ITE TL Block 3 Flashcards
Hydrophilic v hydrophobic opioids used in CSF
hydrophilic = easier absorption -> shorter duration faster onset ex: fent, sufent
hydrophobic = harder absorption -> longer duration, slower onset, and greater migration in CSF
ex: morphine, Dilaudid, meperidine
octanol/H2O partition coefficient
lipid solubility of opioids
-higher = more lipid solubility
first line therapy for pulm atresia w/ intact ventricular septum
Prostaglandin E1 -> keep the PDA open
Medication for PDA closure
Indomethacin
Most significant source of heat loss from body
Radiation
-heat from body travels to vasodilated surface capillaries
a pt status post tonic-clonic sz has a dec RR and is hypoxemic why
central resp depression so dec RR -> build up of CO2 -> inc partial P of CO2 -> inc arterial CO2 tension in alveoli -> cant effectively exchange gas in alveoli -> dec O2
Alveolar gas equation
PAO2 = FiO2 x (Patm - PH2O) - (PaCO2/R)
R: respiratory quotient
Status epilepticus
> 5 minutes of continuous sz activity or >2 consecutive sz w/o intervening recovery of consciousness
When using the term nitrogen handling in setting of liver damage what does that mean
metabolism of nitrogenous wastes, mainly ammonia
-if active GI bleed and breakdown and absorption of amino acids from Hg -> inc ammonia -> can overwhelm a cirrhotic liver to eliminate N compounds -> worsening hepatic encephalopathy
Tx for hepatic encephalopathy
Lactulose: laxative that prevents absorption of ammonia
Rifaximin: abx w/ bactericidal activity against ammonia-generating organisms in gut
25 YOM larygnospasm then in PACU 85-90% on room air w/ well controlled pain and normal RR why?
negative pressure pulm edema
-b/l fluffy infiltrates on xray
-tx: supportive w/ suppl O2, diuresis and PPV if severe
What causes overdamping in an art line
Factors that inc compliance or resistsance in circuit
-adding stopcocks, air bubbles or pliable tubing
-causing systolic BP to be lower than it actually is
Underdamping
-tubing should have a very high natural frequency -> if too low, resonance of the system will add to the pressure form -> underdamping
Controlled hypootension
MAP of 50-65 or 20-30% below baseline
-used for certain surgeries incl cranial aneurysm repair but risks must b econsidered
-done w/ CCB, direct vasodilators, BB and anesthesia
Renal test most reliable indicator of acute renal failure
Cr conc inc >100% from baseline
What causes artifical inc in BUN
reduced effective circulating blood volume
catabolic state: GI bleeding, steroid use
high protein diet
tetracycline use
Decrease in BUN
liver dx
malnutrition
sickle cell anemia
SIADH
If you give 2L NS what labs change immediately after
hyperchloremic metabolic acidosis
-bicarb dec
-Na inc
-K inc
dilutional dec in Hct and albumin
labs in hyperosmolar hyperglycemia
high glucose
low K
no acidosis
-osmotic diuresis due to elevated glucose
TURP blurred vision and minimally reactive pupils, whichh irrigation solution
glycine
(amino acid and Neurotransmitter)
-large amounts metabolized to ammonia
TURP with hyperglycemia, whichh irrigation solution
Mannitol
Lytes intracellular v extracellular
Majority of K is intracellular (157), so is Mg (20) comparatively
The other ions Cl, bicarb, Ca, Na higher extracellularly
Hyperk EKG changes
peaked T waves, prolonged PR interval and widened QRS
Rhabdo complications
DIC -> inc PTT, dec fibrinogen, dec plts
AKI (ATN from myoglobin)
Arrhythmias: hyperK
Normal AG met acidosis causes
normal: ~13
diarrhea, renal tubular acidosis, biliary drainage, large infusions of NS
CI to extracorporeal shock wave lithotripsy
Pregnancy (risk of harm to fetus)
Untreated bleeding d/o
active UTI
extracorporeal shock wave lithotripsy and AICD
not a CI, but should be shut off before with alternate defibrillator ready
Complications of enteric feeds
compl due to placement (aspiration)
long-term indwelling (sinusitis, otitis media)
hyperosmolar feeds cause diarrhea
obstruction from thick feeds
constipation
high gastric residual feeds
Lytes refeeding syndrome
HypoP
HypoMg
hypoK
hypoCa
-also skeletal m weakness: resp weakness, dysphagia, leg cramps, and constipation
What causes diarrhea w/ enteral feeds
hyperosmolar feeds
hypoalbuminemia
rapid administration
bacterial contamination of feeds
MC complication of enteral feeds
- high residual volumes
- constipation
- diarrhea
Three stages of liver transplant
preanhepatic
anhepatic
neohepatic
What happens post reperfusion in liver transplant
-large release of K and H+ into circuation w/ inc preload and inflammatory mediators-> cardiac arrhythmias, hypoTN, pulm HTN, and R heart strain
(can be postreperfusion syndrome)
-hypothermic
-coagulopathic (washout of tPA from organ)
tx of postreperfusion syndrome
pressor support
Na bicarb to neutralize the acid
Ca Cl to stabilize cardiac myocytes
What factors need Vit K to be active?
