2nd test anestesio Flashcards
hx of ketamine
intoduced in 1970
syntheiitc drug (not derived from natural product - like propofol and benzos)
part of feniciclidina group
cx of ketamine
anesthetic agent - can be used unico for that
analgesia
not volatile
liposoluble derivative of fenciclidina
ketamine mechanism and action
not well understood
only EV that gives inhbition and excitation and simultaenously - selectively in one organ CNS (aka DISSOCIATIVE ANESTHESIA - keeps some reflexes intact and others depressed - other EV have to wait for px to close eyes not ketamine - produces fixed gaze tho scared - doesnt blockeyeball like oethers where eye rolls up - ketamine can cause nystagmus tho -)
excites limbic systrm, inc HR, VC, psychiatric deliriums (maybe resistant to others)
depresses cortex and thalamus
inetrrupts pain - anesthesia
blocks AcH at cortex
we think ketamine acts at same opiod rec due to reversal same
but also act in serotonin rec, NE rec, and muscarinic Ach rec
(@ muscarininc thats why salivation increases) -
maintain swallow reflex - px can cough, maintains suction reflex - defense mechanisms
@ NE rec liberates catecolamines, VC peripheral and increases BP
@acute processes dehydrated, hypotense state hypovolemic shock px give ketaine with anesthetic inductor helps cardiac precharge
produces hipnosis actina @ cortex BUT DIFFERENTLY and like barbs with excitation right before (not calm, agitated - unlike propofol)
analgesia > anesthesia –>
(need less inhaled gas) & (no pain at immediate postqx
antagonista puro de opiodes
naloxone
desireaed and undesired effects
FD ketamine
dissociative anesthesia ( suppresses some reflexes while others not)
maintains cough and corneal, suctionz
coordinated movements but not conciosu
eyes open, fixed gaze, nistagmus
potent hipnotic and analgesic
iincreases ICP
blood flow of brain
cerebral O2 cconsumption …metabolsm and intraocular pressure
can we measure depth of coma in ketamine
noooo
effect of ketamine on VC system
acts at NE rec and thats why it increases systolic arterial P 20-40mmHg - causes peripheralVC - more volume reaches heart (precharge) - CO increases as well
increases HR (increases LV work)) and O2 consumption of that muscle - so not good for px with coronary problems
elebates pulmonar vasc resistencees
relaxes bronquial SM - BD (@ asma px, BC px - ideaal_
secondary to increase in sympathetic activity
hepatic px (transplant px)are VD pysiologically, others VD from drugs (propofol, barbs, opiods) - ketamine ideal for VD px (NE causesVC)
anything that increases work of ventricle increases O2 consumption
not best in coronary px
BD (relaxes SM there)
ketamine @ resp
minimal effect - doesnt depress giving it biosecurity
problems alot of time when its used with another drug like opiods
transitory apnea < 5min
seen after intubation dose
relaxes broncial SM
betters pulm compliancy in anesthetic px
FK metabolism of ketamine
very liposoluble - used EV have effects in 1min
crosses BBB
duartion ketamine
10-15min (1min initiation)
IM effect by 5min (absorbs well)
produces qx anesthesia in 30-60sec
20 peak
oral dose produces max sedation in 20-45min
indications of ketamine
IV anesthetic inductor - can be alone
useful in hypovoelmic acute shock
good for kids - cardiac congenital (R to left), bronchial hyperactivity (BD)
used as inducgion agent in kids - IM
(before sevorane)
px with cardac tamponade
px with cardiac congenital diseases with right left shunt
px with reactive bronqual disease severe due to BD effect
useful in kids as an inducctor for less deliriums than in adults
IM inducer in px arent cooperating (with EV, studies)
can cause conscious sedation in kids that are doing minor procedures, como curas o cambios de apositos, desbridamiento of wounds, xray
IN these proceudres causes excellent analgesia wihtout respiratory depression
px that have to go everyday to get anesthesia for qxs
studies where we cant be in contact iwth px or px needs to be stilll/calm - CT, MRI, RT -good to canalize kid for short proceudres no resp or CV depresison
CI ketamine
px with ICP, mass in brain, cerebral infarct hx
NE rec @ chronic shock are depeleted so nooo, opposite effect , more VD (NE, epi wont work!)
px with open ocular lesions , glaucoma, (because ketamine increases intraocular pressure) ophtalmological qx
in px with coronary disease or pulm HTN, HTN,
in px with catecolamine depletion (in px with critical prolonged disease) - ketamine has
cardiodepressor effect which can manifest
bedridden px
px with psychiatric alteratiooncs - causes hallcuincations (auditive or visual), delirium
narcotrafficked, pleasure use-
ketamine interactions
potentiates relaxers NDNMRS
hipotension with halotane
prolongs inhaled anesthesia aka reduces CAM
dosis ketamine
IV
IM
recta;
oral
induction 0.5-2mg/kg IV (1mg/kg)
4-10mg/kg/IM (5 is enough)
maintenace 30-90mg/kg/min
10-20mg for concious sedation
benzodiazepines
dizepam, lorazepam, midazolan
preqx to sedate px - antianxiety
PROLONGED amnesia and good sedation - px wont remember
used in preanesthesia, preinduction, preqx to calm px down
EV anesthetics (right before qx)
also IM, VO (night before), parcho
NO ANALGESIA
NOT FOR INDUCTION OF SLEEP/ANESTHESIC
sturctures of benzos
diacepam and loracepam have similar structures
biodisposition diacepam
high liposoliblituy , hipofilic wait CNS initation
crosses BBB faster than midazolam (more hydrosoluble)
IM irritattes, hurts, acido bensoto, EV also irritates
somnolence, hipnosis slow irregular
very insoluble in water
slow initiaion - not ideal preinduccion
30min
slow recuperation
all EV decrease flow in hard organs
liver kidney bazo
all EV eliminate thru liver (benzos, opiods) - all prolonged if liver messed up…. except ketamine
keatmine doesnt decrease flow!!!!!! - can be used in px with pathologies of these organs
meatabolizes at liver (even at decreased flow or pathology, clears up well) eliminaeted life stays the same
metabolites of diacepam
3hidroxidicepan
oxacepan
dismetilodacepan
WITH sedative and pharmacological activity
like opiods , benzos use oxydation to metabolize
liver
duration of action of diacepam coorelates with these metabolites
in order for these metabolites to eleiminate undergo
2nd bioptransmformation to elimiante not oxidation this time , conjugation
forming acido glucoronico without farmacological activityg
fk DIACEPAM
1.5LT/k C - distribution volume
CLEARING 0.2-0.5CC/KG/MIN
ELIMINATION HALF LIFE 20-40hr
midazolan
most recent benzo
1995-97s
more soluble in water - less irritant via IM
fast initation action
effect on CNS fast
mx depresion > 1-3min
IM absorbs well - effect at less 30min
faster sedation
mech of action of all benzos (like opiods)
@ CNS potentiloze GABA in different areas,
rec of benzos of CNS @ cortex, black sustancia, hipocampo (these others are IIor presynaptic).. cerebelo (has postsynaptic aka type I rec) , medula espinal.
rec are post synaptic or presynaptic (so benzos can be type I or II))
increase clorine ion conductance in synapsis which hyperpolarizes cell - inhibitory
unlike barb, benz increases aperture o fCl- channels
frprnf on lovslxsyion
farmacological action of benzos
decrease necessity for inhaled agent
b/c they are sedatives
@ CV benzos..
