ITE NOTES

MONITORS:
-EKG: II = pwave & SR, V5 75%Sn for ant/lat ischemia
- II measures voltage bw red and white - III bw red and black - AVR bw white and red/black combo
-BP q5m; small cuff overestimates; more distal = dec DBP, inc PP
- automated cuff accuracy: MAP>SBP>DBP (mvmt alters DBP)
-Fluorescine = yellow-orange = no effect on SpO2
-Hgb (high to low) =660nm (abs red light)= blue; Blue abs 660nm = lower SpO2 readings
-HgbO2 (low to high) = 940nm (abs infrared) = red
-SBP/DBP inc/dec by 7.4mmHg/10cm height change
-PE = dec EtCO2 but in A-a gradient bw PaCO2 & EtCO2 (no transfer of CO2 into alveoli)
-REVIEW EtCO2 shape: 1 deadspace gas exhaled→ 2 transition bw airway/alveolar gas→ 3 alveolar
plateau→ 4 inspiration; COPD = prolonged phase 2 and upslope phase 3
-Apnea = inc EtCO2 6mmHg after 1min, 3mmHg qmin thereafter
-Adequate CPR: EtCO2>10 (unless CO2 embolism); DBP>20 on Aline
-Temperature: thermal input from Adelta = cold; Cfibers = warm preprocessed in SC and brainstem→ preoptic anterior
hypothalamus (central thermoreg center); thermal output: skin temp→ behavioral resp (shelter, voluntary mvmt); core temp→ ANS
resp = shiver, sweat, vascular tone; Heat loss with GA = redistribution 1-20 C
Pulmonary artery = core gold standard temp (also distal esoph, TM, NP) ; skin is ~ 2oC of core temp
Hypothermia <36 core body; dec metabolic rate by 8% per 1C; allows CNS protection (trauma/ischemia), inhibit MH, but
-inc infection risk 3x, delayed wound healing, plt/coag probs = bleeding, delays emergence, prolongs CIS block, left shift of
HgbO2 curve, dec inotropy, chronotropy, inc SVR, arrhythmias, EKG intervals, shivering, PACU stay
Interthreshold range: core temp range bw cold-induced and warm-induced responses; normally narrow 36.8-37 (~0.2C); with GA =
33-37 (~4C, 20x, volatiles>propofol) bc inhibited thermoregulation = inc interthreshold range; females = higher threshold for
sweat/vasconstriction
Regional anesthesia also inhibits thermoregulation to lower ½ of body = inc ITR 4x ~0.8C
Anesthesia impaired TR: Phase I = redistribution; Phase 2 = Heat loss>heat prodxn; Phase 3 = EQ
Mechanism to preserve temp: 3
1) Nonshivering thermogenesis: NE/T3/steroids→ brown fat & skeletal m. inc metabolic rate to produce HEAT instead of ATP;
inhibited by volatiles and BETA BLOCKERS
2) Shivering 3) Vasoconstriction
Heat transfer in cold OR: 1) radiation 60% 2) convection 15% 3)evaporation 4)conduction 5%(contact)
- Heat loss thru breathing circuit = evaporation esp in PEDS
Thermal neutral range = environmental temp at which pt’s heat prodxn = heat loss = 27-31C in adults;
32-34C in neonates
After ROSC = induce hypothermia 32-36C x 12-24hrs (can use meperidine to inhibit shivering to dec O2
demand), and rewarm slowly after or else inc ICP/lytes problems
Thermodilution: cold injectate into RA to est volume moving thru PAC (--> CO);
LESS TEMP ∆ = ↑CO
- High CO, high injectate volume, colder temp = less variability in measurements
- Low CO, TR, intracardiac shunts = inaccurate; TR = underestimate CO (reflux of thermal signal); Shunt
(RL)= overest CO bc dilute or shunt signal away to PAC
CHANGE IN TEMP VS TIME; high CO = small narrower peak; low CO = tall wide peak
PACU Shivering: from hypothermia, pain, or volatiles (when MAC dec 0.15-0.3 = pure clonic mvmt), fevers, seizures; shivering inc
O2 consumption (500%), inc CO2 prodxn = inc MV req, inc IOP/ICP/trauma; can Tx with meperidine or NDMBA in intubated pts;
physostigmine could also be used
PONV: if no ppx, ⅓ pts get PONV; RFs: FEMALE>hx of PONV/MS>nonsmoker=volatiles>opioids (area postrema)>young;
opioids target area postrema = PONV
Zofran (HA, QTc)-->decadron (perineal itch)-->prop gtt→ Scop (antiACh, 2-4hr onset, delirium)
Promethazine = blocks H1 and D2→ EPS; Reglan blocks D2 = inc GI motility, inc LES, avoid in SBO/LBO; EPS
Droperidol blocks central D black box warning for inc QTc ; Decadron blocks NTS
Atropine blocks M3 good for epidural induced nausea! (nubain/zofran for epidural ITCH)
 Substance P antagonist (NK1 antagonist, ex. aprepitant) is effective with ATC zofran but expensive; works for posteroir fossa NSGY
& chemo, refractory PONV; give 3hrs before indxn
Ephedrine = 50mg IM - antiemetic; prevents GI hypoperfusion; H2B: cimetidine 300mg IV, ranitidine 50IV preop
NTs/Hormones-->chemoR trigger zone in area postrema (medulla) → parvicellular reticular formation (emetic center, medulla)
Contributions to nausea: volatiles esp nitrous, drugs (neost, opioids), aggressive hydration-->gut edema, >2hr surg; ENT, lap, neuro,
plastic, breast, strabismus
NPO: clears 2hrs, breast milk 4hrs, formula/nonhuman milk/tea/toast 6hrs, fatty meals 8hrs
Nonparticulate antacids: Nacitrate preop
Aspiration pneumonitis if gastric volume >25ccs, pH <2.5
*If intubated, continue TFs unless abd surg or paralysis needed; post-pyloric vs gastric feed = same risk for asp but dec risk of PNA
Allergy: Muscle relaxant>latex>Abx>hypnotics>colloids>opioids
- Allergy to cosmetics related to NH4+, similar to NMBD = inc risk for allergy to vec/pan/roc
- Allergy to latex related to fruit, healthcare, spina bifida, urogenital syndr (prune belly)
If allergy to PCN<10yrs ago, don’t give PCN or ancef; cross reactivity = R1 side chain; cefs 1st/2nd gen = 1% cross reactivity; in
general 0.1% risk of ceph allergies
Type I: IgE
Type II: IgG cytotoxic against antigen (blood transfusion)
Type III: Immune complex = local arthritis, serum sickness
Type IV: cell-mediated Th1 cytokines→ MACs, Tc; contact dermatitis, graft rejection
Anaphylaxis: consider NE or vasopressin gtt; epi 10-100mcg; tryptase peaks <60m (neg in 35% case), histamine peaks<30m; monitor
24hrs bc biphasic phenomenon, refer for allergy testing
O2 GREEN (itnl = WHITE) : E cylinder max =660L = 2200psi; 1000psig = ½ full = 330L; lbs/sq in gauge
Nitrous BLUE L/G: critical temp is above room temp 36C so liquid/vapor ratio doesn’t change and pressure stays the same until
only ¼ or 16% left; 1590L & 745psig= full tank; WEIGH; 253L
- Critical temp is temp above which liquid/gas can’t exist and gas can’t be liquefied no matter pressure; so if critical temp <room temp,
gas will never liquefy even if pressure in very high
- Nitrous and CO2 = wet gases = liquid and gas in cylinders; vs other subst are gases only
- Critical pressure: minimum p needed at critical temp to cause g→ l; nitrous = 1050 psi
CO2 GRAY: 1590L 838psig L/G
AIR = yellow 625L 1900psig, He = brown 500L 1600psig, N2 = black
Pinsafety index applies to H&E cylinders only
Wall connectors = diameter index safety system and color coding
1st stage regulator decrease E cylinder pressure so wall O2 enters system
2nd stage regulator dec gas pressure before it enters flowmeters
Automatic variable bypass system: adjusts to increase temp via dec resistance to flow thru bypass chamber (less thru vaporizing
chamber) = constant [gas] delivered despite temp changes; adjusts for ALTITUDE ALSO
- Divides total FGF into 1) bypass path and 2) vaporizing chamber (varrier gas); ratio FGF = splitting ratio which changes with
concentration dial and ambient temperature
Desflurane vaporizerDEREASE @ high altitude
O2 analyzers: 3 types
- Paramagnetic, no calibration needed, uses switched magnetic fields = changes in pressure, can diff bw expired/inspired O2; NEEDS
BATTERY; FASTER THAN CLARK
- Galvanic (fuel): measures current (cathode/anode); REQUIRES CALIBRATION; 1yr lifespan, No battery needed! Pb, Au
- Clark = polarographic: needs frequent CALIBRATION and BATTERY; moisture = inaccurate; 3yr lifespan bc teflon gets coated
w/protein; Ag, Pt
Infrared reflection absorption spectroscopy: only works for polar mls (so not O2, N2, need ABG); Co2, N2o and volatiles
measured with IRAS based on absorption of diff wavelengths
- CO2 max absorbance in 4200nm
ABG ANALYSIS: Cold sample = high pH, low PaO2
- Delay: dec PaO2/pH/base excess; inc PaCO2 (fr RBC/WBC metabolism)
- Air in sample: PaO2 approaches PO2 room air (159mmHg, 21% Patm), dec PaCO2
- pH = sanz electrode; Co2 = Severinghouse; O2 = CLark; HCO3 = calculated
Minimal FGF should equal basal O2 consumption 3-4cc/kg/m or 8-10cc/kg/m in premies
PVC = most combustible; silicone = least combustible
 Clean procedures: no resp, GI, genital entry
Clean Contaminated: operative wounds with entry of above
Contaminated: fresh open wounds
Dirty/infected: old traumatic wounds, perforation
Abx PPX: usually ancef; vanc if true PCN allergy, clinda if PCN allergy in ENT surgery; cardiac with prosthetic = ancef + vanc
CRC, appy: ancef + flagyl (or flagyl + cipro if PCN allergy), or cefoxitin
Urology: clean contaminated = cefoxitin; if prostehtic→ gentamicin
Ancef 2g, 3g>120kg; clinda 900mg q6h/30m; vanc 1g <80; 1.5g 100-120kg; 2g>120kg q12h/30-60m
Unasyn 3g q2h; cipro 400g q8h; gent 5mg/kg q12; flagyl 500mg q12h
Endocarditis ppx if procedure criteria below AND condition below: (amp 1-2g IV AND gent 15mg/kg 30mprior; if PCN allergy =
cefazolin/ceftriaxone 1g or clinda 600
1) Procedure: gum/mucosa perforated, respiratory tract with incision or biopsy, pts with infected skin or joint (AKA NO NEED FOR
GU/GI PROCEDURE)
2) Condition: prosthetic heart valve, previous IE, CHD that is unrepaired, CHD that is repaired with prosthetic material @ 1st 6months
after procedure, CHD repaired but with defect; heart transplant pts with valve pathology
Line isolation monitor: beeps @ 5mA; primary circuit attached to ground, 2nd circuit isn’t; monitors ungrounded power source; if
beeps, unplug most recently plugged in device

