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193 Cards in this Set

  • Front
  • Back
Properly do a Mallapati classification
Patient sitting head neutral position
open mouth maximally (nml 50-60mm)
stick out tongue as far as possible

Do not say "Ahh" - makes it better
DO not arch tongue - makes it worse
airway eval
Atlanto occipital joint extension
Nml 35 degrees
If cannot do this and anesh tries to extend neck, get bulge pushing larynx anterior, cant see glottis.

Extension of only 11 degrees ~ Grade III or IV View
airway eval
Anterior mandibular space eval
Ask pt extend head to max
measure thyroid cartilege notch to tip of mentum/chin.

If under 6cm, harder to line up to intubate. (small mandible, short muscley neck.
If over 6cm Good sign.

The distance from the inner surface of the mandible to the hyoid bone during neck extension should be at least two large fingerbreadths in adults. If the thyromental space is examined, the comparable distance is 50 mm, which is about three large fingerbreadths. There appears to be no difference in the results of using the hyomental or thyromental distances, except that the thyroid cartilage may be easier to locate. These areas are important because the laryngoscope displaces the tongue into this space, and exposure of the glottis may be inadequate if the space is narrowed or noncompliant. A receding or hypoplastic mandible results in a situation often referred to as an anterior larynx or high larynx by clinicians. An inability to bring the lower incisors edge to edge with the upper incisors (i.e., impaired mandibular protrusion) is an important warning that laryngoscopy may be difficult.[10] Conversely, if the lower incisors can be brought forward to bite the upper lip beyond the vermilion, mandibular displacement can be expected to aid intubation. The latter case would seem to diminish the impact of the Mallampati score.
Med conditions altering airway mgt
table from Miller
Table 42-3 -- Selected pathologic states that influence airway management
Pathologic State Difficulty
Infectious epiglottitis Laryngoscopy may worsen obstruction.
Abscess (submandibular, retropharyngeal, Ludwig's angina) Distortion of airway renders mask ventilation or intubation extremely difficult.
Croup, bronchitis, pneumonia (current or recent) Airway irritability with tendency for cough, laryngospasm, bronchospasm
Papillomatosis Airway obstruction
Tetanus Trismus renders oral intubation impossible.
Traumatic foreign body Airway obstruction
Cervical spine injury Neck manipulation may traumatize spinal cord.
Basilar skull fracture Nasal intubation attempts may result in intracranial tube placement.
Maxillary or mandibular injury Airway obstruction, difficult mask ventilation, and intubation; cricothyroidotomy may be necessary with combined injuries
Laryngeal fracture Airway obstruction may worsen during instrumentation.
Endotracheal tube may be misplaced outside larynx and may worsen the injury.
Laryngeal edema (postintubation) Irritable airway, narrowed laryngeal inlet
Soft tissue, neck injury (edema, bleeding, emphysema) Anatomic distortion of airway
Airway obstruction
Neoplastic upper airway tumors (pharynx, larynx) Inspiratory obstruction with spontaneous ventilation
Lower airway tumors (trachea, bronchi, mediastinum) Airway obstruction may not be relieved by tracheal intubation.
Lower airway is distorted.
Radiation therapy Fibrosis may distort airway or make manipulations difficult.
Inflammatory rheumatoid arthritis Mandibular hypoplasia, temporomandibular joint arthritis, immobile cervical spine, laryngeal rotation, and cricoarytenoid arthritis make intubation difficult and hazardous.
Ankylosing spondylitis Fusion of cervical spine may render direct laryngoscopy impossible.
Temporomandibular joint syndrome Severe impairment of mouth opening
True ankylosis
False ankylosis (burn, trauma, irradiation, temporal craniotomy)
Scleroderma Tight skin and temporomandibular joint involvement make mouth opening difficult.
Sarcoidosis Airway obstruction (lymphoid tissue)
Angioedema Obstructive swelling renders ventilation and intubation difficult.
Endocrine or metabolic acromegaly Large tongue, bony overgrowths
Diabetes mellitus May have reduced mobility of atlanto-occipital joint
Hypothyroidism Large tongue and abnormal soft tissue (myxedema) make ventilation and intubation difficult.
Thyromegaly Goiter may produce extrinsic airway compression or deviation.
Obesity Upper airway obstruction with loss of consciousness
Tissue mass makes successful mask ventilation unlikely.
Airway Mgt
Nml mouth opening
Adults should be able to open their mouths so that there is a 30- to 40-mm distance (about two large fingerbreadths) between upper and lower incisors.
Airway Mgt
Indications for Orotracheal intubation
Prevent aspiration (recent meal, obstruction)
Need freq suctioning
Need Pos Pressure Vent lungs (thoracotomy, NM blockade planned)
Any position other than supine planned
Site on head, neck, upper airway
Mask is hard (no teeth, linebacker)
Upper airway dz (cancer)
Airway Mgt
How
1. Raise table so pts face at level of your xiphoid cartilege so you don't have to bend over.
(CRicoid pressure at induction. Thumb and index finger posteriorly against vertebra.)
2. Patient's crown on pillow. Extend OA about 80 degrees to line up open throat with neck/pharynx tube.
3. Use right thumb to push down pts mandible, use index finger to roll away lower lip so not crushed by blade.
4. L-scope in left hand at junction of blade and handle. Insert at right side of mouth to sweep pts tongue off to the left.Dont crank on teeth esp. max incisors. NEVER LEVER HANDLE TOWARDS YOURSELF.