depression of myocardium
increase HR
@ resp benzos
benzos cause transityry apnea
more pronounced if used opiod before (like propofol)
at dosis of 0.75 of midazolan or 0.015mg/kg of dizepan there will be no resp effects
uses of local anesthesics
residents
paramedics
anesthesiologits
everyone
@ colonization saw indigenus using oja de coca - adornacimiento on wounds and oropharynx,
used in clinic after development of jerninguilla
advangestes of LA
biosecurity
sold without perscription
cheap for alot of qx procedures - regional anesthesia
reuptake of NE causes by LAs
VC
stops bleeding of a wound
(also causes analgesia)
definition of local anesthetic
chemical substances that reversibly block, inhibiting gneration, and nerve umpulse conduction of nerve impulse without LOC (dont cross BBB)
peripihral regional nerve block
remove sensibility of a certain area of the body
presentation of LAs
can be tablet, parche, aerosol, etc all types (depending on objective)
(TODAY WE ONLY USE LIDOCAINE AND BUPIVACAINA)
with and without adrenaline added
without/with hypertonic dextrose –> hyperbaric anesthesia = known as anesthesicos pesados pesados
(deposit @ LCR and have higher baricidad than LCR)
cx necessary for local anesthetics
be reversible latency period adquate duration that will guarantees qx (a bit longer than qx) local toxicity minumum potente de acuerdo a clincial use stable ante light and heat elimination and excretion in totality can sterilize(50, 20ml containters with leftovers to not waste)
protein union of LAs @ nerve
procaine - 6%
lidocaine un 67%
ropivacaine - 94%
Bupivacaine un 97% (double duration time)
B fiber block
accion - increase of T and VD - one of the first MC of px (@ subaracnoid, epidural)
one of the smallest
smallest first to block, thickest last to block
@ dehydrated hypovolemic , VD px shock, it is CI to use LAs –> decreaases cardiac return –> hypotension
block of fiber A-delta and C
loss of sensation of T and pain sensibility
px cant differentiae hot from cold
use aguja to ask if px feels pain or not, vs gota de alcohol
blockage of fiber A-gamma
loss of propioception
dont know position of leg
dont move px until this is blocked??? - last px was in is what theyre in for whole qx in their memory
done when cant lift leg
block of fiber A-beta
loss of sensation al tact and prssure’
after can put bendaje elastico
block of fiber A -alfa
loss of motricity
px feel no deep pain
LAs
no shock, hydrated px necessary…. decrease venous return so first MC = hypotension
represent lack of sensbility in a certain area of the body
give analgesia in different parts of body when applied topically, injection in vecinity of nerve endings (principals ) or in epidural or subaracnoid
clinically useful LA agents
amino eteres or amino amines
primary action LAs
inhibition of peripheral nerves
very selective on which nerve fiber you want
when LAs are systematically administrated they can also affect
functions of cardiacl skeletal muscle and SM
asi como toda la transaccion de los impulsos en el CNS and in system speciliazed system in heart conduction
@ EV can affect purkinje1
most available antiarrythmic (or for tachycardia)
lidocaine
block purkinje to modulate cardiac rythm
2 presentations
constituents of nerve membrane, LA mechanism
…90% of constitutyents of a nerve membrane is lipid and 10% proteins
LA block sodium exit/flow, nerve transmission, depolarization
keep it repolarized
potency of LA depends on`
its liposolubility and duration of its effect (due to ala protiein affinity)
for LA to have an effect should
block no less than 3 nodules of ranvier or 3micras of diabmeter of a no mielinazed fiber
> 0.2 diameter mielinizado
only anesthetic local natural
cocain
cocaine cx
alcaloide with VC properties due to it blocking recatacion of NE in motor simpatico terminal nerve endings
2 groups of LAs…before
amino eteres derived = procaines , cloro proacina, tetracaine
amino- amine dervied -mepivacaine, prilocaine, lidocaine, bupivacaine, etidocaine
differentiating LAs
by metaboslims (where, some in plasma - those caused hpersensibility),
aminos, amina metabolize from hepatic microsomal (used today - at overdose can affect other tissues)
amino eteres from ataraza plasmatica
LAs depedning on duration are classfified into
low potency - procaine and cloro procaine (not really used) < 30min
intermediate - prilocaine, etidocaine - 60minn
high - bupicaina, tetracaina 120min
closer ph normal plasmatic to pka
will ahve more nonionized moleciels - pharmacological activity - faster intiation
further apart - less - prolonged intitation
if u give with bicarbonate (10cc-20cc lidocaine - 1cc of bicarbonate) = increase ionized molecules- more effeectivity - accelerates
what is pka
constant at which drug dissociates
choosing an LA depending on following factuors
duration of qx
duration of anesthetic should be > 50% on qx duration
type of regional anesthesia that will be done
size, constutution, general state of px and metabolic alteration
farmacocinetic
absorption, districution, excretion of LAs can say that oesnt mater where depsosited because distribution patter, metabolism and eliminatin is similar - althoug their velocities in these parameters is different
what does absorption of LAs depend on
whwere there was deposited and grade of preception of each zone
@ peripheral level, max plasmatic concentation reached within 15-30min , when applied EU reach these elvels immediatley
also depends on aditional VC drugs and fisciochemical properties of drug
in relation to plasma concentratio nfor every 100mg of lidocaine (intercostal very vascularized)
1mg of () PHM
(1.5 @ intercostal)
SC = 0.2
max plasmatic dose required to present toxic effect (of lidocaine)
5mcgxdl
we can dedcuce that max lidocaine we can put is 500mg of lidocaine with epn and 400mg without epnef
max at intercostal 350mcgxdl
plasma concentration depends on
lugar of block
Ej: in intercostal level for every 100mlg of lidocaine will have 1.5mcg of { } plasmatico
in a B . epidural = 0.1mg {}plasmatic
in a B. plexo b. will have 0.6mg {} plasmatic
in a B. Plexo cutaneo will have 0.2mg { } plasmatic (can put mroe in places with less irrigation -
these places take into account using adrenaline can cause damage, infection, necrosis - nasal, pabellon oreja, dermis of skin - dont use too superficially - put it SC )
LA metabolism and excretion
destoxicaiton and excretion of local anesthesics are metabolized in liver or in plasma ,
metaboliztes are excreted in urine
VC decreases velocity of venous clearing of LA, from site of injection
this duration is more attenduated in block of peripheral nerve where injectio sites are avascular
local block inititation accelerates with
use of carbonated solutiones combined with LA producing more free particlses
cardiav toxicity of LAs
CV system is more resitent to toxic effects of LAs, (CNS more sensitive)
dose to cause CV depresion is > than dose to provoke depresion in CNS
this doesnt happen with bupivacain, the mostcardiotoxic toxic…
Signs and Symptoms of LA cardiac toxicty
EKG: increases PR interval
prolonges QRS complex
sinusal bradicardia
severe ventricular arrythmia (give lidocaine)
ventricular fibrillation (doesnt happen with lidocinae) - so attached to proteins hard to revese - make sure when giving it youre not in luz of vazo - can kill px
higher threshold when pre give benzo but not level of CNS
tx to toxic response
maintenance, resp route PERM, circulatory assistence
tx convulsion w/ small doses of EU short acting barbituric like triopental in 1-2m/kg and sucinil coline in 0.5mg/kg dose
if maintenace of respiratory airways is compromised with convulsions.
