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side effects of nitrous-Diffusion hypoxia (n2o washes out all the oxygen in lungs = hypoxia and decreases drive to breathe) = prevent with 100% o2 at the end of the caseabsolute contraindications of nitrous-deficiency of enzyme or substrate in methionine synthase pathway
-potential toxicity from expansion of gas-filled space (emphysema, pneumothorax, middle ear surgery, pneumocephalus, air embolus, bowel obstruction)
-increased ICPrelative contraindications of nitrous-pulm htn
-prolonged anesthesia >6 hours
-first trimester of pregnancy
-high risk PONVISO MOA-Unknown
- thought to be due to multiple receptor interactions and diverse ion channels; immobility = thought to be inhibition of excitatory pathways = glycine, Na, and NMDA receptor actionDES MOA-Unknown
- thought to be due to multiple receptor interactions and diverse ion channels; immobility = thought to be inhibition of excitatory pathways = glycine, Na, and NMDA receptor actionSEVO MOA-Unknown
- thought to be due to multiple receptor interactions and diverse ion channels; immobility = thought to be inhibition of excitatory pathways = glycine, Na, and NMDA receptor actionISO
MAC
BG
OGMAC: 1.2
BG: 1.4
OG: 99ISO PD-Increases CBF and decreases CMRO2 = uncoupling
-SSEPs = increased latency and decreased amplitude
-decreases MAP the most
-dilates coronary arteries the most
-can produce irritant effects at high MAC like desinhalational agents that can cause emergence delrium in kidsdes and sevoDES
MAC
BG
OGMAC: 6
BG: .42
OG: 18.7inhalational agent that needs a special vaporizer and whydes, due to high vapor pressure = could boil at normal tempsdes PD key points-Increases CBF and decreases CMRO2 increased = uncoupling
-airway irritant
-increases HR (at high doses >6%) and BP
-decreased SVR
-supports CI best at high doses
-SSEPs = increased latency and decreased amplitudecaution with desmost likely to cause CO formation with co2 absorbers; airway irritantsevo
MAC
BG
OGMAC: 2
BG: .6
OG: 50inhalational agents used for inhalational inductionssevo and nitrousPD of sevo-Increases CBF and decreases CMRO2
-Produces bronchodilation
-Produces the least vasodilation, least heart rate changes
-SSEPs = increased latency and decreased amplitude,
-does not increase CVPcaution with sevocan cause compound a when degraded in soda lime
-most flouride ion production= use with caution in renal insufficient ptsavoid sevo with these populations-kids with hx of seizures = sevo can augment seizures
-renal insufficient patientsMOA/class of midazolamMOA: GABA allosteric agonist = Binds to the benzodiazepine receptor site. Enhances affinity of the GABAa receptors for GABA. Increases the frequency of channel opening.
Class: benzoproperties of midazolam: Y/N
anxiolytic
muscle relaxant
anticonvulsant
analgesic
sedative
hypnotic
amnesicanxiolytic - Y
muscle relaxant -Y
anticonvulsant -Y
analgesic -N
sedative -Y
hypnotic -Y
anterograde amnesic -Yproperties of propofol - Y/N
anxiolytic
muscle relaxant
anticonvulsant
analgesic
sedative
hypnotic
amnesicanxiolytic - Y
muscle relaxant - N
anticonvulsant -Y
analgesic -N.
