exam 1 Flashcards
DEFINITION OF GENERAL ANESTHESIA:
A state of unconsciousness produced by a process of controlled, reversible,
intoxication of the central nervous system (CNS), whereby the patient
neither perceives nor recalls noxious (or other) stimuli
mechanism of anethetics
- Must be lipophilic to have action within the CNS – cross BBB
- Interaction with inhibitory pathways:
- Gamma amino butyric acid (GABA A) in the BRAIN
- Glycine in the SPINAL CORD
the triad of general anethesia
-unconsciousness
-analgesia
-muscle relaxation
depth of anesthetics and how they effect autonomic and somatic nervous system
-anesthetics: lead to , CVS, resp and CNS depression. CNS depression leads to->
-autonomic: hemodynamic, respiratory, thermoregulatory (BAD)
* Somatic = proprioceptive reflexes and muscle relaxation (good)
CNS depression under anesthetic
- Loss of consciousness
- Damping of reflexes:
- Cardiovascular → Hypotension
- Respiratory → Hypoventilation
- Thermoregulatory → Hypothermia
- Postural → Reduced muscle tone
- Central modulation of nociception
main objectives of general anesthesia
- To maintain tissue perfusion, with delivery of oxygen and removal of waste products.
-There are NO SAFE ANESTHETICS – there are only SAFE ANESTHETISTS
-risk linked to health status graded 1-5, must do pre aneshetic exam
important phases of anesthesia
-pre operative assessment
-premedication
-induction
-maintenance
-recovery: aftercare
PRE-ANESTHETIC PREPARATION: FOOD AND WATER
-Dogs, Cats, Horses – fasted at least 6 – 8 hrs (12 hrs common):
-Horses may have small amount of hay to prevent ileus for short procedures
* Ruminants fasted 24 – 48 hours:
* No water last 6 hrs; gorging with water increases volume of rumen contents
* Less than 18 hours fasting increases the risk of bloat
* Very prone to regurgitation
CNS stats for surgery
-surgery performed at stage III, plane 2
-6-12 breaths/ min
-ETCO 35-45Hg
-BP minimal 80/40 (60) mmHg
-HR not predictable of anesthetic depth
-monitor every 5 mins.
eye reflexes dog
-light plane: central eye, palpebral present, shiny cornea.
-surgical plane: ventral eye, no palpebral, dry cornea
-too deep: dilated pupil, central eye
eye reflexes horse
-at surgical plane: inhalation: central eye, sluggish palpebral.
-injectiable: central eye, rapid palpebral.
-too light: tearing, nystagmus, blinking
Vitals during anesthetic
Light = muscle tone +++ rigidity, fast deep breath, holding.
Surgical plane = muscle tone ++, rhythmic breath. * Ruminants may have fast and shallow (tachypnea) breathing pattern at surgical anesthesia = normal
Deep plane = Muscle tone +
* Can assess ‘jaw tone’ in cats and dogs
* Too much relaxation can compromise lung ventilation
Differentiate pain from nociception
-pain arises in the brain, a conscious, complex sensation. Pain is a signal which produces reflex and conscious preventive
response to protect the body from actual damage.
-Nociception is sensory (afferent) information that is relayed via ASCENDING pathways. the neural mechanism of encoding and processing harmful stimuli.
-NOCICEPTION CAN OCCUR WITHOUT PAIN
Phases of nociception
- Transduction – proteins and voltage-gated ion channels that convert thermal, mechanical, or chemical energy into an action potential (AP)
- Conduction – AP moved through pain fibres to depolarize the pre-synaptic terminal
- Transmission – Post-synaptic membrane activated, and signal is relayed in spinal cord
- Modulation - an adaptive process involving both excitatory and inhibitory mechanisms (peripheral and central modulation)
- Perception - the integration of sensations, emotions and cognition that results in the unique perception of pain
neural pathways in transmission of noxious stimuli
-the neural pathways are sensory afferent going ascending to the brain. Sensory neurons sense nociception in the PNS.
-nociceptors sense mechanical, thermal and chemical stimuli.
Characteristics of nociceptors
- Numerous and ubiquitous
- Polymodal
- High threshold
Conveyed by A-delta and C axons.
how is the pain experience relayed to brain
-the nociceptor synapses on the pain relay neuron in the spinal cord which travels to the brain. (cerebral cortex, limbic system, hypothalamus and brainstem)
-the state of excitability of the pain relay neuron determines how much noxious stimuli is transmitted to the brain.