CURVED BLADE/MAC
1. life towards pts feet.
ACLS
after shock?
if pulse ?
do CPR after shock
if pulse check BP
ACLS
asytole
ECG gain up and check leads
epi, no shock
atropine 1 mg/kg alternate with epi
ACLS
v fib and v tach
shock
5 cycles of CPR for 2 minutes
(during this get airway and fluids)
At end of CPR check rhythm
shock epi
amiodarone 300 mg then 150 mg



OR

lidocaine 1 mg/kg then 1/2 @ 5-10 min intervals
ACLS
PEA
(ECG can be anything except v fib or vtach)
5 cycles of CPR
epi no shock
Repeat epi 1mg every 3-5 min as long as cardiac arrest.

atropine 1 mg if brady (rate <60) 1 mg every 3-5 min up to 3 mg lax dose



H's and T's
hypovolemia
hypoxia
Hydrogen ions acidosis (Rx Na bicarb)
hypoglycemia
Hyperkalemia (Rx Na bicarb)
Toxins - drug OD TCA OD (Rx Na Bicarb)
tamponade cardiac
tension pneumo
thrombosis : cardiac or pulm
trauma
ACLS
slow pulse under 60 bpm
symptomatic
0.5 mg atropine and transcut pacing
ACLS
fast pulse over 150
symptomatic and stable
vagal manuver (valsava, no carotid massage)

narrow QRS and reg rhythm : adenosine

symtomatic and unstable : synch cardiovert
ACLS recus
laryngospasm vs bronchspasm
Both give epi 50 mcg IV

succ will only help laryngospasm
For laryngospasm:
* pos pressure vent until opens
* if unconsc succ

Bronchspasm usually asthma or peanut allergy give epi 50 mcg Iv and be ready to repaeat dose in about 3-5 minutes.
May need nebs albuterol or racemic epi.
ACLS recus
what can cause checst wall tightness and can't ventilate and what is treatment ?
opiods esp synthetic
fentanyl at induction

can't ventilate even with bag, person unresponsive, can't move arms sometimes.

IF unconscious : succ
If consc : reverse opiod with naloxone
ACLS
anaphalaxis
O2 so sat >95%
moniter cardiac rhythm
Epi subQ 0.3 ml of 1:1000 (or IV 50 mcg) and hypotension/severe resp distress
If bronchospasm or wheezing : albuterol nebs
IV saline
Benadyl IV/IM
If BP sys below 80 and severe distress repeat epi
If in 5 min still hypotension repeat epi
if still low BP, dopamine
ACLS seizures
check glu -> Rx IV glucose D50 or IM glucagon
narcan
versed 2-5 mg/min IV/IM
pKa of local anesth
Figure 14-2 The fraction of local anesthetic in the protonated, cationic form in aqueous solution at physiologic pH (7.4) as a function of the pKa of the drug. The drug with the lowest pKa, lidocaine, has the smallest fraction of its molecules protonated and the largest in the neutral form, and vice versa for the local anesthetic with the highest pKa, chloroprocaine. Individual drug molecules become protonated and deprotonated in thousandths of a second in solution.
Inhal An
Rise in alveolar conc of anesth is faster w/ soluble or non-soluble ?
Name soluble and non-soluble anesthetics ?
Figure 5-2 The rise in alveolar (Fa) anesthetic concentration toward the inspired (Fi) concentration is most rapid with the

least soluble anesthetics, nitrous oxide and desflurane,

and slowest with the most soluble anesthetic, halothane. All data are from human studies.
what is 2nd gas effect ?
Figure 5-3 A, The rectangle represents a lung filled with 80% nitrous oxide plus 1% of a second gas. B, Uptake of one half of the nitrous oxide does not halve the concentration of nitrous oxide, and the reduction in volume thereby increases the concentration of the second gas. C, Restoration of the lung volume by addition of gas at the same concentration as that contained in A increases the nitrous oxide concentration and adds to the amount of the second gas present in the lung.
what is 2nd gas effect ?
Figure 5-4 In patients, administration of 65% nitrous oxide produces a more rapid rise in the alveolar concentration of anesthetic/concentration of inspired anesthetic (Fa/Fi ratio) for nitrous oxide than administration of 5% (i.e., concentration effect, two solid lines). The Fa/Fi ratio for 4% desflurane rises more rapidly when given with 65% nitrous oxide than when given with 5% (i.e., second gas effect, two dotted lines).
Inhal
If you increase ventilation what is effect on conc inhal anesth ?
For what gases does this matter more ?
Figure 5-5 The alveolar concentration of anesthetic/concentration of inspired anesthetic (Fa/Fi ratio) rises more rapidly if ventilation is increased. Solubility modifies this impact of ventilation; the effect on the anesthetizing partial pressure is greatest with the most soluble anesthetic (ether) and least with the least soluble anesthetic (nitrous oxide).
inhal
what about changing CO?
Figure 5-7 If unopposed by a concomitant increase in ventilation, an increase in cardiac output will decrease alveolar anesthetic concentration by augmenting uptake. The resulting alveolar anesthetic change is greatest with the most soluble anesthetic. Fa/Fi is the alveolar concentration of anesthetic/concentration of inspired anesthetic.
inhal
what effects recovery from an ?
Figure 5-18 Both solubility and duration of anesthesia affect the fall of the alveolar concentration (Fa) from its value immediately preceding the cessation of anesthetic administration (Fa0). A longer anesthetic slows the fall, as does a greater solubility, and the effects are shown for the increasingly soluble desflurane, sevoflurane, and isoflurane (A to C). The horizontal lines designated (a), (b), and (c) indicate 80%, 90%, and 95% decreases, respectively, in the alveolar concentration from the concentration at the end of anesthesia.
inhal
what is diff hypoxia ?
At end of anesh, when turn off nitrous, as it leaves blood, get hypoxia. Prevent by giving 100% O2 at end of anesth.



Figure 5-23 At time zero, the inspired gas was changed from 21% oxygen/79% nitrous oxide to 21% oxygen/79% nitrogen. Arterial oxygen subsequently fell in association with the outpouring of nitrous oxide.
inhal
effect of inhal an on vent ?
Figure 6-13 Comparison of mean changes in resting Paco2, tidal volume, respiratory rate, and minute ventilation in patients anesthetized with halothane (H), isoflurane (I), enflurane (E), sevoflurane (S), desflurane (D), or nitrous oxide (N). Anesthetic-induced tachypnea compensates in part for the ventilatory depression caused by all volatile anesthetics (i.e., decreased minute ventilation and tidal volume and concomitant increased Paco2). Desflurane results in the greatest increase in Paco2, with corresponding reductions in tidal volume and minute ventilation. Isoflurane, like all other inhaled agents, increases respiratory rate, but isoflurane does not result in dose-dependent tachypnea.
NMB
dur of effect ?
Figure 13-19 Percentage of peak effect after a1 × ED95 dose of succinylcholine, rapacuronium, rocuronium, atracurium, mivacurium, vecuronium, and cisatracurium at the adductor pollicis muscle. Times (mean ± SD) in seconds to 95% of peak effect are shown in parentheses.
nmb
Binding site of non depol vs depol nbm ?
Depol are agonists.
NonDepol are compet antagonists.


