Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
114 Cards in this Set
- Front
- Back
|
halothane is what type of molecule
|
halogentated hydrocarbon
|
|
|
halothane is a ______ derivative
|
alkane
|
|
|
how is halogenation accomplished
|
by substitution of a hydrogen atom with a halogen (either a fluorine, chlorine, bromine or iodine)
|
|
|
what does halogenation influence
|
*anesthetic potency
*MAC .75% |
|
|
what are the arrythomegenic properties of alkanes with 5 halogens compared to ethers with 6 halogens
|
they are more prone to induce arrythmias
-so halothane is more likely to produce an arrythmia than isoflurane or enflurane |
|
|
what is the flammability of halothane
|
NON-flammable
(b/c halogenated) |
|
|
how is halothane stored
|
in amber colored bottles
(not stable in light) |
|
|
does halothane need a preservative
|
YES--it is the ONLY IA with a preservative
-preservative is thymol -preservative prevents spontaneous oxidative decomposition |
|
|
which is halothane absorbed in more polyethylene or rubber
|
rubber more than polyethylene
|
|
|
what is the vapor pressure of halthane
|
243/244
|
|
|
what is the relationship b/t CMR and CBF with halothane
|
they are UN-coupled
|
|
|
does halthane increase or decrease ICP
|
may increase it
|
|
|
how can changes in ICP caused by halothane be prevented
|
by PRIOR hyperventilation to < 30 torr PaCO2
|
|
|
what kind of change in there in CMRO2 with halothane
|
dose dependent DECREASE
|
|
|
normally CBF is auto-regulated between what range
|
a MAP of 60 to 140-150 torr
(180-200 torr with HTN) |
|
|
what happens to auto-regulation of CBF with halothane
|
it is lost
|
|
|
CBF is what with halothane
|
pressure dependent
|
|
|
evoked potentials are used to monitor what
|
function of spinal cord, brain stem and cerebral cortex
|
|
|
evoked potentials reflect what type of impulses
|
impulses through specific pathways
|
|
|
evoked potentials are measurements of what
|
electro-physical response to a stimuli
|
|
|
BAEP monitors function of what
|
cranial nerve VIII
|
|
|
how does halothane affect BAEPs
|
does NOT affect the ability to monitor
|
|
|
VEP monitors the function of what
|
the optic nerve
|
|
|
when are VEP monitored
|
*during removal of pituitary tumors or other lesions near the optic nerve
*optic chiasm |
|
|
how does halothane affect VEPs
|
it DOES affect the ability to monitor
|
|
|
SSEP monitors what
|
function of the spinal cord
|
|
|
when are SSEPs used
|
for carotid, aortic or intracranial aneurysms
|
|
|
how does halothane affect SSEPs
|
it DOES affect the ability to monitor
|
|
|
how is production of CSF affected by halothane
|
it is DECREASED
|
|
|
how is absorption of CSF affected by halothane
|
it is DECREASED
|
|
|
how do volatile agents affect baroreceptor reflex control of arterial pressure
|
they depress it
|
|
|
how do volatile agents affect overall sympathetic nervous system activity
|
reduce it
|
|
|
how do volatile agents affect sympathetic responses to declines in arterial pressure
|
attenuate it
|
|
|
halothane, enflurane and isoflurane do what to preganglionic sympathetic efferent activity
|
inhibit it
|
|
|
halothane does what to postganglionic sympathetic nerve activity
|
reduces it
|
|
|
enflurane does what to postganglionic sympathetic nerve activity
|
reduces it
|
|
|
isoflurane does what to postganglionic sympathetic nerve activity
|
reduces it
|
|
|
halothane does what to postsynaptic nicotonic receptors in the stellate ganglion
|
blocks them
|
|
|
enflurane does what to postsynaptic nicotonic receptors in the stellate ganglion
|
blocks
|
|
|
isoflurane does what to postsynaptic nicotonic receptors in the stellate ganglion
|
blocks
|
|
|
what is halothanes effect on NE release from postganglionic sympathetic nerves
|
induces reductions in
|
|
|