-AP is Na+ channels needed for propagation. this is what we block in local anesthetics.
allodynia
-pain experienced in response to normally non-noxious stimuli
inflammatory pain
-Inflammatory pain: leads to increased firing frequency of nociceptors due to inflammatory mediators.
-neural plasticity is done by peripheral and central sensitization.
-an adaptive response to tissue damage. Temporary only while inflammatory mediators are present. A protective mechanism.
neuropathic pain
severe damage to the neural structures of the CNS or PNS.
* pain hypersensitivity due to damage to the nervous system
* a maladaptive response (regenerative) and not normal. Regrowth of neurons and axons which isn’t perfect so leads to too many or inappropriate connections which lead to an inappropriate perception of pain.
-not temporary, can be permanent called learned pain.
-manifests as: hyperalgesia,, allodynia, spontaneous pain.
2 mechanisms of neural plasticity
-peripheral sensitization: in PNS, decreases threshold from inflammatory process so increased excitability of nociceptors. lower nociceptor threshold. greater pain response/ firing.
-central sensitization: in CNS, increased excitability of spinal pain relay neurons, initiated by sustained firing of nociceptors.
They get a hyperexcitable state in the CNS which sends more frequent info to the brain.
what determines how much info of the nexious stimuli is transmitted to brain.
The state of excitability of the
pain relay neuron determines how much information about noxious stimuli is transmitted
to the brain.
how peripheral sensitization leads to central
The Peripheral sensitization from tissue inflammation will send repeated input to the central sensitization which changes the excitability of the neuron in the CNS which leads to an increased pain reception even with less input.
-Animals with chronic pain will have a lower pain threshold.
-Animal may have WINDUP pain, ex. Broke leg 3 days ago comes into clinic so animal will be really painful and has heightened perception of pain. May need more pain medication than an acute injury.
approaches to reduce pain hypersensitivity by using balanced multimodal analgesia
-inhibit perception (opiods)
-inhibit transmission (local anethetics)
-transduction inhibit PNS (NSAIDS)
-modulation of spinal pathway inhibit CNS (a2 agonists)
Pain-modulating region in the midbrain: =
-Periaqueductal grey matter (PAG): sits in and around the central aquaduct and receives information up the spinal cord to the PAG and then to thalamus. Also get information from other higher brain structures which convey the emotional state, attention ect. Which lead to how the animal perceives pain. Also responsible for risk assessment and fear and aggressive behaviors.
how Opioid receptors in brain
-opioids are released from the PAC and binds opioid receptors on the post synaptic cells and inhibit the cell from making an AP so the pain signal is not transmitted to the higher brain centers and the level of brain is reduced (bupenorphine).
NE as a neurotransmitter in pain
-NE released in brainstem and binds receptors on the pre and post synaptic cells. this will cause hyperpolarization and stop them from having AP. which blocks pain transmission. (NE and a2 agonists eg. xylazine.)
Factors Influencing the Assessment of Pain Behaviors
- Species - Breed
- Environmental factors: hospital setting, presence of perceived predators, confinement
- Concurrent diseases
- Anxiety: predisposes animal to worse pain, important for pain management
- Drugs
- Evaluator
Physiologic Indicators of Pain
- Related to activation of the sympathetic nervous system
-increased HR. BP, RR, Temp, pupil dialation
-increased biomarkers such as B-endorphin, catecholamines, cortisol
-influenced by factors such as anxiety, stress, fear, drugs
-look at behavior, posture, facial expression
the challenges of pain assessment
- Pain is a dynamic, complex, multi-dimensional experience involving sensory and
affective components - Uniquely personal experience
- Use of proxy (DVM or owner)
- Observer assess somebody’s subjective experience
- Respondent bias
- Variation in pain response
-species, environmental and different types of pain.
CMPS – SHORT FORM pain score
- High practicality, clear repeatable format
- For assessment of acute pain (orthopedic and soft tissue surgery, medical conditions)
- Behavioral assessment:
- Observation
- Mobility (if appropriate)
- Palpation
- Overall assessment
- Reduced interobserver variability
- Validated: has been tested at multiple hospital settings
-intervention analgesia at 6/24 or 5/20.
