Fluid Therapy Risks and Physiology

• Fluid therapy can be risky due to fluid overload
• A >10% increase in body weight indicates potential fluid overload
• Fluids dilute out important components like protein and RBCs
• Excess fluid can cause complications like pulmonary edema, gut edema, and tissue edema

Fluid Physiology

• Total body water is 60% of body weight
• Intracellular fluid accounts for 40% of body water
• Extracellular fluid makes up 20% of body water, with 15% interstitial fluid and 5% plasma
• Fluids nourish tissues and can be actively/passively exchanged
• Stroke volume plus heart rate yields cardiac output Venous blood constitutes 70% of blood volume, while atrial blood is 10-15%
• The Starling Equation involves capillary colloid osmotic pressure and capillary hydrostatic pressure, governing transvascular fluid flux
• Endothelial glycocalyx is a membrane in the vascular system that is a major gateway for fluids and if destroyed from disease state can lead to edema
• Lymph circulation moves fluid from major GI organs, muscle, brain, and skin to caudal vena cava via the thoracic duct in lungs
• Fluids are not normally resorbed from capillaries except in the gut, kidneys, or during acute hypotensive episodes
• The interstitium is a dynamic, fluid-filled reservoir made of flexible connective tissue
• Elimination is an important aspect of fluid physiology

Fluid Disposition

• Why give fluids: Perfusion, O2, Electrolytes, A/B
• Fluids help maintain hydration and treat or prevent dehydration - dehydration is largest reason, but needs to be done slow and is clinically relevant at 5-6%
• Dehydration can be identified by skin tent, eye position, MM, CRT, and signs of shock
• Can't replenish with just water
• Fluids treat hypovolemia and hypotension by stabilizing blood pressure and blood volume, normalizing electrolytes and pH
• Hypotension during anesthesia is commonly caused by drugs wiping out homeostatic reflexes and vasodilation

Types of Fluids

• Osmolarity = toxicity; a solution's solute concentration affects water movement across membranes and determines if isotonic, hypotonic, or hypertonic relative to plasma
• Oncotic pressure is exerted by plasma proteins like albumin, pulling water into the circulatory system
• Isotonic fluids have a similar osmolarity to plasma (~275-295 mOsm/L) and do not cause fluid shifts
  • Examples: normal saline, lactated Ringer's, and Plasma-Lyte; used for fluid resuscitation and maintaining blood volume
• Hypotonic fluids have a lower osmolarity than plasma (<275 mOsm/L), causing water to move into cells and cell swelling
  • Examples: half-normal saline and dextrose 5% in water; used for cellular dehydration cautiously due to risk of overhydration
• Hypertonic fluids have a higher osmolarity than plasma (>295 mOsm/L), causing water to move out of cells and cell shrinkage
  • Examples: hypertonic saline and dextrose 10% in water; used for severe hyponatremia, cerebral edema, or hypovolemic shock with careful monitoring
• Oxygen Delivery (DO2): The amount of oxygen delivered to tissues per minute
  • DO2 = Cardiac Output x Arterial Oxygen Content;
  • Affected by fluid therapy, supporting cardiac output and oxygen transport

Fluids as Drugs

• Fluids mimic drugs & have a half life, Vd, and Cl
• Fluids include: Electrolytes and concentrations, osmolarity, tonicity, Ac-Ba, colloid osmotic pressure, viscosity, oxygen delivery, and caloric value
• Volume Kinetics (VK):
  • Volume Kinetics (VK) = Fluid Distribution: Maintain blood pressure, and perfusion; Rapid exchange occurs around normal interstitium pressure

VK is an extension of pharmacokinetics, applied to fluids, helping understand fluid movement and optimize therapy

Fluid Spaces

• Intravascular space (plasma) is the blood volume within circulation (~5-7% of body weight)
• Interstitial space is the fluid surrounding cells (~15% of body weight)
• Intracellular space is the fluid within cells (~40% of body weight)
• Crystalloids distribute quickly between intravascular and interstitial spaces, with only ~25-30% remaining intravascular after 30-60 minutes
• Colloids have higher oncotic pressure and stay in the intravascular space longer, pulling fluid from the interstitial compartment

Monitoring Fluid Responsiveness

• Fluid responsiveness is the cardiovascular system's ability to increase stroke volume or cardiac output with IV fluid administration
• Fluid responsiveness helps determine need for more fluids or alternative treatments
• Heart rate and blood pressure can be static parameters
• Central venous pressure is not a reliable indicator of fluid responsiveness
• Pulse Pressure Variation & Stroke Volume Variation are dynamic parameters
  • A significant variation can be indicative of needing higher fluids
• Passive Leg Raise or Abdominal Compression Test can assess transient venous return

Indicators of Fluid Responsiveness

• Lactate Clearance: Decreasing lactate levels after fluid administration indicate improved tissue perfusion
• Capillary Refill Time: Slow CRT suggests poor perfusion
• Urine Output: Oliguria suggests hypovolemia

