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Anesthesia > IV Anesthetics > Flashcards

IV Anesthetics Flashcards

1
Q

Name the 3 benzos commonly used and how are they different?

A

Differ in duration of action from short to long (half-lives):

Midazolam (2hrs)

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2
Q

Name the mechanism of action of benzodiazepines and its effects

A

α1 and α2 subunits of the GABAA receptor –> conformational change to allow GABA to bind and open channel for hyperpolarization (ceiling effect)

α1 subunit –> sedation, anticonvulsant activity, and anterograde amnesia

α2 subunit —> anxiolysis and muscle relaxation

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3
Q

Name the two pathways of benzodiazepine biotransformation in the liver.

A

microsomal oxidation
- impaired by advanced age, cirrhosis, and enzyme induction

glucuronide conjugation

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4
Q

Name the two benzodiazepines with active metabolites.

A

Diazepam - oxazepam and desmethyldiazepam
- enterohepatic circulation prolongs its effect with a secondary peak in concentration 6-12 hours later

Midazolam - hydroxymidazolam, which may lead to prolonged sedation in renal failure

Metabolites are excreted in the urine

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5
Q

For sedation, which benzodiazepine is most potent (greatest receptor affinity)?

A

Lorazepam 1mg = midazolam 2.5mg = diazepam 5-10mg

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6
Q

What is the effect of benzodiazepines on respiration?

A

reduction in resting ventilation (but lower than barbiturates)

reduction in the ventilatory response to hypoxia and hypercarbia

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7
Q

Compare the effects of different benzos on respiration.

A

Midazolam has significantly more respiratory depressant effects than diazepam or lorazepam at equipotent doses.

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8
Q

What is the effect of benzodiazepines on the carbon-dioxide response curve?

A

downward shift of the carbon-dioxide response curve.

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9
Q

What is the effect of benzodiazepines on circulation and BP?

A

modest effects
- decrease in systemic vascular resistance and ventilation –> slight decrease in arterial blood pressure

  • no effect on contractility or HR
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10
Q

What is the effect of benzodiazepines on cerebral metabolic rate (CMRO2)?

A

Decreases

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11
Q

What is the induction dose of midazolam?

A

0.15-0.25 mg/kg

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12
Q

What are some contraindications to using benzos?

A

Acute intermittent porphyria

HIV medications
- Midazolam and efavirenz compete for CYP3A4 –> midazolam toxicity

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13
Q

What are the side effects of benzos?

A

Resp depression
Delayed emergence
Delirium in elderly

Lorazepam has propylene glycol –> metabolic acidosis
Long term –> tolerance and dependence
Withdrawal –> Insomnia, anxiety, restlessness, seizures

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14
Q

What are two good options for providing anxiolysis without respiratory depression?

A

Ketamine or dexmedetomidine (requires 10min to load)

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15
Q

Describe the effects of benzos based on receptor occupancy % - 20%, 30-50%, 60%

A 
(20%) = amnesia and anxiolysis
(30-50%) = sedation
60% = unconsciousness
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16
Q

Which benzo is water soluble but becomes lipid soluble at physiologic pH?

A

Midazolam

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17
Q

What subunit is responsible for benzos sedative, amnestic, and anticonvulsant effects?

A

alpha-1 subunit

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18
Q

What subunit is responsible for benzos anxiolysis and muscle relaxation effects?

A

alpha-2 subunit

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19
Q

What are the common additives and formula of propofol?

A

Propofol + 10% soybean oil + 2.25% glycerol + 1.2% egg lecithin

Diprivan - disodium edentate and sodium hydroxide (pH 7-8.5)
Generic - sodium metabisulfite (pH 4.5-6.4)

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20
Q

What is the mech of action of propofol?

A

Activating GABA-A –> keeps Cl- channels open –> hyper polarization and inhibition of post-synaptic neuron

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21
Q

What properties of propofol explain its fast onset and recovery?

A

High lipid solubility

Rapid distribution from brain (highly perfused) to less well perfused tissues (muscle, fat)

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22
Q

Where is propofol metabolized?

A

Liver –> water soluble sulphate and glucuronic acid –> eliminated by kidneys

May have some 30% metabolized by lungs

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23
Q

Why do children require a higher induction dose and elderly a lower induction dose?

A

Kids - larger central distribution and higher clearance rate

Elderly - opposite

Hypothermia dec metabolism

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24
Q

How do you explain rapid awakening following a long propofol infusion?

A

Diffuses slowly from periphery to central –> rapidly metabolized so it’s half life is less than 40 minutes

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25
Q

How does propofol affect blood pressure?

A

Dec systemic blood pressure

  • myocardial depression
  • dec systemic vascular resistance + venodilation –> red preload

Dec baroreflex –> smaller inc in HR for given dec in BP

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26
Q

What is the effect of propofol on the ventilatory response to hypoxia and hypercarbia?

