Exam 3 Part III Flashcards
liver receives ___________% of CO
25
hepatic artery supplies ___________% of blood flow to the liver, and the portal vein supplies _______% of blood flow to the liver, both supplying ____% of O2
25; 75; 50
prior exposure to _________________ can cause hepatitis with a current exposure to another (different) volatile
halothane
what is volatile induced hepatotoxicity
- decrease hepatic blood flow + increased O2 demand of enzyme induction –> liver dysfunction 2. develops 2/2 decreased hepatic blood flow 3. can occur hours - days post anesthetic
T/F: all volatile inhalational agents have very little liver metabolism
TRUE
s/sx of volatile induced hepatotoxicity
- fever 2. jaundice 3. increased LFTs
volatile induced hepatotoxicity is aka __________________
halothane hepatotoxicity
all volatile anesthetics produce a ___________________ relaxation of skM EXCEPT ___________ which may cause skM rigidity
dose-dependent ; N20
all volatile anesthetics _______________ the effects of DMR and NDMR
potentiate
mechanism at which volatiles produce skM relaxation
- decrease neural activity within the CNS 2. decrease effect at the NMJ (Predominantly post-synaptic membrane)
NDMR doses are decreased by _______________% in the presence of a volatile gas
15-50
time dependent potentiation of NDMR via volatile agent begins in ___________ min
10-May
after 30 minutes of exposure to sevoflurane, recovery from vecuronium to 25% of baseline is prolonged __________%
89
after 60 minutes of exposure to INH agent, the recovery from NDMR to 25% of baseline is prolonged by ________%
100
effects of Iso on: CO SVR MAP HR
CO - decreased SVR - decreased MAP - decreased HR - increased
effects of Sevo on CO SVR MAP HR
CO - maintained SVR - decreased MAP - decreased HR - maintained
effects of desflurane on: CO SVR MAP HR
CO - maintained SVR - decreased MAP - decreased HR - increased
effects of N20 on: CO SVR MAP HR
CO - decreased SVR - increased MAP - maintained HR - increased
ISO, SEVO, and DES ______ MAP, CO, CI via a ______ in SVR 2/2 ________________
decrease; decrease; reduction in intracellular free Ca
Halothane decreases MAP by?
direct myocardial depression
which volatile inhalational agent is SUPPORTIVE of HD
N2O
inhalational agents will cause dose dependent depression of what cardiac activity?
- myocardial contractility 2. peripheral vascular smooth muscle 3. inhibition of ANS activity
HR effects of inhalational agents
- antagonism of SA node automaticity 2. modulation of the baroreceptor reflex 3. SNS activation
which INH agent increases HR the most
desflurane
INH (ether) agents reduce intracellular free calcium this has what effect on the myocardium and peripheral vasculature
depression of myocardium and dilation of peripheral vasculature
inhalational agents, esp ____________ should be cautioned in those with ________ 2/2 HR effects
des; CAD
increase in HR with inhalational agents can be modulated (but not ablated) with ______________ 5 min prior to induction before an increase in desflurane concentration
fentanyl
what dose of fentanyl can give up to 70% modulation of increase in HR prior to increase desflurane concentration
1.5-4.5 mcg/kg
_________________ will block the increase in HR but not the decrease in MAP with inhalational agents
esmolol
INH agents effects on coronary blood flow
- produce vasodilation 2. cause coronary steal syndrome in diseased coronarys
which INH agent causes vasodilation the LEAST
sevo
which INH agents may be used in pts with hx of ischemic heart disease
- iso 2. sevo 3. des
common arrhythmias with inhalational agents
bradycardias and AV conduction abnormalities
which INH agents produce arrhythmias the most
sevo and halothane
sevo and halothane are c/i if the patient has what arrhythmias
2nd degree AV block type II, complete heart block
what is “sensitization” (with arrhythmias)
reduction in catecholamine threshold necessary to produce arrhythmias
_______________ may protect the myocardium from coronary steal syndrome
50% N20
what is hypoxic pulmonary vasoconstriction
- natural compensatory mechanism in response to hypoxia or atelectasis 2. pulmonary arterioles constrict w/ alveolar hypoxia –> diversion of blood flow away from poorly ventilated alveoli 3. reduces pulmonary shunt, reduces V/Q mismatch
when are INH agents at risk of decreasing hypoxic pulmonary vasoconstriction?
in one lung situations
Enflurane CNS effects
- increase CBF 2. increase ICP 3. increase CSF 4. produces seizure activity
MAC of enflurane
1.7
B: G solubility of enflurane
1.9
Vapor pressure of enflurane
175
% of enflurane that is metabolized
8-Feb
enflurane is toxic to the _______________
kidneys
T/F: enflurane is stable and not effected by light, has no preservatives
TRUE
which agent causes coronary vasodilation more than any other INH agent?
