Anesthesiology Test 1

Important to conduct prior to any anesthetic treatment.

Signalment / history, general inspection (mentation check), physical exam. Want to determine if there is altered pharmacokinetics or pharmacodynamics.

Systems of greatest concern with anesthetics.

Cardiovascular, respiratory, nervous (target), hepatic, renal.

Components of stroke volume.

Preload (venous return = blood volume), contractibility, and afterload (systemic vascular resistance, which approximates mean arterial pressure).

Impact of vascular tone on cardiac output.

Inverse relationship: vasodilation decreases afterload & systemic vascular resistance, improves stroke volume / cardiac output.

Components of arterial oxygen content.

Hb-bound oxygen and dissolved oxygen.

Calculation for alveolar ventilation (V_A).

P_ACO₂ = k x (VCO₂ / V_A), where

P_ACO₂ is alveolar CO₂, which approximates arterial CO₂ content.

k is 0.863, used to convert units to mmHg.

VCO₂ is CO₂ production.

Calculation for tidal volume (V_T).

Measures volume of air in the airways.

V_T = V_A + V_D, where

V_D is deadspace ventilation / volume, the portion of air that remains in the conducting airways, and should make up 40-50% of total tidal volume.

Calculation for minute ventilation (V_E).

Measures volume of air moving in and out of the lungs each minute.

V_E = V_T x RR, where

RR is respiratory rate.

Partial pressure of oxygen in alveoli at sea level.

100mmHg.

Measure of oxygenation in a patient.

SaO₂ (percent hemoglobin saturation in arterial blood), or PaO2 (partial pressure of oxygen in arterial blood).

Relationship between ventilation and CO₂ levels.

Hypoventilation increases PaCO₂, hyperventilation decreases PaCO₂.

Normal oxygen and carbon dioxide levels in arterial and venous blood.

PaO₂ = 95 mmHg. PvO₂ = 40 mmHg.

PaCO₂ = 40 mmHg. PvCO₂ = 45 mmHg.

Calculation for alveolar air (PaO₂).

PaO₂ = FiO₂ (P_atmos – P_water) – (PaCO₂ / R), where

PaO₂ is partial pressure of alveolar oxygen.

FiO₂ is inspired oxygen concentration, purer is closer to 1.

P_atmos is total atmospheric pressure, P_water is partial pressure of water

PaCO₂ is partial pressure of arterial carbon dioxide.

R is ratio of CO₂ to O₂ consumption, usually 0.8.

Calculation for A-a gradient (P(_{A – a})O₂)

(P(_{A – a})O₂) = alveolar mmHg (usually 100) – arterial mmHg (usually 95)

Gradients < 10mmHg are normal, > 30 indicates gas exchange impairment.

Tests conducted prior to anesthetic administration.

Quick assessment tests (QATs) such as PCV, plasma protein, glucose, and BUN. In patients with noted abnormalities, CBC, biochemistry, and urinalysis may be conducted.

Classification of anesthetic risk

On a scale of 1 (healthy) to 5 (unlikely to survive), based on level of systemic disease.

Length of withholding for food and water of monogastrics.

Food: 6-12 hours.

Water: 2-4 hours, or until premedication period.

Length of withholding for food and water of ruminants.

Food: 24-36 hours.

Water: 8-12 hours.

Three major classes of sedatives

Phenothiazines, benzodiazepines, alpha2 adrenergic agonists.

Acepromazine – indications

Sedation. Antiemetic, antiarrhythmic, antihistaminic, antipruritic, but only as side effects (not main indication for administration).

Acepromazine – MOA

Antagonises post-synaptic dopamine receptors in the CNS (inhibits release / increases turnover), as well as serotonin, a1, histamine, and muscarinic receptors.

Acepromazine – cardiovascular and respiratory effects

Hypotension (due to peripheral vasodilation) with same or unchanged HR, decreased SV, CO, PCV, platelet function. Only minimal respiratory effects.

Acepromazine – neurological effects

Not an analgesic (must be combined with opioids, which it potentiates). Generalised depression, anxiolysis, decreased chemoreceptor trigger zone (vomiting), decreased thermoregulation.

Acepromazine – side effects

Muscle relaxation, delayed gastric emptying, rarely equine penile prolapse.

