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199 Cards in this Set
- Front
- Back
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a gauze sponge pad soaked is how many mLs?
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10-15mls
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a big lap pad soaked is how many mLs
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about 50mLs
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what classifies something as an anesthetic complication?
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DEATH
shorter life long recovery injury to staff expense |
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normal blood pressure
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systolic: 120
MAP: 90-100 diastolic: 80 |
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minimum acceptable MAP
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60-65mmHg
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when does hypotension happen?
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inhalant anesthetics
excessive anesthetic depth hemorrhage |
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BP=_____ * ______
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CO * PVR
(CO= HR*SV) |
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clinical signs of hypotension
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tachycardia
weak pulses (maybe) Pale MM |
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how do you respond to hypotension?
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check your patient !!!!!!
change anesthetic depth? appropriate fluids (crystalloids, colloids) +/- inotropes +/- vasopressors |
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how do we classify hypoxemia
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low O2 tension in the blood (PaO2 <60)
SPO2 is a more common measure SPO2 <95% = mild <90%=severe |
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Why do we care about hypoxemia?
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because EVERY tissue needs O2 to survive
it is an emergency under anesthesia we can prevent it |
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when does hypoxemia happen?
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Beginning/End of anesthesia
sometimes in the middle |
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Clinical signs of hypoxemia?
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Cyanosis- won't always see
tachycardia arrhythmias bradycardia "gasping" death |
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Cyanosis happens when?
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5gm/dL deoxyHb
SpO2 DOES NOT define cyanosis Polycythemic patient Anemic patient |
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Causes of hypoxemia?
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Low FiO2
VQ mismatch Shunt Hypoventilation Diffusion impairment |
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How do you respond to hypoxemia?
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Check your patient!!!!!
supply oxygen intubation (do it/check it) attempt to ventilate check your machine |
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Hypercarbia/hypercapnia
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excessive CO2 levels in the blood
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What are the 2 causes for hypercarbia/capnia?
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poorly eliminated
Produced excessively |
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What is normal and what is acceptable for CO2 levels?
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normal: 35-45
acceptable: 55-60 |
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Clinical signs of hypercapnia/carbia?
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increased respiratory rate
tachycardia increased BP!!! dark pink MMs eventually - narcosis |
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what is the general approach to arrhythmias?
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do I need to treat?
what is the likely cause? how should I treat? |
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what causes sinus bradycardia?
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opioids
hypothermia vagal stimulation ----hypotension in very young patients |
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treatment for sinus bradycardia?
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anticholinergics
warming |
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what is sinus bradycardia?
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complexes are normal but slow
-----make sure to check what is slow for this patient induced by several anesthetic agents/conditions |
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what is sinus tachycardia?
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complexes are normal but fast
----make sure to check what is fast for this patient significant tachycardia reduces ventricular filling time may indicate pain, light anesthetic plane |
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treatment for sinus tachycardia?
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---find the cause first!!!
analgesia increased depth |
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what is second degree AV block?
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normal?
anesthetic induce block (alpha 2 agonists, opioids) |
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what is treatment for second degree AV block?
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do it only if appropriate
usually an anticholinergic |
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third degree AV block
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complete dissociation between atria and ventricles
associated with significant bradycardia treat with pacemaker will come up on a pre-op exam!!!!!!! |
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What are ventricular complexes?
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wide
bizarre biphasic indicate ventricular origin |
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What are Ventricular Premature Complexes (VPCs)
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singles
ibgeminy runs (V-tach vs AIR ---its all about rate) multiform treat if indicated lidocaine is most common choice |
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what are ventricular escape beats?
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ventricular origin
NOT premature Lidocaine is contraindicated!!!! raise heart rate- anticholinergics are first choice!!!! |
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What are rhythms of death?
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Asystole
ventricular fibrillation electro-mechanical dissociation/pulseless electrical activity |
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what is hypothermia?
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below-normal core body temperature
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Why do we care about hypothermia?
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decrease MAC of inhalent
arrhythmias delayed wound healing prolonged recovery shivering is painful and physiologically exhausting |
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What are the heat loss mechanisms?
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conduction
convection radiation evaporation |
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What can we do about hypothermia?
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acknowledge the problem
prevent heat loss actively warm |
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What are the different classifications/causes of emergence excitement?
