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IV induction agents
| Question | Answer |
|---|---|
| Reticular Activating System | in brain stem responsible for maintenance of wakefulness |
| Barb pharmacokinetics | A: genl IV indux D: highly lipid soluble, highly protein-bound, quick recovery (M>T)d/t redistr to muscles B: liver (M>T) E: renal |
| Barb geriatric considerations | greater CNS effects. decr dose 30-40% d/t incr Vd (protein bidning) |
| Barbs in the brain | constrict cerebral vasc--> decr blood flow and ICP incr CPP (relative to decr ABP) decr cerebral O2 consumption protects against transient focal ischemia |
| Thiopental induction dose | 3-6 mg/kg IV |
| Methohexital induction dose | 1-2 mg/kg IV |
| Grand mal seizure control | benzos & barbs x Methohexital |
| Which benzo is water soluble? | midazolam (at pH <6) |
| propylene glycol in which agents | diazepam lorazepam |
| half lives of benzos | midazolam quickest hepatic clearance r/t other benzos |
| therapeutic effect of benzos r/t receptor occupancy | 20% anxiolytic 30-50% sedation 60+% unconsciousness |
| benzo potency/affinity for receptors | lorazepam>midazolam>diazepam |
| sedation dose for midazolam | 0.5-2.5 mg IV steep dose response curve |
| CNS effects of benzos | anterograde amnesia, hypnosis, sedation, & anxiolysis prevents/controls grand mal seizures (esp diaz) muscle relaxation at spinal cord (not NMJ) decr cerebral blood flow/ICP |
| CV effects of benzos | HR may incr d/t vagolytic effect or remain wo change. mild systemic vasodilation and decr CO (pronounced changes if rapid push or with opioid) |
| benzo distribution | large Vd, quickly crosses BBB small, lipid-soluble, weak base, highly protein-bound relatively slow use as indux agents |
| MOA benzos | high affinity for GABA receptors in CNS esp cerebral cortex Cl- ion in --> hyperpolarization (minimal circulatory effects) |
| diazepam seizure dosing | 0.1mg/kg to abolish seizures r/t locals, ETOH, and status epilepticus |
| benzo +valproate | psychotic episode |
| diazepam + heparin | heparin displaces diazepam on proteins --> increased free [ ] |
| midazolam + erythromycin | midazolam metabolism inhibitied -->longer duration |
| opioids + benzos | synergistic~ decr BP, decr BP apnea risk |
| benzos + pregnancy | no! B HCG before benzos to any female of child-bearing age. risk cleft lip/palate, fetal depression |
| MOA flumazenil | competitive antagonist to benzos. onset 2 mins, peak 10 mins 45-90 mins duration (need to redose as benzo outlasts). dose 0.3 mg IV Q 30-60 seconds MAX 5 mg |
| Flumazenil cautions | contraindicated TCA overdose, benzos for seizure, control benzos for incr ICP. caution if long-term benzo use d/t withdrawal |
| poorly managed HTN with barb induction | wide swings in BP |
| what agents are highly protein bound | barbs. etomidate. benzos. opioids (fent, sufent, alftent) low albumin--> incr Vd |
| ketamine causes what type of anesthesia? | dissociative anesthesia- appears conscious but unable to process or respond to sensorium. thalamus is dissociated from limbic cortex which is resp for awareness of sensation |
| safest induction choice for cardiac pt | etomidate cause minimal CV effects (sl decr in PVR/BP). high dose opioids |
| Ketamine biotransformation | short half-life (hepatic extraction ratio =0.9). biotransformed to sevl metabolites. elimination T1/2= 2 hr |
| ketamine distribution | very high lipid solubility and low protein binding (r/t thiopental). quick cerbral uptake and redistribution |
| Ketamine CV effects | incr BP, HR and CO. d/t central stim of SNS and inhibition of norepi reuptake (adrenergic receptors) |
| Ketamine Resp effects | potent bronchodilator. upper airway reflexes remain intact. |
| Propofol pharmacodynamic for turnover | quick onset and awakening d/t high lipid solubility. lesser hangover and antiemetic=quicker recover |
| Popofol and LMA | depresses upper airway reflexes wo paralysis. |
| propofol MOA | increases activity at GABA synapses used for sedation, induction and maintenance |
| propofol biotransformation | hepatic metabolism. plasma clearance exceeds hepatic blood flow. minimal cumulative effects even if liver or renal dysfunx. |
| propofol and CNS | decr CPP, CBP, and ICP. anticuonvulsant properties. no analgesia |
| propofol and CV effects | decr BP (more so than thiopental). exag in hypovolemia, elderly, cardiac compr...esp if large, rapid admin. HR genl unchanged. can have bradycardia 2/2 heart block. |
| propofol and resp | depress ventilation with inhib to hypoxia and hypercarbia response. Bronchodilation in COPD pt! some histamine release. upper airway depression. |
| propofol induction dose | 1-2.5 mg/kg IV expect hypoTN |