Table top Flashcards

(80 cards)

1
Q

Propofol properties:

A

Lipid emulsion with pH of 7-8.5
Has Disodium edetate - preservative to inhibit bacterial and fungal growth

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2
Q

Generic prop contains what?

A

Sodium metabisulfite or benzyl alcohol - both preservatives to inhibit bacterial and fungal growth

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3
Q

What can sodium metabisulfite cause?

A

Allergic reaction specifically in patients w asthma

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4
Q

Opened syringes of prop should be discarded within___

A

6 hrs

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5
Q

Prop MOA:

A

GABAa receptor activation - causes Cl- to enter the cell resulting in hyperpolarization –> decreases action potential

Propofol DIRECTLY stimulates gaba (GABA MIMETIC) and causes increase in Cl in cell inhibits AP’s

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6
Q

Prop pharmacokinetics: Onset/duration

A

Distributes rapidly to brain (VRG)
Onset - 5-30 seconds

Rapid redistribution - duration of action 5-15m

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7
Q

prop pharmakokinetics Metabolism

A

In liver by CYP2B6, UFTHP4, CYP2C6

HIGHLY PROTEIN BOUND (98%)
- If given to patient plasma protein levels may increase increase the free active fraction and in turn increase effects

Elim half likfe - 1-2hrs

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8
Q

Prop Pharmacodynamics in brain

A

Decreases CBF, CMRO2, ICP, CPP

DUE TO decrease in MAP, metabolic rate, cerebral vasoconstriction

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9
Q

Prop dynamics CV

A

Decreases sympathetic tone and vasodilates –> lowers BP

Predictors - ASA III + IV
Age >50 - REDUCTION in dose by 50% in elderly over 80
Baseline MAP <70mmHG
Coadministration with fentanyl

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10
Q

Prop Respiratory dynamics:

A

DECREASE Tv

Minimal bronchodilating effect

Apnea - based on dose, speed of injection, patient characteristics and other resp. depressants

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11
Q

Prop other systems dynamics:

A

-Antiemetic effect - due to decreases in serotonin levels

Antipruritic effect

Pain on injection - reduced by Lidocaine 20-40mg pre-injection AND use of antecubital vein (Larger vein)

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12
Q

PROP numbers:

A

Induction Dose: 1-2mg/kg
Onset: 5-30 seconds
DOA: 5-15 mins
Elim half life: 1-2Hrs

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13
Q

Coadministration of prop with ____ can cause increase in propofol concentrations:

A

Midazolam - may also decrease metabolic clearance

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14
Q

Etomidate MOA:

A

GABA mimetic

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15
Q

Etomidate pharmacokinetics:

A

Lipid soluble

Distributes rapidly to brain and VRG - Onset - 5-30 seconds

Rapid redistribution - DOA - 5-15min

76% protein bound

Metabolized in liver by hepatic enzymes AND PLasma esterase - ester hydrolysis

Elim half life - 2-5 hours

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16
Q

CNS dynamics of etomidate:

A

Dose depenent CNS depression

Decreased CBF, ICP, CMRO2

CPP Remains the same - due to no decreases in MAP with adminstration (see cardiovascular effects)

Causes MYOCLONIA - sudden, generalized, asynchronous muscle contractions

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17
Q

Etomidate dynamics CV:

A

Hemodynamic stability when compared to prop - no sign. changes in HR, PAP, CI, SVR, SBP

ACTS as an agonist at alpha2 adrenoreceptors which can increase blood pressure

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18
Q

Etomidate dynamics respiratory:

A

Dose-dependent resp. depression

Decrease in MV, RR

Can cause apnea

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19
Q

Etomidate and adrenal gland:

A

Cause suppression of plasma cortisol for up to 24 hours after induction dose of etomidate due to inhibition of 11bhydroxylase enzyme

NEED to take caution when giving to septic patients

Septic patients - have adrenal insufficiency 2-3 times as long as nonseptic patients

Etomidate may increase mortality

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20
Q

Adverse effects of etomidate:

A

Myoclonia
Pain on injection (90%) d/t prop glycol
N/V (30-40%)

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21
Q

Contraindications of etomidate:

A

known sensitivity
Adrenal suppression
Acute porphyria

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22
Q

Etomidate numbers:

A

Induction dose: 0.2-0.3mg/kg
Onset: 5-30s
DOA: 5-15m
Elim halflife: 2-5hrs

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23
Q

Ketamine MOA:

A

Water soluble w a pH of 3.5-5.5

Class: Phencyclidine derivative

NMDA Antagonist - selective depression of afferent signals of pain perception to thalamus and cortex

Blocks GLUTAMATE from binding to receptor and causing rapid influx of NA, CA, and K

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24
Q

What is ketamine helpful in preventing?

