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;
64 Cards in this Set
- Front
- Back
most potent inhaled anesthetic
|
isoflurane
|
|
least soluble anesthetic
|
desflurane
|
|
least irritating anesthetic
|
sevolfurane
|
|
what is diffusion hypoxia
|
washout of nitrous oxide can lower alveolar concentrations of oxygen and carbon dioxide
|
|
Definition of MAC
What is the MAC for loss of awareness, what is MAC awake |
alveolar concentration of an inhaled anesthetic at one atmosphere that prevents movement in response to a surgical stimulus in 50% of patients. Concentrations of inhaled anesthetics that provide loss of awareness and recall are about 0.4 to 0.5 MAC.
Mac awake is about 0.2 |
|
how does MAC change w/ age
|
decreases about 6% each decade ( excluding kids less than 1 yr old)
|
|
what is vapor pressure?
|
At equilibrium, the pressure exerted by molecular collisions of the gas against the container walls, as long as any liquid remains in the container, the vapor pressure is independent of the volume of that liquid.
|
|
vapor pressure and temp?
|
proportional relationship.
|
|
what is partial pressure?
|
For any mixture of gases in a closed container, each gas exerts a pressure proportional to its fractional mass.
|
|
Dalton's law regarding total pressure of a container?
|
The sum of the partial pressures of each gas in a mixture of gases equals the total pressure of the entire mixture
|
|
what is the ideal gas law?
|
each gas in a mixture of gases at a given volume and temperature has a partial pressure that is the pressure it would have if it alone occupied the volume. The entire mixture behaves just as if it were a single gas according to the ideal gas law.
|
|
what does the concentration of any one gas in a mixture of gases in solution depend on?
|
(1) its partial pressure in the gas phase in equilibrium with the solution, and (2) its solubility within that solution.
anesthetic gases administered via the lungs diffuse into blood until the partial pressures in alveoli and blood are equal |
|
what is Fi
|
fractional concentration of a gas leaving the circuit
|
|
what is FA
|
fractional concentration of a gas in the alveoli
|
|
what is partition coefficient, δ
|
the ratio of dissolved gas (by volume) in two-tissue compartments at equilibrium.
|
|
factors that increase the rise of FA/FI
|
1.Low λB, The lower the blood:gas solubility
2. Low Q, The lower the cardiac output 3. High V.A, The higher the minute ventilation 4. High (PA - Pv), pulmonary arterial and venous blood partial pressure difference in partial pressures. |
|
overpressurization definition
|
analogous to an intravenous bolus. This is the administration of a higher partial pressure of anesthetic than the alveolar concentration (FA) actually desired for the patient. Inspired anesthetic concentration (FI) can influence both FA and the rate of rise of FA/FI
|
|
second gas effect
|
Along with the concentration of potent agent in the alveoli via its uptake, there is further concentration via the uptake of nitrous oxide,
|
|
factors affecting recovery from inhaled anesthetics?
|
anesthetic solubility, cardiac output, and minute ventilation. Solubility is the primary determinant of the rate of fall of FA
|
|
partial pressures in muscle and fat depend on
|
the inspired concentration during anesthesia, the duration of administration, and the anesthetic tissue solubilities
|
|
diffusion hypoxia def
|
washout of high concentrations of nitrous oxide can lower alveolar concentrations of oxygen and carbon dioxide. The resulting alveolar hypoxia can cause hypoxemia, and alveolar hypocarbia can depress respiratory drive, which may exacerbate hypoxemia. It is therefore appropriate to initiate recovery from nitrous oxide anesthesia with 100% oxygen rather than less concentrated O2/air mixtures.
|
|
molecular structure of isoflurane?