endotraqueal intubation is urgent
also that will avoid bronco respiration of gastric secreionts
first step to prevent toxicity of LAs
use in small quantity for any regional anesthetic
if toxic reaction of bupivacaine and cloro procain shoudl consider using slow injection or fractioned dosis in particular for epidural block to reduce leaste toxiiity potential in am maccidental IV injection
premedication with benzodiacepine like diazepam 1-2mg/kg increases toxic threshold in CNS, nevertheless, influences in CV toxicity
subaracnoidal anesthesia
used with LA base
seen daily, gynacologists for cesarean, hacer mama
regional block of hemicuerpo
raquianesthesia - thru vertebral column
have to do LP (need to know where medula finishes)
localizing spots isnt too hard
blocks different nerve fibers depending on size (thinnest first - A beta ) –> VD –> hemodynamic changes, hypotension –> changes T (cant differntiate)
doesnt feel sensitivity nor motor
where does medula finish
L1-L2 - lesioned causes pernmanaent damage, less sensibiliy
L2-L3 - inadult inferior border
all should be below L2
neonate - until S2
covered by PAD w/ LCR
absolute CI of subaracnoid anesthesia/ LP
vessels in the way,factors to bleeding –> grand hematoma - compresses medula with irreversilbe medula damage - altered coag factors to form trauma
infectious process @ SKIN and puncture area - can cause bacterial translocation
px denies
labor attitutes
deformities of spine (palapate spinooous apofisis)
elements to go thru
skin (insulin, LAs with bigger agujas)
between apofisis espinosasa - interspinous ligament
yellow ligament
epidural space (another site for block)
dura madre
exit of LCR - must happen to know youre in subaracnoid space *cx of liquid
important subaracnoid, osmolarity
isovaric (LCR = osmolarity) vs.. hipovaric (nerve block under where yo u adminstetered -) vsl. hyperovaric (block will be above where administered - to block T10 - the higher the block more VD - more hemodynamic changes more hypotension)
isovaric bloacks in same place of deposition
election depends on which block level you desire
subaracnoide casues regional anesthesia - hemicuerpo (not specific limb)
lidocaine 1min (heavy , hypervarica - have dextrosa hypertonic, adrenaline_
surgeon has to mark exact of qx excision - ombligo T10 - block fibers above it too T8
first 5min
incline head of px - physical effect to diffuse faster - anesthetic osmolarity is decreasing (hypervaric evenutally becomes isovaric = se fijo - doesnt increase more thant that no matter what more you do to head - wont ascend more)
duration depends on which used
lidocaoine 1 min
bupiv - 2hr
lidocaine pesado , hypervaric with hypertonic dextores
can use adrenaline to increaseduration 30%-40%
max # of LA (volume) can deposit to avoid hypertension of toxicity of any drug
4ml
max lidocaine to avoid toxicity
100-(200mg)
100 i smax @ subaracnoide
postanesthetic cefalea
not always feminine multiple tries of finding space aguja was too big not appropriate hydration of px
NOT because px walked or due to pillow or sat up
differnt types
sat or awake NOT when laying down
anesthesia causes weight occiptofrontal sensation
do a differentaial )hx of anesthesia from 24hr -14d
vs pulsatile in temporo parietal (if vascular headache)
hard in kdis and oldies (more in normal fertile age - anesthesia cefalea)
tx cefalea
hytdration
steroids
meningeal irritation or no?
parche hematico - not really used , risky
advantatges of epidural anesthesia
analgesic (less dose) and anesthesic (more dose)
relaxes less than subaracnoide
al depends on dose
today we are using opiod subdural for analgesic
LAs, lidocaine are not used as analgesics in subaracnoide but they are used in epidural dpeending on dose
any level - doesnt cross dura madrea - wont injur medula
thicker neeedle and catheter can go thru (this determines headage) - can be there 1 wk - long duraion
px can feel pressure but not Pain
much slower or resistent to hemodynamic changes (firssst MC in subarachnoide) USE FOR CESAREA - hypotension affects fetus
much more selective on where to block
complications fo subaracnoide not present here (doesnt perforate dura madre)
of anesthesia depends on how high block (the higher the block, # of anesthetic will be less)
px that dont need too much muscle relaxation - epidural is ideal
plastic surgery
more sensitive block - feels hand of dr but no pain
the higher the block, the less # of anesthetic needed why because the spacers are diffferent (higher medula occupoes mroe aguerjo below more space)
desambular faster - recovers faster
can block 2 places at once
blocking of braquial plexus
we want to decrease risk for px
fast recuperation
specific anatomical block = to inhibit pain transmission @ calcium channels that liberate @ nerve fibers
in px with severe pulm or cardiac px - can just block hand - putting them full to sleep is a bit risky for that kind of px
can go straight home
what forms form first primary trunk
(roots/raizes) C4, C5, C6
DRAW
segundo tronco primario is formed by
C7
tercer tronco primario is formed by
C8, T1
innervation of hand
C4-T1
each primary trunk has
anterior and posterior branches
anterior branch of first trunk unites with
anterior branch of second primary trunk to form tronco secundario anterinterno
anterior branch of thrid trunk forms..
tronco secoundario anteroexterno
3 anterior branches from 3 troncos form
tronco secundario posterio
from tsai
medial
cubital
musculocutaneo
ECM
tsae
raiz external of medial
coracobraquial nerve
another he forgets
tronco secunario posterior
radial nerve
raizes come out of osea where i sthe braqueal plexus
agujeros de puncion? in neck between anterior and medial scalenes
then passes under clavicle (already in paquete with veins and artery) - hueca supracavliculara a nivel de la sida
3 levels of blocking brauql plexus
interexcalenico - at raiz exit
hueco supraclavicular
axilar
advantages of interecalenico
can block entire plexus - all roots
of anesthesia needed is less
px doesnt have to move hurt arm
disadvantages of interecalenica
need paresthesia - with aguja #22 superficially, px feels sensation when it touches nerve - thats when you deposit anesthesia - around cricoid thyroid
(now we have electric stiulators)
can block vago and frenico
cant do parrallel, bilateral
supraclavicular tecnhique
has been discontinued
@ inspiration vertix of lung comes up and can cause a neumotorax even if done correctly
axillar techinqieu avantages
can be done bilaterally
no need for paresthesia
disadvantages of axillar technique
need large volumes for blocking all plexus
blocks can be partial (T1 not fully blocked)
can easily punture artery or vein of axillar, if put anesthesics in luz of vessel causing intoxication when looking for nerve - orient with pulse
px would have to move injured arm
smelly
if you puncture vessel just go all the way throught, nothing out, dont move needle
dont take it out and try again
IV blocks
thru vein
antebrazo is the only place to do it
effective, useful
exsanguinate all forearm, presure bandage to avoid reflux perfusion (180mmhg/ 2 tourniquetse)
take 1% lidocaine , 20cc, thru acatherer that was put earlier
(without adrenaline) or bupivacaine
arm is asleep
used most for hand, trauma. lavado qx, phalangeal fractures
risk of IV block
if tourniquets get lose,
lidocaine through circulation can cause cerebral toxicitu
how long for tourniquet max
1.5hr
no perfusion to arm
qx should be over by then (1hr lidocaine should be absorbed up by now)
lidocaine presentation
2%
every ml/cc there is 20mg
dilute with saline solution
1% - every cc - 10mg
max dose of IV block without epi
400mg max of lidocaine
more 5mg/dl
today we can do selective blovks of specific nerve fibers of plexus - most popular
cubital and radial
especially when working on hand
organ according to books that most gets injured
the hand
where to block cubital
funny bone area
fossa epitrofia/craneal?
