Inhalational agents - effects on MSK, neuro, hepatic, renal, and metabolism Flashcards by Linsley Lloyd

inhaled volatile agents cause a dose dependent _______ ______ _______

relaxation of skeletal muscle

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but ______ has no effect on skeletal muscle relaxation

N2O

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the higher the MAC multiple, the greater the _____ ____ ______

fade on tetanus

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inhaled anesthetics can be used instead of ________ or to enhance the effect of ______

NMB
NMB

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this enhanced effect of NMB may be from _____ or _____-______ effects or from effects on the spinal ______ _____

pre or post-synaptic
motor neurons

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agents inhibit ______ receptors incompletely at MAC

nicotinic

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practical application of inhaled anesthetics (4)

decreases doses of nondep NMB 25% (50%)
decreases frequency of redosing
myasthenia gravis patient - give NO NMB
patient with hepatic or renal impairment

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Roc has a ______ duration depending on the volatile agent interaction:
Des ___ mins
Sevo ___ mins
Iso ___ mins
Prop ___ mins

longer
Des 90 mins
Sevo 59 mins
Iso 35 mins
Prop 35 mins

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Roc duration explains the prolonged ______ from ______ when volatile concentration is maintained

recovery from NMB

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One study examined the effect of decreasing the concentration of volatile on the twitch height when a vecuronium infusion was maintained. As the % concentration decreased, the twitch height ______, although the vecuronium infusion was ________.

increased
unchanged

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Eger demonstrated the “substitution” of ___ ________ for NMB with an abdominal surgery in which muscular relaxation was desired by the surgeon

9% Desflurane

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Effects on neuromuscular system: _______ results with ______ agents

different
different

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Effects on neuromuscular system: may be explained by ______ of _____

methodology of study

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Effects on neuromuscular system: with cisat and roc, _______ caused a prolonged block, and ______ didn’t

sevo
iso

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Effects on neuromuscular system: with vecuronium, _____ and _____ both prolonged block

sevo and iso

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Effects on neuromuscular system: all volatile agents have an ______ effect with ______

additive effect with succinylcholine

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Effects on neuromuscular system: iso causes more rapid shift from ______ to ________ block with succ infusion

phase 1 to phase 2

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Effects on neuromuscular system: TIME-dependent enhancement of _________

non-depolarizing NMB (recovery of ToF 1 twitch)

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Effects on neuromuscular system: sevo 30 mins delayed recovery from vec ____

89%

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Effects on neuromuscular system: sevo 60 mins delayed recovery from vec _____

100%

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Effects on neuromuscular system: volatile agents can cause impairment of ______ of ________ NMB

reversal
non-depolarizing

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Effects on neuromuscular system: take home message

CAREFULLY administer NMB, use your twitch monitor, and consider using relaxant effect of volatile in lieu of NMB, if possible

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Uterine smooth muscle: volatile anesthetics cause dose-dependent ________ of the uterine smooth muscle

relaxation

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Uterine smooth muscle: ___ ____ - modest relaxation

0.5 MAC

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Uterine smooth muscle: ____ ____ - significant relaxation

greater than 1 MAC

Uterine smooth muscle: positive implication - desirable relaxation for ______ of ______ ______

removal of retained placenta

Uterine smooth muscle: negative implication - contribute to increased _____ ______ with uterine ______

blood loss uterine atony

Uterine smooth muscle: _____ does not alter uterine contractility in doses used to provide analgesia during vaginal delivery

N2O

Uterine smooth muscle: N2O can be useful to ______ volatile and ______ benzodiazepines/opioids

decrease avoid

Effect on uterine blood flow: ______ in maternal blood flow

decreases

Effect on uterine blood flow: decreases in uterine blood flow - maintain ____ _____ - evidence of _____ ______ not present

< 1.5 MAC fetal distress

Effect on uterine blood flow: ______ with no neonatal distress

amnesia

Effect on uterine blood flow: amnesia with no neonatal distress - ____ MAC with ____ ____ - consider avoiding _____ in fetal distress