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disorientation
dysphoria pain |
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what can we do for emergence excitement?
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handle with care
treat pain reassess |
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What is pain?
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unpleasant sensory and emotional experience (perception) associated with actual or potential tissue damage or is described in term of such damage
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What is nociception?
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the reception, conduction, and central nervous system processing of nerve signals generated by the stimulation of nociceptors. this process leads to the perception of pain.
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where is perception in the pain pathway?
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cerebral cortex
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where is modulation in the pain pathway?
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spinal cord
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where is transmission in the pain pathway?
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sensory nerves
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where is transduction in the pain pathway?
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sensory nerve endings
nociceptors |
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What is tranduction?
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free A-delta and C nerve endings or nociceptors convert the mechanical, chemical or thermal energy (noxious stimuli) into electrical impulses
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What are A-delta nociceptors?
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composed of mechanoreceptors and mechanohermal receptors
- low threshold (<75%) - high threshold (<25%) --- respond only to tissue-damaging stimulation discharge at a higher rate than C-fiber nociceptors --- provide more discriminative info to the CNS --- responsible for pricking and sharp qualities of "first pain" |
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What are C-fiber nociceptors?
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almost all are high-threshold and respond to different types of stimulation
activation is responsible for slow-onset ("second") pain that occurs after the initial insult ----burning and aching qualities ----signals tissue damage and inflammation that initiates self-preservation behaviors such as avoidance and guarding and disuse |
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What are silent or sleeping nociceptors?
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A-delta fibers and C-fibers contain "sleeping" nociceptors activated by tissue damaging events
important role in peripheral sensitization |
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what substances can cause activation of nociceptors?
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histamine (from Mast cells)
bradykinin serotonin prostaglandin K+ substance P (from Mast cells or blood vessels |
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What is Transmission in the pain pathway?
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electrical signals are transmitted by the nociceptive fibers to the spinal cord
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A-delta fibers
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small diameter 1-4 micrometers
myelinated fast conduction transmit well localized prickling, sharp pain "first pain" |
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C-fibers
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smaller diameter (0.4 - 1.2 micrometer)
unmyelinated slow conduction transmit poorly localized dull or aching pain "second pain" |
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What is modulation in the pain pathway?
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amplification or suppression of the peripheral sensory nerve impulses at the level of the spinal cord
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modulation causes activation of....
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excitatory or inhibitory interneurons
propriospinal neurons involved in segmented reflex activity projection neurons extending to supraspinal centers (midbrain and cortex) |
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What is perception in the pain pathway?
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end result of neuronal activity or pain transmission
pain becomes a conscious multidimensional experience |
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In perception, multiple cortical areas are activated. The responses include...
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the reticular system
somatosensory cortex limbic system |
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Perception: Reticular system
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autonomic and motor response and warning to do something (move away from insult)
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Perception: Somatosensory cortex
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identifies intensity type and location of pain and relates to past experiences and memory
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Perception: limbic system
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emotional and behavioural responses to pain (attention, mood and motivation)
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what is the descending pathway?
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cortex, amygdala and thalamus --> descending signals --> periaqueductal grey matter (PAG) --> inhibitory input through --> endogenous opioids (dynorphins, endorphins, enkephalins) --> descend from brainstem to dorsal horn of the spinal cord --> inhibition of transmission of impulses
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What is central sensitization?
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alteration in the excitability of neurons in the brain and in the spinal cord caused by severe or chronic painful stimuli that activates A-delta and c nociceptors
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How do we classify pain?
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duration and origin
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duration of pain: acute
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results from an abrupt and brief event usually related to trauma, surgery or infection
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duration of pain: chronic
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pain persists beyond a reasonable time for the course or an acute disease or an injury to heal
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what is somatic pain?
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originates from damage to somatic tissues (bone, joints, muscle, and skin)
sharp and well localized |
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what is visceral pain?
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arises from visceral injury
is not well localized can be associated with nausea and vomiting |
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What is neuropathic pain?
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direct damage to peripheral nerves or spinal cord
described as burning or shooting pain usually difficult to treat |
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Why do we treat pain?
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pathophysiological effects
psychological effects |
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What are pathophysiological effects caused by pain?
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inc. anxiety
inc. depression inc. heart rate inc. respiration inc. coagulability dec. metabolism dec. immune function |
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How is the immune system affected by pain?