SNOT
Seven
Nine
10
Two
Enzyme targeted by warfarin
Vitamin K epoxide reductase
-so Vit K dpt factors can’t be activated b/c active Vit K not being made so can’t act as cofactor
how is coag factor III produced
tissue factor/thromboplastin
-secreted by damaged vascular endothlium or plts
NOT liver
Citrate and lytes
HypoCa and hypoMg -> chelates both
which blood products have more citrate
FFP and plts
What inc rate of citric toxicity
hypothermia
liver dx/transplant
peds pts
hyperventilation (alk)
massive blood transfusion
When does Ca decrease from blood tranfusion?
6 units per hour (35 cc/min)
When does hyperK occur from blood transfusion?
120 cc/min or more
Citrate intoxication signs
hypoTN
narrow pulse pressure
inc VEDP
inc CVP
When does INR normalize post liver transplant if you’re a donor
post op days 5-7
INR trend post liver transplant for donor
w/ partial removal of liver -> loss of syn fxn, so inc peaking post op days 2-3 usually no higher than 2
-returns to normal post op 5-7
Liver metabolism of drugs depends on 3 facotrs:
- intrinisic liver fxn
- hepatic blood flow
- drug extraction ratio
Phase I biotransformation of drugs in liver
hydrolysis, oxidation or reduction
-goal to make more hydrophilic (so easier to eliminate)
-carried out by cytochrome p450
Phase II reactions in drug biotransformation
conjugation reactions, addition of a polar functional group
-continuing to make more hydrophilic
Extraction ratio for drugs and hepatic BF
ER: portion of drug removed from liver as it passes through
(100% -> all of drug that passes through liver in blood is removed)
-based on protein binding and efficiency of drug metabolism
-high ER more dpt on hepatic blood flow, low ER less dpt on hepatic blood flow
relationship b/w succ and obesity
need larger doses b/c
obese pts have inc in pseudocholinesterase activity and inc extracellular fluid volume
how to dose maintenance infusion dose of propofol
actual total body weight
how to dose succ
actual total body weight
how to dose thiopental
lean body weight
how to dose induction dose of propofol
lean body weight
how to dose fentanyl
lean body weight
how to dose rocuronium
ideal body weight
how to dose vecuronium
ideal body weight
volatile anestetics and hepatic BF
<1 Mac: all preserved
> 1 Mac: iso decreases HBF in dose dept
What IV anesthetic inc hepatic blood flow
Propofol
IV anesthetics and hepatic BF
neutral/small decrease: benzos, barbs, dex, etomidate
no change: ketamine
inc: prop
first-pass metabolism
before onset of drug
-breakdown or modification of drug or prodrug in GI tract or liver before systemic circulation
(why oral drugs have higher dosing than IV drugs)
Drug therapeutic index
ratio of the toxic dose (TD50) to effective dose (ED50)
-higher, safer drug
Adenosine and liver
Adenosine is a potent vasodilator
-it is a byproduct of the liver that is produced in the space of Mall (surrounds hepatic vasculature)
-washed out by portal v from space of Mall -> when flow dec, it builds up -> hepatic a dilation
Most sensitive lab test for acute changes in liver
PT
(synthetic fxn)
Measure excretory fxn of liver
alk phosphatase
gamma-glutamyl transferase (GGT)
bilirubin
measure of hepatocellular injury
AST, ALT
-ALT more liver specific, AST also found in heart, muscles, brain, and kidney
What is 2,3-BPG
2,3-diphosphoglycerate
-binds to Hg changing its conformation to allow O2 to leave, shifts O2 disassociation curve to the R
-higher in anemia and hypoxia
Body compensation for anemia
-inc cardiac output
-arteriolar vasodilation (inc nitric oxide from tissue hypoxia and acidosis)
-dec blood viscosity -> less shearing in microvasculature -> dec vascular resistance -> dec afterload
-inc 2,3 DPG and acidosis -> R shift of O2 curve
Where are the cell bodies of motor neurons located
ventral horn of the spinal cord
what’s at the dorsal horn of the spinal cord
first-order somatosensory afferent n terminate
dorsal root ganglion
cell bodies of somatosensory neurons
lateral horn
T1-L2
b/w dorsal and ventral horns
-cell bodies of the sympathetic NS
How n depolarize
ACh released from presynaptic n -> binds to nicotinic ACh receptor on postsynaptic membrane -> conformational change allow Na and Ca into cell -> miniature end-plate potential -> if several occur at once -> m depolarized -> action potential and m contraction
if you put iso in a sevo vaporizer
iso has a higher saturated vapor pressure -> in a sevo vaporizer a higher concentration will come out than intended
What color protective eyewear for neodymium:yttrium aluminum garnet laser
Nd:YAG
-green filter
what color filter for carbon dioxide laser
clear
what color filter for argon laser
orange
what color filter for potassium-titanyl-phosphate-Nd: YAG
orange-red
where is the sympathetic trunk
L1-L5 posterior to IVC on R and lateral and slightly posterior to aorta on L
What levels are the celiac plexus block
T5-12
-innervates all the abd organs
SE of lumbar plexus sympathetic blocks
-prob w/ ejaculation in men (esp if b/l)
back pain
accidental blockade of genitofemoral n or lumbar plexus in psoas m -> numbness in groin, thigh or quads -> neuralgia and burning pain
earliest sign that a lumbar symp plexus block is successful
vasodilation and temp changes
CMR and CBF of volatile anesthetics at MAC > 1.1
dec CMR with inc CBF “uncoupling”
b/c vasodilation from volatile anesthetic wins
nitrous oxide on CMR and CBF
both inc
ways to measure EtCO2
capnography, capnometry or mass spectroscopy
-and must have a low end-tidal CO2 alarm
ASA required monitors
EtCO2 w/ disconnection alarm
O2 analyzer w/ low O2 conc limit alarm
continuous EKG
continuous pulse ox w/ variable pitch pulse tone and low threshold alarm
BP monitored every 5 minutes
Temp if expecting changes
Recommended skin prep for central line placement
> 0.5% chlorhexidine w/ alcohol is BETTER than iodine or 70% alcohol
Brugada syndrome
inherited mutation in Na channels MC in southeast asian men
-high risk of ventricular arrythmias and sudden death
-ICD mainstay of therapy
EKG for brugada syndrome
pseudo RBBB (wide QRS, terminal R wave in V1, wide or exaggered S wave in V5-6) and ST elevations in V1-V3 with negative T wave
Anesthesia considerations for Brugada syndrom
-propofol infusions and bupivacaine are assoc w/ lethal arrythmias
-ICD
-high risk for lethal arrythmias
-avoid class I antiarryhtmic meds and beta blockers -> trigger or worsen arryhtmias
Delta wave and short PR interval on EKG indicates what?
