Sorry, saturated hydrocarbons that are extensively halogenated, such as halothane, chloroform, and Freons, are generally not flammable.

Go back to Item XI and choose again.

Sorry, halothane will, but nitrous oxide cannot, produce respiratory arrest, - i.e. Stage IV anesthesia - under the conditions given.

You'll have to go back to Item XVI and try again.

Sorry, wrong choice. It is hard to see why facilitated AV conduction could predispose to occurrence of ventricular arrhythmias, and, in any case, the direct effect of general anesthetic agents is to slow or impair AV conduction. One might have expected that, perhaps, knowing the effect of anesthetic agents on cell functions generally. You might review this matter as it is presented in your text, even in your textbook of physiology!

Now go back to Item XIII and try again.

Of course, you're perfectly correct. Tubocurarine, too, acts to stabilize the post-junctional membrane, but specifically to the stimulant effects of acetylcholine released from the pre-synaptic nerve terminal and competing with tubocurarine for the same receptors. Succinylcholine - true to its chemical nature - acts like acetylcholine at the neuromuscular junction and causes depolarization of the cell subsequent to the drug's combination with receptors in the post-junctional membrane. Hence, ether acts additively, synergistically, with tubocurarine, and antagonistically to succinylcholine.

Under what circumstances might tubocurarine act synergistically with succinylcholine? Antagonistically?

It's time to go on to Item XVI.

Very good; not many students make this their first choice, by the way. You've recognized that at equilibrium Pa=PsK, and that potency, by definition, is inversely related to dose, or Pa, in this case. You need not have known the Pa for cyclopropane exactly; you may have known only that it's a gas at standard temperature and pressure and hence has a higher vapor pressure than 760 mmHg at 20°C. Hence it's more volatile and less potent than MF.

You know already, I'm sure, that concentration, expressed as volumes percent, is directly proportional to the partial pressure (P) of the gas in the gas-mixture. In fact, VOL% = P/760mmHg, or torr, at standard pressure.

The relationship Pa=PsK is, of course, a way of writing Raoult's Law - or Henry's Law, for that matter - in which K represents the mole fraction of anesthetic agent in solution. It can be read in this way, remembering that K is essentially the same for all anesthetic gases and vapors: at equilibrium, when the concentration of anesthetic material to which an organism is exposed is sufficient to produce anesthesia, the concentration relative to the vapor pressure of the material has a constant value, regardless of the agent. According to the ideas of Ferguson, when a certain fraction of, e.g., a cell is occupied by anesthetic agent, anesthesia is produced; this fraction (mole fraction) is the same for all inert, volatile materials used as anesthetics, expressed as a fraction of the vapor pressure of the pure agent.

Now go to Item V.

Right you are! Generally speaking post-operative nausea and vomiting occur when there is a relatively slow recovery from anesthesia, a relatively slow recovery of willful or involuntary control over vomiting mechanisms. I think we've agreed recovery from ether tends to be slower than recovery from the equivalent degree of anesthesia produced by nitrous oxide; if we're not agreed to this, I suggest you review Item VIII. In addition, of course, ether is by far the more irritating to the mucous membranes of the oro-pharynx and the tracheo-bronchial tree and the gastrointestinal tract (all the anesthetic gases pass into the gas bubbles that always exist inside the gastrointestinal tract); these factors - in addition to its sometimes unpleasant smell - would contribute to vomiting following ether, but not nitrous oxide, anesthesia.

Good, go on to Item XIII.

I'm afraid not; other things being equal, rate of onset of anesthesia is related inversely to the solubility of the anesthetic agent in the blood. The blood acts as a "buffer" between the concentration of agent in the alveolus and its concentration in the tissues. Therefore, in the case of ether and TF...

Go back to Item VII and make another choice.

You're right. Pa=PsK. At the higher temperature the vapor pressure of TF would be higher than at normal body temperature (37°), the partial pressure for anesthesia would be higher, and the potency would be lower in the hyperpyrexic patient. And it works out that way; See Anesthesiol 26: 764, 1965 and papers since then such as Fed. Proc. 33: 495 (#1605) 1974. You can now probably predict correctly the effect of hypothermia on anesthetic dose. Another thing that works out all right, as you may have noticed, is the fact of Pa=PsK, even though Ps may be given at 20°C instead of at 37°C, the temperature at which the pharmacologic action of general anesthetics and similar materials occurs. Needless to say the results turn out "better" when the vapor pressure and partial pressure are determined at the same temperature.