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increased cortisol levels impair wound healing and decrease immune system function
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How is the neuroendocrine system affected by pain?
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activated by pain
gluconeogenesis is favored impaired metabolism results in catabolism and cachexia |
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how is the GI system affected by pain?
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sympathetic stimulation can cause shunting of blood, decreased motility and decreased mucosal integrity
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how is the cardiovascular system affected by pain?
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===activation of the renin-angiotensin system
fluid retention elevated blood pressure decreased renal perfusion increased HR, SV, CO, and myocardial O2 consumption |
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What are the psychological effects of pain?
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patient's quality of life decreased
owner gets angry, guilty and fearful of procedures caregivers feel guilt or lack of compassion if unable to treat it |
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How do you recognize pain?
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history (input from owner)
observation of behavior physical exam (fourth vital sign) interaction with patient assessment tools |
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what are losses of behavior that occurs with pain
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decreased ambulation or activity
lethargic attitude decreased appetite decreased grooming (cats) harder to assess in the hospital |
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What are some abnormal behaviors that are expressed with pain?
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inappropriate elimination
vocalization aggression dec. interaction with other pets or family members altered facial expression altered posture restlessness hiding (esp. in cats) |
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what reactions to touch might a patient have if in pain?
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increased body tension or flinching in response to gentle palpation of injured area an dpalpation of regions likely to be painful (neck, back, hips, elbows)
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What are physiologic parameters that are used for signs of pain?
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elevations in:
heart rate respiratory rate body temp blood pressure ---pupil dilation |
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What is the dynamic and interactive visual analog scale (DIVAS)?
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observation from a distance undisturbed
approached, handled, encourage to walk palpation of surgical incision and surrounding area final overall assessment of sedation and pain |
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What are th ecategories used in the Glasglow Composite Measures Pain Scale?
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posture
comfort vocalization attention to the wound demeanor and response to humans mobility and response to touch |
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How do we inhibit perception?
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anesthetics
opioids alpha 2 agonists benzodiazepines |
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how do we inhibit central sensitization (modulation of spinal pathways)?
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local anesthetics
opioids or alpha 2 agonists tricyclic antidepressants cholinesterase inhibitors NMDA antagonists NSAIDs |
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How do we inhibit impulse conduction (inhibit transmission)?
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local anesthetics
alpha 2 agonists |
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How do we inhibit peripheral sensitization of nociceptors (inhibit transduction)?
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NSAIDS
Opioids Local anesthetics |
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Systemic Opioids: Mu agonists
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use for moderate to severe pain:
morphine oxymorphone fentanyl meperidine hydromorphone methadone |
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Systemic Opioids: partial Mu
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use for mild to moderate pain:
buprenorphine |
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Systemic Opioids: agonists-antaonists
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use for mild pain:
butorphanol |
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How do NSAIDs work?
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inhibitors of COX-1 and COX-2 --- prevents conversion of arachidonic acid into prostanoids
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What are contraindications of NSAIDs?
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renal or hepatic insufficiency
low effective circulating volume (dehydration, hypotension, shock) active GI diseases coagulopathies current use of corticosteroids or other NSAIDs pregnancy |
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Alpha 2 agonists
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central opioid like effect
analgesia low doses (cardiovascular effects still present) duration (use CRI?????) |
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Local Anesthetics
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prevent transduction and transmission
use in local and regional blocks IV lidocaine (NOT BUPIVACAINE) -good visceral analgesia in horses (colic) adjunct to systemic opioids decreases about 25% MAC of inhalent anesthetics |
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Low Dose Ketamine
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block of glutamate action at NMDA receptor (NMDA antagonist)
can prevent and treat central sensitization central sensitization and hyperalgesia common in burns IV, SQ, IM, epidural |
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What is preemptive analgesia?
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not only previous (preventative analgesia) to surgical stimulus but also during and after stimulus
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Opioid constant rate infusion
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plasma levels more consistent
eliminates the need for repeated administration from traditional routes (IV, IM, SQ, and oral) |
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What do use for buccal transmucosal pain med?
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---Buprenorphine
cats dogs pH of the mucosa NOT ORAL no first pass effect |
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What are some drawbacks to transdermal administration (Fentanyl and Lidocaine)?