A

Dose dependent respiratory depression

More likely to induce apnea than other induction agents - etomidate, ketamine

Blunts the ventilatory response to hypoxia and hypercarbia

Decreases tidal volume and respiratory rate

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27
Q

What is the effect of propofol on cerebral blood flow and intracranial pressure?

A

decreases cerebral blood flow
decreases CMRO2
decreases ICP
does NOT affect monitoring of somatosensory and motor evoked potentials.

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28
Q

What is propofol infusion syndrome?

A

Rare often fatal
o Critically ill, high doses and long-term infusion
o Acute refractory bradycardia → asystole
o Rhabdo, tachycardia with metabolic acidosis, cardiomyopathy with failure and lipemia
o ? mitochondrial toxicity

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29
Q

How can you minimize the pain with injection of propofol?

A

Larger vein

Prior administration of lidocaine or potent opioids like fentanyl or remi

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30
Q

What is the relationship between propofol and egg allergy?

A 
Allergy = egg white (albumin)
Propofol = lecithin (yolk)
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31
Q

What is the induction dose of propofol?

A
  1. 0 - 2.5 mg/kg adult

1. 0 - 2.0 mg/kg elderly

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32
Q

What is the GA maintenance dose of propofol?

A

100-300mcg/kg/min

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33
Q

What is the induction dose of propofol for kids?

A

2.5-3.5mg/kg IV

34
Q

How does Forpropofol differ from propofol?

A

Water soluble = no pain, HLD, PE or sepsis risks

Onset and recovery prolonged

35
Q

How does methohexital differ in onset and recovery than thiopental?

A

Cleared more rapidly, faster, more complete recovery

Also more stimulating –hiccups

36
Q

With what disease must you avoid barbiturates?

A

Acute intermittent porphyria

- aminolevulinic acid synthase inc porphyrins

37
Q

What happens when you mix NMBs with barbiturates?

A

pH 10 = precipitates when mixed with acidic drugs like NMBs → irreversibly block IV lines

38
Q

Describe barbiturates effects on CMRO, CBF and ICP

A

Decreases
• Possible neuroprotection from focal cerebral ischemia
• Methohexital – activates epileptic foci = used in ECT

39
Q

Describe barbiturates effects on HR, MAP

A

Baroreceptor reflex blunting but inc in HR → transient dec in MAP

40
Q

Describe barbiturates effects on ventilation

A

Dec TV, RR –> dec MV

Dec response to hypercapnia, hypoxia

41
Q

What are the side effects of barbiturates?

A

Intra-arterial injection = excruciating pain, vasoconstriction → gangrene

Garlic or onion taste with induction

42
Q

What barbiturate is used for ECT and why?

A

Methohexital - produces longer seizure duration

43
Q

What is the mechanisms of action of ketamine?

A
  1. Non-competitive NMDA antagonist
  2. Mu-opioid agonist
  3. Antagonize muscarinic acetylcholine receptors
  4. Inhibits Na channels (modest local anesthetic effect)
  5. Inhibits Ca channels (cerebral vasodilation)

May also have effects on cholinergic, nicotinic

44
Q

Describe the onset of ketamine and its unique properties

A

Profound analgesia
Stim symp nervous system
Bronchodilation
MINIMAL resp depression

45
Q

What is the induction dose of ketamine?

A

1.0 - 2.5 mg/kg IV

5 - 10 mg/kg IM

46
Q

What is the dose of ketamine for infusion with and without nitrous oxide?

A

15-45 ug/kg/min infusion w/ NO

30-90 ug/kg/min infusion alone

47
Q

What are some of the side effects of ketamine?

A

Dissociative amnesia

  • eyes open, nystagmic gaze
  • some reflexes intact but may not be protective

Inc lacrimation and salivation

Emergence reactions

  • hallucinations, vivid dreams, fear, disorientation, euphoria
  • reduced w/ midazolam 5min b4
  • inc w/ droperidol and atropine

NOT recommended in pregnancy

48
Q

Describe the effects of ketamine on CBF and ICP and EEG waves

A

Cerebrovasodilator = INC CBF > CMRO2 –> inc ICP
These effects can be blunted by maintaining normocapnia

excitatory CNS effects –> EEG theta waves

49
Q

Describe the effects of ketamine on cardiac function

A

Inc MAP, HR, CO
Inc CNS SNS stimulation
Direct myocardial depressant
Can be blunted with co-admin of opioids, benzos, gases

50
Q

Describe the effects of ketamine respiratory system

A

Little respiratory depression
Bronchial smooth muscle relaxation
INCREASES PAP (avoid in pul HTN)
Inc secretions –> airway obstruction

51
Q

What are risk factors for developing emergence reactions with ketamine?

A 
Risk greater when >15yrs
female
>2mg/kg dose IV
psychiatric hx
atropine use
52
Q

What is the mechanism of action of etomidate?