Top: The action of the normal agonist, acetylcholine, in opening the channel. Bottom, left: A nondepolarizing blocker, eg, rocuronium, is shown as preventing the opening of the channel when it binds to the receptor. Right: A depolarizing blocker, eg, succinylcholine, both occupying the receptor and blocking the channel. Normal closure of the channel gate is prevented and the blocker may move rapidly in and out of the pore. Depolarizing blockers may desensitize the end plate by occupying the receptor and causing persistent depolarization.
nmb
ToF and tetanus response to depol and non-depol nbm ?
Fade: indicates NON-depol block, may show pre-junct action of NMB reducing amt of Ach. when fade is gone -> sign of clin recovery.

Post-tetanic facilitation : when do tetany (long 5 sec stim) and then twitch and see greater twitch response = 'POST TETANIC FACILITATION. See in partial non-depol block.
Shows partial inc in Ach from tetanic stim.

A phase I block (succ, depol) in contrast, no fade, no ToF, no post-tet facilitation.But if keep giving succ, changes to phase II block which ressembles a non-depol block.

In the train of four (TOF) pattern, four stimuli are applied at 2 Hz. The TOF ratio (TOF-R) is calculated from the strength of the fourth contraction divided by that of the first.
In the double burst pattern, three stimuli are applied at 50 Hz, followed by a 700 ms rest period and then repeated. In the posttetanic potentiation pattern, several seconds of 50 Hz stimulation are applied, followed by several seconds of rest and then by single stimuli at a slow rate (eg, 0.5 Hz). The number of detectable posttetanic twitches is the posttetanic count (PTC). (*, first posttetanic contraction.)
iv
thiopental : time to redist to VRG ? fat ?
local
ester vs amide ?
Structures of two prototypical local anesthetics, the aminoester procaine and the aminoamide lidocaine. In both drugs, a lipophilic aromatic group is joined to a more hydrophilic tertiary amine base, by an intermediate amide or ester bond.
local
channel binding state ?
Functional and structural features of the Na+ channel that determine local anesthetic (LA) interactions. A: Cartoon of the sodium channel in an axonal membrane in the resting (h gate open), activated (h gate open), and inactivated states (h gate closed). Recovery from the inactivated, refractory state requires opening of the h gate. Local anesthetics bind to a receptor (R) within the channel and access it via the membrane phase or from the cytoplasm.
local
types of injections near spine ?
iv
type of opiod receptors ?
opiods MOA ?
Act inside and outside CNS
potency : ~ afficnity for R , levo-iso more effective

MOA: dec neurotransmission as PRE-SYN inhib of NT (Ach, subt P).

Also opiod R activation inc K+ conduction so cell hyperpolarized.

Mu-1 : supra-spinal anal, spinal, euphoria, miosis, urine retain

Mu-2 : spinal, vent depression, bradycardia, constipation, phy dependance

Kappa : supraspinal , spinal, dysphoria, sedation, miosis

Delta : supraspinal, spinal, vent depression, urine retain, phy dependance
airway
how insert LMA ?
A: The laryngeal mask ready for insertion. The cuff should be deflated tightly with the rim facing away from the mask aperture. There should be no folds near the tip. B: Initial insertion of the laryngeal mask. Under direct vision, the mask tip is pressed upward against the hard palate. The middle finger may be used to push the lower jaw downward. The mask is pressed forward as it is advanced into the pharynx to ensure that the tip remains flattened and avoids the tongue. The jaw should not be held open once the mask is inside the mouth. The nonintubating hand can be used to stabilize the occiput. C: By withdrawing the other fingers and with a slight pronation of the forearm, it is usually possible to push the mask fully into position in one fluid movement. Note that the neck is kept flexed and the head extended. D: The laryngeal mask is grasped with the other hand and the index finger withdrawn. The hand holding the tube presses gently downward until resistance is encountered
airway
proper placement Mac blade ?
airway
view w. curved blade / Mac
airway
diff airway algo
inhal
what effects uptake of gas ?
Inc rate of induction:
inc anesth conc
inc fresh gas flow
inc alv ventilation
** dec COoutput (alveolar blood flow, predispose to anesthetic ODose)
2nd gas effect
non rebreathing
** low blood:gas SOLUBILITY
(diff in part pressure of alv gas and venous blood)

GREATER the uptake of anesth agent, greater diff between inspired and alveoli conc, and slower the rate of induction.

NB :Slows induction :shunt whereas wasted ventil to nonperfused alv no change
PreOp
General
testing :
when do ECG ?
Hgb ?
glu and creat/BUN ?
When CXR ?
PFT ?
when do ECG ? General An men over 40 and women over 50
Hgb ? gen all women ; men over 50
glu and creat/BUN ? Over 65
CXR ? over 74
PFT ? COPD and upper abd sx


NB 2-7% labs abn
PreOp labs
MAC or regional
Over 50 : Hgb in last 6 mnths

Over 65: Hgb (6 mnths)
ECG: last year

Over 74 : In last 6 mnths hgb, creat/BUN, glu, AND ECG
PreOp

ASA for :
poorly cont HTN
DM vascular comps
angina
prior MI
pulm dz that limits activity
ASA 3
severe systemic dz limits funtional activity
PreOp
ASA for controlled
and mild (no severe comps)
HTN
DM
chrn bronchitis
morvod obesity
exteme age
ASA 2
mild well controled dz no functional limitations
PreOp
unstable angina
CHF
adv pulm, renal, liver dysfunction
ASA 4 : severe systemic dx constant threat to life.

