Pre-Meds I Flashcards
What are the basic aims of premedication?
- relieve anxiety/fever
- facilitate handling
- counteract side effects of anesthetics
- reduce anesthetic dose
- contribute to perioperative analgesia
- contribute to smooth recovery
What are the 3 classes of sedatives and tranquilizers we use for pre-meds?
- phenothiazines
- benzodiazepines
- alpha2 adrenergic agonists
What common analgesics are used as pre-meds?
opioids and NSAIDs
Which 6 classes of anti-emetics and GI protectants do we use as pre-meds?
- NK-1 antagonists
- D2 antagonists
- 5-HT antagonists
- PPIs
- Anti-H2
- Buffers
What are the 3 hypnotics we use as pre-meds?
- Alfaxalone
- Ketamine
- Tiletamine
What is the MOA and effect of anticholinergics on each body system?
MOA: competitive antagonists MAchR (M1-M5)
- CV: +/- paradoxical bradycardia (IV), incr HR
- Lungs: bronchodilation, reduced secretions (incr viscosity)
- Eye: mydriasis, +/- incr IOP
- GI: antisialogue, decr motility/ileus
- CNS: sedation/hallucinations (hum)
What type of drug is atropine?
an alkaloid anticholinergic
What type of drug is glycopyrorlate?
a quaternary ammonium anticholinergic; low lipid solubility and does not cross BBB + placenta
Does atropine cross the BBB?
Yes
How is atropine metabolized?
- Dogs + humans = hydrolysis + excreted unchanged
- Cat + small ruminants = hepatic and renal esterases
- Atropinase = 30% of rabbits
How is glycopyrrolate metabolized?
- no species variability
- excreted unchanged in urine
- effective in rabbits
- slower onset/longer duration than atropine
Why use anticholinergics as premeds?
- prevent bradycardia
- reduce salivation
- reduce bronchial secretions
What are the disadvantages to using anticholinergics as premeds?
- thickening of saliva + bronchial secretions
- decreased GI motility
- incr myocardial O2 consumption/arrhythmias
- no study to prove benefit
Given what we know about the disadvantages of using anticholingergics as premeds, should we use them to treat bradyarrhythmias and hypotension?
YES - these are life-saving drugs!
My anesthetized patient is bradycardic and hypotensive, what should I do?
A. Bradycardia and hypotension are not a problem
B. Anticholinergics can cause bradycardia, so I wouldn’t use them
C. Administer an anticholinergic
D. Tell the surgeon it is time to wake the patient up
C
What is the MOA and effect of phenothiazines on the various body systems?
MOA: D2, alpha1, H1, MAchR antagonists
- CNS: tranquilization, + opioids = neuroleptoanalgesia, decr MAC, anxiolysis?
- CV: vasodilation, +/- antiarrhythmic
- T°: hypothermia
- GI: antiemetic, relax LES, delay gastric emptying
- Hematologic: decr HCT (20-30%), decr PLT aggregation?
- Antihistamic
How is acepromazine metabolized?
hepatic metabolism, lasting up to 12 hours!
T or F: acepromazine can be antagonized
False
What types of patients should acepromazine be avoided for?
pediatric, geriatric, debilitated, hepatic dysfunction, or hypovolemic (causes low BP)
Why should you only use low doses of acepromazine?
the dose-response curve reaches a plateau with no increase in sedation, but it lasts longer
T or F: acepromazine is more reliable than alpha2 agonists and is a good choice for aggressive/excitable patients
False - poor choice and less reliable
Why should acepromazine be avoided in breeding stallions and bulls?
it causes priapism
What is one reason brachycephalic breeds might be at extreme risk when using acepromazine as a premed?
it may cause CV collapse (and potentially vasovagal syncope)
I gave my patient acepromazine, and now it is tachycardic and very hypotensive. What do I do?
A. Administer an anticholinergic
B. Reverse acepromazine
C. Administer a fluid bolus
D. Turn off all monitors
C; cannot reverse and anticholinergics cause tachycardia
What is the MOA and effect of benzodiazepenes on various body systems?
