Pre Medication 2010

8/3/2019 Pre Medication 2010

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Premedication

Goals of premedication: – Calm and sedate the patient

– Reduce stress of handling

– Smooth anesthetic induction,

maintenance and recovery – Reduce induction and

maintenance drugs required

– Provide pre-emptive analgesia

and muscle relaxation – Decrease airway secretions

and salivation

– Obtund autonomic reflexes



• Hypnosis:

– A depth of sedation fromwhich the patient is not

easily aroused – Loss of ability to

maintain a patent airway

– Lack of response to

surgical stimuli – Propofol, ketamine,

thiobarbiturates,etomidate

– Indistinguishable fromgeneral anesthesia withvolatile anesthetics

• Sedative

– Drug that relieves anxiety

– “Conscious” sedation

– Drowsiness

– Benzodiazepines andalpha-2 agonists



• Tranquilizer:

• A drug with apredominant action inrelieving anxiety without producingundue sedation.

• These drugs are also

called anxiolytics orantianxiety drugs.

• An example of this typeof drug would be

diazepam and otherbenzodiazepines



Anti-cholinergics

• Competitivelyantagonize Ach atcholinergic

postganglionic muscarinic receptors (parasympatholytic)

• Receptors found in:

– Heart – Salivary glands

– Smooth muscles ofthe GIT and UT

• Postganglionic nicotinicreceptors located at the NMJ

and autonomic ganglia• Anticholinergics are

selectively anti-muscarinicand only anti-nicotinic at toxic

doses





• Atropine is an alkaloid ofbelladonna

• Semi-synthetic

belladonna alkaloids(e.g., glycopyrrolate) arequaternary ammoniumderivatives which aremore potent

• Glycopyrrolate does notcross the BBB, so has noocular or CNS effects

• Atropine crosses the BBBand cause sedation,excitement, andmydriasis

• Potent antisialogouges

• Reduce salivary and bronchial

secretions

• Mydriasis (atropine)

• Central AnticholinergicSyndrome (rare)



Parasympatholytic

• Competitively antagonizes Achat cholinergic postganglionicmuscarinic receptors

• Decreases vagal tone andprevents vagally inducedbradycardia

• Increases and maintains HRand improves CO

• Sinus bradycardia, sinusarrest, sinus block, 1o,2o, and 3o AV blockade

• CPR = atropine

• Bronchodilation

Cardiac Output = HR x SV



• Gastrointestinal Tract

– Reduced motility and ileus

– Avoid in ruminants and horses – Increased sphincter tone

– Decreased gastric H+ secretion

– Decreased tone of smooth

muscles of the biliary tract

• Urinary tract

– Decreases tone

of smoothmuscles of theureters andthe urinarybladder

– Reduces spasmof ureters

– Increases toneof the bladder

sphincter -urinaryretention



Clinical Use

• Included as pre-medication:

• Maintain heart rate and CO

• Offset vagal reflexes

• Decrease GIT, salivary and respiratory secretions

• To treat sinus bradycardia, sinus arrest, sinus block, andfirst, second, and third degree atrioventricular blockade

• Contraindications:

– Pre-existing tachycardia

– GI motility problems (horses, rabbits, ruminants)

Asystole = Atropine!



Tranquilizers and Sedatives

Phenothiozines

Benzodiazepines

Alpha-2 agonists and antagonists



Acepromazine

• Dopamine (D2) andalpha1 (a1) receptorantagonist (blocker)

• D2 receptors: – CNS (arousal)

– Basal ganglia(coordinatemotor function)

– CTZ (nauseaand vomiting)

– Hypothalamus(temperature

control)• Alpha-1 receptors:

vasoconstriction

EliminationHepatic metabolismElimination half-life is 3 hours;

detectable in plasma > 8 hours



Cardiovascular Effects - Ace

• Respiratory effects

– Minimal effects

• Dose dependent decrease in blood pressure due to:

– Alpha1 R blockade - vasodilation

– Depression of CNS vasomotor centers – CV collapse in patients with high SNS tone or

hypovolemia

• Epinephrine reversal

• Anti-arrhythmic• Decreases sensitivity to catecholamines

• Cardiac output and heart rate minimally affected a lowdosage rates



CNS Effects of Acepromazine

• Sedation (prolonged period of sedation – at least 4 hours)

• Anxiolytic (likely not)

• Muscle relaxation and decreased motor activity

• Third eyelid prolapse

• Reduces required dosages of other drugs, includinginhalants (MAC reduction)

• Anti-emesis (CTZ)

• Inhibits hypothalamic thermoregulation

• Rigidity or tremors with overdosage (Extra-pyramidal orParkinsonian-like signs)

• Acepromazine has the reputation for lowering the seizurethreshold, but there is little evidence to support this.