isoflurane
which agent causes coronary steal more than any other agent
isoflurane
which INH agent is the most potent (of commercially available agents in US)
isoflurane
______________ increases CBF and ICP @ 1 MAC
isoflurane
which agent increases CBF less than any other INH agent
isoflurane
which agent decreases CMRO2 less than any other INH agent
isoflurane
which INH agent is considered cerebral protective
isoflurane (means the CBF at which ischemic changes occur on EEG is lower with isoflurane than other agents)
respiratory effects of isoflurane
- decrease TV 2. increase RR (slight) 3. decrease MV 4. increase PaCO2 5. bronchodilator
what is the most widely used INH agent
isoflurane
metabolism of isoflurane
0.20%
isoflurane _________ RBF –> ______ GFR and UOP
decrease; decrease
what is the only volatile that undergoes reductive metabolism
halothane
which agent decreases MAP from direct myocardial depresson
halothane
which agent increases the incidence of ventricular arrhythmias
halothane
which agent has NO impact on SVR
halothane
which agent increases the arrhythmic potential of epi
halothane
respiratory effects of halothane
- bronchodilator 2. increased RR 3. decreased TV 4. decreased response to CO2 (less than other agents) 5. hypoxic drive severely depressed
CNS effects of halothane
- increased CBF 2. increased ICP (more than all other agents) 3. decreased CMRO2 4. autoregulation is blunted and completely abolished at high concentrations
which INH agent increases ICP the MOST
halothane
which INH agent is metabolized more than any other agent
halothane (20%)
which agent is the most hepatotoxic
halothane
which inhalational agent is metabolized via oxidation/reduction reactions
halothane
______________ is added as preservative to halothane to enhance stability
thymol
major metabolites of halothane
- trifluoroacetic acid (TFA) 2. free bromide 3. free chloride
T/F: metabolism of halothane increases with repeated exposures
true - 20% first exposure, increases from there
which inhalational agent is the LEAST potent
desflurane
which INH agent is the least soluble
Desflurane
which INH agent (other than N2O) has the highest MAC
desflurane
which INH agent is the most expensive
desflurane
CV effects of desflurane
- rapid increase in des –> transient increase in HR 2. does NOT increase coronary artery blood flow
why does desflurane require a special heated and pressurized vaporizer
because vapor pressure is so high (664) and close to atmospheric, it is a gas at room temperature
____________________is pungent, airway irritant that has high risk of coughing and laryngospasm if administered while pt is awake
desflurane
__________________ is a great gas for pts who are super morbidly obese and/or have liver dz
desflurane
which INH agent is the LEAST irritating to the airway
sevoflurane
sevoflurane is __________% metabolized
5-Feb
metabolites of sevoflurane
- inorganic fluoride 2. hexafluoroisopropanol
what gas is a methyl isopropyl ether
sevoflurane
sevoflurane will spontaneously degrade in _______________ bottles, so must be kept in ___________ or __________ bottle
glass; plastic; metal
what is the MAC of Xenon
71%
what is the B:G solubility of Xenon
0.14
why is xenon not able to be used as an inhalational anesthetic
because MAC = 71% so you would only be able to use 29% O2
induction and emergence with xenon is _________________ x faster than desflurane or sevoflurane
4-Mar
xenon advantages as inhalational agent
- non-explosive 2. minimal cardiac depression 3. no metabolic effects 4. not harmful to the environment
disadvantages of xenon as inhalational anesthetic
- potential risk of recall 2. extremely high cost 3. MAC of 71%
________________________ has hindered the acceptance of xenon into clincial practice
extremely high cost
anesthetic effects of N2O and other volatile agents are _________________
additive
N2O usually used in concentrations of __________ - ___________% to reduce the requirement of more potent agents
50; 70
basic characteristics of N2O
- stored as a liquid and a gas in pressurized tanks (@ 50 atm) 2. Non flammable 3. BUT DOES support combustion 4. least potent of all gases 5. minimal toxicity 6. stable at room temperature 7. does not react with soda lime or other anesthetic drugs 8. almost entirely eliminated through the lung
analgesic effect of 50% N20 is approximately equal to __________
10 mg morphine
approximately __________% of N20 undergoes metabolism
1
absolute c/i of N20
- known deficiency of enzyme or substrate in methionine synthase pathway 2. potential toxicity from expansion of gas filled space (emphysema, pneumothorax, middle ear surgery, pneumocephalitis, air embolus, bowel obstruction)
relative C/I to use of N20
- increased ICP 2. pulmonary HTN 3. prolonged anesthetic (> 6 h) 4. first trimester of pregnancy 5. high risk PONV
CNS effects of N2O
- increased CBF- potent cerebral vasodilator (not good for neuro cases) 2. minimal increase in CMRO2 3. minimal EEG changes 4. no effect on cerebral autoregulation 5. big increase in PONV (d/t activation of CTZ and vomiting center)
CV effects of N20
- no effect on HR, CO, BP 2. no significant changes in EKG 3. mild, transient, stimulation of SNS 4. increase PVR (issue with pulm htn)