|
halogenated methyl ethyl ether that is a clear
|
|
whic inhaled anesthetic has lowest blood:gas solubility
|
desflurane
|
|
metabolism of sevo
|
results in inorganic fluoride
sevoflurane is not metabolized to trifluoroacetate |
|
Sevo and dry CO2 canisters
|
Sevoflurane can form carbon monoxide during exposure to dry CO2 absorbents, and an exothermic reaction in dry absorbent has resulted in canister fires
|
|
what is compound A
|
Sevoflurane also breaks down in the presence of the carbon dioxide absorber to form a vinyl halide called compound A. Nephrotoxin in rats, not in humans. Negligible formation at higher gas flows
|
|
Xenon
mac? |
nonpungent, and odorless, and thus can be inhaled with ease
MAC 71% has analgesic properties |
|
Nitrous
- mac - controversy for use? |
MAC = 104%
does not produce significant skeletal muscle relaxation, analgesic effects - flammable, B12 vit inactivation, nausea, potential MI, expantsion of gas bubbles, teratogen |
|
some factors that increase MAC
|
Increased central neurotransmitter levels (monoamine oxidase inhibitors, acute dextroamphetamine administration, cocaine, ephedrine, levodopa)
Hyperthermia Chronic ethanol abuse (determined in humans) Hypernatremia |
|
what is hysteresis?
|
that it quite consistently takes 0.4 to 0.5 MAC to lose consciousness, but less than that (as low as 0.15 MAC) to regain consciousness. This may be because of the speed of alveolar wash-in versus wash-out
|
|
what is MAC-BAR?
|
alveolar concentration of anesthetic that blunts adrenergic responses to noxious stimuli, has likewise been established and is approximately 50% higher than standard MAC.13 MAC also has been established for discreet levels of EEG activity, such as onset of burst suppression or isoelectricity.
|
|
Administering 0.5 MAC of a potent agent and 0.5 MAC of nitrous oxide is equivalent to
|
1 MAC
|
|
Factors that decrease MAC
|
Increasing age
Metabolic acidosis Hypoxia (PaO2, 38 mm Hg) Induced hypotension (mean arterial pressure <50 mm Hg) Decreased central neurotransmitter levels (α-methyldopa, reserpine, chronic dextroamphetamine administration, levodopa) α2-Agonists Hypothermia Hyponatremia Lithium Hypo-osmolality Pregnancy Acute ethanol administration Ketamine Pancuronium Physostigmine (10 times clinical doses) Neostigmine (10 times clinical doses) Lidocaine Opioids Opioid agonist-antagonist analgesics Barbiturates Chlorpromazine Diazepam Hydroxyzine Δ-9-Tetrahydrocannabinol Verapamil , Anemia (<4.3 mL O2/dL blood) |
|
factors that do not alter MAC
|
including duration of inhaled anesthetic administration, gender, type of surgical stimulation, thyroid function, hypo- or hypercarbia, metabolic alkalosis, hyperkalemia, and magnesium levels
|
|
Sevoflurane and EEG
|
High, long-lasting concentrations of sevoflurane (1.5 to 2.0 MAC), a sudden increase in cerebral sevoflurane concentrations, and hypocapnia can trigger EEG abnormalities that often are associated with increases in heart rate in both adults and children. maybe not best for pt w/ epilepsy
|
|
Potent agents and CBF
|
all incrase
Isoflurane, sevoflurane, and desflurane cause far less cerebral vasodilation per MAC-multiple than halothane |
|
what is uncoupling w/ respect to CBF and inhaled agents?
|
The increase in CBF with increasing dose caused by the potent agents occurs despite decreases in CMR.
|
|
effect of potent agents on brain autoregulation?
|
Because the volatile anesthetics are direct vasodilators, all are considered to diminish autoregulation in a dose-dependent fashion such that at high anesthetic doses CBF is essentially pressure-passive
|
|
volatile agents and effect on ICP?
|
Like isoflurane, both sevoflurane and desflurane >1 MAC produce mild increases in ICP, paralleling their mild increases in CBF
|
|
which agent depresses CSF production
|
sevo at1 MAC depresses CSF production up to 40%
|
|
volatile agents and EEG
|
All three currently used agents at <1 MAC and N2O at 30 to 70% can produce shifts to increasing frequencies. Between 1 and 2 MAC the potent agents produce shifts to decreasing frequencies and increases in amplitude. At >2 MAC, all of the potent agents can produce burst suppression or electrical silence.
