Sorry, wrong choice. "Moment-to-moment control" is just another way of talking about rapidity with which the depth of anesthesia can be changed.
I think you'd best go all the way back to Item VII.
Wrong choice, I fear. Atropine might produce pupillodilation by blocking the effects of the parasympathetic nervous system on the circular muscles of the iris, but probably not in this low dose. The pupillodilation seen in deep anesthesia is the result of both a "neurogenic" effect and the effect of the agent on the muscles of the iris themselves; it's like the pupillodilation of a completely denervated eye. It's not prevented by atropine, and is, ultimately, more intense than that produced by even maximally effective doses of atropine. Hence, atropine won't interfere with detecting the ocular signs of deep anesthesia. Obviously other signs of deep anesthesia - and its consequences - are of more clinical importance than eye signs such as pupillodilation.
Go back to Item XIX and choose again.
Very good; you've remembered that the rate limiting factor in induction of anesthesia with volatile and gaseous agents is the blood/gas solubilities of the agents. Other things - such as concentration - being equal, rate of onset of anesthesia is inversely related to the relative solubility of drug in blood. The greater the solubility of the anesthetic agent, the longer it takes to saturate this reservoir, and the longer it takes for drug to "spill-over" from blood in to the tissues where the agent has its desired - and, perhaps, some undesired - effect. BF has a lower solubility in water (blood) than does ether; hence the onset of anesthesia would be more rapid with BF than with ether.
Go on to Item VIII
Incorrect: Ether and tubocurarine act synergistically with each other ar the neuromuscular junction. Sorry, you'll have to go back to Item XV and try again.
Sorry, you've made an incorrect choice. The less potent an agent is, the greater the concentration required to produce a given effect, i.e., the greater the partial pressure required to produce anesthesia (Pa). Pa is proportional to vapor pressure. Therefore, the greater the vapor pressure, the larger the CT index, when concentrations are determined for equal times of exposure and the concentration-latency curves are parallel. Maybe it would help to sketch the curves involved here.
Go back to Item X and choose again.
Sorry, wrong choice; but before you go back to Item XVII to choose again, I suggest you review Item VIII.
Sorry, saturated hydrocarbons that are extensively halogenated - as the Freons are, and as halothane and chloroform are - are generally not flammable. Of course, ether and cyclopropane are highly flammable. Go back and make another choice from Item XI.
Very good; MF and TF have boiling points a little higher than room temperature as diethyl ether does and, therefore, all three could be stored under similar conditions: in tightly closed containers but at ambient atmospheric pressure.
Go on to Item II.
Sorry; gallamine acts synergistically with ether at the neuromuscular junction. Since gallamine acts antagonistically to succinylcholine, at least when administration of gallamine precedes administration of succinylcholine, it seems reasonable to suspect that ether acts antagonistically to succinylcholine - at least to the manifestation of succinylcholine's intrinsic activity. And that's actually what happens!
Back to Item XV and try again.
Incorrect: The direct effect of the agent would be, I think, to prolong the atrial refractory period and (or while) increasing the threshold of the atrial muscle to stimuli.
Please go back to Item XIII and choose again.
Wrong choice, I fear. May I suggest that you consider again that Pa=PsK and that Ps changes with temperature and reaches a maximum of 760 mmHg at the boiling point of the material?
Go back to Item V and choose again.
Good. The diffusion constant for a molecule is inversely related to the square root of its molecular weight - over a wide range of weights - and O2 certainly has a lower molecular weight (32) than does ether. Given equal partial pressure differences and equal areas for diffusion (one lung's worth) diffusion of molecular oxygen will be more rapid than diffusion of ether.
You'll remember, of course, that for normal subjects with normal lungs, diffusion of drug across the alveolar membrane is not the rate limiting factor in induction of anesthesia. What is?
TF wasn't included in any of the choices for this item. You'll observe that the implied direct proportionality between molecular weight and vapor density - seen nicely in the case of MF, BF and ether - doesn't hold true if TF is included in the series. Maybe the differences in vapor density of TF and BF couldn't be discriminated well with the method used to get the data reported here; certainly their molecular weights indicate that their densities should be close together. Maybe our generalization is too general for the case of agents with such similar weights. Go on to Item VII.
Very good, this is the correct answer. Back to reality or at least to real, clinically useful anesthetic agents. The rate at which recovery would occur depends on the rate that drug will pass from tissues to blood to the pulmonary alveoli, and to the exterior of the body, in that order. To the extent that an agent is soluble in blood (or, roughly speaking, water) the reservoir of the blood is not readily emptied, the concentration difference between tissues and blood is small, agent leaves the tissues slowly, and anesthesia is prolonged. Since ether is more soluble in water or blood than are either nitrous oxide or cyclopropane, under the conditions given, recovery would be slower with ether than with either of the other two.
The most important point, perhaps, is that you don't have to remember isolated facts such as the solubilities of nitrous oxide and cyclopropane. You know that cyclopropane and nitrous oxide are gases at standard temperature and pressure, i.e., they have high vapor pressures at room temperature. According to Raoult's Law, the solubility of an inert gas, in dilute solutions, is inversely proportional to the vapor pressure of the liquid solute at the given temperature. Raoult's Law applies perfectly only to ideal dilute solutions, but it applies well enough to anesthetic materials under conditions of use to permit the generalization that the clinically useful anesthetic gases are less soluble in blood and water than the clinically useful anesthetic vapors and rates of induction and recovery from anesthesia for these two groups vary accordingly. Among the vapors and among the gases, respectively, Raoult's Law, as given, is not a sure predictor of solubility.