sedative -Y
hypnotic -Y
amnesic - Yetomidate properties Y/N
anxiolytic
muscle relaxant
anticonvulsant
analgesic
sedative
hypnotic
amnesicanxiolytic - Y
muscle relaxant - N
anticonvulsant - N
analgesic - N
sedative - Y
hypnotic - Y
amnesic - Yketamine properties Y/N
anxiolytic
muscle relaxant
anticonvulsant
analgesic
sedative
hypnotic
amnesicanxiolytic - Y
muscle relaxant -N
anticonvulsant - N
analgesic - Y
sedative -Y
hypnotic -Y
amnesic -Ymidazolam dosing, OOA, DOA, and half lifedosing
Preoperative: IV: 0.02-0.04 mg/kg
PO: 0.4-0.8 mg/kg
Induction: IV: 0.1-0.4 mg/kg
OOA: IV: 30-60 sec
PO:30 minutes
DOA: 20-30 minutes
Half life: 2-4 hrsMidazolam absorptionCharacterized by a pH dependent ring-opening phenomenon
Rapid GI absorption
Slow effect site equilibrationmidazolam distribution95% protein bound
Highly lipid soluble (rapid distribution/redistribution)
high VDmetabolism of midazolammetabolized by CP450 (CYP3A4) in liver
Active metabolites: 1 hydroxymidazolam - Ā½ activity and 4-hydroxymidazolam
Cleared by kidneysexcretion of midazolamMetabolites are excreted mainly as conjugated
45-57%1-hydroxymidaz excreted in urine as a conjugatemidazolam active metabolites1 hydroxymidazolam - Ā½ activity
4-hydroxymidazolamPD of midazolam key points-decr. CMRO2 and CBF (induction dose)
-cerebral vasomotor responsiveness to CO2 is preserved
-no change in ICP
-POTENT ANTICONVULSANT (status)
-paradoxical excitement can occur (tx with flumazenil)
-spinal mediated skeletal muscle relaxation (antispasmodic)
-provide anxiolysis
-does NOT provide analgesia
-min CV response
-dose dependent decrease in ventilation (induction dose)
-Does not prevent blood pressure and heart responses evoked by intubation of the tracheaside effects with midazolam-CYP450 inhibitors = slow metabolism of midaz
-Competes with fentanyl for metabolism
-hepatic clearance midaz> lorazepam> diazepam
-COPD and combination with fentanyl - greater ventilatory depression
-depression of the swallowing reflex and decrease in upper airway activity
-decrease BP with opioids/heart disease/ elderlytype of effect of midaz with opioidsSYNERGISTIC effect of respiratory depressionMOA/class of thiopental-barbiturate
-GABAa agonist, may act on glutamate, adenosine, and neuronal nAChR
-used for inductiondosing of thiopental-Induction dose: 2.5-5 mg/kg
-ā in peds
ā in elderly, pregnancy, premedication w/ benzo/narcotic, liver disease, HF, shock, severe anemia
-Long half-life (10x propofol)
ā in peds d/t rapid hepatic clearance
ā in pregnancy d/t ā protein bindingdistribution of thiopental-Rapid distribution accounts for rapid termination of effects after a single induction dose.
-Increased lipid soluble and greater hypnotic potencymetabolism of thiopentalmetabolize in the liver by oxidation.
Metabolizes into pentobarb.
Depends on hepatic metabolism.
Low hepatic extraction ratio - capacity dependentexcretion of thiopentalvia the kidney
-rapid onset and awakening. Rapid distribution and redistributionbarbiturates PD-burst suppression on EEG
-decr. CMRO2, CBF, ICP
-reverse steal effect
-monitor SSEPs
-decr. MAP and CO, but increase in HR
-central apnea, not as much bronchodilation, airway reflexes maintained
-can cause bronchoconstriction d/t histaminethiopental indications-used for induction
-maintenance infusions of barb coma in pts with increased ICP after acute TBIbarbiturates contraindications-Enzyme induction can cause accelerated metabolism: anticoag, phenytoin, tricyclic antidepressants, endogenous substances (corticosteroids, bile salts, vit K).
-can exacerbate intermittent porphyriaMOA/class of methohexitalbarbiturate
GABAa agonist, may act on glutamate, adenosine, and neuronal nAChRbarbituatesmethohexital and thiopentaldosing of methohexital-Induction does: 1-2 mg/kg
(Rectal in peds) 25 mg/kg
(Sedation/GA) 50-150 mcg/kg/min
-Long half-life (10x propofol)
ā in peds d/t rapid hepatic clearance
ā in pregnancy d/t ā protein bindingexcretion for methoheixtalvia kidney
-rapid onset and awakening. Rapid distribution and redistribution.metabolism for methohexital- metabolized in the liver by oxidation. Depends on hepatic metabolism. Low hepatic extraction ratio - capacity dependentdistribution of methohexitalRapid distribution accounts for rapid termination of effects after single induction dosemethohexital key point-increased hypnotic potency and decreased seizure threshold (causing myoclonus on induction)indications for methohexital-induction agent of choice for a pt undergoing ECT.
-therapeutic effect related to duration of sz
-induction agent, infusions for general anesthesia, prolonged infusions can cause seizuresmeperidine MOA/class-opioid agonist
-Binds to mu and kappa opioid receptors
Mu produces analgesia, while stimulation of kappa receptors decreases shivering thresholdindictation for meperidinePost-op shiveringdosing/DOA/half life of meperidine12.5 mg IV (for shivering)
DOA: 2-4 hours
half life = 3-5 hoursmeperidine PKA: potency: 1/10th of morphine
M: extensive first pass metabolism
Normeperidine is Ā½ as active as an analgesic, produces CNS stimulation
60% bound to plasma proteins.meperidine metabolite/sigNormeperidine is Ā½ as active as an analgesic, produces CNS stimulation = can cause seizuresPD of meperidineIncreases HR- has a mild atropine-like effect on the smooth muscle
Delirium and seizures with the accumulation of metabolite normeperidine
Serotonin syndrome. Avoid use in pts taking MAOIs or fluoxetine. Autonomic instability... HTN, tachycardia, diaphoresis, hyperthermia, agitation, hyperreflexia
high doses, negative inotropy and histamine release.contraindications of meperidineElderly, renal, pts taking fluoxetine or MAOIsMOA/Class of fentanylopioid agonist
Binds to mu, kappa, and delta receptors to produce analgesiafentanyl dosing/effect site time1-2 mcg/kg IV
effect site time: 6.4 mins
Large Vd d/t high lipid solubility
Continuous infusion >2 hours increases the context-sensitive half timePK of fentanylA: more rapid onset and shorter duration than morphine. Highly lipid soluble. Effect site equilibration time 6.4 minutes.