Wolf-Parkinson White
-this short PR interval w/ delta wave -> widened QRS completed
Pt w/ known WPW and SVT tx
procainamide, ibulitide or cardioversion
NO Beta blockers
What causes a LBBB
aortic stenosis
dilated cardiomyopathy
LV MI
lyme carditis
aortic regurge
Pacing at RV
dx?
LBBB
dx?
RBBB
Def of long QT
> 480 ms
What happens to body when drowning in freezing water
hypothermia -> diving reflex: slowing of HR and constriction of peripheral arteries to shunt blood to heart and brain -> dec metabolic demand of tissues -> delaying hypoxia and acidosis
-breath holding and air hunger -> hypoxemia 2/2 laryngospasm and aspiration of water -> LOC and irreversible brain injury
-cardiac dysrhythmias -> sinus tach to brady to PEA to asystole
-asp fluid washes out surfactant -> pulm dysfxn
axillary n block view
A: median n
B: ulnar n
C: radial n
D: musculocutaenous n
when to use axillary block
fingers, hand, wrist and forearm surgery
-musculocutaneous not blocked
-if tourniquet is required, need to block intercostobrachial n
position for axillary n block
supine, abducted 90 degrees, externally rotated and elbow flexed at 90 degrees
when musculocutaenous n spared by axillary n, where to block it seperately?
b/c biceps brachii and coracobrachialis
Atrial natriuretic peptide
released by cardiac myocytes w/ inc atrial stretching (inc extracellular volume or volume overload)
-dec BP b/c vasodilator (inc cGMP)
-diuretic and natriuretic effects: suppresses effects of aldo, ADH and renin
Lung volume changes in pregnancy
dec FRC
dec ERV
dec RV
inc IRV
only slight dec in TLC
How does MV inc in pregnancy
progesterone inc TV w/ minimal inc in RR
-inc arterial O2 tension and dec CO2 arterial tension
P50 O2 curve
oxygen tension at which Hg is 50% saturated
normally: 26.7 mmHg
Causes of R shift of O2 curve
Dec pH
inc H+
inc 2,3 DPG (phosphate, so if low phosphate would go to the L)
inc temp
–> dec affinity of Hg for O2
How long is fetal Hg peristant?
2-4 months of age
-completely gone by 6 months
Cardiac changes w/ insufflation
inc in systemic and pulm vascular resistance
-pneumoperitoneum -> inc intraabd pressure -> compressed vessels in splanchnic vasculature -> inc in venous return -> inc preload and cacrdiac output
-hypoTN w/ insufflation + PPV
-vagal activation w/ pneumoperitoneum -> arrhythmias
how to minimize renal damage w/ abd insufflation
lower intraabd pressures and intravascular volume load
Type I hepatorenal syndrome
acute and rapid renal failure (Cr x2) assoc w/ precipitating cause (SBP, surgery, sepsis)
-responds to medical therapy and stabilizes after medical therapy is d/c
-w/o tx survival is 2-4 weeks
Type II hepatorenal syndrome
insidious onset of renal failure b/c of portal hypertension
-dec intravasc volumte from splanchnic dilation and ascites -> renal vasoconstriction -> activation of RAAS, sym act, and vasopressin
-survival is ~6 months
Terlipressin
vasopressin analogue
Tx for type II Hepatorenal Syndrome
Vasoconstrictors: midodrine, octreotide, NE, vasopressin analogues
Volume expanders: albumin
-definitive tx: liver transplant
-depending on how far gone, liver transplant will improve kidneys
Hemolytic Uremic Syndrome
thrombocytopenia, acute renal impairment, and microangiopathic hemolytic anemia
-plt microthrombi in small bllod vessels, nonimmune hemolytic anemia, thrombocytopenia, and clots get caught in kidneys
-usually post GI (E Coli) or resp (S pneumo)
What lab is the strongest predictor of periop outcomes in pts receiving TPN
serum albumin
Prolonged TPA causes what lab changes?
trace metal depletioni: Zinc, copper, Mg
When d/c TPA what is likely to happen to labs?