Note: ASA does not count dz being operated on that will be fized by opeartion. IE Gb dz for GB sx
PreOp
ASA
ruptured Aneur
PE
head injury w/ high ICP
ASA 5
moribund, will die without operation
PreOp
ASA
brain dead organ donor
ASA 6
PreOp
Plan
What is regional anesth ?
Epidural / spinal / caudal
Pt conscious
+ : GI and skel m relaxed
Use for lower leg and GI sx
-: may not have enough sens anal,
See drop in BP esp if hypovolemic
PreOp plan
peripheral N block
when :
sx on arm or leg
+: keep airway reflex so good pts lung , kidney, heart dz
Sx: AV shunt
-: occ not enough sens and motor anal
Poor choice drunk/agit as key to it is technique and skill at block.
Intub
drugs
preox
LOC : propofol / etomidate
+/- opiod blunt pressor resp to intubate
+/- lido
paralyze: succ/rXXX
intubate
PreOp
how to check intub in trachea
capnograph > 20 mmHg CO2 with exhale

pulse ox over 95%
Pre Med
why clonidine ?
sedate
blunt ANS (HTN, tachy, catach from anx and surg stim)
PreMed
why anti-hist
promethazine w/ mepiridine to augment sedation w/o inc Resp depression.

diphenhydramine with cimetidine to dec chance of allergy (contrast dye in atopic pt)
PreMed
Who gets anto-acid meds
pregnant
GERD
Sx reflux
obese
diff airway
PreMed
metoclopromide
IV acts in 1-2 min use for emergency sx in pts who ate

PO : 30-60 min pre
DM preg recent ate and nonGI sx, diff airway
SE : can go to brain EPS
PreMed
for anti-sial effects only
glycopyrrolate
strong anti-sial (vs atropine) and 2 duration
PreMEd
anti sial and sedation
scopolamine
SE CNS toxicity delerium esp elderly as crosses BBB. Also mydriasis/cyclo.
PreMed
When use atropine
Kids to prevent vagal bradycardia with propofol and other anesth

Has antisial, sedative, CNS toxicity. Can cause tachycardia.
PreOp
Fasting
food
breast milk
formula
fast light meal 6 hrs
non human milk "
formula "
BREAST milk 4 hrs
clears 2 hrs
(ice chip, gum, candy) 2 hrs
PreOp
anti nausea meds

More nausea :
female, h/o,
Sx: gyne, eye, cosmetic, ortho shoulder, general >regional
phenergan : histamine

ondasertron 5HT3 blocker

droperidol low dose, dopamine blocker, SEDATES, give after benzo or dysphoria. Droperidol can SEDATE but pt still anxious.

scopolamine anti-chol

Decadron/corticosteroid
IV
effect on BP ?
Drop BP:
* thiopental
* propofol

Minimal to no drop:
* etomidate
midozolam

INCREASE BP
* ketamine
IV effect on HR ?
Dec HR
none

increase HR
thiopental (as drop BP)
ketamine
IV effect on ICP ?
increase ICP :
ketamine

dec :
** thiopental : barbs used as Rx for high ICP
propofol
etomidate
midozolam neutral to dec
IV effect ventilation ?
all depress ventilation except ketamine which has dose dep depress of ventilation.
At low doses, does not but since you give with Versed, do see depression of vent.
IV Na and Vomiting ?
Dec in N/V:
propofol

Increase:
etomidate
ketamine
IV adrenocort supress ?
etomidate and some midozolam
IV
barbs
effect of adding sulfer methyl
sulfer : (thiopental, thiaamytal)
more lipid soluble, hypnotic, rapid onset and sht duration

Oxy: methohexitol
shortens duration

NB: MOA depress retic activating system and transmission thru sym ganglion as dec rate of dissociation of GABA from R. ALSO hyperpol mmb post-syn so inhibit post-syn neurons
IV barbs
PK
awake as redist
elim due to metab
Distribution : lipid solubility and tissue blood flow
change EEG ?
barbs : isoelectric EEG w/ hypnosis also dec ICP and CBF and CMRO2

benzo: isoelectic

etomidate: activate epiletic foci with myoclonus

ketamine: myoclonus but NO seiz on EEG
IV
Methohexital
histamine
CV: mild dec BP with mild tachycardia, dec CO and contractility
RR: trans stim then apnea, less responsive to CO2, dec RRATE and TVol, can see bronchospam/laryngospams at light depths,
Brain: dec ICP and CBF and CMRO2

methohexital VS thiopental
more un-ionized
2.5x as potent

Neg: no skel m relaxation, occ excitatory, hangover, CI poryphries
IV
propofol
a phenol
MOA
GABA -R
dec dissociation
prolonged opening Cl ch hyperpol mmb
no impulse conduction
IV
propofol PK
Onset: rapid LOC in 30 sec
Rapid awake
Redist, clear, metab fast:
clearence faster than hep blood flow.
Can give cont IV infusion, no cum effect.
Iv
propofol
CNS
RR
CV
AE
Propofol
CNS : dec ICP CBF CMRO2; keeps tuoreg to CO2 level
RR: dose dep dec resp and transient apnea, bronchodilation
CV: dec SVR, dec MAP, neg inotrope, No change in HR, depressant CV more than thiopental esp older pts, hypovol, those on ACE-I
IV
propofol Allergies
has egg
soybean oil
sulfite
glycerol
Iv
etomidate
a carboxylate imidazole

