Preanesthetic and Perioperative Medications


Preanesthetic and Perioperative Medications


Pre and postanesthetic (perianesthetic) medications are essential to safe anesthetic management. When used appropriately, they minimize stress, cardiopulmonary depression, and the deleterious effects produced by IV and inhalant anesthetic administration. Preanesthetic medications almost always reduce the required dose of injectable or inhalant anesthetics and postanesthetic medications improve the quality of recovery.

Preanesthetic medications generally include combinations of drugs from multiple categories: Anticholinergics (atropine, glycopyrrolate) limit salivary secretions and emesis and limit or prevent bradycardia, particularly vagally induced bradycardias. Phenothiazine tranquilizers (acepromazine) reduce anxiety (anxiolytic), produce calming, and generally enhance the central nervous system (CNS) depressant or analgesic effects of other anesthetic drugs. Benzodiazepines (diazepam, midazolam) produce anxiolytic, anticonvulsant, and muscle relaxant effects. α2Agonists (xylazine, dexmedetomidine) produce sedation, stupor, analgesia, and muscle relaxation without producing general anesthesia. Opioids (morphine, butorphanol) produce analgesia; some produce sedation. The combination of an α2-agonist or tranquilizer with an opioid (neuroleptanalgesia) produces marked calming, muscle relaxation, and analgesia and light stages of anesthesia, especially in young or old animals. Postanesthetic medications are generally administered to hasten or improve recovery and include Analeptics (doxapram), CNS stimulants, generally used to stimulate respiration. Analgesics can include α2-agonists, opioid and nonopioid analgesics (meloxicam, tramadol), and specific drug antagonists including but not limited to benzodiazepine (flumazenil), α2-(atipamazole), opioid (naloxone), and peripheral neuromuscular blocking drug antagonists (neostigmine).

Purposes of Preanesthetic and Postanesthetic Drugs

Preanesthetic drugs

Facilitate physical restraint by modifying behavior (Fig. 3-1)

Reduce anxiety, fear, and stress

Produce muscle relaxation

Reduce or prevent pain before, during, and after surgery

Decrease the dose of drug required to produce sedation, muscle relaxation, analgesia, or general anesthesia

Facilitate safe and uncomplicated induction, maintenance, and recovery

Minimize or prevent the adverse and potentially toxic effects of concurrently administered drugs

Modulate autonomic reflex activity, whether of sympathetic or parasympathetic origin

II Postanesthetic drugs

Drug Categories

Anticholinergics (e.g., atropine, glycopyrrolate)

Competitively antagonize acetylcholine at sites innervated by postganglionic, parasympathetic (cholinergic) nerve fibers and on smooth muscles that are influenced by acetylcholine but lack innervation; referred to as parasympatholytics, anticholinergics, or antispasmodics

Primarily used to limit salivary secretions, prevent bradycardia, or deliberately increase heart rate

Inhibit bradycardia caused by reflex increases in vagal tone (e.g., laryngeal or ocular stimulation and vasovagal reflexes)

1. Increasing heart rate generally increases arterial blood pressure (BP) and cardiac output

2. Parasympatholytics may induce a sinus tachycardia or occasionally precipitate ventricular arrhythmias. Anticholinergic drugs may cause sinus bradycardia then progress through first- and second-degree atrioventricular block before the establishment of a faster sinus rhythm (Fig. 3-2).

3. Atropine sulfate may stimulate vagal nuclei in the medulla and, thus, induce an initial sinus bradycardia; not seen with glycopyrrolate

4. Vagal reflexes (bradycardia) produced by traction on visceral organs or during ocular surgery can be but are not always successfully treated with parasympatholytic drugs

5. General anesthetics, opioids, α2-agonists, digitalis glycosides, hyperkalemia, acidosis, and injection of calcium salts augment vagal effects and may precipitate bradycardia

Gastric pH is increased (i.e., less acidic); gastrointestinal (GI) motility and contractions of the bladder and ureters are reduced; intestinal motility can be decreased for several hours in horses, an effect that could cause colic. Ruminal atony (bloat) can occur in ruminants

Reduce glandular secretions of the respiratory tract, GI tract, oral and nasal cavities

Produce bronchodilation (increased physiologic dead space) and mydriasis

Atropine and scopolamine may produce drowsiness and potentiate the effects of CNS depressant drugs; large doses may stimulate cerebral areas, leading to restlessness, disorientation, and delirium, an effect more common in ruminants and elephants

Glycopyrrolate, a quaternary ammonium drug, does not cross the blood-brain or placental barriers

Administer intramuscularly (IM) or subcutaneously (SQ) (IV for emergencies)

1. Atropine (20 to 40 µg/kg) or glycopyrrolate (10 µg/kg) increases heart rate and dries secretions in small animals. The duration of action of atropine is 60 to 90 minutes; the duration of action of glycopyrrolate is 2 to 4 hours.

