1 Flashcards
male DLT sizing
39 F (if < 170 cm)
41 F (> 170 cm)
female DLT sizing
35 F if < 160 cm
37 f if > 160 cm
male and female DLT depth
male- 29 cm
female 27 cm
peds dlt sizing
8-9 F = 26
10-12 = 28
12-14 = 32
where do you clamp dlt
distal to y piece and open air vent
what is applied to non dependent lung and what is applied to dependent with DLT
cpap 40 cmh2o for 8 seconds non depedent (up) lung
peep 5-10 cmh2o to dependent lung
what can bronchial blockers NOT do
-ventilate isolated lung
-suction secretions, blood or pus
-isolate contralateral lung infections
what can bronchial blockers do?
-lung isolate peds < 8-10 yo
-insufflate o2 to isolated lung
-isolate for nasal intubations
-suction air from isolated lung
bronchial blockers indications
-peds < 8 yo
-nasal intubation w isolation
-tracheostomy
how do you place a bronchial blocker
intubate with single ETT- insert BB through ETT- place in lung to isolate
complications/ risks of mediastinoscopy
- hemorrhage
- pneumothorax
what side should pulse ox/ a line be on with mediastinoscopy
r arm- looking for r inomminate artery compression
what should be on L side with mediastinoscopy
nibp
iv should be in lower extremity
prbc in room
contraindications to mediastinoscopy
absolute: previous MEDS
reltive: tracheal deviation, thoracic AA, svc obstruction
tracheal resection: upper vs lower lesion
-upper tracheal lesion- advance standard ETT distally before trachea is open may do distal 2nd ett after trachea is open
-if lower lesion: place ETT above lesion. after trachea opened 2nd ett placed in L main bronchus to ventilate while surgeon sutures tracheal anastamosis. 2nd L mainstem ett is removed and origional ett gets advanced past anastamosis into L bronchus
ards lung strategies
-pcv
-vt 4-6 ml/kg IBW
-peep fio2 <50
-plateau pressure < 30
-RR to allow permissive hypercapnia
-i:e 1:1 for restrictive or 1:3 for obstructive
-pao2 55-80 and spo2 88-95%
ards berlind definition
pao2 / fio2 ratio
mild= 200-300
moderate= 100-200
severe < 100
who should not get a needle cric
peds <6 yo
c/i to tracheostomy
none
airway exchange catheter. what can you do through it?
etco2, jet vent, o2 insufflate through AEC
what cant you do through airway exchange catheter
suction
airway exchange catheter is usually __ at lip
25
what is autopeep and who is at risk
obstructive air trapping
elderly, copd, emphysema, asthma
what can cause angioedema and how do you tx it
ace-i and c1 esterase deficiency
give ffp and c1 inhibitor concentrate, ecallatide, icatibant
1 cause of nerve injury in LMAs
cuff overinflation (lingual, hypoglossal and RLN at risk)
when is an LMA okay with laproscopic
< 15 minutes, <15 degrees trend, abd pressure < 15 mmhg
max pos pressure and max lma cuff volume
max pressure: < 20
max LMA cuff volume: <60
proseal lma
has gasric drain
reusable
built in bite block
lma supreme
gastric drain
disposable version of proseal
fasttrach lma
can intubate through it
cannot go into mri
flexible lma
wire reinforced
head and neck surgery
igel lma
no cuff- for spont ventilation
gastric decompression
combitube
gastric drain/ suction port
double lumen/ double cuffed
king tube
gastric drain- single lumen and cuff
indications for retrograde intubation
-unstable c spine
-upper airway bleeding
-mandibular fracture
c/i to retrograde intubation
-cannot access CTM
-goiter
-neck deformaties (tracheal airway tumors that would block path of wire)
-tracheal stenosis
-infection: ludwigs angina
-coagulopathy
how do you retrograde place
-puncture CTM with 14g needle
-aspirate air to confirm in trachea
-pass wire cephalad and out of mouth
-clamp wire, load ett and advance
-once ett cannot be advanced anymore, withdraw wire and advance ett to final position
nasal intubation c/i
lefort ii, iii
basilar fx
coagulopathy
nasal fx (cribiform plate fx)
nasal intubation depth
men 27
women 25
who is bullard laryngoscope good for
small mandible
-pierre robin, goldenhar, treacher collins, cri du chat
limited mouth opening (need at least 7 mm)
limited c spine mobility
c/i to bullard laryngoscope
none
who is the bullard great for
PEDS - bullard is faster than FOB- less cervical displacement than DL