INHALATIONAL AGENTS: iso = purple sevo = yellow, des = blue, halo = red, enflur=orange
-reverse inh agents with 1.25 physostigmine
-partial pressure in blood (not concentration) yields effect; at higher altitude, same [gas] = lower pp in blood (more escapes) = less
effect
-Volatiles inc rhabdo in DMD/BMD; MH not associated with DMD/BMD
-Vapor pressure: H240 I238 S160 E175 D665 N2O1550s
-rate of Fa/Fi rise = speed of induction; high CO = slow induction
- low CO = risk overdose bc faster Fa/Fi (less blood dilution of gas pp) esp halo/iso
- inc MV = inc rate of Fa/Fi rise esp Halo/iso; infants have ↑MV:FRC vs adults = FASTER INDXN
- R→ L shunt = slow onset (doesn’t change Fa/Fi rate!, just more blood to dilute); esp Des/nitrous (ex of shunt = MAINSTEM) (vs
IV induction RL shunt will inc speed bc bypass lung circ)
- L→ R = no change
- FAT (fatty meal, HLD) slows indxn
-INC B:G solubility = DEC rate of FA/FI rise = slower indxn/emergence; adults have high B:G vs infants = SLOWER INDXN
-H 2.3 I 1.4 S 0.69 D 0.42 N 0.47; des is lowest B:G coeff
-2nd gas effect: N2O augments uptake of 2nd gas (inc relative [gas]) d/t rapid N2O uptake into blood
-MAC: H0.75 I1.2 S2.1 D6 N104
-MAC awake: prevent resp to tactile/verbal stim; volatiles MAC 0.4, nitrous MAC0.6
-MAC mvmt = 1MAC
-MAC EI: prevent laryngeal response to ETT ~1.3MAC
-MAC BAR: blunt ANS response ~1.6MAC
-MAC highest@6months, then dec w/age ~6% per decade after 40yo
-decrease MAC: benzos, verapamil, Lithium, acute EtOH, age, hypothermia, hypoxia, hypercarbia, anemia, sepsis, hypoNa,
hyperMg/Ca, pregnancy, chronic cocaine/TCA, opioids dec MAC by 60%
**MAC normalizes 72hrs postpartum; MAC dec by 1/3 at 8wks (inc plasma, dec alb)
-increase MAC: acute cocaine/meth, chronic EtOH, hyperthermia, hyperNa, red hair, infant
- AWARENESS: more common if EtOH/drugs; higher in PEDs; avoid w/versed, minimize paralysis, use Inh over TIVA; if TIVA use
EEG-->BIS 40-60, Sedline 25-50 2 min lag time
-1/MAC = potency = lipid solubility oil:gas coeff (ex. Des/nitrous not potent, but D more potent vs N)
-HISED inc CBF/ICP @ >1.5MAC (uncouple CBF/CMRO2), dec CMRO2 @ even low concentration; hyperventilate to avoid
ICP; @ low [iso] = no chnages to CBF
*burst suppression = ↓↓↓CMRO2 (for aneurysm clipping)
-N2O INCREASES CMRO2; ketamine inc CBF more than inc CMRO2
Xe blocks NMDA, DEC CMRO2, inc CBF/ICP
-all volatiles blunt hypoxic vasoconstriction = inc shunt & V/Q mm; dec cilia fxn; inc RR, dec TV = preserved or dec MV (n2O
doesn’t dec MV)
 -bronchodilate distal>prox
-N2O does not dec SVR; HISED dec SVR/inc HR so CO maintained; halothane = bradycardia & dec contractility; INCREASE
QTc
-if rapid increase of Iso/Des @ indxn = inc BP = HTN, inc HR especially DES; Des = HTN
-all volatiles except nitrous = muscle relaxation potentiation INCLUDING UTERINE RELAXATION!
Des 60%>sevo/iso 40%>halo>TIVA esp with ROC/VEC/PAN (steroids); des up to 60%, sevo/iso 40% bc dec Sn of post jxn
skeletal m. cells to depol; des is not potent = high conc @ MAC 1 @ NMJ
- dec freq, inc amp EEG
-H/S not pungent = good inhalation indxn
-Metabolism (fluoride prodxn = nephrotoxic): Halo 20% to trifluoroacetic acid; Sevo 5%; Iso 0.2%; des is minimal biotransf
-Halo: hepatotoxic (immune mediated), dec contractility, brady; preservation of hepatic blood flow least to greatest: H<D<I<S
-Enflurane: seizures, nephrotoxic, dec contractility 2% metabolism
-Methoxyflurane: nephrotoxic, extensive metabolism
-Nitrous: NMDA antagonist = analgesic, no muscle relaxation, preserved MV, inc SNS/CMRO2, low potency, low solubility,
diffusion hypoxia, PONV, expansion in air cavities (tracheal injury, SBO, brain surg, PTX), dec contractility, prolonged use =
p.HTN, PN (dec myelin), BM suppression, dec DNA synth, teratogenic; N2O 34x more soluble vs N2 = into spaces; PTX 2x size in
10m, 3x size in 30m!!!
-Iso: cheap, pungent, 2nd most potent!, coronary steal, @1.5MAC = burst suppression, @2MAC = silent EEG
-Sevo: ½ potency of iso; Compound A with sodalime (NaOH, CAO)/BaOH but not CaOH; nephrotoxic in rats; new sodalime/ old
baralyme = inc compound A
-Des: high VP = boils @ sea lvl = special vaporizer affected by high altitude; very pungent = breathholding,
laryngo/bronchospasm, cough, salivation; rapid indxn = inc SNS/HR; forms CO fr old dry BaOH, less with sodalime
CO2 Absorbent: ethyl violet = color indicator when pH<10.3; silica, CaSo4, added to absorber to harden granules, dec resistance and
inhalation of toxic fumes; high temps = CO, CA

IV ANESTHETICS: GABA A = Cl, GABA B = K, EtOHglycineR, caffeine inhibits glycine

-Propofol and barbiturates: dec rease of dissociation of GABA to GABA-A-R (duration)
-Benzos: inc efficiency of GABA binding Cl- channels (frequency); bind alpha unit of GABA-A at POSTSYNPASE OF
CORTEX; min resp dep by itself, but synergistic with opioids; relaxes muscles
-Etomidate:GABA-A, least cardiac depression, min pulm effect; propylene glycol = pain on inj; PONV, myoclonus (EPS sys), inh
11BOHase = adrenal suppression 4-8hrs, nonionized@phys pH = fast onset; hiccups, anticonvulsive, thromboplebitis; preserved
CPP; 0.2-0.3mg/kg; metabolized by liver esterases, dec hepatic blood flow; highly protein bound; dec ICP, inc AMP/latency
SEP!!!
*Baclofen = GABA- B
-Ketamine: NMDA antagonist = analgesic, no respiratory depression, inc PVR, bronchodilation, inc secretions, IOP; inc SSEP
amplitude, inc CMRO2, questionable eff on CBF/ICP; stimulates SNS but direct myocardial depressant = worse in depleted NE/E
situations (CHF, CAD) = hypotension; active metabolite norketamine
-Precedex: PERIPHERAL AND CENTRAL alpha2 agonists (more selective vs clonidine 1600:200) @ locus ceruleus = NREM sleep-
like; hypnotic and analgesic; transient HTN fr alpha2B agnoism, then hypoTN fr alpha2A agonism; brady (not tachy)/heart block,
dry mouth, nausea, dec dose if liver/kidney probs, 2hr ½ life, dec CBF/CMRO2/TV, no change to MV; dc can cause rebound HTN;
gtt 0.4-1.2mcg/kg/hr; bolus 0.3mcg/kg
-Propofol: dec CMRO2/CBF/ICP, dec contractility/SVR/RR, antiemetic, anticonvulsant, kids = inc Vd and clearance; inc clearance
in KIDNEY/uremic pts (prob fr inc liver fxn compensation); egg yolk lecithin (not egg white so unlikely allergenic); 12 hr
expiration; PRIS if >4mg/kg/hr = rhabdo, myogl, heart/lung issues, MA fr impaired mito/FA metabolism; inc triglycerides = risk of
pancreatitis postop, high mortality in kids; can cross placenta but short DOA = safe in preggo; phenol = green pee; no change to
hepatic blood flow like etomidate; blocks CYP3A4
1) Propofol completely met by liver on single pass!! Emergence fr propofol bc redistribution, then liver met, then LUNG metabolism
2) Fospropofol = hydrophilic (vs prop lipophilic) = no lipid emulsion = no pain on injection; goes to liver for metabolism to propofol +
formaldehyde = slower onset
-Thiopental: dec CMRO2/CBF/ICP, dec RR/SVR/contractility; ppt w/acidic fluids (LR, roc, vec), vasoconstriction = thrombosis,
necrosis; Tx papaverine, lido, sympathetomy/stellate ganglion block, heparin; pH = 9 hides in tissues, prolonged effect
-Midazolam: no EEG burst suppression; imidazole ring= water/lipid soluble; active metabolite = accumulate in CKD; high protein
binding (adjust if liver dz)
-Lorazepam=proplyene gycol toxicity; diazepam =pain on injection
-Flumazenil 0.2mg q1m w/max1mg, shortacting 0.7-1.3hrs = resedation
Temaz, loraz, oxaz OK in liver dz and old ppl bc only phase II conj metabolism

