208 terms


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Halothane side effects (2)
(1) fulminant hepatic necrosis
(2) sensitization of the myocardium to the dysrhythmogenic effects of catecholamines.
Methoxyflurane side effect
dose related nephrotoxicity
Enflurane side effect
evidence of seizure activity on EEG
- MAC 1.2%
-Less toxicity, more rapid onset and faster awakening than earlier volatile gases
Halogenated exclusively with flourine
Sevoflurane and desflurane
minimum alveolar concentration of anesthetic required to suppress movement to a surgical incision in 50% of patients
Inhaled anesthetic mechanism of action
Enhances inhibitory ion channels leading to hyperpolarization of the neuron and blocking the function of excitatory ion channels preventing depolarization
Variable bypass vaporizer
- two streams of inflowing fresh gas - one contacting the reservoir (sump) and the other bypassing the sump
halothane, sevoflurane and isoflurane
Tec 6 vaporizor
special vaporizer for desflurane
compound A
produced from breakdown of sevoflurane and is nephrotoxic after prolonged exposure
airway anatomy
Standard deviation of MAC
10%: so 1.1 MAC should be effective for 95% and 1.2 should be effective for 99% of the population.
concentration effect
The higher the concentration of gas administered, the faster the alveolar concentration of that gas approaches the inspired concentration. In modern practice is only relevant for nitrous oxide since other inhaled anesthetics are delivered at much lower concentrations due to their higher potency.
second gas effect
When a constant concentration of an anesthetic like halothane is inspired, the increase in alveolar concentration is accelerated by concomitant administration of nitrous oxide, because alveolar uptake of the latter creates a potential subatmospheric intrapulmonary pressure that leads to increased tracheal inflow
high blood-gas partition coefficient
a large amount of anesthetic must be dissolved in the blood before the Pa equilibrates with the PA
Inhaled anesthetics effect on MAP
- decreases due to decr SVR with desflurane, sevoflurane, isoflurane
- decreases due to decr CO w/halothane
- stable ti incr MAP w/Nitrou Oxide
Desflurane circulatory effects
Above 1 MAC causes transient circulatory stimulation (seen to a lesser extent with isoflurane, abrupt increase in sevoflurane is associated w/slight decrease in HR)
propofol induction dose and duration
1-2.5 mg/kg, 8-10 minutes
etomidate dose
0.2-0.3 mg/kg
ratio of fractional concentration of alveolar anesthetic to inspired anesthetic (FA/FI)
• Uptake into the bloodstream is the primary determinant of FA
• The greater the uptake (in blood), the slower the rate of rise of FA/FI
• The gases with the lowest solubilities in blood (i.e. desflurane) will have the fastest rise in FA/FI
Nitrous oxide
• Low potency (MAC 104% - can never reach 1 MAC!)
• Insoluble in blood
- Facilitates rapid uptake and elimination
-- used as adjunct
• Half as potent as isoflurane (MAC 1.8%)
• Lowest blood:gas solubility coefficient (lower than N2O)
• Very fast uptake and elimination
• Low potency (MAC 6.6%)
(1) MAC-Awake (a.k.a. MAC-Aware)
(3) MAC-EI
(1) - The MAC necessary to prevent response to verbal/tactile
- Volatiles: ~0.4 MAC; N2O: ~0.6 MAC
(2) - The MAC necessary to blunt the autonomic response to a noxious stimulus
- ~1.6 MAC
(3) - The MAC necessary to prevent laryngeal response to
endotracheal intubation
- ~1.3 MAC
(Neosynephrine) = alpha 1 receptor agonist (start at 100 mcg)
- Direct vasoconstrictor
- Use in vasodilated state with tachycardia
- Will cause reflex bradycardia
•Ephedrine = alpha 1, beta 1, and beta 2 (less so) agonist (start at 5 mg)
- Direct and indirect adrenergic stimulation via NE release
- Use in vasodilated, bradycardic, low CO states
neostigmine dose (glyco dose)
40-5- mcg/kg (20% of neo dose)
thoracic vertebra anatomy
spinal epidural landmarks
(+ interspinous ligament)
caudal anesthesia
sacral hiatus is in the sacrococcygeal ligament (missing in 8% of adults)
landmarks in spinal anesthesia
- C7 is spinous process at the lower end of the neck.
