ITE TL 2022-23 Flashcards
Blood:gas coefficient
ratio of gas dissolved in the blood and the alveoli at equilibrium
-larger -> higher solubility in blood -> slower onsent of action
second gas effect
rapid uptake of nitrous oxide into the blood -> second gas inc in conc due to loss of volume of nitrous oxide -> more rapid uptaek of 2nd inhaled anesthetic (more concentrated)
B:G coefficient Des, iso, Nitrous oxide, sevo
Des: 0.42
Nitrous: 0.46
Sevo: 0.65
Iso: 1.46
Vecuronium metabolism
metab by liver w/ byproduct w/ 80% potency -> metabolite (3-desacetyl-vercuronium) can build up in pts w/ renal insuff or liver failure
Vecuronium onset/duration
onset: 3-4 minutes, duration: 25-50 minutes
Pancuronium metab
Active metabolite -> build up in hepatic/renal failure -> prolongation of NMB
Cisatracurium metabolism
Hofmann elimination and ester hydrolysis (spontaneous degradation in plasma) -> inactive metabolite
Mivacurium metabolism
metabolized by pseudocholinesterases into inactive metabolites
Rocuronium metabolism
excreted unchanged by biliary and renal systems
-small amount metabolized by liver -> 17-OH roc -> minimal NMB activity
Potentiating NMB w/ inhalational gases, which the most?
DES!
Des > Sevo > Iso > nitrous oxide
Does that gas potentiate the NMB? Yes it DES!
Perip fluid management peds
Healthy peds pts elective surgery: 20-40 cc/kg over 2-4 hours LR,NS, plasmalyte
12 hrs post-op: 2-1.05 cc/kg/hr if not tolerating PO
When to use glucose containing solutions in peds
neonates, infants <6 months old, malnourished children, undergoing cardiac solution 1-2.5% dextrose
-be sure to monitor glucose!
Digoxin MOA
Glycoside -> positive ionotropic and negative dromotropic and chronotropic effects
-inc myocardial contractility, inc phase 4 depolarizations, and shortens action potential
-dec AV node conduction velocity, and prolongs refractory period of AV node
Digoxin toxicity symptoms
nausea, vomiting, diarrhea, abd pain
-vision changes yellow -> green, blurry vision,
=vent tachyarrythmias, and atrial tachycardia w/ AV block
-EKG: ST depressions, dec QT interval, inc PR interval, T wave inversions (normal w/ digoxin, not necessarily toxicity)
Digoxin toxicity inc risk
advanced age, worsening renal function, hypokalemia, low body weight, med noncompliance
beta-blocker toxicity
bradycardia, hypotension, hypoglycemia, hyperkalemia, wheezing,
severe: sz, deliriuum, and coma
PONV guidelines
-if any risk factor -> multimodal ppx
-RF: female, hx of PONV or motion sickness, postop opioids, non-smoker
-volatile anesthetics, nitrous, GA, long duration, young, gastric, gyn, or laparoscopic surgery
-1-2 RF: 2 interventions
-3-4 RF: 3-4 interventions
Jugular bulb venous O2 saturation monitoring
-put a catheter in retrograde and measure mixed venous sats at the jugular venous bulb
-measure of GLOBAL cerebral oxygenation, not local
(no change in stroke b/c local ischemia)
global cerebral oxygen supply and demand
supply: CBF, arterial oxygen content, and Hgb
demand: CMRO2
Cardiac myocyte action potential phases
phase 0: Depolarization
-VG Na channels open -> influx of + Na => membrane -90 to +20
phase 1: early rapid repolarization
-Na channel inactive, K ions exit cell -> dec in membrane potential
phase 2: plateau
-Ca active, Ca moves intracellularly, balancing out K leaving -> slows rate of decline in AP
phase 3: repolarization
-Ca inactive, K permeability inc -> AP decline
phase 4: resting potential
-normal cell permeability restored, Na-K-ATPase pumps K in and Na out
post-heart transplant heart
Denervated -> isolated from recipient nervous system
-only resp to direct myocardial adrenergic -> isoproterenol, epi, dob
-no resp to atropine, no resp to hypovolemia, no reflex for phenylephrine
-resting HR: 90-110
-accelerated rate of atherosclerotic disease
-no angina b/c denervated
tingling lateral surface of lower leg and dorsum of feet and toes, weakness w/ eversion of foot, what n?
Common peroneal nerve
-likely due to lithotomy position -> to dec minimize pressure at fibular head
Tramadol metabolism
PRO-DRUG
-metab by cytochrome p450 2D6 and 3A4
Tramadol MOA
After metabolism (pro-drug)
+ enantiomer: mu opiod agonist
- enantiomer: SNRI ( serotonin and NE reuptake inh)
Stages of liver transplant
preanhepatic, anheptic, and neohepatic
Preanhepatic
incision to cross-clamping of protal v, hepatic a, IVC or hepatic v
Anhepatic
cross clamping -> anastomosis are made and perfusion starts
Neohepatic
Unclamping of portal v when reperfusion starts -> hepatic a, biliary duct anastomosis, and abd closure
Changes during ischemia of liver
-lack of ATP -> can’t maintain ion gradients -> swelling
-alterations in Ca homeostasis
-hepatic cell death
-dec in cytoprotective substances
Reperfusion of liver possible issues
-build up of ischemic products (lactate, H+, K+), preservation solution released
-blood through graft -> release of microemobli
-hypoTN or arrhythmias
Postreperfusion syndrome
First 5 minutes after reperfusion -> systemic hypoTN and pulm HTN
-ischemia-reperfusion injury b/c low ATP and glycogen -> Na/K pump failure -> extracellular Na ions move into cells and cause swelling
-vascular permeability inc -> dec ATP and adenylate cyclase activity dec
Blood alteration if IgA def
washed RBCs
Acute hemolytic transfusion reaction
IgM antigen-antibody complex activating complement
Standard deviation percentages
SD 1 68%, 2 95%, 3 99%
CBF changes with hypothermia
for every 1 degree decrease, CMRO2 dec by 6%, proportional dec in CBF
PaCO2 and CBF
1 mm Hg in PaCO2, CBF changes by 3%
CBF and PaO2
constant for PaO2 >50-60
-inc dramatically when below 50
CBF and MAPs
CBF constant b/w 50-150
Specificity
TN/ (TN + FP)
“rules in” a disease
-confirmatory test
Sensitivity
TP/ (TP+FN)
-screening test
Which coronary cusp
Non-coronary cusp
-is always located next to the inter-atrial septum
-LCC is next to the pulm artery
-RCC is anterior most and faces RV
Which coags go down/no change in pregnancy?