Hypoglycemia (b/c inc insulin production 2/2 TPA)
Elemental diets v polymeric feeds
elemental diets are more expensive and may inc hospital length of stay and mortality
Enteric feeds w/ glucose and carbs dose this to body:
-red of gluconeogenesis and lypolysis
-stim insulin -> protein synthesis and dec lipolysis
-hyperglycemia
Why are lipid emulsions important in TPN
lipid oxidation is the predominant energy-prod pathway in stress (sepsis, burns, and surgery)
-adequate nutrition is key to healing
Complications of TPN
HypoMg
after d/c -> high insulin -> hypoglycemia, hypoK, hypoP
cholestasis due to a lack of enteric
**use enteric feeds whenever possible
When you decrease the glucose-to-lipid ratio
-dec risk of steatosis b/c dec carbs
-dec risk of hypoglycemia
Etomidate and liver
Decreases hepatic blood flow due to dec in hepatic arterial vascular resistance
Best IV anesthestic for concern w/ hepatic encephalopathy
Propofol: doesn’t dec hepatic blood flow, may increase due to splanchnic vasodilation
-midaz can accumulate, same w/ dex
Labs typical for DIC
inc D-dimer
dec factor VIII
dec fibrinogen
low plts
Best test for DIC in end stage liver dx
factor VIII (b/c d dimer elevated in ESLD anyway so hard to tell apart)
clotting factors not produced by liver
factor III, IV and VIII
What inc hepatic blood flow
Inc venous return (inspiration)
inc arterial bloood flow (inc CO)
inc portal blood flow by spanchnic vasodilation (after eating)
What dec hepatic BF
dec venous return (PPV) and R heart failure
dec art BF (HF)
redistribution of splanchnic BF (exercise and catecholamine release)
dec BF (shock)
Why hypoxia inc w/ laparoscopy
pneumoperitoneum causes shift of diaphragm (restricts lung expansion) cephalad -> dec lung expansion -> vent/perf mismatch -> intrapulm shunting
In crisk of normal pt getting postop hepatic dysfxn
abd procedures (dec BF to liver), preop asymp elevation of liver enzymes
pre-exiting liver dx
Autonomic dysreflexia
-Injury above T5-7 (takes wks to months)
-when stimulation below level of SC -> massive symp resp -> massive HTN, severe vasoconstriction below leevel of injury
-carotid sinus senses HTN -> severe bradycardia, heart block
-parasymp resp above injury: bradycardia, HA, flushing above injury
Tx for autonomic dysreflexia
deepen anesthetic
stop stimuli
vasodilators: NG, CCB, hydralazine
Carotid body v carotid sinus
body: senses composition of arterial BF: pH, CO2, temp, PaO2
sinus: baroreceptor by CN IX (glossopharyngeal) detect, respond and regulate BP
body-senses
sinus-BP
When does sympathetic NS use ACh at NT?
at postgang sweat glands
sym v parasymp stimulation at pulm vessels
sym: pulm constriction
parasym: pulm dilation
parasym and symp at bladder: detrusor v trigone
trigone: area near urethra
detrusor: bladder muscle
parasym: trigone relax, detrusor contract
sym: trigone constrict, detrusor relax
ciliary m in eyes symp v parasymp
sympathetic: relaxation for far vision
parasymp: contraction for near vision
What levels artery of adamkiewicz
T9-12
What tracts supplied by anterior spinal a
spinothalamic (pain and temp)
corticospinal (motor)
intermediolateral (autonomic)
Inc risk of postop vision loss
Surgery: prolonged hypoTN, long duration of surgery, large blood loss, large volume of crystalloid, anemia/hemodilution, inc IOP from prone position
Pt: HTN, DM, atherosclerosis, obesity, male, tobacco
Two types of postop vision loss
central retinal artery occlusion: unilateral vision loss, direct pressure on globe during surgery
ischemic optic neuropathy: prolonged duration of surgery, obesity, blood loss, hypoTN, male
Duchenne Muscular Dystrophy: MOA, and cardiac implications
defect in dystrophin: pseudohypertrophy of m, m cells broken down and replaced by fat
-occurs in myocardium too -> dilated cardiomyopathy, regional wall abnormalities, vent arrhythmias
-X-linked recessive
EKG Duchenne’s Muscular Dystrophy
sinus tach
inverted T waves
Q waves in precordial leads
tall R waves in R precordial leads
highest risk of prob w/ ped sedation
Under 6 months of age
remote location (MRI)
developmental delays
invasive procedure: DL, endoscopy
RF for optin n damange w/ retrobulbar blocks
myopic eye (axial length longer than 25 mm) -> longer eye lentgth -> RF for optic n damage or globe penetration
Dedfinition of inc IOP
> 25 mmHg
cataracts
opacification nof lens of eye
retinal detachment and visual loss
no capillaries supply retina -> choroid layer provides O2 and nourishment -> retina detachment from choroid layer -> blindness
Inc risk of relapse after training in substance use d/o
hx of major opioid use
IV admin of drugs
family hx of substsance abuse
psychiatric d/o dx
periop fluids peds
20-30 cc/kg of isotonic fluid over 2-4 hrs (reduce ADH)
-if <6 mo, neonates, malnourished, cardiac surgery: give glucose-containing fluids
Morphine hydrophobic or philic
Hydrophilic
-avoids first-pass uptake and retention by lungs, stays longer in SC
opioids and lung uptake/retention
hydrophobic/lipophilic opioids taken up by lungs on first-pass -> will only be released when plasma conc decreases
-fent, sufent, and meperidine have a high first-pass uptake/retention
-morphine is hydrophilic so it does not
Tx for digoxin OD
Digoxin-specific antibody fragments
N/V/D, abd pain, anorexia, bradycardia, hx of afib, weakness dx?