here only covered with skin
with 3-5cc withoutepi
need paresthesia
need asepsia
causes of ER infections
poor asepsia (block cubital first)q
medial nerve blockage
between palmar major and palmaro minor - on sides
laterally punctinging medial nerve
dont need paresthesia
5cc of lidocain without epi
radial nerve block
easily blocked by
agujera thru tabacera anatomica under skin and pentrate needle max and then administer
fine needle
know which fingers are innervated by it
ALWAYS ASPIRATE before infiltrating to makre sure youre not in an artery
interdigital blocks
2 cc o f lidocaine blocks all distal phalanges
pudendal nerve blocks
also done
crystalloides (aka suero)
anesthesiologists regulate hydration
were used for hemodilutions
similar to plasma
substances with water, electrolyetes and or sugars in different pro-portions and osmolarities (dextorse) - may or may not contain dextrose
(some substances have only dextrose and water - hypertonic solutions)
water with disorbente universal and electrolytes
basis for hadningl px hydration
water or electrolytes
know normal rnage of elecrolytes
normal Na+
135-145meq/dl
most abundant electrolyte
command osmolarity of solutions - decides
> 145 = hypernatrmic/hyperosmolar solution
K+ normal
3.5-4.5
Cl- normal
107ish
calcium normal
8-10
magnesium normal`
1.7-2
if you give 1000ml distributes in coporal liquids as
2/3 to IC space (666ml) and 1/3 to EC space (333ml)
since EC space is divided into intersticial and intravascular (250ml to intersticial - 75% and 83ml to IV space 25%)
takes 2-4min to diffuse to diffeent spaces
capacity for crystaoilds o expand volume is related to
consentration of sodium in solution and this sodium is what provokes osmotic gradient between Extravasuclar and intravasuclar space
different for each solution - depends on how much sodium
hypernatremic drags more water from EV space to IV space (osmosis - ability to mbilize liquid from one space to antoerh)
IV is where we want liquid in hypotense VD px, to imrpove precharge
crystaloids are considered …
non toxic, no eadverse effects,
dont cause allergies,, are not vitamins, dont need refridgeration or light
dont interact with regular blood components
only should maintain equilibrium
can present certian alterations related to indiscriminated use and without control of medical team -
hyperhydration can cause
edema in all tissues and membranes
normal osmolarity of plasma
280-300
nutrient in orgnaism
dextrose
types of dextrose in water
for every g of dextrose 4kcal
5% - 5g
10%, 50% for food formulas
energy only in hypoprotein px
hypernatremic px needs…
WATER
give 0.45% saline
Ringer lactate (130 Na+)
dextrose in water
px losing cl- and na+ , bleeidng, acute hypovolemic
give normal saline
drags water , osmosis, less liquid needed
careful for saline solutions
in px with cardiopathies
adverse effects of ringer lactate
has bicarbonate (to elimate has to be CO2 and H2O)
in px with hepatopathies will cause metabolic alkalosis form too much lactate in blood
has calcium - can cause hypercalemia in renal px with high infusions
dont use in px with liver and kidney probems
adverse effects of normal saline solution
too much cl - hypercloremia
hypercloremic acidosis in px with poor renal function
hypernatremia in renal px
edema (all solutions cause this)
hypertonic saline solution
hypernatremia
metabolic acidosis
hypocalemia
cerebral dehydration with ingracraneal blleed
mielinolisis pontica from abrupt changes in sodium concentration
pulm edema in cardio px
dextrose in water adverse effects
water intoxication due to overdose of glucosalated solution
hyperglicemia -dont use in diabetics
addison px can cause crisis due to cell edema and water intoxication
cell dehydration in cerebraltrauma
hypotonic solutions
have less solute concentrations than other solutions
solutions with osmolarity less than plasma ( < 280mOsmol/l)
used for hypernatremia
saline 0.45, 0.33?
dextrose 2.5, 5
isotonic solutions
solutoins that have the same concentration of solutes as other solution
an isotonic solutoin has an osmolarity similar to plasma between 272-300mosmol/l
most cardiotoxic LA
bupicavaine
low potency LA
procaine
cloro procaine
initiation of procaine vs cloro procaine
1 (procaine)
cloro procaine (0.8)
pka of procain vs cloroprocain
procaine (8.9)
cloro procaine (8.7)
low potency LA with protein uniont
procaine - 5.8
intermediate potency LAs
mepivacaine
etidocaine
prolocaine
lidocaine
initations of intermeidate potent LAs
mepivacaine - 1.5
etidocaine - 8
prolocaine - 1.5
lidocaine - 0.8
pka of intermediate potency LAs
mepivacaine - 7.6
all the rest are 7.7
etidocaine
prolocaine
lidocaine
7.7 lidocaine - 7.4 normal plasma pka - 64% particles
protein union of intermediate potency LAs
mepivacaine - 77
etidocaine - 94
prolocaine - 55
lidocaine - 64
high potency LAs
tetracaine
bupivicaine
intitation of high potency LAs
8 both tetracaine
bupivicaine
oka of high potency LAs
tetracaine - 8.5
bupivicaine - 8.1 (initation action will be slower 20% noninonized particles)
decide by duration of qx
protein union of high potency LAs
tetracaine - 76
bupivicaine - 95
max dose of lidocaine wihtout toxicity
we can dedcuce that max lidocaine we can put is 500mg of lidocaine with epn and 400mg without epnef
LAs pH
local anesthetics are drugs of weak bases, when their PKA > pH will have a > # of ionizaed molecules
year that cocain was clinically introduced and use
1884
topical use
polvo prep
max dose of cocaine
200
year benzocaine was introduced in clinic and use
1900
topical use
pomada and aerosol prep
year procaine was clinically introduced and use
1905
spinal use
prep sol 10/20g/ml
max dose of procaine
1000
year tetracaine was clinically introduced and use
1930
spinal use
sol 10/20g/ml
max dose of tetracaine
200
year lidocaine was clinically introduced and use
1944
2 presentation types
????? periphral neve block, epidural
10/20g/ml
max dose 500
spinal
topica = pomada 2.5
history and use of mepivacaine
1957
epidorual and peripharl nerve block
sol 10/20g/ml
max dose of mepivacaine
500
prilocaine histoy and use
1960
epidorual and peripharl nerve block
sol 10/20g/ml
max dose of prilocaine
900
bupivicaine history and use
1963
epidorual and peripharl nerve block
sol. 2.5 and 5mg
max dose of bupiviaine
200
cx of class C fibers
myelinic? - no
D-M (0.3-1.3)
conduction velocity 0.7 - 1.3
sympathetic, func. auto post gan diverso
cx of class D fibers
myelinic? - no
D-M 0.02
Veloc-conduction 0.1-2.0
pain temperature and tact
cx of class A alpha fibers
myelinic (> 0.02 are myelinic….he said)
D-M (6-22) - thickest
cond vel 30-120
motor
cx of beta A fibers
myelinic
D-M (6-22) - biggest
cond vel 30-120 metro por milecima seg
motor
cx of gamma A fivers
myelinic
D-M (3-6)
cond vel 15-35
muscular tone
cx of delta A fivers
myelinic
D-M 1-4
conduction velocity 5-25
pain and temperature and tact
cx of B fibers
myelinic
D-M -3
conduction velocity
3-15 pregnagionar sympathetic
diverse autonmaous functions
where do LAs act
act in n. membrane
(what they do is the inhibit the flow of sodium acting on specific receptros responsible for changes in conductance of sodium channels)
specifically in internal channesl is blocked by local anesthetics used in clinics
duration of anesthetic effect can lengthen how
increasing the dosis or by abolition of VC like adrenaline or fenilatrine
3 main benzos with special interest for anesthesia
dizepam, lorazepam, (he doesnt use) midazolan
diazepam and loracpam have similar structures
midazolan is completely different
what differentiates midazolam from diazepam since each molecule has hydrogen atoms also has a ring strucuture called….and its importance in midazolan
imidazol
( i think this is only in midazolan….the imidazol in midazolan converts this drug to hydrosoluble with a pH < 4)
midazolan different (dormicun) (doesnt irritate, less liposoluble than diazepam immidasol ring) - BBB fast, fast initiaion imidazol ring
but we cant explain why midazolam is faster initation
why does diacepam irritate
prepared in benzoic acid which irritates alot
loracepan prepared in what solution
propilenglicol acid
solubility of loracepan
just as insoluble in water as diacepam
flumacenil
inidication
revert depressive effects of benzos @ central level
dose of flumacenil for an overdose of benzos
bollus of 0.2mg
@ 30min
0.3
then 0.5 until reacing 3.0mg
Pedro Cieza de leonn - described that incas chewed coca (kunka) sukunka means faringe adormecida
1532
charles gabiriel prevaz, crystal jeringa
1853
alexander wood, aguja hypodermic
1885
who and when was cocaine isolated
1860 - Nieman
who and when describes pharmacology of cocaine
1878 - anrep describes farmacology of cocaine
who and when show first clinical demonstration of cocaine in ocular conjuntiva
1884 - k. koler and sigmund freud
who and when realized first block with cocaine
1885 - Halsted
who and when used frist time adrenaline to prolong a regional block
1903 - Braun , uses adrenaline to prolong regional block
when and by whom was logfren synthesized
1943 - logfren synthethizes lidocain
when was bupivacaine synthesized
1963 - synthesizes bupivacaine
in respect to plasma crystalloids can be
can be hypo, hyper or isotonic
components of cloruro de sodio of 0.9% (normal saline) vs 0.45% (SS al medio)
saline 0.9% only has Na+ and Cl- (154 each) - hypercloremica, hypernatremica_ - mild hypertonic - 308 osmolarity (mosm/L)
put if losing sodio (hiponatremia_), bleedning (improve hemodynamic state of px), acute hypovolemic px
saline 0.45% 77,77, hyposomlar, hypochloric, hyponatremic - 154