OPIOIDS: DOSE BY LBW

naloxone 0.4mg/ml dilute in 9cc = 0.04mg; give 0.04mg q2min, max 0.2mg, wears off w/in 2hrs; dose of 0.04-0.08mg can reverse
resp dep without affecting analgesia
Alvimopan/Methylnaltrexone = opioid antagonist doesn’t cross BBB = prevent periph Sxs (GI/constipation); Naltrexone = PO
bioavailable; Naloxone = no oral bioavailability
Clonidine = Tx for opioid withdrawal
Opioid1st pass lungs; block AC = dec cAMP  PLC
Potency = lipid solubility (sufentanil)
Onset = pKA (alfentanil pka 6.5)
DOA = protein binding (fentanyl = long context ½ life)
Opioids inc K conductance, dec Ca conductance = hyperpolarize → post synaptic
inhibitory potentials
Vasodil bc of histamine release AND block SNS = dec SBP/hypotension, bradycardia
DEC MV, INC TV
Chest wall rigidity = CENTRALLY mediated, common with lipid soluble opioids (fent, remi), can be blocked by NMBs
Mu in PAG and substantia gelatinosa: itch possibly fr receptors in medulla and trigeminal nucleus (not always related to histamine!);
miosis, brady, hypotension
-mu1 = muscle rigidity, dec GI motility/LES, ↑prolactin, pruiritus (meperidine & morphine!); dependence, miosis
-mu2 = resp depression by blocking CO2 responsiveness in MEDULLA, inc apneic threshold;
-kappa: sedation, spinal anesthesia, dec shivering (meperidine), dec CO2 response, ADH
-delta: analgesia, behavioral, epileptogenic; NAUSEA/VOMITING
-sigma: dysphoria, hallucinations (KETAMINE), antidepressant
ALL effects except CONSTIPATION/MIOSIS demonstrate TOLERANCE; tolerance and hyperalgesia from downregulation of
opioid receptors and from ?NMDA agonistic properties; opioids = hypogonads = osteoporosis
-Review %peak effect over time; dilaudid 2-4hr, morphine 4-5hr
-opioids = weak BASES (so lower pKA = more neutral = cross BBB = faster onset)
-Potency = lipid; onset = pKa; DOA = protein binding
Mep 0.1 morphine 1 alf 10 fent 100 remi 300suf 1000
-Sufentanil is 2x more lipid soluble vs fent = 10x more potent vs fent, 1000x morphine
lipid solubility: morphine<alfent<fent<sufent
pH: alf 6.5 morphine 7.9 suf 8 fent 8.4
-Elim ½ life: Remi (10m), alf (30-90m), morph/mep/suf/fent, methadone (34hrs); fent context sens; R<S<A
-Alfent: 1-2m, 5-10mDOA (rapid redistribution); fastest onset bc pka 6.5 (cross BBB fast despite high protein binding = lowest
Vd; use for brief intense stim; more n/v, chest wall rigidity, resp dep; met by esterases; 4x faster vs fent but ¼ DOA/potency
-Remifent: onset 3-5m, DOA 5-10m; plasma esterase met (not pseudocholinesterase!); AGE = dec clearance; not affected by
pseudochol deficiency
-Sufent: 3-5m, 20-45m; gtt when sign surg stim and sign postop pain; turn off 30m prior to end of case; most lipid soluble = very
potent = bradycardia; fentanyl has longer context Sn ½ life vs sufent
-Fentanyl: lipophilic=onset 3-5m, DOA 30m-1hr; long context ½ life bc inc protein binding and lipid solubility!!; no active
metabolites = OK in CKD; no effect on CBF, CMRO2
-Hydromorphone onset 5-10m, DOA 2-4hrs; H3G=noanalgesia but neuroexcitation; no histamine
-Morphine: hydrophilic!= onset 10-20m, slower peak, longer DOA (4-5hr); histamine release; m3g>m6g M6G = analgesic more
potent vs morphine but less afinity for u receptors, RESP DEP, hypoTN; M3g neuroexcitatory/allodynia; accum in renal dysfxn
-Methadone: onset 10m, DOA 24hr; longest terminal ½ life, accumlates; racemic L-meth = opioid agonist, D-meth = NMDA
antagonist; BLOCKS 5HT reuptake→ 5HT syndrome with MAOi (so does tramadol, meperidine, methylene blue,
dexmethorphan!!!!) (U, NMDA, 5HT); serial EKG bc inc QTc
-Meperidine:local anesthetic properties; kappa = Tx shivering; similar to atropine = antiAch = tachycardia, mydriasis; avoid with
MAOi (mu blocks 5HT reuptake, or else 5Ht syndr = ataxia, hyperreflexia), histamine, euphoria, less resp dep; normeperidine =
analgesia, renal toxic = seizures; N/V/ITCHHHHHHHHHYYYY
-Codeine met by CYP2D6
Tramadol = SNRI, u, NMDA
-Buprenorphine = no apnea but dec MV; DOA = 10hrs (partial U)

MUSCLE RELAXERS: Lithium is additive w/ sux, synergistic w/ NDMB, ↓MAC bc block brainstem NE/D/E
NMB = large poor lipid soluble = cross placenta slowly
AChnR: bind 2 ACh mlcs to paired alpha units; choline+acetyl CoA = ACh met→ acetate + choline in cytoplasm
-succinylcholine: 2 ACh mlcs joined by methyl group = ACh-R agonist = depol = inc K 0.5meq; intub 1-1.5mg/kg, laryngospasm Tx
20mg; onset 1m, lasts 10m; met by pseudocholinesterase; 1:3K pts with abnormal pseudochol = 3-8hrs
-Phase I TOF ratio >0.7; TOF/tetany/doubleburst =constant/nofade; absent posttet potentiation
-Phase II (high repeated dose, resembles NDMB): TOF/tetany/doubleburst=fade; present posttet potentiation; Tx phase II
sux paralysis with neo 0.03mg/kg
SUX can inc tracheal tone, masseter m rigidity esp in kids with strabismus; OK in MG/LES; not OK in MS, GBS, ALS, DMD,
myopathies, burns 24hrs-2years
-PTP = inc ACh release after brief high freq AP
-Dibucaine: % of pseudochol inhibited by dibucaine (inhibits NL pseudochol); NL = 80; 20= homo 4-8hrs DOA, 50 = heterozyg =
30m DOA; contraind: hyperK, UMN (stroke/tumor), dystrophies, MH hx, open globe (inc IOP); SE: fasciculations (min w/roc
0.03m/kg 3m prior but doesn’t prevent inc IOP or CV side effects, need higher sux dose after), myalgias esp women/ambulatory pts
(less in kids, older ppl, muscular pts), bradycardia in kids (have atropine ready), tachycardia, ANAPHYLAXIS (1:5-10K), trismus,
inc ICP/IOP/LES/gastric pressure = aspiration risk
Myalgias: 50% pts, lasts 1-2d, more fit = less; prevent w/NDMB, Cagluconate/lidocaine (stabilize membr), vitC
-Pregnancy and liver dz = inc Sux DOA; -Esmolol, pancuronium, cyclophosphamide, phenelzine inhibit pseudocholinesterase = inc
sux DOA
NDMB: hydropilic, inhibit ACH-R @NMJ & also blocks presynpatic ACHR which normally mobilizes ACh vesicles; blockade
@presynaptic AChR = FADE!!!!! Fade = phase II
*can also inhibit muscarinic AChR@ large doses = autonomic margin of safety; ex: roc ED50>3-5x blocks PNS; ED50>10 blocks
SNSn
E95 = average dose to produce 95% suppression of twitch height in 50% population
-intubating dose = 2xE95; larger dose = faster onset, longer DOA
-priming dose. = 10% of ID 3-5m prior (to speed onset)
-ROC RSI = 1-1.2mg/kg
-ID: sux 1, roc 0.5, vec 0.1 cis0.15 atra 0.5 miv 0.2; vec onset 3-4m, cis 5-7m
-Vec 3-OH metabolite fr liver = 75% biliary, 25% renal excr= 80% potent = prolonged in renal failure
-Roc = no metabolites (biliary excr; LIVER DZ = no roc excr!!); low potency = faster onset
-Pancuronium = prolonged in LIVER FAILURE, 80% excr urine; potentiates SUX
-Roc/VEc = acidic ppt with thiopental (so does Lactated ringer)
-Benzylisoquinolinium: urium =CAM = HISTAMINE esp ATRA & MIV > CIS
-Aminosteroid: onium = vagolytic P>R esp PAN; Vc = no vagolytic properties; OH snaps SNS
-Reovery fr paralysis d/t DISTRIBUTIONmostly
- if NDMB gtt needed in ICU pts, use cisatracurium; vec gtt = prolonged weakness and neuropathy for months
-Anticholinesterases inhibitors (neo, echothiophate, donepezil) = Inc ACh = hard for NDMB to work, potentiates sux (potentiates
phase I, reverses phase II)
-Esmolol, pancuronium, cyclophosphamide, phenelzine inhibit pseudocholinesterase
-Phenytoin/carbamazepine = resistance to aminosteroids (pancuronium); cyclosporine inc DOA NMB
-Recovery: TOF ratio>0.9 or 5s of sustained tetanus without fade
-TOF 3 = 75% block, 2= 80%block. 1=90% block
-Most R to most Sn: vocal cords>diaphragm>corrugator supercilli (assess block)>abd m> AP (assess reversal)
-Paralysis potentiated by: Mg(pregn), hypoK, hypoCa, acidosis, hypothermia, neonates, volatiles (not N2O), Li, verapamil,
autoimmune dz (SLE)
-AChR upreg (fetal AChR) = Sn to sux, R to NDMB = SCI, stroke, burn, immobility, MS, ALS GBS (demyelin), CP (NL to sux, R to
NDMB), prolonged NDMB exposure; paralyzed limb = inc ACHR = higher TOF (high resistance to blockade)
-ACHR downreg= R to sux, S to NDMB: MG, LES, ACHase poisoning, organophosph poisoning
-Reversal = nicotinic and muscarinic effects so need Anti-M3 to prevent bradycardia
-Neo: 0.3-0.05mg/kg if 2-3 twitches; 0.015-0.02 if 4 twitches wo fade; max 0.07mg/kg or 5mg; ceiling effect = paradoxical weakness
w/large doses or when given near full recovery; onset 5m, peak 10m, DOA >1hr
 -Glyco = ⅕ neo (3 neo = 0.6 glyco); quaternary amine = big can’t cross BBB = no mydriasis or CNS Sxs = OK in narrow angle
glaucoma
-Atropine tertiary crosses = restless, hallucinations, delirium; not OK in narrow angle glauc
-Scopolamine tertiary crosses = sedation, amnesia, euphoria; not OK in narrow angle glauc
-neo, pyrido, erdro = cant cross BBB; physostigmine crosses = reverse central antiACh syndr (atropine, scop, volatiles),
benzo/volatile/morphine resp dep, PO shivering
- Neo crosses placenta but glyco cannot; use atropine in preggo pts!!!!!!
- erdro/atro (fast); neo/glyco (IM); pyridost/glyco (slow)
- Erdro is fast, short acting, and least potent (1/10th neo); least muscarinic
- Pyrridostigmine is slow and 1/5th neo potency, LONGEST DOA
-Sugammadex: gamma-cyclodextrin w/hollow core = traps ROC/VEC; don’t use if severe CKD; increases PT/PTT 25% for 60m;
don’t mix in line w/zofran, verapamil or ranitidine; anaphylaxis; 7d addl contraceptive to hormonal; uses:
-cant vent/intub after roc (use 16mg/kg)
-deep blockade or inadequate reversal by neo
-pregnancy bc doesn’t cross placenta
-1twitch or PTP 2= 4mg/kg; 1-2 TOF 2mg/kg
-CIS = hoftman elim yields laudanosine which is metabolized by liver and excreted in kidneys;laudanosine = neuroexcitation = inc
MAC if accum; CIS DOA prolonged if hypothermia (dec hoftman elim)
Cis + roc = synergy
Cis + atra = additive
Pan/Vec 0.1, cis 0.15, miv 0.2, atra 0.5, roc 0.6