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variable plasma levels
skin reactions nausea anorexia potential human exposure ingestion by the animal |
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Intraarticular injection
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local anesthetics
opioids --- opioid receptors on peripheral terminals of primary afferent neurons ---inflammation increases number of receptors |
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Epidural Opioids / Local anesthetics
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preservative free drugs
advantages: prolonged segmental analgesia minimal sedation reduces inhalation anesthetic requirement disadvantages: technical expertise spinal needle required |
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Side Effects to epidural opoids/LA
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pruritis
urinary retention delayed respiratory depression? vomiting hypotension from LA |
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complications from Epidural opioids/LA
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ineffective analgesia
epidural hematoma epidural abscess |
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What are contraindications for Epidural Opioids/LA?
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sepsis
coagulopathies |
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What is the indication for a brachial plexus block?
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procedures within and below the elbow
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Intercostal nerve block
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indications:
lateral (intercostal) thorocotomy rib fractures ----- inject two spaces cranial and caudal to injury site ----- caudal border of rib ----- near intervertebral foramen |
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What are the indications for interpleural analgesia?
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thoracotomy
rib fracture thoracic wall, pleural, or mediastinal metastasis pancreatitis cholecystectomy |
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Lidocaine is what kind of local anesthetic?
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amide
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Procaine is what kind of local anesthetic?
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ester
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Amides used as local anesthetics
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longer acting than esters
lidocaine -- rapid onset of action, lasts 1 to 2 hours, causes neurotoxicity mepivicaine -- rapid onset of action, lasts 2-3 hours, joint blocks on LA bupivicaine -- slow onset, lasts 3-4 hours, causes CARDIOVASCULAR TOXICITY -broken down by the liver at a slower rate than esters -first pass pulmonary uptake |
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_________ is converted to orthotoluidine which results in methemoglobinemia
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Prilocaine
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Bupivicaine
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slow onset, lasts 3-4 hours
-causes cardiovascular toxicity (malignant arrhythmias) -be supremely careful b/c giving it IV will kill your patient -prevention: use 2 mg/kg (1/2 dose if cat) -if you give way too much, give Lipid Rescue (lipid reversal agent) |
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Esters
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procaine, benzocaine, chlorprocaine, tetracaine, cocaine
-broken down in minutes by pseudocholinesterase -PABA, a metabolite, can cause an allergic reaction |
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Why is cetocaine spray (procaine) not recommended in cats?
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causes methemoglobinemia
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Which local anesthetic would likely have the slowest absorption, all else being equal?
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Bupivicaine
- MOA - block the function of Na channels, physically plug, alter conformation; the drug knows where to go b/c it knows where the Na channels are being asked to open |
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Mechanism of action - locals
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prevent neuronal depolarization
block the function of Na channels --physically plug -- alter conformation ------frequency dependent blockade |
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nerve types: class and function
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A:
Alpha- proprioception, motor beta: touch, pressure gamma: muscle tone delta: pain, temperature B: preganglionic autonomic C: dorsal root - pain (slow) |
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local anesthetics block sodium channels in what conformation?
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resting-closed
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Local anesthetics: pharmacology
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poorly water soluble alone
marketed as water soluble hydrochloride salts other formulations: continuous release patch liposomal encapsulation creams, gels, sprays EMLA cream |
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Local anesthetics act locally, so ________ usually signals the end of their action?
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absorption
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Injection site of Local anesthetics: absorption
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more vascular site --> faster absorption and a higher peak blood concentration
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Drug-tissue interaction: absorption
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more potent, more lipid soluble, lower blood concentration
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Addition of vasoactive agent -- epinephrine : absorption
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vasoconstriction -- less absorption, longer duration
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Dose: absorption
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greater dose: higher concentration, then higher peak blood concentration
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Metabolism of Esters
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pseudocholinesterase
rapid (minutes) PABA - allergic reaction |
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Metabolism of Amides
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hepatic cytochrome P450
slower ---- lidocaine t1/2: 1.5 hours ---- bupivicaine t1/2: 3/5 hours first pass pulmonary uptake prilocaine --> othotoluidine: methemoglobinemia |
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Which local anesthetic causes neurotoxicity?
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lidocaine
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Which local anesthetic causes cardiovascular toxicity?
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Bupivicaine
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Cetocaine spray is not recommended in cats b/c it can cause what problems?