- iliac crest is at L4
-T7-T8 at at lowerlimits of the scapulae
-L2 terminal portion of 12th rip
-S2 is posterior iliac spine
(spinal cord terminates at lower border of L1 in adults)
Artery of Adamkiewicz
enters vertebral canal through the L1 intervertebral foramen. Blood supply to lower two thirds of the spinal cord (damage causes anterior spinal artery syndrome of bilateral lower extremity motor loss)
oculocardiac reflex - most often encountered during strabismus surgery, or eye regional anesthetic nerve block. Hypercarbia, hypoxemia and light planes of anesthetic depth augment
strabismus surgery
- high incidence of intraoperatice OCR
- increased risk for malignant hyperthermia
- marked prevalence of postoperative nausea and vomiting
-vagal stimulation of the superior laryngeal nerve
-Tx: 100% oxygen, deepen anesthesia, small doses of succinylcholine (0.25 to 0.5 mg/kg)
Spinal location
Allowable blood loss calculation
ABL= [EBV x (Hi-Hf)]/Hi
- EBV = kg x ABV
- ABV men = 70
- ABV women = 60
EKG intervals:
PR 0.12-0.20 sec
QRS 0.06-0.10 sec
QT < 0.4 sec
Hemodynamic variables
Pulmonary artery waveform
CVP waveform
abnormal CVP
-tricuspid regurge, stenosis, afib, ASD, restrictive pericarditis, 1st degree HB, complete HB
dibucaine number
- inhibits the activity of normal pseudocholinesterase
- identifies individuals with substitution on the butryl cholinesterase enzyme (does not inhibit these abnormal enzymes)
- 80 percent inhibition and above is normal
- 40-60 is heterozygous
- 20 is homozygous - abnormal
defasciculating dose of Roc
0.03 mg/kg 3 min prior to sux
Two classes of non-depolarizing NMBA
(1) benzylisoquinoliniums "uriums"
(2) aminosteroids "oniums"
Alveolar gas equation
-Arterial O2 content
-venous O2 content
CaO2 = (Hb x 1.36 x SaO2/100) + (PaO2 x 0.003)
- nml = 20 ccO2/dl
CvO2 = (Hb x 1.36 x SvO2/100) + (PvOx x 0.003)
O2 delivery
DO2 = CO x CaO2
- nml = 1 L 02/min
Fick equation
= O2 consumption
= VO2 = CO x (CaO2-CvO2)
-nml = 250 ccO2/min
O2 extraction ratio
ER(O2) = VO2/DO2 x 100
- nml 22-30%
oxygen consumption
250 mL/min
FRC and lung volumes and capacities
atmosphere components
E gas cylinder capacity
(E is standard transport cylinder size)
O2 - 625-700L = 1800-2200 PSI
Air - 625-700L = 1800-2200 PSI
N2O - 1590L = 745 PSI
remaining time for O2 in a cylinder calculation
time in hours = PSI/(200 x flow rate in L/min)
Poiseuille's law
capnography waveform
curare cleft
caused by lack of synchrony between diaphragm and intercostal muscles in a patient who has received neuromuscular-blocking agents and in whom muscle strength is returning
arterial O2 saturation measurement vs
SaO2 = HbO2/(HbO2 + HHb + metHb + COHb)
HbO2 = oxyhemoglobin
HHb = deoxyhemoglobin
metHB = methemoglobin
COHb = carboxyhemoglobin
functional oximetry measurement
SpO2 = (HbO2/(HbO2 + HHb)
pulse oximeter (also effect of COHb and metHb)
HHb absorbs light in the red band (600 - 750 nm) and HbO2 absorbs light in the infrared band (850 - 1000)nm. Pulse-ox probe emits light at 660 nm and 940 nm. Because there is additional blood during systole the pulse ox isolates blood during this phase and measures only arterial blood.