what is enfluranes effect on NE release from postganglionic sympathetic nerves
|
induces reductions in
|
|
|
what is isofluranes effect on NE release from postganglionic sympathetic nerves
|
induces reductions in
|
|
|
halothane may have what effect on reflex vasoconstriction in peripheral blood vessels
|
may contribute to depression of
|
|
|
enflurane may have what effect on reflex vasoconstriction in peripheral blood vessels
|
may contribute to depression of
|
|
|
isoflurane may have what effect on reflex vasoconstriction in peripheral blood vessels
|
may contribute to depression of
|
|
|
halothane does what to vagal efferent activity
|
depresses it
|
|
|
what is halothanes effect on reflex bradycardia in response to increases in arterial pressure
|
inhibits
|
|
|
halothane and isoflurane have equivalent or unequivalent depression of PNS and SNS
|
EQUIVALENT
|
|
|
volatile agents have what effect on the PS nervous system
|
depression
|
|
|
with halothane there is what type of depression of myocardial contractility
|
dose-related
|
|
|
regarding depression of myocardial contractility what is the order of depression between the following agents:
deflurane, enflurane, halothane, and isoflurane |
halothane & enflurane > isoflurane or desflurane
|
|
|
halothane has what type of effect on LV preload and afterload in pts with heart failure & CAD
|
beneficial decreases
|
|
|
isoflurane has what type of effect on LV preload and afterload in pts with heart failure & CAD
|
beneficial decreases
|
|
|
negative inotropic effects of halothane and enflurane are d/t what
|
alterations in intracellular Ca+
|
|
|
the negative inotropic effects of halothane and enflurane cause what effect
|
depression of BP
|
|
|
though halothane and enflurane can have negative inotropic effects what is still recommened to be continued with pts
|
*continue all routine medications including b-blockers & ca-channel blockers
|
|
|
b-blockers and ca-channel blockers with halothane or enflurane might cause what to occur
|
increased magnitude of BP depression
|
|
|
despite negative inotropic effects of halothane what stays very stable
|
HR
|
|
|
what effect does halothane have on HR
|
*slow the rate of SA node discharge by direct or indirect effects on SA node automaticity
*prolong atrioventricular conduction time & refractoriness |
|
|
halothane has the potential to produce bradycardia or tachycardia
|
bradycardia
|
|
|
with peds and use of halothane what should always be available
|
atropine
|
|
|
halothane sensitizes the myocardium to what
|
the arrhythmogenic effects of epi
(both exogenous and endogenous epi) |
|
|
halothane reduces the hearts threshold for what
|
atrial and ventricular arrythmias
|
|
|
with halothane escalating doses of epi could cause what
|
PVC's and sustained ventricular tachyarrhythmias
|
|
|
what should be avoided and if cannot be avoided the dose limited with halothane
|
EPI
|
|
|
what are the safe dosages of epi with halothane
|
*0.1 mg
10 mls of 1:100,000 in 10 min *0.3 mg 30 mls of 1:100,000 in 1 hr |
|
|
how does lidocaine given with epi change the dosage that can be safely given with halothane
|
doubles the safe dosage
(secondary to the protective effect of lidocaine) |
|
|
halothane has what effect on the response to hypoxia
|
PROFOUNDLY depresses it
|
|
|
when does halothane place the pt at greater risk for hypoxia
|
in the absence of stimuli
|
|
|
what is apneic threshold
|
3-5 torr < PaCO2 for spontaneous ventilation
|
|
|
halothane has what effect on GFR and renal blood flow
|
decreases
|
|
|
enflurane has what effect on GFR and renal blood flow
|
decreases
|
|
|
isoflurane has what effect on GFR and renal blood flow
|
dereases
|
|
|
halothane has what effect on urine output and why
|
*decreases it
-d/t decreased CO & decreased BP |
|
|
enflurane has what effect on urine output and why