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methemoglobinemia
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topical route for local anesthetics
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absorbed across mucous membranes (corneal, laryngeal)
generally poorly absorbed by intact skin --- exceptions are EMLA cream and Lidoderm patch |
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Local anesthetics: Local infiltration
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infiltrate SQ w/ local anesthetic around/under surgical site
----small lumps/bumps ----small lacerations ring blocks inverted L block watch total dose!!! |
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Local anesthetics: peripheral nerve blocks
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infiltrate local anesthetic adjacent to peripheral nerve
blocks area innervated by that nerve armed w/ anatomy book, you can block nearly any peripheral nerve prep the skin before injection ALWAYS ASPIRATE BEFORE INJECTION be conscious of local/vasoconstrictor mixes |
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Maxillary Nerve block
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maxillary molars and all teeth/tissues rostral
aim just under the zygomatic arch |
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Infraorbital nerve block
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third premolar and forward
soft tissue rostral to upper 4th premolar |
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Inferior Alveolar (Mandibular) nerve block
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all teeth in mandible
mandibular hard and soft tissues (extraction and fracture repairs) slight misdirection may impair tongue function (careful!) |
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Mental nerve Block
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Mandibular incisors
surrounding soft tissue |
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Retrobulbar Nerve block
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especially good for enucleation
Blocks: occular movement through the abducens, oculomotor, trochlear sensation to the eye (opthalmic branch of trigeminal) Be careful of oculocardiac reflex |
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Risks with the Retrobulbar nerve block
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hemorrhage
globe rupture CNS infiltration -> arrest (aspirate before you inject - if you see straw color fluid - don't inject |
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Intravenous Regional (Bier Block)
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useful for lesions on distal extremities
place IV catheter place tourniquet inject lidocaine block is gone shortly after removal of tourniquet time limited by tourniquet |
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What are the 3 regional blocks?
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epidural
intrathecal brachial plexus |
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Epidural injection is recommended for:
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hind limb/end procedures
abdominal incisions background analgesia for anywhere |
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Epidural injection: cranial spread determined by...
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site of injection
quantity of drug volume injected |
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Relative contraindications for Epidural injections
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CHAINS
-coagulopathy -hypotension/hair -anatomic abnorm./allergies -Infection -neurologic disorder (meningitis or assessment required) -septicemia |
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Brachial Plexus Block
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clip and prep similar to epidural
insert spinal needle medial to scapulohumeral joint aim needle lateral (up) to avoid thoracic cavity blind technique (advance needle to half length of humerus) electrostim technique: target nerves always aspirate before injecting |
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What drug is good to use for CRIs in local anesthetics
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lidocaine --- but NOT IN CATS
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Mortality rate under anesthesia
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humans: 1/10,000
dogs: 1/250, 40/10,000 horses: 1/100 or 100/10,000 |
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Horses _______ have a good CPR success rate.
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DO NOT!!!!!!!!!
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Steps to General Anesthesia in the Equine
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patient assessment and planning
equipment set up and check IV catheter placement clean the mouth and feet sedation induction maintenance recovery complete record |
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Equine: sedatives and analgesics
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acepromazine +/- alpha 2 agonists +/- opioid
Acepromazine + opioid alpha 2 agonists +/- opioid |
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Equines: Morphine
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full mu-agonist = more profound analgesia and side effects
used for seere pain (usually orthopedic) more likely to cause GI discomfort can cause histamine release when given IV so give diluted and slowly while observing BP more likely to cause excitement, better to sedate with alpha-2 prior to admin can be used as CRI excellent for epidural analgesia can be used in joint for analgesia |
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Equine: induction of anesthesia
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only induce if horse is well sedated
do not induce if horse is not well sedated!!!! =can be done in the field as free-drop or behind a gate in an induction room at the hospital |
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Equine: induction drugs - dissociatives
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mechanisms of action not completely understood -- NMDA antagonists
- good for induction and recovery qualities -do not cause tissue necrosis if outside vein -analgesia -small volumes -controlled substances -used in assoc. w/ other drugs -mild resp. depressants (transient apnea) -direct myocardial depressants, but indirect stimulants -no reversal agent available |
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Equine induction drugs: Ketamine
