Set the Language

We weren't able to detect the audio language on your flashcards. Please select the correct language below.

Front

Back

Related Flashcards

Flashcards
»
Anesthesia Exam I

Anesthesia Exam I

by c.a.childs9, Feb. 2014

Favorite

Add to folder

Flag

Shuffle
Toggle On

Toggle Off
Alphabetize
Toggle On

Toggle Off
Front First
Toggle On

Toggle Off
Both Sides
Toggle On

Toggle Off
Read
Toggle On

Toggle Off

Reading...

Front

Card Range To Study

through

Play button

Progress

1/1018

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

1018 Cards in this Set

Front
Back

	Why give General Anesthesia to Large Animal?	-Unconsciousness -Amnesia -Muscle relaxation -Immobility -Analgesia
	Types of Procedures for Anesthesia in large Animal	-Orthopedic procedures --arthroscopy --fracture repair -Soft tissue procedures --tie back --castration --hernia repair -Emergencies --colic surgery --difficult lacerations --C-section
	Steps in Anesthetizing a Large Animal	1. Patient Evaluation --Hx, PE, Identify the problem 2. Patient Preparation 3. Equipment set-up 4. Sedation --drug choice --environment 5. Induction --drug choice --induction style 6. Maintenance 7. Monitoring 8. Recovery --drug choice, species, style 9. Long-term recovery
	Patient Evaluation for Anesthetizing a large Animal	-Signalment -Presenting complaint -Estended history -Current history -Patinent status -COMPLETE physical exam -Diagnostics available --bloodwork --imaging -ASA physical status
	Pre-operative fasting in large Animal	-Horses: 4-6 hours no food --free choice water -Pigs: 8-12 hours --free choice water -Ruminats: 18-36 hours no food --12-24 hours no water --worry about bloat -Camelids: 14-18 hours no food --8-12 hours no water
	Large Animal Patient Preparation	-Catheter placement --jugular vein (most common) --cephalic vein --lateral thoracic vein --ear -Use sedation and restraint for safety -Clean and prep area for surgery while animal is still standing -Wash mouth to get rid of food particles
	Equipment pre-anestheia	-Anesthesia machine --set-up and pressure check -Endotracheal tube -IV fluids all set -Ropes and hobbles available
	Large Animal Sedation	-Calm and comfortable animal -Reduce anxiety for animal -Less stressful environment lends to a safer environment for both animal and personnel
	Sedation for Large Animals	-Drugs and protocols are species-dependent -Phenthiazine: acepromazine -A2 agonists: xylazine, romifidine, detomidine, dexmedetomidine -Opioids: butorphanol, morphine -Benzodiazepines: Diazepam, midazolam
	Aceproamzine in Large Animals	-Healthy, anxious animals -Ace is never enough for induction of a large animal --have to use with something else -Adult horse -Adult bull/cow -Takes 15-20 min to start working --give ahead of time if needed
	A2 agonists for Large Animals	-Reliable sedation -Need a healthy patient -Horses, cows -Give lower dose for sick animals -Small ruminants can be used, but may cause pulmonary edema -Avoid in neonates due to concern for bradycardia -Not in pregnant animals, will cause vasoconstriction
	Opioids	-Safe for most patients -Give with other drugs, as adjunct for most patients -Morphine and Butorphanol are most common -Morphine: horses and pigs --avoid in ruminants, slows GI and causes bloat -Butorphanol: safe for all large animal species --good for young patients
	Benzodiazepines in Large Animals	-Sedative for camelids, pigs, and neonates -Not used as sedative for horses, cows --used as muscle relaxant ONLY --become ataxic --can use for induction but not for sedative
	Induction of a Large Animal	-Beginning of anesthesia, loss of consciousness -Hospital and drug settings are different -Common drugs: --ketamine --propofol --telazol --Inhalant (pigs or goats most likely) --Thiopental
	Induction of Horses	-Head and tail rope induction -Swing gate induction --don’t need a wall of people -Sling induction --fractures --neurologic horses
	Induction of Large Ruminants	-Ropes against the wall -Swing gate -Table induction -Protect airway from regurgitation! --Maintain sternal recumbency for intubation
	Induction of Small Ruminants	-Camelids, pigs, small ruminants -Can intubate on/next to table --similar to a small animals -Pre-oxygenate -Maintain in sternal recumbency --avoid aspiration
	Intubation of Large Animals	-Maintain a patent airway --protects lungs --allows for mechanical ventilation -Can do via blind intubation, direct visualization, or palpation
	Swine intubation	-Make sure you can see arytenoids
	Position of Large Animal on the Table	-Very important due to weight of the patient -Dorsal or lateral recumbency -Sternal recumbency puts a lot of strain on legs -Ensure proper placemnt of legs --avoid myopathy or neuropathy
	Maintenance for Surgery in large Animals	-Inhalant anesthesia: delivery of a gas to maintain the animal as unconscious --isoflurane, sevoflurane, desflurane -IV drugs --xylazine ketamine --good for procedures that are less than 1 hour, field castrations
	Monitoring Large Animal Patient	-Depth of anesthesia -Respiratory parameters --RR --capnography -Cardiovascular parameters --HR, rhythm, BP -Oxygenation --pulse-ox --arterial blood gas
	Monitor and Record	-Report every 5 minutes -Maintain a legal record -Have complete patient info --signalment, history, PE, bloodwork -Record drugs used and effects -Record comments for better understanding and future reference
	Pain management for Large Animals	-Pain prolongs hospitalization -Painful animal is depressed, anxious, aggressive, has weight loss -Analgesia is part of the protocol! -hard to assess in large animals, do not show pain -Careful with opioids
	Recovering a Large Animal patient	-Depends on procedure --length, pain scale, species -Species dependent -Certain breeds are calmer during recovery than other breeds -Also depends on drugs used
	Recovering a Horse	-Give time to clear inhalant gas --if not enough time, will go through delirium phase -sedate during recovery with A2 agonist or aceproamzine --gives more time to clear inhalant -Free recovery -Sling recovery -Pool recovery -Inflating pillow -No recovery method has been proven to be better than any other method
	Head and Tail rope Recovery for Horses	-Most elective cases and emergency surgeries -Supports horse while they stand -Keeps horse balanced -Horse stays in one position --easy to enter stall and re-sedate if needed -Need people to help
	Pool Recovery for Horses	-Use for fractures -Difficult recoveries -Special concerns of owner -Can make sure the animal is TOTALLY awake -VERY controlled environment -VERY expensive! -Not tolerated well by some patients -Horse is in sling in raft in pool, awkward environment
	Recovery for ruminants	-Cows are very easy --calm, no sedation needed --Stay down until they are ready to get up -Small ruminants are also very easy -Camelids and pigs --watch for respiratory obstruction due to edema in nose --be prepared to re-intubate or re-anesthetize
	Long Term Recovery of large Animal	-Check on patient night of surgery -Check on patient the next day -Look for post-op complications --facial nerve paralysis --corneal nerve ulcerations --lacerations -Add anything to the record
	Extended history of a Patient	-Previous or chronic illnesses --may not be the presenting complaint, but still important -Medications -Known allergies -Previous anesthetic history --drugs used -Current history
	Patient Evaluation before Anesthesia	-Patient status --temperament -Pain status -Complete physical exam --cardiovascular --respiratory --musculoskeletal -Diagnostics: bloodwork and imaging
	Pre-operative fasting for the Small Animal patient	-Dogs and cats: no food 8-12 hours -Young patient (less than 2 months old): no food 2-4 hours -Neonate: no fasting needed -Free choice water for dogs and cats
	Physical Status of the Small Animal patient	1. Normal and healthy patient 2. Patient with mild systemic disease 3. Patients with severe systemic disease 4. Patients with severe systemic disease that is a constant threat to life 5. Moribund patient, not expected to survive E: emergency
	Problem List for a patient	-Cardiovascular -Pulmonary -Renal -Hepatic -Musculoskeletal -Hydration Status -Pain status -Perceived complications during procedure
	PLAN	-Drugs to be used --sedation, induction, analgesics -Fluids -Possible complications -Equipment needed
	Sedation Use	-Reduces stress for the patient and the handlers -Provides analgesia for painful patients --can be pre-emptive analgesia also -DEcreases induction agent dose --decreases side effects
	Acepromazine Case selection in Small Animals	-Blocks A-receptors -Decreases SNS stimulation -great drug for the healthy patient in elective procedures --spay, neuter, orthopedic procedures -Avoid use in hypovolemic patient, neonates, older patients, excited patients/high SNS patients, or risk of cardiovascular collapse
	Alpha2 Agonists Case Seletion in Small Animals	-Good drug for healthy patient for elective procedure -has a big effect on the heart -Avoid use in patients with cardiovascular disease or young patients -Causes CNS depression
	Diazepam and Midazolam in Small Animals	-Not a reliable sedative in dogs --can cause dysphoria -Works well as sedative in old, calm, or sick dogs -Not reliable sedative in cats, can cause dysphoria, aggression, or excitement -Works well in sick cats
	Opioid case selection in Small Animals	-Usually a poor sedative when used alone -Can be combined with another sedative -Can be used alone in painful, sick, young, or old patient
	Sedation basics	-Route of Administration: --SQ, IM, IV --Need proper restraint of patient, muzzle if necessary -Allow time for drugs to take effect --quiet environment for the patient -ALWAYS monitor premedicated patients
	IV catheter in small animals	-Size depends on patient and procedure -With pre-placed catheter, make sure they work! -Catheters are cheap, easy, and life-saving -Can give drugs or fluids very easily
	Steps prior to induction of the Small Animal	1. Catheter is placed and flushed 2. ECG leads are placed and no arrhythmias are present 3. Patient is pre-oxygenated for 3-5 minutes -Be prepared! Have anesthesia machine ready to go
	Induction of the Small Animal	-Reach state of unconsciousness -Can do IV, IM, Mask induction, or chamber induction -Drugs: ketamine, propofol, etomidate --choose drug based on patient and environment
	IM Induction in Small Animals	-Done in special cases --aggressive animals --Wildlife patients --exotic patients -IV access is not an option -Use ketamine or telazol
	Mask Induction in Small Animals	-Sick patients -Unable to place the catheter -Inhalant anesthetic --iso, sevo, des
	Chamber induction of Small Animals	-Aggressive patients -Very nervous patients or stressed patients -Zoo or wildlife patients -INhalant anesthetic -Be careful!
	INtubation of Small Animals	-Done to establish and control an airway -Protects airway and lungs --gastric reflux, fluids -Inflated cuff prevents gastric stuff from getting into the lungs
	Maintenance of General Anesthesia in Small Animals	-Inhalant: Connection to an anesthesia machine and breathing circuit --keeps animal anesthetized -PIVA --inhalant and injectable intravenous drug -TIVA --injectable intravenous drug only
	Partial Intravenous Anesthesia PIVA	-INhalant connected to anesthesia machine and breathing circuit -IV drug giving CRI
	Total Intravenous Anesthesia TIVA	-IV anesthesia ONLY -INjectable anesthesia only, maintained through CRI -May or may not have intubation also -May use anesthesia machine for O2 supply and ventillation, but no inhalant used
	Monitoring of the Small Animal Patient	-Vitals (RR, HR) -ECG (heart rhythm) -Capnography (End-tidal CO2) -Pulse Ox -Blood pressure (perfusion) -Temperature
	End of General Anesthesia in the Small Animal	-End procedure -Move patient to the recovery area -Have post-op analgesia plan -Stop anesthetic that results in general anesthesia -Disconnect monitoring equipment -Be prepared to re-intubate if necessary -Move patient to recovery cage
	Small Animal Recovery	-Animal is no longer anesthetized but still under effects of anesthesia -Want quiet and calm recovery -Proper analgesia -May need to use sedation -Extubate when the animal is ready --animal can swallow or has lots of movement
	Critical period in recovery	-Recovery is when most issues happen! -Requires close monitoring -Hypoventilation, hypoxemia, hypothermia, low blood pressure
	Inhalation Anesthetics	-Current use: --isoflurane --sevoflurane -Minor use: --Desflurane -NO is majorly small use
	N2O	-Inorganic gas -Pressurized tank to flow meter -No vapor pressure because it is a gas at room temp
	Halogenated Ethers	-Basic chemical structure of inhaled anesthetics -All have ester bond -Volatile Anesthetics -Delivered via vaporizer, picks up O2
	Delivery of Inhalant Anesthetics	-Gas vs. Vapor -N2O is a gas -Volatile agents are in vapor form, have to go through vaporizer
	Generic Variable Bypass vaporizer	-Has bypass track and vaporizing chamber -Bypass track does not collect any anesthetic -Vaporizing chamber contains anesthetic in liquid form --Any fresh gas that goes into vaporizing chamber picks up anesthetic --mixed with fresh gas to outlet -Isoflurane and sevoflurane --NOT desflurane, works differently due to low boiling point
	Gas Laws	-Anesthetics are gasses and obey basic gas laws -Important for how gasses move into body, distribute in body, and are eliminated form the body -Dalton's Law -Boyle's Law -Charles' Law Guy-Lussac's law -Henry's law -Solubility increases as temperature increases
	Henry’s Law	-Pressure of gas= Cgas*K -Solubility co-efficinent is temperature dependent --Solubility decreases with increasing temperature
	Diffusion of Gasses	-Diffuse from areas of high partial pressure to areas of low partial pressure -Does not matter what concentration of gas is -Only depends on partial pressure gradient
	Physio-chemical Characteristics of Inhaled Anesthetics	-Vapor Pressure -Boiling point -Partition co-efficients -Saturated vapor pressure is WAY too high for patients --need much less to anesthetize patient -Desflurane will evaporate very quickly, has low boiling point --need a different type of vaporizer
	Vapor Pressure of a gas	-Pressure that vapor molecules exert when liquid and vapor phases are in equilibrium -Meaningless if you don’t measure the temp -Increases as temperature increases -measured in VP, mmHg, or Pa
	Flow Pattern of Inhalant Anesthetics	-P delivered ⇒ P circuit ⇒ P inspired ⇒ P alveolar -P alveolar ⇒ P arterial ⇒ P tissues ⇒ P venous ⇒ P alveolar -P alveolar ⇒ P expired
	Partition co-efficients	-Affect how quickly can achieve anesthetic depth and how long it takes patients to recover from anesthetics --lower coefficient allows for faster changes -Blood/Gas partition coefficient -Oil/Gas Partition coefficient -Real value is in comparing Partition coefficients -Capacity of blood to act as a sink for anesthetic -More blood in sink, delays absorption of anesthetic from alveolus
	Blood/Gas partition Co-efficient	-capacity of blood state vs. gas state at equal partial pressures -Compares how many particles are in blood vs. gas
	Oil/Gas Partition Co-efficient	-Oil is a gas, speaks to lipid solubility -Increased lipid solubility, increased redistribution of anesthetic to fatty body tissues -Want decreased lipid solubility, tissues will have absorbed less --body can eliminate anesthetic faster --faster recovery
	Flow Pattern of Inhalant Anesthetics	-Pressure that is delivered= pressure of anesthetic that exist the tank --Change by changing vaporizer setting --Does not change concentration in breathing apparatus
	Factors contributing to a FAST Rate of Rise of inspired Anesthetic	-low circuit volume, less volume to fill -high fresh gas inflow rate, will fill compartment faster -high vaporizer setting, increase partial pressure of anesthetic delivered to tissues
	Time Constant and Rate of Rise of inspired anesthetic	-Capacity/flow -1 time constant is the time it takes partial pressure to equal 63% of vaporizer output -Takes about 3 time constants for partial pressure of anesthetic to be 95% of vaporizer output
	Main factors affecting uptake and elimination of inhalant Anesthetics	-Gradients of anesthetic partial pressures --Alveolar pressure vs. venous partial pressure --Blood:tissue partial pressure -Properties of Anesthetics --Solubility in blood --Solubility in tissues -Physiological factors --alveolar ventilation, CO, pulmonary elimination
	Uptake and Elimination of Inhalant Anesthetics	-Total uptake of anesthetic is proportional to solubility of anesthetic -Pulmonary uptake -Distribution via blood stream --certain areas have higher perfusion --certain areas have smaller vessels -Tissue uptake --CNS vs. Lean tissues vs. fat -Pulmonary elimination
	Factors increasing rate of blood uptake of anesthetic	-Increased alveolar pressure --increased by increasing alveolar minute ventilation --decrased functional residual capacity -Increased CO -Increased blood solubility
	Lean tissues and Inhaled Anesthetic uptake	-Lean tissues have larger volume or capacity -Perfusion is not as great as vessel-rich group
	Fat and uptake of inhaled anesthetic	-Fat is last tissue to equilibrate -Never actually reaches equilibrium
	Alveolar Ventialation and Inhaled Anesthetics	-Anesthetic needs to reach alveolus first in order to get into blood -Builds up certain partial pressure in alveolus, comes into equilibrium with partial pressure in alveolus -Favors drive of inhaled anesthetic from alveolus into the blood
	Rate of Blood Uptake of Inhaled Anesthetic	-Increases with faster respiration -Decreased volume or functional residual capacity results in faster uptake -Increased CO results in increased uptake
	Increasing anesthetic is NOT the same as increasing anesthetic depth	-Anesthetic depth is the amount of anesthetic in the CNS -Eventually CNS is in equilibrium with alveolar gas --many steps removed, and takes some time --Delayed equilibrium -Increasing uptake from alveolar gas to blood stream takes away anesthetic from alveoli --decreases alveolar partial pressure of gas --delays changes in anesthetic depth -Increased CO opposes increases in alveolar pressure and pressure in CNS
	Rate of Uptake of Inhaled Anesthetic in Tissues	-Increases with increased tissue solubility -Increases with increased tissue perfusion
	Capacity or Effective Volume of Inhaled Anesthetic	-How soluble is inhalant in tissues? -More mass or greater solubility means tissues have greater capacity to absorb inhalant -Vessel rich group of tissues has small mass but excellent perfusion --small mass equilibrates very quickly -Lean tissues have larger mass with less perfusion --takes longer for tissues to equilibrate -Fat has poor perfusion, does not equilibrate under clinical circumstances
	Elimination of Inhaled Anesthetic	-Factors that govern rate of uptake apply to elimination -Faster elimination with low blood solubility and tissue solubility -Faster elimination with increased alveolar ventilation -Faster elimination with increased CO -Shorter anesthesia time will give faster elimination -Hypothermia results in slow elimination --solubility increases
	Speed of Recovery from Volatile Anesthetics	-Mostly based on tissue solubility
	Biotransformation of Inhalant Anesthetics	-Limited importance -Sevoflurane has more anesthetic recovered as metabolites, NO has least
	Why use anesthetics?	-To do procedures that would cause pain or discomfort to animal or personnel -Protect veterinarians from animals -Sedation (IM, IV, SQ, PO) -General anesthesia is IV or Inhaled --can be assisted or unassisted ventilation
	Questions for Developing an Anesthetic Plan	1. What effect do you want? -What drug will provide effect? -What are side effects and toxic effects? 2. What dose is recommended in average healthy animal? --volume of distirbution 3. How long will effect last? --clearance 4. How does drug work? --mechanism of action 5. Do you need to adjust the dose for your specific patient? --pharmacogenomics and disease factors
	Volume of Distribution	-Measure plasma concentration of the drug -Vd=(dose)/(concentration in plasma) -Gives an idea of where drug is going --can compare to target concentration
	Drug Distribution	-Most are lipophilic --need to go through BBB, diffuse across membranes -Lipophilic substances Have large volume of distribution -Hydrophilic/acidic/large molecules have small volume of distribution
	Clearance	-Volume cleared of drug per unit time -How body gets rid of the drug -Kidney and Liver, lungs for volatile drugs -Skin and intestines play role in non-anesthetic drugs -Lots of ways to calculate clearance -Adding clearance of all body systems gives total body clearance -Maximum clearance is equal to CO of patient
	Clearance Calculation	-Volume cleared of drug per unit time -Clearance= (volume of distribution)* (Elimination Rate Constant) --kel -Clearance units: L/min/kg
	Half-life	-Time it takes for 50% of drug to be removed from plasma -T1/2= 0.693/kel -Assume that after 5 halflives, 96% of drug is removed
	Calculation of T1/2	T1/2= (0.693*Vd)/Cl
	Changes in Halflife	-As clearance decreases, halflife increases --hepatic disease, renal disease, inhibition of CYP450 enzymes -As clearance increases, halflife decreases --coadministration of drugs and upregulation of CYP450 -Increased volume of distribution will increase halflife --inflammation -Decreased volume of distribution will decrease halflife --dehydration
	Drug elimination variations	-Varies by individual patients
	Distribution Half-life	-Drug is distributed into highly perfused organs quickly -Precipitous drop in plasma concentration due to 2nd phase --movement into adipose tissue and muscle -3rd phase is distribution to liver and kidney
	Elimination Half-life	-MUCH longer that initial distribution half-life
	Volume of Distribution at Steady State	-Combines initial and secondary volume of distribution
	Single Bolus Technique	-Drug concentration declines over time -Dose depends on target plasma concentration
	Repeated Dosing	-Less predictable anesthesia --Concentrations will fall and go back up often -Can calculate dosing interval
	Constant Rate Infusion	-Once steady state is achieved, rate of removal of drug from plasma equals rate of administration -Rate of removal=rate of administration -Can accurately hit target plasma concentration CRI=Cl*Target Concentration -Will have delayed induction -Takes 5 half-lives to reach equilibrium -Can give loading dose to immediately get concentration up to target
	Context Sensitive Half-life	-Longer administration of drug, longer it takes for animal to remove 50% of drug after infusion is stopped -Half-life does not appear to be constant -LOTS of binding sites in tissues --volume of distribution is ENORMOUS -Dose to counteract redistribution of drug, not elimination/clearance of the drug --longer infusion fills up more binding sites in tissue --tissues serve as source of drug
	Ketamine and Norketamine Context-sensitive Halflife	-Norketamine active metabolite accumulates in the tissues -Prolongs action of Ketamine, increases effective half-life
	Saturation and CRI	-Infusion dose stays the same, but you are giving more and more drug overall -Risk saturating enzymes -Can significantly change the half-life for the drug
	Sources of Variability in Anesthesia	-Genetics -Species or breed differences -Hepatic disease -Renal disease -Obesity -Hydration status -Drug-drug interactions -Differences in pharmacokinetics are more of a factor than differences in pharmacodynamics
	Greyhounds and Anesthetics	1. Propofol -Decreased propofol clearance due to decreased rate of hepatic metabolism -Majorly decreased in relation to other breeds 2. Thiopental --decreased clearance, most likely due to CYP450 saturation
	Ruminants and Xylazine	-Give MUCH lower dose, very sensitive -Do not metabolize slower than other species --not pharmacokinetic sensitivity -Not due to receptor binding -Binding of drug on receptor itself causes change in response in ruminants
	Key Points of Anesthesia	1. Develop a Plan 2. Use drug’s target plasma concentration and volume of distribution to calculate dose --use t1/2 to calculate dosing interval --use Cl to calculate CRI 3. Context sensitive half-life is important for anticipating length of recovery of patient 4. Intra and inter species differences in Pk and Pd --also be aware of renal and hepatic diseases 5. Learning is on-going
	Importance of Intubation	-Establishes an airway -Allows proper ventilation, can mechanically ventilate patient if necessary -Safer! -Protects the airway from regurgitation and aspiration or inhalation of foreign material -Allows effective delivery of inhalant, less pollution
	Intubation	-Can be done several ways -Orally -Nasally (horses) -External pharyngotomy -Tracheostomy
	Endotracheal Tube Material	-Polyvinyl chloride (PVC) --most common in small animal anesthesia -Silicone --large animal tubes -Rubber --not used anymore
	Ideal endotracheal tube	-Clear plastic, can see what is in there -Radio-opaque line to see tube on radiographs --want to be able to see exact placement or artifacts from tube
	Reinforced endotracheal tube	-Has spiral wire inside that prevents kinking -Adds strength and flexibility -internal diameter is smaller due to spiral wire --less space
	Markings on the Endotracheal Tube	-Numbers on outside are lengths of the tube --measured in cm -internal and outer diameter --Tubes are sized based on internal diameter
	Endotracheal Tube Cuff	-Inflatable end of the endotracheal tube -When inflated, forms seal with tracheal wall --protects airway --allows for positive-pressure ventilation --does not let anything through --Prevents inhalant pollution, inhalant getting out of the patient -Inflated via pilot balloon --one-way valve --have to specifically deflate -Pilot balloon inflates as the cuff inflates, but not proportionally related
	Types of Endotracheal Tube Cuffs	1. Low pressure High volume --PVC tubes --Takes more air to inflate --More evenly distributed over larger surface area, less risk of mucosal damage --higher risk of leakage 2. High pressure low volume --Does not take a lot of air to inflate --creates a high pressure --Better seal against tracheal wall --Higher risk of ischemia and tracheal damage
	Endotrachal Tube Connector	-Connects ET tube to breathing circuit -Small animal: one end size specific to fit tube diameter --Side that connects to the endotracheal tube changes based on tube --Side that connects to breathing circuit is 15mm fixed diameter -Large animal: side connected to ET changes based on tube diameter --side connected to breathing circuit is 22mm fixed diameter
	Murphy-Type Endotracheal Tube	-has opening at end of the tube called "murphy eye" -In wall opposite bevel of tube -Allows flow even if end hole of ET is occluded -Can be cuffed or uncuffed tubes -ALWAYS have murphy eye
	Cole type endotracheal tube	-Always uncuffed -Shoulder near distal end of the tube --thinner part goes through the larynx, rests on arytenoids
	Choosing appropriately sized Endotracheal Tube	-Best way to assess is to palpate trachea -Larger tube is usually a better choice, largest tube that will not damage the trachea --decreases resistance to flow --higher radius, lower resistance -Breed differences exist --bulldogs need smaller tubes than same sized dogs --dachshunds can take a bigger tube -Always select 3 tubes
	Intubation Techniques	-Have a good holder -Extend the neck of the patient -Open mouth, move tongue out of the way --do not cut the tongue! -Can use lube, but do not put lube in murphy eye -Need good plane of anesthesia, intubation is VERY stimulating -Place laryngoscope under epiglottis
	Airway assessment while intubating	-Quick exam of larynx -Look at soft palate displacement -Think about what to expect during recovery and extubation -Record abnormalities
	Endotracheal tube Positioning and securing	-Measure tube from point of shoulder to canines --Record the length of the tube to know if it moves -Secure tube using gauze, tie behind ears or to nose -Avoid movement of the tube during any procedure --inflated cuff rubs against the trachea --Disconnect the patient if you are going to flip or move the patient -If tube moves during the procedure, deflate cuff before readjusting
	Endotracheal Tube Cuff Pressure	-Do not want to just inflate to maximum --will prevent blood flow in tracheal mucosa -Hyper-inflation will cause mucosal damage, ischenic injury, tracheal stricture -Inflate to 20-25mmHg -Cuff should leak at 20cm H2O, seal at 15cm H2O
	Laryngoscope and Endotracheal Tube Placement	-ALWAYS use a laryngoscope -Can see better and examine airway while intubating -Several blades and sizes available -Miller and Wisconsin are most commonly used
	Dog Intubation	-Easy to see airway -Use laryngoscope with good light -Laryngoscope should not touch the epiglottis or arytenoid -Sternal position is best, lateral can also work -Do not put tip of laryngoscope on the epiglottis, will damage --go under epiglottis -Tube sizes should be 3-14, depending on breed -Do not extubate until dog is swallowing
