Medical brain notes 7

  The gases Only two anesthetic gases (as opposed to vapors) deserve to be mentioned: nitrous oxide and xenon. Cyclopropane and ethylene are two explosive gases used in the past. Nitrous oxide Nitrous oxide has been around for centuries and is still widely used. Yet you will often hear it said that, if nitrous oxide were to be introduced today, it would never pass the FDA’s muster. For this jaundiced view, we can cite several reasons. ·             The gas is a weak anesthetic with a MAC of 105%. Thus, it would require a hyperbaric chamber to administer that concentration with enough oxygen to make it safe. In concentrations up to 70% in oxygen, it is an analgesic rather than a reliable anesthetic.   ·             Because it is such a weak drug, in the past people tended to give high concen-trations of it, which is another way of saying that it was given with marginal ...

  Comparing effects on heart, lung, and brain   All anesthetic vapors affect consciousness and have analgesic effects. They depress ventilation, as judged by decreasing minute ventilation and increasing levels of arterial carbon dioxide, with increasing depth of anesthesia. A few words about generally subtle differences between these drugs: Inhalation induction The older halothane and the newer sevoflurane have established for themselves a special niche because they are less irritating to the upper airway than the others. Particularly in children, who abhor needle sticks (and whose veins are more easily cannulated when the child is asleep), anesthesia can be induced quite gently by inhalation of nitrous oxide/oxygen together with either one of these two drugs. Cardiovascular effects All volatile agents depress myocardial contractility and cause peripheral vasodi-latation. As long as baroreceptors function normally, heart rate will increase in response to hypotension. In deep a...

  The opioids (Table  12.7 ) Today, narcotics play a major role in general anesthesia. Their advantage lies in their potent ability to abolish pain without depressing the heart. Their principle  side effect remains powerful respiratory depression resulting in a decreased res-piratory rate and finally respiratory arrest (Fig.  12.4 ).  This side effect can be tol-erated if we are prepared to ventilate the patient’s lungs, as we do routinely when patients receive neuromuscular blocking drugs and thus require mechanical ven-tilation. Unchecked respiratory depression and elevation of arterial carbon diox-ide can reduce resistance in the arterial bed of the cerebral circulation, leading to increased intracranial pressure. Chemoreceptor depression by opioids reduces the respiratory response to hypoxemia; however, the administration of oxygen to a hypoxemic patient may further depress ventilation, demonstrating that chemo-receptor activity still contributes to the resp...

  Neuromuscular blockers and their antagonists (Table  12.11 ) Even though the title presents the official name, we will call them muscle relax-ants with the understanding that we are talking about drugs used in anesthesia to facilitate tracheal intubation and to ease the surgeon’s work. The good news about muscle relaxants is that they affect only striated, voluntary muscles, but not the myocardium and the smooth muscles under autonomic control (including the uterus). Being quaternary ammonium compounds, all muscle relaxants carry a charge and thus do not readily cross the blood–brain barrier (no effect on the brain) or the placenta (no effect on the fetus). The bad news is that the relax-ants do not spare the muscles of ventilation. That fact has cost many lives when partially paralyzed patients became hypoxemic because inadequate ventilation was allowed to persist during and particularly after anesthesia. Do not forget that muscle relaxants have no anesthetic effect, that a...

  The local anesthetics (Table  12.13 ) Instead of flooding the whole system, from head to toe, with an inhalation or intravenous anesthetic, we can inject an anesthetic locally; directly on a nerve; place it into the epidural or subarachnoid space, catching several nerves at once; or paint or spray it on mucous membrane as a topical anesthetic. Local anesthetics come in two chemical classes: esters and amides, with tetracaine (Pontocaine®)  being a well-known ester and lidocaine (Xylocaine®) an even better known amide (Fig.  12.7 ).  A trick for remembering the class of local anesthetics: if there is an ‘I’ before the “caine” it is an amIde. The trick to the trick, though, is this only works for the  generic  name of the drug, e.g., bupivacaine is an amide, even when found in a bottle labeled Marcaine®.   Local anesthetics interfere with nerve conduction by blocking ion fluxes through sodium channels. This blockade occurs from the inside of the c...

  Bicarbonate As mentioned above, we add bicarbonate to those drugs prepared at a particularly acidic pH (lidocaine, chloroprocaine) to speed onset of anesthesia (it also reduces burning when making a skin wheal). Epinephrine We might add epinephrine to the local anesthetic solution to (i) prolong the dur-ation of anesthesia, particularly for vasodilating local anesthetics such as lido-caine; (ii) reduce peak plasma concentration of the local anesthetic, also more important for vasodilating agents; (iii) increase the density of regional anesthetic blocks (by an unknown mechanism); and (iv) as a marker for intravascular injec-tion. Because of epinephrine instability in an alkaline environment, commercial local anesthetic preparations containing epinephrine are highly acidic. We can add bicarbonate, and/or use plain local anesthetics to which we add epinephrine ourselves. Remember that 1:200 000 epinephrine is only 5 mcg/mL – use a tuber-culin syringe and measure carefully! Important...