Other EffectsAcepromazine• Anti-emetic (CTZ)

• Anti-histamine

• Hypothermia

• Penile prolapse and priapism in stallions

• Splenic sequestration of RBC’s

• Prolonged sedation (4 to 8 hours or longer)

• Premedication prior to anesthesia

• Contraindicated in head trauma, increased ICP

• Contraindicated in neonates, elderly, shocky patients

• Caution in Boxers; always combine with an anticholinergic

• Lower dosages in larger animals

• Caution with aggressive animals



Benzodiazepines

• Distribution &Elimination

– Highly protein

bound (96-98%)

– Unbound drugcrosses theblood brainbarrier and isactive

• Metabolism

– Hepatic with

renal excretionof metabolites

• Mechanism of Action

– Receptors in cerebral cortex,hypothalamus, cerebellum,

midbrain, hippocampus, medullaand spinal cord

– Increase GABA and glycine

– Sedation due to increased

GABA activity in the CNS – Anxiolysis & muscle relaxation

due to increased glycine activity

– Mild analgesic effects - possiblydue to increased GABA

– Retrograde amnesia



CNS Effects-Benzodiazepines

• Anticonvulsant• Very mild sedation or

even excitement whenused alone in dogs, cats,

horses• Mild to profound sedation

in sick animals

• Mild sedation in ruminants

• Muscle relaxation (spinallymediated)

• Analgesia (mild)

• Appetite stimulant



Benzodiazepines

• Respiratory

– Minimal effects

– Respiratory depression whencombined with opiates orother anesthetic agents

• Cardiovascular

– Minimal effects

– Slight increase in HR



• Diazepam (Valium)

– Water insoluble (dissolved in propylene glycol)

– Pain on injection

– Mixes poorly with other drugs (except ketamine)

• Diazepam usually given IV, but can be given orally

– Unreliable absorption when given IM or SQ

• Midazolam (Versed)

– Water soluble at low pH

– Given IM, IV or subcutaneously

– 2-3 x’s more potent than diazepam

– Shorter acting than diazepam – No pain on injection

– Can be mixed with other drugs



Benzodiazepines

• Zolazepam

– Found only combined withTiletamine as Telezol

– Only benzodiazepinelicensed for use inveterinary patients

• Flumazenil - reversal agent forall benzodiazepines



Clinical Usage:

• Rarely used alone in healthy patients as sedation ispoor and excitement may occur

• Often combined with ketamine to induce anesthesia

• Administered with opiates for sedation of higher riskpatients (neurolept anesthesia)

• Sedative affects are good in debilitated, sick patients,especially if combined with an opiate

• Generally used for sedation of pediatric, geriatric, andcompromised patients



a2- Adrenoreceptor

Agonists

• Alpha2 receptors:

– Decreased SNSoutflow:

• Inhibition of NErelease fromterminal axons

• Inhibition of firing

of NE neurons(hyperpolarization)

• Decreased NEturnover in CNS

Peripheral effects:

• Vascular smoothmuscle contraction

(post-synaptic a2 R) – Vasoconstriction

• Inhibition of insulinrelease from pancreas

– Hyperglycemia



a2- Adrenoceptor Agonists

• Decreased SNS outflow in the CNS results in:

– Sedation (Alpha-2 receptors in the locus ceruleus)

– Analgesia (spinal a2 receptors)

– Muscle relaxation (spinal a2 receptors)

– Cardiovascular depression (centrally mediated)

• Bradycardia

• Decreased contractility

• Vasodilation

• Decreased CO



Cardiovascular Effects• Administration results in initial vasoconstriction, followed by

reflex bradycardia, then centrally mediated SNS depression• Bradycardia, vasodilation, decrease in CO, tissue perfusion

• Dysrhythmias

• Xylazine causes premature ventricular contractions (PVC’s);

other a-2 agonists decrease PVC’s

• All cause sinus arrhythmias, bradycardia, sinoatrial block, 1stand 2nd degree A-V block

• Respiratory

– Mild respiratory depression

– More significant with opiates

– Hypoxemia in cattle and sheep





CNS Effects

• Analgesia

• Comparable to opioids in efficacy for visceral pain andact synergistically with opioids

• Duration of analgesia is much shorter (around 1 hour)

than duration of sedation

• Significant reduction of doses of other drugs used foranesthesia, including volatile anesthetics (MACreduction)

• Reversal agents available – alpha-2 antagonists



Unwanted Effects

• Vomition in dogs and cats (xylazine) • Decreased GI tract motility, resulting in ileus

• Inhibition of insulin release from pancreas resulting in hyperglycemia and osmotic diuresis

• Sweating and piloerection in horses • Increased myometrial contractions in cattle with xylazine,

which can lead to abortion in the third trimester

• Bradycardia -reversed with alpha-2 antagonists or

atropine or glycopyrrolate only if life-threatening• Indications: Young to middle-aged, healthy, exercise-

tolerant animals



Contraindications:

• Pre-existing CNS depression• Pre-existing cardiovascular disease

• Gastric or intestinal or urinary obstruction

• Diabetes mellitus

• Avoid xylazine in cattle in the last trimester of pregnancy

• In any animal that does not have normal cardiovascularand respiratory function



a2- Adrenoceptor Antagonists

• Increase SNSoutflow and NErelease from CNS

• Reversibility is an

advantage

• Specificity for a2 receptors:atipamazole >

idozoxan >yohimbine >tolazoline

N l t l i



Neuroleptanalgesia • Goal: production of a tranquil, calm patient with some

dissociation from environment and analgesI• Combination of a tranquilizer or sedative with an opioid

• A tranquil and analgesic state due to synergism of ananalgesic and a tranquilizer or sedative

• Better sedation results in:• -- Better restraint and decreased dosages of other agents

used (injectable and volatile anesthetics)

• Addition of the opiate allows decreased dosage of sedate

• Less CV depression with additional sedation• More rapid elimination of drugs when differing metabolic

pathways involved

• More rapid elimination and recovery because of lower dose

Documents

Pre Medication 2010