where does the ETT sit with bullard
to the R of the blade
should you have pt in sniffing position with bullard
no
bullard laryngoscope how do you increase glottic exposure
life anterior
symptoms of epiglottitis
4 d’s: drooling dyspnea dysphonia dysphagia
epiglottitis is the #1 cause of
meningitis < 5
is croup viral or bacterial
viral
ludwigs angina
cellulitis infection of submandibular space from dental abscess-> complete upper airway obstruction
how to intubate ludwigs angina
need awake FOB or nasal intubation
retrograde intubation C/I
larygeal papilloma
benign neoplasm from hpv
cystic fibrosis is a mutation of what
chloride regulation mutation- tenacious mucus/ secretion production in lungs, liver, pancreas, gi tract
is cystic fibrosis obstructive or restrictive
obstructive
what other comorbid are common with CF
DM and hepatitis- check BG and coags
what is the number 1 risk for viral infection following blood transfusion
cytomegalovirus
alpha 1 antitrypsin deficiency
-early onset 25-50 yo COPD like emphysema from liver not producing alpha 1 antitrypsin
-leads to loss of elastic recoil, alveolar tissue destruction, airway collapse, and air trapping
PISS vs DISS
piss- wrong cylinder
diss- wrong pipeline
what are the numbers for oxygen, air and n2o
air= 1,5
n2o= 3,5
o2= 2,5
what does the oxygen analyer do
-detects pipeline crossover / flowmeter leak
-o2 analyzer = inspiratory limb
o2 pressure failure device
o2 pressure, not concentration
what is o2 consumption
250 ml/min
jet ventilation
15-30 psi via 14g needle cric
o2 flush valve
35-75 L/min at 50 psi
when do the bellows move
during expiration
-ascending bellows rise during expiration
soda lime turns purple at what pH
10.3
what si the most sensiitve indicator of absorber exhaustion
elevated fico
what inhibits hpv
mac >1.5, vasodilators (ntg, snp), pde inhibitors, dobutamine, ccb, acei
what is in the aldrete score
activity, neuro status, oxygen sat, respiration, circulation
what ones contain gastric ports
igel, supreme, proseal
what blade is the modified mac with levered tip to lift up epiglottis
mccoy
what blade is straight blade with wider spatchula/ belly
wisonsin
what blade is straight blade with side overhang best for cleft palate
oxford
what blade is modified mac with steeper 135 degree mount angle for limited neck mobility and lg breasts
polio
look at pics of lmas
Fast Trach = Intubating
I Gel = Spontaneous breathing, no cuff
Supreme = Single use, Gastric Tube, Bite Block
ProSeal = Reusable, Gastric Tube, Bite Block
Protector = Cuff Pilot allows pressure monitoring
Gastro = Helps passage of Endoscope
Air-Q
what lmas are safe for mri
lma classic, supreme, igel
what materials are safe for mri
stainless steel, titanium, aluminum and copper
most likley cause of injury with LMA placement
cuff overinflation
how does a nebulizer work
venturi
where should the hme filter be placed on a known patient with active infection/ pathology
expiratory limb
where is precordial placed
between 2 and 4th interspaces L sternal border
what does cbf autoregulate at
50-150
cmro2 decreases _ for every 1 degree of hypothermia
7%
1 site for herniation
temporal uncus (CN 3 oculomotor)
is peep good or bad for high icp
bad - avoid it
how fast should you get tpa or embolectomy for ischemic stroke
tpa w/in 4.5 hrs. embolectomy w/in 6
what is tripple h therapy for SAH
hemodilution (hct < 30%), hypervolemia, HTN
how to reverse warfarin
ffp, prothrombin complex, factor 7a
what should you avoid for tbi
steroids! glucose, albumin, n2o, hyperventilation
what anticonvulsants cause resistance to NDMR
phenytoin, valproic acid, carbamazepine
-cyp 450 inducers
s/e of abrupt withdrawl of gabapentanoids
seizures
s/e of carbmazepine
aplastic anemia
s/e of valproic acid
bleeding/ hepatic toxicity
tx for alzheimers
cholinesterase inhibitors
fxn of cholinesterase inhibitors
inhibits pche - prolonged doa of sux
whats wrong with parkinsons
low dopamine and excess ach. excess gaba at thalamus-> eps
s/s of parkinsons
pill rolling, skeletal muscle rigidity, postural instability and bradykinesia (slow movements)
what drugs do you want to avoid for parkinsons