- COHb is interpreted as 90% HbO2 and 10% HHb and will overestimate SaO2 in someone exposed to CO
- metHb is dark and absorbs equal amount of red and infared which will extrapolate to 85% (caused by sodium nitroprusside, antimalarial agents, nitroglycerine, nitrites and nitrates)
MAC to prevent awareness
NMBA inhibit which receptors?
acetylcholine nicotinic receptors
Preganglionic sympathetic neurotransmitter
Postganglionic sympathetic neurotransmitter
NE (except sweat glands and blood vessels in muscles: Ach)
Postganglionic parasympathetic neurotransmitter
percentage of blockade possible w/normal tidal volume vs headlift
80% vs 30%
arterial oxygen content
CaO2 = (Hb x 1.39 x SaO2/100) + (PaO2 x 0.003)
oxygen consumption (Fick Principle)
VO2 = CO x C(a-v)O2
apprx 250 mL/min for an adult
oxygen delivery
DO2 = CO x CaO2
oxyhemoglobin dissociation curve
Hb 50% saturated at 26.7 mmHg
Haldane effect
deoxygenated blood has a greater cpacity to carry CO2 than does oxygenated blood
2 types of local anesthetic
3 important aspects of local anesthetics:
(1) lipid solubility - effects potency
(2) pKa - effects onset
(3) protein binding - effects duration of action
useful pressers in PAH
(1) vasopressin increases SVR without increasing pulmonary artery pressure
(2) norepinephrine increases SVR more than PVR
malignant hyperthermia
unexplained rise in end-tidal CO2 with unexplained tachycardia. Temperature rise is late feature (DDx includes thyroid storm)
autonomic nervous system and neurotransmitters
autonomic nervous system and neurotransmitters
2 most common sympathomimetics
(1) phenylephrine - direct acting - stimulates alpha 1 receptors. Reflex bradycardia common
(2) ephedrine - indirect acting - produces norepinephrine release -stimulates alpha 1 and beta 1. Repeated doses cause tachyphylaxis. Should not be used with tricyclic antidepressants, MAOi, acute cocaine intoxication (can cause severe hypertension)
nonselectibe beta blocker, also has selective alpha 1 blocking properties and is potent antihypertensive.
alpha blockers
results in vasodilation, non-selective have reflex tachycardia. Selective alpha blockers = prazosin
Non selective alpha blocker = phentolamine and phenoxybenzamine
muscarinic antagonist
mydriasis, bronchodilation, increase in heart rate, inhibit secretions, central acting can cause delerium.
Atropine, scopolomine, glycopyrrolate (peripheral acting), ipratropium bromide
intraoperative management of pheo
Pts are volume deplete and at risk for severe hypertensive crises. Need alpha blockade and rehydration. Phenoxybenzamine is commonly used. Beta blockers administered after alpha blockers, often labetolol. Intraoperative hypertension infuse phentolamine or nitroprusside
normal FRC
1.7-3.5 L
closing capacity
Volume during expiration where small airways close:
1/2 FRC while standing
2/3 FRC while supine
CC = FRC in the supine individual at 44 yo
CC = FRC in the standing individual at 66 yo
alveolar gas equation
PAO2 = FiO2(Pb - PH2O) - PaCO2/RQ
Pb = 760 at sea level
PH2O = 47
RQ = 0.8
at sea level on room air PAO2 = 99.7
FRC under general anesthesia
reduce by 400 mL
supine decreases it by another 800 mL
anatomic dead space in adult spontaneously breathing
2 mL/kg
= ratio of physiologic dead space to tidal volume = nml is 33%
= (alveolar PCO2 - expired PCO2)/alveolar PCO2
shunt fraction
Qs/Qt = (CiO2 - CaO2)/(CiO2 - CvO2)
CiO2 = ideal arterial oxygen concentration
CaO2 = arterial oxygen content
CvO2 is mixed venous oxygen content
oxygen content of blood
CaO2 = 1.34 x hgb x SaO2 + (PaO2 x 0.003)
CO2 and breathing
CO2 (indirectly) and hydrogen ions (directly) work on the chemosensitvie areas in the brainstem. CO2 is a stronger regulator than O2
O2 and breathing
interacts with peripheral chemoreceptors located in the carotid and aortic bodies.
henderson-hasselbalch equation
henderson-hasselbalch equation
anion gap metabolic acidosis
lactice acid, ketones, toxins (ethanol, methanol, iron, salicylates, ethylene glycol, propylene glycol), uremia
acid-base compensation formulas
Using PaCO2 of 40 and HCO3 of 24 as baseline
- resp acidosis (acute) = HCO3 increases by 0.1, pH decreases by 0.008
- resp acidosis (chronic) = HCO3 increases by 0.4
-resp alk (acute) = HCO3 decreases by 0.2, pH increases by 0.008
- resp alk (chronic) = HCO3 decreases by 0.4
-met acidosis = PaCO2 decreases 1 - 1.5
- met alk = PaCO2 increases 0.25 -1
what is pH?