XI, XIII: down
II, V: no change
all the rest procoag inc, anticoag decrease
Major RF for PONV
female sex, motion sickness, postop opioids, hx of PONV
Tetanus toxin MOA
prevents release of inhibitory neurotransmitters
-SNARE cleaved by tetanus prevents vesicle fusion and prevents release of GABA and glycine
Autonomic symptoms tetanus
Autonomic dysfunction: sweating, vasoconstriction, severe tachycardia w/ HTN may rapidly alternate w/ bradycardia and hypoTN
-abnormally high epi and NE -> exagg symp NS
-major cause of morbidity and mortality
Where tetanus acts
travels via retrograde axons from peripheral ro central neurons
-prevents GABA release in synaptic cleft b/w inhibitory interneurons and motor neurons
-enters brainstem to affect SNS
Botulinum toxin
only affects peripheral motor neurons, and prevents release of ACh into NMJ -> flaccid paralysis
Kartagener syndrome
primary ciliary dyskinesia
-can be associated w/ situs inversus, recurrent sinusitis, bronchiectasis
Bronchiectasis
-issue w/ mucociliary clearance -> recurrent lung infxn and inflammation -> localized and irreversible dilation -> dialted bronchial malacia -> airway collapse and impair mucus clearance
-w/ progression can have dec FEV1/FVC ratio
Bronchiectasis tx
prevention w/ aggressive antimicrobials
-inhaled corticosteroids may dec sputum production and inflammation
-chest PT
-if hemoptysis or recurrnt PNA, lung resection can be indicated
**treat like COPD, lots of PEEP
Nerve agents
Inhibit AChE
-SLUDGE Mi: Salivation, Lacrimation, Urination, Defecation, GI Upset, Emesis, Miosis
-arrhythmias, typically bradycardia but can be any
-ACh at nicotinic rec at NMJ -> fasciculations, twitching, fatigue, and flaccid paralysis
Why hypothermia in OR?
Anesthetic induced impaired thermoregulatory control, internal redistribution, red in head development, cold OR
Pattern of heat loss
initial rapid decrease then slow, linear reduction, then stabilization and plateau
Consequences of hypothermia
-coag impaired -> defect in platelet fxn
-dec drug metabolism
-***wound infxn inc (impairs immune fxn and dec wound O2 delivery)
-shivering -> hypoxia and ischemia
Prevention of hypothermia from redistribution
preop pre-warming -> inc preipheral temp before vasodilation
heat loss radiation
radiates heat to surrounding environment, heat transfered to from core to subq vessels -> lost to environment
**major loss type
heat loss convection
thin layer of air adjacent to skin acts as an insulator -> since air exchanged every 15 min in OR -> loss of insulator
heat loss conduction
transmission of boy heat through conducting medium (contact w/ mattress)
heat loss evaporation
liquid -> vapor lowering of kinetic energy
-when sterile prep solutions applied
RF for postop hospital admission
age over 65, long op times (>120 min), ASA III or IV, OSA, vascular dx
Thyrotoxicosis
Hypermet state from high thyroid hormone
-sym: nervousness, irritability, tremors, tachycardia, arrhythmias, fever, vomiting, diarrhea
Tx of thyrotoxicosis
PTU and Methimazole: inhibit production of thyroid hormone
-PTU: prevents peripheral conversion of T4 to T3
-can be used as a therapy or bridge to tx w/ surgery or radioactive I
radioactive iodine
used to destroy thyroid gland
-SE: inc hyperthyroid sym the first few days b/c destroy gland -> hormone release
-pre treat w/ methimazole or propanolol
-CI: breast-feeding, pregnancy
Complications w/ periop hyperglycemia
-immunosuppression -> dec WBC fxn
-inc infections
-stim of sympatho-adrenergic activity
-osmotic diuresis
-red skin graft success
-inc catabolism in burn pts
-delayed wound healing
-delayed gastric emptying
-exacerbationo f brain, SC, and renal damage by ischemia
-increased mortality
-risk of postop cognitive dysfxn following CABG
What’s in cryoprecipitate
vWF, fibrinogen, fibronectin, factor VIII, and factor XIII
Indications for cryo
-microvascular bleedingw/ low fibrinogen (ex DIC)
-bleeding due to uremiathat is unresponsive to DDAVP
-factor XIII def
-ppx before surgery or tx of bleeding w/ congenital dysfirinogen, VW Dx, Hemophilia A (if factor concentrates unavailable)
-use in firbin sealant production
SE of high dose oxytocin
-Oxytocin mimics vasopressin -> dec urine excertion
-volume overload sensed by atria -> ANP -> natriuresis -> hypoNa
-hypoTN -> N/V
Normal fetal pH
7.32 to 7.38
Normal pregnant mother pH
7.43 -> chronic resp alk
Fetal ion trapping
low fetal pH
-crosses placenta in un-ionized form, accepts aH ion in more acidic environment -> drug accumulates and then b/c ionized can’t cross back
why does lidocaine accumulate w/ ion trapping
pKa is 7.8 -> once in pH lower than 7.8 it accepts a H ion
Determines if drugs cross placenta
-Size: drugs <500 Da cross easily, >1000 Da (heparin, protamine, insulin) don’t cross
-Degree of lipid solubility, ionized (succ, NDMR) don’t cross, lipophilic (fent) do
-Protein binding: highly protein bound less likely to cross
-Maternal drug conc: higher conc morel ikely to cross
Drugs that do NOT cross Placenta
He Is Going Nowhere Soon
Heparin
Insulin
Glycopyrrolate
NDMR
Succinylcholine
Reversal of MR in pregnant pts
Neo and atropine
-Neo crosses, glyo doesn’t -> fetal bradycardia
Lowest blood:gas coefficient
Des < N2O < Sevo < Iso
blood: gas partition coefficient
ratio of the concentration of inhaled anesthetics in blood to conc in alveoli at equilibrium
-Lower = faster onset
Why is nitrous faster than Des
Des has a lower blood: gas coefficient, but “concentration effect” -> nitrous has a bigger concentration
B:G coefficients
Des 0.42
nitrous 0.46
sevo 0.65
iso 1.46
Secondary HSV active gental wounds what to do
C/s
-no invasive fetal monitoring
Conn Syndrome: cause and tx
Primary hyperaldosteronism: excess secretion of aldosterone from adrenal adenoma
tx: Spironolactone, anti-HTN, supplemental K
Sym of primary hyperaldo
fatigue, m cramps, weakness, polyuria, HA
(from HTN and hypoK from excess aldo)
Midodrine MOA
alpha 1 rec agonist
Octreotide
Somatostatin analogue
-used in acromegaly (supp GH production)
Congenital Diaphragmatic Hernia
-L side more common, more common in females
-Triad: dyspnea, cyanosis, and dextrocardia
-assoc w/ congenital heart dx and intestinal malrotations
TEG parts
R time: clot initation
K and alpha angle: clot kinetics
MA: clot strength
Ly30: fibrinolysis, clot stability, breakdown
TEG R
t=0 to initial clot formation
-dpt on clotting factors
-tx: FFP
TEG K and alpha angle
strength of clot formation, alpha measures speed of clot formation
-dpt on fibrinogen
-tx: cryoprecipitate
TEG MA
strength of clot, and maximum width of TEG
-dpt on plt number, function, and fibrin cross linking
-tx: plts
Desmopressin uses
When fxnl issue w/ plts (dec MA on TEG)
-causes release of endothelial cell stoes of factor VII and vWF, inc plt glycoprotein expression
-used for uremic bleeding or vWD
Normal TEG values
Rule of 6’s
R time: 6 minutes
alpha angle: 60 degrees
MA: 60mm
Ly30 6%
location of landmark interscalene block
behind the lateral border of SCM at level of cricoid cartilage
Coverage for interscalene block
Ventral rami of C5-C7, and supraclav (C1-3)
