Q

When estimating blood loss, average adult human fist covers a surface area equivalent to approximately _____ml.

A

20

132
Q

How many ml of blood can the following sponges carry (when they are saturated)?
3 x 3
4 x 4
Lap sponge

A

3 x 3: 3.25 ± 1.25 mL
4 x 4: 10 ± 2 mL
Lap sponge: 150 mL

133
Q

What is death diamond composed of?

A

Acidosis
Hypothermia
Coagulopathy
Hypocalcemia

134
Q

Cellular shock - pathogenesis

A
  1. altered pH
    ATP hydrolysis produces H+ that can’t be shifted into the elctron chain
    usually shifted out of the cell with lactate via MCT co-transporter but in shock overwhelmed so intracellular acidosis.
    Also CO2 still produced by remaining oxydative metabolism.
    Ultimately low intracellular pH = enzymes dysfunction
  2. deranged ion flux
    without ATP Na/K pump dysfunctional = increase Na intracellularly = swelling and depolarization with opening of Ca++ channels = apoptosis and mitochondrial damage
  3. IRI and Fenton reaction with intracellular storage of Fe++ and copper
  4. adenosine release
    from ATP metabolism
    produced in large amount so leaking out of the cell
    acts as a messenger acting on A1 (Gi) causing bradycardia and on A2 (Gs) causing vasodilation
    Also further reactions extracellularly forming urate which can’t be re-transported back into the cell + washed out by RBCs and blood flow –> lack of substrate to re-synthetise ATP once shock reversed
  5. gene expression
    adaptive response with HIF-1, Glut-1 and iron transport molecules synthesis
135
Q

List two main causes of endothelial dysfuction in hemorrhagic shock

A
  • endothelial glycocalix damage
  • intercellular tight junctions dysruption (VE-Cadherin:VE-PTP interaction)
136
Q

Syndecans and HA are exclusive of glycocalix

A

False

HA is also present in the interstitium
SYN is also present on leukocytes

Important to considered when used as biomarkers

137
Q

What does the current human evidence indicate between a liberal vs restrictive IVFT approach?

A

No difference in mortality between the two strategies. However moderate IVFT (4L/day) has been shown to significantly decrease mortality in septic patients.

In short avoid giving less than 2L/day or more than 5L/day in septic patients.

  • only exception is in septic patients with CKD (CLOVER reanalysis) in which restrictive approach gave a survival benefit
138
Q

List 5 macro/systemic perfusion parameters

A
  1. CO
  2. BP
  3. Lactate
    Limitations: hyperlactatemia B and long half-life
  4. Central and mixed venous oxygen saturation
    Influenced by many parameters
    Decreases during tissue perfusion disorders
    Can be elevated despite low tissue perfusion (i.e. cryptic shock)
  5. ΔPCO2 = venous PCO2 – arterial PCO2
    Increased in hypoperfusion due to the accumulation of CO2 on the venous side
139
Q

Name 4 microcirculatory/regional perfusion parameters

A
  1. Skin temperature
  2. Difference between tissue and arterial CO₂
  3. Photoplethysmography (perfusion index = pulsitile component (stroke volume) / nonpulsitile component (vascular tone))
  4. Microscopic visualization of microcirculation
140
Q

Define loss of hemodynamic coherence and list two examples

A

Discrepancy between the status of the micro vs macro circulation.
Typical of sepsis and traumatic hemorrhagic shock (SIRS/coagulopathy)

141
Q

Optimal Hb level in TBI and why

A

7-9 g/dL

In a normal brain anaemia up until 6g/dL can be compensated by vasodilation, but in injured brain max vasodilation is achieved at 8-9g/dL

Also important to avoid high Hb level due to increased viscosity

ECVECC Board Exam (24 decks)

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