LOCAL ANESTHETICS: BASES, ionized form bind inactivated>resting channels @ alpha unit of VGNC = no Na influx = no
AP; ONSET determined by pKA and concentration; premix w/Epi = acidic = slow speed
DURATION is INVERSELY ~PROTEIN BINDING (diff fr opioids)
- Alpha aminoglycoprotein binds LA more than albumin does, carries away for metabolism
Low pKA = faster onset (just like opioid bases); nonionized form cross membr; ionized form binds VGNC
pKA: Mepi/lido/prilo = 7.6/7.9; Bupi/ropi 8.1; tetra 8.5; chlorpro 8.7; pro8.9
Onset: lido = rapid; mep = med; chlorpro/pro = rapid; bupi/ropi/tetra slow
Max dose/with Epi: Mep/Lido 5/7; Bupi: 2.5/3; Ropi 4/n/a; chlorprocaine 10/15; tetra 1.5/n/a
*Epi is stored in acidic sln so -->BH+ can delay onset if premade mixture; epi has alpha2 = analgesia unrelated to LA; epi addn =
early detection of systemic absorption and inc max allowable conc
Bupi is highly protein bound and lipophilic = long DOA & epi has little effect!! cardiotoxic bc binds to resting + inactivated NaC
and slower dissociation fr channel @ diastole, TW elevation-->prolong PR/QTc; 2 enantiomers R+ binds heart very tightly = ACLS
resistant/ wide complex bradycardia!!; Levobupi and Ropi S- isomer only = similar efficacy but less cardiotoxic; liposomal
bupi=higher conc =longer ½ life but same cardiotoxic
Tetra + epi = extends duration by 30m
Bupi/Ropi/Tetra = 1.5-2hr block
Chlorprocaine = short
LIdo/Mep = intermediate, epi extends by 90m
Adding fentanyl to spinal = faster onset due to lipophilic, synergistic and intensifies sensory block
Procaine/Chlorprocaine: high pKa but fast onset bc higher concentration used (low systemic toxicity)
3 Structures: 1) aromatic benzene = lipophilic 2) ester or amide 3)tertiary amine (hydrophlic)
Benzocaine, prilocaine (metabolite o-toluidine), lidocaine (met xylidine) → metHg (Tx methylene blue)
ESTERS: met by pseudocholinesterases and RBC esterases except for COCAINE which is liver→ urine; → PABA = allergy
AMIDES: met by LIVER (aromatic hydroxylation, N-dealkylation, amide hydrolysis); has preservative methylparaben = allergy
LA affect first→ last: SNS-->sensory→ proprioception → motor
Sensory: A-delta = small diameter & myelinated concentrated at nodes of Ranvier
Max lido tumescent 1% = 55mg/kg; epi = 0.055mg/kg
Rate of absorption: IV>tracheal>IC>caudal>paracervical>epidural>brachial plexus>axillary>sciatic>SQ
LA to CNS: dec CBF/CMRO2; CNS excitation by blocking inhibitory pathways→ seizures/coma; lightheaded tinnitus, tongue
numb metallic taste
LA to heart: block NaC (dose dep) = distupr condxn = brady, arrhythmias; rmm bupi = TW elev first
 Need 3x [LA] to produce CV effects vs CNS toxicity; Tx CNS toxicity with benzos (*methohexital doesn’t inc sz threshold aka not
helpful! But useful in ECT)
LAST: benzos for sz; epi<1mcg/kg = less than code dose!!!, no vasopressin/CCB/BB!!; 20% intralipid 1.5 cc/kg bolus x 3, gtt
0.25-0.5 cc/kg/m (vs dantrolene for MH 2.5-10cc/kg bolus q5m, 0.25cc/kg/hr
Malignant hyperthermia: Ryr-1 mut (Ca release @ SR); autosomal dominant with variable penetration; triggered by
VOLATILES (not nitrous) and SUX; first tachycardia and tachypnea, HTN, muscle rigidity (trismus), inc EtCO2; temp = late
symptom inc 1-2C q5m, metabolic acidosis→ DIC, renal failure, hyperK; TX: hyperventilate, TIVA, NaHCO3 for acidosis,
Ca/insulin/glucose for hyperK, diuretics, alkalinization; Dantrolene 2.5-10mg/kg q5m, 0.25mg/kg/hr x24hrs bc 25% rate of
recrudescence; Dantrolene vial = 20mg (need to dissolve in 60cc sterile H2O, sln has mannitol); Ryanodex = 250mg/vial in 5cc
sterile H2O pushes until stable; AVOID CCB(hyperK, dec CO) just like in LAST; cool if temp>39; refer to MHAUS, biopsy center
Gold standard for MH suscp testing: caffeine-halothane contracture test = fresh muscle biopsy (thigh) and exposre to triggers; Sn
97%, Sp 80-93%; if CHCT+, then genetics test of Ryr1 mut (high Sp)
Lido 3-4hrs Mep 4-6hrs +4hrs if clonidine+90m 40-80% if epi
Chlorprocaine 60-100m bupi/ropi 12-14hrs
CARDIAC:CNS ratio: Bupi/levo/ropi 2 Mep/Lido 7

Other PHARM/PHYSIO:
BB: hypoglycemia (B2 block), antinociception (dec opioid use), dec AQ humor, dec T4→ T3 peripheral
Glucagon: inc cAMP = inc PKA = antidote to BB
Alpha1= Gq = PLC = IP3 = Ca release fr SR; blocks insulin, lipolysis; mild inotropy, inc afterload, neg chrono
- NE inc SBP and DBP; E inc SBP, min eff on DBP
Alpha2 = Gi = dec cAMP = inhibit insulin release; blocks NE release fr presynaptic terminals
Phenoxbenzmine = irrev alpha1&2 blockade = can inc HR/BP(bc of alpha2 block)
B1: cAMP lipolysis, HR, contractility, lusitropy, RENIN
B2 = cAMP = Ca into SR; vasodilation, bronchodilation, glycogenolysis, insulin release
Insulin: anabolic = inc glycogen/protein (inc aa uptake), inc GLUT4, inc Na/K pump
REg insulin, onset mins 1U dec Gluc by 25pts; 5U = 125pts
SQ insulin onset 15m, lasts 4-6hts; NPH = 1-4hr onset, lasts 18hrs
Tyr→ dopa→ NE→ E
Tryptophan: 5-HT, melatonin
Alanine: pyruvate, glutamate transport; glucose→ pyruvate→ alanine (ALT, uses N2, 2ATP) travels to liver: ala-->pyr→ gluc =
negative nitrogen balance
Leucine/lysine = ketogenic → acetyl CoA but no pyruvate/glucose
Phe/Isl, thr, tryp, tyr = keto/gluco
LIVER: COMT→ MAO; NEURONS: MAO→ COMT
Dopamine: low dose= DA1 = inc RBF/UOP but no renal protection
- high dose = alpha1>>>D1 = inc SVR, dec RBF
Dobutamine: B1>>>B2 = alpha1; inc HR less vs dopamine
Dopexamine: B2>>>B1 = inc CO in CHF, can exacerbate hypotension; potent D1
Phentolamine blocks alpha 1 and alpha2
NTG(v>a) and nitroprusside(a=v, $$$, CN toxicity) in ICH!!!
- Nitroprusside causes MetHgb bc ferrous→ ferric; Tx with methylene blue
- Nitroprusside→ CN toxicity bc breaks down into NO and CN-; Tx Na-nitrite = sink for CN = inc met Hgb; methylene blue to Tx
cyanometHgb, then give sodium thiosulfate
Milrinone: PDE3inh = inc cAMP (no breakdown)--> PKA Fenodolpam: D1
NO dec PAP via Gprotein→GC→ cGMP = vasodilation Sildenafil inhibits PDE5 = no cGMP breakdown
Nesiritide ~BNP = inc GC/cGMP/vasodilation
IV admin→ vessel rich→ vessel poor organs; dec clinical effects fr alpha phase of REDISTRIBUTION; then equilibriate bw vessel
rich and vessel poor; subsequent doses inc plasma levels; dec clinical effects from beta phase of CLEARANCE rate
Volume of distribution Vd is SMALLER for hydrophilic vs lipophilic drug
½ life INVERSELY proportional to CLEARANCE RATE and PROPORTIONAL to Vd
Lipid solubility ~onset speed and inversely proportional to EFFECT DURATION but not related to ½ life
-Fentanyl long elim ½ life bc inc protein binding and lipid soluble
Clonidine: cross BBB = dec SNS outflow fr brainstem, dec PAIN transmission= ANALGESIC
 Dexmethorphan = anticough, NMDA antag (like methadone, ketamine), has local anesthetic effects like meperidine, SSRI effect = can
ppt 5HT syndr like tramadol, meperidine, methylene blue, methadone!
Methadone: u agonist AND NMDA antagonist!
SSRI blocks CYP2D6: converts
- hydrocodone to hydromorphone (4x analgesia)
- oxyc-->oxym (2x)
- codeine-->morphine
RAS→ thalamus→ cortex; Almost all anesthetics block RAS; KETAMINE acts on THALAMUS and DISSOCIATES RAS FROM
CORTEX
Review Reponse Vs DOSE curve; horizontal shift = potency; vertical shift = efficacy
Esmolol = RBC cytosol esterases and pseudocholinesterase; NL ½ life 10m, 15m if psc def
LA = esterases and pseudocholinesterase
Miv and Sux: pseudocholinesterase
Remi = esterases (not pseudochol)
Esmolol, pancuronium, cyclophosphamide, phenelzine inhibit pseudocholinesterase
1% = 10mg/ml = 1:100
Allergies to LA: esters = PABA metabolite; amide = methylparaben preservative; EPAM!!!
HyperK periodic paralysis mut VGNC: ppt by FASTING (NPO), respiratory acidosis, and hypothermia; no pulm or cardiac issues
bc no involved channels there; exercise is good; admin glucose, CaCl; Sx weak trunk and extremities, diaphragm preserved!!!!!
HypoK paralysis mut VGCC: ppt by hypothermia; Tx KCl, diamox, reversis hypothermia and reverse alkalosis
Glycine irrigation = inc NH3, hypoNa, inc glucose, transient blindness fr CNS depression
Organ procurement: vasodilation, NE/E stimulation = exhausion; diabetes insipidus from HPA dysfxn; 3-drug Tx with steroids,
thyroid, vvasopressin; MAP>60, UOP >1cc/kg/hr; LVEF 45%, Hct 30