	Cat intubation	-Easy to see airway -Always use laryngoscope with good light -Laryngoscope should not touch epiglottis or arytenoid -Use local anesthetic over arytenoids, cats have a lot of laryngospasm -Use careful dose of lidocaine with cat -Best to intubate when cat is in sternal -Size 3-5, 4.5 is most common -Extubate when cat is able to swallow
	Cat Laryngospasm	-Cats will close arytenoids and prevent intubation -Can use guide tube or tip of ET tube to spread arytenoids open --stay ventrally and wait for arytenoids to open -Do not force!
	Apneustic Breathing and endotracheal intubation	-Animal holds breath during inhalation -Take breath, hold arytenoids open -Makes intubation easier
	Horse Intubation	-Blind intubation -Can use PVC pipe as a mouth gag -If difficult, can use stomach tube as a guide tube -Can use endoscope if needed -Usually 26mm tube, can be 20-30mm tube -Can also have horse nasally intubated (22mm tube) -Intubate in lateral recumbency, sternal also works -Resistance on intubation is arytenoids --pull back, rotate tube, re-try --Should not take a lot of force to intubate!
	Horse mouth and intubation	-Always wash first, may have hay around mouth or in teeth -Do not want hay in lungs!
	Cow Endoracheal Tube Intubation	-Wash mouth -place speculum after induction -Keep animal sternal, cow will regurgitate in lateral -Put hand and endotrachal tube into larynx --should be able to feel arytenoids --Can use guide tube if necessary -Inflate cuff right away to prevent issues with regurgitation and aspiration -Make sure cow is fully anesthetized --stimulation will activate regurgitation! hand is in mouth, bad news -Intubation should be done efficiently, decrease risk of aspiration of ruminal contents -Extubate when animal is very awake, holding head up and shows that oral and pharyngeal reflexes have returned
	Active vs. Passive regurgitation of anesthetized cows	-Passive regurgitation is OK -Active regurgitation will happen in animal is not properly anesthetized
	Small Ruminant Intubation	-Always use laryngoscope -Guide tube should be used if view of larynx is impaired due to little space in oral cavity --ET tube is passed over the guide tube -Can be done sternal or lateral --sternal is best, keep head and neck extended -Animal should be deeply anesthetized to avoid active regurgitation -Inflate cuff quickly in case of regurgitation
	Swine Intubation	-Difficult to intubate --mouth does not open widely, larynx is small and slopes ventrally, small larynx and trachea --Small Endotracheal tube is needed --trachea has ventral diverticulum -Put in sternal with head extended -Use laryngoscope -If intubation is difficult, use a mask -Intubate in sternal position
	Rabbit intubation	-Hardest patient to intubate -use small laryngoscope and lidocaine, and guide tube -Can do in sternal or dorsal recumbency -Can do blindly if good at it --capnography needed
	Confirming Tracheal Intubation	1. Direct view and laryngoscopy 2. Inflation of chest with positive pressure intubation 3. Movement of rebreathing bag 4. Capnography --presence of endotracheal CO2 is most accurate confirmation --gold standard
	Switching Endotracheal Tubes during procedure	-Leak present, need to see larynx -Use stylet or guide tube --place stylet or guide tube before extubating -Stylet may be obstructing gas flow, do not keep in for too long
	Complications during Intubation	-Lacerations to gums and tongue -Epiglottis or arytenoid damage -Tracheal damage --necrosis --tear that results in SQ emphysema -Avoid rotating the animal when the ET tube is attached to the breathing circuit --disconnect and re-conenct
	Bronchial Intubation	-Go too far during intubation and tube is in the bronchial -Will only get inflation of 1 lung -Be sure to measure tube to carina -Ascult bilaterally to make sure ventilation is on both sides
	Esophageal Intubation	-Does not last very long, animal does not stay anesthetized -Make sure there is movement of the rebreathing bag -Need to see endotracheal CO2 on the monitor
	Involuntary extubation	-Patient moves or wakes up -Sudden arousal -Tube comes out in the middle of the procedure
	Endotracheal Tube in Surgical Site	-Procedure requires access to mouth, larynx, trachea -May have to do nasotracheal intubation --possible in horses, camelids, cows -May have to do tracheostomy
	Tracheostomy	-Done when endotracheal tube is in way of surgical site -Last chance option -Oral intubation is needed to perform tracheostomy -Replace tube through tracheostomy site -Between upper and middle 3rds of the neck -Can pre-place or place in case of an emergency
	Bronchoscopy	-Need access to trachea, cannot intubate the patient -Most likely will use total intravenous anesthesia (TIVA) -Provide oxygen insufflation through scope or through catheter/airway -Always have endotracheal tube available in case of emergency and to intubate at the end of a procedure --be ready to intubate!
	Mask	-Pre-oxygenation is always a good idea -Increase oxygen concentration of functional residual capacity -Mask may stress patient -If using TIVA, can use mask and O2 -Post-op, can give supplemental O2 while animal is still sedated -High flow is needed to flush out expired CO2 -If connected to insufflation, allow space for expired gas to flow into atmosphere
	When to use a mask	-If intubation fails --does not provide airway protection -Can be used to induce anesthesia --make sure there is a good seal, otherwise will get lots of pollution
	Management of the Difficult Airway	-Oral mass -Tracheal Mass -Laryngeal paralysis -Fractured mandible -Bonded teeth -Use stylet or guide tube
	Stylet for difficult airways	-Malleable metal wire -Used for difficult intubations -Can help conform the tube to a specific shape
	Guide tube for Difficult Airways	-Smaller diameter tube -Allows for better view while passing through larynx -Has to be 2-3x length of endotracheal tube -Guide tube sits inside ET tube
	Using Bronchoscope or Endoscope fort Intubation	-Always an option -Helps with visualization of arytenoids -Good for horses with laryngeal hemiplagia or dogs with dental bond -Pass scope through the endotracheal tube and guide tube through the larynx
	Retrograde intubation	-Pass hypodermic needle through skin and into trachea between 2nd and 3rd tracheal ring -Wire is threaded through the needle -Pass wire cranially through larynx and into oral cavity -Wire can be used as guide tube
	Lateral Pharyngotomy	-Good for cases that need oral-pharyngeal access -Intubate normally, then remove connector --cut near the angle of the mandible --Use hemostats to pick up tube and bring tube out through side of the head
	Blood Pressure Monitoring for Anesthesia	-historically done during anesthesia -Arterial blood pressure, force of the blood against the artery walls -Always in reference to atmospheric pressure, at the level of the heart -Return of blood gives a lot of blood pressure
	Arterial blood pressure	-Force of the blood against the artery walls -Not a driving pressure -Always in reference to atmospheric pressure at the level of the heart -Half of the area under the BP curve is the mean arterial pressure
	Arterial catheterization for blood pressure	-Gold standard for anesthetic blood pressure monitoring -Measures directly the pressure changes
	Invasive technique for blood pressure monitoring	-Arterial catheterization in animals
	Non-invasive techniques for blood pressure monitoring	-Manual methods: operator dependent --Auscultatory methods --Doppler -Automatic Methods: less operator dependent --Oscillometric
	Auscultation of Korotkoff's Sounds	-Method used in Humans -Characteristic sound when artery is occluded and released -Difficult and not reliable in animals --distribution of arteries and distribution of elastic fibers in arteries
	Ultrasonic Doppler technique to monitor BP	-Uses doppler effect to detect blood flow in the artery -Measures systolic blood pressure ONLY -Small ultrasound probe over the peripheral artery --lines need to be perpindicular to the artery -Uses acoustic energy, ultrasound --wave goes into blood vessels and hits RBCs, bounces back --sound wave reverberates as sound -Tells you that there is flow in the artery, gives idea of flow
	Using Ultrasonic doppler	1. inflate cuff above transducer -compresses artery and occludes flow 2. slowly release pressure from the cuff -flow returns, can hear sound again -Measures systolic blood pressure
	Advantages of Ultrasonic Doppler	-Easy to use -Portable -Works on small animals -Works on awake animals -Inexpensive -Audible monitor of pulse and peripheral blood flow
	Info from Ultrasonic Doppler	-HR -Heart rhythm -Presence of an arrhythmia -Presence of blood flow
	Disadvantages of Ultrasonic Doppler	-Underestimates Systolic Arterial Pressure in cats by 15mmHg --better to underestimate than overestimate -Does not measure diastolic or mean BP -Need an operator to take each BP --operator variability and inexperience can give incorrect readings
	Blood Pressure Cuffs	-Correct size and placement are key factors -Diameter of the cuff needs to be 40% of the circumference -Big cuff will over-estimate blood pressure -Small cuff will under-estimate blood pressure -Don't put in high-motion areas -Make sure the limb is at the level of the heart for even hydrostatic pressure
	Automated Non-invasive Blood Pressure Monitoring	-Different methods for operation -Most measure the pulse rate -Mostly oscillomeric principle --also other methods exist -Machine is tightly regulated in human medicine -Measures mean BP, and extrapolates other BP through algorithms -Will give SBP, DBP, mean BP, pulse rate
	Using Automated Non-Invasive BP	-Inflate the cuff until pulse is occluded -Cuff pressure decreases in linear manner -Cuff pressure decreases blood flow in the artery --oscillations are detected by the monitor -Magnitude of oscillations increase to maximum and then decrease
	Automated Non-invasive Blood Pressure Cycle	-Have manual cycle and automatic cycle -Automatic cycle gives BP at designated intervals -Various settings give maximum pressure for the cuff --good for patients of different ages -Have alarms
	Advantages of Automatic Non-Invasive Blood Pressure monitors	-Easy to use, simple to place -Automatic cycle -Non-invasive -Works on all limbs and the tail -No interference --noise --cauterization units -Gives most reliable reading when everything is normal
	Disadvantages of Automatic Non-invasive Blood Pressure monitors	-Inaccurate with arrhythmias, vasoconstriction, movement (shivering), cuff dislodgement -Overestimates BP if animal is hypotensive --do not want to overestimate hypotension! -Need to interpret carefully with small animals -Specific devices have specific limitations
	Invasive BP monitoring	-Continuous beat by beat monitoring -Requires arterial catheterization --need to know how to place -Need specific equipment --heparin-saline filled tube transmits pulse pressure wave to pressure transducer --transduced transforms pulse wave into electrical signal -Displays on monitor as pressure waves and numbers -Gold standard for pressure monitoring, but still has downfalls
	Advantages to Arterial Catheterization Invasive BP monitoring	-Gold standard for BP monitoring in animals -Beat-by-beat monitoring -Ideal for critical patients -Gives information on hypovolemia and response to fluid therapy
	Disadvantages to Invasive BP monitoring	-Lots of complications related to catheter placement --thrombosis --hemorrhage from catheter --hematoma --skin necrosis --infection -Subject to errors in technique and equipment -Difficult to place catheter -Expensive
	Capnography	-Graphic measurement and display of instantanous CO2 vs. time
	Pulse Oximetry	-Non-invasive measurement of O2-hemoglobin saturation -Alternative to assess arterial blood oxygenation -Gives Hemoglobin-oxygen dissociation curve -Absorption and reflectance of Hb is affected by oxygenation --allows for optical method of measurement of Hb-O2 saturation of blood
	Hb Dissociation curve	-Not a linear relationship between Hb and oxygen in the blood -Due to changing affinity -More O2 that is bound, the easier it is for other O2 to bind to Hb --stereochemistry of Hb changes when O2 binds and makes it easier for other O2 to bind -Left shift: increased affinity --decreased temp, decreased DPG, decreased concentration of H+ -Right shift: decreased affinity: --increased temp, increased DPG, increased concentration of H+ -Useful tool when breathing room air, less useful when breathing 100% O2
	4 types of Hb	-Oxyhemoglobin -Reduced hemoglobin -Methemoglobin -Carboxyhemoglobin -Each type of Hb has different light absorption -Pulse ox can only see OxyHb and reduced Hb
	Use of pulse oximetry	-Early warning of hypoxemia -Helps assess effectiveness of treatment to increase O2 saturation -Can monitor post-anesthetic periods --thoracotomy --brachycephalic dogs --upper and lower airway problems -Can be used to measure systolic BP
	Factors Influencing Measurements of Pulse oximetry	-Ambient light -Low perfusion --amplified signal -Patient motion --causes pulsation of venous blood
	Pulse Oximetry Probes	-specific probes for veterinary medicine -Have tongue clips -Wrap clips -Rectal probes for horses
	ECG	-Measures electrical activity of the heart -Need electrical-mechanical coupling for the heart to beat -Can have normal ECG with heart beating, need doppler to confirm that the heart is beating -Amount of electrical activity over a length of time
	ECG waves	-P: atrial depolarization -QRS: ventricular depolarization -T: Ventricular repolarization
	Use of ECG monitor	-Helps diagnose dysrhythmias, ischemia, conduction defects -May be able to find ventricular enlargement
	ECG leads	-3 leads -Esophageal leads exist, are very convenient -Can be placed in many parts of the body --just need to form a triangle with the heart in the middle
	Mean Pressure	-NOT Halfway between systolic and diastolic pressure --generally closer to diastolic pressure -Heart spends more time in diastole, skews mean -Normal systolic: 100-160 mmHg -Normal diastolic: 60-90 mmHg -Normal mean: 80-120 mmHg
	Autoregulation of Blood Flow	-Can occur in certain organs -Want to keep BP in autoregulatory range to maintain adequate perfusion to tissues
	Large Animal BP	-Can end up with myopathies and neuropathies during recovery if BP is in 60s (low)
	Calculation of Blood Pressure	-BP = CO x Systemic vascular resistance -CO = SV x HR -SV = venous return x contractility
	Increases in Systemic vascular resistance	-Increases preload -Can decrease SV and CO
	Starling's Law	-As myocardial fiber length increases, pressure during systole increases -At a certain point, myocardial cells are at maximum length --pressure and contractility will fall
	Cardiac arrhythmias and Hypotension	-Can affect how well the atrium feeds blood to the ventricle
	Regulation of Blood Pressure	-Based in autonomic nervous system
	Atrial Kick	-Atrial beat should come before ventricular beat -Atrial volume is not fed into ventricle
	Peripheral Receptors to regulate BP	1. baroreceptors (stretch receptors) --carotid sinus and aortic arch 2. Mechanoreceptors (volume receptors) --atria and ventricles 3. Chemoreceptors --aortic body and carotid body --play a minor role
	Regulation of Blood Pressure	-Balance between symathetic nervous system and parasympathetic nervous system -Sympathetic Nervous System: --NorEpi is main NT --Epi, ACh, serotonin, dopamine, and neuropeptide Y also -Parasympathetic Nervous System: --Cholinergic --ACh is main NT --long pre-ganglionic axon, short post-ganglion
	Parasympathetic nervous System	-Cranial and sacral spinal cord segments -ACh is main NT released --ACh released from ganglionic connection and post-ganglionic connection -Long pre-synaptic fiber, short post-synaptic fiber -Cardiovascular effects due to Vagus (CN X) --affects rate and AV node conduction --does not really affect contractility --Decreases HR and AV conduction
	Sympathetic Nervous System	-Thoracic and Lumbar spinal segments -short pre-ganglionic fiber and long lost-ganglionic fiber -ACh is released at ganglion -NorEpi and Epi are released at adrenal gland -NorEpi released to act on heart, smooth muscles, glands -ACh released to act on sweat glands
	Epi vs. NorEpi	Epi: Primarily circulating catecholamine released from the adrenal gland NorEpi: Primary neurotransmitter released at neural effector junction
	Atropine	-Parasympatholytic agent -only affects parasympathetic nervous system -Anti-muscarinic
	NorEpi re-uptake	-Main mechanism for getting rid of NorEpi in the synaptic cleft -Some is broken down by MAO, some by COMT -Cocaine inhibits NorEpi re-uptake
	ACh breakdown	-Broken down by ACh-esterases in synaptic cleft -Plasma cholinesterases are also found in the blood --Etomidate broken down by pseudocholinesterases in blood
	Vagus Nerve action on the Heart	-Decreases HR -Decreases AV conduction -Has minimal effects on vascular tone or contractility -May have prolongation of P-R interval (1st degree AV block) -2nd degree AV block: P-wave with no QRS following --common in anesthesia
	Horse Resting Vagal Tone	-Horses have high resting vagal tone -before using a2 agonist (increases 2nd degree AV block) make sure dropped beat goes away with activity
	Symathetic Nervous System Effects on the Heart	-Affects SA node and AV node -Oppose vagal effects to increase heart rate -Increases contractility in atria and ventricles
	A2 agonists	-Decrease sympathetic outflow from CNS to the heart -Can make 2nd degree AV block worse
	Sympathetic Nervous System effects on the Vasculature	-Normal resting sympathetic tone -Maintains systemic Blood Pressure -Controls distribution of blood flow
	B1 receptors in the heart	-Stimulated by Epi and NorEpi -Increases HR -Increases contractility -Increases conduction velocity (dromotropy)
	B2 receptors on bronchioles and blood vessels	-Airways and vasculature (skeletal muscles and coronary arteries) -Stimulated by Epi -NorEpi has no efect on B2 receptors -Causes bronchodilation -Causes vasodilation
	Anesthesia causes Hypotension	-Patient is asleep, decreases sympathetic tone --causes vasodilation and hypotension -Baroreceptors do not work normally due t inhalant effects --not triggered -Specific drugs have specific effects on cardiovascular system --acepromazine (vasodilation) --Opioids (bradycardia) --A2 agonists (bradycardia, changes in SVR)
	Acepromazine	-Vasodilator
	Anesthetic Hypotension by Species	-Horses get hypotensive easily under anesthesia -Ruminants do not, maintain good blood pressure with anesthesia
	Young animals ans anesthetic hypotension	-Young: less than 3 months -heart does not have high contractile mass -ventricle is not very compliant -CO is rate-dependent, only way to maintain CO is through HR -Sympathetic system is not fully developed --do not vasoconstrict very well -Can get cold quickly -baroreceptor response does not work very well
	Old animals and anesthetic hypotension	-Ventricles do not work well, CO tends to be a little lower --decreased ventricular compliance --decreased CO -Cardiac disease is more common -Decreased elasticity of vasculature -Do not have problems under anesthesia, but if there is a problem they are hard to get out of the problem --less responsive to catecholamines -Need more finesse, do not want to get into a problem to begin with
	Effects of Patient history on Hypotension	-What is the presenting complaint? -Known medical conditions --cardiovascular disease --respiratory disease --endocrine disease --neurologic disease -Previous anesthetic history
	Effects of Medications on Hypotension	-Vasodilator therapy (enalapril) -Antiarrhythmics -Tricyclic antidepressants --MAO inhibitors, increase NorEpi release and inhibition of re-uptake --parasympatholytic -Antibiotics (neuromuscular blocking activity)
	Cardiovascular exam for hypotension	-Check HR and rhythm -volume status/tissue perfusion -Character of peripheral pulses -Murmurs heard -Exercise intolerance
	Pulmonary exam for Hypotension	-Auscult lungs on both sides
	Electrolytes and Hypotension	-Main one to worry about is K --Hyperkalemia -K determines where resting membrane potential is -If patient is hyperkalemic, will repolarize to less negative resting potential --not all K channels re-set --rate of depolarization is slower -As rate of depolarization becomes slower, patient becomes bradycardic
	Changes in Venous return as a cause of Hypotension during Anesthesia	-Hypovolemia is most common cause of hypotension under anesthesia -Can be due to bleeding, dehydration -Can have absolute fluid deficits due to bleeding or relative deficits due to vasodilation
	Normal Blood Volume	Dog: 90 ml/kg Cat: 60 ml/kg Horse: 90-100 ml/kg
	Normal maintenance fluids	2-4 ml/kg/hour -Evaporative loss is increased by: --dry anesthetic O2 --Exposed body cavities --3rd space losses with surgical manipulation -Have to increase normal maintenance fluids during Sx due to increased evaporation -Maintenance fluid for patient in surgery should be 6-12 ml/kg/hour
	Venous Return	-Vena Cava can be compressed when animal is placed on their back -Horses esp have long, sloping diaphragm and lots of intestines
	Positive Pressure Ventilation	-Breathing for the patient during surgery -Every time you give breath and positive pressure to chest, change gradient for blood to flow back up to chest --giving a breath decreases venous return --next few beats have decreased CO --the more hypovolemic a patient is, the more pronounced the effect
	Surgery and Venous Return	-ANYTHING a surgeon does can affect venous return
	Recognition of inadequate volume	-Look at diastolic pressure -heart is beating well, have good upstroke of pressure wave -With vasodilation, diastolic pressure will get low between each beat
	Factors affecting arterial pressure or wave form	1. Diastolic pressure and dicrotic notch 2. Positional changes 3. Positive pressure ventilation
	Central Venous Pressure	-Measure of filling pressure -Dependent on many things -If contractility increases, CVP decreases -Can change based on patient positioning
	How to treat inadequate venous return	1. Make sure they are getting fluids --give fluids IV 2. Change patient positioning --move from dorsal to lateral, tilt head down 3. Change positive pressure ventilation 4. Adjust depth of anesthesia 5. Correct electrolyte abnormalities 6. Give pressure support via pharmacokinetics
	Fluid Replacement questions	-How much? -How fast? -What route? -What type? -What is an allowable blood loss?
	Crystalloids	1. Crystalloid Solution: basic balanced electrolyte solution -Tend to be smaller molecules --NaCl --Lactated ringers --Plasmalyte -1/3 stays in vessels, 2/3 goes extravavascular
	Colloids	-Dextran -Hetastarch -Vetstarch -Solutions made up of larger molecules --molecules stay in vascular space -Give at 1:1 ratio -Easier to give quickly -Can cause coagulopathies, anaphylactic reactions, renal failure
	Catheters for FLuids	-Use biggest catheter possible -Rate of fluid is inversely proportional to radius of catheter ^4 -Diameter of catheter is really important for how fast you can give fluids
	Halothane	-Myocardial depressant
	Anesthesia inhalants	-All vasodilators -All affect venous return -giving fluids will not do much if patient is deep under anesthesia --have to lighten anesthesia a little bit for fluids to have an effect --give fentanyl, opioid CRI, bolus with oxymorphone or hydromorphone to keep patient asleep
	Opioids	-Are good for maintaining blood pressure -Can give when turn inhalant down -Fentanyl, oxymorphone, hydromorphone, butorphanol
	Etomidate	-Least effect on blood pressure -Changes tidal volume a little bit, but does not change BO
	Sympathomimetic Amines	-A1 -A2 -B1 -B2
	Alpha 1 and 2 receptors	-Cause vasoconstriction -Purpose for using alpha receptors is vasoconstriction -NorEpi -Epi -Phenylephrine -Dopaime -Dobutamine (just a little)
	Beta 1 Receptors	-Mostly affect the heart -Increase HR -Increase contractility -NorEpi -Epi -Dobutamine -Dopamine -Phenylephrine just a little
	Beta 2 receptors	-Cause vasodilation -Do not want in a "pressor" drug -Will also increase contractility -Epi -Dobutamine -Dopamine -Epi just a little -Phenylephrine not at all
	Vasopressors	-Drug that will cause vasoconstriction -Affects alpha receptors -Phenylephrine -Norpeinephrine -Epinephrine (as a bolus) -Dopamine -Vasopressin/ADH
	NorEpi as a Vasopressor	-Alpha effects -Beta 1 effects -Minimal Beta 2 effects -Used as a pressor -Not the first choice, very potent -Good for use in sicker patients that are not responding to other drugs
	Epi as Vasopressor	-Alpha effect -Beta 1 effects (effects the heart) -Beta 2 effects also -Give as bolus when patient is arresting --in high doses is very good vasoconstrictor --recussitates the patient -Not used as a pressor so much because it has B2 effects
	Phenylephrine as a Vasopressor	-Alpha agonist -Minimal B1 and B2 effects -Very good vasopressor agent
	Dopamine as a Vasopressor	-Good vasopressor to start off with -Very dose-dependent --low doses, affects dopamine receptors and acts as vasodilator --increasing doses, get mostly beta effect (increased HR and contractility) --in high doses, get mostly alpha effect, more pressor effect -Effect is partly dependent on NorEpi release -Good for a normal patient that isn't doing well under anesthesia -not good for sick patient that has run out of endogenous catecholamines
	Dobutamine as a Vasopressor	-B1 effect and some B2 effect -Increases HR and contractility -Causes vasodilation --BP may not rise at all, may decrease --OK for patient with DCM -Not a "pressor" so much
	Ephedrine	-Bolus -Takes a few minutes to work -More of a beta-agonist, not really a pressor
	Vasopressin	-ADH -Works through vasopressin receptor -Does not work through catecholamine receptors --no Alpha or Beta receptors -Good for sick, septic patients where nothing else is working
	Drugs for Changes in Myocardial Contractility	-Alpha-2 agonists: decrease sympathetic outflow --cause changes in contractility -Xylazine -Medetomidine -Dexmedetomidine -Detomidine
	Opioids and Contractilty	-Do not change myocardial contractility
	Meperidine	-Demerol -Designed as anti-cholinergic -Active as an opioid also -Has some direct effects on left ventricular function -Not used very often, but still around
	Ketamine and myocardial contractility	-Indirect effect is CV sparing --HR increases, pressures stay the same, CO increases --Causes catecholamine release --can be supportive of BP -Direct effect is CV depressant --can't be reversed if there is a problem
	Thiobarbiturates and Myocardial contractility	-Can cause transient decreases in myocardial function that can be dose and rate dependent
	Propofol and Myocardial Contractility	-Probably causes the most hypotension -have to be careful with use -Decreases in contractility and BP are dose and rate dependent -give slowly! -Avoid use in sick patients
	Inhalants and Myocardial Contractility	-Potent inhalants can affect myocardial contractility -Not too much of an issue with newer inhalants --iso, sevo, des
	Patient Factors that cause release of Myocardial depressants	-Ischemia and reperfusion injury -Sepsis -Manipulation of the pancreas -Hyoxemia -Acidosis -Hypocalcemia -underlying cardiac disease
	Alpha 2 agonists and Myocardial contractility	-Affect CO more than contractility -Cause increase in afterload
	Recognizing decreased CO in anesthesia	-Changes in arterial pressure or wave form 1. low CO will have low pulse pressure, "thready" --hard to tell the difference with vasoconstricted patient --Low CO artery feels flaccid, vasoconstriction artery feels like a hard tube 2. Auscultation via doppler
	Changes in venous return	-Use Pressors, alpha agonists
	Myocardial contractility and CO issue	-Want to stimulate B1 receptors --cause increase in Ca currents in cardiac cells -B2 will also have effect, B1 are more important
	NorEpi to increase myocardial contractility	-Can be used, does have B1 effects, but more of a alpha agonist/vasopressor
	Epi to increase myocardial contractility	-Good B1 agonist
	Phenylephrine to increase myocardial contractility	-Will not have effect
	Dobutamine to increase myocardial contractility	-Classic B1 agonist -Pure B1 with a little B2
	Dopamine to increase myocardial contractility	-At low-range doses will affect dopamine receptors -At mid-range will affect beta receptors -At high range acts as a pressor Dose-dependent
	Inotropes	-Beta-1 agonists -Epinephrine -Dobutamine (also B2 effects) -Dopamine (also B2 effects)
	Factors affecting Cardiac Output	1. Stroke volume: --venous return --changes in contractility --changes in afterload --arrhythmias 2. Heart rate --parasympathetic vs. sympathetic tone --baroreceptor response
	Ventricular Bigemeny	-Seen after thiobarbiturate use -Beats come in couplets
	Ketamine and arrhythmias	-Causes catecholamine release and beta-effects -Causes arrhythmias
	Drugs causing cardiac arrhythmias	1. Thiobarbiturates (ventricular bigemeny) 2. Ketamine, causes catecholamine release 3. Sympathomimetics, beta-agonists --cause catecholamine release and beta-effects 4. Potent inhalants (halothane)
	Tachycardia and Anesthesia	-Can be major compensatory response to hypotension caused by anesthesia -Inadequate anesthesia -Poor ventilation and CO2 is too high -O2 is too low -Hyperthermia, hypermetabolic -Awake and feeling pain -Anticholinergic -Sympathomimetic