- 0.5 MAC with 50% N2O (total equivalent of 1 MAC) - consider avoiding N2O in fetal distress

Malignant Hyperthermia: ____ ____ agents can trigger MH (even without ______)

all volatile succinylcholine

Malignant Hyperthermia: _______ is the most potent trigger

halothane

Malignant Hyperthermia: ______ is a much weaker trigger and is on the MHAUS safe list

N2O

Malignant Hyperthermia: is a pathologic change in _____, ________ state

muscle hypermetabolic

Malignant Hyperthermia: exposure to triggering agents cause the ______ ______ to release calcium from the ______ _____ to enter the muscle cell

ryanodine receptor sarcoplasmic reticulum

Malignant Hyperthermia: muscle contraction occurs due to interaction of _____ and _____

actin and myosin

Malignant Hyperthermia: both aerobic and anaerobic muscle metabolism increase producing massive amounts of _____, _____, and ______

heat, CO2, and lactate

Malignant Hyperthermia: muscle membrane permeability allows ______

leakage

Malignant Hyperthermia: time to onset with volatile agent trigger only - Des ____ minutes - Iso _____ minutes - Halo ____ minutes

- Des 260 mins (pt could even be home at this time) - Iso 140 mins - Halothane 35 minutes

CNS: CMRO2 requirements decrease at approx. ______ as the patient moves towards unconsciousness

0.4 MAC

CNS: reduction in CMRO2 is _____ ______

dose dependent

CNS: once an ______ _____ is produced, further increases in the agent concentration do not further decrease CMRO2

isoelectric EEG

CNS: - CMRO2 - ______ ______ 60% + _____ _____ 40%

electrical activity cellular homeostasis

CNS: CMRO2 decreases normal response with no volatile anesthesia: brain _____ (____) its blood flow with its ______ ______

matches (couples) metabolic requirements

CNS: CMRO2 decreases when ______ _____ decrease, blood vessels _______, and _____ decreases

metabolic demands constrict (CVR increases) CBF

CNS: 2 opposing factors with volatile anesthetics - vasoconstriction from _______ of _____ - vasodilation from _______ _____ _____

- reduction of CMRO2 - anesthetic agent directly

CNS: no uncoupling if ______ of des or iso

less than or equal to 1 MAC

CNS: ________ can occur at higher doses

uncoupling

CNS: N2O causes increased ______ and _____.

CMRO2 and CBF

CNS: However, with N2O there is still _______ due to the greater increase in ______ than ______

uncoupling CMRO2 CBF

CBF: may ______, remain _______, or _______ - different studies

increase unchanged decrease

What affects change in CBF? (5)

1. dose of volatile 2. other drugs administered (prop, opioids, barbiturates, nitrous) 3. rate of change of concentration of volatile 4. ventilation (hyper- ) 5. animal used in study she alluded that this was a test question

CBF: volatiles cause dose-dependent ______ in CBF

increase

CBF: normocarbia, > 0.6 MAC causes (4 things)

1. cerebral vasodilation 2. decreased CVR 3. increased CBF (potential increased ICP) 4. OBTW: decreased CMRO2 (coupling should result in decreased CBF)

cerebral vasodilation: ____ = ____ > ____

iso = des > sevo

increase in CBF occurs _____ _____ of administration of inhaled agent

within minutes

increased CBF is independent of _____ and can be sustained for as long as ___ ____ during an anesthetic