Clinical Measurement Instruments for chronic pain
-ask owners
* Evaluate behaviors in a natural setting, such as:
- Going up or down stairs
- Eating
- Grooming
- Ability to jump in the car
- Difficulty in Rising
-Inappropriate urination or defecation
pain definition
: An unpleasant sensory and emotional experience (a perception) that
elicits protective motor actions, resulting in learned avoidance, and is
capable of modifying species-specific behavior, including social
behavior”
THE PAIN EXPERIENCE COMPRISES
- Detection of tissue injury by the nervous system (NOCICEPTION)
- Conscious perception of pain (noxious stimulus)
- Behavioral responses or changes which occur to protect the individual from further discomfort
what happens if pain goes untreated
-acute pain can lead to chronic pain which is the disease itself.
Can lead to:
-peripheral and central sensitization
-hyperalgesia: primary and secondary
-wind up pain
-allodynia
TECHNIQUES TO TREAT AND REDUCE PAIN:
1. Pre-emptive analgesia:
- 1st key strategy when pain is anticipated
- Providing analgesia BEFORE the insult can significantly reduce both intra- and post-operative analgesia requirements
-PREVENTS SENSITIZATION
Multimodal analgesia:
- Combines analgesics from two or more drug classes or analgesic techniques
that employ different mechanisms of action, targeting different (peripheral or
central) pain pathways, thus achieving a synergistic effect at lower analgesic doses.
nociceptive pathways and whats happening
-transduction: noxious stimuli (chemical, thermal, ect.) are transformed into electrical signals.
-transmission: conduction of impulses from peripheral pain receptors to spinal cord.
-modulation: amplification or suppression of pain impulses by spinal cord.
-perception: processing and recognition of pain by the brain.
ANCILLARY PAIN MANAGEMENT TECHNIQUES
- Manipulative Therapies:
- Temperature – application of heat (improve circulation) or cold (decrease
inflammation) - Massage
- Alternative Techniques:
- Acupuncture
- Laser Therapy
WHY USE PREMEDICATION?
- Relieve anxiety and stress in the patient
- To smooth induction of anesthesia
- To smooth the maintenance phase of anesthesia
- To smooth the recovery from anesthesia
- Anesthetic sparing – reduce the dose of induction and maintenance anesthetic agents and thus reduce their side effects
- To provide analgesia
- To reduce muscle tone
AN IDEAL PREMEDICATION SHOULD
- Relieve fear and anxiety
- Be easily administered
- Have reasonably quick onset of action, and reasonable duration of action
- Be antagonizable (reversible)
- Be predictable (dose-dependent) and reliable
- Be safe and effective in all species
- Produce minimal cardiovascular, respiratory, and other side effects
- Provide some analgesia and muscle relaxation
- Possibly provide amnesia
PRE-ANESTHETIC MEDICATIONS*
- Phenothiazines (acepromazine), Butyrophenones, Alpha2 agonists: sedation to calm, anesthetic sparing.
-anticholinergics: prevent side effects (bradycardia/ vasodialation) - Opioids, Alpha2 agonists, Ketamine: Provide analgesia (pre-emptively)
-all sedatives have cardio and resp effects which are dose dependent.
injectable agents mechanism
- Majority of these drugs mechanism of action is via:
- Potentiation or facilitation of GABA, by their actions at GABAA receptors in the
CNS - Need a high concentration of drug to rapidly reach the site of action
(THE BRAIN) for a titratable effect
When to use an injectable solution?
SEDATION: low doses
INDUCTION: main use to get into surgical plane for endotracheal tube
MAINTENACE: top ups, keeping under
EMERGENCY: supplement if animal rapidly wakes
best route of administration for injectable drugs
-Intravenous: accurate, titratable, rapid-acting in 20-60 seconds
-rapidly acheives surgical plane of anesthesia stage 3 and can bypass 1/2
PHENOTHIAZINES
(acepromazine)
-anti-adrenercic (a1 blocker)
* Anticholinergic (muscarinic blocker)
-NO ANALGESIA
-hypotension /hyperthermia
-can cause penile prolapse in horses don’t use In breeding stallions
* 30 – 40 % anesthetic sparing effect
benzodiazepines:
-no analgesia
-anticonsolvent
-(diazepam, misazolam)
-muscle relaxation
-over dose causes coma.
DIAZEPAM a pre medication
-sensitive to light, adheres to plastic
-painful on IM injection
-crosses placenta
-do not use for C-sections
-better for IV
-no analgesia
-enhance affinity for GABA receptors –> axiolysis and sedation.
MIDAZOLAM a premedication
-don’t use IV
-2-3x more potent than diazepam.
-popular in exotics
-no anelgesia
-enhance affinity for GABA receptors –> axiolysis and sedation.