Acepromazine – use

Given to dogs, cats, horses in IV, IM, or SC, onset in 20-30 mins and lasts 2-6 hours. Metabolised by hepatic conjugation with glucuronic acid.

Acepromazine – pros and cons

Pros: decreases other anesthetic requirements, doesn’t cause respiratory depression, cheap.

Cons: irreversible, long-lasting, causes hypotension and hypothermia.

Benziodiazepines – indications

Sedation, anxiolysis, muscle relaxation, and anticonvulsant effects.

Benzodiazepines – MOA

Potentiates effects of GABA in CNS, by increasing their Cl- channel opening frequency to cause neuronal hyperpolarisation.

Diazepam – cardiovascular and respiratory effects

Minimal at normal doses, but if given with propylene glycol vehicle (injectable form) may cause cardiopulmonary depression or venous thrombosis.

Diazepam – neurological effects

Mild sedation, anticonvulsant effects, muscle relaxation. May cause paradoxical excitement (disinhibition), hepatic failure in cats repeatedly given PO.

Diazepam – use and metabolism

Given to dogs and cats IV, lasts 4+ hours. Hepatically metabolised by demethylation.

Midazolam - indications

Same indications as diazepam, with similar effects on the cardio, respiratory, and neuro systems.

Midazolam – use and metabolism

Given to dogs, cats, exotics, and neonatal foals IV, IM, or SC. Lasts 1-4 hours. Hepatically metabolised, but produces inactive metabolites.

Benzodiazepines – pros and cons

Pros: minimal cardiovascular and respiratory depression, reversible.

Cons: variable sedative effect, may cause paradoxical excitement, not analgesic.

Flumazenil – use

Benzodiazepine antagonist (high GABA affinity), reversing the CNS, anticonvulsant, and cardiopulmonary effects. Rapid acting (2-4 mins, lasts 60).

Alpha 2 agonists – indications

Sedation, analgesia, muscle relaxation, sympatholysis.

Alpha 2 agonists – MOA

Binds a2 receptors in CNS to inhibit norepinephrine release, and in blood vessels to cause vasoconstriction.

Alpha 2 agonists – cardiovascular effects

Biphasic on blood pressure – hypertension occurs initially due to peripheral vasoconstriction, then reduced NE causes hypotension and bradycardia due to reduced blood pressure. CO also decreases due to decreased SV and HR (mainly in peripheral tissues, so may turn mucous membranes grey).

Alpha 2 agonists – respiratory effects

Reduced rate and tidal volume (dose-dependent), additive with other drugs such as opioids.

Alpha 2 agonists – CNS effects

Sedation, muscle relaxation, analgesia, changes in personality.

Alpha 2 agonists – side effects

Emesis, GI or urinary issues, decreased thermoregulation, hypoinsulinemia, increased uterine tone (premature birth in pregnant animals).

Xylazine – use and metabolism

Used in any species IV, IM, or SC, with an onset within 3-15 minutes and duration up to 60 mins for sedation (less for analgesia). Extensively hepatically metabolised, excreted in urine.

Detomidine – use and metabolism

Used in horses and cattle IV, IM, or SC, with an onset within 2-15 minutes and duration up to 120 minutes for sedation (60 for analgesia). Extensively hepatically metabolised, excreted in urine. Expensive.

Dexmetatomidine – use and metabolism

Used in dogs and cats IV, IM, SC, transmucosal, most A2 selective (minimal side effects). Onset 2-15 minutes, duration up to 90 minutes for sedation (less for analgesia). Extensively hepatically metabolised, excreted in urine.

A2 adrenergic agonists - pros and cons

Pros: decrease anesthetic requirements, induce sedation, muscle relaxation, analgesia, and are easily reversible.

Cons: cardiovascular and respiratory depression, GI illness.

Reasons to reverse A2 agonists

Atipamezole – use

Very selective A2 antagonist, relatively safe but can only be given IM. May cause excitation, tachycardia.

Opioids

Act on opioid receptors (mu, kappa, delta) in the CNS and peripheral tissues, providing analgesia and enhancing sedatives.

Opioids – MOA

Activate G-protein coupled opioid receptors in the CNS to reduce Ca+ influx and increase K+ efflux, decreasing neurotransmitter release and hyperpolarising neurons.

