VNSA11 Flashcards
What does general anaesthesia provide?
Muscle relaxation
Analgesia
Unconsciousness
Define general anaesthesia
The reversible immobile state that induces amnesia
Name anaesthetic types
General anaesthetic
IV induction agents
Inhalation gases
Epidural
Local anaesthetic
Dissociative
Topical
Regional
Local anaesthesia
Used alongside GA
Temporarily blocks conduction in sensory nerve fibres preventing nociceptibe info to be received.
Mode of action - inhibits sodium channels in neuronal membranes, preventing influx of sodium ions into nerve axons.
Nervous function lost in order: pain, cold & warmth sensation, touch, deep pressure, motor function
Pharmacokinetics of local anaesthetics
Absorption: depends on dose, site on inj and if there’s a presence of a vasoconstrictor
Distribution: affected by degree of protein binding. Free drug exerts effects and is metabolised. Metabolism via liver and lungs, excreted via kidneys.
Local anaesthetic can cause vasodilation (often used with adrenaline to delay absorption and lengthen action). Vasoconstrictors can cause localised ischaemia so not used in distal areas as potential necrosis.
Effects: lipid soluble and low molecular weight (cross blood-brain barrier). At therapeutic range these are of great use (anticonvulsants, sedatives and analgesia) at high levels can induce seizures and cause CNS depression. Can slow myocardium conduction causing vasodilation, hypotension, bradycardia and cardiac arrest. Cats and exotics are more susceptible to this than dogs
Local anaesthetic drugs
Lidocaine: rapid onset of activity, good tissue penetration. Short duration of activity (45 mins without adrenaline & 1-2hrs with). Good for regional blocks and general surgery.
Proxymetacaine: topical analgesia of eye, rapid onset but duration only 15 mins. Causes less initial sting than other agents.
Bupivacaine: slow onset of activity (15 mins) but longer duration (6-8 hrs). Potency 4X stronger than lidocaine. Good for epidural analgesia and post-op. Don’t give IV as cardiac toxicity risk.
Topical anaesthesia (local)
Eg sprays, drops, gel or cream
Limited to analgesia of nasal mucous membranes, eye, larynx, penis, vagina, rectum and urethra.
Perineural (regional) block
(Local anaesthetic)
Injected directly around the nerve, reduces motor side effects and risks of systemic absorption and subsequent toxicity.
Nerves must be palpable and easily accessible - use of nerve stimulators and ultrasounds
Eg:
Intercostal nerve block: injected caudal to ribs
Brachial plexus block: analgesia distal to elbow
Maxillary and mandibular nerve blocks: dental and jaw surgery, nerves blocked as exit jaw bones
Intra-articular block (local anaesthetic)
Local anaesthetics or opioids injected into the joint cavity following surgery or arthroscopy.
Used as part as multimodal analgesia
Asepsis to prevent introduction of infection into the joint.
Epidural (local anaesthetic)
Performed by vs only
22G needle, or a 17G/18G tuohy needle
Inserted 90 degrees into skin surface and advanced slowly, stylet removed as it nears epidural space.
Eg; lumbosacral epidural, analgesia to structures caudal to thoracolumbar junction.
Bupivacaine used as long duration of action. Preservative free morphine can be used for analgesia of 18-24hrs
Local infiltration block (local anaesthetic)
Intradermal or subdermal tissue infiltrated by injection of local anaesthetic agent.
Uses: minor procedures used with sedation and or restraint.
Sterile needle injected into area. Draw back on hub to ensure no accidental vascular access. Inject small amount of local, creating a wheel effect.
If each injection is made at the periphery of the previous site the patient will only feel 1 injection.
Adrenaline may be used to delay local absorption and lengthen duration of action
Intravenous regional anaesthetic (Bier block)
(Local anaesthetic)
For surgical procedures in the body’s extremities, eg; toe removal.
Local is injected IV into area below or between two tourniquets (Esmarch bandage) on a limb.
Rapid onset of local in this area
Dissociative anaesthesia
KETAMINE
Has minimal effect on the respiratory system whilst creating analgesia and amnesia.