	Decreases in HR with anesthesia	-Can be due to increase parasympathetic/vagal tone --may be increased relative to sympathetic tone -Opioids cause bradycardia in dogs --not so much in cats and horses, and "morphomania" -Alpha-2 agonsists: decrease sympathetic outflow --increases relative parasympathetic tone --decreases HR
	Oculo-cardiac reflex	-Use anti-cholinergic to prevent ocular-cardiac reflex
	Hypoxemia and HR	-Initial tachycardia, trying to keep CO up -Sudden bradycardia, then arrest -If there are sudden changes in HR, make sure everything is OK with your patient!
	Hypothermia and HR	-Can really affect HR! Will cause bradycardia
	Treatment of a sudden bradycardia	-Give atropine or glycopyrrolate
	Cardiac Arrhythmias and Anesthesia	-Identify if rhythm is atrial or ventricular -Was arrhythmia pre-existing to anesthesia? -Frequency: changing? -Multifocal or unifocal -Effects on blood pressure
	Causes of Cardiac Arrhythmias	-Underlying disease -Sympathetic vs. parasympathetic tone imbalance -Myocardial ischemia -Acid-base or electrolyte imbalance -Drug induced
	Treatment for Cardiac Arrhythmias	1. Premature ventricular contractions or Ventricular tachycardia: --lidocaine --procainamide --amiodarone 2. Supraventricular tachycardia/ Atrial fibrillation --digoxin --diltiazem --amiodarone --quinidine 3. Sinus bradycardia/ AV block --atropine --glycopyrrplate
	Ventricular Afibrillation in Anesthesia	-Not too common -May occur in horses -DO NOT GIVE ANYTHING TO INCREASE AV-NODE CONDUCTION --No anticholinergic -Want to keep everyhthing status-quo
	Phenothiazine Tranquilizers	-Acepromazine -Decrease BP -HR may increase -Vasodilators -Alpha-blockers
	Butyrophenone Tranquilizers	-Vasodilators
	Guaifenesin	-Not used in small animal anesthesia -Used in large animal anesthesia as muscle relaxant during induction -Can cause vasodilation
	Propofol and Hypotension	-Causes most significant hypotension -Can cause animal to turn blue --venodilation and decreased contractility
	Potent Inhalants and SVR	-Vasodilators -Iso is potent vasodilator
	Epidural anesthetics and SVR	-Block peripheral nerves -Acts as Na channel blocker -Blocks all nerves in area of epidural -Blocks nerve according to size --motor nerves are biggest, hardest to block --Sensory nerves are smaller --sympathetic nerves are even smaller -Blocking sympathetic nerves causes vasodilation -Epidurals cause significant vasodilation --do not give to a patient that is shocky or hypotensive
	Histamine and SVR	-Histamine is a vasodilator -Drugs causing histamine release --opioids: meperidine, morphine --atracurium --mast cell tumors --protamine --species/breed predilection
	Beta-2 agonists and SVR	-Cause vasodilation -isoproterenol -Epi and epi reversal
	If pressure is low, turn up fluids	-As increase fluids, flush Pt with O2 and lighten inhalant -Switch to injectible opioid
	Adequate BP does not ensure adequate tissue perfusion	-If patient is hypovolemic, may be decreasing perfusion of vital organs
	Tissue Perfusion Indicators	-Mucus membrane color and character -Capillary refill time (less than 2 sec) -Peripheral pule quality -Temperature of extremities -Urine production -Blood lactate -pH -Central venous oxygen saturation
	Managing Perianesthetic Arrhythmias	1. Identify the arrhythmia 2. Identify the cause of the Arrhythmia --why does the animal have an arrhythmia 3. Determine the significance of the Arrhythmia 4. Treatment necessary? if yes, what?
	Common causes of arrhythmias	-Autonomic imbalances -Anesthetic drug effects or interactions -Systemic disease -trauma -Sudden hypertension/hypotension -Electrolyte abnormalities -Acid-Base abnormalities -Myocardial hypoxemia/ischemia
	Important factors in determining the significance of the Arrhythmia	-Origin -Effect on peripheral blood flow --CO= SVxHR -Effect on myocardium --excessive O2 consumption --reduced coronary perfusion -Potential to deteriorate to a more severe arrhythmia
	Anti-arrhythmics	1. Bradycardia: atropine, glycopyrrolate 2. Rapid atrial arrhythmias: digoxin, procainamide, quinidine, b-blockers, Ca channel blockers 3. Ventricular tachycardia -lidocaine, magnesium sulfate, procainamide, quinidine
	Identifying an Arrhythmia	1. What is the HR? --normal? slow? fast? 2. Rhythm regular or irregular? --regularly irrregular or irregularly irregular 3. P-waves: normal? all the same? 4. QRS complexes: normal? all the same? 5. P wave for every QRS complex and QRS complex for every P wave
	2nd degree AV block	-Atrial depolarization and P wave present with no QRS complex or ventricular depolarization -"Dropped beat" -Common in horses due to high resting vagal tone -Can occur due to xylazine
	Xylaxine	-Reduces amount of sympathetic outflow from the CNS -Increases relative amount of parasympathetic activity --can cause AV blocks -Also causes big increase in BP due to peripheral vasoconstriction
	Causes of AV block	-Autonomic imbalances, changes in sympathetic/parasympathetic tone -Anesthetic drug effects
	Effects of AV block on peripheral blood flow	-Decreases HR, and probably decreases CO a little -Do not expect to deteriorate and turn into something alarming
	Treatment for Excessive Vagal Tone	-Atropine --need to give a big dose -Epinephrine: increases AV conduction quickly --works within seconds
	Dobutamine	-Sympathomimetic drug with B-adrenergic activity -In horses increases cardiac contractility -Can also affect heart rate
	Cause of Sinus Tachycardia	-Autonomic imbalance due to surgical stimulation or light anesthesia -Anesthetic drugs: Atropine, glycopyrrolate, Ketamine --sympathomimetics: dobutamine, dopamine, epinephrine, ephedrine --anything with B1 activity -Sudden hypotension and response of baroreceptors to increase HR
	Significance of Sinus Tachycardia	-Originates in Sinus node -Increases peripheral blood flow (increased HR) -Results in excessive oxygen consumption and probably reduced coronary perfusion -Has potential to deteriorate to a more severe arrhythmia
	Premature atrial contractions	-Source is ectopic focus somewhere in the atria -Not from the sinus node -Common rhythm in horses under anesthesia --not common in awake horses -Caused by dobutamine?
	Significance of Premature Atrial Contractions	-Atrial in origin -Has no affect on peripheral blood flow or CO --can sometimes be higher -Does not affect myocardium -Will not develop into something more serious, no more severe arrhythmia -No treatment!
	Atrial Tachycardia	-4 or more premature atrial contractions in a row -Can be sustained: stays in atrial rhythm for long periods of time -Can be paroxysmal: starts and stops randomly --short runs of atrial tachycardia within the normal sinus rhythm
	Paroxysmal Atrial Tachycardia	-Short run of premature atrial contractions -Originates in the atria -Increases peripheral blood flow by increasing HR -Probably no affect on myocardium -Will not develop into something more severe -Does not need treatment
	Atrial Fibrillation	-Irregularly irregular rhythm with no distinct P-waves -Can be pathogenic in dogs, associated with heart disease -Not significant in horse or cow -Atrial in origin, usually occurs because the atria is enlarged -CO nd blood flow may be reduced --high HR increases cardiac muscle work, may reduce coronary perfusion -Echocardiography is needed for definitive answer -Treat based on echo findings
	Equine Atrial Fibrillation conversion	-Quinidine can be used -Elecrtocardioversion an be done --Use electrode catheters down jugular vein and into heart
	Sinus Tachycardia with premature ventricular contraction (VPC)	-Caused by sudden hypotension, acid/base abnormalities, and myocardial hypoxemia/ischemia -Indicates the heart is under stress -Significant arrhythmia! tachycardia is probably more important than a single VPC -treatment: lidocaine --address underlying issues, blood transfusion to restore blood volume and oxygenation
	Ventricular Premature Complexes	-Ventricular ectopic focus fires before the impulse from the atria can get into the ventricles -Ventricle "interrupts" p-wave -Occasional VPCs are not all that significant in young, healthy animals -Can be significant in older or diseased animals -Unifocal vs. multifocal can be important
	Paroxysmal ventricular premature contractions/tachycardia	-Run of ventricular premature contractions -Starts and stops all of a sudden -More dangerous than atrial tachycardia --ventricular in origin, bigger deal -Have to look at bloodwork for cause --electrolyte abnormalities --acid base abnormalities -Causes increased myocardial work and decreased O2 delivery -Treat with IV fluids, Ca, and bicarbonate --can also give lidocaine for ventricular premature complexes --Myocardial hypoxemia/ischemia
	Anesthesia Machine	-Gas delivery system -Delivers inhalant of choice to patient -Allows precise gas mixtures to be delivered to patient
	Basic anesthesia machine components	-Source for medical gas --O2, N2O, medical air -Regulator/flow meter for each gas -Vaporizer for inhalant of choice -Compatible with many different breathing circuits
	Flush Valve	-Delivers O2 to patient directly -Bypasses vaporizer, no inhalant to patient -part of INTERMEDIATE pressure area on anesthesia machine
	Anesthesia machine Pressure divisions	-System is divided into high, intermediate, and low pressure areas 1. High pressure: accepts gas from the tank --delivers gas to regulator 2. Intermediate pressure: accepts pressure from pipelines/regulator, conducts to flush valve and flow meters 3. Low pressure: conduits between flow meter and common gas outlet
	High pressure area of Anesthesia machine	-Delivers gas from tank to regulator -Gas cylincers -Hanger yokes -High pressure hoses -Pressure gauges (read pressure of O2) -Regulators Pressure is as high as 2200psi (pressure in O2 tank) -Anything above 55 psi
	Intermediate pressure area of Anesthesia machine	-Accepts gas from central pipeline or regulators on anesthesia machine -Conducts gas to flush valve and flow meters -INCLUDES FLUSH VALVE -Pipeline inlets -Power outlets for ventilators -Tubing inside the machine, pipes you do not see, to flowmeter -Flowmeter assembly (half of flow meter) -O2 flush apparatus Pressure is between 37-50 psi, depending on machine -
	Low Pressure area of Anesthesia machine	-Conduits between flow meter and common gas outlet -Slightly higher than ambient pressure -Flow meter to breathing circuit -Part of flow meter -Piping from flow meter to vaporizers -Vaporizer -Piping from vaporizer to common gas outlet -Common gas outlet to breathing circuit Pressure is slightly higher than ambient pressure
	Components of the Anesthesia Machine	-Medical gas source --pipeline or cylinder -Pressure gauge -Regulator -Flowmeter -Flush valve -Vaporizer -Common gas outlet
	Medical gas sources	1. Hospital central gas supply --more economical, acts as primary source of gas --bank of large compressed gas cylinder --pipelines distribute gas to areas of the hospital --bulk tank of liquid O2 --Oxygen concentrating system 2. Cylinder attached to the machine --can be used for transporting patient in a hospital --good for emergencies --more expensive
	Hospital pipeline system	-Goes from central unit somewhere in hospital to terminal unit throughout the hospital -Station unit is where anesthesia machine is connected to hospital gas --specific to gas you are using --has mechanism to prevent incorrect attachment of gas
	Non-interchangeable gas specific connector	-Only allows corresponding receptor to be attached -Prevents incorrect attachment
	Gas Cylinders	-All anesthesia machines should have cylinders attached for safety -Attach to hanger-yoke assembly -All have pin index safety system --prevents attachment of incorrect gas cylinder to machine --different gasses have different spaces between pinholes
	Gas Cylinder characteristics	-Classified by lettering system --Alphabetical from small to large tank --E tank: attaches to machine --G and H tanks are in central supply -Color coded, but based on country --not universal! -Identify tanks by label, do not use a tank without a label
	E- Tank	-Has 660L of oxygen at 1900 psi
	H-tank	-Holds 6900 L of oxygen at 2200 psi
	Oxygen Tank	-Pressure is proportional to volume -If pressure gauge reads 1100psi, indicates only 1/2 of tank is remaining (350L) -Green cylinder in USA
	Nitrous Oxide	-Pressure in E,G, and H tanks are always the same --volume changes per tank -Pressure: volume is not proportional due to liquid/gas phase --when tank is full, everything is liquid --pressure does not change until all liquid is gone and only gas is in tank --25% contents left in tank -Pressure will read 745 psi until only 25% of tank is remaining
	Pressure Gauge	-Each compressed gas should have a corresponding pressure gauge on anesthesia machine --has name and color of corresponding gas -Indicates how much pressure (and volume) is left in tank -And sometimes measure wall tank pressure
	Regulator on Anesthesia machine	-Reduces high and variable pressure from cylinders to lower and more constant pressure -Makes pressure appropriate for machine -Maintains constant flow to flowmeter as pressure in tank changes -Valve that separates high pressure from intermediate pressure -Wall pressure is a little higher than regulator pressure
	Flowmeter on Anesthesia machine	-Measures and indicates rate of flow of gas to patient -Allows precise delivery of O2 to common gas outlet and vaporizer and patient -Calibrated as a unit for each individual gas --Cannot be used for a different gas or with different parts -Assembly unit is intermediate pressure -Tube itself is low pressure
	Flowmeter In Action	-Gas enters from bottom, flows through flow control valve --changes from intermediate to low pressure -Tubing is larger at top than at the bottom --allows greater volume of gas to move around indicator
	Types of flowmeters	1. Single taper: graduations are constant through length of the tube 2. Double taper: allows increased accuracy in lower part of the tube --has 2 changes, not a gradual change --abrupt change in the middle somewhere --can be accurate for small AND large amounts
	Scale of the Flowmeter	-Can be ml/min or L/min -Indicator can be float, ball, or bobbin --read ball in middle
	Flush Valve	-Delivers intermediate pressure flow -37-75 L/min -Straight to common gas outlet or straight to breathing system -Bypasses vaporizer! -DO NOT use with a rebreathing system! Do not flush the valve! Will over-pressurize patient's respiratory system
	Vaporizer	-Deliver inhalant anesthetic to maintain patient under anesthesia -Halothane -Iso -Sevo -Des -Designed to change liquid anesthetic to vapor form and add specific amount of vapor to carrier gas
	Classification of Vaporizers	1. Method out output regulation 2. Method of vaporization 3. Location 4. Mechanism of temperature compensation 5. Agent specificity 6. Resistance
	Vaporizer Regulation of Output	1. Measured flow: measures flow going into vaproizer -also measures flow that never entered the vaporizer -Need to calculate the different flows 2. Variable bypass: all fresh gas goes through the vaporizer -vaporizer divides flow into inhalant chamber and bypass chamber -Most vaporizers are variable bypass
	Vaporizer Method of Vaporization	1. Flow over: gas picks up inhalant from vaporizer -direct carrier gas over the surface of liquid anesthetic -Surface area may be increased with a wick 2. Bubble through: gas comes from bottom of liquid inhalant, bubbles through liquid inhalant 3. Injection: delivers a known amount of liquid anesthetic into a known gas volume
	Vaporizer location	-Can be in circuit or out of circuit -Today, most vaporizers are OUT of circuit --are not part of breathing circuit, are part of anesthesia machine
	Vaporizer Temperature Compensation	-Heat is needed to make inhalant go from liquid to vapor state -as vapor is used, temp decreases 1. can apply heat to maintain temperature 2. Can use high-termal conductivity material to maintain stable temperature 3. alter flow of carrier gas --temp decreases, less vapor is produced, flow needs to be higher --vaporizer does it on its own
	Vaporizer agent specificity	1. Vaporizers are agent-specific! --Use with one single inhalant anesthetic 2. Multipurpose vaporizers are used with any volatile liquid anesthetic --make sure you do not mix inhalants!
	Common Gas Outlet	-Leaves anesthesia machine and connects to breathing circuit -Combination of gas from flowmeter, vaporizer, and flush valve -Flush valve gas will not be included unless flush valve button is pressed -Connection between anesthesia machine and breathing circuit
	Transition between anesthesia machine and Breathing circuit	-Anesthesia machine: prepares precise gas mixtures -Breathing circuit: allows delivery of precise gas mixture to patient -Connection: common gas outlet to fresh gas inlet --"fresh gas inlet" on breathing circuit side
	Types of Breathing circuits	1. Rebreathing circuit: circle system -whatever the patient inspires is expired and re-used by the patient -gas is re-used 2. Non-rebreathing: whatever the patient expires exits system through pop-off and is never inhaled by patient again
	Rebreathing Circuit	-Part or all of the exhaled gas is re-used by the patient after the CO2 is extracted --O2 and inhaled anesthetic are re-used -More economical, conserves O2 and inhalant -Conserves heat and moisture -Can be used with patients over 8-10 kg -What patient inhales is a mix of fresh air and recycled air through the absorber
	parts of Re-breathing circle	-Fresh Gas inlet -Inspiratory one-way valve -Inspiratory corrugated tube -Y-piece (patient) -Expiratory corrugated tube -Expiratory one-way valve -Pop-off valve (into scavenger) -Rebreathing valve -Rebreathing bag -Manometer -Absorber
	Fresh gas Inlet	-Connection between anesthesia machine and breathing circuit -AKA common gas outlet -Provides fresh carrier gas (O2) and inhalant to the circuit
	Inspiratory one-way valve	-Directs flow toward patient during inspiration -Prevents inspiration of the exhaled gas -Gas enters the valve from below, raises disk, and passes under the time into inspriatory tube -Increases resistance in system, resistance to breathing --not a major problem for the patient --not the biggest source of resistance for the patinet
	Inspiratory corrugated Tube	-made of rubber or plastic, very flexible -Very low resistance --makes it easy for the patient to breathe -Corrugations allow bending without obstructing flow -Add length and volume to the system, but not dead space -22mm diameter for small animals -55mm diameter for large animals -Always consistent! Allows plugging into one post
	Y-piece	-Connects inspiratory and expiratory tube -Mixing of gas occurs
	Expiratory corrugated tube	-Same construction as the inspiratory tube -Does not matter which tube gets plugged in where!
	Expiratory one-way valve	-Helps maintain flow towards the patient on inspiration, away from the patient during expiration -If does not function, allows patient to re-breathe CO2 -Disk can become stick with moisture, check to make sure it is working! --Likely spot for problems
	Pop-Off Valve	-Vents excess gas to the scavenger system -prevents build-up of excessive pressure within the circuit -Vents gasses at pressures more than 1-5 cm H2O --allows easy leaking, prevents pressure build-up -Whatever is in the flow meter is probably more than what the patient needs --extra gas has to go somewhere, goes out pop-off valve -Should ALWAYS be open!! --Closed pop-off: pressure checking machine for leaks or closed system ventilation
	Reservoir Bag	-Gas that does not go out through the pop-off valve -Size should meet at least 1 tidal volume of the patient -- (body weight x 10) x 4 = size of the bag -Size of the bag is only an issue if it is too small --too large adds volume to circuit, but not bad for patient --too small, patient can collapse bag, which is very bad for the patient! -Allows mechanical ventilation of patient if needed -Part of system that adds extra compliance
	Manometer	-Pressure gauge -Reading of the pressure within the breathing system -Calibrated in cm H2O -Should read 0 at all times, unless providing positive pressure ventilation
	Absorber	-In plastic cannister -between 2 one-way valves -Adds resistance, want patient to exhale into the bag first -Exhaled gas can enter top or bottom of canister -Volume between granules in canister should be equal to or more than the tidal volume of a pateint --airspace is 50% when canister is filled
	Absorption of CO2	-Sodalime or Barium hydroxide lime -Causes chemical reaction, between granules and CO2 -Produces water and heat --canister is warm to touch -Once granules are used, they become hard --turn into CaCO3 -fresh granules are broken down very easily, crushed easily -Color change can also indicate used-up granules -Change absorbant once 2/3 of canister has changed color
	Choosing Fresh Gas Flow	-Flow meter allows you to choose whatever flow you want -Pt has minimum O2 demand -Smaller patients need proportionally more oxygen per minute than larger patients --total amount is greater for bigger animals, but ml per minute is smaller
	Formula for patient O2 demand	O2 demand = body weight (0.75 x 10) ml per minute
	Closed System	-Whatever fresh gas flow is administered to patient is what the patient is consuming -No gas is leaving the system whatsoever -In theory, can close pop-off -Economical, conserves heat and moisture -Takes longer to establish plane of anesthesia --patient should not be started on low flow, start high then dial down O2 flow
	Low flow Circuit	-Fresh gas flow 5-10 ml/kg/min -Slightly above the patient's requirement -Pop off valve should be open! -Economical, not wasting a lot of fresh gas or inhalant -Conserves heat and moisture -Need to start patient on higher flow -Takes a long time to change the plane of anesthesia due to low flow
	High floe circuit	-Fresh gas flow is 30 ml/kg/min -MUCH higher than the patient's O2 requirement -Can establish plane of anesthesia very fast, and can change plane of anesthesia -More expensive, lots of waste
	Changes in Oxygen Flow	-Vaporizer dial setting (%) --What comes out of vaporizer is what the percentage says --Will deliver the same percent no matter what the flow rate is -In re-breathing system, is not actually same percentage because it is mixing with what the patient is expiring/what is recycled by absorber -Deliver larger amount, amount patient is exhaling makes less of a difference --dilution is less -If fresh gas flow is low, more of it is recycled
	Non-rebreathing Circuit	-Systems that do not use chemical absorbent -Depend mostly on fresh gas flow rates to flush exhaled gas -Do not remove CO2, not re-using gas -Need high fresh-gas flow rate, very high -Mostly used for smaller patients due to waste --less than 8 kg -Patient never inspires same gas again -Very easy to use and clean, inexpensive -Less resistance for patient to breathe -Minimal dead space -Quick change of anesthetic depth -Needs very high flow, wasteful -Will have drying of respiratory tract and potential hypothermia
	Mapleson Systems	-For non-re-breathing systems -Classified based on position of fresh gas inlet, location of overflow, presence of a reservoir, and corrugated tubing
	Bain Coaxial System	-Non-rebreathing circuit -Modified mapleson D -Tube within a tube --Internal tube brings fresh gas to patient --external tube takes exhaled gas away from patient to reservoir bag or Pop-off valve -flow rate is 100-200 ml/kg/min, very high flow! --amount is patient dependent --always need to run at least 1L -If rebreathing is noticed (increased inhaled CO2), flow should be increased -High flow is needed to "flush" the system with each breath, push exhaled gas out of the expiratory tube
	T-pieces system	-"Mapleson E" and "Mapleson F" -Fresh gas enters T-shaped tube from the side --perpindicular to the direction of gas flow during ventilation -One end of T-tube connects to ET-Tube, other end connects to expiratory corrugated tube -Flow rate needs to be 2-3x patient's minute volume --pushes at least 1 tidal volume away, exhaled gas is pushed away
	Managing Oxygen Flow in non-rebreathing	-Flow is always constantly high, from start to end -Expired gas is wasted -Whatever is dialed on the vaporizer is what the patient is breathing --pure iso right out of the vaporizer! -Easier to anesthetize and wake-up patient
	Universal F Circuit	-Rebreathing system with only 1 limb -Inspiratory tube on inside, expiratory tube on outside --allows conservation of heat and moisture -Tube also has one-way valves -Less bulky than conventional 2-tube method
	Pressure Checking Anesthesia Machine	-Entire machine should be checked at the beginning of the day -Breathing circuit should be tested before anesthetizing each pateint -Close pop-off valve, turn on flow meter,let pressure build up to 20 cm H2O --drop in pressure over 30 seconds should be less than 5 cm H2O -If leak is present, need to figure out where gas is lost -Can turn flow meter on to see how much is leaking
	Tank Induction	-Used for oxygenation and induction of anesthesia -Good for aggressive cats, exotic patients, lab animals -Use inhalant anesthetics alone -HUGE contamination of inhalants into room -May be less stressful for patient, less restraint -No catheter or tracheal tube present, if there is an issue there is not quick approach -Risk of airway obstruction and corneal damage -Should be clear tank, size of chamber should not be larger than needed --tank should also have way to scavenge inhalant -Need really high flow rates! -Practical, but still not safe -Patient should be watched the entire time -not good for all patients, esp. patients with airway pathology, patients with low cardiac output
	Primary Function of the Respiratory System	-Gas Exchange -Transports gas -Allows CO2 to diffuse out and O2 to diffuse in -Ventilated areas have to be perfused --Need Perfusion and ventilation to match
	O2 and Partial pressure Gradients	-O2 moves down partial pressure gradient from atmospheric pressure to capillaries
	Partial Pressure of a gas	-The pressure a gas exerts in a mixture of gasses -The fraction of the total pressure of gas contributed by the percent concentration of the gas -Measured as mmHg
	Fractional Concentration of gasses	-N: 78% -O: 21% -CO2: .004% (not a lot of CO2 in room air) Comes from by-product of metabolism -Inert gasses: .007%
	Oxygen Uptake	-Barometric pressure -Fractional concentration of inspired O2 -Ventilation -Diffusion -Ventilation/perfusion mismatch -Shunting: areas that are perfused and not ventilated --blood leaving lung is still mixed venous blood
	Barometric Pressure	760 mmHg at sea level 253 mmHg on Mt. Everest
	Tracheal gas	-Have to take into account partial pressure of water vapor that is in the trachea --47 mmHg at sea level -Causes partial pressure of O2 to be a little bit less than 21%
	Partial Pressure fo Oxygen in Alveoli	-Lower because gas is constantly being removed
	Tidal Volume	-The amount of gas you move in and out of the lung with normal resting breathing -10-15 ml/kg -Measured via spirometer
	Intrapleural Fluid	-Acts as a lubricant for lungs -Causes lung and thoracic wall to be attached to each other and also gives lubrication to decrease friction
	Functional residual Capacity FRC	-Volume of gas left in the lung after a breath -Equilibrium point where the tendency of lung to expand is the same as the tendency of the lung to collapse -Fair amount of gas is left in the lung -Gasses become important during anesthesia --parts of the lung can collapse during anesthesia in certain species
	Respiratory Minute ventilation RMV	-Volume moved in and out of the lung each minute = tidal volume x respiratory rate -Small animal patient: 150-250 ml/kg/min
	Causes of decreased RMV	-Medullary depression: anesthetics or increased ICP -Restriction of the lungs or chest wall --chest trauma --abdominal distention --obesity --respiratory muscle fatigue --surgeon sitting on the patient
	Factors affecting Respiratory centers in the brain	-Arterial CO2, peripheral and central chemoreceptors --increased CO2 is the primary drive to breathe --brain does not want to get acidotic -O2 plays a role, but only after O2 levels fall below 60 mmHg
	Respiratory centers in the Brain under Anesthesia	-Can get change in threshold and change in slope of CO2-response curve -Inhalant anesthetics decrease the slope of the line --higher concentration of anesthetic in the lung, the more respiration is depressed --Iso, sevo, and des are likely to depress respiration --N2O is least likely to depress respiration
	Narcotics and Respiration Depression	-Changes partial pressure of CO2
	Causes of Decreased RMV	-Respiratory obstruction -Neuromuscular blockade --paralytic agents --spinal cord lesions -Inadequate mechanical ventilation
	Alveolar Ventilation	-Volume of Fresh gas that reaches the alveoli per minute -Very important! -ONLY volume effective at maintaining gas exchange -Not the same as respiratory minute ventilation --respiratory minute ventilation includes dead space in trachea and upper airways -Takes dead space into account! = (tidal volume-dead space)* respiratory rate = (Vt - Vd)* f
	Intubation and Deadspace	-Lumen of the ET tube is narrower than trachea --decreases deadspace -Also decreases the amount of dead space in the pharynx -If ET tube is too long, increases amount of dead space