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give IV (doesn't work well other routes)
donkeys and mules req. more frequent redosing maintain strong palpebral reflex and occasional nystagmus can be used as CRI: triple drip, or adjunct to gas anesthesia |
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Equine induction drugs: Telazol
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combo of tiletamine and zolazepam
onset: up to 2 min., duration: 15-45 min usually used as a single bolus good induction quality can cause excitement during recovery |
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Equine Maintenance: Adjuncts to inhalant anesthesia (CRIs)
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morphine
lidocaine butorphanol xylazine ketamine |
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Equine Monitoring: corneal reflex
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light: brisk
adequate: present deep: absent |
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Equine Monitoring: palpebral reflex
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light: brisk
adequate: slowed deep: absent |
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Equine Monitoring: lateral nystagmus
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light: present
adequate: absent deep: absent |
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Equine Monitoring: unstimulated blinking
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light: present
adequate: absent deep: absent |
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Equine Monitoring: eyeball position
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light: centered
adequate: rotated deep: centered |
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Equine Monitoring: Tearing
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light: present
adequate: absent deep: absent |
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Equine Anesthesia: Support
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ventilation
Inotropes/vasopressors: B-agonists vs a-1 agonists -dobutamine vs dopamine phenylephrine vasopressin norepinephrine Fluid therapy: 10mL/kg/h (~5L/h for avg horse) |
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Equine Anesthesia: Recovery
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sedation
oxygen airway support (oral or nasal tube) empty bladder cover eyes nasal decongestion (vasoconstrictors) |
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Equine Anesthesia: complications
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hypotension/CV collapse
hypoventilation V/Q mismatch myopathy nerve paralysis fractures airway obstruction (nasal swelling - obligate nasal breathers) excitement |
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Equine Anesthesia: conclusion
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high mortality rate in equine anesthesia
every detail is important adequate analgesia is warranted |
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Important things to consider with bovine anesthesia
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big and heavy
rumen frequent eructation fairly docile very sensitive to: alpha 2 agonists, dopamine, and dobutamine |
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Fasting Bovines for anesthesia
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depends on rumen size
-adults 18-24 hours if possible -milk fed calves just a few hours |
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Bovine: Common sedation protocols
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alpha-2 agonist ---REMEMBER lower dose (xylazine)
alpha 2 agonist +butorphanol alpha 2 agonist + ketamine ----local anesthetics are the mainstay of analgesia (lidocaine, bupivicaine) |
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Bovine Induction
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ketamine
ketamine + diazepam ketamine + GG Thiopental Thiopental + GG |
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How to intubate a cow
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take off your jewelry
prepare to get messy palpate the arytenoids pass tube -- +/- stomach tube as stulet -- inflate cuff (important to do immediately) -- have suction ready secure the tube -- ties will get WET so tie to both upper and lower jaw |
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Bovine Anesthesia: positioning
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heavy
pointy prone to regurgitation plan for voluminous secretions (pad under shoulder to allow for a mountain like incline of neck and head) pad like crazy (under shoulders and between legs) rumen down if possible |
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Bovine: normal parameters
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HR: 60-80 bpm
RR: 20-30 breaths per min eye position - ventral rotation indicates surgical anesthetic depth -central position could indicate too light OR too deep blood pressure: same as other mammals --- normotension is important to prevent myopathy |
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Bovine: Anesthetic complications
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tympany
regurgitation - atropine not useful to dec. secretions -- just makes em thicker hypoventilation movement hypotension --- uncommon complication --- very sensitive to dobutamine's tachycardic effects |
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Bovine Anesthesia: Recovery
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accustomed to lying down
--- position in sternal ASAP --- they have little to no excitation during recovery extubate only when they have good airway control |
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Small Ruminant Anesthesia: special considerations
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very narrow dental arcade
relatively long face and thick tongue regurgitate often -- may need to be deeper at induction -- cuffed ET tube important!! -- atropine not useful to dec. secretions b/c just makes em thick may bloat under anesthesia eye position less useful than pupil size/shape |
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Small Ruminant Anesthesia: common complications
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hypoxia
rumen tympany hypotension |
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Small ruminant anesthesia: common protocols -- sedation/analgesia
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alpha 2 agonist