-100% block ipsilateral phrenic nerve -> hemidiaphgramatic paralysis
-covers shoulder and proximal upper extremity -> ulnar spared so no forearm or hand
Interscalene block landmark technique w/ n stim
at level of cricoid cartilage, posterolateral to SCM, in interscalene groove, insert needle, move caudad -> until movement of deltoid, triceps, biceps or pectoralis gets a response
-make sure stim at 0.4 mA, if stim at < 0.2 mA intraneural, pull back
hyperparathyroid and NMB
thought is hyperparathyroid -> inc Ca and inc in ACh rec -> hyposens to NDMR but resp is variable and unpredictable
Gold standard for core temp
pulmonary artery via pulm artery catheter
Acceptable alternatives for core temp
nasopharynx, distal esophagus, tympanic membrane
Pregnancy factor level changes
INCREASE: factor I (fibrniogen), factor VII, smaller inc in others
DECEASE: anticoag: antithrombin III, and protein S
Normal coags in pregnancy labs
20% decreasein PT, PTT
-dilutional effect on plts dec
Gestational thrombocytopenia
plts < 150k
Which factors procoag DEC in pregancy
XI, XIII
Pregnancy TEG
dec R time, K, alpha angle, MA
hypercoag
TX for congenital long QT syndrme
BB: propranolol, nadolol
QT prolongation leads to
syncope, cardiogenic sz, MI, sudden cardiac death -> all from polymorphic tachyarrhthmia, torsades
Tx for QT prolongation causing torasades
unsynchronized cardioversion and 2g Mg sulfate
Myasthenia Gravis risk for postop ventilation
-Diagnosis > 6 years
-Vital capacity < 2.9 L
-Daily dose > 750mg
-chronic respiratory illness
secondary:
-EBL >1L
-BMI >28
-advanced stage of MG
-hx of MG crisis
-Anti-ACh titer > 100 nmol/mL
-pronounced decremtanl resp (18-20%) on low freq repetitive n stim
Myasthenia gravis and NMB
-very sensitive to NDNMB
-resistant to succ
Change for CBF and temp
6-7% change by 1degree C in temp
Hypothermia body changes
-dec in speed of chemical and enzyme rxns -> less metabolism
-peripheral vasoconstrictin -> inc SVR and inc BP
-if <32 cardiac conduction slows -> bradycardia
-diuresis -> contraction of blood volume -> inc Hct and viscosity
-leukocyte and plt fxn dec
-dec in insulin sensitivity and secretion -> hyperglycemia
-arterial partial P of O2 and CO2 dec b/c soluble in blood
inhalational agents and fetus
cross placenta esaily b/c higher lipid solubility and low molecular weight
Possible SE of inc intra abbd pressure from repairing gastroschisis
-abd compartment syndrome
-compress IVC -> hypoTN
-compress liver and kidney -> altered drug metabolism
-prevent diaphragm excusion -> red lung compliance -> inc peak and plateau pressures
-inc in ICP (inc in intrathoracic pressure reduces cerebral venous return)
Inc in peak pressue w/o inc plateua pressure
inc in airway resistance -> bronchospasm, ETT obstruction, mucous plugging, kink in circuit, retrained secretion
Inc in peak and plateau pressure
PTX, pulm edema, ARDS, PNA
Labetalol half life, effect on BP
1/2 life: 6 hours
effect on BP: 16-18 hours
Labetalol MOA
antagonism to alpha 1: arteriolar vasodilation
antag to beta 1: dec HR and dec contracility
antag to beta 2: arteriolar vasodilation
Labetalol metabolism
hepatic glucuronide conjugation w/ excretion via urine and feces
Esmolol half life
9 minutes
Esmolol metabolism
metabolized by RBC estereases -> short 1/2 life
-useful to tx acute tachycardia => dose dpt response
-used for DL to attenuate symp response
Abx that do NOT affect NMB
PCN and cephalosporins
Abx that inc NMB
aminoglycosides (Gentamycin), polymixins, lincosamides: clindamycin
-gluoroquinolones and tetracyclines
Prolong NMB
-inh gas: des most
-Lithium (activates K inhibit ACh release)
-Mg (block Ca)
-CCB
-acute antepileptics
Chronic antiepileptic drugs and NMB
inc conc of serum glycoproeins and postynatpic nAChR -> more rapid clearance and shorter duration of action
What’s blocked in adductor canal block
vastus medialis is the ONLY muscle, remaining sensory block (saphenous on)
boundaries of adductor canal
vastus medialis laterally, sarterius anteriorly (roof), adductor longus (superior) or magnus (inferior)
Fascia iliaca block
Blocks femoral and LFCN
-large volume
Zero-order kinetics
Will eliminate a constant amount of drug per unit time, regardless of plasma conc
-ethanol, cisplatin, phenytoin, high dose salicylates
First order kinetics
eliminate a constant fraction of drug per unit time (decreases exponentially)
-higher conc, faster clearance
LFCN
L2-L3 n roots, sensory innervation to anterolateral aspect of thigh
-blocked for surgeries w/ femoral neck or skin grafting on thigh, or muscle biopsies of lateral thigh
LFCN location
emerges from lateral border of psoas, crosses iliacus m toward ASIS, behind/through inguinal ligament, in front of sartorius
LFCN block
ASIS, -1 cm medical and 1-2 distal, advanced until pierces fascia lata
Meraglia paresthetica
d/o LFCN -> pain, parethesia, hypesthesia in anterolateral thigh assoc w/ n compression
-LFCN n block is diagnostic
Intravascular injxn of caudal anesthesia symp
inc in 25% or more in T-wave amplitude
inc HR and BP (T waves more reliable b/c not guaranteed when under GA)
Layers to femoral block
Skin, subq, fascia lata, and fascia iliacus
Temp and CMRO2
each degree C < 37, CMRO2 dec by 6-7%
gold standard of cerebral temp
jugular bulb venous temp
Oxygenator arteial outlet temp
measures temp of the arterial blood leaving CPB circuit and entering body via aortic cannula
NG and dec myocaridal demand
preferentially dilates Venules -> dec preload
v > a
NG onset and 1/2 life
onset: 1-3 minutes, 1/2 life 2-3 minutes
metab by liver
NG MOA
smooth m: activates guanylyl cyclase to inc cGMP -> inh Ca into cells -> smooth m relaxation
Artery of Adamkiewicz supplies
anterior 2/3 of SC T9-T12 -> loss of motor fxn of lower extermities, loss of pain and temp 1 level below lesion, sexual dysfxn, urinary and fecal incont
-proprioception and vibration intact (posterior a)
spinal n
anterior: motor, posterior: sensory root
Anatomical landmarks for dermatomes
Dermatomes
surgery post DES
elective is 6 months
surgery post bare metal stent
30 days
anatomy near stellate ganglgion
carotid a anterior to at level of C6
anterior to neck of the first rib and C7 transverse processes
lateral: scalene muscles
posterolateral: vertebral arteries
Obesity changes on lung volumes
Dec compliance -> shallow breaths, inc WOB, and limited max VC
-dec FRC (dec ERV), dec TV, dec TLC
-RV unaffected
-FEV1 and FVC slightly decreased, ratio preserved or slightly inc
-nc O2 consumption and CO2 production due to inc adipose tissue
NG MOA
enters endothelial cells from the bloodstream and are converted to nitric oxide intracellularly -> smooth m relaxation (incl uterine smooth m)
-nitric oxide -> cGMP -> sequesters intracellular Ca
SE of NG
tachycardia, hypoTN, flushing, and HA
Mg Sulfate preterm labor
tocolytic and neuroprotection
-blocks intracellular Ca
Terbutaline MOA
selective beta 2 activation -. beta 2 rec complex is Gs coupled -> activation of adenylyl cyclase and inc cAMP
COA NG
PDE 5 inh (sildenafil, tadalafil, vardenafil)
-potentiate nitrates b/c prolongation of cGMP activation -. hypoTN
cardiac arrest pulseless v fib post cardiac surgery, next?