digoxin toxicity
-vision changes (yellow or green) MC
-hyperK
-hyperCa -> proarrythmic -> premature contractions
N/V/D, abd pain, anorexia, bradycardia, hx of afib, weakness dx?
digoxin toxicity
-vision changes (yellow or green) MC
-hyperK
-hyperCa -> proarrythmic -> premature contractions
when can you give activated charcoal
1-2 hours of suspected OD
Antidote for Beta blocker OD
Glucagon
CBF and PaCO2
w/i 25-75
1-2 cc/100g/min for each 1 mmHg
-if above or below, resp is diminished
-if hypoTN, responsiveness is reduced
region from soft palate to epiglottis
oropharynx
region from base of skull to cricoid
pharynx
region b/w epiglottis and cricoid cartilage
larygnopharynx or hypopharynx
skull base and soft palate region
nasopharynx
posterior to nasal cavity
Why hypoxia when you place mobidly obese pts supine
Dec FRC -> closing capacity above FBC -> small airways closing, V/Q mismatch, R to L shunting
Miosis and Mydriasis symp v parasymp
Miosis: parasymp activation
Mydriasis: symp activation
Why inc in MAP and SVR w/ abd insufflation
CO2 absorption -> symp response
-dec in renal BF -> activation of renin, angiotensin, aldosterone system
-AT II causes a direct vasoconstriction effect
-vasopressin causes a vasoconstriction effect and causes an inc reabsorption of water
vasopressin level inc is the primary inc in SVR and MAP, dec venous return is NOT directly responsible
Metabolic resp to surgical stress
immunosuppresion
-release of epi, NE, cortisol
-breakdown of glycogen stores
-insulin resistance in tissues -> hyperglycemia
-m catbolism and proteolysis (cortisol)
-lipolysis
which are cutting and not cutting needles spinals
cutting: Quincke
not cutting: Whitacre, Sprotte
Parkland formula for resuscitation after burns
Replacement = TBSA burned (%) x weight (kg) x 4
-1/2 over 1st 8 hours
`1/2 over next 16 hours
**leave % as a whole number not a decimal
supraclav n block
-supclavian a and first rib view -> brachial plexus tranks in relation to artery?
lateral
what level does infraclav block target?
level of cords next to axillary artery does block axillary and musculocutaneous n
-level of cords
TAP block between what layers
internal oblique and transversus abdominis
What n does the TAP block block?
anterior rami of the thoracolumbar spinal segment n from T7-L1
-subcostal, ilioinguinal and iliohypogastric blocked
***somatic postop pain, not visceral
What n provides sensory inervation over the sole of foot?
posterior tibial n
-behind medial malleolus
what innverates skin over dorsum of foot
superficial peroneal
what innervates lateral ankle and foot
sural n
-inject behind lateral malleolus
ankle block
possible complications for TAP block
LAST: large volume **calculate*
peritoneal puncture
bowel perf
liver/spleen lac
retroperioneal hematoma
what n block is phrenic n paralyis a complication
interscalene
What n block is PTX a complication
supraclav and infraclav
symp blockade is a complication of what n block
thoracic paravertebral block
ilioinguinal/iliohypogastric n block
-used in orhidopexy and hydrocele repair in kids
-ASIS located
-needle b/w internal oblique and transversus abdominis m
which eye block causes more chemosis
peribulbar
which eye block is faster with greater analgesia
retrobulbar
which eye block as a higher risk of retrobulbar hemorrhage, subarachnoid injxn, eyelid hematoma, globe perforation
retrobulbar
sub-tenon block
eye block -> quick onset but akinesia variable
-blunt cannula inserted via incision in the conjuctiva and tenonn capsule
-dec risk of perforation and subarachnoid injxn (b/c blunt)
-but inc risk of chemosis
-CI: eye infxn
what n injured during proximal humerus fx
axillary n
axillary n block anatomy
muscles surrounding: latissmus dorsi, biceps muscle, coracobrachialis muscle
deep peroneal n sensation
first web space of the foot
deep peroneal n relative to extensor hallicus longus tendon
n is lateral to tendon
post single shot caudal pt hypoTN needing pressors, post emergence apneic, weakness, fixed dilated pupils, dx?
total spinal blockade
Signs of intravascular injxn instead of cadual
peaked T waves
inc in heart rate
inc in BP
why total spine w/ caudal higher in infants ?
dural sac extends to S3-4, so close to puncture site (adults S1-2)
Rectus sheath block b/w what layers
rectus abdominis and posterior rectus sheath
where does probe go for interscalene block
level of cricoid cartilage (C6)
-SCM medial, and middle scalene laterally
interscalene block anesthetizes what?
ventral rami of C5-C7
interscalene block anesthetizes what?