FLUIDS
Hypovol if IVC<1.7cm or 50% variation
Pulse pleth variability index PVI
PPV>10-13% (can’t use if not SR, if open chest, if not on PPV or if TV>8cc/kg)
TBWater = wtx0.6males, 0.5females; 5% intravasc, 15% interstitial, 40%intracell
CRYSTALLOIDS: 1:4 intravasc
NS: pH 5.5 NS 308osm, 154Na, 0K; exacerbate hyperK fr metabolic acidosis
LR: pH 6.5, 273osm, 130Na, 4K, 3Ca, 3lactate (risk of hypoNa, LR metabolized to GLUCOSE, lactate met to HCO3 in liver; Ca
interferes with citrate chelation of RBCs)
Plasmalyte: 294osm 140Ns, 98Cl, 5K, 3Ca, 1.Mg, acetate, glucose
3%Saline 308osm, pH 5-6 154/154
D5W: 253osm, 50g/l glucose
COLLOID: 1:1; longer intravascular time; inc coagulopathy DEXTRAN>HES
Albumin 5% for hypovol; 25% for hypovol if pt is restricted Na/IVFs; theoretical risk of PRION DZ
HES: max daily 20cc/kg, branched chain glucose degraded by amylase, elim by kidney; INC PTT, DEC F8/VWF = plt dysfxn;
anaphylaxis
Tetrastarch: 50cc/kg max
mIVFs: if>20kg, 40+weight; other 4:2:1 (10,10,rest), give ½ /hr, ¼, ¼ ; then ongoing fluid loss w/surg: if minimal tissue trauma, 0-
2cc/kg/hr; if severe tissue trauma 4-8cc/kg/hr
BURNS: avoid glucose-continaing IVFs bc large volumes and stress can cause hyperglycemia!!! Use LR;
Parkland formula=Volume = %BSAx4cc/kg give ½ over 8hrs, then ½ over next 16hrs
%BSA = rule of 9%, hand = 1%; good resusc will cause dilutional anemia
First deg burn epid/upperdermis; BAD if 3rd-4th deg >10% BSA, 2nd deg >20-25%, burns to hand/feet/perineum/face, or if all burns
in pts with severe preexisting cdns; ARDS compartment syndr
PRBCs:
Type: ABO, antiD (rh), direct = detect Ags in recipient’s blood using antibodies
Screen: indirect = detect Abs in recipients’ blood using known Ags
T&S: if using T&S only = <1% risk of hemolytic rxn; takes 30-120m, lasts 72hrs
T&C (after negative T&S) = 30-60m
-immediate phase: direct recip serum Abs + donor cells (to detect Ags) ~5m
 - incubation phase: incubate from first test to look for incomplete recipient Abs to donor (Rh)
- indirect antiglobulin test: Ab serum of first two tests to look for incomplete recipient Abs to Rh, Kell, Duffy, kid
1PRBC inc Hgb by 1g/dl, inc Hct 3%; don’t run blood in LR bc clot formation d/t Ca; don’t run in D5W bc hypotonic = LYSIS
10% of RBCs hemolyze after transfusion = jaundice if Gilbert’s
Citrate-phosphate-dextrose sln@4deg = 21 days; CPD-adenine = 35days; Adsol = 42days, warmer
Citrate = anticoag metabolized by LIVER; phosphate = buffer; dextrose = energy; adenine for ATP synth
PLATELET: Rh tested only, can give ABO incompatbile; Rh sensitization can occur bc small amt of RBCs present ; transfuse if
plt<50K
Platelet concentrate (PC) = 1 donated unit = 5K-10K plt = 50-70ccs
Apharesis unit: fr single donor ~250ccs ~50K plt
Reverse Plt dysfxn with DDAVP 0.3mcg/kg in 50ccNS over 30 min
FFP: fluid portion fr whole blood, has all coags except Plt; need to be ABO compatible but Rh incompatible is OK; stored FROZEN
= need 30m thaw & use w/in 24hrs; AB = universal donor (vs O = universal donor in RBCs); give if INR>2, excessive microvasc
bleed, massive tranfs (1:1), urgent warfarin reversal (or use PCC), correct factor def, heparin resistance in pts needing heparinization
(ex. Antithrombin III def)
CRYO: a component of FFP, fraction of plasma that ppt when FFP is thawed; factor I (fibrinogen), 8, 13, VWF; 1 unit of cryo has
5x more fibrinogen than 1U FFP; 0.1U/kg inc [fibrinogen] by 100mg/dL; use w/in 4-6hrs after thawing if want to replace factor 8;
give if [fibrinogen]<100 with bleeding, massive transf, bleeding VWF deficient pts, congenital fibrinogen deficiency
Allowable blood loss: (Hctinitial - Hctallowed)/ Hctinitial x EBV
- EBV males = 70cc/kg; females = 65cc/kg; 1-6yo= 75cc/kg; term = 90cc/kg; premie = 100cc/kg
Massive transfusion: defn >1blood volume (10U) in 24hrs; complications:
- Hypothermia fr cold storage → coagulopathy (use warmer)
- Dilutional coagulopathy (ex Plt<100K after 10U PRBC); factors ⅝ labile in stored blood
- Citrate toxicity = chelates Ca and binds Mg = hypoCa (give Ca); rapid transf >65cc/min = acute hypoCa, hypoMg
- Acidosis fr Co2 prodexn (ventilate to eliminate)
- HyperK
- Impaired O2 delivery capacity bc stored blood = dec 2.3DPG = left shift, Hgb holds onto O2
Infection: CMV (1:100K)>HBV(1:300K)>HCV>HIV>HTLVII
Bacterial RBC: 1:38.5K Yersinia stored at 4deg; Bacterial Plt 1:5K bc stored in Dextrose @ room temp
Blood screened for HCV/HBV core/HIV1/2, HTLV, syphilis, Zika
HBV primary ppx: 3series vax; most acute infxn resolves, 10% progress to chronic carriers; PEPPx = Ig and vax
Transfusion reactions:
Febrile nonhemolytic: residual donor WBC/Plt, avoid w/leukoredxn; Tx tyl, benadryl, slow transf
Anaphylaxis: in IgA def pts; avoid with washed to dec plasma proteins; Tx IVF, epi, ACLS, benadryl
Acute hemolytic: ABO incompatibility = hematuria, flank pain, fevers chills; Tx = stop, alkalinize urine (bicarb, mannitol, lasix, IVF)
Delayed hemolytic: non-AB donor Ags w/in 2-21 days
TACO: circulatory overload; order volume reduced for pts with CHF
TRALI: 4-6hrs after; Plt/FFP>RBCs; donor Abs against recipient WBC (like graft vs host) = leading cause of transf-related
mortality; rule out sepsis, volume overload, ADHF; Tx as in ARDS (lasix not helpful)
Autologous transfusion: collect blood 4-5wks before surg
CellSaver: blood-->reservoir-->mixed with heparin, debris removed; contraind if Cx/sepsis
Normovolemic hemodilution: take 1-2U blood, store in CPD bag, replace with crystalloid for goal Hct 20-25%, glood given back
after blood loss