Pain Mechanisms

• Definition of Pain: An unpleasant sensory and emotional experience associated with actual or potential tissue damage
• Sensory Physiology: detection mechanisms for specific stimuli

Pain Transmission

• Nociception: Sensory system encoding noxious stimul Nociceptors detect environmental changes (mechanical/chemical) in skin, muscles, and inner organs
• Nerve fibers transmit pain signals

Types of Nerve Fibers

• A-alpha: Proprioception, myelinated, 13-20 diameter, 80-120 conduction speed
• A-beta: Touch, myelinated, 6-12 diameter, 35-90 conduction speed
• A-delta: Pain (mechanical and thermal), myelinated, 1-5 diameter, 5-40 conduction speed
• C: Pain (mechanical, thermal, and chemical), non-myelinated, 0.2-1.5 diameter, 0.5-2 conduction speed
• Plasticity: Changes in nervous tissue amplifying pain signals

Pain Pathways

• Layers 1, 2, and 3 consist of: mechanical/thermal/chemical pain, mechanical/thermal pain, and touch pain
• Wide dynamic neurons respond to innocuous and noxious mechanical stimuli and exhibit a frequency-dependent progressive increase
• Perception is the brain involving ascending/descending pathways from the spinothalamic tract and limbic system, with the locus coeruleus inhibiting action

Physiologic Pain

• Nociceptor Mediated: activation of high threshold of pain receptors by painful stimuli

Pathologic Pain

• Promote, intensify and prolong pain Amplify response, create chronic pain state
• Pain Processes that promote, intensify and prolong pain:
  • Peripheral sensitization: -inflammatory cytokines desensitize nociceptors
  • Primary hyperalgesia:
    • response with severe or chorninc pain
    • NMDA-R
  • Central Sensitization/Activation of NMDA-R:
    • caused by increase in membrane excitability, synaptic efficacy, reduce inhibition, CNS plasticity
  • Activation of Silent Nociceptors:
    • respond during inflammation and tissue
    • TRPV1, TRPV3, TRPV4, TRPV8 targets
  • Disinhibition:
    • inhibitory nerves are inhibited, constant insult, GABA/Glycine modulators
  • Neuroinflammation/Glial Cell Activation:
    • surround the cell body, main types being Schwann cells, satellite cells
  • Stress and Pain (PTSD):
    • stress induced

Collateral Sprouting

• After nerve injury, C-fiber terminals atrophy, A-beta sensory axons sprout superficial

Adaptive Pain

• Pain serves a beneficial role as it protects the body
• Activation of nociceptive pathways
• Nociceptive Pain: Arises from actual tissue damage, detected by nociceptors (pain receptors)
• Somatic Pain: Sharp, localized pain (e.g., cuts, fractures)
• Visceral Pain: Diffuse pain in internal organs (e.g., abdominal pain from inflamation)
• Inflammatory Pain: Results from immune responses that sensitize nociceptors
  • Function: Alerts injury and prevents harm.
• Promotes healing

Maladaptive Pain

• Persists beyond protective function
• Neuropathic Pain: Nerve damage
• Central Sensitization: Hyperexcitability
• Allodynia: Pain from non-painful
• Hyperalgesia: Exaggerated pain
• Persistent or spontaneous pain: Pain without trigger

Algesia Key Characteristics

• Adaptive Pain: protective, promotes healing, temporary
• Maladaptive Pain: serves no benefit, persistent or chronic

Taxonomy of Pain

• Location: Somatic, visceral
• Severity: Mild, moderate, severe
• Mechanism: Inflammatory, neuropathic

Pain Assessment

• Scoring and Scaling
• Subjective: Behavior activity
• Objective: pain scales

Multimodal Analgesia

• Use one or more methods
• Goal: additive synergistic analgesic effects, less side effects
• NSAIDS and Alpha 2 Agonists are used
• Opioids work in dogs and pigs, worst in horses and cats
• Synergism complimentary or routes of administration
• Local anesthetics include lidocaine, bupivacaine, ropivacaine, mepivacaine
• Transdermal topical includes lidocaine patch
• NSAIDS includes carprofen, meloxicam, robenacoxib, aspirin
• Opioids+sedation, inhibits adenylyl cyclase and open k+ channels and membrane hyperpolarization
• Alpha-2 Agonists includes xylazine, detomidine, dexmedetomidine
• Ketamine and Magnesium: block NMDA
• Anti NGF like Librela and Solensia
• Neutracueticals used for OA: omega 3's, ascorbic acid, vitamins D and E, ginger, glucosamine, hyaluronic acid, turmeric

Overview of potential risks including fluid overload, dilution of blood components like protein, and edema. Discussion of total body water distribution, intracellular and extracellular fluid balance, and the starling equation. Endothelial glycocalyx in vascular system