MAP 4 hours

greater decrease in CMRO2 by ______ may explain why CBF is not significantly increased at ____ _____

isoflurane < 1 MAC

lower metabolism = ____ _____ production, _____ ____dilation

less CO2 less vasodilation

CNS: ______, ______, & _______ maintain the cerebral vascular reactivity to CO2 at less than __ MAC

desflurane, sevoflurane, and isoflurane < 1 MAC

CNS: Iso, Des, and Sevo at ___ ____ preserve autoregulation of _____

1 MAC CBF

CNS: Halothane _____ ______

eliminates autoregulation

CNS: at 1.5 MAC _____ preserves autoregulation better than ____

sevo iso

CNS: as dose increases above 1 MAC, _______ is affected (CBF is more dependent on _____)

autoregulation MAP

CBF is maintained (unchanged or higher). CMRO2 is _____. (iso>halothane) = _______ at ______ doses

decreased uncoupling at higher doses (> 1 MAC)

CNS: _____ may blunt necrotic processes resulting from ______ ischemia due to transient _____ ischemia during ______ ______

isoflurane cerebral regional carotid endarterectomy

CNS: bc isoflurane may blunt necrotic processes, cerebral _____ _____-_____ ______ is improved

oxygen supply-demand balance

cerebral vasodilation and increased CBF raise risks of ______ _____

increased ICP

CNS: hyperventilation to decrease the _____ to ____ mmHg counters the increased ICP

PaCO2 to 30 mmHg

CNS: iso, sevo, des - start hyperventilation with _____ ___ _____

start of agent

CNS: halothane - start hyperventilation ______ _______ _____

before agent is started

CNS: iso does not change production of ____, but decreases resistance to ________

CSF reabsorption (increases reabsorption)

CNS: the result of iso increasing CSF reabsorption is only _______ ______ in ______ (even if CBF increases)

minimal increases in ICP

CNS: des may _____ or not change CSF production

increase

CNS: sevo ______ CSF production

decreases

CNS: N2O ___ ____ in CSF production

no increase

CNS: normal response to hypocarbia and PaCO2 goal

vasoconstrict goal is PaCO2 30-35 mmHg - effective 4-6 hrs

CNS: normal response to hypercarbia

vasodilate

CNS: differences in literature (3)

1. type of surgical procedure 2. pathophysiology 3. coexisting diseases

EEG effects: less than 0.4 MAC, ______ _____ and _____

increased frequency and voltage

EEG effects: at 0.4 MAC, activity shifts to ______ portions of the brain, transition from ______ to _______

anterior excitement to unconsciousness

EEG effects: typically, ______ voltage and ______ frequency at about 1 MAC

increased voltage decreased frequency (bigger slower waves)

EEG effects: the deeper the level of anesthesia, _____ ______ occurs (1.5 MAC) and possibly _____ _____ (2 MAC)

burst suppression flat EEG

EEG effects: exception - ________ does not produce burst suppression at clinical levels

halothane

EEG effects: des, iso, and sevo can suppress ______ activity related to drugs like ______

seizure lidocaine

EEG effects: however, _______ has been associated with seizure activity but MOA is uncertain

sevoflurane

EEG effects: sevo associate with seizures - increased incidence with higher concentrations (__ ____), ____carbia, repeated auditory _____, and pre-existing _____ _____

2 MAC hypocarbia stimulation seizure disorder

EEG effects: question regarding a possible link between this seizure tendency and increased risk of ______ on emergence with sevo

delirium

Evoked Potentials is monitoring the transmission of the impulse from the _______ to/through the _____

periphery cord

Evoked Potentials are typically utilized with ____ _____ for _____

spinal fusions for scoliosis (monitoring to protect the spinal cord)

Evoked Potentials: ALL potent inhaled anesthetics depress ______

SSEP

Evoked Potentials: inhaled anesthetics have a dose-dependent ______ in evoked potentials with _____ _____ being the most sensitive and _______ _____ being the most resistant

reduction visual EP brainstem EP

Evoked Potentials: an increase in _______ or decrease in _______ are indications of ischemia OR can be related to the volatile agent

latency (time of stimulus in periphery and onset of EP recorded by scalp electrode) amplitude