2. Parasympatholytics are of questionable value in horses and ruminants because of side effects (bloat, colic) or lack of effect, respectively

Untoward reactions

1. Atropine may slow heart rate transiently after IV administration

2. Cardiac arrhythmias: first- and second-degree atrioventricular block progressing to sinus tachycardia can be observed after IV administration of atropine or glycopyrrolate in animals with sinus bradycardia; ventricular arrhythmias may occur after IV administration

3. Sinus tachycardia increases myocardial oxygen consumption and can precipitate heart failure or pulmonary edema in animals with preexisting cardiovascular disease (heart failure) if heart rate becomes excessively rapid

4. Atropine may cause CNS depression in dogs and cats; it may cause restlessness, delirium, and disorientation in ruminants and elephants

5. Slows intestinal transit time and is thought to cause ileus and colic in horses

II Tranquilizers and sedatives (e.g., phenothiazines, butyrophenones, benzodiazepines, α2-agonists; Table 3-1)

Phenothiazines (e.g., acepromazine, promazine), butyrophenones (e.g., droperidol)

1. Mode of action

2. Physical properties

3. Produce mental calming, decrease motor activity, and increase threshold for responding to external stimuli

4. Cardiopulmonary effects

a. α-Adrenergic blockade results in vasodilation and a decrease in arterial BP (hypotension). Subsequent epinephrine administration may cause a paradoxical drop (β2 effect) in arterial BP because α receptors are blocked.

b. Heart rate usually decreases as the animal becomes calm; however, reflex tachycardia may occur if the animal becomes hypotensive

c. Antiarrhythmic effects: phenothiazines block α1-receptors, produce quinidine-like effects, and decrease central sympathetic, ganglionic, and peripheral (adrenal) activity, reducing the incidence of ventricular arrhythmias

d. Dose-dependent depression of the myocardium and vascular smooth muscle

5. Reduce respiratory rate; may decrease tidal volume when administered in large doses; decreases respiratory center sensitivity to increases in carbon dioxide (CO2)

6. Potentiate the ventilatory and cardiovascular depressant effects of α2-agonists, opioids, and drugs used to produce general anesthesia

7. Useful as antiemetics. Acepromazine and droperidol administered 15 minutes before opioids lower the incidence of vomiting.

8. Most have antihistaminic properties; phenothiazines and butyrophenones should be avoided when skin testing for allergies

9. Most phenothiazine tranquilizers cross the placental barrier relatively slowly

10. Many phenothiazine tranquilizers, including acepromazine and promazine, may cause erection (priapism) and temporary or permanent prolapse of the penis in stallions or geldings. Potentially reversible by administering benztropine (20 µg/kg IV).

11. Butyrophenone tranquilizers produce calming and antiemetic effects (see above)

12. Primary organ of metabolism is the liver; should be avoided in animals with moderate to severe liver disease or portocaval shunts

13. Clinical effects are present for 4 to 8 hours but residual effects may last up to 48 hours or longer in older animals or animals with liver disease

14. Acepromazine is the most popular and safe phenothiazine used in veterinary practice; butyrophenone tranquilizers are rarely used in veterinary medicine (Tables 3-1 and 3-2)

15. Side effects

a. Tachycardia or (rarely) bradycardia

b. Hypotension; decreases in BP may result in transient decreases in packed cell volume and plasma total protein

c. Hypothermia secondary to peripheral vasodilation

d. Acepromazine significantly decreases platelet numbers and their ability to aggregate; however, this does not produce hemostasis problems in otherwise normal animals. Avoid in animals with von Willebrand’s disease or other clotting abnormalities.

e. Akathisia: restless condition in which the patient needs to be in constant motion

f. Acute dystonic reactions: hysteria, seizures, ataxia

g. Tranquilizers alter behavior, generally producing calming and depression but can increase anxiety and produce restlessness and occasionally aggression in some dogs and cats. Their effects on the reticular formation of the pons and medulla (extrapyramidal effects) can lead to akinesia (inability to initiate movement) and akathisia (inability to remain motionless) particularly in aged animals.

Benzodiazepines (e.g., diazepam, midazolam, zolazepam) are centrally acting muscle relaxants (see Table 3-1)

1. Mode of action

a. Exert many of their pharmacologic effects by enhancing the activity of CNS inhibitory neurotransmitters (gamma-aminobutyric acid [GABA], glycine) by binding to the benzodiazepine site of the GABAA receptor and opening chloride channels, thereby hyperpolarizing membranes. This effect is produced by combining with CNS benzodiazepine (BZ1, BZ2) receptors. Effects can be antagonized by the benzodiazepine antagonist flumazenil.

b. Depress the limbic system, thalamus, and hypothalamus (reducing sympathetic output), thereby inducing a mild calming effect and disorientation

c. Reduce polysynaptic reflex activity, resulting in muscle relaxation and antiseizure effects

d. Stimulate appetite and pica

2. Physical properties

3. Recommended doses produce minimal sedation in normal animals; calming effects are observed in sick, depressed, or debilitated animals

4. Cardiopulmonary effects

Sep 6, 2016 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on Preanesthetic and Perioperative Medications

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