Raoult's Law has come up before in Item IV, when we were concerned with anesthetic potency. This law or relationship among partial pressure, vapor pressure, and solubility (mole fraction of solute in solution) applies to questions of potency when we're concerned with solution of agent in a target cell, and applies to questions of rate on onset and waning of anesthesia when we're concerned with solution of agent in blood, the medium which transports agent to the target cell. Disregard all other factors for the moment, including the fact that anesthetic agents can't act as perfect gases under conditions of use; still, it's no coincidence that the three agents once used clinically which are gases at STP (cyclopropane, ethylene and nitrous oxide) were of low potency, more rapid onset, and shorter duration of action than the volatile agents were.
Now, of course, only nitrous oxide is used clinically.
That was a long one. Why don't you go on now to Item IX?
Sorry, the probabilistic model explains selectivity of action in terms of the probability that information will get through a neurone chain, regardless of the cellular mechanism by which the function of individual neurones might be altered.
Go back to Item II and try again.
Sorry. Whatever the Freons might do, enflurane and isoflurane don't characteristically induce cardiac arrhythmias more frequently than does halothane. You'd do well to review the cardiac effect of anesthetic agents as given in the textbook before going back to Item XII and making another choice.
Too bad. Neither of these materials undergoes substantial biotransformation in the body. I suspect your memory on these points needs refreshing, by referring to your text.
Back to Item XIV and another choice.
Right. And any of a number of mechanisms, direct and indirect, have been suggested as accounting for the association of hypercarbia and ventricular arrhythmias. The association was apparent particularly in deep cyclopropane anesthesia: respiratory depression produced by the drug led to hypercarbia that was not accompanied by - or signalled by - the signs of hypoxia, since the concentration of oxygen in the inspired gas mixture (70-80%, or more) was more than adequate even though tidal exchange was reduced.
As for mechanism, try this one: Hypercarbia is associated with acidosis, and this leads to an increased concentration, locally at least, of ionized calcium. Calcium ions themselves decrease the SA rate; calcium ions (acting synergistically, additively, with the anesthetic agent in this case) also lead to slowed AV conduction. Under this combination of circumstance, the inherent rhythmicity of the ventricle can be manifest and ventricular arrhythmias are observed.
During hypercarbia, both epinephrine and cellular potassium are released into the blood stream by mechanisms which are not entirely clear; these agents may play a role in inducing ventricular arrhythmias during hypercarbia as they do under other circumstance.
Maybe your textbooks of pharmacology and physiology have more light to shed on this subject. By the way, regardless of their clinical usefulness, what drugs might facilitate production of ventricular arryhthmias during hypercarbia? Might militate against their occurrence?
After a moment's thought on that, why don't you go on to Item XIV?
Sorry, MF would volatilize nicely - possibly too nicely - under conditions of the "open-drop" method, since its boiling point is just a bit above room temperature ; MF also has a vapor density greater than that of air and MF vapors would "fall" nicely through the mask used in the open-drop technique. And, of course, ether was administered by this technique with good success clinically, for many years.
Go back and select another choice from Item I.
Absolutely true; now would you like to make an additional choice or two from Item XVIII?
Good, this is the correct choice, reasoning by analogy. One of the hazards in the use of chloroform and trichloroethylene - particularly in industry, where they are used as solvents and degreasing agents - is the formation of phosgene from the agents in the presence of heat. Carbon tetrachloride is guilty of having the same property; it may no longer be used in fire-extinguishers; too many victims avoided injury or death from fire, but succumbed later to the effects of phosgene, which produces pulmonary edema - and a succession of consequent effects - by virtue of its properties as a pulmonary irritant.
Go on to Item XII and remember phosgene; anesthesiology and industrial hygiene have more in common than the CT index!
Sorry, atropine provides protection against some of the vagal reflexes that occur during anesthesia, but doesn't protect much against such severe and biologically significant stimuli as traction on the viscera.
Might it be useful to review the pharmacology of atropine?
Go back to Item XIX and try another choice.
Sorry, you'll have to make another choice. Under the conditions described, rate of recovery, like rate of induction, is related to the water/gas or blood/gas solubility coefficients of the agent. TF is less soluble in water than ether, and recovery from anesthesia with TF would be more rapid than recovery from ether anesthesia.
Go back to Item VIII and choose again.
Very good; all these effects would be produced by the mechanisms suggested and would be observed during the course of deep clinical anesthesia.
Carry on, and try Item XIX
I'm afraid not. Diffusion constant is inversely proportional to the square root of molecular weight - over a wide range of weights - and inversely related to the square root of vapor density. ( You can almost see heavy molecules moving sluggishly). Therefore, with equal concentration differences and equal areas for diffusion, the diffusion rates of MF and ether should be in the proportion of...
Go back to item VI and try again.
Too bad, wrong choice. Before going back to Item XVII to make another choice, why don't you review Item VIII; I think it might help.
Sorry; under the conditions described, recovery from anesthesia proceeds rapidly to the extent that agent readily passes out of the tissues, through the blood (as it were), and into the pulmonary alveoli, preparatory to exhalation. If the agent is relatively soluble in the blood, the blood "reservoir" is not readily emptied, the concentration difference between tissues and blood remains small, and agent leaves the tissues slowly, i.e., the anesthetic state is prolonged. Therefore, after comparing the solubilities of BF and ether, we'd conclude that...
Go back to Item VIII and make another choice.
Stop! Ether acts synergistically with tubocurarine at the skeletal neuromuscular junction. Since gallamine has the same mode of action at that site as does tubocurarine, it follows that ether should act synergistically with gallamine. Indeed, it does. Back to Item XV, and try a different choice.