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PT2 B1 > Lecture 4 - IV Anesthetics > Flashcards

Lecture 4 - IV Anesthetics Flashcards

1
Q

Name the IV Anesthetics

what are the three goals of a balanced anesthetic technique?

A

Propofol

Ketamine

Etomidate

Dexmedetomidine

Benzodiazepines

Barbituates

Balanced technique: Amnesia, Analgesia, Muscle Relaxation. Not acheived By IV anesthetics alone; must use combination of drugs

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2
Q

Propofol

  • mechanisms
  • considerations upon administration of the drug
A

mechanism: Potentiation of chloride current mediated through the GABA Type A receptor complex; increases this conductance therefore further inhibiting the post synaptic cell and inhibiting AP

Considerations: have to use with sterile technique; Must use within 6 hours after opening; Do not give to persons with egg allergies

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3
Q

Propofol

- pharmacokinetics (lipid solubility, metabolism, excretion, redistribution)

A 
Highly lipid soluble 
Rapid onset 
			Rapidly metabolized by the liver 
			Excreted by the Kidneys 
			Redistribution -- wake  up 8-10 minutes after induction bolus
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4
Q 
Propofol -- 
CNS effects
CVD  effects
Respiratory effects 
GI
A

CNS – AMNESIA with NO ANALGESIA properties.
deceased CNS blood flow and metabolic rate
Decreases ICP
Anticonvulsant
Neuro protective

CVD – Vasodilation; Decreased systemic blood pressure

Respiratory – Depressant; suppresses upper airway reflexes

Anti-emetic

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5
Q

propofol Side effects;

what is propofol Infusion syndrome?

A

Pain on injection;

Propofol Infusion Syndrome: —
lactic acidosis via an unclear mechanism
Reversible in early stages

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6
Q

propofol Clinical uses:

A
  • Induction of anesthesia — but NOT ANALGESIA
  • Maintenance of anesthesia — As an infusion , in combination with volatile anesthetics and opioids (balanced anesthesia regimen) or with opioids and benzodiazepines (total intravenous anesthesia technique)
  • Sedation – Repeated boluses and/or intravenous infusion for procedure like endoscopy, MRI, dental extractions etc
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7
Q

Ketamine –
mechanism –
Pharmacokinetics (solubility, onset, duration, metabolism, excretion)

A

Mechanism: Antagonist of the NMDA Receptor (+some direct mu related activity). inhibits the effects of glycine and glutamine; inhibiting the Action potential

lipid soluble, low protein binding
Rapid onset, relatively short duration
Metabolized in the liver to Nor ketamine ( less potent)
Excreted in the urine 
Wake up is due to redistribution
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8
Q

Ketamine effects:
CNS
CVD
Resp

A

CNS Effects – Dissociative Anesthesia, + ANALGESIA, increased Cerebral blood flow and metabolitic rate, can produce seizure like activity (Not used for neurosurgery)

CVD - Sympathetic stimulation; Increased BP, HR, C.

Resp – No effect on rate; (apnea with rapid infusion); bronchodilator (good for asthmatics); Can increasd salivary and bronchail secretions (therefore given with glycopyrolate)

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9
Q

Ketamine –
Primary side effect:
how can this be managed?

A

Emergency Delerium; Nightmares hallucinations (decreased with benzos)

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10
Q

Clinical Uses of ketamine

how is it administered

A

• Induction of anesthesia:
IV or IM

Maintenance:
Sedation:
Post op pain

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11
Q

Etomidate
Mechanism
Pharmacokinetics (BBB penetrance; peak onset; protein binding; metabolism; excretion)

A

Mechanism of action: (similar to propofol) – potentiates GABA receptor conductance

Pharamacokinetics – rapid BBB penetrance; peak onset of 1 minute; 76% bound to albumin; Metabolism by ester hydrolysis; excreted in urine and bile

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12
Q

Etomidate effects

  • CVD
  • resp
  • CNS
  • endocrine
A

CVD – minmial changes in BP, HR; good for patients who are cardiovascularly unstable

Resp – Minimal depressant effect

CNS - cerebral vasoconstriction; decreased blood flow and metabolic rate

Endo – Adrenocortical suppression due to 11 beta hydroxylase inhibition

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13
Q

Etomidate

best clinical use

A
  • Clinical Uses:

* Induction of anesthesia — mostly for patients with cardiovascular issues

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14
Q

Dexmedetomidine -
Mechanism
Pharmacokinetics

A

Mechanism: Agonist of Alpha2 receptors in the pons; decreases NE secretion

Pharmacokintics: Water soluble; short term sedation?

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15
Q

Dexmedetomidine effects
CNS
CVD
RESP

A

CNS – Analgesia, Sedation; no effect on cerebral metabolic rate

CVD – Depression; brady cardia, hypotension

Resp System – Minimal depressant effect

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16
Q

Dexmedetomidine

clinical use

A

§ Sedation:
• Short-term sedation of intubated and ventilated patients in the ICU
• Radiological procedures, MRI and interventional radiology

general – loading dose followed by infusion

17
Q 
Benzodiazepines
name them; 
Mechanism
Pharmacokinetics 
(differences in metabolism)
A

Midazolam, Diazepam, Lorazepam (Ativan)
Mechanism of action -
Enhance affinity of the GABA receptor for GABA
HOWEVER There is a specific binding site

Pharmacokinetics
§ Highly protein bound to albumin
§ Highly lipid soluble
§ Hepatic metabolism:

Midazolam – metabolite is inactive
Diazepam – 2 metabolites are both active; patients have a “hangover” – not a preferred drug

18
Q

Benzodiazepines
effects

CNS
RESP
CVD

a negative side effect

A

CNS: Sedation, hypnosis, anterograde amnesia
Anticonvulsant

RESP: minmal resp depression

CVD – slight decrease in systemic vascular resistsnace and BP

Pain with injeciton with Diazepam (like propofol) —

19
Q

Benzodiazepines
how is it adminstered
best clinical use ?

A

Pre-operative Medication –
• Midazolam – can be given IV, PO, Rectally, Intranasal
• Diezepam – PO

20
Q

Barbituates

name a few
Mechanism
Pharmacokinetics –

A

Thiopental, Methohexital

Mechanism: GABA receptor potentiation

Pharmacokinetics – Metabolized in the liver, excreted in the urine; enhanced effects with alcohol

21
Q

Barbituates

CNS effects - (general effects; which one can activate epileptic foci)
CVD
RESP

A 
CNS effects:  Sedation, anesthesia
NO ANALGESIA 
↓CBF, ↓ICP, 
↓CMRO2 ;
Methohexital activates epileptic foci

Cardiovascular system:
• Peripheral vasodilatation with modest ↓ in BP

Respiratory system:
Respiratory depressant effect: ↓minute ventilation, tidal volume and respiratory rate
↓ventilatory responses to hypercapnia and hypoxia

22
Q

Barbituates

  • consideration take when giving bolus through a line? (why?)
    a primary side effect
    exacerbation of what disease?
A

Precipitation when mixed with acidic drugs in an IV line, due to its Alkaline pH

		* Pain, intense vasoconstriction and gangrene on intra-arterial injection
		* Exacerbation of acute intermittent porphyria;
23
Q

Barbituates

clinical uses?

A

(BUT NOT USED ANYMORE)
Induction of anesthesia:

Neuroprotection:
Treatment of raised intracranial pressure
Treatment of focal cerebral ischemia

PT2 B1 (38 decks)

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