Opioids, IV anesthetics Flashcards
(27 cards)
Barbituric acid
Cyclic compound
Formed from condensation of urea and malonic acid
No intrinsic CNS activity alone
Replacing both H atoms at position 5 with alkyl- or arylgroups
produces sedative hypnotic action
do barbiturates have analgesia?
no. it is possible to give enough to get an analgesic effect but they are not analgesics
Etomidate
Carboxylated imidazole derivative CNS effect results in hypnosis No intrinsic analgesic properties Offers CV stability with a wider margin of safety and less ventilation impairment Gaba agonist Gaba antagonists can antagonize etomidate effect **good for unstable patients**
Etomidate-Side Effects
Pain on injection(30-80%) Myoclonia (shock-like contractions of part of muscle[entire or group]-looks like convulsion)—33% Hiccups (1-10%) Adrenocortical suppression Nausea and vomiting
Adrenocortical suppression
suppression of catecholemine release
catecholimines start what response?
sympathetic response
repeated exposure to etomidate may have what effect?
decreases CV stability of the drug
Dextro goes to the
right
Levo goes to the
left
Most important clinical pearl of Etomidate
your patient may not go apneic after induction dose
Ketamine
Chemical structure 2-(O-chlorophenyl)-2-
methylamino) cyclohexanone
Pka 7.5-partially water soluble
3.5-5.5 pH
Produces “dissociative anesthesia” -Eyes remain open with slow nystagmic gaze -Patient noncommunicative -Amnesia -Intense analgesia -EEG evidence of disconnect between thalamus and limbic system -Controlled substance
Response to visual, auditory and pain stimuli are not what we expect in normal circumstances (hallucinogenic effect)
May bind to opioid receptors
Does not interact with GABA receptors
why use glyco with ketamine
to reduce the salivary increase of ketamine
Ketamine Metabolism
Biotransformation: hepatic microsomal enzymes
Primary path: Ctyochrome P-450 demethylation
metabolite I,norketamine
Hydroxylationhydronorketamine metabolites 1,2,3
Eliminated primarily renal
Ketamine IM route
Peak plasma concentration occurs within 22 minutes Dosage 3-5mg/kg Onset 2-3 min “Ketadart” 2mg/kg Ketamine 0.2mg/kg Midazolam 0.02mg/kg Glycopyrrolate
Ketamine Pt population uses
Combative children especially in dental (consideration
give glycopyrrolate)
Down’s Syndrome patients
Burn patients (debridement)
Obstetrics (just before delivery or an adjunct to regional anesthesia) high doses increase uterine tone and possible loss of consciousness
Ketamine Uses
Sedation for kids away from OR- cardiac catheterization, radiation
Glycopyrrolate important-decrease salivation
Preferred children with tetralogy of fallot.
Not used in pts with WPW syndrome
Propofol Dosage and Admin
Only given intravenously
General Induction
1.5-2.5mg/kg ASA I-II
May consider decreasing the dose in ASA III-IV
General Continuous Infusion
100-300mcg/kg/min
Propofol MAC bolus
10-20mg titrated to effect
Be careful not to induce apnea
Wait 60 seconds before additional dose
Propofol MAC Continuous infusion
25-100mcg/kg/min
Bolus is not necessary or recommended by
manufacturer
Myocardial depression
the heart literally pumps weaker
preload drops
blood pressure deviation goal
20-25%
Propofol CV considerations
Decreases SVR and systemic B/P more than
equipotent doses of pentothal
Thought to be inhibition of sympathetic nervous
system mediated vasoconstrictor nerve activity
Negative inotropic effect
Inhibits intracellular calcium uptake
Heart rate remains unchanged
Questionable association with bradycardia
Propofol Advantages
Fast onset-less than a minute. Duration 4 minutes
Low incidence of excitatory phenomena
Less N &V
Fast recovery with less “hangover” effect
Recovery of psychomotor function is rapid
Propofol Disadvantages
Incidence of apnea is greater with propofol than with
pentothal
Cardiovascular effects similar or even greater than
pentothal. Combo with fentanyl increases hemodynamic depression
Neuromuscular blocking agents-increasing blockade in steady state infusions but does not increase duration