negative logarithm of the hydrogen ion concentration (normally 40 nmol/L). The negative log of this value is 7.4
correct AG with a hypoalbumiemia
Corrected AG = observed AG + 2.5 x (normal albumin - observed albumin)
Serem osms calcualtion
2(Na) + glc/18 + BUN/2.8
hypotension and blood loss
30% of blood volume lost before hypotension
coronary distribution
coronary artery distribution
-RCA system dominant in 80-90% of people
-Supplies RV, SA node, AV node. Terminates in posterior descending artery (PDA) in 84% of people
-Left main artery divides into circumflex and left anterior descending - supplies septum and LV wall.
- When circumflex ends in PDA it is a left dominant circulation - left coronary supplies AV and septum.
- 40% of people circumflex supplies SA
coronary blood flow
225 mL/min = 5% of CO
myocardial oxygen demand
-wall tension (T) and contractility
-T = PR/2h (pressure x radius/2 wall thickness
3.6 mL/kg/min oxygen uptake.
Ability to climb 3-4 flights of steps = 4 METs
ST segment depression or elevation, T wave inversion, Q wave = old MI
- changes in II, III, AVF = RCA
- changes in I and AVL = circumflex
- changes in V3, V4, V5 = LAD
Vitamin K dependent factors
II, VII, IX and X
-factor VII has shortest half life, used in extrinsic pathway only
Warfarin mechanism of action
Competes with vitamin K for binding sites on hepatocytes. Administration of vitamin K reverses deficiency in 6-24 hours.
FFP can be administered for immediate hemostasis
Heparin mechanism of action
Accelerates interaction between ATIII and factors II, X, XI, XII and XIII, neutralizing the factors. Its half life is 90 minutes. Pts who are ATIII deficient are resistant to heparin
Different coagulation tests
- platelet phopholipid added to measure intrinsic pathway
- tissue thromboplastin added to measure extrinsic pathway
cryoprecipitate contents
factor VIII, vWF, fibrinogen, and factor XIII
- one unit per 10 kg of body wt increases fibrinogen by 50 mg/dL
innervation of the larynx
Laryngeal nerves are branches off Vagus
-internal branch of superior laryngeal = sensory above vocal cords
-external branch of superior laryngeal = motor to cricothyroid muscle and tensor of vocal cords.
-recurrent laryngeal = sensory below vocal cords and motor to posterior cricoidarytnoid muscles (abductors of vocal cords) - cough reflex
-glossopharyngeal (CN IX) = innervates the valecula - gag reflex
(arteries are superior laryngeal and inferior laryngeal - branches of thyroid artery)
Narcan dose
increcmental doses of 40-80 micrograms to a cummulative dose of less than 400 micrograms
Opioid receptors
MOR receptor functions
mu1 = analgesia
mu2 = respiratory depression
mu3 = opioid induced immune supression
opioid endogenous receptors
methadone receptors
opioid analgesic and antagonists at the NMDA receptor (there fore it is clinically useful in reducing opioid tolerance and opioid-induced hyperalgisia
tramadol receptors
opioidergic and monoaminergic activity at the doral horn spinal synapses of the nociceptive pathways
potent analgesic with reduced GI and CNS side effects. Active at the MOR at spinal and supraspinal sites and as a norepinephrine reuptake inhibitor at the spinal cord.
pain pathway
Thalamic nuclei receive the nociceptive inputs and pass the information to key brain pain reception sites such as the periaqueductal gray (PAG), amygdala and somatosensory cortex.
Activation of MOR sitmulates analgesia by activating descending inhibitory pathways.
Opioid-induced hyperalgesia: seen with remifentanil. Attenuated by morphine (0.1 to 0.25 mg/kg) 45 - 60 minutes before remi turned off. Or low dose ketamine drip 10-30 mg/hr
lipophilic vs hydrophilic opioids
lipophilic: fentanyl and sufentanyl
hydrophilic: morphine and meperidine
Lipophilic opioids penetrate faster and achieve higher conc into the spinal cord.