-anticonsulvent
FLUMAZENIL: BENZODIAZEPINE ANTAGONIST
-ANTAGONIST at benzodiazepine binding site on GABAA receptor
-* Increases muscle tone to normal – improves ventilation
-used in exotic anethesia. 30-60mins
BEHAVIOUR MODIFIERS: TRAZODONE
- Serotonin receptor antagonist and reuptake inhibitor.
-antidepressant
-possible hypotension’
-oral.
-decrease stress
BEHAVIOUR MODIFIERS: GABAPENTIN
-before visit and chronic pain treatment
-inhibitory effect on voltage gated Ca+ channels in neural tissues decreasing glutamate.
pharmacokinetics of IV bolus infection
-a phase: blood goes from blood to vessel rich tissues. brain, heart, lungs. uptake to CNS is rapid. REDISTRIBUTION. from brain to blood.
-B-phase: elimination from central compartment to blood.
-injectables have an anesthetic effect lasting 4-10 minutes
goal of induction
-goal is to achieve stage 3 anesthesia and bypass the excitement phase (stages 1 and 2)
-titrate to effect in small animals (20-80% dose reduction)
-physical status of patent
-slow injection 60-120 sec
-give whole dose for large animals for saftey
Total IntraVenous Anesthesia (TIVA)
-One or more drugs can be used, Can be slow to change depth of anesthesia
- Partial IntraVenous Anesthesia (PIVA):
-Use injectable drugs to supplement inhalational anesthesia
injectable anesthetic drug
-propofol
-great for c-sections and patients with decreased liver function.
* Acts on GABAA receptors in CNS to produce
Anesthesia
-no analgesia
* Used for induction and maintenance (TIVA).
* Onset 40 – 90 seconds and one dose lasts 5 – 10
minutes
-DD cardio depression and resp.
ALFAXALONE CD-RTU - Neurosteroid
-injectable anesthetic
- Acts on GABAA receptors in CNS to
produce anesthesia - Good muscle relaxation
- Produces reliable sedation in cats when given IM
- Excellent in reptiles (IM)
-* Onset 15 – 45 seconds and one dose lasts 5
– 10 minutes
-TIVA
-no analgesia
-pain on injection
-DD effects
ketamine injectable anesthetic
-interrupts info from reaching higher centers in the brain.
-maintains CNS reflexes.
-slow onset 30-90 sec. long duration 20-30 mins .
-used for induction and maintenance/ analgesia.
-sedation
-muscle rigidity ALWAYS COMBINE WITH MUSCLE RELAXANT
-avoid in cats with compromised renal function or HCM.
-rough recoveries
-used with other drugs to limit side effects.
KETAMINE/DIAZEPAM
(“Ket – Val”)
-IV induction agent in dogs, cats, foals, cattle.
-slow onset 30-90 sec.
-do not use for C-sections
-minimal effects.
⍺2 AGONIST + KETAMINE
- Xylazine + Ketamine:
- Good combination in large animals (horse, cattle) (IV)
- Reliable for wildlife immobilization (IM)
- Analgesia, muscle relaxation and narcosis
-not for dogs and cats - Potent cardiopulmonary depression
⍺2 AGONIST + KETAMINE
- Dexmedetomidine – Ketamine – Opioid:
- “Kitty – Magic”
- Wildlife, game ranch animals
- Supportive care (provide O2)
- Monitor closely
- ⍺2 reversible (Atipamezole)
iNDUCTION APNEA
- Usually observed after rapid bolus of IV induction agent
- Apnea or Hypoventilation result in:
- Poor uptake of maintenance inhalant anesthetic
- Poor transition to maintenance phase (stable plane) of inhalant anesthesia
- Once IV induction agent is redistributed – animal wakes up
- Assist ventilation until spontaneous ventilation returns – ensure plasma inhalant
concentration is adequate - Once induction agent wears off – inhalant plasma concentration should be
enough to keep patient anesthetized - Apnea can be avoided by titrating to effect
-alpha 2 agonists
: provide sedation, analgesia, muscle relaxation, anxiolysis
-examples (dexmedatomidine, xylazine)
- ALPHA2-AGONISTS method of action in sedation
-act both centrally and peripherally and their actions depend on:
* Interaction with ⍺2 (and ⍺1) receptors
* Interaction with imidazoline (I1 and I2) receptors (Dexmedetomidine)
-inhibit NorEpi release, decrease sympathetic, inhibit release of neuotransmitters AChm serotonin, dopamine.
