Fluid Therapy & Shock Flashcards
Examples of Synthetic Colloid Solutions
VetStarch
Hetastarch
What is a Colloid Solution (Properties)
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
Shock bolus (Isotonic)
Canine
Feline
Canine: 90 mL/kg
Feline: 40-60 mL/kg
Comes from blood volume
Maintenance rate
Canine
Feline
Canine: 60 mL/kg/day
Feline: 50 mL/kg/day
Examples of Natural Colloid Solutions
Plasma
Albumin (only human and canine available)
Examples of Oxygen Carrying Colloid Solutions
Whole blood
PRBCs
Synthetic Colloids: effect on IV volume
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
Why use Colloids?
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
VetStarch and Hetastarch:
Physiochemical properties-structure
Hydroxyethyl Starch; similar to glycogen (less likely to have adverse reaction)
VetStarch and Hetastarch:
Elimination half-life determined by:
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)
Hydroxyehtyl Starch Solutions:
Adverse effect
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)
Hetastarch (HES 450/0.7)
Properties
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)
Hetastarch (HES 450/0.7)
Side Effects
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
What part of the coagulation cascade is factor VIII & vonWill a part of?
Intrinsic pathway: APTT
Hetastarch will elevate APTT (slight is okay)
When APTT increases 1.5-2x then more likely to hemorrhage
Hetastarch (HES 450/0.7)
Recommended dosage
Canine: 20 mL/kg/day
Feline: 10-20 mL/kg/day
Can always be less
Hetastarch (HES 450/0.7)
Administration
Bolus (shock)
Canine: 5 mL/kg
Feline: 2.5-5 mL/kg
CRI (in hypoproteinemia cases)
VetStarch (HES 130/0.4)
Properties
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
VetStarch (HES 130/0.4)
Side Effects
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
VetStarch (HES 130/0.4)
Recommended dosage
Canine: 20-50 mL/kg/day
Feline: 10-20 mL/kg/day
VetStarch (HES 130/0.4)
Administration
Bolus (shock)
Canine: 5 mL/kg
Feline: 2.5-5 mL/kg
CRI (24 hour)
Plasma
What is it?
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)
Plasma
Disease sate that contraindicates
IMHA
Patients are anemic however blood volume is normal
Safer to administer RBCs otherwise make them hypercoaguable
Plasma
Properties
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
Why use plasma?
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)
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
If a patient needs platelets what should be administered?
Fresh whole blood for greatest improvement
Plasma
Side Effects
Allergic/hypersensitivity (Type and Cross-Match)
Fluid overload
Infectious diseases
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
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
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%
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)
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
What is obstructive shock?
Extracardiac obstruction of blood flow; low CO
Need to increase cardiac output
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)
Clinical Signs of Shock
Hypotension Tachycardia Poor pulse quality Prolonged CRT Pale mucous membranes Hypothermia Tachypnea
What type of fluids do you avoid giving to a patient in shock?
Hypotonic crystalloids; does not support IV expansion
What increases microvascular permeability?
Immune mediated diseases
Sepsis
Vasculitis
Anaphylaxsis
When should you administer colloids over crystalloids in a shock patient?
Hypovolemic, Distributive, or Obstructive shock
Increased microvascular permeability
Decreased COP
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
Three main things to consider when treating a hemorrhage shock patient
- External? Internal?
- Fluid therapy: aggressive in external hemorrhage patients, volume-limited in internal hemorrhage pateints
- Values:
External; achieve normal
Internal; achieve subnormal
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
Nontraumatic Hypovolemic Shock Fluid Deficit
Intravascular (Interstitial/Intracellular)
Nontraumatic Hypovolemic Shock Pathophysiology
Decreased blood volume with concurrent dehydration
Nontraumatic Hypovolemic Shock Microvascular Permeability
Normal
Nontraumatic Hypovolemic Shock Plasma Oncotic Pressure
Normal
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
Traumatic Hypovolemic Shock Fluid Deficit
Intravascular
Traumatic Hypovolemic Shock Pathophysiology
Decrease blood volume
Traumatic Hypovolemic Shock Microvascular Permeability
Normal to increased
Increased: use colloids (b/c of large MW)
Traumatic Hypovolemic Shock Plasma Oncotic Pressure
Normal to decreased
Decreased: use colloids
When would you use hypertonic crystalloids?
Traumatic hypovolemic shock potentially
Augments IV compartment
Beneficial in treating head trauma by reducing ICP
Septic Shock
Fluid Deficit
IV (relative depletion)
Septic Shock
Pathophysiology
Maldistribution of blood flow
Septic Shock
Microvascular Permeability
Increases
Septic Shock
Plasma Oncotic Pressure
Decreases
What is shock?
Main goal of treatment?
Shock is the inadequate delivery of oxygen to your tissues
Main goal: improve patient’s perfusion
Can a patient be in shock and have normal blood pressure?
Yes
Compensated Shock
Tachycardia with poor perfusion
Patient compensates for low cardiac output with tachycardia and increase in systemic vascular resistance
Decompensated Shock
Frank hypotension
Early organ dysfunction changes
Azotemia, oliguria/anuria, hyperbilirubinemia, and DIC
Difficult to bounce back from
Compensatory Shock in the Dog
Manifest as hyperdynamic and hypermetabolic response (brick red mucous membranes)
Tachycardia, tachypnea, hyperemia, decreased CRT and pyrexia
Compensatory Shock in the Cat
Often already headed to decompensated shock
Lethargic, bradycardic, hypothermic, hypotensive, pale mm, weak pulses
Cardiogenic Shock: Causes
Pump failure (CHF) Arrhythmias Decreased contractility (DCM) Ventricular outflow obstruction (SAS) Acute valvular failure (endocardiosis)
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
Lidocaine dosage for ventricular tachycardia
2 mg/kg
1 mL/10 kg
Drugs that you can use 1 mL/10 kg dose
Lidocaine
Atropine
Epinephrine
Diazipam/Valium
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
Obstructive Shock: Pathophysiology
Blockage of venous return -> decrease stroke volume -> decrease CO -> decrease perfusion of tissue -> shock
Causes of Hypovolemic Shock
Causes:
Hemorrhage
Severe dehydration (GI loss, burns)
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
Abdominocentesis
Spleen or free fluid?
Spleen: the sample will clot
Free fluid: abdomen or thorax the fluid will not clot
What decreases first: PCV or TP? Why?
TP will because of splenic contraction
Distributive Shock Causes
Anaphylaxis
Sepsis
Heart worm disease
Saddle thrombosis
Cold or hot extremities (depends on cause; sepsis will be hot)
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
Can a patient have more than one type of shock?
Yes!
Just figure out which one is primary
What is COHDe?
Cardiogenic
Obstructive
Hypovolemic
Distributive
Blood flow during cold shock
Blood flow goes to non-vital organs (skin, GI) opposed to vital organs (heart, kidney, brain)
