Anesthesia & Analgesia

Question 1

Reflex bradycardia is associated with __ administration, and is caused by

Answer 1

Dexmedetomidine; increased SVR

Question 2

Hypoventilation can occur when __ are administered with other drugs (ie, opioids, ketamine, propofil)

Answer 2

Alpha-2 agonists

Question 3

Dexmedetomidine produces profound

Answer 3

Sedation and muscle relaxation

Question 4

Analgesia provided by alpha-2 agonists has been shown to be synergistic with __

Answer 4

Opioids

Question 5

Dexmedetomidine duration of action

Answer 5

1-3 hours

Question 6

Administration of alpha-1 agonists commonly results in a __ blood pressure response: initially the patient is ____ with __ but with time the __ may decrease, resulting in ___ with continued ___

Answer 6

Biphasic; bradycardic with elevated BP, but then SVR may decrease, resulting in hypotension with continued bradycardia

Question 7

With alpha-2 agonists, in addition to bradycardia, a variety of ___ may be observed

Answer 7

Dysrhythmias

Question 8

Atipamezole has been successfully used __ in cats

Answer 8

Off-label (it’s labeled for IM use in dogs)

Question 9

Atipamezole administered IV is contraindicated because it may

Answer 9

Result in rapid relaxation of vascular tone, which, coupled with bradycardia could result in cardiovascular collapse

Question 10

It is recommended that atipamezole and anticholinergics

Answer 10

Not be used concurrently, as both can cause significant increases in heart rate

Question 11

ASA PS 1

Answer 11

Normal; no disease, elective procedure

Question 12

ASA PS 2

Answer 12

Mild systemic disease (eg, skin tumor or fracture) without shock

Question 13

ASA PS 3

Answer 13

Severe systemic disease limiting activity but not incapacitating (eg well-controlled DM)

Question 14

ASA PS 4

Answer 14

Incapacitating systemic disease that is a constant threat to life (eg, perforated small intestine and severe hypovolemia)

Question 15

ASA PS 5

Answer 15

Moribund patient not expected to live 24 hours without Sx (eg severe trauma & shock)

Question 16

The state of general anesthesia consists of

Answer 16

Unconsciousness, muscle relaxation, amnesia, analgesia, and absence of reflex responses

Question 17

Acepromazine duration of action

Answer 17

4 to 7 hours (longer with compromised hepatic function)

Question 18

Acepromazine adverse effects

Answer 18

Vasodilation (alpha-1-adtenergic blockade) –> hypotension (avoid in in hypovolemic/hypertensive patients)
Hypothermia (inhibits thermoregulation in hypothalamus via D2 receptors)

Question 19

Potentially beneficial effects of acepromazine

Answer 19

Anti-arrhythmic, anti-emetic, anti-histamine

Question 20

Phenothiazines (acepromazine) block ___ receptors

Answer 20

Dopamine-2 and alpha-1 receptors

Question 21

Acepromazine has __ effects on oxygenation/ventilation

Answer 21

Minimal

Question 22

Benzodiazepine MOA

Answer 22

Increase GABA and glycine (inhibitory) activity in CNS, resulting in sedation

Question 23

GABA and glycine receptors are found in

Answer 23

The cerebral cortex, hypothalamus, cerebellum, migraine, hippocampus, medulla, and spinal cord

Question 24

While acepromazine is considered a sedative, it is likely not an

Answer 24

Anxiolytic

Question 25

CNS effects of acepromazine

Answer 25

Sedation, muscle relaxation, ataxia, decreased motor activity, 3rd eyelid prolapse

Question 26

The increased glycine activity of benzodiazepines results in (overall effects)

Answer 26

Anxiolysis and muscle relaxation

Question 27

CNS effects of benzos

Answer 27

Anticonvulsant, sedation, muscle relaxation, (very mild) analgesia, appetite stimulation, retrograde amnesia

Question 28

Cardiopulmonary effects of benzos are __

Answer 28

Minimal, but respiratory depression if used with opiate or other anesthetic

Question 29

Benzos are rarely used in healthy patients because

Answer 29

Sedation is poor and excitement may occur

Question 30

Alpha-2 receptor agonist MOA

Answer 30

Post-synaptic alpha-2 receptor activation: vasoconstriction (vascular smooth muscle contraction) Pre-synaptic alpha-2 receptors: inhibition of NE release from terminal axons, inhibition of NE neuron firing b/c of hyperpolarization, and decreased NE turnover in CNS

Question 31

The decreased SNS outflow from alpha-2 agonists results in

Answer 31

Sedation, analgesia (spinal alpha-2 receptors), muscle relaxation (spinal alpha-2 receptors), CV depression (bradycardia, decreased contractility, vasodilation after vasoconstriction)

Question 32

CV effects of alpha-2 agonists

Answer 32

Initial vasoconstriction followed by reflex bradycardia then centrally mediated SNS depression: bradycardia, vasodilation, decrease in CO and tissue perfusion All alpha-2 agonists cause sinus arrhythmias, bradycardia, sinoatriral block, 1st & 2nd degree AV block