	Dead Airspace in the Anesthesia Machine	-In the Y-tube right next to the patient -Everywhere else is 1-way flow of O2, does not allow for dead-space
	Accommodating Dead Space	-In an awake patient, increase in dead space can usually be off-set by a corresponding increase in respiratory minute ventilation -Under anesthesia patient takes smaller tidal volumes and slightly greater RR --each breath has less and less fresh gas due to dead space
	Dead Space Ventilation in Cats	Normal TV: 10-15 ml/kg Frequency: 20 bpm RMV awake: 200 ml/kg/min --30% deadspace --60ml dead space, 140 ml fresh gas Right angle adapters add 9ml of dead space to calculation -Increase of dead space is a major issue with small patients -Can use non-rebreathing circuit, has less dead space
	Physiologic Dead Space	Anatomic Dead Space Alveolar Dead Space --pulmonary emboli
	Causes of Hypercarbia (too much CO2)	-Decreased RMV -Increase in dead space with no change in minute ventilation -Increase in CO2 in inspired air -Increased CO2 production with fixed RMV, increased metabolic rate
	Dead Space in Lung	-Areas that are ventilated but not perfused -Hypotensive or bleeding lung may result in lower lung perfusion -Increases dead space in patients that are cardiovascularly unstable
	Accurate Assessment of Ventilatory Status	-Made by measuring Arterial CO2 -Gold Standard: measure Arterial CO2 -Arterial CO2:
	Arterial CO2	-Gold standard measure for ventilatory status -Normal volume: 40mmHg -Depends on how much CO2 is being produced (metabolic rate) relative to how well patient is ventilating -Changes in arterial CO2 from the normal value are used to define alveolar ventilation -Increases in arterial CO2 means patient is Hypoventilating -Decreases in arterial CO2 means patient is Hyperventilating
	Hypoventilation Signs For when Arterial CO2 blood gas is not available	-Increased or decreased respiratory effort -Tachypnea or dyspnea -Tachycardia -Hypertension -Cardiac arrhythmias -Peripheral vasodilation -Indicates blood gas PaCO2 is more than 45mmHg
	Spirometer	-Put on expiratory limb of the anesthesia machine -Each time patient expires, needle moves and tells you volume of the breath
	Capnograph	-Measures end tidal CO2 -CO2 sampling line in the rebreathing circuit --directly hooked up to breathing circuit -First expired gas will not have a lot of CO2 --fresh gas left over from inspiration -End tidal reading gives info
	Sidestream Monitor for CO2	-Continuously suctions a small amount of gas from anesthesia circuit and tests for CO2 -Sucks between 50-150 ml/min --can be an issue for small patients with low tidal volume -Endotracheal tube adapter has side-port --reduces dead space -Make low-flow closed circuit anesthesia difficult
	Closed Circuit Anesthesia	-Delivering the amount of O2 that the patient is consuming --4-6 ml/kg/min, O2 consumption rate of the patient -Nothing goes out of the pop-off valve -Exhaled air goes through soda-lime and is cleared of CO2 -Less waste, less expense
	Mainstream CO2 monitoring	-Monitor has infrared analysis -Does not suck the gas at all, just reads gas as it goes through breathing tube and device -Does not remove gas from the circuit -Need adapter for ET tube, adds a little bit of dead space -Good for closed-circuit anesthesia
	CO2 curve	-Start of expiration has a little lag due to fresh air in the trachea dead space -End tidal volume is the maximum CO2 -Inspiration looks like a steep drop in CO2
	Leak in Hose and CO2 curve	-Causes fresh gas influx -Will not get CO2 plateau
	End Tidal CO2 vs. Alveolar CO2	-End Tidal CO2 is generally 5-10 mmHg lower -Due to dead space gas -Every time the heart beats it puts a little more CO2 into the lung -End tidal CO2 is affected by how well patient is ventilating, also affected by perfusion --Can use End Tidal CO2 as cardiac monitor and respiratory monitor --End tidal CO2 will go down with heart failure because CO2 is not being delivered to the lung for removal
	End Tidal CO2 and Hypoventilation	-Drop in End Tidal CO2 can indicate hypoventilation -Accurate assessment of centilatory status needs CO2 measurement
	Importance of High CO2 Hypercarbia	-Acidemia -Changes in cerebral blood flow -Sympathetic nervous system stimulation -Arrhythmias -Narcosis -Respiratory depression -Decreased myocardial contractility -Shift in O2 dissociation curve
	Alveolar Gas Equation	Alveolar concentration of O2 = inspired concentration of O2 - (O2 uptake/Alveolar ventilation) Concentration of gas in the alveolus depends on inspired concentration of O2 relative to how much O2 you are taking up relative to how much O2 is being delivered PaO2 = PiO2 - (PaCO2/R) PiO2 = FiO2 (Pb-H2O)
	Respiratory Quotient	-How much CO2 patient produces relative to how much O2 is being consumed VCO2/VO2 -Omnivore= .8 -Herbivore= Higher than .8, eating mostly carbohydrates -Carnivore= less than .8. eating more meat and less carbohydrates
	Alveolar gas Equation	PaO2 = PiO2 - (PaCO2/.8) Arterial PaO2 is usually 5-10 mmHg lower
	Aa Gradient	-Alveolar-arterial oxygen difference =PalveolarO2-ParterialO2 -In room air is about 5-15 mmHg -Ventilation and perfusion are never completely matched in the lung, ratio is never perfect 1:1 -Bronchial circulation puts mixed venous blood into pulmonary vein --adds deoxygenated blood to oxygenated blood in pulmonary vein
	Alveolar PaCO2 60	-On knee of curve of Ox-Hb dissociation curve -O2 saturation is 90 -Not a good place to be! -Any further hypoventilation will cause PaO2 to fall -If possible, try to reverse the patient -Can also give patient supplemental O2 until they are more awake
	Quick way to calculate PaO2	Take %O2 patient is breathing and multiply by 5
	Influences on O2 uptake and delivery to the lung	-Changes in FiO2 -barometric Pressure -Ventilation -Diffusion -V/Q mismatch -Shunt
	Diffusion abnormalities are rarely a cause of hypoxemia in patients	-Unless the system is stressed
	Fick's Law	-Determines the velocity of diffusion of gas across a membrane -Proportional to: --the surface area available for diffusion --Diffusion co-efficient (depends on solubility and MW) --driving pressure for diffusion -Inversely proportional to the thickness of the barrier
	Lung Surface Area	-Exponential increase in cross-sectional area of the lung after initial divisions -LOTS of space available for diffusion
	Blood Gas Barrier Thickness	-0.3 microns -Very thin! -Has thin side and thick side --thick side has capillaries, edema accumulates on thick side --Most diffusion occurs on thin side
	Alveolar Diffusion Abnormality	-Thickening of the Blood-gas barrier -Occurs with pulmonary fibrosis -Only really occurs when the system is stressed -Never a cause of hypoxemia
	Pulmonary Edema	-No diffusion abnormality -Get flooding of the alveolus -Areas are perfused but not ventilated --SHUNT -Causes problems with gas exchange
	Pulmonary Disease Hypoxemia	-Ventilation/Perfusion mismatch is main cause V=0 SHUNT
	Shunt	-Ventilation =0 -No ventilation -Venous mixed blood goes into section of lung and is not re-oxygenated --leaves as venous mixed blood
	Lung as a Low Pressure system	-Mean pressure is 15 mmHg -No major muscular systemic arterioles -Only 60% of pressure drop occurs on arterial side --40% on venous side -Hard to tell the difference between pulmonary vein and pulmonary artery --Very dependent on gravity
	Distribution of blood flow to the lung Zone 1	-Not a lot of blood flow to the top of the lung -Area of dead space where alveolar pressure is greater than arterial pressure is greater than venous pressure --If pressures are low for some reason, dead space increases --giving positive pressure ventilation also increases dead space
	Distribution of blood flow to the lung Zone 2	-Arterial pressure is greater than alveolar pressure is greater than venous pressure -Start recruiting new vessels
	Distribution of Blood flow to the lung Zone 3	-Areas where the venous pressure is greater -Blood flow continues to increase due to distended vessels --not a lot of muscle
	Blood flow increases from top of the lung to the bottom of the lung	Ventilation also increases from the top of the lung to the bottom of the lung
	Intrapleural pressure variation	-Ventilation increases from the top of the lung to the bottom of the lung - -10 cm H20 at the top of the lung - -2.5 cm H2O at the bottom of the lung -Alveoli are going to be bigger at the top of the lung -Alveoli are on different parts of the compliance curve
	Compliance Curve	-Basically a pressure volume curve -What kind of change in volume do you get for a given change in pressure -The more compliant something is, get a bigger change in volume for a given change in pressure -Allow alveoli in the top of the lung to be bigger
	Alveoli at the top of the lung	-Are bigger -At the top of the compliance curve -Become less complaint when a breath is taken
	Top of lung vs. bottom of lung	-Blood flow increases towards the bottom of the lung -Ventilation increases towards the bottom of the lung -Do not increase at the same rate -Results in areas at the top of the lung that have a lot of ventilation relative to available perfusion -Areas in the middle of the lung are close to ideal -Areas at the bottom of the lung have a low ventilation relative to perfusion
	Areas with High V/Q	-O2 is higher -CO2 is lower -Approaches what is found in inspired gas -Less perfusion going to areas with high V/Q -O2 content is not changing very much due to Hb dissociation curve
	Areas with low V/Q	-O2 and CO2 is closer to that of venous mixed blood -O2 is lower -CO2 is higher -More blood going to areas with low V/Q
	Mixing samples of Blood	-Does not mix PO2 -Mixed Contents -Oxygen content/saturation will be half way between O2 content --results in lower PO2 due to non-linear nature of Hb curve -Not adding a lot of content -Areas of lung that are not getting any blood are not changing
	Hypoxic pulmonary vasoconstriction	-Areas of the lung where alveolar PO2 is less than 70, pulmonary arterioles are constricted -Arteriole PO2 will be 60 mmHg --on knee of Hb dissociation curve! -Different strength of response between species -Response decreases when animal is on anesthesia --increases mismatch between ventilation and perfusion --anesthesia causes increase in dispersion between ventilation and perfusion -Increase in alveolar dead space occurs due to increased distribution of ventilation to areas with high V/Q
	Shunts under Anesthesia	-Causes huge increase in shunt fraction -Common, especially in horses --can have PO2 of 60-70 due to huge shunt -will have Areas of normal function and Areas where mixed venous blood comes in and leaves as mixed venous blood -If there is not ventilation, will not fix issue no matter how much O2 animal gets via machine -Normally right to left shunt --affects oxygenation
	Horses and Shunts under Anesthesia	-Very common -Horses have long sloping diaphragms -Often are on their backs -Over time get absorption atelectasis, areas of alveoli that start to collapse
	Positive End Expiratory Pressure PEEP	-Best method to decrease shunt fraction -Add positive pressure so at end expiration positive pressure never goes back to zero -Try to change areas of shunt to areas of V/Q mismatch --might not be perfect, but at least some gas is getting to areas --giving 100% O2 will make a difference -Positive pressure decreases CO, decreases venous return
	Problem with PEEP	-Increasing pressure decreases CO and venous return to the heart -As blood goes by tissues, tissues need to extract more of the available O2 -Decreases mixed venous O2 saturation --Not helpful! -Add Inotrope to increase CO
	Inotrope with PEEP	-Horse: dobutamine -Add something to increase CO
	Pulse Oximeters	-Measures differential absorption of light in pulsatile flow -Put on the tongue -Method for measuring PaO2 without doing an arterial blood gas -Gives oxygen saturation, NOT PO2 -Should read 95-100 --almost never reads 100, needs to sense a pulse to work --PO2 should be 400-500 -good for patients in recovery or for patients on room air -If it senses a low flow, it cannot get a good reading
	Pulse Oximeter Function	-Device sends out flashes of light and compares what is absorbed to normal light -Red, infrared, ambient light -Oxygenated Hb absorbed less light in the red range than non-oxygenated Hb --Red light is reflected back -Non-oxygenated Hb absorbs less infrared light, reflects more infrared light back to sensor -Measures Differential absorption of light in pulsatile flow
	Normal Values for Arterial Blood gasses	-When patient is breathing 100% O2 -PaO2 > 500 mmHg -PaCO2 = 40 mmHg -pH = 7.4
	Cyanosis as indicator for Hypoxia	-Bad indicator! Late-presenting sign
	Factors affecting Oxygen status	-Oxygen uptake -Oxygen transport -Oxygen release -Tissue Oxygenation
	Factors affecting Oxygen transport	-PaO2 -Hb -SaO2 -CO
	Oxygen Content	-Every gram of Hb carries 1.34 ml of blood
	Henry's Law	(1.34 x Hb x SaO2) + 0.003 PO2
	Oxygen Delivery	= CO x Oxygen content
	Gas Exchange in the Lung	-Need to be able to get the O2 in and CO2 out
	Important things with O2 uptake	-PaO2: PO2 in the alveoli
	PAO2	-Depends on alveolar ventilation (not minute ventilation) --how much fresh gas is getting down to alveoli -Need fresh gas to be getting down into the lung to have gas exchange -Ideally 100 -Depends on concentration of fresh gas (room air vs. pure O2)
	Minute ventilation vs. alveolar ventilation	-Minute ventilation: amount of gas moving in and out of the lung every minute --Tidal volume x RR -Alveolar ventilation: amount of fresh gas getting down into the lung --(Tidal volume - dead space) x RR --Need to take amount of dead space into consideration
	Factors increasing amount of dead space	-Hypotension -Positive pressure ventilation
	Partial Pressure of Inspired Oxygen	=FiO2 x barometric pressure -Depends on barometric pressure -Humidity of air -Depends on fractional concentration of inspired O2
	FiO2	-Fractional concentration of inspired O2
	Ventilation and Perfusion	-not always matched -Normal V/Q ratio = 0.8 --more perfusion than ventilation --Never have ideal 1:1 -Changes in ratio are common cause of hypoxemia with pulmonary disease -Areas in the top of the lung have relatively high V/Q ratio --O2 will be higher than 100, CO2 will be lower
	PaCO2	-Ideally 40
	Room Air	-FiO2: .21 -Barometric pressure: 760 mmHg -Water vapor pressure: 47 mmHg .21 (760-47) = 150 mmHg = PO2 in trachea at end inspiration
	Alveolus that is not getting perfused	-PO2 coming in = 150 -CO2 coming in = 0 -Will not change if there is not perfusion -DEAD SPACE
	Dead Space	-Area that is ventilated but not perfused -All capillaries in the lung are not perfused all of the time -Areas in the top of the lung are less perfused --will get some blood getting into area --some O2 and some CO2 is introduced --Blood leaving the top of the lung will have relatively high O2 and low CO2
	Areas with relatively high V/Q	-Top of the lung -Blood leaving areas will have higher than normal O2 and lower than normal CO2 -Cannot make up for areas of low V/Q --More blood goes to bottom of the lung --Relationship between PO2 and Hb saturation is not linear (sigmoid relationship)
	Areas with relatively Low V/Q	-Bottom of the lung -Some ventilation occurs, but less than at the top of the lung -Oxygen will be lower than 100, more like 65-70 -Normal in the lung -More blood goes to the bottom of the lung, to areas with low V/Q
	Shunt	-Area with perfusion but no ventilation -Mixed venous blood comes in and leaves as mixed venous blood -No ventilation, no gas exchange is occurring -Big shunts cannot be made better by giving lung 100% oxygen (give PEEP)
	Normal partial pressures in mixed venous blood	PO2 = 40 mmHg --75% saturated PCO2 = 46 mmHg
	PO2 = 60	-Oxygen saturation is around 90 -Not a good thing, right on the "knee of the curve" -About to start dropping quickly
	PO2 = 100	-Oxygen saturation is 98
	PO2 = 40	-Oxygen saturation is
	PO2	-Pressure that dissolved oxygen is exerting in blood -Oxygen saturation is more important than PO2, is bound to hemoglobin -Mixing volumes of blood results in mixing oxygen contents
	Optimizing O2 Delivery	-Optimize with Hb -Make sure hematocrit high or at least adequate --do not anesthetize anything with PCV less than 20 -Can add PEEP (Positive and Expiratory Pressure) --allows keeping alveoli open, changes areas that are completely collapsed to areas of V/Q mismatch
	Inotrope	-Drug that increases cardiac contractility -Dobutamine -Dopamine at low dose
	Things that shift O2/Hb dissociation curve to the right Bohr Effect	-Increases in metabolic rate --increase in CO2 --decrease in pH --Increase in temperature -Unload more oxygen at tissue level
	Changes in venous blood gasses	-Difference between O2 on arterial blood vs. venous blood -More oxygen demand in tissues, tissues pull more O2 out of the blood --results in a lower oxygen pressure in veins -SVO2 increases, CO increases, delivering more blood to tissues so tissues do not need to extract as much O2 from blood -CO decreases, SVO2 decreases
	SaO2 SvO2	SaO2: Saturation of O2 on Hb on arterial side SvO2: Saturation of O2 on Hb on venous side Determine where animal is on Hb/O2 dissociation curve Determines how saturated the animal is
	Oxygen Content Equation	= (1.34 mlO2) x (Hb concentration g/100ml) x (O2 saturation) 1.34= O2 carrying capacity of Hb --mlO2 per gram Hb
	Normal Aa Gradient	5-15 on room air 150 on pure O2
	Alveolar gas Equation	= PiO2 - (PaCO2/0.8)
	Mechanical Ventilation	-Spontaneous respiration is replaced or assisted by a device or machine -Replaces or assists natural ventilation
	Vt	Tidal Volume
	Ve	Minute volume
	SV	Spontaneous Ventilation
	Barotrauma	Injury due to high airway pressure
	Volutrauma	Injury due to over-inflation of the lungs
	Compliance	Measure of distensibility Measured in ml/cm of H2O
	WOB	Work of Breathing
	CMV	Controlled/Continuous Mechanical/mandatory Ventilation Ventilator is doing all of the breathing
	IMV	Intermittent mandatory ventilation -Supportive ventilation by ventilator
	Assisted ventilation	Patient tried to breathe, tidal volume was probably not big enough -ventilator supports patient's breathing -Allows patient to have a deep enough breath
	PEEP	Positive end-expiratory pressure
	CPAP	Continuous positive airway pressure
	Indications for Mechanical Ventilation	-Apnea, no breath -Hypoventilation: PaCO2 is more than 60 mmHg -Hypoxemia: PaO2 is less than 60 mmHg --Some hypoxemia will not be helped by mechanical ventilation, some can be -Open-chest surgery (patient cannot breathe on their own, not able to generate negative pressure) -Space-occupying brain tumor -Increase in work of breathing -Stabilization of anesthesia -Post-CPR, may not see enough breathing from patient
	Hypoventilation	-Anesthetics, sedatives --decrease frequency and tidal volume of breathing -Decreased functional residual capacity, less air left in the lungs at end expiration -Neurologic disorders -Muscular disease (myasthenia gravis)
	Factors contributing to Decreased Functional Residual Capacity	-Can be due to anesthesia -High abdominal pressure (GDV, colic, pregnancy, bloat, severe ascites) -Pulmonary issues (pneumothorax, pleural effusion) -Laproscopy, endoscopy, or thoracic surgery --increase pressure by inflating the stomach -Position of the animal --dorsal, head-down, lateral (especially in large animals) -Diaphragmatic hernias, results in less space in pleural area
	Spontaneous Ventilation	-Animal makes negative pressure in thoracic cavity by moving diaphragm -Increases volume, decreases pressure -Need to establish a pressure gradient, negative pressure -Air goes down into lungs, down pressure gradient -Eventually reach equilibrium, indicates end fo inspiration -Expiration is mostly passive, except in horses (slightly active exhalation)
	Mechanical Ventilation	-Squeezing bag creates positive pressure -Causes positive pressure in the lungs, airways, trachea -Positively pushing air into the lungs, complete positive pressure
	Advantages of Mechanical Ventilation	-Can maintain good minute volume (Tidal volume x frequency or respiration) -Can do manually -More stable and deeper anesthesia -Easy to control PaCO2 level -Important for patients with space-occupying brain tumors
	Anesthetic Depth under Mechanical Ventilation	-Minute volume is constant -Inhalant anesthetics need to be inhaled by the patient, mechanical ventilation ensures patient is inhaling --if not enough ventilation, inhalants do not get to the brain -Hypoventilated animals may not be anesthetized with inhalant anesthetics as much as you expect -Inconsistent ventilation can cause unstable anesthesia depth
	Increasing Ventilation	-Increases gas-exchange surface area --increases inhalant uptake --increases depth of anesthesia
	Disadvantages to Mechanical Ventilation	-Decreased CO -No "feeling" sensation, cannot feel breath or changes in the lungs and pulmonary system -Hyperventilation -Lung injury -Malfunction of ventilator -Human error due to incorrect setting, inadequate knowledge of ventilator -Infection with more than 48 hours of continuous ventilation
	Decrease in CO with mechanical ventilation	-Blood flows due to pressure gradient -Right atrium pressure = 0, allows all blood to flow back to the heart -During positive pressure ventilation everything in the chest is pressurized --Blood does not go back to the heart due to loss of pressure gradient -Biggest issue is in INSPIRATORY phase --increase in thoracic pressure, decreased blood returning to the heart, decreased SV -In expiration phase goes back to 0, not an issue -Can try to reduce inspiratory time -Can reduce mean airway pressure (MEAN pressure is the big thing)
	Hyperventilation and Mechanical Ventilation	-Leads to hypocapnia, low PaCO2 -Has effect on cerebral blood flow, decreases -Increases sympathetic tone and increases catecholamine release --low SVR, low HR, low contractility -Acid-base imbalances leading to respiratory alkalosis -Increases respiratory drive
	Hyperventilation and Cerebral Blood Flow	-Can occur during mechanical ventilation -As PaCO2 increases, cerebral blood flow increases -If PaCO2 decreases, cerebral blood flow also decreases -With hyperventilation, PaCO2 decreases, causes cerebral blood flow to decrease -Causes brain ischemia
	Lung Injury and Mechanical Ventilation	-Ventilator-Induced Lung Injury -Ventilator-Associated Lung INjury
	Ventilator Induced Lung Injury	-Microscopic level injury -Occurs on level of the acinus -More likely due to volume trauma, over-inflation of the lung -Over-inflation causes the lung to release inflammatory mediators, increase in shear stress, and depletion of surfactant -Volutrauma
	Ventilator-Associated Lung Injury	-Injury to lung due to barotrauma, too high pressure in the lung -Depends on the compliance of the lung and chest wall --highly compliant lung, might not have effect --non-compliant lung can be damaged with just a little bit of excessive pressure -Induced by mechanical ventilation -Pneumonia
	Power Source for Mechanical Ventilation	1. Electric: piston-driven ventilator 2. Pneumatic: compressed gas, high-pressure gas --high pressure gas compresses the bellows --O2, medical air, or mixture 3. Both Electrically controlled pneumatic ventilator is most common
	Singe-circuit Mechanical Ventilator	-Patient-gas circuit only -Pneumatic ventilator or piston-driven ventilator -Tubing or cylinder is the "reservoir bag" --machine squeezes the bag
	Double-Circuit Mechanical Ventilator	-More common type of circuit -Driving gas circuit -Patient gas circuit -Bellows act as the "reservoir bag" -has "spill valve" in bellows that lets excess gas into the scavenger system
	Styles of Bellows	1. Ascending: goes up during exhalation --smaller work of breathing --shorter inspiratory time --Easier to find leak in ascending bellows 2. Descending: goes down during exhalation --more work of breathing, have to bring bellows up to inhale --harder for the patient --longer inspiratory time, less ideal for cardiac output --Common on older machines (easier to make?)
	Safety System in Mechanical Ventilators	-high pressure alarms go off -Low pressure alarms if machine is leaking -Pressure-limiting mechanism --pressure is set, machine will not give higher pressure than setting --prevents barotrauma
	Targeted Mechanical Ventilation Settings	1. Volume targeted: set target tidal volume to give to the patient 2. Pressure targeted: set peak inspiratory pressure for each breath
	Volume targeted Mechanical Ventilation	-Fixed Tidal Volume, constant tidal volume -Check peak inspiratory pressure -Depends on compliance of patient lung -Can cause barotrauma
	Pressure Targeted Mechanical Ventilation	-Peak inspiratory pressure is set for each breath -check tidal volume -Depends on compliance of chest and lungs -No potential for barotrauma -Variable tidal volume may result in hypo/hyperventilation --high compliance, not enough volume --low compliance, too much volume
	Cycle for Mechanical Ventilation	-Determining the end of inspiration -Time-cycled -Volume-cycled -Pressure-cycled
	Recommended Machine Ventilation setting for Small Animal	-Tidal volume: 10-20 ml/kg -RR: 6-12 -Inspiratory time: 1-1.5 seconds
	Recommended Machine Ventilation setting for Horses	-Tidal Volume: 10-15 ml/kg -RR: 4-8 -Inspiratory time: 1.2-3 seconds
	Recommended Machine Ventilation Setting for Ruminants	-Tidal Volume: 8-12 ml/kg -RR: 6-15 -Inspiratory time: 1.2-3 seconds
	Dead Space in Mechanical Ventilation	-Increasing tidal volume decreases dead space --Anatomical dead space volume will not change --Increasing gas exchanging area -Increasing tidal volume increases lung volume, area for gas exchange --proportionally anatomical dead space becomes smaller
	Dead Space ratio	=Dead space/tidal volume
	Rule of 4- normal arterial blood gas	-pH: 7.4 -pCO2: 40 -HCO3-: 24 -Base Excess: +/- 4 Always have a 4!
	Normal Arterial Values	-pH: 4 -pCO2: 35-40 mmHg -HCO3-: 24 mmol/L -Base excess: +/-4 Sample arterial blood in anesthetized patients -Need to assess oxygenation and ventilation -arterial blood gas gives OXYGENATION status
	Normal Venous Values	-pH: 7.35 -pCO2: 40-45 mmHg -HCO3-: 24 mmol/L -Base Excess: +/-4 CO2 acts like an acid, more CO2 in venous blood causes lower pH -Sample venous blood in awake individual -Only gives info on ventilation
	Hypoxemia	-PaO2 less than 80 mmHg Severe hypoxemia: PaO2 less than 60 mmHg -Saturation of Hb with O2: SaO2 less than 90% -After 90%, start anaerobic metabolism --heart and brain suffer
	Approaching an Acid/Base case	1. Look at the pH 2. Look at pCO2 --figure out of CO2 is causing acidity or basic blood 3. If CO2 does not explain blood pH, look at HCO3-
	Base Excess	-Amount of acid or base that would need to be added to a liter of blood to bring pH back to 7.4 -Assumes CO2 is 40 -How much extra acid or base there is -True metabolic component
	Bicarbonate	-Derived from pH and CO2 -Influenced by CO2 -Normally between 20-24 mmol/L -If low, depletion is occurring from buffering H or loss of HCO3 (vomiting, diarrhea, renal losses)
	Compensating CO2	-High CO2: respiratory acidosis -Low CO2: respiratory alkalosis Compensates for acid/base imbalance elsewhere
	Acid/Base Compensation	-Metabolic disturbance will have a respiratory compensation -Respiratory disturbance will have a metabolic compensation -Compensation never fully corrects acid-base disturbances -Predictable vales for compensation
	Mixed Acid-Base Disorders	-Compensatory change fail to explain pCO2 and HCO3- in mixed acid-base disorders -Normal pH in the face of disturbances in pCO2, HCO3-, and base excess -2 or more acid-base disorders can coexist
	Anion Gap	-Not a real gap -based on laws of electro-neutrality -Cations and anions are in equilibrium so electroneutrality occurs in the body -Usually only have to measure Na+, K+, Cl-, and HCO3- --if measured and the value is different from what you expect, there is another ion that we have not yet accounted for --something else is throwing off the balance
	Increased Anion Gap	-Indicates metabolic Acidosis -Can be due to presence of organic acids --lactic acid, ketones, renal failure, toxins -Metabolic acidosis with high anion gap, think toxin and ethylene glycol
	Metabolic acidosis with no anion gap	-Hyperchloremic acidosis -Acidosis is due to loss of bicarbonate --GI tract or renal loss -To maintain electro-neutrality, loss of bicarbonate is compensated by chloride gain
	pH less than 7.2	-metabolic Acidosis -Life threatening! -Direct myocardial depression -Impaired tissue perfusion -Arrhythmias -Altered coagulation -Altered mentation -Multiple organ failure
	Treating Metabolic Acidosis	-Just giving bicarbonate will not fix patient -have to treat the underlying cause of acidosis -Maintain Oxygen delivery to the tissues --restore perfusion and maximize oxygen carrying capacity -Give IV fluids -Improve CO -Maximize oxygen carrying capacity --give O2 and maintain adequate PCV
	IV fluids for Metabolic Acidosis	-Alkalizing solutions -PLA -Lactated ringer's solution -Normosol-R -Give half-strength of any fluids depending on Na concentration -DO NOT give NaCl, will administer Cl in excess
	Look at Na to give you info about H2O	If Na is very high or very low, correct slowly -Especially low Na, do not correct too fast --can cause demylenization in the brain, will occur 3 days later