PULMONARY/OXYGEN: shunt = atelectasis, mainstem, pulm edema etc (doesn’t improve w/O2 if shunt burden is 40%)
PaO2 = FiO2 (Patm - PH2O) - PaCO2/0.8; 0.21(760-47) - 40/0.8 = 100mmHg; can dec water vapor component via hypothermia
(dec PH2O)
PaO2 60/SpO2 90; 90/97 80/92 60/90 50/80 40/70 27/50; 60 50 40 / 90 80 70; NL PaO2 = 103 - age/3
PO2 vs SpO2 curve:
-LEFT shift: alkalosis, hypothermia, hypocarbia, dec 2,3DPG (stored RBCs), CO-Hb, Met-Hb, Sulf-Hb, Fetal Hgb, myoglobin
-RIGHT shift: acidosis, hyperthermia, hypercarbia, inc 2,3DPG, sickle cell, pregnancy, volatiles, chr anemia
A-a gradient: should be <10 if FiO2 21%, <60 if FiO2 100%; <age/4 + 4; a/A >0.75; @ high PaCO2, A-a gradient DECREASES
Thebesian, bronchiolar, and pleural veins bypass right heart and empty into LA = shunt!
CvO2 = 15cc O2/dl (assuming SvO2 = 75%)
 CaO2 = HgbO2x1.36x%SpO2 + PaO2x0.003; 15x1.36x1 + 100x0.003 = 20cc O2/dl
O2 consuption = FICK EQ: VO2 = COx (CaO2-VaO2) = 5L/min (20-15) = 250cc O2/min
O2 delivery = DO2 = COxCaO2 = 5L/min x 20cc O2/dl = 1L O2/min
O2 Extraction ratio: ERO2 = VO2/DO2 x 100 = 25% (NL 22-30%); coronary extract more ~80%
Bohr: @ tissues, right shift to unload O2 fr Hgb
Haldane: @ alveoli where O2 binding promotes CO2 unloading from Hgb
Extubation:
1) Rapid shallow breathing index RSBI = RR/TV <105 = ideal
2) NIF <-20mmHg
3) TV>5cc/kg, SpO2>90, FiO2 <40%, PaCO2<50, RR<30
4) Headlift >5s, sustained tet >5s
Inspiration = inc RH load, dec LV preload, inc LV afterload
Type II pneumocytes outnumber Type I; makes surfactant and differentiate into Type I; macrophages
90% resistance fr conducting airways = upper airways to terminal bronchioles (non cartilage, highest proportion of smooth
muscles); upper airways = turbulent>laminar; term bronchioles = asthma
- Reynolds: inc R = inc turbulence = inc resistance
JET VENTILATION: 12-16G @ cricothyroid membrane, min-max PSI 15-55psi, recommended 35psi; passive expiration (inc E
time to avoid air trapping); contraindicated in trauma, altered anatomy; relative contraindication in COPD, coag problems
Transillumination: lighted stylet→ glow @ cricoid cartilage; helpful if secretions/blood; avoid if obese or trauma
Fiberoptic for difficult airways from neck mobility issues
Airway Exchange catheter: HOLLOW tube ~ bougie but also allows O2/ventilation, can connect to jet or circuit, etco2 monitor in
extubated pt for rapid re-intubation if needed; fits over flex bronch
Altitude: dec FiO2 = PaO2 = inc vent = dec PaCo2 = inc pH
Review AV vs PaCO2 graph; same slope shift right = ventilation depressants; shift right AND downward slope = dec venilatory
response to CO2 (high dose opioids, volatiles @1MAC)
Lung zones: 1 = high V/Q (deadsp), 2 = V/Q 0.8, 3 = low V/Q(shunt);
- 1: PA>Pa>Pv 2: Pa>PA>Pv 3) Pa>Pv>PA
Normal SV: ⅔ TV for ventilation, ⅓ TV is deadspace
Mechanical vent: same perfusion but increase alveolar pressure so inc V/Q = ½ TV deadsp
Review flow volume loops:
- Restrictive lung dz = shift right and smaller
- COPD = larger volume and concave expiratory limb
- Variable extrathoracic obstruction (vocal cord dysfxn) = flattened inspiratory limb
- Variable intrathoracic obstruction (tracheomalacia) = flattened expiratory limb
FEF25-75% = early indication of disease (before FEV1/FVC changes!!!
FRC lowest @ 12hrs postop=shunting; FRC = RV+ERV
Abdominal surgery = dec ERV 25%>TV/TLC 20%; inc RV 10%
Pregn: unchanged VC from inc IRV/TV, dec FRC(dec RV/TLC)
Plateau pressure = STATIC, related to system compliance (chest wall, lungs)
PEAK pressure = dynamic related to AIRWAY resistance
- Inc plat and peak = ARDS, obesity, endobronchial ETT, inc TV
- Inc peak but not plateau = upper airway, asthma, anaphylaxis, bronschospasm, inc FGF
Closing capacity: volume remaining in lungs during exhalation when alveoli start to close = closing volume + residual volume
COPD ECG: low voltage from hyperinflation
Smoking cessation at least 2 months= improves operative outcomes; cesation for <1 day = dec carboxy Hgb to normal levels and inc
O2 carrying capacity
Muscles of inspiration: diaphragm, strap muscles (scalenes = NL insp, SCM = deep insp), external intercostals
Muscles of expiration: NL passive, but effort = internal intercostals, abdominal muscles
NEgative pressure pulmonary edema: 0.1% incidence under GA, RF = young, male, fit, HEENT surg, symptoms (frothy sputum)
immediately after relief of obsturction; pathophysiology involves increase in preload and afterload
NITROUS inc PAP; NO dec PAP via Gprotein→GC→ cGMP = vasodilation

ANATOMY:
CN IX: sensory pharynx, tonsils, tongue(posterior ⅓); block via anterior tonsillar pillar (lingual, tonsillar, pharyngeal branches only)
 SLN internal br: sensory above vocal cords; block near inferior aspect of great cornu (hypohpharynx); if too lateral or inferior = will
accidentally block external br of SLN
SLN external br: motor above vocal cords and cricothyroid m.( which tenses for pitch)
RLN: sensory below vocal cords and motor to all intrinsic m except cricothyroid; note that posterior cricothyroid = abduct; RLN
injury = unopposed cricothyroid (extSLN) = adduction; transtracheal block = block RLN sensory but SPARES motor innervation!
Most Sn indicator for difficult ETT - MP3-4 (Sp 80-90%)
- Sternomental <12.5cm
- Interincisor <3cm
- Thyromental <6.5cm
Mask vent difficulties: previoius neck rad, beard, OSA, male, MP 3-4, obesity, neck circ >60cm
Narrowest part of adult airway = glottic opening; of neonate is @cricoid cartilage under cords
RUL bronchus is 2cm below carina (T4/T5, sternal angle)
Laryngospasm(closure of true VCs +/- false VCs): affernt = SLN int br, efferent = RLN; ETT>LMA>face mask; URI <1mo, peds
3x>adults; can be caused by hypoCa; Tx jaw thrust, suction, CPAP, bag mask, deepen aneshtesia; suc 10-20mg IV or IM, monitor
for NPPE (young ASA I-II, 80% males, frothy sputum, large A-a gradient, pulm edema on CXR)
Jaw thrust:
Sniffing: oral axis perp to pharyng and laryng axes; flex C-spine, extend alanto-occipital jt
SNS = T1-L3; T1-T4-->stellate ganglion (lvl C6) → cardiac nerves
Sensory for lungs = vagus nerve
Brachial plexus is bw anterior scalene (ant, med) and middle scalene (lat, post); subclavian artery is also bw middle and anterior
scalene (BP is lateral, post, sup to SCA); SCV is anterior to ant scalene; phrenic n anterior to anterior scalene = dec ventilation by
25% if affected
- 100% phrenic n palsy with interscalene block; 40$ w/supraclavicular block
- NPPV helpful in phrenic n palsy
Interscalene block: spares ulnar C8/T1 and proximal cutaneous shoulder (req superficial cervical block to cover incisional pain)
- vertebral artery if too deep/cadual (immediate seizure vs carotid)
- Carotid artery and phrenic n if too anterior
- Stellate gang/Horners if near chassaignac’s tubercle
- Spinal/epidural if caudal and medial
Supraclavicular block: usually covers ulnar C8/T1; more risk for PTX than infraclavicular
Axillary nerve block: excludes musculocutaneous = lateral forearm, block separately within coracobrachialis muscle
- axillary artery reference: radial n = lateral/bicep, median n = anterior, ulnar n = medial and posterior
Left subclavian approach is highest risk for thoracic duct injry (TD exits where SCV meets IJV)
IJV courses bw anterior and posterior heads of SCM
Chylothorax Tx: chest tube, high protein/carb and low fat diet, PEEP
Internal carotid artery ICA gives rise to MCA
Spinal cord blood supply: ASA syndrome = paraplegic but intact sensation
- 1 ASA artery supplies ant SC (+posterior ICs anastomoses) to thorax and L&S spine; @ T8-L1 aorta gives rise to Adamkiewicz for
addl supply; upper thorax is watershed area
- 2 PSA supplies post SC
Spinal cord terminates (conus medullaris) @ L1 in adults, L3 in neonates; celiac plexus @ L1
Dura sac: @S1 in adults; S3 in neonates
C8 nerve root below C7
T4/T5 = lvl of carina = sternal angle
T7 = inferior tip of scapula
C7 = vertebra prominens
C6-C7 = lvl of stellate ganglion; block - Horners, vasodilation, stuffy nose, flush, inc pulses fr vasodilation, ptosis, miosis,
enophthalmos, anhidrosis
L4 = superior aspect of iliac crests
Interspace bw spinous processes are leveled in L spine but T spine has downward sloping spinous processes
Facet joint innervation is by medial br of posterior division of spinal nerves
Lateral upper arm = axillary nerve, radial nerve
Musculocutaneous nerve block = lateral forearm sensation
Median nerv = palmar 1st to laterl 4th digit; wrist flexion and elbow extension
Radial nerve: dorsum of hand; wrist extension
Ulnar nerve = pinch; prolonged prone = ulnar n entrapment; 28% claims; RF = very THIN or OBESE pt, male, long bedrest, old age,
hyperflex elbow; KEEP ARM SUPINATED TO AVOID; if motor prob = consult neurology, if sensory, resolves ~5d; EMG is
NORMAL immediately (takes time for abn signals)
Antecubital fossa = median nerve which is medial to brachial artery
Sensation of thigh: mostly femoral, medial thigh AND KNEE = obturator, lateral thigh = lateral femoral cutaneous
Lower leg sensation: mostly sciatic nerve, except medial lower leg and medial ankle which is saphenous nerve (a branch of femoral
n) and not covered in sciatic nerve block!!
Sciatic gives rise to tibial n and common peroneal nerve
Posterior lateral lower leg and lateral ankle= sural nerve, a br of tibial n
Superficial peroneal n = foot dorsum except intersp bw 1st/2nd toes by deep peroneal n
Tibial nerve: plantar foot; sural nerve = lateral ankle
TAP between tranversus abdominus and internal adbominal oblique
Obturator reflex: stimulate lateral bladder wall = thigh adduction; prevent with GA and NMBA
Oculocardiac reflex: afferent = V (ophthalmic br); efferent = X