reponer with nutrition not to hydrate
@ hypernatremc px
know what px needs at rehydration
other saline solution components 0.21 vs 3% vs 5%
0.21%
Na and Cl - 34 each
68 mosm/L
3% - 513 each
1026mosm/L
5% 856 each
1712 mOsm/L
components of dextrose in water (5 vs 10 vs 50%)
dextrose in water - only to give energy and nutrients @ hypoglicemia, for heart and brain, no other electrolyte
5% has 50g of glucose /L with 252 osmolarity
10% - 100g/L, 505mosm/L
50% - 500 g/L - 2525mOsm/L
@ hypernatremic px
energy only in hypoprotein px
components of Ringer solution
Ringer solution has 148 Na+, and 156 Cl-,
K+4,
Ca 3
(310mosm/L)
ringers lactate or Haartmann (baxter) solution components
lactate ringer Na+ 130, - hyponatremic Cl 109, 28 bicarbonate, K+ 4, Ca - 3, (272 mildy hypotonic) @ hypernatremic px
Components of dextrose in 5% saline solutoin
= SOLUCION MIXTA = 154, 154, Na+ and Cl-
50g of dextrose (560mosm?L)
slaine 9 + dextrose 5 together
dextrose/glucosated solutions are CI in
CI - diabetic px
use for hypotonic solutions
used to correct electolytic anomalies like
in px with hypernatremia from loss of free water
in diabetic px
or px with chronic dehydration donde prima IC volume loss
examples of isotonic solutions
SSN (normal saline solutoin) al 0.9% and Ringer lactate
hypertonic soltions
those that have higher concentraiton of solutes than other solutoins and higher osmolarity than plasma ( >300mosm/L) and higher sodium concentration
dextrose in distilled water al 5% (DAD 5%)
is a hypotonic solution between 252-261mOsmol/L of glucose
energy only in hypoprotein px
main 2 indications for DAD 5%
rehydration in hypertonic dehydrations and as an agent to give energy
gives significant calories to reduce proteic catabolism and acts as a producer combustible of tissues that most need it likw CNS and myocardium
every L of DAD5% gives what
50g of glucose = 200kCal
dextore in distilled water al 10%,20%, and 50%
these are hypertonic glucsolated soltions that same as 5% glucose once they metabolize they give energy and transform in water
only for food boli
also glucose is considred as an indirect provider of K+ to the cell because it mobilizes sodium from the cell to the EC space and K+ in the opposite direction
most importnat indications of dextorse in distilled water al 10, 20, 50%
tx circulatory collapse
cerebral edemas
pulm edema
because glucose produces cell dehydration and attracts water to vascular space decreasing the pressure of CSF liquid and lung
colloid solutoins
contain particles in suspension of high molecular weight that dont cross capillary membrane
so they are capable of increasing osmotic pressure in plasma and retaining water in IV space
basicllay they increase oncotic pressure and effectivity of movement of fluids from intersitical space to deficient plasmatic compartment aka they are PLASMA EXPANSOR AGENTS
hemodynamic effects of crystaloids vs colloids
colloids produce hemodynamic effects faster and more sustained than crystaloids in less amount
precisandose less volume than crystaloids
cost is much higher
ARS makes you justify use of these synthetic solutions
cx that coloidal solution should have
should have the capacity to maintain osmotic coloidal pressure for some hours
lack of other farmacological actions
lack of antigenic effects, alergenic or pirogenic effects
lack of interference with tipification or compatbilization with blood
stability during prolonged periods of storing y bajo amplias variaciones of temperature
easy sterilization
cx of viscocity that are adequate for infusions
classification of coloids… 2 types
natural coloidal solutoins - only one
artificial coloidal solutoins
natural coloid sollutions
albumin
albumin is produced where
in the liver
albumin
responsible for 70-80% of oncotic pressure of plasma making it an effective colloid
molecular weight of albumin
its molecular weight osscilates between 66.3 and 66.9
distributioin of albumin
between IV compartnemtn (40%) and intersticial 60%
albumin synthesis stimulated by
stimulated by coritol and tyroid hormones
while albumin decreased when there is a decrease ? in oncotic pressure of plasma - edema to peripheral tissue
normal concentration of albumin in serica in suero
3.5-5g/dL
it correlates with nutritional state of subject
<3.5 - hipodenutrido
1gr of albumin increases plasmatic volume by
18ml,
more mobliity of liquid form one space to another
100ml of albumin al 25% increases plasma volume by
una media de mas o menos 465 +/- 47 mL
20gr albumin - 455-500cc in plasma
1L of ringerlactate increases plasma volume by
194cc +/- 18mL
90% of administrated albumin stays where
plasma for 2hr
after this it equilibrates between intra and extravascular spaces for a period of 7-10d (1gr)
75% dissapears from plasma by 2d
catabolism of albumin
in digestive tract, kidney, mononuclear phagocytic system
clinical condutions thtat can be associated with decrased albumin prodcution in blood include
malnutrition cirrosis - hepatopata qx trauma hypothyroidism inflammatory systemic states like sepsis
less albumin produced in all these states because albumin is simualted by cortisol in liver, malnutrat…
possible benefits of albumin
capacity to decrease edemas
improving oncotic vascular pressure avoiding edema in lung and other organs
not justified for NUTRITION - even tho measured for that $2500 por frasco
artifical coloidal solutions
dextranos
HEA (hidroxietil-almidon)
Pentalmidon
dextranos orgin
polysaccarides with bacterial orgin (Leuconostoc mesenteroids)
solucion hemased - helafundi?? commercial names
capacity of dextranos
oncotic protperties are adequate but cant transport oxygen
fast glumerular fast
elimination of dextranos
renal
dextranos on kidney
concentrated infusions of low molecular weight rapidly cross glomerular filter and can increase urine viscocity causing renal insufficiency from tube obstruction
this is reversible if you rehydrate px (IR)
HEA
hetaalmidon is a synthetic almidon prepared from amilopectine using hydroxietil eter groups in glucose residus
Pentaalmidon clearance - advantage
90% is cleared in 24hr and is practically indetectable in 3d
pentaalmidon
volume expander takes longer than albumin - 12hr effect
due to incrased oncotic pressure (40mmhg) - expands more than albumin 5% or hetaalmidon 6%
duration of pentaalmidon
12hr
lactate ringer or Hartmann solution (vs SSN)
isotonic solution with 51mEq/L of Cl less than SSN generating only transitory hypercloremia so less possibility to cause acidosis
its a balanced electrolytic solution - part of sodium of isotonic saline solution is replaced with calium and potassium
use when hartmann or ringer lactate
when we need to administer massive amounts of crystaloid solutions
hypertonic saline solution actions
expands IV volume by extracting liquid from extravascular compartment
inotropic and pulm VD affect as well
use for hypertonic saline solution
in burned px
decreases edema and supplies well hydric demands
hypertonic saline solution mechanism
increase in sodium concentration and osmolarity when infusing hypertonic serum in extracelular space
gel derived solutions history
first used in WWI due to increasing viscosity and low freezing point
how to buffer psyychiatric affects of ketamine
buffer with benzo
methods of metabolism
oxydation,
conjugation reduction, hydrolysis
elimination can be transcutaneous, pulmonary, urine
who shouldnt use diazepam
accumualtes in fetal blood risk for RN - cross BBBand placenta
px with IR, IH, VD px dont use , but if u have to pseudosis to relax
these px have increased GABA rec # so more sensible to EV anesthesics
prolongs action duration
fk midazoloam
decrease volemu similar to others 1-5lt/kg and clearance 4-8ml/kg/min - higher
half life of elinianted 2-4hr therefore much shorter
dissapears faster
metabolism midazolam`
metabolizes in liver - oxidation
metabolites hidroximetil midazolan - excreted thru urine - not farcaologically active
best sedatin
midazolam
dont wake up fucked like with diazepam
smooth relaxation properties
amnesia of diazepam vs midazolam
diacepam more amnesia thqan mid midazolam
use what to revert resp affects of benzos
revert with flumazenil
dosis dependent
causes of high doses of diacepam
\
high dosis can cause severe cerebral depression
suicide method
only ev anesthetics with analgesic affects
opiods and ketamine
not barbs, not benzos, not propofol
best EV anesthesia for biosecurity margin
ketamine
wont cause ventialatory arrest (like propofol and benzos and opiods - wrost, barbs)
1 cause of death from EV anesthesia
resp arrest
only EV and IM of same effectivity
ketamine (maybe initaion action a little longer)
nuvaine opiod SC
only drug that can inhibit or excite at same time
ketamine
reversing ketamine side effects
same opiod reverser = naloxone
we think it involves opiate rec due to reversion of efects of ketamine from naloxone
we think ketamine acts in same opiod rec
(antagonsita puro de opiode to revert_
naloxone
how to decrease salivation effects of ketamine
decreaseed with anticholinergic drugs- atropine, –> broncoaspiration
if px needs itcant use in px with isquemia, myocardial infarct
coronary infartc unstable angina problem you fuck up giving them ketamine - they have excess salivation - dont double fuck up and give atropine - increase HR even MORE
give glicopirulato (exclusive salival rec) - atropine has rec in heart and salivary or give psuedosis of atromine (0.1mg) b/c salivary galnds are very sensitive to atropine so pseudosis is enough
anticholinergics
….