ventral rami of C5-C7
what change in anatomy does cricoid pressure cause
lateral displacement of esophagus
consequences of cricoid pressure
dec LES tone
poorer laryngoscopic view
longer time from induction to intubation
anatomy
A: middle scalene
B: anterior scalene
C: carotid
D: SCM
roots seen: C5-C7
Types of regional that is inhibited w/ recent use of apixaban
neuraxial blocks and paravertebral blocks
PEC I and II blocks
PECs I: injxn only b/w pec major and minor
PECS II: 2 locations, between pec minor and serratus anterior and second pec major and pec minor
Why is bupivacaine the most cardiac toxic
stronger affinity for resting and inactivated Na channels in myocardium
cardiac-to-CNS dose toxicity ratio
normally LA cause CNS toxicity before cardiac
-cardiotoxicity is related to potency and higher lipid solubility
-bupivacaine has the highest
u/s of the neck carotid a relative to v position
v is lateral and superficial (superior) to artery
what muscles does the external branch of the superior laryngeal n innervate?
cricothyroid muscle
-affects voice pitch
What muscle sit he primary abductor of the VC?
posterior cricoarytenoid m
-RCLN innervation
what keeps LA around the femoral N?
fascia iliaca
gag reflex afferent/efferent in posterior pharynx
afferent: CN IX
efferent: CN X
pupillary light reflex afferent, efferent
afferent: CN II
efferent: CN III
First 2 reflexes lost during gerenal anesthesisa
oculocephalic (doll’s eyes): eyes open and head turned briskly and held -> normal is eyes move to opposite direction, abrnoaml, eyes follow rurning
corneal
Why does spinals last longer w/ older age
Dec CSF volume
N more sensitive to lcoal anesthetics
Absolute CI to spinal
pt refusal
infxn at site
severe coagulation problem
inc ICP due to mass lesion
presenting sign of subcutaneous emphysema after abd insufflation
extensive hypercarbia and crepitus
-no assoc w/ high inspiratory pressures
RF for subq emphysema
longer opeartive times
greater number of prots
higher insfflation pressures
retroperitoneal laparoscopy
lower BMI
older age
post spinal anesthesia, have discomfort aching pian in lower back that radiates down leg, no longer neuro sym
dx and tx?
transient neurologic symptoms (exact not known, possibly trauma to local structures, drug tox, and n root irritation)
NSAIDs -> opioids 2nd line
SE of loop diuretics
hypoNa
hypoK
hypoMg
hypoCa
sulfonamide hypersentivity (abx)
ototoxicity
eplerenone MOA
K sparing diuretics
Furosemide MOA
inhibitor of Na-K-2Cl cotransporter in thick ascending loop of Henle
recurrent laryngeal n monitoring during neck surgery
specialized ETT -> doesn’t need a neuromonitoring tech
-doesn’t require TIVA
-can’t use muscle relaxants
-no definitive decrease in injury been shown
which NMB has same metabolism similar to succ
mivacurium
if you give roc first then succ, any changes to succ dosing?
succ dose must be increased
hypoP and Hg dissociation curve
L ward shift (dec 2-3 biphosphoglycerate)
Ca and phosphate repletion
replenishing phos can cause hypoCa b/c P binds Ca -> despositio in tissues
Phos and granulocytic phagocytosis and chemotaxis
severe low Phos diminished ability of immune system to have energy to move it’s cells -> inc infxn risk
how does ventilation affect phos?
hypervent -> resp alkalosis -> inc pH -> activates phosphofructokinase stimulating glycolysis and consuming ATP
(makes sense, breaking too fast, need energy to keep it up)
why is hyperglycemia assoc w/ worse outcomes w/ cerebral ischemia
worsens lactic acidosis (anaerobic resp w/ hyperglycemia -> inc production of lactate)
inc cortisol resp w/ hyperglycemia -> stress resp worsening ischemia
enhanced glu-Na exchnage
Part of primary pattern generator for neural initiation of phasic respiration
subparabrachial nucleus
parabrachial nucleus in the pons
ventrolateral medullary complex
rostral and caudal ventral respiratory groups in the medulla
-cause rhythmic ventilation through reciprocal inhibition and modulate according to chemoreceptors, wakefulness and anesthesia
why is digoxin toxicity occur in hypoK
binds at the Na, K ATPase jate the same site as K -> when K is low, less competition and toxicity potentiated
dromotropic
affects conduction speed
mixed venous O2 in sepssis
high due to increase dcardiac output
what type of shock:
hypotension, high cardiac ouptu, low SVR
septic
what ppx helps succ myalgias
NSAIDs
fects w/ succ
pretx w/ anticholinergics
atracurium metabolism
ester hydrolysis and hofmann elimination (same as cisatracurium)
which inhaled anesthetics produced fluoride
des iso and sevo in liver via cytochorome p450 2E1
-highest in sevo***, lowest in des
Bezold-Jarish reflex
reduced preload sense low ventricular pressure -> inc vagal tone -> dec HR
MC assoc w/ severe bradycardia after spinal (HR < 40)
male gender
baseline bradycardia (,60bpm)
Assoc w/ bradycardia after spinal (HR <50)
male
baseline bradycardia
younger age
nonemergent surgery
beta-blockers
longer operative duration
Lithium and surgery
d/c 24 hours prior
prolonged NMB (reduces release of ACh)
lower anesthetic requirements (reduced release of NE, epi, DA)
-hypoNa and NSAID cause lower excretion -> inc risk of toxicity
nitrous oxide and cobalamin
cobalamin = B12