ACTION AT THE ALPHA1 RECEPTORS
- CNS stimulation:
- Arousal, excitement, restlessness
- Can exacerbate pain
- Smooth muscle constriction
- Vasoconstriction
- Increased peripheral resistance
- Increased blood pressure
- Mydriasis
- Relaxes GIT smooth muscle
- Contraction of uterus and bladder sphincter
- Bronchoconstriction
- Decrease insulin secretion
ACTION AT THE ALPHA2 RECEPTORS
- Anxiolysis and sedation
- Anesthetic sparing effect
- CNS depression
- Anticonvulsant activity
- Neuroprotectant - ↓ total intracranial blood volume
- Analgesia
- Muscle relaxation
- Increase uterine tone
ALPHA2 AGONISTS – CARDIOVASCULAR EFFECTS
-Peripheral vasoconstriction and increased blood pressure (hypertension):
* Activation of peripheral post-synaptic ⍺2 receptors
-baroreceptor-> bradycardia. DO NOT TREAT WITH ANTICHOLINERGICS.
-decreased preload
ALPHA2 AGONISTS – RESPIRATORY EFFECTS
- RR may be reduced – compensate for this by increasing tidal volume
- Blood gases remain virtually unchanged
- Take care in patients with CNS depression
ALPHA2 AGONISTS – OTHER EFFECTS
- Musculoskeletal Relaxation: Manifests as ataxia or recumbency
- Endocrine (Diuresis): Reduced ADH-> diuresis
-hyperglycemia
-reduced GI motility
-hypothermia
-decreased BF to kidney and liver.
alpha 2 and opiods in anelgesia
- ⍺2 adrenergic and opioid receptors are intimately related: Combination of ⍺2 and opioid produces profound synergistic analgesia. Work well together.
- Widespread location of ⍺2 receptors – stimulation may suppress nociceptive
signals at various points in the pain pathways: inhibit neortransmitter release.
Inflammation and alpha 2 agonists:
-Analgesic and antihyperalgesic effects are most pronounced during inflammation.
* Greatest effects are often in the middle of the inflammatory process
* Up regulation of ⍺2 or imidazoline receptors
ATIPAMEZOLE: ALPHA2 ANTAGONIST used for reversal
- Most selective ⍺2 antagonist available
- Competitive antagonist
- Occasionally accompanied by:
- Muscle tremors, tachycardia, over-alertness, transient hypotension, panting, defecation, vomiting
- Reversal of both sedation and ANALGESIA, give dose and then wait for effects before you redose, you can always go up.
- Only labelled for IM administration
dexmedatomadine
-alpha 2 agonist
-most used in small animals
-highly selective a2.
-always combine with opiod.
-onset IM: 15 mins- 1 hr.
-DD resp and cardio depression.
what drug reverses all a2agonists
Atipamezole
Xylazine
-large animals a2 agonist
-onset minutes, duration 45 mins.
-rare to reverse, can use tolazoline in cattle.
-great for standing procedures.
-reflex bradycardia transient for 5 mins.
Detomidine
-a2 agonist used in horses longer standing procedures.
-onset minutes, duration 45 mins.
-good sedation slightly more ataxia/ depressed than with xylazine.
- Often combined with an opioid (butorphanol) for standing procedures
Dexmedetomidine
-alpha 2 agonist for sedation great for minor procedures.
-small animals
-combine with opiod or local block for better effects.
-reversible
-when added with local anesthetic prolongs duration of the block.
INFUSION IN THE POST-OPERATIVE PERIOD: DEXMEDETOMIDINE
- Benefits – analgesia and sedation
- Indications:
- Anxious dogs that need to be kept calm
- Fractious dogs that need to be in the ICU for post-operative care and handling
- Painful dogs that require something more than an opioid
- Dose in dogs: 1 – 5 μg/kg/hr IV
dexmedetomidine EPIDURALS LARGE ANIMALS
-not used in small animals
-prolongs duration of blockade.
-dose not produce motor blockade.
-often combined with other drugs, local anesthetics and opiods.
-analgesia
-adverse effects (ataxia, recumbency) – can be reversed.
-systemic absorption occurs -caution
different epidural agents in horses
-xylazine: 2.5 hr of perineal analgesia no hind limb ataxia.
-detomidine: analgesic and sedative effetcs. ataxia and recumbency/ CV effects. analgesia will spread cranially to T14. 2 hr duration. diaresis occurs.