MOA: allosteric modulator of GABA @ GABAA rec
- No direct action
- Incr susceptibility to GABA –> incr Cl- conduction –> decr excitability
-
Effects: sedation, anxiolysis, anticonvulsants, MM relaxants
- Minimal CV effects
- mild dose-dependent resp depressant
T or F: Benzos may cause excitement in healthy dogs and cats
True, potentially due to a decreased learned inhibition
Benzodiazepines are reliable sedatives in what types of animals?
- very young
- very old
- very sick
- small ruminants
- pigs
What type of metabolism do benzos undergo?
hepatic
What are 2 benefits of using benzos as a premed?
they reduce your anesthetic requirement and can be antagonized
What do benzos need to be paired with for a reliable effect?
opioids or hypnotics
What type of drug is diazepam and what are some features of it?
- benzodiazepine
- insoluble in water
- 35% propylene glycol (–> pain, hemolysis, erractic IM SQ absorption)
- light sensitive
- absorbed in PVC (in syringes)
What type of drug is midazolam and what are some basic features of it?
benzodiazepine
- no propylene glycol
- in vial pH (3.5) = water soluble
- at physiologic pH = liquid soluble (reaches brain and has an effect)
What type of drug is zolazepam and what are some basic features of it?
benzodiazepine
- tiletamine = Telazol (trade name)
- excellent immobilization
- powder = can be reconstituted with small volumes
- metabolism:
- cats, pigs - tiletamine > zolazepam (smooth recovery)
- dogs, horses - zolazepamn > tiletamine (rough recovery)
What is flumazenil and what is a potential side effect of it?
a competitive antagonist for benzodiazepines; can cause seizures!
I was not paying attention in class, so I gave midazolam IV to a young, healthy dog as a pre-medication. The dog is now climbing the wall. What do I do?
A. Administer more midazolam to achieve sedation
B. Administer an anticholinergic
C. Give a hypnotic or an opioid
D. Leave the room
C
What are the effects of alpha2 adrenergic agonists on various body systems?
- CNS: sedation - ruminants alpha2D, touch/sound sensitive, MAC reduction, analgesia
- GI: vomit, decr motility
- CV: biphasic- incr BP, decr HR; decr BP, decr HR; CO reduction (50-66%)
- T°: decr ability to thermoregulate
- Resp: mild depressant, cyanosis, pulm edema in small ruminants
- M/S: central mm relaxant
- Uterus: ecbolic effect
- Renal: incr urine production
- Endocrine: suppression of stress response, insulin (hyperglycemia)
- IOP/ICP: no change, vomit may increase!
Describe MOA of alpha2 adrenergic agonists?
mimics NE at pre-synaptic alpha2 receptors, causing negative feedback and decreased NE release + decr Ca2+ conductance on post-synaptic cells
Where are alpha2A receptors located and what is their effect?
cortex and brainstem; sedation, supraspinal analgesia, central bradycardia, hypotension
Where are alpha2B receptors located and what is their effect?
spinal cord and vascular endothelium; increased SVR = reflex bradycardia
Where are alpha2C receptors located and what is their effect?
spinal cord; impaired thermoregulation
Where are alpha2D receptors located and what is their effect?
2A; ruminants only
Of these alpha2 agonists, which has the greatest alpha2:alpha1 selectivity? The least?
detomidine, romifidine, medetomidine, dexmedetomidine, xylazine
Medetomidine, dexmedetomidine = greatest
Xylazine = least
What are the side effects of alpha2 agonists?
- profound CV effects - transient hypertension, persistent bradycardia, hypotension, decr CO, do NOT give to neonates (relie heavily on HR for CO)
- decr ability to thermoregulate
- emesis
- decr GI motility
- hyperglycemia
- incr urine production
What is the proposed mechanism of alpha2 agonists causing pulmonary edema in small ruminants?