defibrillation x3 prior to any compressions (w/i 10 days after cardiac surgery)
-if no change w/ defib rec to repeat sternotomy for direct cardiac massage (external compressions associated w/ fatal complications)
-if using epi dec doses to avoid HTN
Affects the level of spinal
primary: dextrose content (hyperbaric more influenced by gravity), total drug dose
others: volume of local anesthetic, pt position, pt height, pt age, CSF volume, intra-abd pressure, injxn site, needle bevel direction
clonidine spinal
inc analgesic properties (alpha 2 stimulation)
Epinephrine spinal
inc duration of action of local anesthetic and quickens speed of onset
Morphine spinal
inc analgecis properties, esp visceral pain
-minimally enhance block height
Diagnosis
B-lines
pulm edema
Diagnosis
PTX
-no lung sliding, so when on M mode -> barcode sign
Dx
Normal u/s
-on M mode you see lung sliding: “seashore sign”
Diagnosis
pleural effusion
-M mode: sinusoid sign
-area of fluid b/w visceral pleura and parietal pleura
Dermatome innervates the skin over the lateral malleolus
S1
Dermatome medial aspect of thigh, knee, calf
L3
Dermatome anterior knee and medial malleolus
L4
Dermatome dorsal and lateral foot, toes 2-4
L5
Which local anesthetic has a duration of action that would be prolonged LEAST by addition of 1:200,000 epi
Bupivacaine: more readily absorbed from epidural space indepent of epi vasospasm which negates epi impact
Epi adds a benefit with alpha 1 stimulation, dec bleeding, red toxicity, prolonged duration of action
-epi benefits more pronouned w/ short or intermediate acting local anesthetics
sodium bicarb as a block additive
increases local pH -> inc rate of onset, facilitating nonionized local anesthetic into neurons
LMWH
bind and potentiates antithrombin III, but more selective inhibition of factor Xa w/ minimal inhibition of thrombin
-not reversed w/ protamine
-risk of HIT but lower than UFH
Cardiac effects of isoflurane
dec SVR, dec MAP, dec contracility, prolonged QT interval, inc HR
Which inhaled anesthetics prolong QT interval
sevo, iso, des
Inc in K after succ in normal healthy people
0.5 mEq/L
ppx for postop myalgias due to succ
pretreament with NSAIDs: ASA, diclofenac
Boundaries of adductor canal
lateral: vastus medialis
superior: adductor longus
inferior: adductor magnus
anterior: sartorius
-deep to sartorius is aponeurosis: vasoadductor membrane
UFH MOA
indirectly inhibits thrombin and factor Xa by bing to ATIII -> enhanced degradation of thrombin and factor Xa
Renal adjustments for UFH v LMWH
LMWH metabolized 40% by kidneys, needs adjustment
UFH does not require renal adjustment dosing
UFH monitoring
PTT or ACT
Emergence from nitrous oxide anesthesia
-high conc N2O exits tissue and blood and enters alveoli -> w/i first 5-10 min after discontinuing, inc N2 in alveoli causes less O2 in alveoli -> hypoexemia
-enahnced washout of CO2 as well, causing hypocarbia and dec resp drive
second gas effect
N2O concentrating effect
-due to rapid uptake of N2O in blood, second gas inc in concetration due to loss of volume of nitrous oxide -> more rapid uptaek of second higer conc volatile anesthetic
Airway anatomy
only complete cartilaginous ring in upper airway
cricoid cartilage
trachea cartilage
C-shaped rings of hyaline, open end opposing esophagus
bronchi/bronchioles and carilage
bronchi: complete circular cartilage rings
bronchioles lack cartilaginous structures
site of carina landmark
5th thoracic vertebra
what level disc herniation?
L5-S1
-L5 nerve root could be affected
acute normovolemic hemodilution
occurs before significant blood loss
-whole blood removed from pt while giving back crystalloid or colloid (3:1 for every 1 cc blood removed), blood stored in citrate-containing solution, and stored at room temp for 8 hours or 24 if 4C
-when bleeding occurs, number of RBCs los is lower
-blood transfused back to pt in reverse order of collection (1st unit has highest conc of plts, Hg)
Indication for Acute normovolemic hemodilution
-likelihood of blood transfusion >10%
-preop Hg is >12
-no significant renal, pulm, liver, or conoary dx
-no severe HTN
-no infxn
Body compensation for ANH
inc cardiac output
-in HR b/c anemia
-SV inc due to dec in SVR and afterload
-dec blood viscosity -> dec in shear stress in microvasculature inc flow and venours return to heart
-mild tissue hypoxia and acidosis -> ateriolar vasodilation red afterload
-if Hct <25, 23DPG inc causing R Hg curve shift
When to use cell salvage
Anticipated blood loss of >20% of estimated blood volume
-crossmatch compatible blood not available
-pt refuses allogeneic blood transfusion but agrees to cell salvage
-more than 1 pRBCs is expected
opioids and sz threshold
do not alter sz threshold unless pt has renal failure (accumulate toxic metabolites)
-and no EEG sz activity even if m rigidity or shivering is present
Why muscle rigidity w/ opiods
inhibit GABA release and inc DA production in CNS (like Parkinsons)
morphine and renal failure
inc morphine-3-glucuronide -> neuroexcitation and sz when accumulated after repeat doses
meperidine and renal failure
Normeperidine accumulates -> sz
GI SE of opioids why?
spasming of smooth muscles -> constipation, biliary colic and delayed gastric emptying
-esp morphine which dec peristalsis, and b/c moving slowly, inc in water absorption
-inc tone of pyloric sphincter, ileocecal valve and anal sphincter
sym/parasympathetic changes w/ aging
inc baseline sympathetic activity -> why such big blood pressure lability during surgery
-dec resp to alpha and beta stimulation
-dec parasym activity
heart changes w/ aging
stiffening of myocardium, arteries and veins -> HTN
-conudction changes: blocks and loss of SA node cells
-defective ischemic preconditioning
-baroreflex dec due to dec in HR
-stiff aorta, more stroke volume stays in aorta -> waves back to heart -> inc work of LV -> LVH impairs diastolic filling -> diastolic dysfxn -> so reliant on atrial kick
Pulmonary changes w/ aging
inc stiffness of chest wal and dec stiffness of lung
-inc curve of diaphgram -> harder to generate negative pressure -> inc work of breathing
-dec elastin so lung tissue less stiff, easier to inflate but inc collapsing -> inc closing capacity
-dec response to hypercapnia and hypoxia
-inc risk of upper airway obstruction due to loss of muscle mass, impaired swallowing and dec coughing
Definition of larynx
epiglottis to inferior border of cricoid cartilage (C6) ie start of trachea
Nasopharynx
anterior: nasal cavity
superior: base of skull
posterior: posterior pharyngeal wall
inferior: soft palate
bordered by oral cavity
oropharynx
b/w soft palate and hyoid bone
hypopharynx
pharynx below hyoid bone
-connects oropharynx to esphogus and larynx
Desflurane Boiling point and vapor pressure
BP: 24C
VP 669
-b/c BP is near room temp -> why requires closed storage container and a pressurized and heated vaporizer to allow predictable responses
Isoflurane BP and VP
BP: 49
VP 238
Sevoflurane BP and VP
BP 59
VP 157
what happens if you put isoflurane in a sevo vaporizer?