-romifidine: inconsistant alangesia up to 4 hr. spreads cranially.
epidurals in cattle
-xylazine: onset 10 mins, duration 4 hr. mild effects, ataxia. bradycardia.
-xylazine + lidocaine: onset 5 mins-6 hr. mild sedation, ataxia. bradycardia.
-romifidine: analgesia and sedative effects DD.
breed and species indications with a2 agonists
-beware of brachycephalics and laryngeal paralysis animals.
-increased regurgitation risk.
-good for blocked cats for catheter.
-in diabetics can cause hyperglycemia.
Cardio effects with alpha 2 agonists:
-vasoconstriction leading to hypertension which leads to reflex bradicardia
How low is too low when it comes to HR?
-If its less than 50% of resting HR then check BP.
What ECG abnormalities may you see with a2 agonits?
bradycardia, second degree AV block
opiodid mechanisms
- Any natural, synthetic, endogenous substance with morphine-like properties.
- Inhibition of pre-synaptic voltage gated Ca ++ channels: decreased Ca ++ influx
-> Reduction in neurotransmitter release (Sub P, glutamate, Ach, NE, 5HT)
-> Inhibition of synaptic transmission of nociceptive input - Increased K + efflux -> neuronal hyperpolarization of post-synaptic
spinal cord projection neurons
-> Inhibition of ascending nociceptive pathways
Mu and kappa receptor agonist effects of opiods
-mu receptor: profound analgesia, spinal, resp, bradycardia, sedation, hypothermia.
-kappa receptor: spinal analgesia, mild sedation, diuresis.
opioid effects
-analgesia
-sedation
-anesthetic sparing
-reversible
-bradycardia
-resp depression
-emesis
-abuse potential
-dysphoria
opioid antagonists
-Naloxone:
* Pure μ, δ, κ opioid antagonist
* Can reverse all opioid agonist effects.
-duration 30-60mins
Naltrexone
* Clinical effects last approximately 2x as long as those of naloxone
potency vs efficacy in opioids
- Efficacy: Maximum effect that a drug can produce regardless of dose
- Potency: Amount of a drug that is needed to produce a given effect 50% of max effect.
Opioids clinical use:
- Premedication
- Bolus or infusion intra- and perioperatively
- Dose-dependent analgesia
- Great anesthetic sparing effect
- Analgesia for medical and critical ill patients
- Procedural sedation:
- Combination with sedatives
- Sedation (when administered alone in critical ill patients)
opioids adverse effects
-behaviour changes (euphoria)
-vomiting and nausea
-GER
-bradycardia
-resp depression DD (u receptor agonists)
-antiussicve action depresses cough
-decreased GI motility
OPIOID AGONISTS - Full μ-agonists
- Superior analgesics
- Treatment of moderate to severe pain
1. Morphine -gold standard
2. Hydromorphone
3. Methadone
4. Fentanyl
morphine (opioid)
-full u-opioid agonist
-gold standard
-histamine released IV hypotension.
-vomiting
hydromorphine (opioid)
-full u agonist
-5-10x more potent than morphine.
-DD sedation, rept depression, bradycardia
-vomiting / panting
methadone (opioids)
- Pure μ agonist
- NMDA antagonist
- NE and serotonin uptake inhibitor
- Analgesia ++ to +++
- Clinically similar to morphine
- No vomiting but panting
- No active metabolites
fentanyl -opioid
- 75-125 x more potent than morphine, analgesia +++
- Intra and peri-operative pain
- Fast onset, short half-life.
- Anesthetic sparing:
-DD resp and cardio depression
tramadol (opiod)
- Atypical μ-receptor agonist
- Inhibits reuptake of serotonin and norepinephrine
- Primary analgesic
-not good for dogs
-better for cats
Buprenorphine opioid
- Partial μ-agonist (weak κ-antagonist)
- 1000x higher affinity for μ-receptor than morphine
- Slower onset time than other opioids (15-30 minutes)
- Long duration: 6-8 hours
-mild sedative good for resp destressed.
what do anesthesia machines do
- Delivery of oxygen to patient (most veterinary machines utilize 100% oxygen)
- Delivery of anesthetic gas
- Assistance with ventilation
- Removal of exhaled carbon dioxide from the patient
safety features in oxygen deliver
-green or white always
-pin system PISS for E cylinder
-Diameter index safety system DISS for H cylinders.
regulators pressure reducing valves
-Convert variable high pressure to a constant working pressure (50-60 psi)
* E-tanks: have one-stage regulator on anesthetic machine
2,200 psi down to 50-55 psi
* Pipeline supply: Regulator at O 2source Set to 50-55 psi.