Go on Item VI.

Very good, you've made the correct choice. The dose of agent required to produce anesthesia, for these agents, is proportional to the vapor pressure, of course; you've undoubtedly referred, in your thinking, to the relationship Pa=PsK discussed in Item IV. Since the concentration-latency curves of MF and ether are parallel, by the terms of our problem, at any and all durations of exposure, the Pa, or C, for MF is greater than that for ether, and the CT for MF is greater than the CT for ether for any exposure time, T.

Go on to Item XI, now.

Incorrect: The probabilistic model explains selectivity in terms of the "multiplication" of effects in neurone chains of various lengths, regardless of the mechanism by which the function of the individual neurone is impaired. Sorry, go back to Item II and make another choice.

Sorry; diffusion constant is inversely related to the square root of molecular weight - and the square root of vapor density, too, according to Graham's Law. If the driving force of partial pressure differences and the area through which diffusion occurs are the same for BF and MF, then...

Go back to Item VI and select another choice.

Sorry. Pa=PsK; the partial pressure for anesthesia is proportional to the vapor pressure of the material. Concentration in volumes percent is directly proportional to the partial pressure (Pa) of gas required to produce anesthesia; VOL% = Pa/760 mmHg. Potency, therefore, is inversely related to partial pressure for anesthesia as potency is always inversely related to dose. Therefore MF should be less potent than ether. Go back to Item IV and make another choice.

Too bad, wrong choice. Perhaps you're confusing the properties of cyclopropane, which is not an oxidizing agent but is eminently flammable, with those of nitrous oxide, which is not flammable but is an oxidizing agent. Freons, by the way, aren't oxidizing agents.

Make another choice in Item XI.

Sorry; this is just another way of considering the relationship between vapor pressure for materials like TF, and the concentration of the material required to be inhaled to produce anesthesia. This one is rather like Item IV.

Go back to Item V and try again.

Sorry; you may well have remembered that rate onset of anesthesia is determined by the blood/gas solubility coefficient, but you've misremembered the relationship.

Go back to Item VII and try again.

Too bad. Since "moment-to-moment" control is a reflection of the rate at which depth of anesthesia can be increased or decreased, I suggest that you'd do well to go back to Item VII.

Of course, the probabilistic model explains selectivity of action on the CNS of such agents as these in terms of a "multiplication" of effects on information transmission in chains of differing numbers of serially arranged neurones. Selectivity of such agents for the central nervous system is explained in terms of a lesser sensitivity to the drug of such tissues as have their functional cells not arranged in serial order; in such tissues the effect of drugs on the function of the tissue represents the sum of the effects on individual cells. In any event, the probabilistic model explains selectivity of action in terms of what happens to the function of a group of cells after the function of individual cells has been altered, and, hence, without regard to the cellular mechanism of action of the drug. (See Intern. Anesth. Clinics 2:3, 1963).

Go on to Item III.

Sorry, it's really the other way around: halothane, but neither isoflurane nor nitrous oxide undergoes substantial biotransformation in the body. Might it be useful to review the relevant parts of your textbook?

Back to Item XIV, I'm afraid, and another choice.

True enough; why don't you make an additional choice or two from Item XVIII?

Too bad. Whatever the effects of the Freons on the heart, cardiac arryhythmias and sensitization of the heart to epinephrine are not characteristic of anesthesia with nitrous oxide. Why don't you refresh your memory concerning the cardiac effects of anesthetic agents by referring to your text. Then go back to Item XII and make another choice.

Sorry, unlike scopolamine, atropine has negligible central nervous system depressant effects in doses such as those described. Certainly, any such effects are of a kind and severity that do not permit or require reduction in the "induction dose" of thiopental. Should you review the pharmacology of atropine?

Go back to Item XIX and make another choice.

Stop! Whatever the Freons might do, occurrence of hypertension during surgical anesthesia is not characteristic of halothane. Review the cardiovascular effects of anesthetics with the aid of your text, go back to Item XII, and make another choice.

Stop! Disregarding cyclopropane for the moment, nitrous oxide can't be used under these conditions to produce Stage IV anesthesia.

Go back to Item XVI and please, try again.