|
|
what other than volatile agents influences EEG reading?
|
hypoxia, hypercarbia, and hypothermia
|
|
volatile agents and cortical somatosensory evoked potentials.
|
All of the volatile agents cause a dose-dependent increase in latency and decrease in amplitude in all cortical SEP modalities
|
|
volatile agents and motor evoked potentials?
|
all agents depress them.
|
|
Nitrous and cerebral blood flow and CMR
|
preserved CBF but decreased CMRO2
|
|
Nitrous and neuroprotection?
|
antineuroprotective effect, as addition of N2O to isoflurane during temporary ischemia is associated with greater tissue damage and worsened neurologic outcome
|
|
spontaneous ventilation and CO, HR and SV
|
spontaneous ventilation decreases systemic vascular resistance and increases heart rate, cardiac output, and stroke volume as contrasted to positive pressure ventilation
|
|
volatile anesthetics and pacemaker cells
|
Sinoatrial node discharge rate is slowed by the volatile anesthetics and conduction in the His-Purkinje system and conduction pathways in the ventricle also is prolonged by the volatile anesthetics
|
|
which anesthetic has a potential for coronary steal?
|
iso
Isoflurane (and most other potent volatile anesthetics) increases coronary blood flow many times beyond that of the myocardial oxygen demand |
|
volatile anesthetics and cardioprotection
|
mimic ischemic preconditioning and trigger a similar cascade of intracellular events resulting in myocardial protection that lasts beyond the elimination of the anesthetic. Preconditioned hearts may tolerate ischemia for 10 minutes longer than nonconditioned hearts
|
|
which drugs abolish the cardioprotection?
|
sulfonylurea
hyperglycemia as well, so insulin needs to be started. |
|
Des and autonomic nervous system?
|
increase in resting sympathetic nervous system activity and plasma norepinephrine levels
Adequate concentrations of opioids or clonidine given prior to increasing the concentration of desflurane have been shown to attenuate these responses |
|
Volatile agents and minute ventilation?
|
All volatile anesthetics decrease tidal volume and increase respiratory rate such that there are only minor effects on decreasing minute ventilation
|
|
volatile agents and response to hypercarbia?
|
All of the inhaled anesthetics produce a dose-dependent depression of the ventilatory response to hypercarbia
|
|
what happens to the apneic threshold under anesthesia?
|
It is generally 4 to 5 mm Hg below the prevailing resting Paco2 and unrelated to the slope of the co2 response curves or to the level of the resting Paco2.
|
|
volatile agents and response to hypoxia
|
depressed response
|
|
volatile anesthetics and effect on pulmonary artery pressure?
|
minimal since it doesn't affect the smooth muscle in the PA and depresses the CO
attenuate hypoxic pulmonary vasoconstriction (HPV). |
|
National Institute for Occupational Safety and Health recs for nitrous exposure
|
25 parts per million (ppm) as a time-weighted average over 8 hours. The 1-hour exposure limit for halogenated anesthetics without nitrous oxide exposure is 2 ppm, and with nitrous oxide is 0.5 ppm.
|
|
what is compound A
|
Sevoflurane undergoes base-catalyzed degradation in carbon dioxide absorbents to form a vinyl ethe
|
|
which absorbents cause more compound A production w/ sevo
|
Barium hydroxide lime produces more compound A than soda lime and this can be attributed to slightly higher absorbent temperature during CO2 extraction
|
|
when is CO produced in anesthesia machines?
|
CO2 absorbents degrade sevoflurane, desflurane, and isoflurane to carbon monoxide when the normal water content of the absorbent (13 to 15%) is markedly decreased <5%. Exothermic reaction.
|
|
which gas produces most CO?
|
des
|
|
which gas produces most heat w/ dessicated CO2 absorbers?
|
sevo
|
|
enflurane toxicity?
|
nephrotoxicity presents as a high-output renal insufficiency that is unresponsive to vasopressin and is characterized by dilute polyuria, dehydration, serum hypernatremia, hyperosmolality, elevated blood urea nitrogen, and creatinin
|