Fluid Therapy & Shock Flashcards

(76 cards)

1
Q

Examples of Synthetic Colloid Solutions

A

VetStarch

Hetastarch

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2
Q

What is a Colloid Solution (Properties)

A

Contains large molecular substances which do not readily cross capillary membranes => remains in the intravascular space

Increases colloid oncotic pressure; draws water into IV space (helps with hypoproteinemia cases)

Increases total blood volume

Long lasting effect

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3
Q

Shock bolus (Isotonic)
Canine
Feline

A

Canine: 90 mL/kg

Feline: 40-60 mL/kg

Comes from blood volume

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4
Q

Maintenance rate
Canine
Feline

A

Canine: 60 mL/kg/day

Feline: 50 mL/kg/day

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5
Q

Examples of Natural Colloid Solutions

A

Plasma

Albumin (only human and canine available)

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6
Q

Examples of Oxygen Carrying Colloid Solutions

A

Whole blood

PRBCs

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7
Q

Synthetic Colloids: effect on IV volume

A

Will increase IV volume by more than the volume infused

Example: give I L VetStarch, IV space will pull 370 mL fluid from interstitial space
IV space volume: 1,370 mL

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8
Q

Why use Colloids?

A

Improve intravascular volume (treat hypovolemia and/or hypotension)

Maintain intravascular colloid oncotic pressure (usually due to hypoproteinemia) – minimize tissue edema

Do NOT give in a dehydrated patient

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9
Q

VetStarch and Hetastarch:

Physiochemical properties-structure

A

Hydroxyethyl Starch; similar to glycogen (less likely to have adverse reaction)

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10
Q

VetStarch and Hetastarch:

Elimination half-life determined by:

A

Molar substitution (how many hydroxyl groups are replaced by hydroxyethyl groups)

Substitution C2:C6 ratio (higher the ratio the longer the molecule stays in IV space)

Molecular weight (larger the molecule the longer it stays in the IV space)

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11
Q

Hydroxyehtyl Starch Solutions:

Adverse effect

A

Coagulopathy
Depends on:
Molecular weight
Molar substitution (how many hydroxyl groups have been substituted with hydroxyethyl groups; the more substitutions the more likely patient will become hypocoaguable)

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12
Q

Hetastarch (HES 450/0.7)

Properties

A

Mean MW: 450 kDa
Molar Substitution: 0.7 (70% substituted with hydroxyethyl group)
C2:C6 ratio 5:1
Volume Expansion: >100%
Duration: 24-36 hours (even with a bolus)

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13
Q

Hetastarch (HES 450/0.7)

Side Effects

A

Allergic reactions (vomiting)

Coagulopathies:
Dilutes clotting factors
Inhibits platelet function (less sticky)
Decrease fibrin clot stabilization
Decrease activity of factor VIII & vonWill factor
Accelerates fibrinolysis
Clot may form but is weak

Potentially renal failure

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14
Q

What part of the coagulation cascade is factor VIII & vonWill a part of?

A

Intrinsic pathway: APTT

Hetastarch will elevate APTT (slight is okay)

When APTT increases 1.5-2x then more likely to hemorrhage

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15
Q

Hetastarch (HES 450/0.7)

Recommended dosage

A

Canine: 20 mL/kg/day

Feline: 10-20 mL/kg/day

Can always be less

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16
Q

Hetastarch (HES 450/0.7)

Administration

A

Bolus (shock)
Canine: 5 mL/kg
Feline: 2.5-5 mL/kg

CRI (in hypoproteinemia cases)

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17
Q

VetStarch (HES 130/0.4)

Properties

A

Mean MW: 130 kDa
Molar Substitution: 0.4 (40% substituted with hydroxyethyl group)
C2:C6 ratio 9:1 (high; if lower than would get eliminated quickly)
Volume expansion: >100%
Duration: 4-6 hours

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18
Q

VetStarch (HES 130/0.4)

Side Effects

A

Allergic reactions

Coagulopathies (less likely than Hetastarch)
Dilution of clotting factors
Less effect on factor VIII and vonWill factor

Renal failure less likely due to smaller MW

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19
Q

VetStarch (HES 130/0.4)

Recommended dosage

A

Canine: 20-50 mL/kg/day

Feline: 10-20 mL/kg/day

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20
Q

VetStarch (HES 130/0.4)

Administration

A

Bolus (shock)
Canine: 5 mL/kg
Feline: 2.5-5 mL/kg

CRI (24 hour)

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21
Q

Plasma

What is it?