metoclopramide, droperidol, haloperidol, promethazine
andidopaminergics and muscle relaxants
have no effect on sux or ndmr
risks of deep brain sitmulator
tx for parkinsons
sitting position- risk of VAE (precordial dopler for monitoring)
what si the only CN in the CNS not in pns
cn 2 optic
cn 3 oculomotor controls what eye movements
all except LR6 SO4
ischemic optic neuropathy
1 periop vision loss
from cn2
hypotension in prone
risks: prone, wilson frame, long surgery, lg blood loss, low colloid ratio, hotn
pt risks: male, obese, DM, HTN, smoking, elderly, HLD
central retinal arterial occlusion
external compression on globe in prone position
risks- horeshoe headrest in prone
1 eye complication
corneal abrasion
how long after spinal cord injury should you avoid sux
24 hrs
does MG have normal ach
yes normal ach but dec number of receptors
s/s of MG
muscle weakness that progresses as day goes on; resp weakness is #1 concern
when do you need post op vent for MG
MG >6 yrs, pyridostigmine >750 mg/day, vc <2.9 L, copd, sternotomy
tensilon test
edrophonium 1 mg IV-> weakness worsens= cholinergic crisis- give anticholinergic
if weakness improves= MG crisis- inc ach at NMJ- improved strength
MG and NMB
restatnt to sux -inc dose
sensitive to ndmr- reduce dose by 1/2
eaton lambert
autoimmune destruction of pre synaptic ca channels- dec ach release
skeletal muscle weakness-> s/s similar to MG
tx: 3,4 diaminopyrodine- inc ach release from pre synaptic terminal
eaton lambert and nmb
sensitive to sux and ndmr
MS
demyelination of cns- autonomic instability, bulbar weakness, aspiration risk, sensory deficit
MS and muscle relaxants
sensitive to ndmr
avoid hypothermia and sux -> hyperkalemia in MS (hypothermia prolongs sux)
guillian barre syndrome and neuromuscular
avoid sux- hyperkalemia (extrajunctional receptors)
GBS- sensitive to NDMR
guillian barre
autoimmune destruction of myelin in nerves- from ebstein barr virus- starts with a flu like symptoms-> ascending paralysis-> resolves (tx iv iggg)- no steroids
mh is associaed with which dz
king denborough syndrome, central core, multi core dz
mh tx
-cool them <38 c and correct acidosis - sodium bicarb 1-2
-correct hyperK- cacl 5-10 mg/kg, insulin 0.15 u/kg / d50 1 ml/kg
- dx dysrhtyhmias - lido 2 mg/kg / procainamide 15 mg/kg - no ccb
-uop > 2 ml/kg/hr = fluids, mannitol 0.25 g/kg, lasix 1 mg/kg
cobb angle of what = surgery
40-50
myotonic dystrophy
no sux (sustained contractions), anticholinesterases, hypothermia with myotonic dystrophy
where are third order neurons located (hot spot)
thalmus conencting to cerebral cortex
-1st order: SC
2nd: brainstem
3rd: thalmus
how do these drugs effect seizures?
ketamine
propofol
etomidate
methohexital
lidocaine
ketamine- induces seizures
propofol- reduces seizures
etomidate- induces seizures
etomidate- induces seizures
methohexital- no effect on seizures
lidocaine- reduces seizure threshold/ decreases duration
hyperventilation / hypocapnia will inc seizure duration
a wave form on cvp correlates to what part on ekg
p wave
RA cxn
c wave on cvp correlates to what part on ekg
rv cxn
qrs (isovolumetric cxn)
x on cvp correlates to what part of ekg
ra relaxation
end of qrs / t wave
v wave on cvp correlates to what part on ekg
ra passive filling
end of t wave
y descent
RA empties to LV (mv opens)
t-> p wave
best leads for ischemia/ arrhythmias
lead II and V5
where does hydralazine work
ccb - works in arteries
antiarrhythmic drug classes
class 1: na blockers- lidocaine, procainamide
class 2: beta blockers
class 3: k blockers- amiodarone
class 4: ca blockers- diltiazem, verapamil, clevapine
who needs endocarditis abx prophylaxis
prior ie infection, prostethic ht valve, unrepaired cong ht defect < 6 m old, gingival/ resp infection biopsies, ht tx with valvuloplasty
who does not need abx prophylaxis
cabg, mv prolapse, coronary artery stent
heparin goal before cpb
> 400
who needs retrograde plegia
incompetent aortic valve
1 cause of death with LVAD
sepsis
transcranial doppler
looks at flow through middle cerebral artery
which physiologic factors increase after placement of infra renal aortic cross clamp?