-B12 cofactor for homocysteine to methionine -> methionine involved in the synthesis of DNA, RNA
-in adults nitrous oxide -> megaloblastic anemia
-anemia rare in healthy pts, but in seriously ill pts -> bone marrow changes w/i 2-6 hours
HypoNa and MAC
decreased MAC b/c hypoNa causes CNS depression
HypoNa and MAC
decreascocaine and MACed MAC b/c hypoNa causes CNS depression
HypoNa and MAC
decreased MAC b/c hypoNa causes CNS depression
HypoNa and MAC
decreascocaine and MAC acute and chroniced MAC b/c hypoNa causes CNS depression
acidosis and MAC
decreased MAC
(makes sense, hypovent assoc a/ acidosis -> likely neuro off, dec MAC_
melanocortin-1 receptor gene MAC
inc MAC
seen in pts w/ red hair
Mg and anesthetic requirements
TIVA + Mg = less anesthesia
Mg + gas -> incMAC req
RF for transient neurological symptoms
lithotomy position
lidocaine use
adding phenyleprhine to 0.5% tetracaine
outpt procedures
phenytoin and NMB
acute: longer NMB
chronic: reduced blockade
carbamazepine and NMB
reduced blockade
what metabolite of morphine accumultes in renal dysfxn and causes rep depression
morphine-6-glucuronide
3 looks like a brain, 6 is a g upside down -> assoc w/ lungs
morphine metabolite that accumulates and causes neuroexcitation
morphine-3-glucuronide
3 looks like a brain, 6 is a g upside down -> assoc w/ lungs
Oxymorphone
metabolite of oxycodone
-metabolized by cytochrome P450 2D6
8x more potent
termination of succ
diffusion away from NMJ
degraded by pseudocholinesterase in blood away from NMJ
HyperCa and EKG
prolonged PR interval
shorted QT interval
-Ca extends depolarization when you think about Ca acting w/i Na current, but high Ca leads to contraction of heart -> shorter QT
HyperK EKG
peaked T waves
prolonged PR interval
wide QRS
HypoCa EKG
shortened PR interval
prolonged QT
HypoCa EKG
shortened PR interval
prolonged QT
Where to look for U waves
V4-6 -> vectors monitoring thicker parts of the heart
(hypoK and hypoMg)
what causes PR prolongation
hyPeR
hyPeR-kalemia, calcemia, magnesemia leads to PRolongation of the PR interval
-and opposite happens to QT interval
When should you monitor/check labs for someone on enoxaparin
morbid obesity (BMI >40)
altered GI anatomy (post gastric bypass)
possible drug-drug interaction
-concern over drug adherence
lab: anti-factor Xa activity or drug plasma concentration to assess for proper absorption
What fluid should you be careful of in acute liver failure?
Lactate b/c metabolized in liver to bicarb
Inhaled anesthetics effect on resp system
dec TV
blunt resp to hypercarbia and hypoxia
inc RR
bronchodilation
dec FRC
why does nitrous have a faster onset than des despite blood:gas coefficients
concentration effect
oil:gas coefficient
lipophilicity, and related to anesthetic potency
iso has the highest
what is fent metabolized by
CYP3A4
if a pt almost OD’d on coedine what other meds would be a problem?
oxycodone -> if ultrametabolizer will create more oxymorphone (results of metabolism by CYP2D6) -> more potent opioid than oxycodone
tramadol -> prodrug like codeine metabolized active by CYP2D6
Nitrous oxide MOA
noncompetitive inhibition of NMDA receptors
Effects of nitrous oxide on body
cardiac: may cause myocardial depression, but stim symp NS -> inc SVR and CO
resp: dec TV but inc RR
inc CBF and inc ICP
Sevo MOA
enhancement of GABA on GABA-A receptor
ACE inhibitors effects
prevent conversion of ATI to ATII
-dec in vasoconstriction -> dec BP
-dec in aldo -> red water and Na absorption, limit K wasting -=> hyper K
-dilation of renal arterioles
-inc arachidonic acid metabolites -> inc vasodilation -> dec BP
***hyperK inc in renal dx, DM, or K sparing diuretic use w/
teratogenic effect of ACEinh on pregnant ladies
renal malformations
When do you commonly see Bezold-Jarisch reflex
post-spinal (otherwise symp usually outshine)
-dec preload -> bradycardia
which is which
Confidence interval equation
sample statistic +/- confidence factor *(standard error)
standard error = standard deviation / (square root of sample size)
how to decrease confidence interval
sample statistic +/- confidence factor *(standard error)
standard error = standard deviation / (square root of sample size)
-lower confidence interval
-inc sample size
-dec standard deviation
-dec variation of the sample
GI changes in full term pregnant women
-if NOT laboring -> gastric emptying is NORMAL
-progesterone dec LES tone
-cephalad movement of esophagus -> dec competence of LES, inc risk of regurge, aspiration
-inc gastrin -> more acidic gastric fluids
epidurals and GI pregnant women
epidurals w/ opioids will delay gastric emptying -> preserved if only local anesthetic
what to give pregnant women pre GA
prior to induction, metochlopramide and antacid
When does aspiration risk inc in laboring pts
after 20 weeks
-gravid uterus -> displacement
-hormonal changes
Epi dosing for anaphylaxis
Epi 1 mcg/kg
-max dose is code dose of 0.01 mg/kg
-adult dosing typically 50-100 mcg IV
Tx for anaphylaxis
-reduce contact w/ offending agent
-d/c all meds that could cause anaphylaxis
-intubate if needed
-maintain airway and 100% O2
-IVF 25 cc/kg (up to 50)
-Epi 1 mcg/kg
-d/c all anesthetic agents
if you have allergies to tropic fruits or chestnuts what are you at high risk of being allergic to?