alpha 2 agonist + opioid --- sheep may have idiosyncratic pulmonary edema w/ xylazine--- |
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Small ruminant anesthesia: induction
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ketamine + diazepam
telazol thiopental propofol (smaller animals |
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Small ruminant anesthesia: recovery
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manageable size
usually no excitation |
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Small Ruminant: Normal Parameters
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HR: 40-80 bpm
RR: 20 bpm blood pressure: same as mammals eye position: less useful measure of anesthetic depth; pupil size and shape are indicative other signs: palpebral maintained at adequate depth (sluggish) - spontaneous blink means too light - nystagmus not usually visible |
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Small Ruminant Anesthesia: Recovery
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obligate nasal breathers
prone to regurgitation --- maintain sternal body position --- extubate when swallowing effectively curl necks backward and swing head during recovery normally show little excitation |
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Camelid anesthesia: principles
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accurate weight is vital
difficult to catheterize intubation similar to small ruminants obligate nasal breathers (like horses) |
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Camelid anesthesia: common protocols
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Sedation/analgesia
xylazine alpha 2 agonist + butorphanol alpha 2 + buprenorphine Induction: ketamine + diazepam propofol (smaller animals) Thiopental |
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Swine Anesthesia: Principles
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thick necks
relatively brachycephalic huge size range -- can be big and heavy resent restraint -- LOUD can vomit little body hair, lots of body fat |
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Swine anesthesia: Preparation
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fasting usually recommended: 12-24hrs for adult
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Swine anesthesia:: catheter
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venous access difficult w/out significant sedation
thick skin -- usually fat so..... ear veins are best bet rubber band around ear base to raise vessel |
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Swine anesthesia: intubation
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sternal recumb., neck stretched up, mouth open
laryngoscope to visualize arytenoids --- spray lidocaine ET tube w/ stylet ben at tip into a curve pass tube until you meet resistance, then turn 180 degrees up, advance, and turn back down |
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Swine anesthesia: complications
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malignant hyperthermia:
Landrace, Duroc, and a few others triggered by stress, depolarizing neuromuscular blockers, inhalants (esp halothane) treat by removing all inhalant, actively cooling, ventilate, +/- Dantrolene regurgitation hypothermia hypotension |
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Swine anesthesia: recovery
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monitor temp closely
warming often needed generally smooth |
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Swine anesthesia: premedication
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IM doses
Telazol Telazol + xylazine Ketamine +/- midazolam +/- butorphanol acepromazine not very effective |
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Swine anesthesia: Induction
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IV doses
ketamine +/- diazepam propofol (smaller animals) telazol thiopental (phlebitis in small vessels) |
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Swine anesthesia: Maintenance
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inhalant
CRI of propofol, etc |
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Feline Anesthesia: Preparation
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fasting usually recommended
- 8-12 hours for a full size adult -young kittens may only be 1-2 hours Equipment: non-rebreathing circuit recommended for inhalant delivery |
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Feline Anesthesia: Intubation
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take a deep breath, prepare to be patient
start giving induction drugs "to effect" use laryngoscope to view arytenoids - DO NOT touch epiglottis apply lidocaine to arytenoids pause...allow cat to relax and lidocaine to take effect visualize arytenoids again and slip in your tube ---stylet PRN ---may need more induction drug for this step |
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Feline Anesthesia: Normal parameters
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HR: 120-160 bpm
RR: 10-20 bpm eye position: ventro-medial blood pressure: same as other mammals non-rebreathing circuit for inhalant delivery |
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Feline Anesthesia: complications
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hypothermia: small, little fat
monitor temp during active warming -- can warm up very quickly hypotension: very sensitive to volume overload relatively low blood volume per body weight (60 ML/kg) Bronchoconstriction: underlying asthma reactive airway how does it feel when you squeeze the reservoir bag |
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Feline Anesthesia: recovery
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hyperthermia:
cats get hot young healthy animals many drugs implicated, none proven hypothermia: frequent complication best to prevent it active warming PRN, and temp frequently slow recovery: delayed metabolism is it appropriate to reverse |
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Feline Anesthesia: Kitty bomb or Kitty magic
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ketamine
dexmedetomidine opioid (eg butorphanol, buprenorphine) |
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Feline Anesthesia: Sedation/analgesia
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kitty bomb or kitty magic
acepromazine + opioid ketamine + midazolam +/- opioid |
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Feline Anesthesia: induction
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propofol
diazepam telazol Inhalant -- MAC similar to other animals |