Iso has a HIGHER vapor pressure: 241 (I) to 160 (S)
-PV is the pressuer exerted by the gas phase on walls of container
-b/c iso’s VP is higher, it’s vapor concentration is higher, so at 1atm: iso 241/760 = 32% vapor concentration
-more iso in gas form than sevo -> so if iso in sevo vaporizer -> actual output conc will be higher than indicated by the dial
Nitrous oxide BP and VP
BP: -88 C, which is why it’s a gas at room temp
VP: 38,770
Advantages to postop epidural analgesia
-superior pain control
-red periop inflammation and sensitization of pain pathways\
-red GI hypomotility
-improved visceral BF -> dec MI and bowel ischemia
-dec postop pulm comp (PNA)
-vascular surgery improved mortality
Disadvantages to epidural postop analgesia
-CI: inc ICP, coagulopathy, high risk of infxn
-inc hypoTN intraop
-epidural failure up to 25%
-SE of anesthestic-opioid: pruritis, nausea, urinary retention
-small risk of major compl: hematoma, abscess,
-lower exremity m otor blocks, uncommon but delay mobilization
nasopharynx innervation
maxillary branch of trigeminal nerve
oropharynx innervation
glossopharyneal nerve
superior laryngeal nerve external branch
motor innervation to cricothyroid
airway innervation
Pharmacokinetic compartment models
Movement of drugs b/w tissues w/i body
-central compartment (where drugs get injected to and where they get eliminated/metabolized)
3 phases:
-a step, rapid phase (slow and fast equilibrating compartments take the drug up from the central compartment)
-intermediate phase (fast equilibrated w/ central, but slow stil taking up the drug)
-flat slow elimination phase: all compartments equilibrating toward central compartment as it eliminates
Vd: sum of all the compartment volumes at equilibrium w/ drug
CYP2D6 inhibitors
SSRI: escitalopram, fluoxetine, or paroxetine, SNRIs, Histamine antag (Cimetidine), Chlorpromazine, amiodarone, quinidine
-dec conversion of codeine to morphine
Methadone MOA
racemic mixture w/ opioid analgesic and NMDA antagonist, also SNRI
Cause of malignant hyperthermia
mutation in the RYR1 gene coding for the ryanodine receptor (Ca channel)
-mutation causes abnormal, unregulated release of Ca iosn
muscle rigidity (masseter rigidity), inc O2 production
Malignant hyperthrmia
MH labs
lactic acidosis, rhabdomyolysis, inc CK, hyperK, myoglobinuria
Cyproheptadine
Tx for serotonin syndrome
-blocks serotonin and histamine receptors
Rigidity, hyperthermia, myoclonus, hyperreflexia
Serotonin syndrome
-also get nausea, vomiting, diarrhea
hyperthermia, rigidity, dysautonomia, mental status change
Neuroleptic malignant syndrome
-can tell apart from serotonin syndrome by hyperreflexia (in SS but not NMS)
Inc risk of Mg toxicity w/ pregnancy and preeclampsia
Renal insufficiency
-skip or lower loading dose in renal insuff
Inc risk of Mg toxicity w/ pregnancy and preeclampsia
Renal insufficiency
-skip or lower loading dose in renal insuff
-renal insuff if Cr > 1.1
Therapeutic range for Mg tx in preeclampsia
5-9 mg/dL
Mg toxicity symptoms if Mg < 7
Nausea, HA, lethargy, diminished deep tendon reflexes
Mg sym if Mg 7-12
-somnolence
-bradycarida, hypoTN
-EKG: prolonged PR, QRS and QT
-absent DTR
Sym if Mg > 12
muscle paralysis, resp failure, complete heart block
Sym if Mg > 15
cardiac arrest
Papilledema caused by what electrolyte disturbance
severe hypoCa
ST elevations caused by what electrolyte disturbance
severe hyperCa
acceleromyography
Quantitative nerve monitoring technique
-TOF ratio >.9 to .95 is considered full reversal
-most sensitive compared to qualitative and clinical maneuvers
Mechanomyography
Quantitative NM monitoring
-gld standard for measurement of blockage, but primarily used for research
how do BB slow disease progression in HRrEF
prevention of catecholamine cardiotoxicity
-HF -> dysregulated symp NS w/ inc circulating catecholamines -> adrenergic cardiotoxicity -> cardiac remodeling
-BB interrupt this vicious cycle
Hydralazine MOA, effect on HF
MOA: directly relaxes venous and arterial smooth muscle
-reduces afterload and myocardial work
Sacubitril MOA
Neprilysin inhibitors
-prevents breakdown of natriuretic peptides
Sacubitril effect on HF
Reduce sodium, volume retention, adverse cardiac remodeling
Dapagliflozin MOA
Sodium-glucose cotransporter 2 inhibitors
-promotes glucosuria and natriuresis
EKG changes hyperMg
prolonged PR, QRS duration, and QT interval
HypoK EKG changes
Flat or inverted T waves, U waves
HyperCa EKG changes
shortening of ST segment, can also in a few cases mimic MI w/ ST elevations
HyperCa EKG changes
shortening of ST segment
electrolyte abnormality
hypoK
Normal CBR
50 mL/100g/min
gray matter 80%
white 20%
Hyperthermia on CBF
b/w 37-42 CBR inc
>42 marked reduction in CBF b/c reduction in CMR
CO2 BP and CBF
25-75 CBR inc linearly w/ PaCO2 when normotensive
-when MAP is low, resp to PaCO2 attenuated, and w/ severe hypoTN no changes for PCO2
Infant cyanotic and HR 80 what next?