PK?
MOA:
enahnce GABA
PK:
Onset : LOC in 30 sec
rapid awake as re-dist, no hangover
rapid clearence
metab by hydrolysis
little cm effect
Iv
etomidate
CNS
RR
AE
Etomidate
CNS: dec CMRO2, CBF, ICP, can + seizure foci on EEG but an anti-convulsant,
MYOCLONUS
RR: transient dose-dep dec Tidal vol and inc RRate
CV: modest BP dec due to dec SVR, minimal myocardial depression
AE: myoclonus, pain on inject, bugs, adrenocort supress 11Bhy-ase lasts 4-6 hrs post induction dose.
HIgh % N/V
IV
ketamine
MOA
NMDA R
opiod R
monamine R
muscarinic R
Ca ion ch
NOT gaba R

stimulates central nerv system
stim Sym Nerv system
inhibits reuotake of norepi
IV ketamine
PK
rapid onset: high lipid soluble, easily ionized in body, rapid brain uptake
redist from brain and VRG,
dist t1/2 10 min
metab : microsomal, active metab; induces liver enz (tolerance)
Shrt elim halflife of 2 hr as extensive liver uptake 0.9
IV ketamine
CNS
RR
CV
CNS: VASODILATOR inc CBF and ICP, manage effect w. proper ventilation, MYOCLONUS w/o seizure on EEG, anti-convulsant
RR: min depression of resp, if give IV w/ opiods can see apnea, BRONCODILATION, SALIVATION, HYPERTONICITY upperairway keeps reflex
CV: like SNS stim inc BP, PAP, HR and CO
IV ketamine
and emergence delerium
See with doses > 2 mg/kg Iv
females over 16
personalit d/o and freq dreams

Prevent by predose w/ benzos
IV benzos
useful as adj b/c

MOA
anx reduce
sedate
amnesia
minimal dep CV and resp
anti-convulsant
RELAX SKEL M
rare allergy

MOA: enhance GABA Cl channel, hyperpol ch, usually post-syn nerves in CERBRAL CORTEX

midozolam has 2x affiity vs diaz for R
IV
benzo
PK
lipid sol so rapid to CNS
resdist
metab:
Diaz-> liver to active metabolites t1/2 2-3 days
Midozolam -> liver p450 3A4 inactive metabolite t1/2 1-4 hrs
lorazepam -> not active metabolite, t1/2 10-20 hrs
Iv benzos
CNS
RR
CV
CNS : dec CMRO2 and CBF, isoelectric EEG, no effect ICP, anti-convul, no neuroproective effect
RR: min depr alone but apnea with opiods
CV: stable but esp w/ induction midozolam can get dec SVR which can drop BP
IV benzos
injection rxns ?
diazepam no water soluble, has propylene glycol -> thrombophlebtitis

ativan also thrombo but no prop glycol.

Both hurt with injection. Not water soluble.
Iv benzo reversal
do reverse what?
do not reverse what ?
reverse CNS effect
but not amnesia

DO not see anx, HTN, tachy or stress like with narcan.

Need much less with kids.

adults 0.2 mg titrateup to 10 mg
kid 0.01 mg/kg up to 1 mg
Iv opiods
effects ?
Why good as premed ?
analgesia
no loss of touch, propio or LOC
Good pre-med:
anal lines, no direct myo depres, delays time to need post-op pain med.
IV opiods
morphine
IV
peak onset : 20 min
Effects: smooths out HR to surg stim (less inc)
AE: depress resp at medulla,
Nausea by stim central, ortho hypo as periph vasodil,
IV opiods
fentanyl
fentanyl
Peak onset 1 min
Effects : evens out HR (less rise w. surg stim)
IV opiods

which R do vent depression ?
Mu-1 : supra-spinal anal, spinal, euphoria, miosis, urine retain

*** Mu-2 : spinal, vent depression, bradycardia, constipation, phy dependance

Kappa : supraspinal , spinal, dysphoria, sedation, miosis

*** Delta : supraspinal, spinal, vent depression, urine retain, phy dependance
IV opiods

which R do spinal and supraspinal anal ?
*** Mu-1 : supra-spinal anal, spinal, euphoria, miosis, urine retain

ONLY SPINAL
Mu-2 : spinal, vent depression, bradycardia, constipation, phy dependance

*** Kappa : supraspinal , spinal, dysphoria, sedation, miosis

*** Delta : supraspinal, spinal, vent depression, urine retain, phy dependance
IV opiods

which R do sedation ?
Mu-1 : supra-spinal anal, spinal, euphoria, miosis, urine retain

Mu-2 : spinal, vent depression, bradycardia, constipation, phy dependance

*** Kappa : supraspinal , spinal, dysphoria, sedation, miosis

Delta : supraspinal, spinal, vent depression, urine retain, phy dependance
IV opiods

which R do bradycardia ?
Mu-1 : supra-spinal anal, spinal, euphoria, miosis, urine retain

*** Mu-2 : spinal, vent depression, bradycardia, constipation, phy dependance

Kappa : supraspinal , spinal, dysphoria, sedation, miosis

Delta : supraspinal, spinal, vent depression, urine retain, phy dependance
IV opiods
compare potency of
morphine
meperidine
alfent
fent
remifent
sufent
morphine 1.0
meperidine 0.1 (so 1/10 as strong)
alfent 10-25
fent 75-125
remifent 250
sufent 500-1000
IV opiods effects
CNS
Opiods
CNS: depend on R, dec CBF/ICP as long as not hypovent,
SKEL M RIGID esp synthetics
N/V via central
Mepiridine metabolite can cz seizures
dec MAC of vol anesth
IV
opiods
effect
RR
CV
GI
RR: depress vent via Mu-2 on brainstem, less resp to CO2 and inc PaCO2, dec RRate and inc Tvol,
Some HISTAMINE so inc AIRWAY RESIST, DEC COUGH REFLEX

CV: min depress alone, no heart sens to catach,
MORPHINE : histamine dec BP, others opiods hypotension as blunt response for vasodilation
BRADY: except meperidine (tachy) as stimulate vagus

GI: bil colic, dec gastric empty, constipate,
GU: urine retain,
effect immune system, tolera and phy dependance.
IV opiods
Uses in anesht
anal pre and post sx
induction and main : must give w/ oter drugs for amnesia
inhib reflex sym responses
suppl inhaled anesth (dec MAC needed)

ProS: CV stability, no myocard sens to catech, easy arosal post-op, no end organ toxic, post-op analgesia,

Disad: recall, chest wall rigid, postural hypotens, if under dose during procedure HTN and tachy, N/V, bil colic, urine retention
IV opiods
naloxone
reversibly binds opiod R
non specific effect so careful as might reverse analgesia : see HTN, tachy, pulm edema, N/V