Three aspects of opioid metabolism:
(1) meds that inhibit or induce the CYP450 system may increase or decrease the clinical effect of oioids
(2) opioid metabolites may either b e active or inactive
(3) genetic variation in CYP system has clinical implications
morphine metabolism
phase II (conjugation to specific substrate): turns into M3G and M6G (60% into M3G - no clinical effect). M6G (5-10%) has full clinical effect but it is not relevant in healthy patients. In pts with renal failure, M6G can accumulate
piperdine metaboism
- includes fentanyl, alfentanil, sufentanil and remifentanil
- cross BBB
- alfentanil metablized by CYP3A4 and 5
- metabolized by cytochrome P450 system
- remi metabolized by tissue nonspecific esterases
methadone metabolism
- CYP2B6 - because of pharmacogenetic variablility there is a varied response to the drug
-the delay between peak drug concentration and the peak concentration at the effect site
-described by the plasma-effect site equilibrium constent
gene causing phenotype of red hair, fair skin and increase in MOR analgesia
MC1r gene
codeine metabolism
CYP2D6 to active metabolite of morphine.
- pts with out CYP2D6 have no response
- ultrarapid CYP2D6 metabolizers causes codeine intoxication
rapid equilibrium
= higher diffusible fraction - the proportion of drug that is uionized and unbound, and high lipid solubility
E size oxygen tank
contains 625 L of oxygen at a pressure of 2000 psi
E size nitrous tank
-Will remain at 750 psi until all the liquid nitrous oxide has been used = 75% of the contents
-hold 1590L - when gage begins to drop it has about 400 L left
Endogenous opioids
Endorphin, enkephalins, dynorphins
Opioid agonist-antagonist
Pentamidine, but orphaned, buprenorphine, nalbuphine
Peripheral opioid antagonist that doesn't cross the blood brain barrier. Used to prevent constipation in palliative care opioid use.
Mu agonist and NMDA receptor antagonist, can prolong QT
Codeine analog, acts on mu, kappa and delta also a norepinephrine and serotonin reuptake inhibitor, moderate analgesic without as bad side effects by van lower seizure threshold.
Weak local anesthesia properties, can cause tachycardia, can act on kappa receptors to reduce post-op shivering, contraindicated in pts taking MAOis
Opioid MOA
Bind to Rexed lamina II (substantia gelatenosa) in dorsal horn. Of spinal column. Mu receptors reduce visceral and somatic pain via GABA pathway, kappa reduce peripheral pain via inhibition of substance P
Opioids and cancer
Opioids inhibit cell mediated and humoral immunity in animal models this increases cancer cell growth
metabolism of local anesthetics
- esters undergo hydrololysis by pseducholinesterases
- amides undergo enzymatic biotransformation in the liver.
- lungs also play apart in extracting lidocaine, bupivicaine and prilocaine.
- chlorprocaine has rapid hydrolysis (less likely to cause toxicity)
local anesthetic potency
- determined by solubility (the more soluble, the more potant)
local anesthetic duration
- greater the protein binding, the longer the duration of action.
local anesthetic onset time
- determined by the degree of ionization: the closer the pKA to tissue pH the more rapid the onset time.
max dose of local anesthetic
- lidocaine = 5 mg/kg (7 with epi)
-bupivicaine = 2.5 mg/kg
- procaine = 7 mg/kg
treatment of systemic toxicity of local anesthetic
- 20% lipid, initial bolus of 1.5-2 ml/kg up to 8 ml/kg
- infusion rate of 10ml/min
double lumen endotracheal tubes
- note that the right upper lobe bronchus take off.
local anesthetic associated with methemoglobinemia
transient neurologic symptoms
-seen with lidocaine when used in spinal anesthesia
-seen especially with lithotomy
bronchospasm treatment
subcue epi 300 micrograms q 20 min
1:200,000 of epi means?
1 gram in 200,000 mg = 0.005 mg/ml
(1:100,000 = 0.01 mg/ml, 1:50,000 = 0.02 mg/ml)
effect of altitude on vaporizers
x' = x(p/p')
x' = output in volume percent at new altitude
x = volume percent at altitude calibrated at
p' = new altitude pressure
p = altitude at calibration
how much L of nitrous remain when pressure gage drops below 750?
400 L
spinal vs epidural (vs caudal)
- spinal is an injected in the subarachnoid space at the lumbar region - faster, easier, more intense block. Spinal influenced by kyphosis and lordosis.