only anesthetic that helps CO, pregcharge and causes peripheral VC
adrenaline
stimulated by ketamine
increases BP and HR (not like others that u can use bradicardia to see depth of anesthesia)
how to measure depth of anesthesia with ketamine
incoordinated movments
no way to know if its pain or part of the effect …. cant really know
drug ideal for VD px
ketamine
when do LAs cause cerebral and cardiac alterations
cerebral changes only if overdosage as well as cardiac alterations — so all is well if you stay in therapuetic dosis
nerve fiber composed of what
2 layers of lipid and one protein layer
determines potency of LA
affinity anesthesia has to lipid - liposolubility
duration action of LA depends on
depends on affinity to plasma protein of nerve
are LAs composed of what
organic compounds
carbons, H ions
myelinic vs amyelinic nerve fibers
(amyelinica < 0.03 micra diamter - with)
transmission of pain impulse is all along nerve fiber
various symptoms - tachy cardia, altered glicemia, endocrine MC< CV MC psycoholgical MC, apendicular process like, discomfort
non localized pain
myelinic > 0.03 miras diamter
form of tranmission of pain alatrorio a traves de ranvier nodules
localized pain
transmission velocity is usally in LAs
(usually 20-25 x diabeterm of fiber it blocks
pH affect on LAs
LAs weak to pH changes
dont act at acid envirtonment - cant transform and dissociate into pharmacological parts, ionized/nonionzed part
(odontological proceudres) - also affects initiation action time
at cardiac arrest we look for resp acidosis from bad ventilation it doesnt matter what adrenaline or atropine you give they wont react….thats why ventilation is so important
FK of LAs
all same
absorpption \depends on irrigation of deposit area
lecho venoso - immediatley
peripheral 15min
raiz nervioso - depends on if has adrenaline or not with it (where there isa vein, arenaline caues VC –> passage to bloodstream is slower, 30-40% superior - longer block) - with adrenaline can put more dose - less possibility of toxicity
without adrenaline - immediate passage - less dose allowed
SC less irrigation
CNS adverse affects of LAs
tinnitus
meningeal irritation
no response al cuander vale?
convulsions tonic clonic (give regular meds)
@ lidocaine toxicity causing bradicardia
can give anticholinergic like atropine
important cx of liquid at subaracnoid space
pressure which it comes out
serosanguinolent - abort mission
lechosa - abort - take sample
max bupicaina to avoid toxicity
20mg
complications of raqui
meningitis encefalitis
hypotension manage with hydration
infecting
cefalea post puncture
complications of epidural
catheter folded on itself
cant take it out
more catherer intoduced can fall out of site desired
max LA at lumbar
20cc
max LA at cervical or thorax
10-15cc
apofisis espinosa anatomy for aguja
thoaax and cervix perpendicular
lumbar - they are reactas
use what to block braquial plexus
lidocaine without adrenaine (5…..400 max dose for toxicity)
or bupicaina1
15cc = 350mg
interecalaneico 10cc = 200mg (still below dose)
EV (20cc 1%)
dilute with saline solution (10cc with water and convert 2%usual presentation to 1%)
types of solutions
colloid, blood, crystaloid or , blood derived (total blood, plasma, complete blood)
suero = …
were used for hemodilution
all crystalloids different
depends what px needs
base for handling hydration - reposicion in a px
what is osmosis
ability to mbilize liquid from one space to antoerh
why edema in px
pump problem
depletion of albumin, hypoproteinemic px
px iwth osmotic factor low
cardiopathic px
pulm px
px with too much water
px with IR
discover and tx cause
balanced solution expensive in markets
vaster solution, crystalloid de baster
and
normosol? nono sol - solution prototype very equibilirated - too expensive
tapon system
no bicarbornate for tapon
types of blood derived solutions
blood derived (total blood, plasma, complete blood)
colloid solutions only used for
severe hypotension
improve perfusion in these px
NOT FOR HYDRATION
preanesthesic evaluation objective
drugs with more security, hemodynamic changes, less heapto/neuro/nephrotoxic = best advanceses
qx used to be awful, death
px never met anesthesiologist before
best px conditions before taking to qx sala not IN it
general - bigger integration between professional, family and px
specific - know history and physiological anatomical aspects of px
all this used to be while px was hospitalized the day before surgery…too late really
px taking aspirin , antiplatelets - SUSPEND px better a week before
avoid getting sued by informed px
last filter to make sure they got all their other evavlautions done (endocrinological, cardiological etc)
alst chance to suspend or cancel qx
preanesthetic evaluation divided into 3 aspects (2 parts)
Inform - give infor to px aboust his case and what the deal with anesthesia (type, why that one); familiarity between px and
dr should know all about px (any questions?)
know the risks, conversate with family (he saild pilas not just 2 or 3 aspects)
Mental preparation - px prepared for qx, px will be anxioius, scarier than actual qx - taboos (decrease tensions) - spread good vibes
previously visisint pzx in room to decerease stress
benzos are important for that (10mg of diazemapm)
after infomring medical part begins…
medical history from childhood
family hx - (women gynelogical history)
toxic habits (marijuana or cocaine can inhibit recapatioan of catecolamines) - can modulate tx type, drugs? (som suspended some not)
pathological hx, transfusions, allergics
history of actual disease and subyacentes
physical exam in preanesthetic evaluation
general inspection palpation auscultatoin percusion
all we care about is pulmonary function - how px is ventilating!! (ronco, sibilantes, crepitantes??)