Duration 30-45 min
IV opiods
remifentanyl is special why ?
Not metab in liver like other opiods.
ULTRA SHORT ACTING
ester hydrolsis in plasma,
non-specific enz so pts w. aty enz nml wake up.
pts with liver dz nml wake up
no effect w. long infusion,
still wake up in 3 min
IV opiods and renal failure
pts renal failure and
morphine
mepiridine
can take days to wake up
nor-meprindine can cause seizures and myoclonus not reversible w. naloxone.
IN opiods
2nd peak
fentanyl has 2nd peak
2-4 hrs later
IV
barbs and benzo
neuroprotection
barbs neuroprotect NOT benzos
barbs vasoconst brain
protect cerebral clot local ischemia
prob not global like cardiac arrest
Iv
effect on brain opiods vs b's
Vs benzo and barbs
opiods less of dec in O2 use, CBF, and ICP.
And opiods may not blunt inc ICP seen with intubation if pt not asleep enough.

high doses fent : occ seiz activ might be muscle ridigity
mepiridine : seiz activity
IV
what to dec shivering ?
mepiridine 25 mg
IV
ketamine
Who good for ?
Who bad for ?
Good for asthma , early hypovol shock

Bad for:
Due to inc HR/MAP/CO: CAD, uncontrolled HTN, CHF, art aneur, severe end state shock w. depleted NE stores
PreOp Meds
CI to sedative meds pre-op
severe lung dz
hypovol
impending airway obst
high ICP/intracranial pathology
depr mental status
under 1 yr or elderly
no informed consent to Sx

Also some pts may do ok with some anx, may be better then IM or long hangover for sht ambul sx
PreOp meds
who does well with pre-op sedation
kids for separation
drug abusers to avoid w/drawal
med cond where stress bad: CAD, HTN
Pre Heart sx
Cancer sx / pre-op pain
Regional anesthesia
And pre-op opiods help induction.
nmb
metabolism of depol vs nondepol
Ach: metab by AchEase in cleft
depol : diffuse away, metab psesudoAchE in plasma, nonspecific esterases, or butrylcholesterase
NonDepol : redist, grad metab, excretion by body OR giving reversal agents (except mivacurium)
NMB
Why don't kids get succ?
Hyperkal
rhabdo
cardiac arrest in unrecog myopathy
nbm

potassium and succ
K will rise 0.5 mEq/L
CA rise life threat in:
burn
trauma, hemm shock w/ met acidosis
neuro d/o (GBS, stroke, myopthies like duchennes, encephalitis, severe parkinsons, tetanus, polyneurpathy,
severe intra ab infection
spinal cord injury
prolonged immobiliaztion
ruptured cerbral aneurysm/closed head injury

Reason is immature extrajunct AchR release excess K.
nmb
rule w. potency and speed of onset ?
more potent -> longer onset
nmb
excreted by kidney and prolonged effect in renal failure ?
doxacurium
pancuronium
pipecuronium
(vec)
nmb
effect of CHF or cirrhosis ?
larger Vd and smaller plasma conc for given dose.

So may need larger starting dose and then smaller main dose
NBM
cisatra and atra metab ?
nonspecific Hoffman elim
to laudanosine
no NMB but CNS excitement
nmb
mivacuronium ?
special ?
like succ metab by plasma psuedochlEase

tiny bit by Achase

Prolonged in pts aty enx or low levels
nmb
pancuronium special ?
vagolytic
catech release from adren N

-> HTN and tachy
nmb
long term use vec in ICU ?
days long NM blockade on wake up
active metab accum OR devel of polyneuropathy
NMB
which drug is like succ ?
Rocuronium 0.9-1.2 mg/kg
onset like succ in 60-90 sec
for RSI but has longer duration
NMB
succ
prolonged by
onset 30-60 sec, low lipid soluble
duration 10 min , as serum levels falls drug diffuses away

Prolonged only modestly in :
preg, hypothermia, liver dz

DRUGS:
echothiophate, neostig, pyridostim
phenelzine (MAOI)
cancer drug (cyclophosphamide)
metoclopromide
esmolol
pancuronium
OCP

abx -mycin, glycosides, cycin, linc
inhal anesth, LA,
lithium
Mg citrate
anti-arrthy
NMB
gene varients and succ
Abn genes
hetero 1/50 pts 20-30 block, dibucaine inhibited 40-60%

homo 1/3000 pts 4-8 hrs, dibucaine inhib 20%

(nml enz inhib by dibucaine 80%)
NMB
nondepol
drug effects
DECRASED response:
*** echothiophate, neostig, pyridostim UNLIKE SUCC
anti-seiz meds

prolonged
abx -mycin, glycosides, cycin, linc
dantrolene
inhal anesth, LA, ketamine
Mg citrate
anti-arrthy'
NMB
effect of cholinesterase inhibitors ?
non depol
succ
ON EFFECT OF OTHER 3?
Ex neostimgine and pyridostigmine

Prolong depol succ Phase I block :
- inhibit AchE so more Ach in terminal so more depol
- reduce hydrolysis of succ by inhibit pseudocholAse
Organophos pesticides prolong succ to 30 min

NonDepol blockers:
- sm doses occupy some Ach R so partly block succ phase I depol effect
- Exception is pancur which augments succ by blocking
pseudocholAses

Succ will reduce doses needed of nondepol blockers for up to 30 min, if if give enough succ to create phase 2 block, a nonpol will creat paraylsis
NMB
succ and fasciculations
Seen in adults not kids and elderly
Prevent with pre-treat small dose non-depol
This antag the block with succ so need more succ.
NMB
random odd AE succ?
inc IOP so no use open globe
myalgias : pretz rocur/NSAIDS and occ myoglobinuria
Intragastric pressure inc
masseter M ridgid
malig hyperthermia
myotonic pts get myoclonus
slight inc ICP but not as much as intubation
slight histamine
NMB
release histamine
atracur
mivacur
nmb vagal block
pancur
nmb liver
pan and vec metab by liver : have active metab