CARDIOVASCULAR:
BP = MAP-CVP = CO (HRxSV)xSVR; infants = fixed SV so change in CO is fr change in HR; NL stroke volume is 70ccs
SVR = 95% of impedance to ejection; P=(COxSVR)/80; SVR(woods) = 80P/CO; SVRx80 = dynes/cm^5; contractility =
force&velocity
VO2 = COx (CaO2-VaO2)
Cardiac Index = CO/BSA NL 2.6-4.2 L/min/m^2; max CI @ HR 120, if HR<40, SV maxed out and CI starts to dec; SV max occurs
@ HR 60
CO: liver>kidney>brain@ rest
PP NL = 40@rest, 100@exsc; narrow<25 = AS, coarct, tesnion PTX, ADHF; wide>40 = AR, atheroscl, PDA, inc CO states
-SC lesion above T5 = severe autonomic hyperreflex = HTN; below T10 = mild; SNS = T1-L3
-Tx intraop HTN: prop or volatiles or opioids (analgesic, histamine = vasodil); clevidipine = shortacting; avoid NTG(v>a) and
nitroprusside(a>v, $$$, CN toxicity) in ICH!!!;BB
Review Drugs
-REVIEW Tx CN toxicity
-increase QTc: hypoK, hypoCa, hypoMg
SA node: 4034; Na, Ca, K; 0 = calcium
Ventricle: 01234 Na, K, Ca, K RMP; 0 = sodium
PNS to heart mediated by dorsal vagal nucleus
SNS T1-T4-->stellate ganglion (lvl C6) → cardiac nerves
Bezold Jarisch = left ventricle receptors detect low pressure/sudden dec preload = empty heart→ vagal tone = brady, hypoTN,
coronary vasodiliation; AKA DEC VOLUME = DEC HR
**esp in SPINALS bc cardioaccelerators @T1-T4 blocked!; higher block = dec HR
Bainbridge reflex: atrial reflex to an increase in volume (ex. bolus) = dec vagal tone = inc HR fr medulla input & SA stretch = inc
automaticity = inc HR; AKA INCREASE VOLUME = INCREASE HR
Baroceptor reflex: carotid Sinus→ CN 9→ Hering nerve → medulla → inh SNS, inc PNS; chemoR are more SN than baroR to
anesthetics and can influence ventilation!
Alpha1= Gq = PLC = IP3 = Ca release fr SR
B1: lipolysis, HR, contractility, lusitropy, RENIN
B2 = cAMP = Ca into SR; vasodilation, bronchodilation, glycogenolysis
NO → GC = inc cGMP = improves V/Q and dec PAP
ANP + EtOH inhibits ADH = diuresis
Troponin binds actin and covers myosin-binding sites on actin; Ca binds troponin to displace trop; myosin-ATP is unbound to actin,
hydrolysis → release P = myosin binds to actin, then releases ADP = power stroke, and myosin is stuck to actin until another ATP
comes
LaPlace: T = Pr/2h(wallthickness)
Pouseuille: Q = Pr^4/8nl n = visc, l = length of tubing
Boyles PV (basis for Tx of gas emoblus with hyperbaric O2); Charles V/T; GayLussac P/T
Starling: Q=kA(Pc-Pi) - o(nc - ni)
 CAD and surgery: thrombosis of BMS less likely to yield SCD vs thrombosis in DES; BMS = low incidence of early thrombosis but
higher rate of late thrombosis (>1-3mo)
- If ACS and no intervention: wait 2 months before elective surg
- DES for ACS: DAPT 12 months before elective surg; 6mo if issues with delaying surg
- DES after angina/routine test: DAPT 6mo before elective surg
- BMS: DAPT for 1 month
- Balloon angioplasty: 14d
Aflutter Type 1: ablate isthmus bw IVC & TV annulus
Cardiac X Syndrom: clean coronaries but angina fr microvasc dz of very distal regions
ECHO: pressure difference = 4v^2 (v = velocity); dp/dt = LV contractility; can use MR jet velocity @ isovolumetric contraction
(independent of afterload)
- Sphericity index = LONG AXIS: SHORT AXIS; >1.5 is normal; DEC with dilated CM
TTE better than TEE for pulm valve vs PV is so anterior
CVP tracing: ACxVy; A& Y = diastole; CV = systole
- C = isovolumetric contraction & TV bulge (lost in TR)
- V = atrium filling against closed TV; occurs after Twave
- X atrium relaxing mid systole
- Y = ventricle filling TV opens; LOST IN TS
CABG: better FLOW but dec O2 carrying capacity; also machine is primed with crystalloid = dilute and dec viscosity =
hypotension; Q ~ D^4 ~1/viscosity; if NL HCt, blood is 3x as vscious as water
PM = no MRI (IUD is OK); Magnet turns off tachyarrhythmia therapy but not PM!, defaults to VOO = risk of R on T in pts who are
not completely PM dependent; paced rate needs to be HIGHER to dec risk of R on T
- Avoid monopolar
- <10s of cautery at a time
VENOUS AIR EMB: 100ccs enough for CV collapse; 300-500cc = fatal; Tx = flood field with saline, compress jugular vein, inc
PEEP (inc CVP, dec air) but watch BP, dobuatmine or epi, left lateral position which places RVOT inferior to RV to overcome
airlock, hyperbaric O2, right heart air aspiration from central line = shortest resusc time

ELECTROLYTES
HypoCa, HypoMg = decrease PR, narrow QRS, prolonged QT
HyperCa, HyperMg = prolong PR, widened QRS, short QT
HypoK =dec P wave, prolonged PR, prolonged QT, reentrant, conduction delay, PAC, PVC, SVT, ileus, inc dig toxicity; inc Sn to
NMB (like hyperMg also); can occur fr hyperventilation; replete 10-20 central or 10meq/hr PIV
HyperK EKG progression: Tall Twaves, long PR, low pwave amp, lose pwave, wide QRS, SINE, asystole
K>7 = ascending flaccid paralysis, resp arrest; Tx PIV Cagluconate 10cc/5m; central line CaCl; do not give Ca if digoxin!!!; bicarb,
insulin, albuterol, diuretics, kayexa, sorbitol (oral/rectal), dialysis; cancel elective cases if K>5.5; hypothermia = alkalosis = DEC K
HypoCa: fr renal failure, sepsis, MAG DEF (dec Sn to PTH), ALKALOSIS, PRBC transf, drugs (heparin, protamine, glucagon!),
hypoPTH = prolonged QT, brady, hypoTN, laryngospasm, seizures, stridor, cramps, perioral numbness; 1g of Cagluconate =
4.5meq Ca; 1gCaCl = 13.6meq Ca; avoid alkalosis bc less H+ = more Ca bound to albumin = worsen hypoCa; dont give Ca with
bicarb or else ppt (@ code)
HyperCa: short QT, prlonged PR, HTN, polyuria; Tx hydrate lasix, HD; avoid acidosis
Ca antagonizes K
HypoMg: Gi/renal loss, B agonist shift intracell, theophylline, AGs, AMB, cyclosporin; long QT, PAC, PVC, afib, inc DTR,
excitability, AMS, seizures; if repletion, watch for hypotension and arrhythmias
HyperMg: fr TPN, laxatives, Mg admin, renal failure, hypoT; wide QRS, long PR, brady, dec condxn, relaxes, dec DTRs, paralysis
when Mg = 15-20; resp failure, CHF, vasodil = hypoTN; Tx hydrate/lasix, admin Ca; potentiate NMB (like hypoK)
Mg is treatment for preeclampsia goal Mg 5-9; Mg = NMDA antagonist = dec pain, seizures; 50mg/kg over 15m, then 8mg/kg/hr

RENAL:
LOH: water impermeable w/hypertonic interstitium (blocked by lasix); PT = AQ channels = isotonic absorption
Aldo inc ENaC and Na/K pump
 Low flow or B1 → JGA to secrete renin; renin converts angiotensinogen to ATN I
ATN II = MESANGIAL CELL contraction = aldosterone release from adrenal cortex; also constrict eff>aff
Creatinine clearance = filtered AND secreted = overestimates GFR
Hypophos: dec resp, prolonged NMB HypoMg = inc PR, QT hypoK = flattened T wave, U waves, inc PR, ST dep
Strong ion gap: cations minus anions NL 40; inc SIG = metabolic alkalosis (dec Cl-); Dec SIG = metabolic acidosis (inc Cl-)

GI/LIVER
Vasopressin inc hepatic artery R, decrease portal vein R = useful in portal HTN mgmt
- Blood supply = 20% HA, 80%PV
MELD: I Crush Several Beers Daily; predict periop mortality; INR, Cr, Sodium, Bili, Dialysis
CHILD PUGH: Pour Another Beer At Eleven; PT Ascites Bili Albumin Encephalopathy
Liver synthetic function = PT; Factor 7 = shortest ½ life 4-6hrs
Albumin ½ life = 20d