1st. warming, drying, stimulation
2nd. supplemental O2, suction and open airway
3rd. PPV, pulse ox 60-65% at 1 min, 85-95% by 10 minutes
4th. HR less than 60bpm compressions
5th Epi if no changes
what HR in infants do you start chest compressions
less than 60 bpm
breathing ratio in infants
3 compressions to 1 breath
when to use epi in newborn resuscitation
PPV, intubation, and chest compressions -> epi
APGAR score
HR, resp effort, reflex irritability, muscle tone, color
MOA HCTZ
inhibits Na/Cl transport in distal convoluted tubule
Chlorthalidone MOA
inhibits Na/Cl transport in distal convoluted tubule
-thiazide diuretic
HCTZ electrolyte changes
hypoNa, hypoCl alk, hypoK, hyperCa, and Hyperglycemia
What is phosgene
Phosgene is a chemical warfare agent that is regarded as a potential terrorist threat
-initially attacks type one and two pneumocytes ~> free radical release
-Secondary attack includes release of inflammatory mediators -> Prostaglandins cause vasoconstriction and platelet issues, bradykinin causes increased capillary permeability, thromboxane causes vasoconstriction, and compliment activating enzymes lead to attraction of leukocytes.
Phosgene treatment
Supportive therapy with steroids beta-2 agonist and prophylactic antibiotics (risk of secondary infection)
-Leuokotriene inhibitors and glutathione may lesson respiratory damage
How does phosgene act?
Colorless gas that dissolves slowly in water to form carbon dioxide and hydrochloric acid
-When liquid released, turns into gas stays close to ground and spreads rapidly
-allows phosgene to enter respiratory tissue without significant upper airway damage
-necrosis follows inflammation and airways and alveoli
-alveolar capillary leak produces pulmonary edema
-Can get hypoxia from intense laryngeal or bronchospasm
Blood and oxygen supply to the liver
-hepatic artery provides 25% of blood supply and 50% oxygen supply
-Hepatic vein provides 75% blood supply and 50% oxygen supply
TEE mid SAX view
transfastric midpapillary short axis view
blood supply in 4 chamber view
Which papillary muscle rupture is the most common
Postero medial papillary muscle because of single blood supply from right coronary or LAD
- Anterolateral papillary muscle rapture is less common because of dual blood supply from L a D and left circumflex artery
Effects of spinal anesthesia
Mostly from removal of sym innervation and unopposed parasym
-Cardiac: v and a dilation -> dec in preload and afterlaod
-renal: red in renal perfusion, urinary retention, give fluids
-GI: hyperperistalsis -> N/V and hypoTN to chemoreceptor trigger zone, and red in hepatic blood flor
Myosin – actin interaction with skeletal muscle contraction
- Myosin release from Actin
- Myosin extending attaching to actin through conversion of ATP to ADP (site must be open from calcium binding to troponin)
- Power stroke. ADP released from myosin causing myosin to rotate and move along Actin
- Actin relaxes
CHF and med changes
A. Furosemide
B. ACE inh or NG
C. Milrinone
D. Epi/NE
Medical direction versus supervision for medicare reimbursement
Direction: higher reimbursement than supervision
To meet qualifications for direction you must
-preanesthesic exam/eval
-anesthetic plan
-participate in most demanding procedures of anesthesia
-ensure procedures done by qualified individual
-monitor admin at frequent intervals
-be physically present and available for emergencies
-post anesthtic care
-ratio of CRNAs max 1:4
-can leave to go to OB epidural
-all can be done by different members of anesthesia team
-CANNOT leave to go to ED
when to use epi in PEA arrest
ASAP, w/i 1-3 minutes is ideal
when to use epi in shockable rhythms
defib then 2 min CPR then defib then EPI
IV PCA v on request
inc pt satisfcation, inc quality of analgesia, inc total opioid requirement, inc pruritis, equal resp depression (w/o continuous infusion)
Glucagon what is it and what does it affect
secreted by alpha-cells of pancreas in resp to hypoglycemia and inc alanine, inc epi and cortisol
-CAUSES: gluconeogenesis, glycogenolysis, lipolysis, and inhibits glycogenesis
Glucagon as a treatment for what toxicity
beta blockers
-inc cAMP -> inc intracellular Ca -> inc contractility and HR
What is deep hypothermic circulatory arrest and when to use it
Deep hypothermic circulatory arrest: cooling pt to 15C to 22C and global arrest of blood flow (w/o flow for CPB circuit)
-used for neuroprotection during operations of aortic arch or pulm thromboendarterectomy
when to use retrograde cardioplegia
obstructive CAD, aortic insufficiency, or procedures incolving manipulation/distortion of aortic valve or coronary ostia
Why use leukoreduced blood
decrease risk of alloimmunization (host antigens, important to avoid if need transplant), allergic rxns (soluble antigens in transfused blood cause mild allergic rxns), dec febrile non-hemolytic rxns, and dec risk of CMV (if immunocompromised)
MG and need for mechanical ventilation postop RF
-Disease > 6 years
-chronic resp illness
-pyridostigmine dose > 750 mg/day
-Vital capacity < 2.9L
RF for minimally invasive approach
-BMI > 28
-adv MG (bulbar involvement, slurred speech)
-prior myasthenic crisis
-assoc w/ pulm resection
Regardless of approach
-EBL >1L
-anti-ACh receptor tite > 100nmol/mL
-pronouned decremtal resp (18-20%) on low freq repeated n stimulation
“birds beak” appearance on pressure-volume loop
lungs are overdistended and further inc in pressure will not inc TV
detect venous air embolism in peds crani
precordial doppler ultrasound
-doppled probe placed over or R of sternum at 4th IC space, if prone b/w scapulae
detect venous air embolism in adults
TEE/TTE
EtCO2 venous air embolism
Moderate sensitivity
-consider dx if sudden drop in EtCO2 -> dec b/c air blocked blood flow and reflex pulm vasoconstriction
-wills tart to have physiological changes before EtCO2
treatment of venous air embolism
communicate to surgical team, rapid flood the field w/ saline
-reposition pt supine
-100% O2, d/c Nitrous oxide, give fluids
SE of TURP syndrome w/ glycine
transient blindness
-b/c glycine is inh NT in brainstem/cranial nerves
-breakdown into ammonia -> encephalopathy, N/V
normal saline and TURP
electrical current dispersion b/c balanced salt solution
TURP and sorbitol/mannitol
Sorbitol -> hyperglycemia
Mannitol ->intravsscular fluid expansion
both cause osmotir diuresis
MetHg pulse ox
85% b/c absorbs light at 660 nm and 930 nm equally
Pulse ox nm absorbion
660 nm deoxy absorbs
930 nm ox absorbs
MetHg tx w/ and w/o G6PD def
w/o: methylene blue
w/: Vitamin C (ascorbic acid)
What causes MetHg
Prilocaine, Benzocaine, Metochlopramide, nitrites (nitric oxide, NG)
-aniline dyes, benzene
-fhloroquine, dapsone, suflonamides
Methylene blue change in pulse ox
65% transiently for ~10 minutes
What pulse ox should be used in MetHg
Multi-wavelength co-oximetry
Composition of 1.8% Hetastarch
Na 308, Cl 308
(NS is 154 of each)
What’s only in plasmalyte and none of the otehr fluids
Acetate and gluconate
-acetate oxidized by liver, m and heart into bicarbonate
-gluconate converted to glucose
Considerations for anterior mediastinal masses
-NMB avoided -> maintain spontaneous ventilation (neg intrathoracic pressure helps keep everything open)
-use rigid bronch/ have 911 equipment available
-px ECMO cannulation in high risk pts
-sitting/semirecumbent positions improve vent mechanisms (avoid supine)
Type II error
Incorrect acceptance of the null hypothesis
-More likely to happen when the alpha value is decreased
-Also known as beta error