D: significant first pass pulmonary uptake
M: metabolized by CYP450, inactive metabolites
E: kidneysPD of fentanylModest increase in ICP.
Can be used to attenuate emergence delirium with inhaled anesthetics
No histamine response.
Reduces MAC-BAR
Synergistic with propofol and midazolam
Carotid baro-reflex control of HR depressed
Large doses: skeletal muscle rigidity of chest and abdomen
Myoclonus- depression of inhibitory neuronsmoa/class of senfentanilopioid agonist
Mu agonist
analogue of fentanylsufentanil dosing/effect site time/context sensitive half time0.1-0.4mcg/kg IV
effect site time: 6.2 mins
context sensitive half time: less than alfent, more than remiPK of sufentanilA: highly lipophilic, crosses BBB, pulm first pass = 60%, More protein binding than fent = smaller Vd
D: rapid redistribution
M: liver - sensitive to liver blood flow
E: urine and fecessufentanil adverse effectsLarge doses: skeletal muscle rigidity of chest and abdomensufentanil is used less in what kind of anesthesiacardiac
due to difficult ventilation due to skeletal muscle rigidity, and bradycardiabutorphanol MOA/classOpioid agonist/antagonist
mu antagonist
kappa agonistButorphanol indicationstreatment of migraines and to prevent shivering via the kappa receptorsbutorphanol dosing/DOA/half lifedosing??
DOA: 3-4 hours
Elimination half life: 2.5-3.5 hoursside effects of butorphanolSedation, nausea, diaphoresis, dysphoria, ventilatory depression
Catecholamine release: increased HR, CO, BPbutorphanol contraindicationspatients who are opioid dependent as they may experience withdrawal symptomsnalbuphine class/MOAOpioid agonist/antagonist
mu antagonist
kappa agonistindication for nalbuphineprevent shiveringelimination half life of nalbuphine3-6 hoursnalbuphine PD-Analgesic properties similar to morphine, but ventilatory depression has a ceiling effect (30 mg IM)
-If given before an opioid: reduces efficacy of full agonists peri-op
-If given after an opioid, it can reduce resp depression but maintain analgesiacontraindication for nalbuphineOpioid dependent ptscelecoxib MOA/class-Inhibit biosynthesis of prostaglandins by preventing substrate arachadonic acid from binding to cox enzyme active site = all our drugs hit cox 1 and 2
-Non opioid analgesics
note: partially cox 2 selectivedosing for celecoxib and VDDose: 400mg PO pre op + 200 BID for 5 days post op
LOW vd - 90% bound to albumincelecoxib PKA: complete rapid oral bioavailability
D:
M: liver
E: urine and bilecelecoxib PDNote: COX2 selective
-plt dysfunction due to acting on cox 1 receptor
-GI = upper GI ulcers d/t cox1 inhibition
-CV effects: disruption in pro and anticoag factors balance
-renal: decrease dosing in renal pts
Pulm - increased risk of anaphylaxis d/t inhibition of prostaglandins
-hypersensitivity with nasal polyps or asthmaketorolac MOAInhibit biosynthesis of prostaglandins by preventing substrate arachadonic acid from binding to cox enzyme active site = all our drugs hit cox 1 and 2class of ketoralacNon opioid analgesics; most selective cox 1 NSAID (still both)ketoralac dosing / VDDose: 15-30mg IV Q6 hours
.5mg/kg in peds (due to renal development)
LOW vd - 90% bound to albuminketoralac PKA: complete rapid oral bioavailability
D:
M: liver
E: urine and bileketorlac PD-plt dysfunction due to acting on cox 1 receptor
-GI = upper GI ulcers d/t cox1 inhibition
-CV effects: disruption in pro and anticoag factors balance
-renal: decrease dosing in renal pts
- hypersensitivity with nasal polyps or asthma
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