	Cardio-Pulmonary Arrest Clinical Signs	-Loss of palpable pulse, cannot feel the pulse (main sign of arrest) -No auscultable heart sounds -Apnea, gasping, not breathing -Change in mucous membrane color --cyanotic, pale, pink, gray --can be deceiving, depends on type of arrest -Capillary refill time can also be deceiving -Pupils fixed and dilated within 30 seconds --(not reliable, also looks like deep plane of inhalant anesthesia)
	CPR successful outcome	-Depends on reason for arrest -Size of the patient (horse vs. small dog) -Skill of person doing CPR -Support staff and trained personnel -Speed at starting CPR --faster is better
	Support staff needed for CPR	-Need at least 2 people -3 is ideal -1 to compress -1 to ventilate -1 to do everything else (draw up drugs, get stuff, etc.)
	CPR crash cart	-Needs to be available, organized, labeled -Need to know if cart has been breached --plastic lock that can be broken off --know if something has been removed, know something needs to be replaced -Need a list to know what should be in it -Dose chart needs to be present
	Basic Life Support	-Airway -Breathing -Circulation
	Airway and Intubation	-Need to confirm correct tracheal intubation! --Direct visualization --palpation of ET-tube in trachea, should only be 1 tube --End-tidal CO2
	Breathing for CPR Anesthetized Patient	-TURN OFF VAPORIZER and REVERSE DRUGS!! --most important part of breathing for CPR -Flush system free of inhalant anesthetic -Ventilate using rebreathing bag -Ventilate 8-10 breaths/minute -Peak airway pressure should be less than 20 cm H2O, never exceede! --if possible, use 10 -Overventilating can cause hypocarbia and decrease cerebral perfusion -Ventilate with lowest pressure possible, Do not want to decrease venous return to the heart -Monitor End-tidal CO2
	Breathing for CPR Non-anesthetized Patient	-Need to have an endotracheal tube in the patient! -Ventilate using ambu-bag, 8-10 breaths per minute --ambu-bag does not have manometer, need to monitor airway pressure carefully --look at chest excursions -Monitor end-tidal CO2 --over-ventilation causes hypocarbia and decreases cerebral perfusion
	Chest Compressions and CPR	1. Cardiac Pump Theory --can do in animals less than 15kg --use hand to cup and pump the heart, use body to press against --100-120 bpm "staying alive" 2. Thoracic Pump Theory --compress chest and organs, indirectly compresses the heart as well --patient needs to be at correct height --Do compressions over the widest part of the chest --Lateral recumbency: 5th-6th intercostal space --Dorsal recumbency: caudal sternum --Need stiff surface, no padding -High compression rate is associated with improved survival and increased mean aortic and coronary perfusion pressure
	Chest Compression Specifics	-Change person doing compressions every 2 minutes -Lateral recumbency: 5th-6th intercostal space -Dorsal recumbency: caudal sternum -40-50% of compression relaxation cycle -Depth of compression should be 25-35% of chest width -External compressions only achieve 20% of cardiac output -Go down and come back up! make sure heart gets a chance to recoil
	Intrathoracic Chest Compressions	-Cannot do chest compressions when the abdomen is open --impossible! -Cut through the diaphragm and do compressions on the heart directly -Need to then fix the diaphragm, don't cut in a way that can't be fixed -Can try placing towel clamps on abdomen
	Chest Compression Monitoring	-End Tidal CO2 --assists with evaluating effective compressions --indicates circulation is present, or chest compressions are effective -SpO2 --can be a little deceiving, movement can cause artifact on the probe -Doppler: --doppler flow can pick up adequate compressions --Hard to place a doppler on an arrested patient, cannot hear flow --Put on cornea to hear flow during arrest
	IV access during CPR	-Want IV access BEFORE patient arrests! Always place and IV catheter! -Quick administration for emergency drugs -Use largest more IV catheter possible -Avoid placement in the hind limb --longer way to go to get to the heart -May have to cut down to find the vein -If IV catheter is already present, make sure line is patent --needs to be functional!
	IV fluids during CPR	-Give depending on why patient arrested -Blood loss/hypocolemia/shock patient will need shock rate fluids
	Shock Rate Fluids	-Crystalloids vs colloids vs. natural colloids -Crystalloids: 90ml/kg/hour in dogs (60 in cats) --1/3 stays in intravascular space, 2/3 goes into intravascular space --3ml/1ml blood loss -Colloids: 30ml/kg/hour in dogs (20 in cats) --all stays in intravascular space --1ml/1ml blood loss -Natural colloids: whole blood
	normovolemic Fluids	-Conservative delivery of fluids -Crystalloids: 20 ml/kg bolus
	Why give fluids for arrested patient	-Coronary perfusion pressure = diastolic BP- Right atrial pressure -Give more fluids, will increase right atrial pressure -Increasing right atrial pressure of the pressure is normal will decrease coronary perfusion --do not want to give too much fluids to a normovolemic patient!
	CPR ECG rhythms	1. Asystole/flatline in most patients under anesthesia 2. Pulseless electrical activity --electrical activity is still present, but no muscle contractions --muscle might not have enough Ca to contract 3. Ventricular fibrillation --random depolarization of myocardial tissues, no ordered contraction --usually happens after emergency drugs are given 4. Pulseless ventricular tachycardia
	CPR emergency drugs	-All drugs should be given IV!!! -If IV route is not possible, give intratracheally --except for sodium bicarbonate --be sure to double dose of drug given -Intracardiac administration is not recommended
	Epinephrine as CPR drug	-1st line emergency drug -Use with any type of arrest -Low dose is recommended under anesthesia (0.01 mg/kg) -high dose is rarely used ( 0.1 mg/kg) --dangerous, can cause fibrillation -Repeat low doses every 3-5 minutes -Alpha receptor stimulation predominates --Causes vasoconstriction and squeezes blood into the coronary and cerebral vessels -Gives better outcome for CPR
	Atropine as CPR drug	-Vagolytic -Used in asystole and pulseless electrical activity -Not used in patient with fibrillation or ventricular tachycardia -0.04 mg/kg, start with half dose -Anticholinergic, acts on muscarininc ACh receptors -Crosses BBB, effects can last 12 hours
	Lidocaine as CPR drug	-Used as anti-arrhythmic -Follows 1st dose of epi -Use for ventricular tachycardia or pulseless ventricular tachycardia -ONLY for fast ventricular rates -Not responsive to defibrillation -Increases fibrillation threshold --also makes it harder to defibrillate a patient -Most useful in post-resuscitation arrhythmias -DO NOT give with slow ventricular escape rhythm, may be fatal!!
	Vasopressin as CPR drug	-No proved difference between epi and vasopressin -Only give 1 dose, lasts a long time -Potent vasoconstrictor
	Calcium Gluconate as CPR drug	-Only give if hyperkalemia, hypocalcemia, hypermagnesimia -Blocked cat arrests, can give Ca gluconate -Give very slowly -Use with ECG
	Sodium Bicarbonate as CPR drug	-Controversial use -Only use if there is severe acidosis or prolonged CPR --pH less than 7.1 --CPR longer than 10-15 minutes
	Amiodarone as CPR drug	-Last chance drug -Use when there is pulseless ventricular tachycardia and it cannot be defibrilated -Anti-arrhythmic class III drug with class I, II, and IV properties
	CPR: what to do	1. Call for assistance 2. Designate person in charge 3. Keep track of time --switch up person doing compressions --Drug timing --Open chest time --legal documentation! 4. Turn off vaporizer and flush system 5. Administer reversal agents that are relevant --Nalxone for opioids --Flumazenil for benzodiazepines --Atipamezole for alpha-2 agonists 6. Check ABCs, start compressions 7. Treat according to rhythm after compressions
	CPR treatment for ventricular fibrillation and pulseless ventricular tachycardia	-Shockable rhythms -Defibrillate -3 consecutive shocks in rapid succession -Resume chest compressions for 60-90 seconds -Epi low dose or vasopressin -Repeat defibrillation again
	Successful Defibrillation	-Flatline -Purpose is to get asynchronous myocytes to "reset" -Reset everything, then try to get it all working together
	CPR treatment for Asystole and pulseless electrical activity	-ABCs and compressions -Atropine -Epinephrine low dose or vasopressin (ONCE) -Lidocaine ONCE after initial dose of epi -Repeat Atropine and epinephrine every 2-5 minutes
	Assessment during CPR	-Mucus membranes -ECG -Pulse pressure --femoral pulses, doppler -SpO2 -End tidal CO2 --high levels indicate better perfusion
	Open Chest CPR	-Pleural effusion -Pneumothorax -pericardial effusion -Patient size -If external chest compressions do not work in 2-3 minutes
	Benefits and Disadvantages of Open Chest CPR	-Better cerebral and coronary perfusion -Can visualize intrathoracic disease -Can evaluate cardiac filling -Increased morbidity -Need facility and staff to deal with post-arrest thoracotomy
	Post-arrest Patient	-Cardio-respiratory support, ensure normal ventilatory pattern -Optimize tissue perfusion and BP -treat underlying cause of arrest -Prevent CPR -Check for arrest recurrence -May require ongoing centilation
	Peripheral Neruomuscular Blockade	-Cause skeletal muscle paralysis by acting at the NMJ -Block ACH receptor on motor end plate -Prevent release of ACh from motor nerve terminal -Can enter open ion channels and prevent depolarization of the motor end plate
	Motor nerve Terminal	-Factory for packaging of ACh -ACh is released in bundles, goes across synaptic cleft to ionophore motor endplate -Non-specific cation channel -ACh crosses synaptic cleft and binds to alpha-subunits on ion channel --2 ACh bound, channel opens --causes depolarization of the motor end plate -DEpolarization impulse is transmitted down the neuron to the contractile machinery
	ACh positive feedback	-Released ACh goes across synapse to motor end plate -Also goes to cholinergic receptors on nerve terminal --enhances mobilization of more ACh --prolongs/sustains contraction
	Post-junctional sites of action	1. Receptors on alpha sub-units of pentameric ion channel 2. Inside ion channel --potential block of ion flow
	Pre-junctional sites of action	1. Non-depolarizing blocking agents: cause decreased mobilization of ACh 2. Depolarizing agents: repetitive nerve firing leads to muscle fasciculations
	Effects of Neuromuscular Blocking Agents	-paralysis of the skeletal muscle -Do not provide sedation or analgesia -Generally only used in patients under anesthesia --controlled ventilation
	Clinical Indications for Neuromuscular Blocking Agents	1. Respiratory control -lightly anesthetized patient with excessive muscle tone 2. Thoracic surgery -relax intercostal muscles -immobilize the diaphragm 3. Ocular surgery -position and paralyze the globe 4. Delicate surgeries (brain) 5. C-section, can reduce general anesthetic drug by using local and regional analgesia, neuromuscular blocking agent, and light anesthetic 6. Awake intubation 7. Abdominal surgery: Flank laparotomy
	Neuromuscular Blocking Agents and orthopedics	-Not used very much -Will help relax muscles associated with very recent fracture --can help reduce fracture -Over time muscles shorten, contracture -Neuromuscular blocking agents will NOT relax contracted muscles --only constant tension will relax
	Biochemistry of Neuromuscular Blocking Agents	-Very polar molecules -large molecules, cross membranes poorly -Do not cross into the brain or placenta very well
	Neuromuscular Blocking Agents in Abdominal surgery	-Used in humans, not used in animals -Except for flank laparotomy for equine ovariectomy
	Long-term mechanical ventilation and Neuromuscular Blocking Agents	-Have been used for long-term mechanical ventilation in the ICU -Prevents patient from resisting ventilation -better than sedation alone? -With long-term use can have difficulty reversing effects --residual effects, ion channel block that cannot be reversed -May interfere with some anti-inflammatory pathways important in septic and shocky patients -Not so great for critical care!!
	Neuromuscular Blocking Agents and birds	-Iris sphincter is skeletal muscle (not smooth muscle) -Anticholinergic will not dilate pupil, need to use neuromuscular blocking agents -Can be used topically, intra-camerally to block the iris sphincter muscle -Cause pupil dilation -Good for lens extraction -Topical use has unpredictable systemic effects --have to be prepared to intubate and ventilate the animal
	Reptiles and Neuromuscular Blocking Agents	-Intubation -Immobilization of large crocidilians for non-painful processes -Use succinylcholine, pancuronium, atracurium, Gallamine -Must be prepared to intubate and ventilate -NMBA given IM may be sequestered in poorly perfused tissues --drug returns to circulation with physical activity, causes paralysis
	Succinylcholine and escaped livestock	-Can be used to capture escaped livestock -High solubility (aqueous) --big dose in a small dart -Soluble in tissue -Rapidly absorbed from IM site -Rapid onset of action -Be prepared to intubate and ventilate!
	Planning for Neuromuscular Blocking Agent Use during Surgery	-Who is the patient? what species? -What concurrent diseases, and how will disease affect NMBA -What is the blockade for? which muscles, and how long? -What type of anesthesia will be used? --TIVA, inhalation -Which NMBA and what dose?
	Neuromuscular Blocking Agents Non-depolarizing Agents	-Pancuronium -Vecuronium -Atracurium -Cisatracurium -Rocuronum is less commonly used in vet med -Gallamine is no longer available in US
	Succinylcholine	-Neuromuscular blocking agent -Depolarizing agent, only depolarizing NMBA -Not used very often anymore -Dependent on plasma cholinesterase activity --injected drug is chewed up by cholinesterase in plasma before it can get to the neuromuscular junction --most of dose never makes it to the NMJ unless pseudocholinesterase levels are low
	Things to determine when choosing a neuromosuclar blocking agent	-Potency -Onset time -Duration of action -Elimination pathway -Side effects --cardiovascular, histamine release
	Evaluation of Neuromuscular Blocking Agents	1. Stimulate a peripheral nerve 2. Measure muscle response --mechanical response (tension developed with stimulation) --Electromyography (amplitude of compound muscle action potential --Accelerometer (acceleration of the body part)
	Nerve Stimulator	-3 frequencies --0.1, 2, and 100Hz -Need to find peripheral nerve --peroneal nerve --ulnar nerve --facial nerve, not recommended (resistant to blockade)
	How to evaluate response with Neuromuscular Blocking Agents	1. Mechanomyography: measure tension that is developed -awkward to use 2. Electromyography: measures compound muscle action potential Allows quantification of muscle twitch
	Onset time for Neuromuscular Blocking Agents	-Important for emergency intubation --Succinylcholine will work within 90 seconds --Rocuronium also works within 90 seconds -Atracurium, Vecuroniumm, Pancuronium, and Cisatracurium work in 3-4 minutes --Not fast enough!! --Respiratory msucles get weaker and weaker, animal cannot breath adequately and will become hypoxic before intubation can happen -increasing dose will increase onset, also increases duration
	Required Duration for Neuromuscular Blocking Agents	-D-tubocurarine: long-acting in most animals -Pancuronium, Rocuronium: intermediate to long (20-60 minutes) -Vecuronium ,Atracuronium, Cisatracurium: short acting (20 min) -Succinylcholine is extremely short acting --dose is based on plasma cholinesterase/pseudocholinesterase activity
	Succinylcholine and low plasma cholinesterase levels	-Like giving animal a huge overdose -Not enough enzyme to breakdown drug -Species differences in healthy animals in levels of pseudocholinesterase activity -Pigs and horses have high levels -Cats have intermediate levels -Cows and dogs and low/intermediate levels
	Increased duration of Succinylcholine Action	-Exposure to pseudocholinesterase inhibitors --organophosphates --glucocorticoids --some anti-neoplastic agents
	Neuromuscular Blocking Agents and long duration paralysis	-Use longer-acting agent or repeated doses of short-acting agent --repeat short-acting drugs -Atracurium and vecuronium do not accumulate with repeated doses --duration of paralysis did not increase over time
	Cardiovascular effects of Neuromuscular Blocking Agents	1. Histamine release with D-tubocurarine and atracurium --No histamine release with cisatracurium --Species differences exist
	Autonomic effects of Neuromuscular Blocking Agents	-Bind to cholinergic receptors in autonomic nervous system -Cause tachycardia, hypertension -Cause bradycardia and hypotension
	Effects of Succinylcholine on Autonomic Sites	-has dramatic effects -Hypertension -Tachycardia -Arrhythmias -Hypoxemia -Hypercarbia -Potassium release leading to arrhythmias -Myoglobin release -Probable muscle pain due to fasciculations -Can cause bradycardia in rabbits and dogs -Increases intraocular pressure, important in patients with eye injuries
	Metabolism and Elimination of Neuromuscular blocking agents	-If systems are not working properly, results in increased duration of action -Renal failure: pancuronium -Hepatic failure: curare, Rocuronium -Combined hepatic and renal failure: vecuronium --use atracurium or cisatracurium -Decreased pseudocholinesterase: succinylcholine
	Hoffman Elimination	-Atracurium and cisatracurium -Start to break down as soon as injected into the body -Unstable at body pH and temperature -Need to store at low pH and low temp, or drug will fall apart -Safe for animals with decreased hepatic or renal function --product will degrade in the body regardless of metabolism -Laudanosine breakdown product can cross BBB
	Laudanosine	-Breakdown product of Hoffman Degradation of atracurium and cisatracurium -Crosses BBB -only bad news when used on long-term basis --does not really accumulate under normal circumstances -Can cause CNS stimulation and seizure activity
	Species differences with Non-depolarizing Neuromuscular Blocking Agents	-Big differences in amount needed to produce 80% twitch depression under halothane anesthesia -Sheep take much lower dose than a horse -Lots of differences exist between individuals also --impossible to predict
	Increased Sensitivity to Neuromuscular Blocking Agents	1. Medications: --antibiotics --Local anesthetics in large doses --Cholinesterase inhibitors --Anti-arrhythmic agents --Phenytoin, Dantrolene --Cytotoxic Drugs 2. Respiratory acidosis --if arterial CO2 level is greater than 60mmHg, cannot antagonize non-depolarizing blockade 3. Diseases --myasthenia gravis, hypoproteinemia, hypokalemia, hypocalcemia, hypermagnesemia, metabolic alkalosis, acidosis
	Decreased sensitivity to neuromuscular Blocking Agents	-Peripheral nerve injury -Spinal injury -Disuse atrophy -Extensive burns -Situations result in development of ACh receptors on muscle membrane away from the motor end plate --receptors are spread out all across the muscle membrane --have to block ALL receptors, not just receptors at NMJ -Monitoring limb would appear to be over-sensitive to the drug --can end up over-medicating the rest of the animal
	Absolute contraindications to Succinylcholine use	-nerve injury, crush injury -Spinal or cranial injury -Burns -in 3-180 days from the injury, body will undergo massive K release --development of extra-junctional ACh receptors -Can result in cardiac arrest
	Instituting the Neuromuscular Blockade	1. Choose the drug 2. Determine the dose --remember species differences! 3. Make sure the patient is adequately anesthetized -twitch monitor?
	Muscle sensitivity	-Determines which muscles need relaxation -Ocular muscles are most sensitive --limb --jaw and laryngeal muscles --abdominal -Intercostals and diaphragm are least sensitive
	Theoretical Differential Sensitivity to Blocking Agents	-Most easily blocked area is ocular muscles -Neck and limb muscles next -Larynx -Abdominal musculature -intercostals and diaphragm are least sensitive
	Controlled ventilation with Neuromuscular Blocking Agents	-ALWAYS necessary! -Even low doses of rocuronium cause transient decreased respiratory tidal volume and minute volume --animal was not ventilating adequately
	Neuromuscular Blocking Agent First Dose	-ED80-90: mean dose for 80-90% twitch depression for the species -For longer-duration agents (Pancuronium, curare, rocuronium) use lower ED -Use incremental doses to establish the block --prevent overdosing the patient!! -Repeated doses would be fractions of the initial dose --1/10 or 1/4 of original blocking dose --depends on the duration of the agent, agents can accumulate!
	Monitoring Neuromuscular Blocking Agent Blockade	-Use simple twitch monitor --0.1, 2, and 100 Hz frequencies --single twitch: 0.1 Hz --Slow, repetitive train of four: 2 Hz --tetanic: 50Hz or 100 Hz
	Single Stimulus	-0.1 Hz -"Train of four" stimuli -Will get response in absence of neuromuscular blockade -Responses will not be affected by repeated stimulation -Useful for monitoring partial blockade
	Tetanic Stimuli	-50Hz or 100Hz at 5 second duration -Will affect subsequent responses -Need mobilization of ACh for repeated responses -More sensitive indicator of residual or partial blockade -Used to document full recovery at end of Neuromuscular blocking procedure
	Tetanic Stimulus during neuromuscular blockade	-Not a good idea -Tetanic stimulus causes motor nerve terminal to mobilize more ACh -Enhances responses for several minutes -May make you think you need to give more drugs -Avoid during procedure
	Methods of Evaluation of Neuromuscular Blocking Agent	-Visual and tactile senses can be used but are not as sensitive --Can be used for establishing and maintaining the block -MUST use tetanus for evaluating the recovery --train of four fade is under-estimated -If no twitch monitor, can use clinical signs --loss of palpebral and anal reflex --animal stops "fighting" the ventilator --muscle relaxation at surgical site
	Antagonism of the Blockade	-Use cholinesterase inhibitors --Neostigmine --edrophonium -prevent ACh metabolism, competes for receptor sites with blocking agent -increase ACh at the motor endplate -Decreases time for recovery -MUST document some spontaneous neuromuscular recovery before using NMBA antagonists -Maintain animal on ventilation -Give antagonist at incremental doses ever 3-5 minutes --cholinergic effects are mitigated
	Complications of NMBA antagonism	-Parasympathetic activity and pre and post ganglionic sites -Decreased HR -Decreased BP -Bronchoconstriction -Increased airway secretions -increased GI motility, causes abdominal cramping
	Suggammadex	-Non-cholinesterase inhibiting agent -Cyclodextrin -Chops up rocuronium blockade --Rocuronium vacuum!
	Total intravenous Anesthesia TIVA	-Technique to provide general anesthesia -Uses combination of injectible drugs delivered IV -All anesthesia is IV, no inhalant anesthetics -Only recently has become safer, practical, and popular --pharmacokinetics and dynamics of modern drugs --inhalants are easier to monitor, easier to use, easier to dose -Syringe pumps have made it easier
	Essential components of TIVA	-same as all other anesthetics -Immobility -Unconsciousness -Analgesia -Muscle relaxation -Inhibition of autonomic reflexes No one drug has all components, need to mix drugs and use synergistic effects
	Pharmacokinetics	-what the body of a living organism does to an administered drug
	Pharmacodynamics	-What an administered drug dors to the body of a living organism
	Volume of distribution	-reflects the amount of tissue distribution of the drug -How much the drug wants to spread to the tissues, leave intravascular space and go into tissues = amount of drug administered/ amount of drug found in plasma -Small Vd, drug stays in blood -Big Vd, drug goes into tissues easily Helps determine the loading dose, desired plasma concentration
	Clearance	-Volume of blood permanently cleared of the drug in a unit time -Area under the curve is the clearance -Used to determine maintenance dosing, how much to give to maintain steady state anesthesia -CRI = desired plasma concentration x clearance
	Distribution Phases of a Drug	-Giving a drug in the blood, a lot moves quickly to vascularized parts of the body --steep curve -Slowly equilibrates into other tissues --shallow curve -Last slow phase is dependent on liver and kidney -Can be used to adjust infusion, determine how much of which drug to give when
	Characteristics of Injectable Anesthetics Drugs that make them suitable for TIVA	-Fast onset -Short duration, shorter the better -high therapeutic index -Minimal or no side effects -Insensitive context half-life, no accumulation -Low cost -Long shelf-life
	TIVA drugs commonly used in Small Animal Anesthesia	-Propofol (substitute for inhalant) -Opioids (adds analgesia) --morphine, fentanyl, remifenntianil -Lidocaine -Dexmedetomidine -Ketamine
	TIVA drugs commonly used in large Animal Anesthesia	-Ketamine -benzodiazepines -Alpha-2 agonists --xylazine, detomidine, dexmedetomidine, romifidine -Lidocaine TIVA is more commonly used in large animal anesthetics
	Minimum Infusion Rate	-Plasma concentration of drug necessary to prevent a reaction to a noxious stimulus in 50% of the population -Same concept as MAC for inhalant anesthetics -Cp50
	TIVA techniques	-Single bolus effect -Intermittent multiple boluses -Automated techniques --CRI --Target controlled infusion (TCI), uses computer to calculate right infusion, very precise
	TIVA single Bolus Technique	-Give single bolus of drug of choice -Will have initial high increase, and animal will be in desired effect range -Have a certain amount of time until the animal wakes up -Good for short proceures (X-ray, castration) -If miscalculate and give too much, will be in adverse effect range -Want to stay in target range, for as long as possible
	TIVA intermittent multiple bolus technique	-Drop in and out of desired effect and termination phase -Animal goes in and out, is either too deep, too light, in between -not very precise -Have different wake-up signs for different species -Should not lose palpebral reflex!! If lost, animal is very very deep -User dependent, depends on experience -Good for short procedures (Skin biopsy, castration) -Need to be ready to intubate and ventilate -Using a catheter is always a good idea!
	TIVA CRI technique	-Takes a long time to achieve desired effect --5x half-life -Maintains a steady drug plasma concentration, less dramatic slope of curve -Can use an infusion pump -Can give loading dose to get to target effect faster, then CRI to maintain -Good for longer procedures (MRI)
	Problems with TIVA	-Pharmacokinetic models only using Cl and Vd may not accurately predict plasma levels -Drugs accumulate --"context sensitive half-life" gives long recovery time --fentanyl can last a very long time --Remifentanil has very consistent short hlaf-life (good for patients with imparied liver function)
	Ketamine	-Has active metabolites! -May not have a very long context-sensitive half-life, but has active metabolites
	Target Control Infusion	-Computer targets plasma concentration that it wants to reach -Very regulated, very organized and calculated -Pump is set based on specific pharmacokinetic properties of a drug -Machine does not measure plasma concentration, runs simulation -Considers K values of tissues, clearance, and Vd
	TIVA Advantages	-No pollution -No need for anesthesia machine -Better cardiovascular stability -Propofol reduces ICP -Suitable for prolonged sedation
	TIVA disadvantages	-Need IV access --can be problematic in very small patients -Potential for delayed recovery --drug related -Not possible to measure real-time plasma drug levels, only predictions -Cost of drugs (remifentanil is very expensive!)
	TIVA indications	-Layngeal exams or airway surgery --Working in an animal's mouth --Impossible to intubate during exam -Bronchoscopy --avoids leakage of inhalant --Some patients are too small for endotracheal tube or bronchoscope -Tracheal stents -Thoracotomy: thorax is open, lung will leak inhalant into surgical field -Brain surgery --inhalants increase cerebral blood flow and ICP --propofol maintains coupling of O2 delivery and consumption in the brain
	Regional Anesthesia	-prevents pain! -has effects on respiratory system, cardiovascular system, endocrine system, other systems
	Advantages of Regional Anesthesia	-Less painful, happier patient --better quality of life -Minimum systemic effects -Decreases in post-operative morbidity and mortality --especially in sicker patients for high-risk procedures -Decreases inhalant anesthetic requirement --less side effects of anesthetics
	Disadvantages of Regional Anesthesia	-Complications -Drug toxicity -Need a lot of anatomy knowledge -Proper techniques, high skill level -Need to know pharmacology -Not always effective -May complicate the post-operative analgesic plan --hard to tell when local anesthesia will go away
	Complications of Regional Anesthesia	-Nerve damage, nerve block --Physical and chemical damage -Infection -Hemorrhage -Allergic Reactions -Intravascular injection can cause toxicity -Methemoglobinemia with benxocaine and prilocaine