check oropharynx in case of intubation (save yo ass)
Gabinete studies
hemogram platelets, bleeding times urea creatinina transminases depurinando? CVr risk? HTN, > 60-70yr - do echo, history of angina - stress strength test (qx is one) psycological evalutation/support
know and explain risks
all this to establish anesethetic conduct to someone who has ASA or risk factors
(pre and post anesthetics and trans qx - which drugs to have, what to expect)
ASAs
ASAI - healthy px without other important pathology
ASA II - px that besides prodcedure has other diseases that dont limit physical function (HTN, diabetic - controlled)
ASA III - px depite this problem have another diesase that limits their physical activity (not controlled , unstable BP, not taking meds regularly, angina a year ago - maybe some HF - fatigues after some effort)
ASA IV - px that even at rest presents potentially mortal risk (instable angina) - need ICU
ASA V - moribundo px ( we will do everything possible but idkkkk - no prognosis)
ASA III an dup
alert family
concentimiento
concentimiento legal medical document - px should have signed
specific to anesthsia
if you have to change must explain first - shouldnt have to change
it tells you if you have high risk
premeds
anticolinergic, atropine, ecopalomine, glicopiralate
heparin if risk for pulm emb, nebulziation at asma px
benzo night before or an hour before
gastric juice blocker decrease acidity at fasting (omeptrazol) - H2 blocker antiacid - particulated (leche qu se yo que) or nonparticualted (fervecente)
monitorization of anesthized px to help identfy phenomenon or accumulated events transanesthesic
monitorization should begin since the moment px arrives to OR
consults started
2006-2008
general concepts of resp insufficiency
px in resp insuff when thru arterial gasometry presents PO2, < 80 mmhg (hypoxemia) and PCO2 < 40mmhg (hipocapnea)
mortality of anesthesia
overdose of drugs (when we didnt have BIS, depth of coma, not knowing px)
NOW ITS RESP problems/depresson/px not ventilating. black blood (all drugs we use alters resp. , EV cause apnea, opiods #1 enemy of resp)
worse if px has chronic bronquitis, emphysiema, asma
even after should be handled
relajante, post qx drugs ??? recording
normal oxygen parameters
PO2 - indicates oxygenation of px (partial pressure at blood)
85-95mmHg
@ FIO2 21%
indicator #1 of how px is ventilating
PCO2
35-45 mmHg
if abnormal - affection of gasometry - changes blood pH
normal pH of plasma
7.4
indicates H+ ions in a substance (tells if acid or alkaline) - arterial blood in this case
bicarbonate
…
relation between HCO3 and pH, CO2
any supplement of HCO3 - excesso o deficit de base EB1
hipoxemia can be
leve 75-/80
mod - 60-75
severa < 60
methods to tx resp insuff
canula nasal first to assimilate 3-4L (PCO2 will go up 4mmhg for every L O2 appliled)
so if px came in with 75 O2, and we put 4L we are giving 16 mre = total will be 91 - in normal range no longer hypoxemic
if it kept descending, canula isnt enough so give simple mask - elevates 4mmhg of mercury for every L of O2 applied - can assimilate up to 6 (ppt says 4L) - should give 94 - breathes from mouth and nose
if keeps going down PO2 use mask with resevoir - last element - px can assimilate up to 10 L of O2 (ppt says 8) and PO2 up 4mmhg for every L O2 applied
px that was hyperventilating is now hypoventilation (hypercapnea) hemoglobin curve to the right bemglobin not letting go of O2 to tissues and CO2 isnt being eleiminated its being retain by cells now we have fracaso resp
fracaso resp
px isnt ventilating properllay
geting resp acidosis and hypoxemia severa
RBC nots diong function (retaining CO2 , not giving O2 to tissues)
no longer clinical, px cant change cuadro himself
have to connect px to artifical respiratory until cuadro is fixed
time we dont know how long
PO2 < 60mmhg severe hypoxemia and PCOr > 45mmhg
after 7 days do tracheotomy for profilaxis (undo intubaiton)
evelvate ventilation to take out Co2
100% oxygen
modify based on gasometries
FI O2 (fraction of O2 inspired from environment)
inspirator pressure of O2 of environment in atmosphere of 760mmhg over mar (21%)
PO2 200-300 @ full 100% oxgenation - can cause fibrosis pulmonar?? - we want to keep in normal range - modify FIo2 to get back to normal ranges
most abundant element of environment
nitrogen 78%
others: ice, sulfur, - 1-2%
gasometric changes
- 5 pH - alkalosis
- 3 - acidosis
ventilatory or metabolic - PCO2 tells you
if px has 40 PCO2 - not ventilatory problem - could be metabolic indirectly proprtional ( up when pH descends and vice versa)
PCO2changes 10mmHg for every 0.1 change in Ph
bicarbonate is directly proprtional to CO2 changes (HCO3 up 2 for every q0 PCO2 up) - in ACUTE form not CHRONIC px (asthma, epoc, sedentary, intubated px) bicarbonate changes 4 for every 10 PCO2)
normal HCO3
22-26 (24 average)
deficit de base
\+ or - 2 # of HCO3 lacking in px to evaluate values that px needs ....you wanted 26 and have 20 actually - deficit of 6
thats HCO3 your giving to compensate
resp acid - if nobase deficit - is pure
????
7.5 pH - alkalosis
PCO2 should be 30
HCO3 acute - should have gone dwn two so 22
basse deficit = 0
if px had HCO3 - 18
alk respwith base deficit of 4
if px had HCO3 - 30
px with alk resp with base excess of 8
…..
ph 7.3 PCO3 40 not a ventilatory problem hepatopata, pancreatic, renal px, too much saline solution bicarbonate should be low in this px
thyroiditis
not that common
hyperthyroid –> ey –> hypo –> total recuperation
heterogenous group of thyroid MC with in commun = inflammation even with diff etiology, MC, dx, tx
most are benign
some autolimited and others cause thyroid insuff that can be transitory or definitive
classification of thyroiditis
etiology
pain?
evolution
etiology thyroditis
autoimmune (linfocititca subaguda - sporadic or postpartum or…. linfocitica cronica = hashimoto, granulomatous)
infectious (viral bacterial
destructive (by radiation or trauma)
drug induced (amiodarone, cytokines)
pain classification thyroii=tsis
pain - granulomatous subaguda
suparative or acute
radiation
trauma
the nonpainful
hashimoto, subacutere, drug induced, Riedel
classification by evolution
acute
subacute
chronic (autimmune , hashimoto)
thyroid phases of evolution
normal function –> follicles rupture (liberates preformed hormones increasing peripherla presence of thyroid hormones) –> hyperthyroid (usually insidious MC, subclinical)–> eythyroid –> hypothyroidism –> normal function
acute thyroiditis
aka supurative, bacterial, pyogena
cause of acute thyroiditis
hurt
due to inflammatory process from microbian agent
associated agents in adults - strep pyogenes and staph auresu
kids - strep alfa and beta hemolitico and anaerobes
circulation form distant infectious foci (GI, skin, resp traact), embryonic infeccted restos (cyst of tiroglose conduct, fistula of seno piriforme)
extension of neighboring infections like abscess mastoiditis otitis etc
unsual siutations from bad technique and accidental inoculation , bad fine needle aspiration or centra catheter, truama, esophageal rupture
main cause in kids seno piriform left infection infected from resp infection
68% bacteria 15% fungal mycobact %9 parasite 5% sifilitic 2%
MC of acute thyroiditis
after an high resp infection cuadro
can have presexisiting disease, fisutla seno piriforme, persistent ting, PAAF biopsy
100% neck pain, dysphagia 91%, disfonia 80%, pain at palaption, fever 92%, erithema of skin 80%, concomitant faringits
thyroid protective factors
capsule and muscles
blood and drainage
iodine
(but adjacent structures, from linfatic or hematogenous spread, or penetrating truama can still cause its infection)
labs at acute thyroiditis
leucocytosis > 20-25000
high ERS
tyroid hormones usually normal (depends on phsase)
normal captation at gammagrpahy (if full inflammaed it will be low )
USG can see abcess or edema in area - encapsulation suggesting infection
+ hemoculture (90% + of dx) with MC (aggressive so give these px ATBs right away before waiting on culture)
complications of actue thyroiditis
sepsis thromboembolism septic abcess rupture obstruction of airway larynx edema traqual estenosis tirotoxicosis
tx acute thyroiditis
EV antibiotics, hospitalize and drain lesion
(CS1gen, and aminoglycoside
pen anti st with aminoglycoside
amoxi with clavulinic acid or ampi and sulbactam
quinolones or C3g
drain lesion
subacute de quervain thyroiditis