A

Opioid induced hyperalgesia

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25
Ketamine pharmacokinetics:
Crosses BBB to achieve rapid onset - 3-5mins IV Duration 15-30mins
26
Hepatic metabolism of ketamine:
P450 Demethylation --> metabolite NORKETAMINE (20-30% activity of ketamine Slower elimination half life than prop +etomidate Elim half life of norketamine - 2-3 hrs
27
Ketamine dynamics CNS:
INCREASED CBF, CMRO2, ICP Dissociated state - lacrimation - salivation - eye blinking - airway reflexes intact - skeletal muscle tone increased - emergence delirium - vivid dreaming, sense of floating, illusions hallucinations, combativeness, restlessness
28
CV dynamics ketamine:
Circulatory stimulant via endogenous cat release + inhibition of neuronal and extraneuronal uptake of norepi --> INCREASES in BP, HR, and contractility and CO
29
Respiratory dynamics ketamine:
Ventilation and respirations are preserved Bronchodilating agent - used for asthmatics
30
Ketamine numbers:
Dose - 0.2-0.8 mg/kg IV Onset: 1-2 minutes IV DOA: 15-30mins Elim half life: 2-3 hrs
31
Midazolam properties:
Highly protein bound - 94-98% and highly lipohilic - large volume of distribution Dose 0.02-0.04mg/kg for premedication Onset 1-3 mins GABAa agonists --> INcrease the FREQUENCY of chloride channel opening --> hyperpolarization Has sedative, hypnotic, and anxiolytic and amnestic (Anterograde) properties Allows GABA itself to work, physiological ceiling - limited amount of gaba that can be agonized and bound
32
Kinetics of midazolam:
Midazolam has shortest half life (<6hrs) due to higher rate of clearance Extensive protein binding (95%)
33
Metabolism of midazolam:
P450 METABOLITE - 1-hydroxymidazolam has 20% potency Elim half life - 1.5-3 hours
34
CNS and resp dynamics midazolam
Decrease CMRO2 and CBF Anticonvulsant May decrease upper airway reflexes and central respiratory drive in high enough doses - PREMEDICATION doses typically do not depress resp system Flattens resp curve to CO2
35
Other dynamics of midazolam>
Potential prevention of PONV Minimal local tissue and vein irritation
36
Midazolam numbers:
Dose: 0.02-0.04 mg/kg (IV for premedication - typically 1-2mg IV) Onset: 1-3 mins Duration of action: 20-30 mins Half life: 1.5-3 hours
37
Benzodiazepine reversal and MOA:
Flumazenil - competitive antagonist to benzo's - efficacy depends on free benzodiazepines at receptor sites Dose: 0.2mg IV (Up to 1mg) Onset: 1-2mins Duration: 45-90mins
38
Succ MOA:
Depolarizing neuromuscular blocker - mimics action of Ach at motor endplate
39
Hydrolysis of succ:
By plasma cholinesterase - pseudocholinesterase, T II cholinesterase, Nonspecidific cholinesterase, plasma cholinesterase, false choinesterase
40
Succ pharmacokinetics:
Acts as initial agonist at nicotinic receptor --> causes rapid onset of action - 30-60 seconds Rapid half life - 5-10 mins duration
41
Succ CNS dynamics:
No effect on CNS - quaternary ammonium - water soluble Can increase ICP and IOP indirectly - 10-15mmHg for 5-8 mins after administration
42
CV dynamics Succ:
Initial tachy followed by sudden abrupt brady (repeat dosing) Brady is due to Parasympathetic muscarinic and autonimic ganglia receptor stimulation
43
Electrolytes with SUcc:
Increase K 0.5-1mEq/L for 5-10mins
44
Dibucaine test:
Dibucaine - local amide anesthetic that inhibits typical pseudocholinesterase but not atypical 80 - means 80% has been inhibited (Typical) 20 - means 20 percent typical inhibited - atypical ATYPICAL causes prolonged apnea and mechanical ventilation
45
What do lower levels of typical pseudocholinesterase occur in?
Elderly Pregnant chronic renal disease chronic liver disease
46
47
Succ numbers:
Dose - 1-1.5mg/kg IV Onset - 30-60s DOA: 5-10min
48
Roc class
Non depolarizing NMB - competitive antagonists at the neuromuscular jucntion (directly compete with AcH Aminosteroid class (along with panc/vec) - benzylisoquinolinium class (Atracurium, mivacurium, cisatracurium Ionized hyrophilic compounds --> not lipid soluble --> do not cross BBB
49
Typically for Roc _____ the ED95 is used for intubation doses d/t low potency
2-3x
50