Evoked Potentials: clinically at ____ -____ MAC

0.5-0.7 MAC

Evoked Potentials: research shows sevo and des can be utilized at ____ ____

1.3 MAC

Evoked Potentials: research shows that isoflurane can be utilized at ____-____ ____

0.5-1 MAC

Evoked Potentials: research shows halothane can be utilized at ___-___ ____

0.5-0.7 MAC

Evoked Potentials: _____ may profoundly decrease amplitude of evoked potentials so AVOID

N2O

Awareness: volatile agents do not cause ____ _____

retrograde amnesia

Awareness: volatile anesthetics are ____ _____ in the effectiveness of preventing awareness

not equal 0.4 MAC iso prevents awareness whereas > 0.5 - 0.6 MAC N2O is required

Awareness: ______ may be altered at low concentrations (as low as _____)

learning 0.2 MAC

Awareness: surgical stimulation may increase the concentration required to _____ ______

prevent awareness

Temp Regulation: impairment of ______ ______ of temperature control

cerebral regulation

Temp Regulation: inhaled agents reset the ______ for regulation of temperature control to a _____ level

threshold lower

Temp Regulation: _____ has less of an effect; substitution of ______ impairs the threshold less

N2O N2O

Temp Regulation: inhaled agents cause center for temp regulation to permit a lower range of temperatures to exist before _______ _______ occurs

cutaneous vasoconstriction

Temp Regulation: inhaled agents permit a lower temp before the body attempts to regulate ____ ____ and ____ _____

heat loss and heat production It is DOSE-RELATED

Temp Regulation: _______ can also lead to temp loss

vasodilation

Temp Regulation: vasodilation results in heat transferred from _____ to ______ and this causes a decrease in core temp of 0.5-1 degree celsius in the first ____ ____ of anesthesia

core periphery half hour

Temp Regulation: elderly have greater _____ of temp regulation than other

inhibition

Neuroapoptosis: neurotoxicity in _______

animals

Neuroapoptosis: no predominant mechanism - altered neurogenesis, _____ growth, and _____ formation contributing to remodeling of ____ _____ and _______ remodeling

neurite synapse neuronal circuitry developmental

Neuroapoptosis: ______ deficits, delayed _____

cognitive learning

Neuroapoptosis: impaired memory ______ and ______

formation and retention

Neuroapoptosis: altered _____ and _____ development

motor and behavioral development

Neuroapoptosis: FDA issued a safety announcement advising that repeated or lengthy exposures to anesthetic or sedative drugs prior to age _____ have the potential to harm children's brains

Hepatic Blood Flow: Iso (___), Des, and Sevo _______ total hepatic blood and artery flow

1.5% maintained

Hepatic Blood Flow: iso/des/sevo increased ____ _____ _____ _____

increased portal vein blood flow (hepatic vasodilator)

Hepatic Blood Flow: halothane is a hepatic ______ ______

artery vasoconstrictor

% of anesthetic biodegraded: desflurane

0-0.02%

% of anesthetic biodegraded: isoflurane

0-0.2%

% of anesthetic biodegraded: sevoflurane

5-8%

% of anesthetic biodegraded: halothane

15-40%

% of anesthetic biodegraded: N2O

trick question N2O isnt metabolized in the liver but in the gut by normal flora (0.004%)

Determinants of metabolism: chemical structure (2)

chemical bond carbon-halogen bond

Determinants of metabolism: hepatic enzyme activity (2)

cytochrome p-450 induced or depressed obese - increased fluoride concentrations

Determinants of metabolism: blood concentration - < 0.1 MAC undergoes extensive metabolism in the _____ (less soluble - quicker out via _____)

liver lungs

Determinants of metabolism: all inhaled anesthetics are metabolized, just to _____ _____

varying degrees

Determinants of metabolism: the concern is the ______

fluoride

Determinants of metabolism: the metabolites of concern are ________ _____ and ______ ______

trifluoroacetic acid (TFA) inorganic fluoride

Determinants of metabolism: metabolic pathways are oxidative for ____, _____, _____