autolimited viral infalmation
with genetic prediposition HLA-35, B27 in summer and fall
more in women between 30-50yrs
eneterovirus incidence coorelates
non specific signs of quervain
myalgia
atralgia
fatique low grade fever
specific sign of quervain
thyroid pain
exquisto ini palapation
irradiates to mandible and ear
phases of thyoridis quervain
pain predominates , manifestation s of tirotoxicosis 50%
pain irradiates retro acular
3-6wk
MC of infallmamtion and hyperthyroidism remit for 6-12months
px can be euthyroid
finally can or not have hypothyroidism
5-15% permanent
querviain lab
ERS high 50-100mm/h elevated tiroglobulin high PCR high thyroid hormones low iodine captation anti TPO and anti TG normal
USG - hipoecogenic areas without mass formation and without vascular flow (CUZ OF INFLAMMATION IOU CANT SEE CIRCULATION)
dx quervain
thyroid pain
high ERS and TG
USG and gamma
PAAF in quervain
not alaways
can have varies depends on stage of process
beginning inflammation and disorganzied folicular arquitecture
infiltration of PMN and lymphcytes and macrophages
most cx accumualtion f giant cells and with granoulomous image
coloid ceenter of granulomas
coloidophageia
formation of microabcesses
follicular disrption
tx quervain
AINES
glucocorticoids start with 30mg of prednisone and go decreasing by .2
betablockers (propanolol)
levotyroxine
other subacteute thyroidistis
sporadic silent thyroiditis (autimmune with infiltraiotn more in iodine deficient women, with small painless bocoi in 50% inflmamatory so transitory
5-20% have h=thyoroid rofile altered
anti TPO + 50% low cpatation
evolution occurs in less than a year
10% of recurrence
pos partum
same as sporadic = autommune
can be 1yr postpartum
5-10% of px 30-50yr
HLA DR3/DR4/DR5
clinca: similar to sporadic and postpartum
doest hurt
25-30% can have permanent hypothyroidism
give propanolol to tx symptoms, most thyrodisits are tranistory
phases of hyperthyroidism (TSH supprsed and high T3, T4) tiroglobulin can be up, positive antibodies, captation low)
meds thyroiditism
cytotocixc effect on follicles
litio lesioins cells
cytokines - interferon a tx and IL2
amiodarone causes lesion type I (increases synthessi) or II (rupture)
tx thyroitidis
betablockers of MC of tirotoxicosis and tx hipotyroidism/TSH > 20mU/L (in pure thyroiditis, but if subclinical > 10 treat as well, could be hashimoto or thyroid has been taken out - other wise wait till 20 because transitory)
DONT tx sublicinical hypothyrodisim except (preg ladies and px with other coomorbilities that will also improve - recent infraction, cardiac insuff III,IV - oldies)
amiodarone - only suspend in type I
manage with glucocorticoides 0.5-1.25 mg/kg 3-6wk
meds thyroiditism
cytotocixc effect on follicles
litio lesioins cells
cytokines - interferon a tx and IL2
amiodarone causes lesion type I (increases synthessi) or II (rupture)
tx thyroitidis
betablockers of MC of tirotoxicosis and tx hipotyroidism/TSH > 20mU/L (in pure thyroiditis, but if subclinical > 10 treat as well, could be hashimoto or thyroid has been taken out - other wise wait till 20 because transitory)
DONT tx sublicinical hypothyrodisim except (preg ladies and px with other coomorbilities that will also improve - recent infraction, cardiac insuff III,IV - oldies)
amiodarone (used to tx arrytmia) - only suspend in type I
manage with glucocorticoides 0.5-1.25 mg/kg 3-6wk
at type II dont necessarily suspend but manage with above
hashimoto thyroditis presentation
ddifuse bocio , symmetrical, firm, atrophic in 10%
hashimoto function
normal or elevated
RF of hypothyrodism
no genetic direct associttion (we think tho)
hashimoto asoociated
other autoimmune pathologies (Grave, AAddison, premature ovarian failure)
hashimoto linfoma
fast growing nodules in px with hashimoto
infiltration, encapsulate and form linfoma
riedal thyroiditis
painless hard lenoso o petreo, unilateral slow growing bocio
lots of compressive MC disphagia, disfonia, disnea, estridor
ERS normal or high, AC poitive, or normal thyroid function
can invade other neighboring strcutures
dx reidal
low captation
ERS and thyroid profile normal or altered
PAAF necessary - fibroinflmmation (disscart tumor)
riedel tx
elminante cpmreession with resection
steroids for inflmmation
replace with levothyroxinve
TABLE flow chart
types of thyroid CA
papilar - 80-85% folicular ca - 10% (hurthe) medular ca - 5% anaplasic ca - 3% miscelaneous 1% ( linfoma, fibrosarcoma, hemangioendotelioma maligo, teratoma)
riedel tx
elminante cpmreession with resection
steroids for inflmmation
replace with levothyroxinve
TABLE flow chart
types of thyroid CA
papilar - 80-85%
folicular ca - 10% (hurthe) - good but most metsastaiss
medular ca - 5%
anaplasic ca - 3%
miscelaneous 1% ( linfoma, fibrosarcoma, hemangioendotelioma maligo, teratoma)
can be follicular or parafolicular (type C which make calcitonin - medular from this one :() cells and tis is how they are differentiated
epi of thyroid ca
PCT in women betwen 30-50yrs
folicular CA more common in women between 40-60yrs
differentiated carcinomas have 100% survical at 5yrs if detected on time
papilar CPT
firm cold on gammagraphy solid in US nodule
7% microcalcinomas
in BMN dominating nodules is usually carcinoma
in kids usually in 20-50% linfatic
usually intraglandular extension
slwo growth can delay dx
follicular CFT
small follicles and poor presence of coloid formation
diff from adenomas of follicles because present invation of vessels and capsular
metastasize to LNs anf through hematogenous reaching lung and bone more than CPT
secrete Tg
tx ca
TABLES
after total thryoid ablation tx with L,4 (2.5 mcg/kg/d)
at 3 motnshs during tx with L4 mesure TSH and Tg (glucoprotein with receidos de tirosina if + something in there is producing)
at 6-12hr conretirada of L4 measure TSH and Tg and do a RCT with 2-5mCi of I 131
RCT negative measure Tg ……………
riedel tx
elminante cpmreession with resection
steroids for inflmmation
replace with levothyroxinve
TABLE flow chart
types of thyroid CA
papilar - 80-85%
folicular ca - 10% (hurthe) - good but most metsastaiss
medular ca - 5%
anaplasic ca - 3%
miscelaneous 1% ( linfoma, fibrosarcoma, hemangioendotelioma maligo, teratoma)
can be follicular or parafolicular (type C which make calcitonin - medular from this one :() cells and tis is how they are differentiated
epi of thyroid ca
PCT in women betwen 30-50yrs
folicular CA more common in women between 40-60yrs
differentiated carcinomas have 100% survical at 5yrs if detected on time
papilar CPT
firm cold on gammagraphy solid in US nodule
7% microcalcinomas
in BMN dominating nodules is usually carcinoma
in kids usually in 20-50% linfatic
usually intraglandular extension
slwo growth can delay dx
follicular CFT
small follicles and poor presence of coloid formation
diff from adenomas of follicles because present invation of vessels and capsular
metastasize to LNs anf through hematogenous reaching lung and bone more than CPT
secrete Tg
differentiated thyoi ca
papilar and follicular
agressive cariants
columnar cells
diffuse sclerosante
insular
bethesda
I - …….repeat FNA - no dx , unsatisfactory
II - benign 0-3% risk of malignancy - follow clinic
III - atypucal of uncertain significanse, follicular lesion incertain - 5-15% - repeat FNA
IV - follicular neoplasia 15-30% - lobcomy/tiroidectomy
V - suspect malignity 6-75% - almost total thyroidectomy or lobectomy
VI - malignant 97-99% - total thyroidectomy
TABLe
medular CA
from parafolicular cells
sporadic 75-80%
hereditary 25-20%
3-4% of all thyroid neoplasias
secrete CT and CEA
seen in MENs
sporadic medular
66-75% RET gene somatic more unicentric alone nodule LN metastasis 80% also to liver, skeleton, lung with calcitonin > 5000pg/mL
hereditary medualr
RET
part of MEN2
lesion in hyperplasia of cel C, diffuse or nodular
multifocal
any age
metastasis to local ganglio, higdao pulnon, hueso
MEN 2a
80% MTC hereditary multicentric
feocromocitoma 50% bilateral or unilateral
hyperparathyroidism primary…..pic
Men 2b
[pic
dx CMT
history PE
anatopathological exploration
immunohistoquimica
tumor markters
tx CMT
1st group - localized sisease, < 500 calctonin can cure
2nd group - neck metastasis - possible to cure
3rd - mestastssis to distance - deadman
1st grou p tx
tiroidectom total
dissection of LNs
25% cure
2nd gorup tx
total tiredoicotmy and GL dissection
3rd group
same as second ,
resecar identified disease