Patient presents as not anaesthetised as can swallow and eyes remain open.
Used in brief, superficial procedures or diagnostic processes.
Can be used in trauma patients (low bp) or elderly patients.
Recovery symptoms of dissociative anaesthesia
On recovery patient may present with;
Hypersalivation
Hyperventilation
Tachycardia
Muscle twitches
Paddling of the legs
Curling of the tongue
Physiology of anaesthesia
Produces many effects on the autonomic nervous system
Effects the brain by the anaesthetic agents acting on the receptors in the CNS and cell membrane of neuronal cells.
Anaesthetic agents cause a reversible depression on the CNS function resulting in loss of consciousness.
Blood-brain barrier: this barrier restricts movement of molecules into brain (water, oxygen and carbon dioxide can cross easily others cross more slowly to not at all). This depends on particles molecular size and lipid solubility.
HIGH lipid solubility and SMALL molecular weight crosses EASILY
The EASIER they cross the barrier the MORE potent they are as anaesthetics.
General anaesthesia; effects on the cardiovascular system
Often causes cardiovascular depression due to
Drugs depressant effect on the brain & peripheral effects of the drug.
Reduction in cardiac output — reduction in blood flow around the body — potential for tissue hypoxia
General anaesthesia; effects on the resp system
CNS depression causes a central depression of resp system.
Leads to reduced sensitivity to blood carbon dioxide concentration and reduced resp drive
Hypercapnia = higher blood CO2 than normal
Hypoxia = inadequate O2 delivered to tissues.
General anaesthesia; effects on the liver
Blood reaches the liver via the hepatic artery and portal vein.
Inhalant anaesthetic agents reduce liver blood flow to a degree due to reduction in cardiac output which affects relationship between hepatic artery and portal vein.
General anaesthesia; effects on the kidneys
Kidneys receive ~20% cardiac output
Normal renal function is reliant on adequate renal blood flow
By reducing that blood flow, GA also decreases glomerular filtration rate, urine output and electrolyte function.
Parameters should return to norm ranges within a few hours of a short GA.
Define MAC
Minimum alveolar concentration
What is the minimum alveolar concentration (MAC)
Amount required to suppress movement to noxious stimulant in 50% of patients.
About MAC
A measure of anaesthetic potency
Potent inhalant agents have a lower MAC.
Dependent on: species, age, temp, disease, CNS depressant drugs, pregnancy
Drug MAC levels
Halothane 0.75%
Isoflurane 1.15%
Sevoflurane 2.05%
Desflurane 5-10%
Halothane = most potent
Halothane
High solubility coefficient
Absorbed quickly into the blood, but doesn’t want to come out
Concentration in the brain rises slowly as the blood reaches the brain (slow induction results)
At the end there is an accumulation of drug in the blood and fat and other tissues
Levels fall slowly as agent is slowly released into alveoli and exhaled
Slow recovery results
Isoflurane and sevoflurane
Low solubility coefficient
Slower absorption into blood, but released readily into brain
Rapid induction of anaesthesia
Agents are eliminated quickly by lungs
Rapid recovery
Drug blood-gas solubility
Halothane 2-3
Isoflurane 1.4
Sevoflurane 0.6
Desflurane 0.42
Halothane has a slow induction and Desflurane has quickest recovery
Soluble anaesthetic agents
Slow induction, slow recovery
Insoluble anaesthetic agent
Rapid induction, rapid recovery
Define critical tension
The necessary drug concentration needed in the brain to induce unconsciousness.
(As levels fall below critical tension the animal will regain consciousness)
Define pain
A sensory or emotional experience associated with actual or potential tissue damage
Analgesia
A conscious sensation
An adequately anaesthetised patient will not experience pain
A noxious stimulus is damaging to tissues (thermal, mechanical and chemical)
Nociception causes perception of pain (experienced during recovery)
Activation of pain pathways may cause surrounding tissues to become painful. Sensitivity to pain heightens due to repeated activation of nociceptive pathways
What 3 categories is pain split into?