	Benzocaine and Prilocaine	-Regional anesthetics -Cause methemoglobinemia in cats -DO NOT USE in cats and ferrets and some other exotic animals
	Drug Toxicity and Local anesthetics	-Toxicity is an overdose -Causes severe side effects -Higher concentration gives more toxic effects -Starts with neurologic effects, develops into respiratory and cardiac arrest and death -Prevent by being careful about the dose -hard to tell the difference between anesthetized and toxic -May have to do multiple doses, always think about the TOTAL dose -Always calculate and recalculate doses, be even more cautious with unfamiliar sized patients
	Bupivacaine	-Causes cardiotoxicity! -Toxic to cardiac myocytes -NEVER inject IV -Toxic dose in cats is much closer to therapeutic dise more prone to toxicity
	Regional/Nerve block anesthesia	-Injection of local anesthetic in the vicinity of peripheral nerves -Brachial plexus block -Mandibular nerve block
	Neuraxial Anesthesia	-Injection of local anesthetic in the vicinity of the spinal cord and/or nerve roots -Epidural anesthesia is in extradural space, outside of the dura --filled with muscle or fat, inject into muscle or fat -Spinal/subarachnoid/intrathecal anesthesia goes into subarachnoid space --MUCH closer to the spinal cord --can be more effective than the epidural anesthesia
	Regional Anesthesia Techniques	-Blind (traditional technique) --based on knowledge of anatomy -Peripheral nerve stimulator guided --use needle to give electrical signal, see muscle twitch that nerve goes do --need to know which muscle is supposed to twitch -Ultrasound guided -Ultrasound and peripheral nerve stimulator guided
	Differences in regional anesthesia techniques	1.Blind technique --low success rate --high incidence of complication --cheap --simple in terms of skill 2. Guided technique: --higher success rate --lower complication incidence, can see anatomy better --more expensive --Need more skill, more practice
	Regional Anesthesia needles	-Hypodermic needle -Spinal needle (most common for regional anesthesia) --has stylet that is sharp and can be removed -Tuohy needle: tip is curved and dull -Insulated needle: conducts electrical signal to stimulate muscle -Echogenic needle: needle reflects ultrasound, can see on ultrasound clearly
	Catheters in Regional Anesthesia	-For long-term regional anesthesia -Epidural catheter -Fenestrated catheter: injection comes out through length of the needle, not just the tip -Insulated catheter -Echogenic catheter
	Good Candidate for Regional Anesthesia	-Localized pain, specific spot --Cannot do a regional block everywhere -Not an emergency procedure --extra time is needed to perform regional anesthesia, at least a few extra minutes -Consult with surgeon
	Topical Anesthesia	-Ophthalmic drops --proparacaine, tetracaine -EMLA cream, lidocaine and prilocaine (methb in cats!) --Not very useful, needs dressing for absorption --60 minute onset, duration is 1-2 hours -Lidocaine patch -Spray: lidocaine or benzocaine --good for intubation, reduces laryngeal reflex --use on mucosa -Superficial cooling: icing or ethyl chloride spray
	Infiltration Anesthesia	-Type of local anesthetic -Linear infiltration is really easy: one line of local anesthesia -Filled block: linear infiltration and deposition of drug into deeper tissue -Continuous infiltration anesthesia --fenestrated catheter and infusion pump --can be used long-term
	Benefits of Infiltration Anesthesia	-Simple, easy, quick -No anatomical knowledge needed -Great for small local cutaneous surgeries -Catheter placement -Wound infusion catheter
	Drawbacks of infiltration anesthesia	-Higher volume needed --need to give injection to cover a certain area -Easier to give overdose -Easier to give patchy anesthesia, gap or space that is not covered -Only deals with superficial tissue -Not good for major procedures -With large surface area is likely to become an overdose -Not god for deeper layers
	Oral Cavity Anesthesia	-Infraorbital nerve block at infraorbital foramen --will cover ipsilateral premolar, canine, incisor teeth, associated soft tissues, upper lip -Mandibular nerve block: mandibular foramen --ipsilateral molars, premolars, canines, incisors, skin, mucosa of chin, lower lip -Mental Nerve block at mental nerve foramen --ipsilateral lower lip -Major palatine nerve block at major palatine foramen --bone and soft tissue of ipsilateral hard palate
	Regional Anesthesia for the Eye	-Retrobulbar block -Anesthetizes CN II, III, IV, V, VI -Inferior temporal palpebral retrobulbar block -Splash block after enucleation -When it works, it works great! -ALWAYS aspirate before injecting to make sure you are not injecting into the vessel
	Possible complications of Regional Anesthesia for the Eye	-Intrathecal injection can cause respiratory arrest, accidentally inject into the epidural space -hemorrhage behind the globe -Globe perforation is possible -Nerve damage -Pressure behind the globe resulting in oculocardiac reflex -IV injection -Proptosis, especially in brachycephalic breeds -Temporary blindness
	Thoracic Limb Regional Anesthesia	-brachial plexus block -RUMM block -Declaw block
	Brachial plexus block	-Anesthetizes within or distal to the elbow -Will not block the shoulder area, more distal block -Injection site is medial to the scapulohumeral joint --parallel to the vertebral column towards costochondral junction -Complications: --pneumothorax --phrenic nerve blockade, hemi-diaphragmatic paresis --Horner's syndrome -Low success rate when using blind technique -Avoid a bilateral blockade
	RUMM block	-Blocks Radial, ulnar, median, musculocutaneous nerves -Anesthetized area is distal to the elbow -Inject lateral and medial to mid-humerus -Easy to perform, easier than brachial plexus block and has less complications
	Declaw Block	-3-point or "ring" block -Anesthetizes radial, dorsal ulnar, palmar ulnar, median nerves -Very simple -0.1 ml anesthetic per site -VERY easy to perform, do not need to know anatomy
	Intercostal Block	-Inject 2 adjacent intercostal spaces, both cranial and caudal to incision/injury site --caudal border of ribs near intervertebral foramens --vein, artery, and nerve are all on caudal part of rib, nerve is most caudal -Great for thoracotomy lateral approach and chest tube placement -Major complication is pneumothorax if go too deeply!
	Epidural	-Most common and most useful regional anesthesia -Inject lumbosacral space L7-S1 -Anesthetizes caudal abdomen, pelvis, hind limbs, perineal area --Can even get cranial abdomen and thoracic cavity with larger volume
	Epidural Technique	-Use spinal needle or tuohy needle -Inject in lumbosacral space --pull limb forward to enlarge the space -Iliac wings, L7 dorsal spinous process -Can feel a "pop" when go through the flavum ligament -Also will have a loss of resistance, hanging drop will be pulled into the epidural space -Can do test injection with saline -Don't want to push too far!
	Epidural volume, injection speed, and dose	-Volume and speed are major factors for how far the drug will travel -0.2ml/kg will travel up to L2 -If there is bleeding, stop! --re-do with a new needle -If the needle tip is in subarachnoid decrease injection volume to 1/3 or 1/3 for spinal analgesia
	Epidural Drug choice	-Lipid solubility is key! -Hydrophilic will have longer duration -Lipophilic will have shorter duration -Morphine is a slow onset and long duration (12-24 hours) -Bupivacaine is fast onset and short duration (2-4 hours) -Mixing morphine and bupivacaine will give fast onset and long duration
	Epidural Side effects	-Local anesthetics: --paralysis of pelvic limbs --sympathetic block can lead to cardiovascular collapse -Morphine can cause pruritus, urinary retention -General side effects: spinal cord injury, dellated hair growth, IV injection, sedation
	Contraindications for Epidural anesthetic	-Skin infection -Neoplasia at injection site -Bleeding disorder, no hemorrhage in epidural space -Unresolved hypovolemia -Sepsis, bacteremia -Allergy to drugs -Be careful when an animal has abnormal anatomy
	What Is Pain	-Unpleasant sensory and emotional experience associated with actual or potential tissue damage -Damage does not have to have occurred to feel pain -What's painful for one animal might not be painful for another
	Beneficial Aspects of pain	-Reduces animal's mobility -Encourages rest, healing and recuperation -NOT true! Actually a bad thing! -Immobility is not good -Pain does not promote healing or recuperation -
	Negative aspects of Pain	-Immobility -Decreased pulmonary function -Autonomic nervous System changes -Stress hormone release, increased catabolism -Decreased immune function -Increased coagulability -Behavioral changes -Ileus and inappetence, changes in GI motility -Insomnia -Patient is suffering!
	Gold Standard of Pain management	-No pain! -Pain management should accompany all surgical procedures -Pain assessment performed on all patients regadless of presenting complaint -Pain management is individualized for each patient
	How to Treat Pain	-Opiopid -Local anesthetics -NSAIDs -NMDA receptor antagonists (ketamine, amadtadine) -Alpha-2 agonists -Steroidal anti-inflammatory agents -Neutraceuticals -Tricyclic Antidepressants or anticonvulsants -Alternate therapies (acupuncture, PT, massage)
	Nociception	-Pain is the unique psychology of the individual -Nociception is unique series of electrochemial events that leads to perception of pain -Transduction of signal from receptor to brain
	Aspects of Nociception	-Transduction -Transmission -Modulation -Perception
	Nociceptive transduction	-Noxious stimulus is received on receptors --mechanical --chemical --thermal -Transduced into action potential via receptor -AP is transmitted along primary afferent nerve to dorsal root ganglion on dorsal horn of the spinal cord -At dorsal horn, excitatory and inhibitory inputs modify the signal -Modified signal goes up to brain, final perception of pain occurs -Brain responds to signal -Descending pathways are inhibitory in general
	Types of nociceptive stimuli	1. Cutaneous -Mechanical: incision or injury -Chemical: Inflammatory mediators -Thermal: hot or cold 2. Deep Somatic: muscles and joints -Mechanical -Chemical 3. Visceral: -mechanical -Polymodal (respond to chemical, mechanical, or thermal stimuli)
	Primary afferent Nociceptors	-Myelinated fiber types --A-delta fibers, high threshold mechanoreceptors --need high threshold to get to respond --faster conduction -Unmyelinated fibers --C-polymodal nociceptor fibers --slower conduction --more responsive for dull, diffuse, throbbing pain --up-regulated in hypersensitization and chronic pain -Evenly distributed fiber types in somatic/cutaneous areas -MUCH more C fibers in viscera --pain in viscera is not well-localized
	Visceral pain	-Viscera respond to distention, inflammation, twisting
	Pain synapses in Dorsal Horn	-Tend to synapse in laminae 1 and 2 --superficial -Laminae 5 also -Laminae 2 (substantia gelatinosa) has lots of reception and modulation of pain perception
	Glutamate	-Main NT in dorsal horn of the spinal cord synapses -Interacts with receptors to open Na channels --AMPA/Kainate receptor --Causes membrane depolarization -Allows signal to travel from dorsal horn of the spinal cord to the thalamus and somatosensory corex
	Primary Afferent neuron NTs	-In Dorsal horn of the spinal cord -Transmit pain perception -Glutamate -Substance P -Calcitonin-gene related peptide (cGRP) -Vasoactive intestinal peptide (VIP) -Somatostatin -Tachykinins -Bradykinins
	Lissauer's tract	-Superficial tract going through the dorsal horn of the spinal cord -A-delta and C fibers decussate and travel up or down a few spinal segments
	Nociceptive Pathways	-Synapse on dorsal horn of the spinal cord, decussate, and travel up to brain in anterolateral quadrant -Lateral spinothalamic tract (neospinothalamic): monosynaptic pathway --localizes incoming pain message -Medial spinothalamic tract (paleospinalthalamic): polysynaptic pathway --sends impulses to reticular formation, hypothalamus, diffuse projections to the thalamus --responsible for arousal mechanisms, "fight or flight"
	Ascending Spinal Pathways	-Spinocervical tract --superficial pain --tactile stimulation --discriminative -Spinoreticular tract --deep pain --visceral sensation --poorly localized
	Localization of NT	1. Periaqueductal gray matter (midbrain) -Endorphins 2. Dorsolateral Pons -Norepi 3. Rostrovental medulla -Serotonin 4. Dorsal Horn -Endorphins, enkephalins, dynorphins
	Inhibitory Neurotransmiters	-norEpi (alpha 2) -Serotonin -Endogenous opioids -Neuropeptide Y -GABA -Glycine -Adenosine -ACh
	Peripheral Sensitization	-Pain sensation is not a static situation -Altered excitability of sensory and sympathetic fibers -Vasodilation -Extravasation of plasma protein -Release of chemical mediators from inflammatory cells -Decreased threshold for noxious stimuli -Decreased threshold for non-noxious stimuli --hyperesthesia, allodynia -Increased pain in response to a noxious stimulus (primary hyperalgesia) -Spread to adjacent areas causes secondary hyperalgesia
	Reflex loops	-Stimulus goes to spinal cord -Efferents run through sympathetic trunk, cause stimulation in adjacent areas -Play role in peripheral sensitization
	Central Sensitization	-"Windup" -Instead of sending one pulse up to the brain, nerve sends numerous pulses up to the brain -Electrical events can last months after surgery -AMPA receptor has increased glutamate release -NMDA receptor is usually quiescent, with repeated stimulation Mg ion is kicked out and becomes Ca channel --easier depolarization -Substance P, brain-derived neurotropic factor is more active -Changes in membrane sensitivity -Long-term changes in gene expression -Increased COX-2 activity -Amplify message from dorsal horn going up to the brain
	pre-emptive Analgesia	-Give analgesic before injury -Prevents hypersensitivity reaction from occurring? -Best way is to give local anesthetic epidurally --Na channel blockers, block transmission of the signal -Can also use opioid, etc.
	Therapeutic approaches to Analgesia	-Pre-emptive therapy -Mechanism based approach -Multimodal therapy --balanced analgesia, get synergistic effect -Integrated therapy
	Painful procedures	-Lateral throacotomy -Limb amputations -Ophthamological procedures -Ear surgery -Orthopedic procedures where the joint is closer to the body -Lots of tissue trauma -Colic -Inflammation of the viscera, pancreatitis -Individual differences
	Evaluation of Pain	1. Behavior: --attitude, activity, appetite, vocalization? --response to manipulation, abnormal posturing --in cats, comfort, hiding, grooming 2. Physiology: --HR, RR, BP, Temp 3. Blood Chemistry: (not super helpful) --cortisol, catecholamines
	Visual Analog Scale for Pain	-Score from no pain to most pain possible -Put X on line to determine scale of pain -Not ordinal, sliding scale -Can measure over time to see how animal is doing -Pain scale for a dog is not the same for pain scale for a cat
	Cats in Pain	-hide -Stop grooming -Usually do not vocalize -"not doing cat things" -Pyrexia (inflammatory mediators released) -
	Physiologic Signs of Pain	-Increased HR -Increased RR -Increased BP -Increased temp -Salivation -Dilated pupils
	Behavioral sign of Pain	-Vocalization (can be questionable, dogs bark at anything) --small ruminants vocalize a lot --cats and horses do not vocalize -Restlessness or agitation -Resents handling of area -Depression/inactivity -Insomnia or reluctance to lie down
	Other evaluators of pain	-Inappetence -Aggression -Abnormal posturing -Disuse or guarding -Licking/chewing at painful area -trembling -Facial expression
	How to treat Pain	-Opioids -Local Anesthetics -NSAIDs -NMDA receptor antagonists --ketamine, amantadine -Alpha-2 agonists -Tricyclic antidepressants/tramadol -Gabapentin -Steroidal anti-inflammatory agents -Neutraceuticals -Alternathive therapies
	Small animal pre-medication	-All animals get an opioid! -Horses do NOT get opioid, can have excitability -Cats can get more excited than dogs -Pretty much every dog gets an opioid
	Opioids	-Heterogeneous group of drugs -All bind to Mu, Kappa, and Delta receptors -All receptors provide analgesia -Most effects are due to binding on Mu and Kappa receptors -Mu and Kappa cause analgesia, sedation, some respiratory depression
	Effects of opioid binding to Mu receptor	-Analgesia -Sedation -Respiratory depression -Bradycardia -Euphoria or dysphoria -Emesis, vomiting -Decreased GI motility -Increased sphincter tone
	Morphine	-"Classic" mu Agonist -Active at mu and kappa receptor -Causes histamine release, big issue! --poor induction drug, will get histamine release -Very good sedative -Used as pre-med, post-operative for analgesia -Lasts 6-8 hours, long-lasting -Often used for epidurals
	Hydromorphone and Oxymorphone	-Used as pre-med, induction, post-operatively -Last 2-4 hours -Good for cardiovascular system -Mu agonists
	Fentanyl	-Short-acting opioid -Use IV for induction and as CRI -Also trans-dermal, can be used post-operatively
	Methadone	-Full mu-agonist -Also has NMDA antagonistic effects -Can be used as pre-med, induction, post-operatively -Expensive!!
	Butorphanol	-Agonist/antagonist -Kappa agonist, Mu antagonist -Decreases side effects -Also decreases analgesia, less pronounced -Would not use for a big orthopedic procedure, will not be enough -Good for visceral pain, colics, cats
	Buprenorphine	-Partial Mu agonist, works on certain mu receptors more than others --different affinities for mu sub-units -Some antagonism at kappa receptor -Not a good pre-med, does not give good sedation --difficult to reverse, esp intra-operatively -Post-operatively for analgesia -lasts 6-8 hours, long-lasting -Used commonly in cats (even as pre-med)
	Opioid Advantages	-Cardiovascular stability -Analgesia -Sedation -Reversible (naloxone) -Good for acute pain
	Opioid Disadvantages	-Sedation -Dysphoria -Respiratory depression in brachycephalic dogs -Vomiting and inappetance -DEA scheduling -Bioavailability, immediately metabolized by the liver -tolerance builds over time, poor long-term post-operative analgesia -Opioid-induced hyperalgesia -AVOID in patients with head trauma! Respiratory depression increases PaCO2, will increase ICP
	DEA scheduling	-DEA schedules drugs 1-5 -1: LSD, heroine -2: highly addictive drug with medical benefits -3: ketamine -4: butorphanol, benzodiazepines less addictive
	Opioids in Cats	-Avoid! -Use partial opioid or agonist/antagonist
	Morphine Epidural	-Hydrophilic --Bounces around epidural fat, is not absorbed/sequestered -Gives long-lasting analgesic effect
	Opioids intra-articularly	-Can be given intra-articularly with chronic inflammation
	Fentanyl trans-dermal patch	-Gel in patch goes on clipped area of the body -Over time drug is absorbed --Takes 24 hours in dog --12 hours in cat -Get to analgesic dose -Can last 3 days! -Take patch off, levels fall very quickly -Will get systemic absorption of the fentanyl -Drug absorption depends on where you put it on the body -Absorption is less reliable in dogs --can depend on thickness of skin, how active dog is, how much blood goes to the periphery
	Recuvyra	-Fentanyl droplets -Fentanyl is in alcohol, when applied to skin alcohol dries up very quickly -Fentanyl is in the stratum corneum of the skin, forms depot -Once in skin, slow rate of fentanyl is delivered to the bloodstream -Do not need to worry about touching dog and getting fentanyl on you
	Methadone	-Synthetic opioid agonist -Levo-enantiomer, left handed version has higher affinity for the opioid receptor --10-50x more potent analgesic -NMDA receptor antagonism -Dextro-enantiomer also has NMDA antagnoist effect -Can decrease the development of morphine/opioid tolerance
	NMDA receptor antagonist uses	-Lots of neuropathic pain --limb amputation --back surgery, hemi-laminectomy -Use methodone as pre-med -Can reduce/prevent opioid tolerance -Protection from opioid/induced hyperalgesia
	CRI infusions in anesthesia	-Morphine, ketamine, lidocaine -Morphine, fentanyl, butorphanol
	IV lidocaine	-has associated toxicity -As dose increases, run into increased side effects --muscle twitching, unconsciousness, convulsions, coma, respiratory arrest, cardiovascular arrest -Hard to see changes when animal is under anesthesia -Lidocaine in cats results in higher peak level that stays higher longer --more likely to get toxicity in cats than in dogs --never use lidocaine CRI in cats!
	Lidocaine in Horses	-Can be used during arthroscopy
	Transdermal Lidocaine	-Transdermal lidocaine patch --suspended in gel on felt backing --normal sensation is minimally affected -Different from fentanyl patch -Cut to fit area where you want it -Do not get systemic effect, just local effect -Mesotherapy, local effect
	NSAID pathway	1. Cell Damage 2. Membrane phospholipid is converted into arachadonic acid via phospholipase A2 or phospholipase C 3. Arachadonic acid is metabolized to lipo-oxygenase (inflammatory cytokines produced) or cyclo-oxygenase (classic prostaglandin activation)
	Inflammatory cytokines produced via lipo-oxygenase activation	-Leukotrienes -LTB4: chemoattractant --pro-inflammatory leukotriene -LTC4, LTD4, LTE4: Bronchodilators
	Cyclo-oxygenase prostaglandin activation	-"Classic" prostaglandins -PGG2 -PGE2 -PGF2-alpha -Thromboxane -Prostacyclin
	Platelt function	-has cyclo-oxygenase enzyme and thromboxane synthase -When collagen is exposed due to injury, platelet becomes activated -Aggregate once activated -Arachadonic acid is released, thromboxane A2 is produced --more platelts are activated, more platelts aggregated --causes vasoconstriction -Platelet plug forms at site of injury
	Prostacyclin	-Primary product of arachadonic metabolism in endothelial cells -PGI2 -Vasodilator -Inhibits platelet activation, opposite action of thromboxane -Acts as check for hemostasis, prevents extensive platelet and thombus formation
	NSAID function	-Inhibit cyclo-oxygenase pathway, specifically COX2 isoform -Addresses pain and swelling associated with injury -Anti-inflammatory -Anti-pyretic -Analgesic -Anti-thrombotic
	Steroid function	-Inhibits lipo-oxygenase pathway
	Prostaglandin Function	-Induces platelet aggregation, vasoconstriction -Affects GI integrity via PGE2 and PGI2 --vasodilators, help maintain local mucosal blood flow --increases mucus production to help with repair --decreases gastric secretions --increases gastric epithelial cell turnover -Maintains renal blood flow with decreased perfusion -Maintains liver blood flow
	NSAID toxicity	-GI ulceration and hemorrhage -Platelet inhibition -Nephrotoxicity -Hepatotoxicity possibility
	PGE2 in dorsal horn	-Administering NSAID will decrease feedback look centrally also -Inhibits PGE2 in dorsal horn of the spinal cord
	NSAID gastropathy	-10-20% of people on NSAIDs developed GI issues 1-4% developed serious GI complications (perforations) -16500 deaths anually -Systemic effect is due to inhibition of prostaglandin synthesis -Local effects are also dangerous Topical effects
	Decreasing NSAID toxicity	-Misoprostol has best results --synthetic analog of prostacyclin -PPIs and sucralfate decrease severity -H2 blockers have NO benefit
	COX-1	-Constitutively in the GI tract -In kidney in JG apparatus --important role in renal blood flow -In platelets
	COX-2	-Up-regulated peripherally and in dorsal horn of the spinal cord in response to inflammation -COX-2 in GI tract also present -Role in angiogenesis in circulation? --decreases tumor metastasis?
	COX-3	-Analgesia only?
	Side effects of NSAIDs	-Gi ulceration and intolerance --vomiting and diarrhea -Inhibition of platelet aggregation -Inhibition of renal function --changes in renal blood flow --Na and H2O retention -Can have hypersensitivity reactions
	NSAID grouping	-based on effect on COX enzyme -Have lots of effects on other cell pathways as well
	COX-1 COX-2 ranking	-Can rank NSAIDs to show which is more COX-2 selective -Can measure thromboxane release and platelet release to determin COX-1 activity -Get ratio between COX-1 and COX-2 inhibitory ratios
	COX-2 selectivity	-Balance efficacy and side effects -Different animals respond differently to NSAIDs -What may work in one will not work in a different patient
	Non-selective coxib	-Aspirin -Flunixin meglumine -Phenylbutazone -Ketoprophen
	COX-2 Preferential coxibs	-Piroxicam -Etodolac -Meloxicam -Carprophen
	COX-2 targeted coxibs	-Deracoxib -Firocoxib -Robenicoxib
	Combined COX/LOX inhibitor	-Tepoxalin
	NSAIDs and Cats	-Ketoprophen (not in US) -Meloxicam -Robenacoxib -Cats do not glucuronidate very well! -Do not want to give drugs that need glucuronidation -Renal failure is a big issue for cats with peri-operative NSAID use
	Robenacoxib	-2 hour half-life -Tissue targeted: --highly protein-bound drug --weak acid -As drug circulates in blood, changes ionization of molecule so it stays in the inflamed tissue -Short half-life, but half-life at site of inflammation is 24 hours
	Robenacoxib Pharmacology	-Max plasma concentration in 30 min -Half-life in blood is 1.7 hours -Persists longer in inflammatory exudate
	Reasons not to use NSAID	-Impaired kidney or liver function -Hypovolemia -Pre-existing GI intolerance --evidence of GI erosion or ulceration -Platelet compromise
	Gabapentin	-GABA analog -Anti-convulsant -Binds pre-synaptically to Ca-dependent channels in dorsal root ganglion --Decreases excitatory inputs to dorsal horn of the spinal cord -Can also bind to NMDA receptor -Activates supraspinal decending noradrenergic system -Prevents delayed hyperalgesia, shortens the recovery -Used for neuropathic pain -Well absorbed, 80% bioavailability and peak levels in 1-3 hours -3-4 hour half-life -Effective for cancer pain
	Tramadol	-Centrally-acting analgesic -Synthetic analog of codeine -VERY weak mu opioid agonist -Works via serotonin and epi reuptake inhibition -OK analgesic, not the best -Probably not the most effective drug
	O-desmethyltramadol	-Active metabolite of tramadol -Potent analgesic, more potent than parent compound -Weak mu agonist -Almost way of giving an oral opioid -Minor metabolite, other metabolites are more long-term
	Tramadol Metabolism	-Has active metabolite O-desmethyltramadol -Metabolized via CYP450 system -has numerous active metabolites (22!!) -Efficacy is related to metabolization speed --fast mobilization is more effective
	Tramadol Side effects	-Adverse GI effects --nausea, vomiting, anorexia -Sedation -increased GI bleeding -Hypertension? -Seizures? -Drug interactions?
	Optimizing Pain therapy	-Determine owner's expectations and ability to comply -Counsel owner on what to expect! -Individualize dosage and dosing intervals -Always consider multimodal, preemptive therapy -Reassess and readjust approach regularly!
	Concerns for Equine Anesthesia	-Health status of the patient -Length of the procedure -Safety!! --patient AND personnel -Knowledge of the drugs to be used
	Equine Sedation	-Reliable --provides safety for human and horses --limited selection, alpha-2 are only reliable sedation -Cardiovascular effects -Respiratory effects -Onset time and duration -Cost
	Phenothiazine	-Acepromazine is only phenothiazine available for large animal patients -20-30 minute onset time -Give when animal is still in stall, give animal a chance to absorb drug -4-8 hour duration, long duration -Not reversible -Decreases the animal's anxiety -Provides mild sedation, not great sedation -Minimal ataxia -Not enough sedation for ketamine induction --have to give with another drug to have sedative effect
	Acepromazine Case Selection for Horses	-Healthy adult horse -Anxious horse -Aggressive or difficult horse -Reduces MAC, prolongs recovery time --can use less inhalant -Improves blood flow, causes vasodilation, and increases cardiac output
	Alpha-2 Agonists in horses	-Xylazine (most commonly used) -Romifidine -Detomidine -Dexmedetomidine -Alpha2: alpha1 ratio varies between drugs, Xylazine has most alpha-2 -Have variable onset time and duration -Analgesia and sedation are caused by Alpha-2, higher Alpha-2: Alpha-1 ratio, more analgesia
	Alpha-2 side effects	-Provide great analgesia -have major cardiovascular side effects
	Alpha-2 agonist summary in large animals	-Provides very reliable sedation, used in almost every sedation protocol -Cariovascular effects start with vasoconstriction followed by vasodilation --bradycardia, decrease in CO -Lowers partial pressure or afterial O2 --can be problem in recovery -Slows GI transit time, may cause horse to colic -Can have sudden awakening, use caution around the animal -Onset time is drug-dependent, 2-10 minutes -Duration is drug dependent and based on route --xylazine is shortest acting
	Alpha-2 reversibility	-Can be reversed! -Tolazoline -Yohimbine -Atipamezole
	Alpha-2 agonist case selection for horses	-All adult healthy horses get an alpha-2 -Used in most anesthesia protocols -Avoid in foals and neonates --depend on HR for cardiac output, alpha-2 will decrease HR -Anxious or nervous horse
	Benefits if Alpha-2 agonists in horses	-Reduces MAC --require less inhalant -Provides sedation during recovery --prolongs recovery
	Drawbacks of Alpha-2 Agonists in horses	-Not good for young patients -Reduce dose for sick patients --reduces cardiac output, do not want to decrease too much --avoid long duration of action -Avoid in pregnant mares, depends on stage of pregnancy --causes vasoconstriction, reduces blood flow to the uterus