Opioids – cardiovascular and respiratory effects

Minimal cardio (potentially bradycardia). Significant respiratory depression (dose-dependent increase in CO2 response threshold), decreased centrally mediated breathing rate and tidal volume (initially tachypnea).

Opioids – CNS effects

Analgesia, sedation (dog, human), excitation (cat, horse), antitussion, increased CRTZ activity causing emesis, and decreased thermoregulatory ability. May also change pupil size, cause urine retention, and reduce GI motility.

Opioids – use and metabolism

Used in any species IV, IM, SC, or orally (bioavailability poor) with a drug-dependent onset and duration of action. Hepatically metabolised, excreted in urine.

Morphine – use

Full agonist used for any species, given IV (slow, histaminic), IM,or SC, with an onset 2-20 mins and duration 2-4 hours.

Methadone – use

Full agonist, less side effects than morphine (+ NMDA antagonist). Used in dogs, cats, and horses IV, IM, SC, with an onset 2-20 mins and duration 2-4 hours.

Hydromorphone – use

Fentanyl – use

Full agonist, extremely potent and highly lipophilic. Used in dogs, cats, and horses IV or transdermally, with an onset 1-2 mins and duration 20-30 mins.

Buprenorphine – use

Partial agonist opioid (high affinity, low intrinsic activity). Used in most species with variable formulations (IV, IM, SC, transdermal), prolonged onset and duration 6-8 hours. Not useful for premedication.

Butorphanol – use

Agonist-antagonist opioid (mild analgesia). Used in most species IV, IM, or SC, with an onset 3-15 mins and duration 1-2 hours.

Naloxone – use

Opioid antagonist used in any species IV or IM, with an onset 1-5 mins and duration 15-45 mins (may require redosing).

Anticholinergics - MOA

Competitive inhibitors of Ach via binding to muscarinic, cholinergic receptors of nerves. Treats bradycardia, decreases secretions.

Atropine – cardiovascular and respiratory effects

Increased heart rate and blood pressure changes, decreased respiratory secretions and bronchodilation.

Atropine – CNS and other effects

Crosses BBB, placenta. High doses may cause sedation, CNS stimulation or seizures. Causes pupil dilation, decreased GI motility.

Atropine – use

Used in dogs and cats IV, IM, or SC, with a duration 60-90 mins. Cats, rats, and rabbits undergo extensive hepatic metabolism (atropine esterase), dogs excrete unchanged in urine.

Glycopyrrolate – cardiovascular and respiratory effects

Increased heart rate (minimal tachycardia and arrythmias), blood pressure changes, decreased respiratory secretions and bronchodilation.

Glycopyrrolate – CNS and other effects

Doesn’t cross BBB or placenta, has reduced ocular effects when compared to Atropine, but may cause decreased GI motility.

Glycopyrrolate – use

Used in dogs and cats IV, IM, or SC with a duration 2-4 hours. Excreted mostly unchanged in feces and urine.

General anesthesia

Drug-induced state of unconsciousness caused by controlled, reversible global CNS depression. The patient is unarousable even with painful stimuli.

Sedation

Drug-induced state of reduced awareness caused by effects on discrete CNS receptors. The patient may be aroused by painful stimuli.

Use of injectable anesthetics

For induction of anesthesia, accompanied by an inhalant for maintenance. Or, for induction and maintenance of anesthesia itself (total intravenous anesthesia).

Qualities of an ideal injectable anesthetic

Rapid onset and metabolism, short duration, high therapeutic index, doesn’t accumulate in tissues or release histamine.

Pharmacokinetics

The body’s effect on a drug.

Pharmacodynamics

The drug’s effect on the body.

Redistribution phase

When the quantity of the drug in the blood decreases, and the quantity in other tissues such as fat and muscle increases.

Clearance phase

When the quantity of drug is decreasing in all tissues.

Propofol – properties

Can only be given IV (emulsive form predisposes to bacterial growth) though the shot is painful. Rapid redistribution and clearance (good for CRI) and causes a smooth, fast recovery.

Propofol – pharmacodynamics

Decreases CO and BP, induces apnea (hypoventilation) and anesthesia without analgesia. Usually used in small animals, rarely in large animals except for neonates or occasionally as a co-induction agent in horses.