- epidural is outside the dural sac anywhere along the nueraxis - greater control over intensity, segmental block
- caudal is an epidural into the caudal epidural space through the sacral hiatus.
What the body does to the drug
What the drug does to the body
4 components of pharmacokinetics
(1) absorption (2) distribution (3) metabolism (4) elimination
Local anesthetic used for Spinal Anesthesia
(1) Lidocaine 5% (diluted to 2.5%): T10: 40-50mg, T4: 60-75mg, onset 2-4 min lasts 45-75 min (epi not recommended)
(2) Tetracaine 0.5%: T10: 8-10mg, T4: 12-15mg, onset 4-6 min lasts 60-120 min (120-180 with epi)
(3) Bupivicaine 0.5-0.75%: T10: 8-10 mg, T4 12-15 mg, onset 4-6 min lasts 60-120 min (epi not recommended)
250-300 mL, hematocrit of 70-80%
1 unit increases hgb by about 1 g/dL
crystalloid for blood loss
give 3x the amount of blood loss
cryo uses
hemophilia A and treatment of hypofibrinogenemia
oxygen dissociation curve
heparin mechanism of action
- Heparin potentiates the activity of antithrombin (AT, formerly AT-III), an endogenous serine protease inhibitor that irreversibly binds various coagulant enzymes, such as thrombin and factor Xa. Heparin enhances AT-mediated inhibition of coagulant enzymes more than 1,000-fold by reducing the half-life of the enzymes and by promoting their binding with AT through induction of a conformational change in AT
warfarin mechanism of action
- Warfarin decrease blood coagulation by inhibiting vitamin K epoxide reductase, an enzyme that recycles oxidized vitamin K1 to its reduced form after it has participated in the carboxylation of several blood coagulation proteins, mainly prothrombin and factor VII. Despite being labeled a vitamin K antagonist, warfarin does not antagonize the action of vitamin K1, but rather antagonizes vitamin K1 recycling, depleting active vitamin K1
Pulmonary Hypertension definition
One of the following:
PA systolic pressure > 35mmHg
Mean PA pressure > 25mmHg at rest
Mean PA pressure > 30mmHg during exercise
Parasympathetic nervous system arises from which nerves
CN III, IV, IX, X and sacral segments
Neuromuscular transmission
- action potential of a nerve causes an influx of calcium into the nerves cytoplasm
- influx of calcium releases ACh
- ACh binds to the nicotinic receptor made up of 2 alpha units, a beta unit, a gamma unit and an epsilon unit. ACh binds only to the alpha and each subunit must be bound
- This opens an ion channel: Na and Ca go in and K goes out
- When enough ACh receptors are occupied the perijunctional membrane depolarizes: sodium channels open and the action potential is propagated releasing calcium from sarcoplasmic reticulum causing actin and myosin to interact and the muscle to contract.
- ACh is hydrolyzed by acetylcholinesterase
Depolarizing muscle relaxant mechanism of action
- Resemble ACh and readily bind ACh receptors but are not broken down by AChesterase so their concentration does not fall as rapidly resulting in a prolonged depolarization at the muscle plate
- Continous end-plate depolarization causes muscle relaxation because sodium channels rapidly inactivate with continuing deplarization.
- The end plate cannot repolarize as long as the muscle relaxant is bound: this is called a phase I block.