Physiological
Inflammatory
Neuropathic
Physiological pain
Early warning device of potentially painful stimuli
Pain is proportional to stimulation
Pain experienced is localised
“Normal” pain pathway activation
Inflammatory pain
Pain associated with changes to pain pathway
-heightened pain sensitivity
-skin incision causes inflammation and tissue damage
Control of disease process causing pain hypersensitivity
Neuropathic pain
Clinical pain caused by nervous system damage
-peripheral nerve damage
-“phantom limb” pain following amputation
Clinical pain is associated with hypersensitivity (at site of tissue damage)
Stimuli that wouldn’t normally activate pain pathways will cause other pain
Stimuli normally activating pain pathways will cause a prolonged and larger pain (hyperalgesia)
Peripheral sensitisation
Noxious stimuli at site of tissue injury produces a more intense and prolonged pain response following clinical pain (primary hyperalgesia)
Nociceptors at site of tissue injury becomes more excitable
Central sensitisation
Resulting in secondary hyperalgesia, allodynia and spontaneous pain
Starts where peripheral nerve reaches spinal cord
Causes sudden augmentation of noxious stimuli as transmitted to brain
Pre-emptive analgesia
Analgesia provided before noxious stimuli
Prevents “sensitisation” or “wind-up”
Analgesia that has taken place after this is less effective
Multimodal analgesia
Using multiple analgesic drugs
Controlling pain at different levels and sites
Synergism between drugs means lower levels of each is needed reducing side effects
Adequate analgesia speeds recovery
Physiological effects of pain
Tachycardia
Inc blood pressure
Tachypnoea
Changes in resp pattern
Panting
Pyrexia
Salivation
Pupillary dilation
Shivering and shaking
Assess patients behaviour and demeanour without interference = more accurate
Response to pain
(Spinal, medullary, hypothalamic, cortical)
Spinal - receives the pain message transmitted from nociceptors which is then sent to the brain
Medullary - once in the brain the pain message is processed and responded to
Hypothalamic - releasing hormones which travel in the portal blood to the pituitary gland where ACTH is produced and released into the general blood system.
Cortical - adrenal cortex release corticosteroids under the influence.
Routes for administration of analgesia
IV - rapid action, potent opioids
IM - volume to inject and site considered. Painful.
S/C - onset of action is slower than IV or IM.
Transmucosal - as effective as IV administration of buprenorphine in cats. Some formulations are unpalatable
Transdermal - “patches” used to provide long term non-invasive analgesia. Reservoir of drug, covered with membrane controlling absorption rate. Bioavailability varies (cats 34% and dogs 64%).
Analgesia in rabbits and rodents
Opioids - good analgesia (Buprenorphine), wide safety margin but causes a degree of sedation, can be administered orally, causes pica in rats.
NSAIDs are very effective but higher doses required
Ketamine and alpha-2 agonists used as part of anaesthetic protocols
Analgesia in birds
Opioids used (kappa opioids receptors more effective than uu)
Response between species varies
NSAIDs used - nephrotoxicity and gastric ulceration seen. Repeated doses are unadvisable.
Define tidal volume
The amount of air that moves in or out of the lungs with each respiratory cycle
Define minute volume
Amount of gas inhaled or exhaled from the lungs in 1 minute
Expiratory reserve volume (ERV)
Amount of air you can forcefully exhale past a normal tidal expiration
Inspiratory reserve volume (IRV)
Amount of air that can be taken into the lungs (above the tidal volume) upon forceful inspiration
Define residual volume
The volume of air remaining in the lungs after maximum forceful expiration
Define vital capacity
Maximum amount of air a person can expel from the lungs after a maximum inhalation
(ERV + IRV + tidal volume)
Define total lung capacity
The amount of air the lung can contain at the height of maximum inspiratory effort
(Residual volume + vital capacity)
Define functional residual capacity (FRC)
The volume in the lungs at the end expiratory position
(ERV + residual volume)
Define physiological (anatomical) dead space
Volume of air in the respiratory zone that doesn’t take part in gas exchange
(Tranches down to the terminal bronchioles)