preload and mixed venous o2 sat
where is lead v5 placed
5th ICS L anterior axillary line
what a line placement is most reflective of central/ aortic pressure
femoral
most common vessel cannulated for retrograde cardioplegia
coronary sinus= middle vein
HOT SPOT
what leads monitor ischemia to anterolateral heart
lateral= 1, avl, v5, v6
anterior= v1-v4
efficacy
potency
affinity
potentiation
efficacy- ability of drug to produce effect
potency- dose needed for effect
affinity- ability of drug to stimulate a receptor
potentiation- drug A is efficacious when given with B. drug A owould not work if given alone
bronchial blockers- can they be used to isolate contralateral lung infection
NO
can bronchial blockers be used for nasal intubation
yes
cross clamp- increase.. vs decreases..
increases MAP, svr, svo2, pao2, o2 consumption, coronary bf
decreases renal bf
cross clamping of Artery of adamkiewicz
becks syndrome- anterior spinal a syndrome
-flaccid paralysis of LE- corticospinal tract
-bowel and bladder dysfunction- autonomic nerves
-loss of temp and pain sensation- spinothalamic tract
-touch and proprioception is sparred!!! - dorsal column
what is the first shock with pals
2 J/kg
what does phospholipase c do
vasoconstriction
nitric oxide pathway
L arginine-> NO-> guanylate cyclase -> cGMP-> sm muscle relaxation
what factors increase after infra renal aortic cross clamp?
-preload
-mixed venous oxygen saturation
clearance is inverse to
half life and concentration
clearance is directly r/t
extraction ratio, blood flow, dose
a lipophilic drug has what vd
> 0.6 L/kg
a hydrophilic drug has what vd
<0.6 L/kg
what is pka
ph where drug is 50% unionized and 50% ionized (conjugated acid)
what has the greatest effect on degree of ionization for drugs with pKa closest to physiologic pH
small changes in pH
ionized fraction predominates if
wb in acidic solution. wa in basic solution
hydrophilic and lipophobic
no diffusion across bbb, less hepatic biotransformation, more renal elimination
non ionized fraction predominates if
wb in basic solution
wa in acidic solution
lipophilic and hydrophobic
crosses BBB
more hepatic biotransformation
less renal elminiation
examples of zero order kinetics
more drug than enzymes
asa, phenytoin, etoh, warfarin, heparin, theophylline
drug metabolism phase 1
modification
-oxidation- removing electron
-reduction- adding
hydrolysis- adds water to split apart (esters)
phase 2 metabolism
conjugation
adds highly polar, water solube substrate
example of glucuronidation
morphine (falls under conjugation)
phase 3- elimination
atp dependent carrier proteins transport across cell membrane produced by kidney, liver, GI tract
enzyme inducers examples
etoh, tobacco, phenytoin, rifampin, barbituates
higher dose of other things needed
enzyme inhibitors
grapefruit, ssris, erythromycin, cimetidine, azole antifungals, omeprazole
lower dose needed
what is eliminated by pseudocholinesterases
Ester LA, succ, mivacurium
what is eliminated by nonspecific esterases
esmolol, remi, atracurium, clevapine, etomidate
what NDMR is excreted biliary
rocuroniujm
what enzyme metabolizes inhalation agents
CYP2E1
is it faster on/off if the blood: gas is higher or lower
lower- less gas in the blood
blood: gas tells you what
onset
oil gas tells you what
potency
decreased oil gas means
low potency
what gases cause hepatic dysfunction
iso, des, halothane
concentration effect