- mediated by macrophages -> reversal of alpha2 agonists does NOT improve edema, ONLY reverses sedation
What problematic condition do alpha2 agonists cause in large felids and what is the proposed mechanism behind it?
hyperkalemia (lethal if not promptly treated); postulated mechanism = anti-insulinic effect leads to translocation of K+ to ECF
T or F: xylazine is commonly used as a pre-med drug in small animals
false; used as a pro-emetic in cats
Name one significant adverse effect of xylazine in horses?
seizures following intra-carotid injections
In what animals is Detomidine used most commonly as a pre-med for and in what form?
horses and pigs; oral gel
Detomidine is ______ (more/less) potent and ______ (shorter/longer lasting) than xylazine
more; longer lasting
In what animal is romifidine licensed to be used as a pre-med for? Is it shorter or longer lasting than xylazine?
horses; longer lasting
Medetomidine is most commonly used for what purpose?
capture (with ketamine); no longer used for domestic species
What are common uses of dexmedetomidine?
analgesia and sedation in ICU (as a CRI); in theory 2x as potent as medetomidine
What are the uses of alpha2 antagonists?
- to terminate sedation
- to treat overdoses
- after capture of wild animals
What are some considerations you should have when using alpha2 antagonists?
- analgesia will be reversed too
- alpha2 adrenergic + ketamine = ketamine convulsive action may be revealed
- these may have profound CV side effects
- if used to treat alpha2 agonist-induced bradycardia, HR doesn’t change much but systemic vascular resistance will decrease! (low BP)
What are 3 examples of alpha2 adrenergic antagonists?
Tolazoline, yohimbine, and atipamezole
What are the effects of tolazoline? Side effects?
- Effects: vasodilation, cholinergic, H release
- SE: fasciculations, hypotension, ventricular arrhythmias, death
Rank these 3 drugs from greatest to lowest alpha2:alpha1 receptor selectivity:
tolazoline, yohimbine, atipamezole
Atipamezole >>>> Yohimbine > Tolazoline
Atipamezole has been licensed to only be given by what adminstration method?
IM
I gave my patient dexmedetomidine, and now it is bradycardic. What do I do?
- If patient’s hypertensive,
- nothing
- increase halogenate
- reverse
- If normotensive,
- nothing
- atropine?
- glycopyrrolate?
- If hypertensive,
- Atropine
- Glycopyrrolate
What are the centers of the brain anti-emetics work on?
Chemoreceptor trigger zone (opioids), cortex/thalamus (pain, anxiety) and vestibular system (motion)
Why should you use anti-emetics and/or antacids for pre-meds?
- peri-operative nausea and vomiting (PONV) is frequent in small animal patients
- factors: anesthesia-related, surgery-related
- Gastroesophageal reflux has high incidence in SA patients –> esophageal stricture, aspiration of gastric content (potential sequelae)
What are three commonly-used antiemetics?
maropitant, metoclopramide, ondansetron
What is the MOA of maropitant?
MOA: NK1 antagonist
*PO admin prior to pre-med reduces incidence of alpha2 agonist-induced vomit
(painful given SQ!)
What is the MOA of metoclopramide and what is it commonly used for?
MOA: 5H3 antagonist, D2 antagonist
Used as a pro-emetic and antiemetic (often CRI)
What is the MOA of ondansetron?
MOA: 5H3 antagonist
Name three common antiacids used as pre-meds
Famotidine, omeprazole, Na citrate
What is the MOA of famotidine?
MOA: H2 antagonist
What is the MOA of omeprazole and what is it more effective at doing than famotidine?
MOA: proton pump inhibitor
More effective at incresing pH that famotidine
What is the MOA of Na citrate and how must it be given? What patients should you be careful using it in?
MOA: buffer (converted to NaHCO3)
Must be given orally
Be careful in patients with CKD (metabolic alkalosis) or cardiac disease (risk of CHF due to Na overload)
Which of the following patients is most likely to benefit from an administration of a gastro protectant and an antiemetic?
A. GI foreign body
B. C-section
C. Chronic kidney disease
D. Severely painful dog that has been on opioids and NSAIDs for a week
E. All the above
E