-Conventional set to 10% (because power is set to 90%)
-Decreased by increasing the sample size, increasing the expected effect size, and increasing the precision of a measurement, increasing power
Power experiment
1- beta (type II error), conventionally 90%
-if you increase, decreases type II error
Clomipramine MOA
Tricyclic antidepressant
Desipramine MOA
Tricyclic antidepressant
Doxepin MOA
Tricyclic antidepressant
TCA toxicity
-blocks Ca channels widening QRS (100ms or greater predicative of Vent arrhythmia)
-anticholinergic (tachycardia, mydriasis, hyperthermia), hypoTN, sz
treatment of TCA OD w/ EKG cahnges
sodium bicarb: perserve physiologic Na channel activity
-infuse continuously until QRS narrows
-IV lidocaine/Mg 2nd line
tx of TCA sz
Benzos
-b/c TCA inh GABA receptors -> benzos help potentiate GABA
what does the external branch of the superior laryngeal n innervate
cricothyroid muscle: tenses VC
laryngospasm reflex afferent and efferent
afferent: internal branch of the SLN
efferent: RLN
Phase I reactions (pharm)
oxidation, reduction, and hydrolysis
-goal is to make functional groups thatcan undergo phase II reactions
ex: cytochrome P450 aledhyde and alcohol dehydrogenase
-slower than phase II (if a drug does both, time for elimination dpt on phase I)
-nonsynthetic rxn
-MC occurs in liver
synthetic rxn()Phase II reactions (pharm)
use conjugating enzymes and result in formation of metabolites w/ inc mass (synthetic rxn)
-conjugation rxns using glucuronyl transferase, sulfotransferase, methylases -> form metabolite w/ increased affinity for aqueous environment (inc water-to-lipid partition coefficient)-> eliminated out of body
-faster than phase I
-MC occurs in liver
Des + dessicated CO2 absorbent makes
carbon monoxide and heat
-sevo, iso, and des all make CO, des makes the most) sevo makes the most heat
When is maternal cardiac output the highest
immediately after delivery (2.5x prepregnancy)
-less vena cava compression, uterine contraction causes autotransfusion, and less demand for blood flow to uterus
cardiac ouput and pregnancy
1st trimeser: HR inc, inc in CO by 40%
2nd and 3rd: SV inc, inc in CO by 50%
onset of labor: 110% inc in CO
highest: immediately after delivery
co inc 10% by 2 weeks postpartum
normal 24 weeks postpartum
what to avoid in methylenetetrahydrofolate reductase def
nitrous oxide
-b/c inhibits methionine synthetase -> homocysteine rises -> thrombosis and coronary events
Propofol and mitochondria
Propofol inhibits mitochondrial fxn so avoid in mitochondrial dx
-reason for propofol-related infusion syndrome
etomidate inhibits
11-beta-hydroxylase
cervical spine injury, HR to 22 w/ larygnoscopy why
unopposed vagal tone
-cardiac accelerators T1-T4 -> if injury above neurogenic shock -> severe bradycardia and hypoTN
Bainbridge reflex
stretch receptors in RA wall sense inc pressure -> inh parasympathetic activity -> inc HR
(if you’re crossing a bridge and a big wave is coming, rush the people faster trying to get them out of the way)
Hering-Breuer reflex
When subject to excessive stretching (CPAP/PEEP), pulm stretch receptors trigger the reflex -> prevents inspiration and allows expiration to occur
-no effect on HR
Autonomic hyperreflexia and SC
2-3 weeks after injury
-occurs when stimulation below level of spinal cord injury -> uninhibited symp stimulation
(above T5)
Treatment for acute dystonia reaction after metochlopramide + prochlorperazine
25-50 mg diphenhydramine
1-2mg benztropine
Net ATP production of aerobic and anaerobic respiration
Aerobic: 32
Anaerobic: 2
Aerobic Respiration Steps
Aerobic glycolysis: Glucose -> pyruvate + 2 ATP
-Pyruvate enters mitochondria to generate NADH -> oxidative phosphorylation in ETC to generate 30 ATP
-O2 final electron acceptor
Anaerobic resp
-where and steps
Cells that don’t have mitochondria (erythrocytes)
-Glycolysis -> pyruvate + 2 ATP
-Pyruvate converted to lactate for continued glycolysis to regenerate NAD+
- Can only occur for a limited time due to build-up of lactic acid and acidotic environment
**cannot do ETC b/c location or b/c O2 is final electron acceptor and is limited or absenti n anaerobic
Blood supply for anterolateral papilary muscle
LAD and LCx
LAD supplies blood to what part of the heart
1/2 of LA and LV (anterior aspect)
Branches off RCA
R marginal artery, PDA (R dom), AV nodal artery and sinoatrial artery
R marginal artery supplies what part of the heart
laterval RV and cardiac apex
PDA supplies what part of heart
posterior 1/3 of intraventricular septum, posterior inferior aspect of the heart and the posteromedial papillary muscle
ST elevations in I, aVL, and V5-V6 which artery issue?
L Cx or diagonal branch of LAD
Activation of which pathway causes bronchoconstriction
Act of M3 muscarinic receptors on airway smooth muscle
-influx of intracellular ionized Ca -> inc in smooth m tone and force -> bronchoconstriction
Predisposing factors to develop bronchospasm
hx of asthma, heavy tobacco smoking, active bronchial infxn (bronchitis)
Airway smooth muscle innervation and reflexes
Autonomic N system, basal tone is parasympathetic nerves in vagal centers, cholinergic neurons, M3 muscarinic receptor
-occasional nonadrenergic noncholinergic mechanisms activated by bronchopulm sensory C fibers (include tachykinis, vasoactive intestinal peptide) -> rare, minimal
-pure reflexive vagal stimuli -> bronchoconstriction is larger airways and more central
-beta 2 receptor important in relaxation: efflus of ionized Ca from cell -> SR relax muscles
What is responsible for the determination of dynamic airway resistance
Caliber of the small airways of the lung
Why does nitrous oxide cause air-containing spaces to expand?
Nitrous oxide diffuses from the blood to air-containing spaces faster than nitrogen can diffuse back out -> expansion
When ok to use nitrous oxide in laproscopic surgery
if case is short, no effect on surgical visualization
Nitrous oxide PONV
does not increase risk when used for less than 1 hour
Metabolism in volatile anesthetics
Oxidation mediated biotransformation by cyto CYP2E1 renal and hepatic
Sevo 5% > Iso .2% > Des .02%
-Des/Iso have highly reactive intermediates that bond w/ hepatic proteins -> Ab form against metabolite-hepatic protein complex -> on 2nd exposure Ab activate and cause destruction of liver (still less than halothane)
-Sevo has a 4-6x higher rate of release of fluoride ions during metabolism -> still nopostop renal dysfxn
-nitrous oxide is not metabolized
Nitrous oxide and metabolism
not metabolized, no significant biotransformation in the body
-inhibit methionine synthase by oxidizing cofactor B12 -> hematologic and neuro dysfxn -> inc homocysteine -> vasc inflammation and inc risk of thrombosis
Partial pressure of gases w/ ABG syringes at higher of lower than room temp
-As temp decreases, partial pressure of O2 and CO2 will decreases
-if pt is hypothermic and blood gas is warmed -> ABG will have a higher partial pressure of O2 and CO2
-if pt is hyperthermic and blood gas is cooled -> results will be a lower partial pressure of O2 and CO2
Complication of decrease phosphorous level
Decreased O2 delivery to tissues
-dec P -> dec 2,3-DPG -> L shift of Hg curve -> dec O2 delivery to tissues
-dec in diaphragmatic contraction (dec ATP stores) -> resp compromised and difficulty in weaning off vent (dec FVC)
-profound (<1) -> RBC membrane not stable -> hemolytic anemia, cardiac failure, nero symp b/c dec ATP stores
How does CO2 exist in the body? majority is in what form?