overpressurizing- higher concentration of agent to produce faster rate of rise
ventilation effect
as rate of rise increases, alveolar ventilation decreases as self protection- decreasing fa/fi rate of rise
low solubility of a gas means
faster onset -faster fa/fi equibiliriation
higher solubility of a gas means
slower fa/fi equilibriation- slower onset
rate of hepatic biotransformation and pulmonary (alveolar) metabolism
n2o 0.004%
des 0.02%
iso 0.2%
sevo 2%
halo 20%
best to monitor for intubation
facial n: orbicularic occuli (eye lid), corrugator supercilli (eyebrow)
recovery from nmb best to monitor
ulnar n and tibial n: adductor pollicis (thumb) and flexor hallucis (toe)
how many receptors are blocked if tv is > 6 mL/kg
80%
how many receptors are blocked if vc is > 20 mL/kg
70%
how many receptors are blcoked with tof 4/4 w/o fade
70-75% blockade
how many receptors are blocked with inspiratory force > -40
50%
best indicators of recovery from nmb
tetany > 5 seconds, headlift > 5 seconds, hold tongue blade against force
other names for pseudocholinesterase
plasma cholinesterase, butrecholinesterase, pseudocholinesterase, t2, false pche
extraunctional receptors
reduced pche- hyperk and prolonged action of sux
what has inc sensitivity to sux
guillian barre, ms, huntingtons, als, eaton lamberts
what is resistant to sux
mg
how much does sux inc k
0.5- 1 for 10-15 mins - hyperkalemia
dibucaine number
inhibits normal pche - tests for degree of functional pche avaliable
dibuacine of 70-80
typical homozygous - normal- DOA 5-10 mins
dibucaine of 50-60
heterozygous - DOA 20-30 mins
dibucaine of 20-30
atypical homozygous- DOA 6-8 hrs
which ndmr are aminosteroids
roc, vec, pancuronium
potency most to least
CPAR - cis, pancutonium, atracurium, rocuronium
what drugs produce laudanosine
atracurium and cisatracurium
seziures!!
pancuronium s/e
inc hr
acetylcholinesterase
breaks down ach atb NMJ or nicotonic receptors
acetylcholinesterase inhibitors
indirectly inc ach at receptor/ blocks hydrolysis
inhibit action of pchE = prolongs sux
anticholinergics
antagonize muscarinic/ cholinergic effects of ache inhibitors (sympathetic response)
what anticholinergics are tertiary
atropine, scopalamine
1 anticholinergic for tachycardia
atropine
1 anticholinergic for motion sickness and sedation
scopalamine
1 anticholinergic for antisalagogue
glyco
a delta fibers
fast sharp pain temp
c fibers
slow dull pain
transmission
1st order neuron: dorsal horn/ dorsal root ganglion
2nd: dorsal horn-> thalamus
3rd: thalamus to cerebral cortex
what inhibits pain
gaba and glycine release
where is pain processed and percieved
cerebral cortex and limbic system
inhaled anesthetics and alpha 2 agonists
what part of opioid does anti shivering
kappa agoinst (dynorphin)
what does mu agonist do
endorphin- resp depression, brady, miosis, constipation
what is delta agonist
enkephalin
can you use remi in intrathecal
no! contains glycine powder
s/e of methadone
prolonged QT syndrome-> torsades
iv dose and potency
meperidine
morphine
hydro
alfentanil
remi
fentanyl
dose; potency
meperidine: 100 mg 0.1
morphine: 10 mg 1
hydro: 1.4 mg 7
alfentanil 1000 mcg 10
remi 100 mcg 100
fentanyl 100 mcg 100
what does pka mean
onset
what does solubility mean
potency
what does protein binding mean
doa
closer pka to blood ph=
faster onset
benzene ring
lipophilicity
intermediate chain
allergy potential!!