Biliary excr :
vec and rocur

Liver failure prolongs :
pancur and rocu , less effect on vec
NMB
nondepol
onset
slow onset: doxo 4 min
mod rapid : others 2-3 min
rapid rapid: rocur 1.5 min
NMB
nondepol
duration
duration
short : mivacurium (plas enz) 15-20 min
INTERMED:
atra onset 2.5-3' Dur 30-45'
cisatra Onset 2-3' Dur 40-75'
vec Onset 2-3' Dur 2-3' 45-90 '
roc Onset 1.5 min DUR 35-75 min

LONG: All renal elim
doxa onset 4min Dur 90-150'
pancur onset 2-3' Dur 60-120'
pipe onset 2-3' Dur 80-120'
delayed awakening GA old man
Differential ?
*hypotension to brain (worse if chr HTN)
*stroke
*renal/liver dz less drug clear
*DM hyperosm coma or hypogly
*severe hypothyroid
* Malig hyper: dont see delay awake but can see somnolence, PRIOR OK ANES DOSE NOT R/O malig hyper !!
*home drugs that dec MAC : ldopa
*ethanol intox, old and benzos
*less hepatic flow (cimetidine)
*additive anti-chol effects w/scopol and sedatives like opiods (esp low CO and IM)
*hypothermia
*hyponatermia
* intraop hyperventil so high trigger of PaCO@ to spont breath
* art hypoxia or hypercapnia

Do ABG and serum Na
PE pupils - should not be fix and dilated unless gave atro/scopol
VEntilate, narcan, flumenazil, physostimg (jaw thrust test for paralysis vs coma)




If prior GA and no probs can rule out aty enz
Unlikely low levels of enz (not see apnea)
NMB
nicotinic R

muscarinic R
Nicotinic R
stimulate autonomic ganglia
skel m R
Agonists: Ach, nicotine
Antag : NonDepol relaxants

Muscarinic R
activate end organ effectors
bronchial sm m : bronchoconstrict
salivary glands/gastric glands : secrete
Heart SA node, AV node : dec HR
Smooth m bronchi, GI, bladder, blood vessels

Agonist drugs : Ach, methacholine, bethanechol
Antag: antimuscarinics -
atropine, scopolamine, glycopyrrolate

Carbachol for glaucoma: both R
NMB
neostigmine
AchAse inhibiter
Main use reversal of NMBlockade
MOA: indirectly inc amt of Ach in cleft to compete w/ non-depol agent by irrever bind to AchE enzyme

Neostim has direct weak effect of agonst on nicotonic R pre-syn so might inc release of Ach.

In excess doses, paradoxically potentiate nondep block.

Also potentiate depol block of succ
- inc Ach
- inhibit pseudocholAse

Also have muscarinic SE:
CV: brady and brady arrhy
Pulm: bronchospasm, sec
Cerebral excitation w/ physistigmine only
GI spasm and saliva
GU bladder tone inc
Pupil constritct
inhal
what inc rate of recovery from anesth
inc fresh gas flow
inc alv ventil
non re breathing
low blood gas solubility
low tissue blood solubity
dec duration of anesthetic

Recovery differs from induction as:
no conc effect
metab can dec part pr alveoli
inhal
speed recovery
elim rebreathing
high fresh gas flow
low anesth circit vol / low absorb by circuit
low solubility
high cerebral blood flow
inc ventilation
elements of total anesth for GA
reversible LOC
anal entire body
amnesia
some muscle relax
inhal
potency relates to what ?
lipid solubility
(meyer-Overton rule)
suggests common MOA unitary hypothesis
inhal
halothane hepatitis
obese women with 2 doses
1/ 35,000
family or personal h/o of it
inhal and coronary arteries
Isoflo dilates cor Art but not as much as nitrogly or adenosine.

theory possible cor A steal in times of tachycardia or drop in perf pressure
inhal
des solubility ?
what is give rapid inc ?
Des low soluble fast induction and fast recovery

Rapid inc in dose -> inc HR, BP, catech release in pts, esp bad if CAD. (worse then with iso)
inhal
non stinky
sevo
non pungent
rapid induction wheras for adults generaly other gases not as prefered for induction.
inhal
no change in MAC
duration Or mech of an
gender
thyroid dz
hyper or hypo kalemia
PaCO2 15-90
PaO2 over 38
spine cord injury
inhal
increase MAC
HYPERthermia
Drugs that inc catechol
- MAOI, TCA, coke, acute speed
INFANTS 1yr over
HYPER NATREMIA
possible alcoholism
inhal
dec MAC
- HYPO thermia
- MEDS: preop med, IV anesth, acute ethanol ingestion , opiods in spine, alpha2agonists : clonidine
- Elderly,
- under 1 yr old/neonates
- PREGNANT and post-partum by 3 days
- PaO2 under 38 / HYPOXIA
- hypotension BP under 40
- lithium
- HYPONATREMIA
- Cardiopulm bypass
inhal effects Resp
- dec resp to PaCO2 at carotid body
- rapid breathing / rise in RRate
- shallow / dec in tidal vol
Rise in PaCO2 unless mech vent

dose dep

Not seen with nitrous
inhal
airway resist
inhal bronchodilators as relax sm m
SEVO the most, and halo

Except iso and
esp DES can cause coughing, breathing holding, layrnspasm, secns
inhal effects CV
- direct myocard depression in vitro esp bad if CHF
- iso/des/sevo periph vasodilate -> dec MAP, no change in CO, inc HR, they dec SVR
- halo : dec contractility and dec CO -> dec MAP, no change in HR, no change in SVR

Effect on CVP: all inc except sevo due to inc in pulm vasc resist.
nitrous also inc pulm vasc resist esp in pts with pulm HTN already


Nit : no change in MAP so if mix with vol anes see less of a drop in BP
inhal
effects CNS
All vasodil inc CBF
dec cerebral metabolic rate
inc ICP
inhal
nitrous sym mimetic effects
inc plasma catech
mydriasis
inc body temp
sweaty
inc CVP / R at pressure
vasoconst systemic and pulm system
inhal
renal effects:
liver:
inhal
renal effects: dec blood flow and GRF
liver: dec art and portal flow,
inhal
nitrous
+/-
Pro
fast uptake/elim
min resp and CV depression
nonpungent, no malig hyper