Majority: Bicarbonate ions
-other: dissolved CO2 and with protein as carbamino compounds
MOST likely to predict for difficult intubation
Class 3 upper lip bite test (can’t bite their upper lip w/ their lower teeth at all) >60% likelihood of difficult intubation
-short hyomental distance, impaired neck mobility and high mallampati are only moderate predictors, ULBT was better
What happens if using too much NS in a kidney transplant
hyperK (b/c of non-AG hyperchloremic metabolic acidosis)
-coagulopathy (dilutional plus acidosis worsens)
-dec renal and gastric perfusion
Eaton-Lambert Syndrome cause and symp
Ab: presynatpic VG Ca channels
sym: proximal m weakness, autonomic dysfxn, constipation, dry mouth, erectile dysfunction, dec sweating, orthostatic dysregulation
Eaton-Lambert and NMB
Sensitive to BOTH dep and nondepolarizing paralytics
-no response to cholinesterase inhibitors
Lambert assoc w/ what disease
Small cell lung carcinoma
Myasthenia Gravis Ab and symp
Ab: postsynaptic ACh receptors
-extraocular m weakness (ptosis, diplopia, blurred vision), bulbar m weakness, proximal m weakness, resp weakness
MG and resp to NMB
resistant to dep (use 1.5-2 mg/kg)
sensitive to nondep
MG and assoc dx
Thymoma
paresthesia in thumb and lateral surface of forarm and upper arm, weakness w/ flexion and supinatio of forearm, external rotation of arm, abduction of arm, and wrist extension. Where is the injury?
brachial plexus neuropathy
midback pain, sudden, severe, point tenderness over vertebrae
most likelyl dx and imaging?
Compression fx
initial: lateral radiography of thoracic and lumbar spine
Why 4 hours NPO time for breast milk and 2 hours for clear liquids
higher gastric residual volume w/ breast milk than clear liquids
**why NPO guidelines are the way they are, ALWAYS gastric residual volumes
postoperative vision loss causes and which is MC
retinal artery occlusion, ischemic optic neuropathy, acute glaucoma
-ischemic optic neuropathy is MC
RF for postop vision loss
prone positioning, long surgical length (5 hours or more), obesity, male sex, significant blood loss, external ocular compression, wilson frame use (looks like a half circle under your torso)
-hypoTN alone is not, hypoTN due to blood loss >1L can be
anterior v posterior ischemic optic neuropathy
anterior: common post cardiac surgery
posterior: more common post prone surgeries
If you put an iso vaporizer on the top of a mountain, what will change in output and what wont’?
won’t change: partial pressure of iso (what vaporizer is set to)
will: inc in volume % conc of inhaled anesthetic leaving vaporizer, inc volume of iso entrained by 100 mL of O2, barometric pressure decreases
Des vaporizer and altitude changes
Dual gas blender vaporizer: constant conc of vapor output and not constant partial pressure -> at higher altitudes, will need to inc des vaporizer to maintain same partial pressure
BIS: GA target, burst suppression, sedation
sed: 80
GA: 40-60
BS: 20
0: flatline EEG
BIS & temp
BIS goes down 1.12 units for each 1 C red in body temp (dec CRMO2)
What meds cause BIS to increase
ketamine, nitrous oxide
RF for PPH
c/s, induction of labor, augmented labor, multiple gestations, macrosomia, polyhydramnios, prolonged labor, adv maternal age, HTN or DM in mother, tocolytic meds
SE of oxytocin
powerful vaso constriction in umbilical arteries, veins, and coronary vessels
-hypoTN, tachycardia, and coronary vasoconstriction -> MI
Options for uterine atony and SE
oxytocin: hypoTN, tachycardia, coronary vasoconstriction
methylergonovine: HTN
misoprostol (prostaglandins): bronchospasm
What types of births should oxytocin be given to postpartum?
all of them (ppx for uterine atony)
Cardiovascular effects of ECT
-initial parasymp resp: transient bradycardia -> symp resp from sz: tachycardia and HTN
-sym surge can inc myocardial O2 demand -> MI in some pts
-EF dec for 6 hours following ECT
ECT and CNS effects
inc CMRO2, inc CBF, inc ICP
-MC: disorientation, impaired attention and memory deficits
Lusitropy
rate of active myocardial relaxation
-if POSTIVE lusitropy -> inc LVEDV for a given EDP
(more compliant ventricle w/ greater rate of relaxation)
-shift to A is POSTIVE, shift to B is NEGATIVE
Inotropy def and PV loops
myocardial contractility
-slope of the end-systolic pressure-volume relationship
-POSTIVE is D, NEGATIVE is C
normal EDV and ESV, SV
EDV: 120, ESV: 40-50 mL
SV: 70-80 mL (normal EF is 60-67%)
factors that inhibit hypoxic pulm vasoconstriction
Vasodilator (NG and nitroprusside)
Acetazolamide
phosphodiesterase inhibitors (sildenafil, tadalafil)
ACE inh
metabolic alkalemia
Hypocarbia, hypothermia
Infxn
SEVOFLURANE (modestly by dilating pulm vascular beds at > 1 MAC) usually not clinically relevant
Cistatracurium degradation
spontaenously degrades in plasma by Hofmann elimination and ester hydrolysis
onset 4-6 min, duration 20-50 min
Mivacurium degradation
butrylcholinesterase or plasma cholinesterase or pseudocholinesterase
Succinylcholine degradation
butrylcholinesterase or plasma cholinesterase or pseudocholinesterase
ASA basic physiologic standard monitors
oxygenation: O2 analyzer w/ low O2 conc limit alarm, pulse ox
ventilation: EtCO2 w/ audible alarm, disceonnection alarm
circulation: ECG continously, BP q5mins
temp: when temp changes are anticipated
Normal CVP waveform
a: atrial contraction
c: tricuspid valve elevation into the R atrium
x: downward movement of the contracting RV
v: back pressure wave from blood filling the right atrium
y: tricuspid valve opens in early ventricular diastole
what change in CVP waveform for pt w/ a fib
loss of a wave and prominent c wave
-contractions less effective b/c not synchronized w/ ventricular activity
when do you get a loss of x descent in CVP
tricuspid regurgitation
-due to abnormal systolic filling of RA
When is y descent lost
tricuspid stenosis
-atrial emptying impaired
MOA of gabapentin
binds to calcium channel alpha 2 delta subunit of VG Ca channels
-decrease glutamate release -> dec production of substance P
