Induction agents

Question 1

Name 8 side effects of propofol. Name 2 positive effects.

Answer 1

• decreased chronotropy
• decreased inotropy
• decrease in SVR (venodilation) without increase in HR –> vasodilatory hypotension
• apnea
• hypoventilation
• enhances ability of epinephrine to induce arrythmias
• increased Heinz Body formation in cats –> hemolysis

positive:
* decreased ICP
* decreased cerebral VO2
* initial increase of IOP which then decrases below baseline after 5min

Question 2

What agents cause splenomegaly + a reduction in HCT?

Answer 2

• acepromazine
• propofol
• thiopental

Question 3

Name the cardiovascular effects of ketamine.

Answer 3

centrally medaited sympathetic response + endogenous catecholamine release causes:

• positive chronotropy
• increased BP
• increased CO
• negative inotropy during catecholamine depletion (critically ill) or if sympethetic system is blocked

Question 4

Name 3 beneficial effects of etomidate.

Answer 4

• decreased IOP
• decreased cerebral VO2
• no effects on RR or rhythm

Question 5

What is the MOA of propofol? How is it metabolised + excreted?

Answer 5

• potentiates effects of GABA at GABAA receptor -> increased influx of Cl- –> hyperpolarization of postsynaptic membrane
• possibly reduces the activity of glutamate via blockade at glycine + NMDA receptors

Metabolism: hepatic via glucuronidation + hydroxylation
Excretion: renal

Question 6

What is the MOA of ketamine? How is it metabolised + excreted? Name 2 adverse effects.

Answer 6

NMDA receptor antagonist (binds phencyclidine-binding site) –> reduces receptor activity and release of glutamate

Metabolism: hepatic via demethylation + hydroxylation (C P-450)
Excretion: renal

Side effects:
* increased muscle tone
* increased IOP

Question 7

What is the MOA of alfaxalone? How is it metabolised + excreted? Name 2 side effects.

Answer 7

potentiates effects of GABA at GABAA receptor -> increased influx of Cl- –> hyperpolarization of postsynaptic membrane

Metabolism: hepatic phase I (C P-450) + phase II (conjugation)
excretion: biliary/faeces + renal

side effects:
* hypoventilation
* apnea
* increased IOP
* cardiodepressant effects

Question 8

What is the MOA of etomidate? How is it metabolised + excreted? Name 2 adverse effects.

Answer 8

potentiates effects of GABA at GABAA receptor -> increased influx of Cl- –> hyperpolarization of postsynaptic membrane

Metabolism: hepatic (glucuronidation + hydrolysis)
Excretion: renal

Side effects:
* adrenal insufficiency (hydrocortisone has no effect on outcome)
* hemolysis (Due to propylene glycol vehicle)
* retching + myoclonus if used as sole induction agent

Question 9

What are the effects of ketamine on the respiratory system?

Answer 9

• apneuistic breathing pattern (does not cause resp. depression)
• bronchodilation + decreased airways resistance

Question 10

Name 4 effects how Lidocaine diminished reperfusion injury.

Answer 10

1. inhibition of Na+/Ca2+ exchange + decreased Ca2+ accumulation
2. hydroxyl radical scavenging
3. decreased release of superoxide from granulocytes
4. decreased polymorphonuclear leukocyte activation, migration into ischemic tissues + subsequent endothelial dysfunction

Question 11

What is the MOA of lidocaine? How is it metabolised and excreted? Name 2 adverse effects.

Answer 11

• NMDA receptor antagonist (analgesia)
• action of Na+, Ca2+ and K+channels (analgesia)
• blockage of fast Na+ channels (cardiac)

Metabolism: liver
Excretion: <10% renal (others??)

adverse effects:
* depression
* ataxia
* muscle tremors
* nausea
* vomiting
* seizures

–> no prokinetic effect in dogs

Question 12

What PCV is necessary for adequate oxygen-carrying capacity and DO2 during GA? By what % might PCV decrease during GA?

Answer 12

> 25%
–> may decrease by 3-5%