latex
Anaphylaxis 4 grades
I: cutaneous-mucous signs
II: mild cutaneous-mucous features, may be assoc w/ cardiovascular and/or resp signs
III: cardiovascular collapse or bronchospasm
IV: cardiac arrest
if concerned about an anaphylactic reaction what lab do ou send?
tryptase level
-peak 15-60 minutes then decline
-if increased, suggestive of mast cell activation
-get a 2nd sample 24 hours later to compare to baseline
Equation for total arterial oxygen content in blood
O2 content = (1.34 x Hg x O2 saturation (in decimal)) + (0.0031 x PaO2)
ERAS goal-directed fluild management
-as pt and procedure complexity inc -> more intense modalities to monitor fluid responsiveness
-fluid management when analyzed solo as part of an ERAS protocol does not have any actual impact, but we still do it anyway
-fluid management ALONE outside of ERAS protocol has been shown to decrease ileus and length of hospital stay
cause of adrenal insuff in critical illness in ICU
functional adrenal insuff
-b/c chronic stress, system depleted in the HPA axis and adrenal glands
-def: no obvious structural defects in HPA
Exogenous glucocoritcoids is causes what type of adrenal insuff
tertiary adrenal insuff
How long after taper of steroids does it take for the adrenals to fully recover
6-12months
What medication should NOT be given in thyroid storm
Salicylates = Aspirin
-b/c competes w/ T3 and T4 for thryoid-binding globulin -> inc circulating free hormones
Tx of thyroid storm
-Beta blockers for heart
-coiling blankets, acetaminophen fo rfevers
-PTU for hormonal control (prevents peripheral conversion unlike methimazole, so PTU > methimazole)
-dexamethasone (relative adrenal insuff 2/2 extreme hypermetabolic state)
Bronchopulm dysplasia
most likely to occur in neonates < 32 weeks
-RF: O2 toxicity, sepsis, inflammation, ifxn, barotrauma
-long-term consequence of respiratory distress syndrome
-chronic dx of airways and lung parenchyma
anesthesia considerations of bronchopulm dysplasia
desat fast (lack of reserve and poor lung compliance)
airway reactivity
hyperinflation
resp distress syndrome and bronchopulm dysplasia
RDS –> bronchopulm dysplasia
-b/c when you have resp distress syndrome (implies shorter = syndrome), iif not fixed, will chronically lead to bronchopulm dysplasia (dysplasia = longer Duration)
Expiration in emphysema
alveolar walls and small distal airways are destroyed -> when intrathroacic pressure positive during expiration, can’t stay open as long as normal lungs -> premature closure -> air trapping and hyperinflation
-occurs in smallest airways and thinnest
expiration in dpt and non-dpt lung regions
-dpt lungs will have small airway closure before non-dpt b/c greater pleural pressure in dpt-lung regions (positive P during nexpiration)
-dpt lung regions closer to bottom, non-dpt at top of lungs
resistance to airflow and radius
radius to the 4th power
-so as radius inc, R decreases to 4th power
peak pressure and plateua pressure and statis anc dyanmic compliance
static compliance -> measured during zero airflow = plateau pressure (has to do w/ volume of lung and lung compliance, less volume of lung ventilated, dec lung compliance, dec static compliance)
dynamic compliance = peak pressure-plateua pressure (resistance in airways)
-inc in peak pressure = decreased dynamic compliance
Dec static compliance caused by
-dec volume of lung ventilated, reduced chest wall compliance
-requires greater plateau pressures to maintain similar lung volumes
PTX
pulm edema
PNA
pneumonectomy
endobronchial intubation
abd insufflation
abd distention
thoracic deformities
Endobronchial intubation static and dyanmic compliance
dec static compliance (inc plateau pressure)
no change in dynamic compliance (b/c no inc airway resistance)
PNA static and dynamic compliance
dec lung for ventilation, dec lung volume for a given pressure -> dec statis compliance
inflammation and ractivity in small airways -> inc bronchiolar resistasnce -> dec dynamic compliance
Pulm embolism on static and dyanmic compliance
does not affect gas flow -> no change in either
Dynamic compliance determined by
resistance to airflow through small airways of the lung
Static compliance determined by
ability of lung to expand inn setting of static positive airway pressure admin
How to determine dyanmic compliance
difference b/w peak pressure and plateu pressure
Static compliance estimated
diff b/w plateau pressure and PEEP
HypoCa QT
prolonged QT
-less Ca in SR -> slows Ca-activated K current -> slows repolarization and lengths QT
Tx for hyperCa due to hyperparathyroid intraop
hydrationn w/ Normal saline
diuresis w/ furosemide to dec Ca levels to < 14
Eaton-Lambert Syndrome sensitivity to succ and NDNMB
INCREASED to both
hypokalemic periodic paralysis and NMB
link b/w malignant hyperthermia and hypoK PP -> avoid succ
inc sensitivty to NDNMB
Digoxin ionotropic, dromotropic, chronotropic
POSTIVE ionotrope (inc contractility)
NEGATIVE dromotropic (conduction speed), chronotropic (HR)
Nitrous O2 and ETT and pulm a catheters
at 75% a cuff can double or triple on volume -> pressure on tracheal mucosa
-in pullm artery cathetrer can double w/i 10 minutes