|
*decreases it
-d/t decreased CO & decreased BP |
|
|
isoflurane has what effect on urine output and why
|
*decreases it
-d/t decreased CO & decreased BP |
|
|
the effect that halothane, enflurane and isoflurane has on urine output is NOT an effect of what
|
ADH hormone
|
|
|
with halothane, enflurane and isoflurane autoregulation of renal blood flow is intact or not intact
|
INTACT
|
|
|
halothane does or does NOT cross the placenta
|
RAPIDLY crosses
|
|
|
halothane does what to uterine muscle
|
relaxes it
|
|
|
halothane has what effect on contractions
|
inhibits them
|
|
|
what effect does halothane have on blood loss with c-sections and therapeutic abortions
|
INCREASES blood loss
|
|
|
what MAC of halothane should be used with c-sections and therapeutic abortions to minimize its side effect
|
keep MAC < .5
|
|
|
what is the "typical" dose of halothane for a c-section
|
.4 MAC halothane & .6 MAC N20
|
|
|
what regarding the repoductive system and sx is halothane useful for
|
valuable for uterine relaxation with retained placenta fragements
|
|
|
halothane undergoes what route for metabolism
|
2 routes
1-reduction (low o2 states) 2-oxidative (ample o2 states) |
|
|
with oxidative pathway for halothane metabolism what may be formed
|
triluroacetic acid (metabolite)
|
|
|
how is trifluroacetic acid detected
|
in the urine for many days
|
|
|
which IA can produce trifluroacetic acid
|
all fluroinated volatile IA EXCEPT sevoflurane may produce it
|
|
|
trifluroacetic acid may produce what type of reaction
|
sensitivity reaction=halothane hepatitis
|
|
|
a cross sensitivity for halothane hepatitis type reaction may occur between what volatile agents
|
halothane, enflurane and isoflurane
|
|
|
in genetically susceptible patients what occurs with trifluroacetic acid
|
an antigen is formed that provokes the formation of antibodies and can lead to halothane hepatitis reaction
|
|
|
what agent is least likely to cause hepatic damage
|
the least metabolized IA desflurane
|
|
|
which IA will NOT trigger halothane hepatitis
|
sevoflurane
|
|
|
halothane is associated with what organ damage
|
liver
|
|
|
with halothane what organ toxicity is now accepted as a distinct clinical entitity
|
hepatotoxicity
|
|
|
what is the incidence of the mild form of halothane hepatitis
|
1:5
|
|
|
what forms of halothane hepatitis exist
|
*mild
*fulminant |
|
|
what type of exposure is needed for the mild form of halothane hepatitis
|
repeat exposure NOT necessary
|
|
|
what occurs with ALT and AST with the mild form of halothane hepatitis
|
mild elevation
|
|
|
what type of liver necrosis occurs with the mild form of halothane hepatitis
|
focal
|
|
|
what is the prognosis for the mild form of halothane hepatitis
|
self-limiting
|
|
|
what is the incidence of the fulminant form of halothane hepatitis
|
1:10,000
|
|
|
what type of exposure is needed for the fulminant form of halothane hepatitis
|
multiple exposures
|
|
|
what occurs with ALT, AST, bilirubun and alkaline phosphatase with the fuliminant form of halothane hepatitis
|
marked elevation
|
|
|
what type of liver necrosis occurs with the fulminant form of halothane hepatitis
|
massive
|
|
|
what is the prognosis with the fulminant form of halothane hepatitis
|
mortality rate of 50%
|
|
|
what is formed as a result of the fulminant form of halothane hepatitis
|
antibodies to halothane--altered protein antigens
|
|
|
is halthane a potential trigger agent for malignant hyperthermia
|
YES
|
|
|
what is halothanes current usage in the US
|
none
|
|
|
how is halothane used for children
|
*induction agent
(not in US) *sevoflurane has replaced it in US |
|
|
what type of arrythmic potential has been confirmed with halothane
|
PROarrythmic
|
|
|
how would halothane induced arrythmias be treated
|
with lidocaine
|