des, iso, sevo

Harmful metabolism: metabolism of halothane - principally ______ by cytochrome p-450 enzymes when ______ is present, but _______ metabolism when hepatocyte PO2 decreases

oxidation oxygen reductive

Harmful metabolism: TFA is produced by biodegradation of ____, ____, and _____. It causes acetylation of proteins on the surface of hepatocytes to form ______ to which ______ form

hal, iso, des antigens antibodies

Harmful metabolism: TFA - connection between its hepatic production and hepatotoxicity via an _____ _____

immune pathway

Harmful metabolism: TFA - significant difference in percentage of _____ & ____ metabolized vs ______

iso & des halothane

Inorganic fluoride - nephrotoxicity: produced by the biodegradation of sevo in the _____ and only minimally in the _____. Thus, little effect on the ______.

liver kidneys kidneys

Inorganic fluoride - nephrotoxicity: same level of inorganic fluoride produced as with ________ which causes renal failure, but no evidence of renal injury, even in patients with existing renal damage

methoxyflyrane (50 mcgmol/L)

Inorganic fluoride - nephrotoxicity: _______ production of inorganic fluoride (methoxyflurane) is a bigger problem for nephrotoxicity than inorganic fluoride produced from _____ metabolism (sevo)

infrarenal hepatic

Inorganic fluoride - nephrotoxicity: historically - no renal effects @ ______ subclinical toxicity @ _____ clinical toxicity @ _______

no renal effects @ < 40 mcm/L subclinical toxicity @ 50-80 mcm/L clinical toxicity @ > 80 mcm/L

Inorganic fluoride - nephrotoxicity: level of _____ is the indicator that renal toxicity may occur - however, no _____ _____ even with levels exceeding this level.

50 renal damage

Inorganic fluoride - nephrotoxicity: ____ and _____ are less soluble and exhaled more and less metabolized

Enf and Sevo

Inorganic fluoride - nephrotoxicity: high out put renal failure is unresponsive to ______, and has an inability to _____ urine, _______, hyper______, hyper______, increased plasma _______

vasopressin concentrate polyuria hypernatremia hyperosmolarity creatinine

Renal effects: studies show no renal _____ after ______

necrosis sevo

Renal effects: have been cases of transient impairment of renal ______ ability and increased excretion of ____-____-_______ in patient exposed to sevo and with peak plasma inorganic fluoride levels > ______

concentrating ability beta-N-acetylglucosaminidase (NAG) 50 mcm/L

Renal effects: NAG is an indicator of _____ ____ ____ ____ injury

acute proximal renal tubular injury

Renal effects: no elevation in ______ or _______

BUN or creatinine (not super sensitive indicators)

Renal effects: patients with pre-existing renal disease

no increased risk for damage

Renal effects: renal blood flow is

reduced (may effect urine output intraoperatively)

Renal effects: decreased _____

GFR

Renal effects: decreased ____ ____

urine output

Renal effects: due more to the decrease in ____ and systemic _____. preop ______ attenuates renal effects

CO BP hydration

Renal effects: _____ ____, not inhaled anesthetics, cause release of ADH

surgical stress

Renal effects: fluid status changes might also cause _____ release to contribute to _____ urine output

ADH decreased

Compound A: may cause inability to ____ ____ causing high _____ and decreased response to _____

concentrate urine output vasopressin

Compound A: no ____ ____ has been seen

renal necrosis

Compound A: however, have seen ______, ______, and _______

proteinuria, glucosuria, enzymuria

Compound A: to decrease risk, minimum flows of _____ if case longer than _____

2L/min 2 hours

Compound A: _____ if case is less than 2 hours

1L/min

Compound A: lower concentrations of ______

sevo

Compound A: avoid ____ and _____ in CO2 absorbent

KOH NaOH

Compound A: avoid increased ______ in CO2 absorbant

temperature