Rocuronium elimination:
Mainly through hepatic elim (70%) but the kidenys functionally eliminate 30%
51
Numbers of roc (Doses for RSI too)
Dose: 0.6-1mg/kg IV RSI Dose: (0.9-1.2mg/kg) Onset: 1.5-3mins Duration: 30-70 mins
52
Vec class:
Nondepolarizing neuromuscular blocker - aminosteroid
53
Vec numbers and elimination:
Dose: 0.1mg/kg Onset: 3-4mins Duration: 30-45mins Eliminated via hepatic and renal mechanisms
54
Neostigmine class and function:
Cholinesterase inhibitors: Carbamic acid ester with a quaternary or tertiary ammonium group - IT FORMS a carbamyl-ester complex on cholinesterase which inhibits it --> leading to more ACH around the receptors --> causing ACH to compete against neuromuscular blocker and bind at the site Has a ceiling effect based on TOF
55
Numbers of neostigmine:
Dose: 0.025-0.075 mg/kg Onset: 5-15mins Duration: 45-90mins Elim - 50% renal 50% plasma esterase
56
SE of neostigmine:
Vagal stimulation Bradycardia hypotension bronchoconstriction hypersalivation Diarrhea PONV DUMBBELLS Defecation urination miosis bradycardia emesis lacrimation lethargy salivation
57
Sugammadex class:
Selective relaxant binding agent - encapsulates and forms a tight water-soluble complex at a 1:1 ratio with steroidal neuromuscular blocking drugs Sugammadex - relaxant complex is excreted in the urine
58
Sugammadex doses for each twitch level:
2/4 twitches: 2mg/kg 0 Twitch but 1-2 PTC: 4mg/kg Immediate reversal after 1.2mg/kg roc - 16mg/kg
59
Half life and onset of sug
2-3hours onset - 1-3 mins
60
Adverse effects of sugammadex
N/V Allergy Binding with oral contraceptives
61
Anticholinergics action:
Competitive inhibitors of Ach on Parasympathetic muscarinic receptors FREQUENTLY used with/before cholinesterase inhibitors to prevent side effects
62
Glyco info:
Most frequently used anticholinergic Does not cross BBB Has a better antisialogogue activity than atropine
63
Numbers for glyco:
dose 0.2 for every 1mg of neostig Onset: 1-2 mins Duration: 2-4 hours
64
Atropine info:
STRONGEST anticholinergic for treatment of bradycardia Crosses BBB
65
Numbers for atropine:
Dose: 0.4-0.6mg Onset: 1-2 m Duration 4 hours
66
If low doses of atropine are given_____
May cause transient bradycardia through blockade of presynaptic, parasympathetic M1 receptors
67
Epinephrine class and action:
Naturally occurring cat Stimulates both alpha and beta receptors Used for anaphylaxis and cardiopulmonary resuscitation
68
Beta 1 stimulation:
cardiac stiulation, positive inotropy, chronotropy, and dromotropy
69
Beta 2 stim
Vasodilation, bronchodilation
70
Alpha stim
Vasoconstriction at higher doses
71
Different doses of epinephrine:
0.1-1mg for cardiac resuscitation 5-100mcg IV intraoperative hypotension - not first line choice
72
Phenylephrine class:
Pure alpha agonist - increases peripheral resistance Can cause reflex bradycardia
73
numbers of phenylephrine:
Dose: 40-100mcg IV Onset: <1min Duration: 5-20m
74
Vasopressin class and action:
endogenous hormone that is produced in the hypothalamus and stored in the posterior pituitary Also referred to as antidiuretic hormone ADH Potent vasoconstricor + dilates renal afferent, pulmonary and cerebral arterioles
75
Numbers for vaso:
Dose: 1-2units (IV bolus) or 0.1 - 1.0 unts/min (infusion) Onset: 1-5 min Duration: 10-30min
76
Ephedrine class and action:
Synthetic noncat sympathomimetic STIMULATES alpha and beta receptors directly AND causes indirect release of cats - increases BP, CO, and HR/SVR
77
Numbers for ephedrine:
Dose: 5-25mg IV onset: <1min Duration: 15 min-1.5hrs
78
Esmolol action and numbers:
Selective B1 blocker - targets HR Rapid ONSET AND METABOLISM - due to hydrolysis by nonspecific plasma esterase Dose: 10-20mg IV Onset: 2 mins Duration: 10-15 mins
79
Metoprolol action and numbers:
Selective B1 blocker - targets HR Dose: 1-5mg IV Onset: 2 minutes Duration: 4 hours
80
Labetalol action and numbers:
Nonselective beta blocker - also possesses alpha blocking compenent (Vasodilation) 7:1 ratio of beta: alpha blockade Beta 1 blockade - decreases HR, contractility Dose: 0.25mg/kg but usually given in 2.5-10mg bolus doses IV Duration 2-6 hours