	Alpha-2 Agonist Reversal	-Tolazoline -Yohombine -Atipamezole (dexmedetomidine, medetomidine) -Reverse if there is excessive sedation or prolonged recovery -Record drug and dose --which sedative and when it was given -IV or IM
	Opioids in horses	-Butorphanol and Morphine
	Butorphanol in Horses	-Kappa agonist and Mu antagonist -Provides mild sedation, use as adjunct --Cannot give as the only drug to sedate an animal -Can cause head tossing -Short-acting drug -Dose for sedation and alangesia are different
	Morphine in Horses	-Pure mu agonist -Provides moderate sedation -increases locomotor activity --needs to be combined with another drug! -Good drug for standing procedures -Longer duration of action, 2-4 hours
	Opioid in Horses Case Selection	-Need additional sedation on top of Alpha-2 agonist and Acepromazine -Minimal cardiovascular effects, good drug for sick patients -Good for analgesia pre-induction, helps with pain --colic or lacerations
	Butorphanol vs. Morphine	-Butorphanol is better sedation before induction -Morphine is better for standing sedation -Morphine lasts longer, may still have effect during recovery -Butorphanol sedates foals very well
	Standing Sedation in the Horse	-Procedures that require animal to stand still for hours -Laproscopic procedures --ovariectomy, cryptorchid castration -Orthopedic procedures -Dental procedures -Need to have safe and quiet environment
	Drugs to use for Standing Sedation in Horses	-Alpha-2 agonists will be needed regardless of what you are doing --detomidine is good, long use (increases urination) --Xylazine has short duration of action --Dexmedetomidine for short procedures, needs CRI for long procedures (Expensive!) -Acepromazine, give with alpha-2 --long sedation, calms animal down --can reduce amount of aloha-2 needed -Opioids --Butorphanol or Morphine --give as bolus or CRI
	Benzodiazepines in Horses	-Midazolam and Diazepam -NOT a sedative for large animals -Muscle relaxant -Give with ketamine --increases muscle relaxation --increases TIVA time of anesthesia -Causes severe ataxia, NOT a sedative! -Good sedative for foals, causes recumbency -Diazepam has longer half-life, will be in body for longer time period -Midazolam is cheaper, used more often
	Guaifenesin	-Muscle relaxant -Produces ataxia -Given to effect before induction -Given instead of diazepam or midazolam (benzodiazepines) -IV only!! Causes tissue sloughing --give via catheter -If give more than recommended dose, animal will be un-coordinated during recovery -Given to effect, can be used to buy time
	Induction drugs in Horses	-Ketamine: most common --works well, affordable, reliable
	Ketamine for Induction of Horses	-Most common drug used for equine induction -Works well, reliable, affordable -Animal needs to be very well-sedated, otherwise will cause excitation -Can cause muscle rigidity if animal is not sedate enough --if in question, give more sedative -Sympathomimetic effects, direct and indirect effects -Use with Alpha-2 and guaifenesin or diazepam --sedative and muscle relaxant -Lasts 10-15 minutes -Fairly safe drug
	Ketamine as Sympathomimetic	-Increases HR, CO via sympathetic system -Contractility is reduced in animals with drained adrenals
	Telazol as Induction Agent in Horses	-Tiletamine and Zolazepam -Good for wild animals or exotic species -has prolonged recovery, not used in normal clinical settings -Good for IM injection of an animal you can't get close to
	Inhalant Anesthesia and large Animals	-Use for procedures longer than 45 minutes -Need anesthesia machine --can use small animal machine for animals less than 150-180kg -Iso, sevo, des -Need to monitor the patient -Use invasive arterial blood pressure monitor, doppler will not be useful -Should have ventilator available
	Monitoring Large Animal Patient under Inhalant	-Invasive arterial blood pressure (doppler will not be effective) -Capnography, ET-gas -Pulse Ox -ECG -Temp
	Large Animal Inhalant Recovery	-Animal needs a lot of time to eliminate inhalant -Prolong recovery with sedation -Prevent animal from standing before they are fully ready
	Balanced Anesthesia in Large Animals	-Combination of drugs to maintain Anesthesia -Inhalant and other drugs to decrease the amount of inhalant needed -Can use alpha-2 agonist CRI --dexmedetomidine, detomidine -Lidocaine CRI reduces inhalant needed -Can do single bolus opioid --morphine, butorphanol -Ketamine is good analgesic, reduces inhalant needed
	TIVA in large animals	-Good for short procedures -Xylazine, Ketamine, Diazepam --10-15 minutes of anesthesia -GKX: Guaifenesin, Ketamine, Xylazine --can have variations
	Equine Recovery Drugs	-Need to stay down for recovery! -Xylazine is probably most commonly used --short onset and duration of action --recovery doses are less than induction doses -Acepromazine can also be used --long onset, long duration -Opioid as adjuct --increases locomotor activity, need to use WITH acepromazine or alpha-2 agonist
	Concerns for Ruminant Anesthesia	-Usually calm -Not very handled, hard to move and handle -Usually elective procedures -Need to be sedated to get airway control! --Need to intubate to precent regurgitation -Can use inhalant or TIVA
	Ruminant Sedation	-Acepromazine: not common, animal is calm already --good if animal is hard to handle or anxious -Alpha-2 agonist: Xylazine is most commonly used due to cost --1/10th the dose used in horses!! Very low dose!! --Detomidine is used in animals that are difficult to handle, can give IM -Opioid
	Alpha-2 Agonists in Ruminants	-Give Xylazine IV in the stall prior to induction --animal will go down, gets very sedate -If animal is difficult, give detomidine or xylazine IM --aggressive bulls -Administer once you are ready to induce the animal
	Opioids in Ruminants	-Provides mild sedation -Can cause mild dyspohoria, animal will vocalize -Administer right before inducing the animal
	Benzodiazepines in Ruminants	-Diazepam or Midazolam -Used as muscle relaxant for induction process -Used as sedative for young animals, less than 3 months --only sedates the little guys -Does not have big effect on HR
	Guaifenesin in Ruminants	-Used as muscle relaxant prior to induction -Need to have IV catheter -Lower dose than in horses, will get sedate quicker -Want animal induced but not lying down
	Ruminant Induction	-Ketamine is only drug available --works well, is affordable and reliable --Allows for fast intubation -Animal needs to be well-sedated, ketamine has excitatory effects --give alpha-2 agonist, guaifenesin, or benzodiazepine
	Ruminant Inhalant anesthetics	-Iso, sevo, des -Need proper monitoring, BP -Need ventilator available
	Ruminant Recovery from Anesthesia	-Recovery is calm and slow -Sedation is not required during recovery -Animal will stay down until they are ready to get up on own
	TIVA in Ruminants	-Short procedures, less than 45 min -Transport to the surgery room -GKX: same for horses but lower dose of xylazine --HAVE TO INTUBATE if they regurgitate, they die
	Small ruminant and camelid anesthesia concerns	-Same concerns as for large ruminants -Intubation is main concern, need to be intubated! -Can be hard to handle -Smaller animals, easier to handle -Need to restrain but do not want to stress animal
	Purpose of Sedation in small ruminants	-Main purpose is to decrease the stress -Smooth induction with ketamine --Lower induction dose if animal is well-sedated -Analgesia can be provided with some sedatives
	Alpha-2 agonists in Small ruminants	-NO XYLAZINE in SHEEP AND GOATS --risk for pulmonary edema --can be used if necessary, but worth avoiding -Xylazine is good for camelids
	Benzodiazepines in Small Ruminants	-Good sedative for small ruminants and camelids -Diazepam or midazolam can be used as sedative -minimal cardiovascular and respiratory effects -Dose is high -Reversible with flumazenil
	Opioids for Small Ruminants	-Use as adjunctive sedative -Alone will not get great sedation, used with others can be good -Short acting analgesia, 1-2 hours -Full Mu agonists are rarely used --cause GI stasis, could cause bloat
	Guaifenesin in Small Ruminants	-More used in camelids as muscle relaxant -Adjunct to ketamine -Animal may lay down, need to be ready to induce -Need patent catheter before use, causes tissue sloughing -Give to effect
	Induction for Small ruminants	-Ketamine is most common --works well, is cheap --Use small dose, small patient has higher metabolic rate -Propofol can be used, costs more --heavy sedation is not required with propofol, causes muscle relaxation --will cause period of apnea if given too fast
	Inhalant Anesthetic in Small Ruminants	-Iso, sevo, des -Need to monitor everything
	Pig Anesthesia Concerns	-IV access is difficult -Complete physical exam and blood work is impossible -Intubation is difficult -Sedation is usually needed to work with them -Just give overview of healthy vs. sick
	Sedation for Pigs	-Usually do combination: --benzodiazepine (midazolam) --alpha-2 agonist (dexmedetomidine or detomidine) --opioid (butorphanol) -Give IM with long needle to reach muscle -Give injection behind the ear -Dose needed is expensive, not done on production animals -Need to have reversal agent for drugs
	Pig Induction	-IV access is ideal --can use ketamine or propofol -No IV access, ketamine or telazol IM --will hurt -Can use mask inhalant for induction if needed -30-45 minute sedation
	Pig Inhalant	-Iso, sevo, des -Same monitoring concerns -Any inhalant can cause malignant hyperthermia in pigs, need to be careful!
	Pain Pathway	1. Transduction of Noxious stimulus --becomes chemical signal 2. Transmission to dorsal horn of the spinal cord 3. Modulation 4. Projection 5. Perception
	Treating Pain	-Need to understand the mechanism of pain to treat pain -Nociceptive vs. inflammatory vs. neuropathic pain -Somatic vs. visceral -Mild vs. Severe -Chronic vs. acute -Peripheral vs. central sensitization -Choose drug based on the mechanism of pain involved
	Pain drugs at periphery	1. Opioids 2. local anesthetics --prevent Na channels from opening
	Pain drugs acting in Dorsal Horn	1. Alpha-2 agonists 2. Local anesthetics 3. Opioids
	Drugs used for Analgesia in large animals	-NSAIDs -Alpha-2 agonists -Opioids -Local Anesthetics -NMDA antagonists -Alternative therapies -Everything is species dependent!!!
	NSAIDs in large animals	-Flunixin meglumine is most common -Phenylbutazone -Firocoxib -Analgesic and anti-inflammatory -Inhibit COX enzymes, decrease prostaglandin production -Very good analgesia -Decrease peripheral and possibly central sensitization --important for long-term chronic pain
	NSAID mechanism of Action	-Inhibits COX enzyme -Decreases production of prostaglandin and leukotrienes -Inhibits pain, inflammation, and fever -Removes gastric barrier, puts animal at risk of forming gastric ulcers -Renal blood flow and tubular function is impaired/altered --increases risk of renal damage
	Case Selection for NSAID use in large animals	-Any healthy animal --horses, ruminants, camelids, etc. -Good for treatment of acute or chronic pain -Cannot be used chronically, will cause GI issues -Good for visceral or somatic pain --flunixin: visceral pain --bute: somatic pain
	Case selection cautions for NSAID use in large animals	-Young animals, neonates -Old animals -Renal disease patients -GI disease patients -Patients with a clotting problem
	Alpha-2 agonists for analgesia	-Xylazine -Romifidine -Detomidine -Dexmedetomidine -Efficacy is based on Alpha-2: alpha-1 ratio --lower alpha-1, higher alpha-2, better analgesic --changes onset time, duration of action, and analgesic property -Also act as a sedative
	Alpha-2 analgesic Mechanism of Action	-Work mainly on the dorsal horn of the spinal cord -Work on the brainstem -Can work intra-articular, within the joint capsule -Have a little local anesthetic effect -Work via g-protein coupled receptors --decrease neuronal excitation, decreases amount of excitation
	Case Selection for Alpha-2 agonist analgesia	-Horses -Some large animals -Good for treatment of acute pain (fractures) -Not great for chronic pain, has a lot of side effects and causes sedation -Good for visceral or somatic pain --abdominal discomfort, lacerations -Used intra-operatively for balanced anesthesia --MAC-sparing, decreases amount of inhalant needed -Good for standing surgeries --combine with opioid
	Alpha-2 Agonist analgesia administration	-IV -IM -Epidurally --needs to be preservative free or brand new bottle
	Alpha-2 agonist side effects	-Sedation -Ataxia -Increase in urine production --horse will have big bladder going into recovery, use a catheter to reduce urine in bladder -Cardiovascular effects, vasoconstriction, bradycardia, lowers CO -Respiratory effects, decreases PaO2 -GI effects, slows transit time --can make some horses colic
	Opioids for Analgesia	-Mu agonists: Morphine and methadone -Kappa agonist/Mu antagonist: Butorphanol -Partial Mu agonist: buprenorphine --longer acting --less analgesia than pure Mu agonist
	Opioid Mechanism of Action	-Works in dorsal horn of the spinal cord -Does not block transmission or transduction of pain -Works supraspinal in thalamus, midbrain, and medulla -Works peripherally in joints and nociceptive nerve endings -G-protein coupled receptors --reduces NT release, results in less excitation in the dorsal horn --fewer nerves firing and sending signals up to the brain
	Opioids in Equine	-butorphanol, morphine, methadone -Good for somatic and visceral pain -Decreases GI transit time, careful in colic patients --use butorphanol -Give IV as single bolus or CRI, IM, Intra-articular -Has variable effects on MAC -Good for standing sedation --combine with alpha-2 agonist and acepromazine -Post-operatively give IV or IM to reduce pain after the procedure -Can give epidural of morphine
	Opioids in Large and Small Ruminants	-Butorphanol is most often used --less GI stasis -Good for somatic and visceral pain under general anesthesia -Can be given IV or IM -Can be given post-operatively to manage pain -Can be given epidurally (morphine)
	Opioids in Camelids	-Butorphanol is most commonly used -Good for general anesthesia, somatic and visceral pain -Give IV or IM -Can give post-operatively to manage pain -Can be given epidurally for hindlimb pain (morphine)
	Side effects of Opioids in large animals	-increased locomotor activity -Ataxia -head-shaking (horses mostly) --do not use for standing sedation in horses -Decreased GI motility -Can cause urinary retention if given epidurally
	Local Anesthetics and Analgesia	-Esters: --cocaine, procaine, tetracaine, benzocaine -Amides: --lidocaine, prilocaine, Mepivacaine, bupivacane, ropivacaine -Choice depends on type of procedure and duration -Some drugs cause sensory and motor block, some just sensory --generally do not want motor block, animal cannot move area of the body and may fall down -Dose changes based on tissue blood flow, infection, and inflammation
	Local anesthetics and vasoconstriction	-Lidocaine comes with some epi in it -Advantages: --maintains local anesthetic in the tissue desired, does not spread to the whole body -Disadvantages: has alpha 1, alpha 2, beta 1, beta 2 effects
	Local Anesthetic Mechanism of Action	-Binds to Na channels -Blocks sensory function of the peripheral nerve terminal -Blocks transduction -Insult never becomes a nerve signal -Prevents propagation of nerve cell action potential --AP never reaches spinal cord, no transmitted -Decreases sensitization
	Case selection for Local Anesthetics	-Topical: mucous membrane, eye, laryngeal spray -IV: extremities --used a lot in cows -Infiltration anesthesia: --lacerations, small mass removal -Perineural anesthesia, targeting specific nerves -Spinal anesthesia, target the spinal cord
	When to use local anesthetics	-Whenever possible! -Any species, any case, if you can use local anesthetic you should -Cheap, safe, great analgesia, MAC reduction -Pain never reaches the spinal cord -Inhalant is needed just to maintain recumbency, not for analgesia -Good for standing surgery, block area before cutting
	IV CRI of local anesthetic	-Lidocaine ONLY!! -Can be done in all species -Decreases visceral and neuropathic pain -Decreases post-operative pain -Decreases hyperalgesia -Anti-inflammatory -Improves bowel function -Inhalant anesthetic sparing -Can be used in laminitic horses -Not a great analgesic, but will support other analgesics used
	Local Anesthetic Side Effects	-CNS: seizures, sedation, coma -Respiratory system: depression -Cardiovascular system: Bradycardia, arrhythmias, hypotension -Local effects: tissue irritation -Allergic reactions, formation of methemoglobin (leading to hypoxemia)
	Toxicity from Local Anesthetic	1. Light headedness, numbness of the tongue 2. Muscle twitching, visual disturbance 3. Convulsions 4. Coma 5. Respiratory arrest Will miss most steps if animal is under general anesthesia! -won't see anything until cardiovascular depression -When using CRI of lidocaine, be sure of the dose you are using! --especially with small animals like goats
	NMDA antagonists for Analgesia	-Ketamine -Dissociative, analgesic, anti-inflammatory effects -S-ketamine and R-ketamine --S-ketamine is more potent, has faster elimination, provides most of the analgesia -Can be used as CRI for general anesthesia --Fractures respond well -Can be used in standing sedation -Chronic pain alangesia
	NMDA Mechanism of Action (Ketamine)	-Continuous input from C- nociceptive afferent fibers results in increased NMDA receptors -Stop NMDA receptor expression, will have fewer receptors -CNS plasticity, ability of the CNS to make body more or less sensitive to pain --mediated by NMDA receptors -Has effects in CNS and peripherally -Can be used in local block -Synergistic with other drugs --alpha-2 agonists, gabapentin, opioids
	Blocking NMDA receptor	-Ketamine -Reduces the amount of Ca going into the cell -Results in less excitation and fewer new receptors
	Ketamine Case Selection	-Needs to be used as CRI -Induction dose for ketamine will have no effect intra-operatively --need to give patient CRI to have effect -Lowers inhalant needed -Provides great analgesia -treats severe or chronic pain, somatic pain -Not so good for visceral pain -Use for general anesthesia or standing sedation -Used most in horses -Sympathomimetic, allows for better BP -Synergistic with alpha-2 agonists, gabapentin, opioids
	Side effects of Ketamine	-Ataxia --be careful of the dose! -Excitatory behavior during standing procedures --high dose
	Gabapentin	-Used for analgesia -Decreases Ca influx into neurons via Ca channels -Questionable efficacy -Used when running out of options
	Tramadol	-Mild mu receptor agonist -Works on serotonin receptors -Not used often in large animal patients, not very effective -Inhibits neuronal release and reuptake of serotonin and NorEpi
	Alternative Therapy for Analgesia	-Acupuncture -Chiropractic -Hydrotherapy -Manual therapies --massage, physical therapy, tissue mobilization
	Acknowledging Pain	-Subjective! -Pain is often ignored in animals -Variation in species --Prey species do not want to show pain -Elevated HR, decreased appetite, teeth grinding, nostril flare, rigid posture, reluctance to be handled, depression, muscle fasciculations -Knowing the animal before using anesthesia can help you use the right amount
	Pain Scoring Systems	-Helps raise awareness of presence of pain in animals -Helps guide if animal is improving or not
	Equine Emergencies	1. Colic
	Anesthetizing a Colic Patient	-Signalment: age, breed, weight -Health status: sick vs. stable -Suration of clinical signs: hours, days? -Safety of animal and personnel: based on agitation level of the animal -Treatments already received: fluids? decompression? -Drugs already onboard -Bloodwork: PCV, total proteins, electrolytes, blood gas analysis
	Approach to a Colic Case	-Pertinent history, need to know about the colic -Work up performed already -Complete physical exam is necessary! --cardiovascular esp., HR and quality --respiratory status -Is animal stabilized enough? -Need to know what drugs were given by referring veterinarian!!! Avoid over-dose
	Colic fluids	-Hypertonic saline -Crystalloids -May also give colloids
	Colic Sedation Alpha-2 agonist	-Alpha-2: reliable sedation -causes vasoconstriction and decrease in CO -dose-dependent -Xylazine is shorter acting, detomidine is a better sedative (longer duration of action) -If animal has already had drugs, may need to give less alpha-2
	Colic Sedation Opioid	-Butorphanol IV -Has minimal cardiovascular effect -Allows for a decreased dose of alpha-2 agonist --Helps with xylazine sedation
	Colic Sedation Guaifenesis	-Guaifenesin can be used to decrease needed dose of alpha-2 agonist -can lower arterial BP -Give to effect --MAJOR advantage, can give as much as you need
	Colic Sedation Benzodiazepine	-Causes good muscle relaxation with minimal cardiovascular effects -Give at same time as ketamine --cannot be given to effect, dose given is what it is
	Colic Induction and Intubation	-Stabilize patient prior to induction and intubation if possible -Sternal or lateral recumbency -Continuously assess the patient --pulse quality, mucus membrane color -Check for risk of arresting during induction -Intubate with endotracheal tube and oxygenate as soon as possible
	Colic Maintenance under Anesthesia	-Inhalant anesthetic is best option -Iso, sevo, des -Intermittent positive pressure ventilation may be helpful --ventilator decreases CO --may help with oxygenation -Colic case has high peak inspiratory pressure
	Monitoring for Colic case	-Arterial blood pressure -ET gasses -HR -RR -SPO2 -Temperature -Arterial blood gasses, look for oxygenation, pH, and lactate -Electrolytes pre-op, intra-op, and post-up --Ca, K, Na, Cl, Mg
	Colic Fluids	-Crystalloids are go-to fluid -Need fluid replacement -Plasmalyte, lactated ringers, normosol-R -10ml/kg/hour to start -Check colloid oncotic pressure, protein is being dumped into GI and out of vessels --volume is going from vessels into interstitial space --Watch for edema -Hypertonic saline (give ONCE) for rapid recussitation
	Colic Electrolytes	-Important to watch during anesthesia -Na and Cl will be low usually -Administering crystalloids will help replenish -K is usually low --never exceed 0.5 mEq/kg/hour -Only give bicarbonate if necessary (pH less than 7.2) --ideally treat lack of bicarbonate by treating the underlying disease process -Ca tends to be low under anesthesia
	Hypoxemia during colic	-PaO2 less than 60mmHg -SaO2 less than 90% -Severe GI distension causes alveoli compression, atelectasis, V/Q mismatch, and shunt -With positive pressire ventilation, peak inspiratory pressure will be high
	Improving Ventilation under Anesthesia	1. Albuterol --Beat-2 agonist --few side effects 2. Recruitment maneuver --Very high pressure ventilation that should pop open compressed alveoli --helps with oxygenation --may pop healthy alveoli along with compressed and damaged alveoli --only use when really needed 3. PEEP --keeps alveoli open at the end of inspiration, will not re-open alveoli --keeps some gas stuck in the lungs --need to start with it, or add after recruitment maneuver for PEEP to be effective
	Colics and Hypotension	-Compromised cardiovascular system and decreased cardiac output -Treat by lowering inhalant concentration -Give more fluids -Dobutamine, phenylephrine, or norepinephrine can be used to decrease hypotension
	Colic Recovery	-Usually prolonged, horse is tired! -Usually do not need to sedate during recovery -If sedation is needed, use lower amount than you would for a healthy patient -Padded stall -Keep nasotracheal tube in, edema can close off airway -Give supportive care if needed -Assist recovery with ropes if needed
	Anesthesia for Dystocia and C-section concerns	1. Signalment 2. Condition of the mare 3. Duration of labor 4. Is foal dead or alive 5. multiparous vs. primiparous 6. Safety or personnel!
	Preparing for Dystocia anesthesia	-Be prepared ahead of time -Shorter duration of dystocia improves the outcome --longer duration, higher chance the foal is dead -Quick physical exam -If foal is dead, will have time to stabilize mare and do bloodwork --if foal is alive, no time!
	Dystocia induction	-Xylazine is not the best choice, but only choice! -Alpah-2 is used for sedation in pregnant mares -increases SVR and decreases CO --Not good for the foal, but don't really have any options -Guaifenesin can be given to effect, takes a little longer -Benzodiazepine can cause "floppy baby" and respiratory depression -Ketamine is used, even though it is not so good for the liver --need fast induction
	Dystocia Intubation	-Do as soon as patient is anesthetized -Dystocias tend to go quickly, C-sections take a while -Ventilate if necessary -Peak inspiratory pressure will be high
	C-section anesthesia	-Keep monitoring and keep record -Mare will probably need to be ventilated -Drug administration is still limited, foal is still in the mare --once foal is out, have more options for drugs --major decrease in arterial blood pressure for the mare
	C-section/Dystocia Recovery	-Brood mares are at higher risk of fractures due to decreased bone density and weakness -Clean, padded recovery stall --Avoid lube!! -Quiet recovery -May or may not need sedation -Do not rush mare to stand after anesthesia -Keep foal away from the mare until she is standing well -Assisted recovery with rope is recommended
	Anesthesia for Horse Fractures, lacerations, Septic joints	-Induction and recovery are most important -Condition of the animal is important --most will be healthy animals, may be exhausted after shipping, training, or event -lacerations will be bleeding -Patient may not be totally mobile, have difficulty reaching the induction area --do not sedate animal at all before it is where it needs to be! -Animal will be in pain, have to address analgesia
	Approach to Anesthetizing fracture, lacerations, or septic joints	-Thorough physical exam -Stabilize animal if needed -bring animal into induction area before sedating -Plan induction and recovery!
	Sedation of laceration/fracture	-Animal is usually systemically healthy, have lots of options for drugs -Sedate right where they are going to be induced -Alpha-2, alpha-2 and opioid, whatever
	Induction of laceration/fracture	-Protect the leg!! -Induce in sling so animal does not fall on a broken leg --if needed, protect with a bandage or splint -Avoid using broken leg to hoist animal
	Maintenance and monitoring of Laceration/Fracture case	-Similar to other healthy cases -Inhalant anesthetic for balanced anesthesia -Local blocks are good, work well -IV drugs work well --opioids, ketamine CRI, alpha-2 agonists -Field lacerations can use GKX --need to do in under 1 hour
	Recovery of Fractures	-Sling, pool rope, work with what you have -Give enough time for inhalant anesthetic to get out --empty bladder --provide proper analgesia -Animal should not bang around trying to get up! keep animal down until it is really ready to stand
	Recovery of lacerations	-Quiet and prolonged recovery -Need to ensure reconstruction does not fall apart during recovery
	Hyperkalemic Periodic paralysis HYPP	-Genetic disorder of Na channels -Affects K levels -Genetic disorder of impressive bloodline in quarter horses --mostly halter horses --NH/HH genotype -Always ask when anesthetizing a quarterhorse whether it has HYPP or not -Emergency during anesthesia, HYPP crisis during anesthesia is a big deal!
	HYPP concerns	1. Stress: increased stress level can cause a HYPP event -Maintain calm environment, sedate horse ahead of time 2. Difficulty breathing: issue with larynx causes respiratory obstruction -Alpha-2 relaxes laryngeal muscles, causes increased risk of obstruction 3. Hyperkalemia during operation -recognize signs and be ready to treat 4. Prolonged recovery due to weakness -recovery crisis
	Recognizing HYPP event during operations	1. Changes in ECG --bradycardia due to hyperkalemia --may see tachycardia before bradycardia --increase in T-wave amplitude --increase in P-R interval --Flattening of the P-wave to point where it disappears 2. increase in CO2 due to muscle tremors 3. Muscle fasciculations --check body temperature! If seen, measure K! K more than 5 is an issue!
	Treating HYPP	1. 23% Ca gluconate --restores difference between resting and threshold potential --does not fix the issue, raises normal threshold so difference between resting is normal --stabilizes the heart 2. 50% dextrose --stimulates insulin release, puts K into the cells 3. Give insulin directly --be sure to measure glucose at the same time 4. Na bicarbonate --increases pH, causes H to come out of the cell --H comes out, K goes into cell
	Bladder Rupture in Foals	-Causes increase in K -Signalment is important, occurs in neonates -Due to complications during birth --check for other complications as well -Check condition of the foal --electrolyte imbalance --hypovolemia/dehydration --cardiovascular status --Renal status --Hypoclycemia?
	Approach to Bladder rupture in Foals	-Physical exam -cardiovascular status --check for arrhythmias -Respiratory status -Look for other issues associated with a difficult birth or neonates in general --pneumonia, infected umbilicus -PCV, TP, check electrolytes