Con
combust, closed air space expands, B12 inactivation, lacks potency
inhal
halothane
Pros
potent
STABLE HR

Con
needs preserv
slow uptake and elim
biotrans -> toxic
idio syn hep necrosis
sens heart to catech
trigger malig hyper
inhal
iso
pro
** dec CMRO2
stable CO (slight inc HR maybe )

Con
tachy at greater conc
pungent
trigger MHyper
inhal
des
Pro
rapid uptake and elim

Dis
pungent
tachy w. rapid inc dose
need special vaporizer
$
trigger M hyper
inhal
sevo
Pros
rapid uptake and elim
non pungent
less myocardial depression
stable HR

Dis:
reacts w. CO2 absorber
release Floride
$
trigeer M Hyper
inhal
enflo
Pro
stable HR
** muscle relax

Dis:
EEG seizure
myocardial depression
trigger M hyper
inhal
myocardial depression ?
stable HR ?
myocardial depression ?
Bad : enflu
Less: sevo , nitrous

stable HR :
halo unless catech
enflu, sevo

Tachycardia w. greater conc:
iso, des
nitrous
cant use alone : MAC 105
good analgesia
expands air pockets
does not sens myo to catach
no change in BP
MOA: inhibits NMDA glut ch for Ca
which sens heart to catech
halo
maybe enf and iso
which worse resp depressants
des and enfl
some brochodilate : halo and sevo

irritate : des cough and enfl
a blood gas part co:eff of 0.5 means what ?
it is LOW

INsoluble so fast onset and fast recovery.

LIKE nitrous
des
sevo
what does a MAC of 1% mean ?
??
local
list esters
ESTERS have 2 I's

esters are older and cocaine is older.
procaine
tetracaine occ spinals
tetracaine
ester
very potent 16
high lipid soluble
long duration

USED topical spray for bronchoscope
Cocaine
esters
not as potent
medium duration

VASOCONST unlike others (which dilate)

USe for nasal hemm and for nasal scoping.
benzocaine
topical ester
SE contact derm PABA
methHgb and dec O2 carry capacity
procaine / novocaine
ester
local
sht dur low potency
low lipid solubilty
small
Use IV regional 4/1000 CNS stim -> convulse
Lidocaine
Amine 2 I's
clear by liver
Low Pka and small -> fast onset
med dur

Rx lido seizures :
prophy in toxicity w. benzos
fix acidosis w hyper vent makes ch rested
thiopent / versed
mepivocaine
Amide
slower onset, long duration
low lipid solubility
low potency
(low pka
in general low pka is fast on BUT mepivocaine is )
ropivocaine
Amide 2 I's
mod/ high potency
lipid soluble
long duration

aka naropin
bupivocaine
Pharm ?
tox and Rx ?
aka marcaine

lipid soluble and binds lipids
potent amide
long duration

Given IV : hypotension, AV block, vfib v tack

Rx. lipid emulsion and used to do CB bypass
DO locals vasodil/const ?
Locals intrinsic VASODILATE
lido > mepiv
causes more systemic absorb and shorter duration of lido

except coke

Can add epi to make vasoconst.
Adding epi to local does what ?
vasoconst
prolong local action
limit systemic absorb
sec systemic toxic
same rate of onset
dont add bicarb
local lungs clear ?
liver ?
renal ?
lungs :
lido
bupiv
prilo

LIVER clears amides , P450

None by renal as not water soluble.
what are lipid soluble ?
lipid soluble ones are long duration :
etidocaine
tetracaine
ropiv


VS
lido
procaine
prilocaine
mepivocaine
local in acid tissue ?
more is ionized, kess drug can cross lipid mmb.
local ptn bind ?
etido
bupiv
tetracaine
local binds what order of nerves ?
outside on mantle : proximal
small diameter
MYELIN
faster firing fibers

But in life :
C fibers: sympathetic postgang pain
B sensory
motor last (propio pressure touch)
where is there more systemic toxicity with blocks ?
top is
INTERCOSTAL *
CAUDAL *
epidural
brachial ones : inc scalenes

*most blood flow to region
prilocaine ?
over 600 mg metab o toludine
which makes meth hgb
Rx methylene blue
local
what is seen on EKG with local poisoning ?
long PR
wide QRS
myocardial depression (brady arrhy AV block ) but w/ bupiv vfib to vtach

profound hypotension
later as CNS excite to CNS depression
what is EMLA ?
2.5% lido
prilocaine

"eutectic" means melts on skin and can cross dermis but takes 45 min
PreMed Iv
CV effects
thiopental
BP drops
HR increase
SVR drops
PreMed Iv
CV effects
propofol
dec BP
dec SVR
dec HR
PreMed Iv
CV effects
etomidate
minimal dec all (HR SVR BP)
PreMed Iv
CV effects
ketamine
inc all
HR SVR BP
PreMed Iv
CV effects
versed
minimal dec SVR and BP esp w/ med combos
PreMed Iv
CV effects

which cause N/V
thio none
prop dec N/V
etomidate increase
ketamine increase
versed no change
PreMed Iv
resp effects
thio pent : dec
prop dec
etom dec
ket dose dep when use w. other meds
VERSED : NO
PreMed Iv
ICP / CBF effects
thio DEC
prop DEC
etomidate DEC
ketamine INCREASE
versed no change/MINIMAL
BARBS which first anal or hypnosos ?
muscle changes ?
analgesia then hynosis then EEG changes.
No skel m relaxation.
propofol MOA
hyperpol mmb
acts with GABA R so its dissoc so ch open

rapid clearence exceeds hep liver blood flow
IV
etomidate RR changes ? GI ?
Yes,
FAST SHALLOW
(unlike barbs)

dec TV and inc rate

GI: lots of N/V
IV
how is potency of opiods determined ?
affinity for R
special fast cleared opiod
remifentanyl cleared by plasma esterases non-specific to inactive metab in blood and tissue cells
lipid soluble of opiods
low lipid soluble : morphine, slow onset long duration

high: fentanyl and sufent : rapid onset, sht duration

(lipid sol can be taken up by lungs and then given back to sytem circ)