drug class
metabolism
tertiaryb amine
makes it a weak base
what drugs cause methemoglobinemia
benzocaine, emla cream, cetacain
which way does methemoglobinemia shift curve
L
tx: methylene blue 1-2 mg/kg
what increases risk of methemoglobinemia
g6p reductase deficiency and neonates
what is emla cream
2.5% lido and 2.5% prilo
what type of LA has cross sensitivity and allergy potential
ester (PABA)
is chloroprocaine protein bound
no
benzocaine at physiologic ph
unionized pka 3.5
la uptake based on location
iv > tracheal > intrapleural > intercostal > caudal > epidural > Brachial plexus > femoral : sciatic, sub q
which way should you look during retobulbar block
midline- highest risk of hemorrhage
how long should you wait before and after exparel for lidocaine
after lido- no exparel for 20 mins
after exparel- no lido for 96 hours
are LA weak acids or weak bases
weak bases
what do LA bind to
conjugated acid binds to intracell alpha subunit of na channel
unioniezed base (LA) and conjugated acid (LA+) - cross axolemma- enter acitve channel- intracell portion of active na alpha subunit- na channel remains closed/ inactivated until LA diffuses away
max dose of lido during tumescent anesthesia
55 mg/kg
when should GA be used for tumuscent anesthesia
> 2-3 L of tumescent
what is ebl with tumescent anesthesia
5% of removed fluids
most common cause of death with tumuscent anesthesia
PE
additives to LA that prolongs doa
decadron, epi, dextran
additives to LA that shorten onset
bicarb
additives to LA that add analgesia
epi, clonidine, opioids
LA DOA
short: procaine, chloroprocaine
intermediate: lido, mepivicaine
long: bupiv, ropiv, tetracaine
what is the dose of intralipids
1.5 ml/kg 20% intralipids if < 70 kg
> 70 kg 100 ml bolus
double and repeat 2x
max dose of intralipids
max 12 ml/kg
what dose should epi be kept under for LAST
< 1 mcg/kg
placing lidocaine in what kind of solution inc its degree of ionization
acidic; water soluble and lipophobic
last symptoms in order
resp depression, arrythmia, loc
esophogeal stethoscope depth
28-32 cm- heart of breath sounds depending on depth
what should esophogeal doppler be at
35 cm or t5-t6 or 3rd sternocostal space - where esophagus and descending aorta line up
where is conus medularis in adults / peds
L1-L2 in adults
L3- peds
when do you d/c clopidogrel and ticlopidine before neuraxial
clopidogrel - 7 days
ticlopidine- 14 days
asa and heparin are safe
LA blockade order
b- c- a delta- a gamma- a alpha and a beta
a alpha
motor
a beta
touch and pressure
a gamma
muscle tone
a delta
fast pain and temp and touch
b fiber
preglanglionic and myelinated - site of spinal action
c fiber
post galgnionic unmyelinated - sympathetic- slow pain
block motor, sensory and autonomic
motor
sensory 2 higher
autonomic 2-6 higher than sensory
what impacts spinal spread
baricity, dose, site of injection, positioning
what is the bone most likely to hit during paramedian
vertebral lamina
what is blocked during epidural (and what levels)
sensory 1st-> motor -> NO automatic
sensory 2-4 higher than motor
what affects epidural spread
volume concentration and dose
what is the dose for epidural ___ per segment blocked
1-2 mL
what are better for pdph
sprotte and whitacree - pencil point
what block can be used for pdph
sphenopalantine
what ligament covers sacral cornu (important for caudal block)
saccrococygeal ligament
dose of caudal block for circumcision/ hemorrhoidectomy
0.5 ml/kg
where do you want to block to for caudal block
t10 = 1 ml/kg
what is c6
thumn
what is c7
2nd and 3rd digits
what is c8
4th and 5th digits
what is t4 and what surgeries block here
nipple line- upper abd surgery, c section, cystectomy
t6
xiphoid process- lower abdomen surgery- appendectomy
t10
umbilicus- total hip, vaginal delivery, turp
t12
pubis
L1-L2
lower extrem surgery
L2-L3
foot surgery
L4
anterior knee
s2-s5
hemorrhoidectomy
what surgery is isc block really not good for
forearm/hand- c8-T1 often misses medial proximal upper arm
what nerve causes phrenic n. block
c5 block- hemiparalysis of diaphragm
what nerve causes horner syndrome
c7- stellate ganglion block- ptosis, miosis, anhidrosis
what reflex can be caused with ISB
hypotension and bradycardia in sitting posittion and isb- bezold jarish
supraclavicular
trunks and divisions- upper arm, elbow, forearm, wrist and hand - NOT SHOULDER
forearm big
biggest risk with supraclavicular block
pneumothorax
if pt has cough, dyspnea, chest pain- xray
can still get horners, subclavian hematoa