	Neonate anesthetic concerns	-Immature system! -Drug metabolism is not the same as an adult, need to adjust the dose of the drug -Hypoglycemia is common, do not have glycogen stores --add dextrose to stores -Hypothermia -The mare -Cardiovascular concerns -Respiratory distress -Electrolyte imbalances
	Changes in neonatal Cardiac output	-Poor blood pressure in neonates, do not have ability to change SV or vasoconstrict -CO is maintained by HR -May be hypovolemic and dehydrated -Arrhythmias due to k imbalance --flattening P-waves, peaked T-waves
	Stabilizing neonate before anesthesia	-MUST be done! -Fluid therapy to correct dehydration and Hypovolemia --0.9% NaCl to correct imbalance --no K, high Na and high Cl is good -May drain fluid from peritoneal cavity --improves respiratory rate and oxygenation --improves venous return
	Correcting Hyperkalemia	-Ca gluconate: increased threshold potential -Dextrose for endogenous insulin release -Insulin if needed (IV or SQ) --Monitor glucose levels! -Na bicarbonate if needed --re-check K before inducing
	Foal induction	-Use benzodiazepine and butorphanol for sedation -For induction use ketamine or inhalant anesthetic --can induce with mask or nasotracheal tube
	Foal Maintenance	-Use whatever inhalant you want -Foals tend to ventilate well on own --have slightly higher respiratory rate -Standard monitoring (pulse, respiratory rate, arterial blood pressure, saturation of O2, capnography, ECG, temperature) -Keep patient warm!! -Check electrolytes
	Foal recovery	-Foals are easy to hand recover -Oxygen supplementation may be needed -no sedation needed -Maintain in lateral recumbency --can be in sternal if more awake --help with head and tail rope to stand -Keep nasotracheal/endotracheal tube in until totally recovered
	Anesthetizing the Small animal Patient	-Signalment -Size -Temperament --can you go IM or do you need to go IV? -Every patient gets PE! --heart and lungs are key -Type of procedure
	Preoperative evaluation of the Small Animal	-History --know medical conditions --medications --previous anesthetic history -Physical Exam (esp. cardio, respiratory, and neuro systems) -Lab tests -Additional diagnostics
	Tissue Perfusion in the Small animal patient	-Mucus membrane color and character -Capillary refill time -General skin condition -Temperature of the extremities -Mental status (brain is a tissue that needs to be perfused) -Urine production
	renal perfusion and anesthesia	-Lots of drugs affect renal perfusion -Liver can regenerate, kidney has harder time -Want to know how well the kidneys are perfused during anesthesia -Especially cats, renal disease is common
	Laboratory tests for Small Animal Anesthesia	-CBC: white cell count --anesthesia is immunosuppressive, need to keep in mind -Chemistry screen: check creatinine for kidney function -PCV and TS -BUN and urine specific gravity --need to know kidney is concentrating urine -Coagulation profiles (dobermans, liver disease, shunt concern) -Blood gasses -ECG -Radiographs
	ASA physical status	1: no systemic disease 2: mild systemic disease 3: moderate systemic disease 4: severe, incapacitating disease 5: moribund, animal will die E: emergency
	Catheter and Anesthetizing	-All animals undergoing anesthesia should have a catheter! -Cheap -Easy access to vein and blood supply -Always a good idea to have a catheter -Rate of fluids is inversely proportional to the radius of the catheter to the 4th power --size of the catheter makes a big difference --faster rate with larger catheter --larger catheter the better -Put on front limb if possible
	Small Animal Anesthesia and Fluids	-Use balanced electrolyte solutions -Specific choice is not critical -All patients get fluids
	Preanesthesia for Small Animal Patients	-Provides sedation and chemical restraint -IM or SQ before placing a catheter --IM stays around for a longer period of time -Reduces dose requirements and side effects of other drugs -Opioids are common choice --also provide analgesia
	Anticholinergic Sedation	-Competitive antagonists of ACh -Sympatholytic, decrease activity of ACh -Decreases vagal influences on the heart -Use secondary to surgical manipulation, secondary to other anesthetic agents, or in patients with high resting vagal tone -Good for ocular procedures due to cardiac-ocular reflex -Good for young patients -Use with opioids to cause vagally-mediated bradycardia -Decreases salivation and airway secretions
	Atropine vs. glycopyrrolate	-Atropine: crosses BBB --longer onset time -Glucopyrrolate: has charged nitrogen --does not cross BBB --lasts longer
	Side effects of Anticholinergics	-Decreases vagal tone -Decreased intestinal motility --big deal in horses (ileus) -Increased myocardial oxygen consumption --bad news for patients with hypertrophic cardiomyopathy -Increased incidence of cardiac arrhythmias
	Acepromazine	-Phenothiazine tranquilizer (VERY reliable tranquilizer) -pre-medication for normal healthy patients -Acts via dopamine receptors in CNS -Provides mental calming -Relatively slow onset of action when given IM -Lasts a relatively long time -NO analgesia -Minimal respiratory effects, good for patients with respiratory issues
	Acepromazine side effects	-Alpha antagonist, causes vasodilation -Avoid if volume status or bleeding is a concern --not good for hypovolemic patients -Do not want to prevent local vasoconstriction with bleeding, will decrease clotting -Can cause seizures, not good for seizure cases
	Ketamine as pre-med in small animals	-Dissociative anesthetic -Not used in dogs by itself --causes seizures --seizure threshold is close to therapeutic threshold in dogs -Use with benzodiazepine muscle relaxant and opioid -Used in cats a lot
	Dissociative anesthetics	-Ketamine -Tiletamine -Provides selective analgesia --NMDA receptor antagonist
	Good aspects of Dissociative anesthetics	-Ketamine, tiletamine -Cardiovascularly sparing, has indirect sympathetic response --increases HR and maintains BP -Direct effect: negative inotrope --not great for a sick case, good for healthy cases -Minimal respiratory depression
	Drawbacks of Dissociatives	-Increases ICP --can lead to seizures -Not a great choice for visceral pain, good for somatic pain -Direct myocardial depressant -Increases muscle tone -increases intraocular pressure
	Morphine	-Opioid -Inexpensive -Excellent sedative -Lasts 4-6 hours -Causes vomiting -Causes histamine release -NOT used as an induction agent --used pre-med or post-operative
	Methadone	-Expensive opioid -Not a great sedative when used as a pre-med -Used in combination with acepromazine or alpha-2 agonist works well -Used in dogs and cats -Can use low dose IV for induction -Can use post-operatively for analgesia -NMDA!!!!!
	Fentanyl	-Very lipid-soluble opioid -Not used as a pre-med, not absorbed reliable
	Demerol	-Short-acting -Causes fair amount of histamine release -not used very often
	Hydromorphone and Oxymorphone	-Versatile opioid -Good pre-med opioid -Good for induction -Good post-operatively -Lasts 2-4 hours -Can cause a fair amount of vomiting
	Butorphanol	-Kappa agonist, mu antagonist opioid -Won't get as much analgesia as pure agonist -Good sedative, not a great analgesic -only lasts 1-2 hours -anti-emetic
	Buprenorphine	-Partial mu agonist -Long onset time, 20-30 minutes -Won't get as much analgesia as a pure agonist
	Mu agonist effects	-Analgesia -Sedation -Respiratory depression -Bradycardia -Euphoria/dysphoria -Emesis -Decreased GI motility -Increased sphincter tone
	Kappa agonist effects	-Analgesia -Sedation -Respiratory depression
	Dysphoria with Mu agonists	-Dobermans and huskies -Hunting breeds
	Benzodiazepine	-Diazepam, midazolam -Work via GABA receptor, facilitate GABA neurotransmission -Increase Cl- conductance into the cell, holds pore open for longer --hyperpolarizes the cell -Not very reliable tranquilizer --give in combination with something else -Minimal calming effect, can cause increased agitation -NO ANALGESIA -Very good for cardiovascular system and respiratory system -Good adjuncts for other drugs
	Drugs working on GABA receptor	-Barbiturate -Propofol -Benzodiazepines -Etomidate
	Diazepam vs. Midazolam	-Diazepam (valium) -Midazolam (versed) -Difference is in solubility --Midazolam is water soluble --diazepam is lipid soluble
	High profile High risk wildlife species for Anesthesia	-Safety for humans and animals is a concern! -Giraffes -Hippos -Elephants
	Methods for Delivering Drugs to Wildlife	-Oral -Hand injection -Pole syringe -Projectile syringe -Inhalation/induction chamber
	Oral delivery of Drugs	-Often used to relieve anxiety before injection -Can achieve deep sedation depending on agent and dose -Anxiolytics can make some animals more wary -Mucosal contact time should in maximized for maximum absorption -If given in water, use 2x IM dose -Rumen vs. monogastric, almost all drugs are absorbed in the rumen
	Hand injection vs. projectile injection	-Lower doses needed with hand injection -Dart needs higher dose -Heavy syringes impact animal with a lot of force --cause startle response, pain, catecholamine release --increases CO, drugs go to peripheral tissue beds --Can also form hematoma from injection, results in slow drug absorption, drug sits in hematoma -May not be accurate with dart, have to shoot it!
	Projectile syringe trauma	-Syringe has weight, momentum, and sometimes too high power -May have unintended injection site -Limb fractures due to impact
	Restraint for Hand or Pole injection	-Behavior training is important -Can use a net and rabies pole -Plywood boards, clear plastic shields -Crate, squeeze cage, squeeze chute
	Projectile syringe methods	-Projection: --compresed CO2 --compressed air --explosive charge -Ejection of drug from syringe: --air, butane gas, CO2, explosive charge
	Plastic Syringes for Darting	-lightweight --lower impact, less trauma -Delivery is usually quiet -Reusable -Somewhat fragile -Expensive! -Trajectory is affected by the wind -Not exceptionally long-range -Can be delivered via blowpipe, pistols, rifles, etc.
	Animal safety while darting	-be sure to dart the animal in a safe spot! Do not want animal to fall and hurt themselves -Falling -Drowning -Pastures with lake/pond/stream -Easier for animals to fall downhill when stumbling! -May run into clear fences, use paddocks or stockade if possible -Keep other animals out of the group
	Darting and damage to equipment	-Animals can damage equipment easily!
	Human Safety issues with darting	-High mg potency! -Highly concentrated drugs -High doses -Need to make sure no self-sticking
	Drugs used for Wildlife anesthesia	-Etorphine -Medetomidine -Midazolam -Dangerous to handle drugs without safety protection! -Avoid contact and splashes -May have direct injection or spray from pistol -Handling projectile syringe -Skin contact with injection site
	Drug Safety with Wildlife	-Personal protection -Protection of others -Antagonists immediately available -Emergency equipment and plan -Drug storage and access -Food chain-hunting -Keep local emergency center aware that these drugs are being used -Animal escape protocols -Employee training and practice -Food chain- predation of animals that have been injected
	Over-Dosing for wildlife anesthesia	-Overdose can cause cardiovascular effects and respiratory depression -Long recovery or incomplete antagonism -Re-sedation or renarcotization in 30 min-24 hours
	Under-dosing for wildlife anesthesia	-Protracted excitement period -Rigidity, struggling -Over-heating, increased metabolic rate -Hypoxia, respiratory and lactic acidosis -Capture myopathy
	Dosing and volume restriction for wildlife anesthesia	-Drug potency and concentration -Distance to target -How far will the syringe travel accurately?
	Wildlife anesthetic drugs used	-Opioids: VERY potent! --etorphine --carfentanil --thiafentanil -Medetomidine -Midazolam -Butorphanol
	Time-lag injection to immobilization	-Onset time differs between specific agents -Especially important in free-range animals, can travel very long distances -Higher doses are given to make onset faster
	Animal concerns with darting	-Body temperature --animal will approach ambient temperature --make sure ambient temperature is reasonable weather and time of day -CNS regulation -Peripheral vascular effects -Do not lose an animal at night!
	Wildlife drug recycling	-Re-narcotization after using opiates -Antagonist does not last as long at effect site as agonist --Antagonist is removed and metabolized, agonist has continued effect -Opiates may under enterohepatic recirculation
	Muscle and nerve damage with wildlife anesthesia	-Direct pressure can cause damage -Need to pad animals properly -Capture myopathy: stress related issue -Hyperkalemia --marine mammals, large cats --severe bradycardia and bradyarrhythmias -Hypoperfusion-related myopathy is less likely --have higher BP, perfuse muscles better
	Cardiovascular monitoring for Wildlife	-Monitor! -Be prepared to treat
	Respiratory monitoring for Wildlife	-Big problem -Can intubate smaller things -Larger animals are harder to intubate and ventilate -Monitor and be prepared to give intranasal O2 -May have to use specific receptor antagonists --opiates, alpha-2, benzodiazepines -Doxapram is a general respiratory stimulant
	Regurgitation and vomiting in Wildlife	-Regurgitation and vomiting are important concerns for ruminants -Depends on species, procedure, and drug effects -Can withhold food and water -Place animal in sternal with head up and nose down -Intubate with a cuffed tube
	Ideal immobilizing Cocktail for Wildlife	-rapid onset -no induction excitement -Good muscle relaxation -High potency per mg -high aqueous solubility -Reliable restraint -Wide safety margin -Obvious sign of effect -Specific receptor antagonist or reasonable/reliable recovery time
	Opioid agonists in wildlife	-Hoofstock, -bears -free-ranging marine mammals -VERY potent compared to morphine -Provide reliable signs of restraint -Animal is approachable before immobilization -Animal can often be handled during onset -Cardiovascular support or cardiovascular stimulation -Has specific antagonists
	Cyclohexamines in wildlife	-Carnivores -hoofstock -primates -captive marine mammals -Ketamine and tiletamine
	Negative aspects of potent opioids used in Wildlife	-Stargazing, falling backwards -Induction excitement (can reduce with adjuncts) -Muscle rigidity -Hyperthermia, acidosis -Respiratory depression -Regurgitation in ruminants -Renarcotization
	Potent opioid adjuncts	-Central alpha-2 agonists -Acepromazine, azaperone -Maybe midazolam? -Ketamine -Thiopental -Propofol -Guaifenesin -Volatile inhalants
	Potent opioids and hypertension	-Can blunt by using aceproamzine or azaperone -Guaifenesin -Propofol -Volatile inhalant anesthetics -Alpha-2 agonists increase hypertension
	Opioid Combinations	-Butorphanol (opiate agonist/antagonist) combined with alpha-2 agonist +/- azaperone -Very useful for immobilizing wide variety of species -Provides standing restraint in hoofstock -Butorphanol, azaperone, medetomidine -Butorphanol, midazolam, medetomidine Beware of sudden arousal!
	Benefits of Cyclohexamines for anesthesia	-ketamine, tiletamine -Reliable restraint -Signs are reliable, especially is used alone -Usually cardiovascularly stable -Usually respiratory stable
	Negatives of Cyclohexamines for anesthesia	-Produce seizures in cats -Muscle rigidity -Apneustic respiration -Awkward induction -Awkward recovery -No specific antagonist
	Cyclohexamine adjuncts	-Central alpha-2 adrenergic agonists (medetomidine and dexmedetomidine) -Acepromazine -Benzodiazepine -Bigger cats need different doses --bigger cats need smaller doses
	Medetomidine in Wildlife	-Dramatic decrease in ketamine requirement -excellent muscle relaxation and analgesia -Antagonist allows rapid recovery -Abrupt arousal is possible when ketamine wears off --20-45 min
	Tiletamine-Late reaction	-Occurs in tigers -2 days after an apparent normal recovery -Depression, ataxia, dragging hindquarters -Hyper-responsive to tactile stimuli -Seizures -over-heating -Do not use telazol in tigers if possible! -treat with benzodiazepine (diazepam, midazolam)
	Telazol in Free ranging Lions	-Telazol alone can have up to 13 hour recovery -Can reduce recovery time by giving medetomidine also --recovery 15-60 minutes after antagonism of medetomidine -Makes late-reaction less likely?
	Long-acting Neuroleptics in Wildlife	-Used to reduce excitement, stress, capture myopathy, convalescence -Can be life-saving -Species differences exist
	Exotic Pet Anesthesia Limitations	-LOTS of different species, lots of different anatomy -Minimal information, most is anecdotal information not evidence-based medicine -Dose extrapolation is common, allometric scaling for size and metabolic rate -Species differences -Breed differences -Behavioral considerations --safety, stress, assessment -Anatomic considerations --safety, vascular access, airway -Physiologic considerations -Pharmacological considerations
	Exotic Pet Pharmacological considerations	-Pharmacokinetics: --rabbits have atropine esterase, will not respond to atropine anti-cholinergic --Rabbits have unique ability to clear meloxicam readily --Ferrets cannot glucouronidate NSAIDs -Pharmacodynamics: --avian species and opioid receptor type and distribution
	Exotic Pet Behavior	-Behavior of exotic pets is very different from that of regular pets -Behavior under anesthesia can also be very different with exotic pets -Assess behavior from a distance, maybe even from a different room
	Preanesthetic Assessment for Exotic Animals	-Can be done at a distance to minimize stress to the animal --takes technology and investment -Appropriate housing and husbandry are important to reduce stress --if animal has a buddy at home, give a buddy in hospital -Stress of handling or observation can change vital parameters of the patient -Be sure to get accurate body weight -Check temperament, cardiovascular, respiratory function -Assessment may be limited -Limit blood sampling, have small blood volume to begin with
	Allometric Scaling for Exotics	-Smaller animals have faster metabolism -Need a proportionally higher dose of sedative compared to a larger animal -Not appropriate to use same dosage in smaller species as in larger species
	Respiratory infections in Rabbit	-Can have major impact on anesthetics
	Anesthetic monitoring of Exotic animals	-Personnel is very important! need to know how to interpret information and act -Monitoring may be limited due to size and anatomy of the patient -hypothermia: Animal has small surface area to volume ratio, will get cold quickly -capnography: mainstream vs. side-stream -SpO2 -Monitor may be minimally useful, avoid over-use of monitors
	Small Mammal Anesthesia	-Not encouraged to fast pre-anesthesia --very high metabolic rate, need constant intake of food --make sure there isn't any food in mouth -many do not have the ability to vomit -IV access via cephalic, lateral saphenous, or auricular veins --do not confuse vein and artery!
	Small mammal intubation	-Small size, small jaw range of motion -Takes a lot of practice! -V-gel has been developed for rabbits -Can do via blind intubation, direct visual, or endoscope --depends on species and ability to visualize larynx -Protects airway and provides ventilation -Avoid causing damage!
	V-gel	-Intubation for rabbits -bigger opening at end lays over the larynx and establishes open airway -Comes in different sizes -Easy to place
	Small mammal pre-medication	-Benzodiazepine -Opioids --hydromorphone, fentanyl, buprenorphine, butorphanol -Ketamine: do not need vascular access -Alpha-2 agonists: dexmedetomidine --benzodiazepines are better, have less cardiac effects
	Small Mammal Benzodiazepine	-Consistent effects on Small mammals -minimal effects on cardiovascular and respiratory systems -can be reversed -no analgesia!
	Small mammal Opioids	-Hydromorphone -Fentanyl -Buprenorphine -Butorphanol -Provides great analgesia, reversible -Has variable duration and efficacy -Also has GI effects, decreased motility --can be very dangerous for hind-gut fermenters like rabbits
	Small Mammal Induction	-ketamine (IM or IV) -Propofol -Etomidate -Inhalant --mask or chamber induction --sevoflurane is better for induction, less pollution and less pungent for patient
	Small Mammal Analgesia	-Opioids -Tramadol -NSAIDs
	Tramadol in Small Mammals	-mu-agonist? -Inhibits reuptake of serotonin and norepi -Has variable duration of action variable efficacy -Lots of different mechanisms of action -Lots of unknowns, but is still very popular
	NSAIDs in Small mammals	-Long duration -Not controlled -Do not use in ferrets! Limited ability to glucuronidate --be careful of dose and dosing interval -Can produce renal, hepatic, GI, and bleeding disturbances
	Local anesthetics in Small Mammals	-Very low cost -Most effective analgesic when used appropriately --only medication that actually BLOCKS pain transmission --other agents modify pain but do not block -be careful not to overdose small mammals with local anesthetics -Calculate toxic dose!
	Small mammal recovery	-Keep animal warm! large surface area to volume ratio means they get colder faster -Pain assessment -SQ fluids may be needed to maintain appropriate hydration -Assisted feeding may be needed --hind-gut fermenters, feeding is very important and may need to force-feed during recovery
	Avian Anesthesia	-Fasting for anesthesia depends on specific species -Vascular access via metatarsal, ulnar, or intraosseous route -Bones can be pneumatic, do not want to administer fluids into an air sac! --radius/ulna is good spot for catheterization
	Avian respiratory system during Anesthesia	-Trachea is large relative to size --also have complete tracheal rings, do not inflate the cuff or use tube without a cuff, may cause damage and scarring in the trachea -No epiglottis -Most birds have similar-looking upper airway -Mucus plugs are present, commonly plug ET --monitor patency of tube! -Air sacs
	Avian Premedication	-Opioids --mu agonists vs. kappa-agonists --Use with benzodiazepines -No great way to measure analgesia in birds, hard to determine if pain medication works
	Avian induction	-Inhalant induction
	Analgesia in Birds	-Tramadol has some effect -Opioids -NSAIDs -Local anesthetics (do not overdose!) -No good way to determine if a bird is painful or not, not sure if drugs are working!
	Anesthetic Recovery	-Patient needs to be able to respirate, ambulate, maintain state of awakeness -Stable cardiac and respiratory systems -Need to make sure patient can regulate own temperature
	Definition of the Recovery Period	-Period of emergence from general anesthesia where different elements of consciousness return at different rates -Discharge criteria: --regain control of airway --stable cardiovascular and respiratory systems --are awake --can thermoregulate --can ambulate
	Importance of the recovery period	-Life-threatening complications can occur during recovery period -Most common time for dogs, cats, and rabbits to die under anesthesia -Equines get fractures and myopathies -bad things can happen! -Need to monitor the patient appropriately
	Environment during recovery period	-Depends on circumstances --species, case load, field vs. hospital -Should be calm and quiet -Needs to be safe! --temperature, altitude, humidity are important --padding is a good idea, traction is beneficial -No water hazards -Help animal maintain homeostasis -Remove or reduce predators
	Equipment for Recovery	-Alert system and crash cart -O2 supplementation and scavenging -Induction agents available for re-anesthitization -Thermal support -Monitoring with staff and machinery
	Staff for recovery	-Very important! Need adequately trained staff! -Trained for species behavior -Able to recognize and prevent any issues
	Patient assessment in Recovery	1. Respiratory system 2. Cardiovascular system 3. Pain assessment 4. Temperature 5. Additional support needed
	Respiratory System during Recovery	1. Subjective assessment: --physical exam, look for air flow and respiratory sounds --respiratory pattern and effort --mucus membrane color 2. Objective assessment: --pulse oximetry for oxygenation: --capnography for ventilation and CO2 exhaled --blood gasses: arterial catheterization is gold standard
	Extubation criteria and technique	-Animal needs to be able to protect its airway and maintain an open airway -Lots of species-specific factors -If hemorrhage, flush, or regurgitation is present, delay extubation and leave cuff inflated --prevents fluid from going down the trachea -Degree of personal preference is involved -If patient can pull tongue back into mouth, should be able to protect airway
	Patient considerations with Extubation	-Some species are obligate nasal breathers --horse, camelids, rabbits --do not occlude the nares!! --watch out for edematous nasal passages in horses -Brachycephalic dogs are also special consideration
	Respiratory system during recovery and specific procedures	-Upper airway obstructions --laryngeal paralysis, brachycephalic dogs --have tracheostomy kit on hand, just inc ase -Tracheal collapse -Pneumonia or ventral slot surgery --mechanical ventilation on-hand -Thoracotomy: check chest tube -Neuromuscular blocking agents
	Cardiovascular perfusion parameters during Recovery	-Mentation -Mucus membrane color -Capillary refill time -Heart rate, sympathetic response compensation -Extremity temperature, vasoconstriction at extremities if patient is in shock, cold limbs -Pulse quality
	Cardiovascular assessment during recovery	-Perfusion parameters -Arterial blood pressure -Lactate
	Pain assessment during Recovery	-LOTS of ways to measure pain in patients --none are particularly great -Species differences in pain and exhibition of pain -Remote vs. interactive assessment of pain -When in doubt, give analgesic! --preventative analgesia --multimodal analgesia -Consider duration of action and time to peak effect of analgesia -Glasgow composite measure pain scale, Melbourne pain scale, Colorado pain scale, Numerical rating system, Visual analog scale
	Multimodal analgesia	-Use different drugs with different mechanisms and different sites of activity
	Hypothermia during Recovery	-Most patients will be cold after anesthesia, cannot regulate body temperature under anesthesia -Prolongs inhalant elimination -Shivering increases O2 demand, muscle contractions -Impaired coagulation -Suppresses immune function -Delayed wound healing
	Hyperthermia during recovery	-Hot patients pant and lose body heat --increased work of breathing --careful in patients with upper airway obstruction -Cats can get hyperthermia with opioid administration --generally self-limiting hyperthermia
	Additional support for animals during Recovery	-Consider fluids, continue fluids if used during anesthesia -Empty urinary bladder -Check bandages -Provide padding -Think about appropriate positioning, avoid damage to muscles and nerves -Consider sedation --depends on temperament of the patient --horses require sedation during recovery (alpha-2 or acepromazine) -May need ropes for horses
	Prolonged Recovery	-Common complication from anesthesia -Make sure patient is cardiovascuarly stable --assess perfusion and peripheral BP, oxygenation -Hypothermia will slow elimination of inhalants or clearance of injectable agents -Drug clearance is important --hepatic function and renal function can be factors -Metabolic factors --hypoglycemia and electrolyte disturbances -Pain!
	Oxygen delivery equation	DO2 = CO x CaO2
	Pharmacological considerations during prolonged recovery	-Consider duration of action when turning off anesthetics -increase fresh gas flow rate, more fresh gas flow, faster elimination of inhalant -If patient is otherwise stable, consider reversal
	Reversal for prolonged recovery	-Alpha-2 agonist reversal: --atipamezole, tolazoline, yohimbine -Benzodiazepines: flumazenil -Opioids: Butorphanol, Naloxone, Naltrexone, Nalbuphine -Agents can be short-acting, may get re-narcotization
	Post-anesthetic delirium/Dysphoria	-Common complication of anesthesia -Occurs with many many many agents --benzodiazepines, dissociatives, anticholinergics, costicosteroids, phenobarnital, antihistamines, opioids, inhalants, pain, dopamine, lidocaine, antibiotics -Hard to find an anesthetic protocol that does not have potential for dysphoria --can be difficult to tease out cause for dysphoria -best approach is prevention! -Keep anesthetic Protocol simple
	Avoiding Dysphoria during recovery	-Keep anesthetic protocol simple! -Any animal receiving more than 3 medications has higher chance to show dysphoria --fewer medications the better -Have a calm and quiet environment --minimize stimuli -Consider reversal or sedation as needed
	Record keeping and communication during Recovery	-Very important! Keep appropriate record! -Communication is essential -Patient signalment -Reason for anesthetic and outcome -Drugs administered and prescribed -Complications -Medical conditions and concerns -Patient status and lab work -Discharge criteria -Contact information

Share This Flashcard Set

Set the Language

Related Flashcards

Anesthesia Exam I

Add to Folders

Upgrade to Cram Premium

Card Range To Study

1018 Cards in this Set