- After a period of time, prolonged end-plate depolarization can cause poorly understood changes in the ACh receptor that results in a phase II block (which clinically resembles that of nondepolarizing muscle relaxants
Nondepolarizing muscle relaxant mechanism of action
- Bind to ACh but do not cause a conformational change: they just block the binding site so ACh can't bind and cause a depolarization
myasthenia gravis and muscle blockade
essentially causes a down-regulation of ACh receptors and resistance to depolarizing neuromuscular blockade and increased sensitivity to nondepolarizing agents
muscle denervation injuries and muscle blockade
essentially cause decrease in ACh release and upregulation of ACh receptors, this causes an exagerated response to depolarizing neuromuscular blockade but a resistance to nondepolarizing agents
forms tight 1:1 complexes with steroidal nondepolarizing agents (vec and roc) rendering them inactive
Dibucaine number
Normal is 80%, homozygote for abnormal allele has a dibucaine number of 20
electrolyte abnormalities that potentiate a nondepolarizing blockade
-hypermagesemia (competes with calcium at the motor end plate)
Barbituate mechanism of action
Bind and potentiate the action of GABA(a) increasing the duration of openings of a chloride-specific ion channel
Lipid soluable barbituates (thiopental, methohexital, thiamylal) onset and duration of action
- Onset 30 seconds, last 20 minutes,
- has high lipid solubility, and a high non-ionized fraction which outweighs the fact that it is highly protein bound
- Duration is determined by re-distribution
- Elimination half life is 10-12 hours
- Eliminated via hepatic oxidation
Hemodynamic changes with barbituate induction
- decrease in BP, increase in HR
- Decrease in BP and CO may be dramatic due to uncompensated peripheral pooling of blood and directmyocardial depression
Benzos mechanism of action
-Bind GABA(a) and increase the frequency of openings of the associated chloride ion channel
Midazolam and kidney failure
-may lead to prolonged sedation in patients receiving larger doses due to the accumulation of the conjugated metabolite alpha-hydroxymidazolam
Benzos and cardiovascular effects
-slight decrease in arterial BP, CO and PVR (midaz more than diaz)
Ketamine mechanism of action
- NMDA (subtype of glutamate receptor) antagonist
- dissociative anesthetic: dissociates the thalamus from the limbic cortex (thalamus relays sensory impulses from RAS, limbic cortex is involved in awareness of sensation).
Etomidate mechanism of action
-Binds GABA(a) receptor and increases the receptor's affinity for GABA.
- may have disinhibitory effects on the parts of the nervous system that control extrapyramidal motor activity (which may explain the incidence of myoclonus with induction
Propfofol mechanism of action
- Increases binding affinity of GABA for the GABA(a) receptor
Opioid mechanism of action
-inhibit adenylyl cyclase (reduce cyclic AMP) and activation of phospholipase C.
-inhibit voltage-gated calcium channels and activate potassium channels
- inhibits the pre-synaptic release and the postsynaptic response to excitatory neurotransmitters (Ach, substance P) from nociceptive neurons
-what the body does to the drug
-what the drug does to the body
alfentanil vs fentanyl
-alfentanil has a more rapid onset and shorter duration even though it is less lipid soluble
-has high non-ionized fraction and small volume of distribution
Glutamate receptors
AMPA, Kainate, NMDA
Result in flow of sodium or calcium across channels generating an action potential
Airway innervation
1. anterior tongue: trigeminal mandiublar branch (V3)
2. posterior tongue: glossopharyngeal (IX)
3. soft palate: glossopharyngeal (IX)
4. oropharynx: glossopharyngeal (IX)
5. hypopharynx (below epiglottis): internal branch of superior laryngeal (vagus X)
6. vocal cords: internal branch of superior laryngeal and recurrent laryngeal (X)
7. larynx (below vocal cords): recurrent laryngeal (X)
8 trachea : recurrent laryngeal (X)
intubation nerve blocks:
1. anterior tonsillar pillar (glossopharyngeal nerve)
2. inferior aspect of the greater cornu of the hyoid bone (internal branch of superior laryngeal)
3. transtracheal (recurrent laryngeal)
-selective D1 agonist
- 0.1 to 0.8 mcg/kg/min treat severe hypertension
alpha 1 antagonists
-phenoxybenzamine - irreversible binds alpha 1 receptors, orthostatic hypotension, used in pheochromocytomas
- prazosin
Mu agonist mechanism for pain treatment
"second pain" sensations carried by slowly conducting, unmyelinated C fibers; less effective in "first pain" sensations carried by small, myelinated A- delta fibers
[(MAP-CVP)\CO] x 80
Opens chloride channels, hyper polarizes cell and makes action potential more difficult.
Starling equation
Volume of distribution
= dose/concentration
Volume of distribution
= dose/concentration
Atropine qualities, myocardial depression, local anesthetic properties
Ventilation perfusion ratio
VQI = (1-SaO2)/(1-SmvO2)
(MAP - CVP) / CO (nml 1000)
(MAP -CVP) / CO (nml 100)
Alpha 1 and 2 antagonist - lasts 15 min
Pure alpha 1 antagonist
Posterior Descending Artery
-Supplies inferior surface of the heart
-ECG leads II, III, AVF
-ST elevation and Q waves signify 100% occlusion
NDMB w/vagolytic properties