flowmeters
- Control rate of gas delivery to the low-pressure area
- Determine fresh gas flow (FGF)
- Specific for gas (density, viscosity)
- Color coded
- Liters/minute
- Operated by needle valve
- Precision instrument
vaporizer saftey
- Color coding
- Key-indexed filler systems
- Lock on dial
- Do not overfill
- Do not tip vaporizer
Anesthetic Breathing Systems
- Deliver oxygen and anesthetic gases to patient
- Allow elimination of CO 2
- Allow ventilation of lungs
- Different types based on CO 2 removal
- Non-Rebreathing systems: Use high gas flow to flush out CO 2
- Rebreathing systems: Use chemical reaction to remove CO 2 with absorber
Breathing Bag and Breathing Tube
Reservoir Bag
* Size: 6 - 10 times tidal volume (10mL/kg)
* Reservoir of gases during inspiration
* Allows monitoring of respiratory movements
* Ventilate lungs
Breathing Tubes / Hoses
* Provides connection and reservoir for gases
* Apparatus Dead Space: Potential area for CO 2collection
rebreathing systems
- Allow rebreathing and conservation of exhaled gases
- Used on animals larger than 10 kg bodyweight (5-10kg pediatric circle system)
- CO2 removal depends on passage of gases through CO2 absorber (chemical reaction)
- Allow low/minimal flow anesthesia:
Advantage: - Decreased use of volatile anesthetics (more economical)
- Improved temperature and humidity control
- Reduced environmental pollution
Disadvantages - Difficult to rapidly adjust anesthetic depth
Rebreathing System: Denitrogenization
-required for all rebreathing systems
* Air is 21% O2 and 79% N2 (CO 2 amount low.
-N2 moves down Partial pressure gradient from body to breathing system.
-high FGF used for first 20 mins to flush out N2.
-have one way unidirectional valves.
non rebreathing systems advantage and dis
- CO 2 removal is dependent on fresh gas flow during expiratory pause:
Non-Rebreathing System - Advantages
- Less resistance to breathing
- Less mechanical dead space
- Rapid manipulation of anesthetic depth
Disadvantages - Significantly higher waste of both carrier gas
- High flow of dry cool gas (heat and humidity loss
NSIADS for small animals ALWAYS USE LOWEST EFFECTIVE DOSE
-carprofen: cox 2 selective. for arthritis. vommiting and diahhrea.
-meloxicam: cow 2 preferential, many forms. acute and chronic musculoskaletal pain (not in cats)/ arthritis.
NSAIDS in small animal and equine the COXIBS
-deracoxib: cox 2, chronic arthritis, post op pain. GI perforation at high doses.
-firbocoxib (previcox): cox 2, dogs and horses same absolute dose. cheap, osteoarthritis for dogs and horses.
-robenacoxib: selective cox 2, cats: cat bites, inflammation, arthritis.
dogs: arthritis, surgery pain.
NSAID adverse drug effects
-, vomiting and diarrhea
-idiosyncratic reaction hepatic toxicity
equine NSAIDS
-Phenylbutazone (“bute”): good for musculoskeletal pain (lameness)
-Flunixin meglumine (Banamine®,: good for visceral pain (colic)
food animal NSAIDS
-meloxicam IV: pain on disbudding, c-section, mastitis NOT for castration
-meloxicam oral: for castration only
-Flunixin (injectable) banamine: pyrexia, endotoxemia. injection site irritation if given subQ or IM.
-ketoprofin: no withdrawl time great for dairy. anti-pyretic
-inflammation associated with respiratory infections.
Flunixin (w/ florfenicol) = Resflor
- Indicated for BRD + fever control
- 1 mL / 7.5 kg bw (Cost ~ $25 / 250 kg steer)
-increases effecacy of the drugs rather then by themselves. control of pyrexia
associated with naturally occurring bovine respiratory disease
drugs which cause unconsiousness
Isoflurane, Sevoflurane, Propofol, Alfaxalone, Ketamine
drugs which cause analgesia
Opioids, NSAIDs, Local anesthetics, Ketamine, Alpha 2 agonists
anticonsolvents
-used to treat seizures and epilepsy.