A

Obatained after RBCs have been removed from whole blood

Provides:
Protein (albumin, globulin, fibrinogen)
Coagulation factors and antithrombin
Immunoglobulins (may be helpful in immunocompromised patients; parvo and panleuk)

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22
Q

Plasma

Disease sate that contraindicates

A

IMHA
Patients are anemic however blood volume is normal
Safer to administer RBCs otherwise make them hypercoaguable

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23
Q

Plasma

Properties

A

MW: 66 to 60 kDa

Oncotic properties:
Increases plasma volume by the volume administered (no pull of extra fluid into IV space)

Carrier for hormones, enzymes, drugs

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24
Q

Why use plasma?

A
DIC
Vitamin K deficiency
Congenital clotting factor deficiency
Coagulation disorders from liver disease
Immunodeficiency syndromes 
Low total protein (<4.0 gm/dL)

Does NOT help with hypoalbuminemia (do so through nutrition)

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25
Plasma | Recommended dosage
10-20 mL/kg 10 mL/kg: increase coagulation factors by 20% 20 mL/kg will increase total protein by 1 g/dL Note: the higher the PT and APTT the more plasma needed
26
If a patient needs platelets what should be administered?
Fresh whole blood for greatest improvement
27
Plasma | Side Effects
Allergic/hypersensitivity (Type and Cross-Match) Fluid overload Infectious diseases
28
Packed Red Blood Cells Administration Dosage
Administration: Give in anemic patients with normal protein concentrations and coagulation status Dosage: 1.5 mL/kg of PRBCs will raise PCV by 1% Note: do NOT have to raise the PCV to 45% should be <25% to decrease clincal signs of anemia
29
How much will the PCV increase in a 30 kg dog given 1 unit of PRBCs (255 mL)
5% 1.5 mL/kg * 30 kg = 45 mL 255 mL/ 45 mL = 5.6666
30
Fresh or Stored Whole Blood When to use it Dosage
When to use it: Anemia with hypoproteinemia and/or coagulopathy (factor or platelet deficiency) Dosage: 2.2 mL/kg of whole blood raises the PCV by 1%
31
What is hypovolemic shock?
Most common! Inadequate circulating blood volume; overall fluid loss Patients have systemic vasodilation Does not respond to intrinsic catacholamines (trying to cause vasoconstriction)
32
What is distributive shock?
Maldistribution of blood flow and volume; inappropriate vasodilation, relative hypovolemia Increased vessel permeability Decreased CO due to cytokines Activation of coagulation system
33
What is obstructive shock?
Extracardiac obstruction of blood flow; low CO Need to increase cardiac output
34
What is cardiogenic shock?
Primary pump failure (often have bradycardia); decreased CO Do NOT administer fluids Exception: cardiac tamponade; more of an obstructive shock, pericardial sack is filled with fluid (right sided issue; give fluids to help fill R ventricle)
35
Clinical Signs of Shock
``` Hypotension Tachycardia Poor pulse quality Prolonged CRT Pale mucous membranes Hypothermia Tachypnea ```
36
What type of fluids do you avoid giving to a patient in shock?
Hypotonic crystalloids; does not support IV expansion
37
What increases microvascular permeability?
Immune mediated diseases Sepsis Vasculitis Anaphylaxsis
38
When should you administer colloids over crystalloids in a shock patient?
Hypovolemic, Distributive, or Obstructive shock Increased microvascular permeability Decreased COP
39
When should you administer crystalloids and colloids to a shock patient?
Hypovolemic, Distributive, or Obstructive shock Increased microvascular permeability with normal COP Normal microvascular permeability with decreased COP
40
Three main things to consider when treating a hemorrhage shock patient
1. External? Internal? 2. Fluid therapy: aggressive in external hemorrhage patients, volume-limited in internal hemorrhage pateints 3. Values: External; achieve normal Internal; achieve subnormal
41
Internal hemorrhage patients approach (management)
Stabilize Best to medically manage these patients, may not require surgery at all Values: BP: do NOT exceed 100 mmHg Produce urine Lactate normalize
42
Nontraumatic Hypovolemic Shock Fluid Deficit
Intravascular (Interstitial/Intracellular)
43