NEURO: PVS has eye opening vs COMA

Glutamate → AMPA, NMDA, kainate, Ca; Mg allosteric block, ligand and voltage gated
Brain uses glucose but switches to ketone @starvation
Review CBF vs diff Pressures (PaCO2, MAP (autoreg section), PaO2)
Volatiles (except nitrous) inc CBF and inhibit autoreg so MAP & CBF becomes linear
Iso>des>sevo for inc CBF
Des>Iso>sevo for inc ICP; Des inc CSF, sevo dec CSF, iso = no chnage in CSF
Propofol, etomidate, barbs (thipental), and benzos mildly dec CBF and inc CVR
Sufentanil and fentanyl inc CBF (Controversial)
CSF has less protein than serum
CSF synthesis 500cc/day; synth in lateral ventricle and choroid plexus→ interventricular foramina of monroe-- 3rd ventricle→
CA→ 4th ventr→ Foramen of Magendie/Luschka→ cisterna magnum→ SAS→ arachnoid granulations→ venous system (low protein
in CSF promotes drainage)
Lasix and acetazolamide dec CSF prodxn
Multiple sclerosis: epidural is OK; all other anesthesia (GA, spinal) can exacerbate MS symptoms
A nerves: MYELINATED
A-alpha: motor and proprioception (spindles, jts, Golgi); LARGE, MOTOR/PROP
A-beta/gamma: cutaneous touch, pressure and muscle spindles; TOUCH
A-delta: low activation threshold, FAST CDXN; PAIN/COLD; SMALL; @nodes of Ranvier
C fibers: small non-myleinated SLOW CONDXN, PAIN/HOT AND post-ganglionic condxn
Pain: DRG (1st order) synapse @ dorsal horn SC (2nd order) which crosses contralateral SC thru STT, then synapse @ reticular
formation PAG thalamus to a 3rd order neuron which synapses at sensory cortex of postcentral gyrus
**PAIN/COLD SENSATION = TWO DERMATOMES above level of anesthesia
Posterior nerve root = somatic and visceral sensory
Anterior nerve root = SNS and motor
Pain inc cortisol, ATNII, ADH (SIADH!), Ne/E, cytokines, ACTH, GH, glucagon
Peripheral sensitization: 1st order neuron; nociceptors require less stimulus to fire AP, send more APs when stimulated and receptors
are upregulated and send off APs even after stimulus ends; mediated by bradykinin, histamine, PGs
Spinal Cord Sensitization: same as above but with 2nd order and 2nd order neuron will induce 1st order neuron to incite it further
(wind up); mediatd by AMPA, NK1 (Substance P), NMDA and interneurons!!!!
Preganglionic PNS fibers: LONG, synpase near target organ (ciliary ganglion)
Preganglionic SNS fibers: SHORT, synapse @ paravertebral ganglion (ex superior cervical ganglion)--> postganglion fibers
(short/long ciliary nerve)
LA: SNS-->sensory→ proprioception → motor; LA block preganglionic B fibers of nerve roots = dec SNS
POCD: in both general anesthesia AND regional; anesthetics→ central ACH insufficiency & B-amyloid phosphorylation
Differential block: diff nerve fibers have diff sensitivities via diff spatial separation to local anesthetic (hence SNS→ pain/touch→
motor); @cephalad level, dec [LA] and SNS fibers to not require same concentration to be blocked vs motor nerves; sympathetic
block ~ 2-4 dermatomes beyond the motor block, the pain/touch ~2-3 dermatomes beyond motor block; sometimes temperature
blocked but inadequate sensory block = pain, so use more LA!
Sacral sparing: patchy less dense in L5-S2 distr bc large nerve roots; Tx by bolus in Reverse trendelenberg
 Unilateral blocks: from catheter migration or presence of dura septations
Intrathecal microcatheters: can cause cauda equina syndrome
Lidocaine spinals + lithotomy → transient neurologic syndrome (TNS), can dec risk if aspirate CSF cc equal to cc of injection; Sx =
butt pain, leg burning lasts ~1week
EDTA in chloroprocaine epidurals → severe back pain; **if used in epidural with opioid, interferes and increases postop
pain!!!!!!!
RF for bradycardia after spinal: block ht, age<50, ASA1, betablock use
Spinals are contraindicated in aortic stenosis bc dec aortic diastolic pressure
Morphine = lipophilic = doesn’t cross dura = spends long time in space = inc risk of cephalad spread high thoracic = late resp
depression; no mroe than 300mcg; peak analgesia 6-12hrs; resp dep has 2 peaks early (brainstem) and late (6hrs later, high thoracic
spread)
Normal kyphosis = limit mvmt of LA to T6 level!
Dec CSF = higher block (pregn, ascites, kyphosis, age, OBESITY)
Intrathecal opioid itch: central mech (doesn’t involve histamine) = benadryl is useess; prevent and treat with zofran!!!!!
Epi adds density to SPINALS but not epidurals!
Enoxaparin and epidurals:
- 1x daily or BID prophylaxis = 12hrs after last dose, 12hrs restart, 12hrs removal, then 4hrs restart
- Daily therapeutic= 24hrs after last dose; at least 24-72s after removal
Plavix 7d, ticlopidine 14d, Fondaparinux = no recs, abcixamab 1-2d, tiro/epti 4-8hrs; no contraindiations to ASA or NSAIDs or
ginkgo or garlic!!! Alteplase 10d, dabigatran 3d
Warfarin and epidural: if stopped 4-5days, check INR and don’t place if INR>1.5, PTT>40
Heparin and epidural: if >5d of any type of hep, obtain PLT to r/o HIT; neuraxial block 4-6hrs after ppx dose or else need PTT <40;
restart anytime after
EEG: frequency = x axis; power = y axis, time = z-axis
- Slow <1Hz
- Delta 1-4Hz stage 3-4
- Theta 5-8Hz stage 1
- Alpha 9-12 Hz drowsy
- Beta 13-25Hz awake
- Gamma 26-80Hz awake
- Spindles = light sedation stage 2 (with K complexes)
Stage 2 NREM = delta + bursts of high alpha and low beta
Stage 3 NREM = no spindles
Ketamine = high beta and low gamma (like awake) 25-32Hz; ketamine targets open>closed NMDA channels and inhibitory
interneurons (generally OPEN) = inc excitatory downstream
General anesthesia: slow delta & alpha oscillations (GABA like mech); if volatiles = theta apperances
Sevo: subMAC = slow delta, alpha osc; 1+MAC = theta oscillations appear 5-8Hz (non-GABA mech)
**THETA=characteristic of inhaled anesthetics**
EEG electrocerebral silence if lack of activity >2uv/min (minimum of 8 elecrodes 10cm apart)
Evoked potentials:
- Brainstem: barely Sensory: somewhat Motor: mostly Visual: very
Transcran doppler: measures blood flow velocity (MCA), if redxn >50%, needs shunting; also measures # of atherosclerotic emboli
PAIN CTRL: CEI>PCEA>PCA>PRN for pain control
EMERGENCE DELIRIUM: Tx/ppx clonidine, precedex, fent, ketamine, nalbupphine, prop
Postop ISCHEMIC OPTIC NEUROPATHY: 2 types both PAINLESS
- Anterior ION after heart surgery
- Posterior ION after spine surgery
Microelectrode recordings (MERS) for DBS placement; benzos worsen dyskinesias and obliterate MERs; precedex OK; prop
attenuates but rapid titration makes it OK
SAH grading:
Hunt criteria (clinical): 0 = no rupture 1 = min HA, slight nuchal rigidity 2= mod-severe HA, cranial n palsy
3 = AMS 4= stupor, hemiparesis 5 = deep coma
Fisher = CT based: 1 = no blood 2 = diffuse thin SAH <1mm thick
3 = localized cloth or thick layer of SAH 4 = intraparenchymal/IVH
 **albumin worsens outcomes in SAH!

Miscellaneous:
- CN- Tx: hydoxocobalamin; if alternative: nitritethiosulfate
- Septic shock = vasopressor + lactate>2 despite volume resusc; 20cc/kg kids; 30cc/kg adults
- Fetal scalp ABG: acidosis if pH<7.2, lactate >4.8
- Activated clotting time: intrinsic and common pathways; NL 107; >400 for CABG; 1mg protamine (large Pos) reverses 1mg hep
(largeNeg) (100U); prevents hep binding to AT3
- R 6m = FFP
- Alpha angle 600
- Amp: 60nm; plt fxn/# and fibrin cross link
- Ly30 = rate of fibrinolysis 6%; if high = Txa, ACA (lysine analogs = bind
plasmin/plasminogen = prevent fibrin breakdown)
- K time = speed/strength of blot formation  cryo, fibrinogen

DDAVP: synth/release of vwF from endothelium

- ICP monitoring: intraventricular = gold standard
P1 = percussion wave = arterial pulse
P2 = tidal wave = intracerebral compliance
P3 = dicrotic wave = aortic valve closure
If P2>P1 = ↓intracranial compliance (plateau wave); fr ↑↑PaCO2, ↓vent, painful stim
If ↑P1 = high SBP; if ↓P1 = low SBP
- Cefazolin inc INR bc blocks epoxide reductase
- Mitchondrial myopathies = can’t make ATP bc impaired ox-phos = avoid stressors (hypoglycemia, hypo/hyperthemia); Sxs =
hypotonia, neuro, CM; don’t give LR, give D5NS; avoid sux, reduce NDMB dose; versed, opioid, alpha2 ag, ketamine OK; inc PRIS
bc prop metabolism impaired
- Apgar: 0-2, 5 categories skin color, HR, reflex to stim, muscle tone, breathing
- GCS: Eye opening (1-4) Verbal resp (1-5) Motor resp (1-6)
- Review EtCO2 tracing: single lung xsplant, incom insp valve, incomp exp valve (NL but shifted ↑)
- Mapleson: RB---------APLPt
A: FGF w/ RB B: FGF w/APL C: shorter B D: APL w/RB, FGF near pt (rapid∆ w/FiO2)
E = D wo RB
SV = All dogs can bite (w/A FGF = MV, DEF = 2-3xMV); CV = Dog bites can ache (with D, FGF = 1.5MV); dec FGF can convert
semiclosed circuit to closed circuit (heat/moisture conserved but rebreathing)
Bain circuit = D: 1) conserves moisture bc partial rebreathing 2) warming of FGF by expired gases 3) scavenging is easier fr APL
valve 4) good for when access to pt is limited
Pregnenolone
 17Ohase androgens
 1721DOC11cortisol
 21DOC11 aldosterone
ECT:
- Methohexital dec SZ duration; Etomidate inc SZ activity; Thiopental dec SZ activity; Lidocaine dec SZ threshold!
Status epilepticus Tx:
Midazolam 10IM/IV Diazepam 10mg rectal Lorazepam 4 IV/IM
Disc herniation: relieves with straight back, worsened with bend/sitting down
Spinal stenosis: relieved with bending
VZV: thoracicophthalmic V1maxillary V2cervicalsacral
REVIEW MAPLESON (semiopen) circuits; SV = All dogs can bite; CV = Dog bites can ache; dec FGF can convert semiclosed
circuit to closed circuit (heat/moisture conserved but rebreathing)
Vesicants: diazepam, phenytoin, promethazine, thiopental
MG postop vent needed if: dz 6+yrs, NIF<20, lung dz (COPD), VC<2.9L, daily pyrido >750mg
LES: proximal limb wkness, improves w/exsc, SCLC, Sn to sux & NDMB
MG: eye/facial wkness, fatigue w/exsc; R to sux, Sn to NDMB
Tumescent: max lido = 55mg/kg; epi 0.055mg/kg; no more than 5L removal