-benzodiazepines (diazepam/midazolam)
-alpha 2 agonists
what happens when drugs increase the affinity and actions of GABA
-GABA actions →
anxiolysis and sedation (dose dependent)*
* Central GABA – enhancing activity → anti-convulsant effect
Arterial blood pressure monitoring
-direct assessment of organ perfusion
-two methods: invasive(direct) or noninvasive (indirect)
-indirect: Oscillometric Method (what i used in clinic) Doppler Method (Sphygmomanometry)
-direct: catheter placed in peripheral artery
indirect Blood Pressure Monitoring - CUFF
-ideal cuff 30-40% circumference of the limb.
-cuff too wide-> underestimation of BP.
-cuff too narrow-> overestimation of BP.
-positioned same level as heart.
doppler taking a blood pressure reading how
. Inflate cuff until blood flow distal is occluded and
doppler sound disappears
2. Deflate cuff slowly
3. Pressure at which blood flow recommences:
(Whoosh sound) corresponds to:
* DOGS and CATS: Systolic BP
Oscillometric method adv/dis for blood pressure monitoring
Advantages:
* Non-invasive, automatic, less labor intensive
Disadvantages: Does not work well in case of:
* Cardiac arrhythmias, bradycardia, severe hypotension
* Movement, shivering
* No continues HR monitor
-High Definition Oscillometric devices (HDO)
* Uses advanced software algorithms
to increase accuracy
mucous membrane color CRT
-information on blood oxygenation and tissue perfusion
* Pink (normal) and CRT less than 2 seconds
* Blue (cyanosis)
* Pale (anemia or intense vasoconstriction)
* Red: (vasodilation: hypercapnia: PaCO 2> 60mmHg, endotoxemia, drugs)
respiratory system monitoring
-ensure adequate ventilation and oxygenation
-capnography
-pulse oximetry (decice on tongue with red light)
PULSE OXIMETRY
-measures pulse rate, SPO2 (oxygen saturation) % of arterial hemoglobin that carries O2.
-normal SpO2 95-100%
-based on changes of volume of a tissue bed and Deoxyhemoglobin and oxyhemoglobin absorb red and infrared light differently
-most common (tongue/ear/ toe wed, prepuce or vulva) or rectal or esophageal rod.
pulse oximetry disadvantages
-cant set and forget
-positioning important
-hard to use in patients with poor perfusion, hypotension, vasoconstriction (hypothermia).
-arrhythmias
-movement, shivering
-venous congestion.
CAPNOMETRY
-Measurement and display exhaled: end-tidal CO 2
-Respiratory rate
-Non-invasive technique for assessing adequacy of ventilation
-blood/ end tidal CO2 determined by: metabolism, circulation, alveolar ventilation.
capnometry values
Hypocapnia: paCO 2: < 35mmHg
* Normocapnia: paCO 2: 35-45mmHg (4.7 – 6kPa)
* Hypercapnia: paCO 2: > 45mmHg
Capnometry advantages
- Easy to use and non-invasive
- Provides continuous measurement
§ Confirmation of intubation
§ Monitoring for circuit disconnection
§ Identification of airway obstruction
§ Rebreathing
§ Severe circulatory problems
capnometry problems
-high end tidal Co2 >45mmHg hypercapnia due to hypoventilation, endobronchial intubation, increased Co2 production. hyperthermia.
-rapidly decreasing CO2. impending cardiac arrest, check patient, severe hypotension.
Electrocardiography (ECG)
-monitors electrical activity of heart, not mechanical
-not reliable for basic monitoring
-no info about CO, BP
lipid soluability of local anethetic drugs
-low lipid soluablility (procain) high pka slower onset of action.
-high lipid soluability (mepivicane) low pka penetrate barrers faster good motor blockade
dissociation constant in local blocks
- Determines the portion of an administered dose that exists in the lipid-
soluble (uncharged; unionized).
-more lipid soluable drug form (active form) ionized can have shorter onset of action.
-Need active form to cause effect but need inactive form to go across the cell membrane where it becomes active again and binds Na+ channel and blocks it and stops AP.
non depolarizing NMBA mechanims of action
-competetive inhibition with ach
-sits on receptor so ACH cant open the sodium channel so no AP.
* To reverse NMBA, an increase in the number of ACh molecules in the
area occurs by blocking Acetylcholinesterase (Neostigmine)
NMBAs USED IN VETERINARY MEDICINE
- ATRACURIUM:
- ROCURONIUM
pre medications
1 phenothiazines (acepromazine)
2 butryophones (azaperone)
3 benzodiazepines (diazepam, midazolam)
4 alpha 2 agonists (dexmatatomadine, xylazine)
5 behaviour modifiers (trazadone, gabapention)