Nontraumatic Hypovolemic Shock Pathophysiology
Decreased blood volume with concurrent dehydration
44
Nontraumatic Hypovolemic Shock Microvascular Permeability
Normal
45
Nontraumatic Hypovolemic Shock Plasma Oncotic Pressure
Normal
46
Isotonic crystalloids What do they do (2 things) 1 Adverse response
Expand IV compartment Rehydrate the ISF compartment Adverse response: May worsen interstitial edema or third space loss
47
Traumatic Hypovolemic Shock Fluid Deficit
Intravascular
48
Traumatic Hypovolemic Shock Pathophysiology
Decrease blood volume
49
Traumatic Hypovolemic Shock Microvascular Permeability
Normal to increased Increased: use colloids (b/c of large MW)
50
Traumatic Hypovolemic Shock Plasma Oncotic Pressure
Normal to decreased Decreased: use colloids
51
When would you use hypertonic crystalloids?
Traumatic hypovolemic shock potentially Augments IV compartment Beneficial in treating head trauma by reducing ICP
52
Septic Shock | Fluid Deficit
IV (relative depletion)
53
Septic Shock | Pathophysiology
Maldistribution of blood flow
54
Septic Shock | Microvascular Permeability
Increases
55
Septic Shock | Plasma Oncotic Pressure
Decreases
56
What is shock? | Main goal of treatment?
Shock is the inadequate delivery of oxygen to your tissues Main goal: improve patient's perfusion
57
Can a patient be in shock and have normal blood pressure?
Yes
58
Compensated Shock
Tachycardia with poor perfusion Patient compensates for low cardiac output with tachycardia and increase in systemic vascular resistance
59
Decompensated Shock
Frank hypotension Early organ dysfunction changes Azotemia, oliguria/anuria, hyperbilirubinemia, and DIC Difficult to bounce back from
60
Compensatory Shock in the Dog
Manifest as hyperdynamic and hypermetabolic response (brick red mucous membranes) Tachycardia, tachypnea, hyperemia, decreased CRT and pyrexia
61
Compensatory Shock in the Cat
Often already headed to decompensated shock Lethargic, bradycardic, hypothermic, hypotensive, pale mm, weak pulses
62
Cardiogenic Shock: Causes
``` Pump failure (CHF) Arrhythmias Decreased contractility (DCM) Ventricular outflow obstruction (SAS) Acute valvular failure (endocardiosis) ```
63
Cardiogenic Shock: | Pathophysiology
Body wants to regulate BP (maintain perfusion) Systolic/diastolic dysfunction (increase HR, decrease SV and therefore CO) Decrease perfusion to tissues (decreased BP and increased peripheral vascular resistance) - compensatory systems max out Pulmonary edema; increased pulmonary venous pressure
64
Lidocaine dosage for ventricular tachycardia
2 mg/kg | 1 mL/10 kg
65
Drugs that you can use 1 mL/10 kg dose
Lidocaine Atropine Epinephrine Diazipam/Valium
66
Causes of Obstructive Shock
``` Causes: Physical blockage to venous return GDV (stomach pushes on caudal vena cava; decreases venous return) Pulmonary thromboembolism Tension pneumothorax Cardiac tamponade ```
67
Obstructive Shock: Pathophysiology
Blockage of venous return -> decrease stroke volume -> decrease CO -> decrease perfusion of tissue -> shock
68
Causes of Hypovolemic Shock
Causes: Hemorrhage Severe dehydration (GI loss, burns)
69
Hypovolemic Shock: | Pathophysiology
Decreased effective circulating volume: Blood loss or other body fluid loss (PU/PD, burns, vomiting, diarrhea) Decreased CO: Decrease venous return and SV Decreased perfusion: Decrease blood delivery to tissues
70
Abdominocentesis | Spleen or free fluid?
Spleen: the sample will clot Free fluid: abdomen or thorax the fluid will not clot
71
What decreases first: PCV or TP? Why?
TP will because of splenic contraction
72
Distributive Shock Causes
Anaphylaxis Sepsis Heart worm disease Saddle thrombosis Cold or hot extremities (depends on cause; sepsis will be hot)
73
Vasopressors and what they are used for
Norepinephrine: septic shock Dopmaine: inotrope (causes contraction and vasoconstriction) Vasopressin: no effects on heart just peripheral vasoconstriction Dobutamine (inotrope): cardiogenic shock
74
Can a patient have more than one type of shock?
Yes! Just figure out which one is primary
75
What is COHDe?
Cardiogenic Obstructive Hypovolemic Distributive
76
Blood flow during cold shock
Blood flow goes to non-vital organs (skin, GI) opposed to vital organs (heart, kidney, brain)