Alfaxalone – properties

Can be given IM or IV (if no preservative predisposes to bacterial growth). Rapid redistribution and clearance (good for CRI) and causes a relatively smooth, fast recovery. More $$$ than propofol.

Alfaxalone – pharmacodynamics

Decreases BP but increases HR. Minimal respiratory effects if given slowly. Induces anesthesia without analgesia. Usually used in small animals with a wide therapeutic margin, rarely in large animal neonates.

Ketamine – properties

Can be given IM or IV. Rapid clearance (good for CRI in combo), but if administered solo can cause rough induction / recovery and inadequate muscle relaxation. Induces dissociation.

Ketamine – pharmacodynamics

Increases HR, BP, CO. Induces mild respiratory depression (bronchodilation, apneustic breathing) and anesthesia + somatic analgesia, but also increases intracranial pressure. Used in small animals for co-induction or as a low dose CRI to supplement analgesia. Used in large animals for co-induction, or given IM with other drugs in pigs.

Tiletamine-Zolazepam – properties

Can be given IM or IV. Powder form of Tiletamine (dissociative) and Zolazepam (benzodiazepene), provides similar anesthesia to ketamine-benzo combos.

Etomidate – properties

Can only be given IV and contains propylene glycol (painful injection). Very rapid clearance, but shouldn’t be given CRI due to adrenal cortical suppression. Pro-emetic.

Etomidate – pharmacodynamics

Minimal cardiovascular or respiratory effects, induces anesthesia without analgesia. Rarely causes myoclonus. Not used in large animals, occasionally used for co-induction small animals that are hemodynamically unstable.

Common co-induction agents

Benzos, guaifenesin (GG), lidocaine, fentanyl and ketamine.

Total intravenous anesthesia (TIVA)

Induction and maintenance of anesthesia using IV drugs only – providing hypnosis, muscle relaxation, and immobility. Done via intermittent IV injections or CRI. Analgesia should be provided by other drugs (opioids, A2 agonists).

Indications for TIVA

Field anesthesia, where inhalants are difficult. Airway procedures, where intubation is not feasible. Short procedures. Patients at risk of malignant hyperthermia.

Benefits of TIVA

Less OR pollution and easier portability, improved hemodynamic control, reduced stress response and improved recovery.

Why perform endotracheal intubation

Reduces dead space, keeps upper airways open, prevents aspirations, allows for safer and more efficient volatile anesthetic administration (and controlled ventilation).

Use of low volume, high pressure cuffs (rubber and silicone)

Low compliance. Has a higher risk of injuries (i.e., allergies) and faulty cuffs or pilot balloons.

Use of high volume, low pressure cuffs (polyvinylchloride)

High compliance with thin walls, and a large surface area in contact with the trachea. Applies low pressure to the tracheal mucosa. Easier to use and can be customised to length.

How to reduce breathing work

Choose largest diameter but shortest possible tube, use low velocities (avoid tachypnea).

Induction chamber

For induction only. High, fresh gas flow rate (>5L/min) but also has risks of pollution. Safe for operator, doesn’t require monitoring during induction. Sevoflurane most commonly used.

Facial mask induction

Is less polluting and allows for better monitoring than using a chamber. Increases dead space. Sevoflurane most commonly used.

V-gel supraglottic airway

Forms seal over trachea, designed for rabbits and cats. Should confirm placement with capnography after every movement of patient.

Orotracheal intubation in birds

Glottis should be easy to identify below tongue (no epiglottis), and the larynx is highly mobile. Do not inflate the balloon, due to complete tracheal rings.

Types of laryngoscopes

Macintosh (curved blade, which is placed rostral to the epiglottis).

Straight blade (placed on top of epiglottis, better for large animals).

Fixing endotracheal tube

Can be fixed behind ears or around mandible/maxilla (pay attention to insertion as you tie it to prevent it advancing further). If it’s too far out, the dead space may increase, but if it’s too far advanced you risk endobronchial intubation.

Why pigs are most difficult species to intubate

Long larynx-nose distance, low amplitude of mouth opening, pharyngeal diverticula, post-glottal narrowing, laryngeal angle, tracheal bronchus, and are prone to laryngospasms.

Blind techniques for endotracheal intubation

Perception (feeling for breath or whistle in tube), visualisation (condensation in tube).