A

Potentiates GABA-A

53
Q

Describe etomidate’s uniques properties regarding hemodynamics, N/V, and side effects

A

Hypnotic but NOT analgesia
Minimal hemodynamic effects

  • More PONV*
  • Adrenocortical suppression* – limits infusion ability
54
Q

What is the induction dose of etomidate?

A

0.2-0.3 mg/kg IV

55
Q

Describe etomidate’s effects on the CNS

A

Potent cerebral vasoconstrictor → dec CBF, ICP
No neuroprotection
May activate seizure foci (like methohexital)
Myoclonic activity in 50% of patients

56
Q

Describe etomidate’s effects on the cardiovascular system

A

MAP, HR, CO minimal change

57
Q

What is the mechanism of action of Dexmedetomidine?

A

Alpha-2 adrenergic agonist

58
Q

What is the induction dose of Dexmedetomidine?

A

0.5-1 ug/kg over 10-15min

59
Q

What is the maintenance dose of Dexmedetomidine?

A

0.2 - 1.5 ug/kg/hr infusion

60
Q

What are the effects of Dexmedetomidine on the CNS?

A

Hypnosis – locus ceruleus
Analgesic – spinal cord
Sedation – more closely resembles physiologic sleep
Decreases CBF without much change in ICP, CMRO

61
Q

What are the effects of Dexmedetomidine on cardiovascular system?

A

Mod dec HR, SVR, MAP, CO

Bradycardia may –> arrest

62
Q

What are the effects of Dexmedetomidine on ventilation?

A

Small dec in Tv

Little change in rate

63
Q

What are Dexmedetomidine’s effects pre and post-synaptically?

A

Presynaptic – inhibits NE → sedation (dec MAC)

Postsynaptic → dec symp, BP, HR, need for morphine

64
Q

What is the active metabolite of Ketamine?

A

N-demethylation by CYP450 system –> Nor-ketamine

1/3 the potency of ketamine

Coadministration w/ drugs that require hepatic metabolism –> prolong the action of ketamine up to 30%.

65
Q

What are some of the common indications for using ketamine?

A

respiratory and cardiovascular compromise (except ischemic heart disease)

reactive airway disease

hemodynamic compromise - hypovolemia or cardiomyopathy (not coronary artery disease with active ischemia)

trauma patients

septic shock

congenital heart disease patients, especially w/ propensity for R–>L heart shunting

66
Q

What are contraindications to using ketamine?

A
  1. poorly controlled hypertension
  2. active ischemic heart disease
  3. preeclampsia
  4. elevated intracranial pressure
  5. open eye injuries and procedures.
67
Q

What is the binding site of etomidate?

A

GABA-A potentiator –> enhances ability of GABA to bind –> hyperpolarization

68
Q

What property of etomidate is responsible for its rapid onset of action?

A

lipopilicity

Onset 30-60sec
Duration 3-5min

69
Q

How is etomidate excreted?

A

urine (85%)

70
Q

What is the induction dose of etomidate?

A

0.2-0.4mg/kg

35% propylene glycol

71
Q

How is etomidate metabolized?

A

plasma esterases + hepatic microsomal enzymes

72
Q

What are the common indications for using etomidate?

A

hemodynamic instability - trauma or critical care
retrobulbar block
Cardioversion
ECT - prolongs seizures

73
Q

What are the effects of etomidate on circulation?

A

MAP - stable
SVR - dec 10-15%
HR, PAP, PSOP, CO - minimal changes

74
Q

How does etomidate affect ventilation in comparison to propofol and barbiturates?

A

Minimal rest depression compared to propofol or barbiturates

Dec ventilatory response to CO2

Typically no apnea or only brief

Slight dec Vt but inc RR

Lasts 3-5min

75
Q

How does etomidate affect the CNS and the eyes?

A 
ICP - dec
CBF - dec
CMRO2 - dec
CPP - maintained 
IOP - dec for 5 min
76
Q

How does etomidate affect EEG and SSEPs?

A

SSEPs: Inc amplitude

EEG: activation at [low]; inhibition at [high]

77
Q

Describe 4 side effects of etomidate administration

A
  1. Adrenocortical suppression - for 5-8hrs, inhibited 11-b-OH
  2. Myoclonus
  3. Pain on injection - propylene glycol
  4. Greater PONV
78
Q

Describe 2 common contraindications for using etomidate

A
  1. Patient’s that require intact stress response - septic shock or hemorrhage
  2. Epilepsy/seizure prone patients - Inc excitatory spike frequency
79
Q

What might be the cause of nephrotoxicity from an etomidate infusion?

A

Propylene glycol

80
Q

What are the side effects of flumazenil?

A

N/V = #1

Seizures in chronic bento users or epileptic patients

Shorter 1/2 life than midaz

Poor oral absorption

81
Q

Which benzo can cause phlebitis, thrombosis on injection?

82
Q

What is the onset and peak of Dex?

A

Onset 5min –> peak 15min

Anesthesia (25 decks)

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