4- Neuromuscular blockers

Isoflurane is a respiratory depressant (71). At concentrations which are associated with surgical levels of anesthesia, there is Htde or no depression of myocardial function. In experimental animals, isoflurane is the safest of the oral clinical agents (72). Cardiac output is maintained despite a decrease in stroke volume. This is usually because of an increase in heart rate. The decrease in blood pressure can be used to produce "deHberate hypotension" necessary for some intracranial procedures (73). This agent produces less sensitization of the human heart to epinephrine relative to the other inhaled anesthetics. Isoflurane potentiates the action of neuromuscular blockers and when used alone can produce sufficient muscle relaxation (74). Of all the inhaled agents currently in use, isoflurane is metabolized to the least extent (75). Unlike halothane, isoflurane does not appear to produce Hver injury and unlike methoxyflurane, isoflurane is not associated with renal toxicity. 

ATC M03AC09 Use neuromuscular blocker, nondepolarizing blocking drug... 

Up to 60-min time to recovery with a long-acting neuromuscular blocker (i.e., pancuronium, doxacurium)... 

Factors that Alter the Effects of Neuromuscular Blockers... 

Nondepolarizing neuromuscular blockers may be useful in severe, refractory cases... 

Paralysis usually is reserved for cases in whom sedation alone does not improve the effectiveness of mechanical ventilation. Neuromuscular blockers may lead to prolonged skeletal muscle weakness and should be avoided if possible. Patients requiring neuromuscular blockade are to be monitored and intermittent boluses should be utilized. 

The answer is c. (Hardman, p 1022.) Pyrantel pamoate is an antihelminthic that acts primarily as a depolarizing neuromuscular blocker. In certain worms, a spastic neuromuscular paralysis occurs, resulting in the expulsion of the worms from the intestinal tract of the host. Pyrantel also exerts its effect against parasites via release of acetylcholine and inhibition of cholinesterase. 

The answer is d. (Hardman, pp 142—M3.) ACh will stimulate both muscarinic and nicotinic receptors. Skeletal muscle contraction is mediated through NM receptors, and ganglionic stimulation is an effect of NN receptors All of the other effects listed in the question occur following muscarinic receptor activation and will be blocked by atropine and scopolamine, both of which are muscarinic receptor antagonists. Skeletal muscle contraction will not be affected by these drugs rather, a neuromuscular blocker (e.g., tubocurarine) is required to antagonize this effect of ACh. 

Halothane exerts a pronounced hypotensive effect, to which a negative inotropic effect contributes. Enflurane and isoflurane cause less circulatory depression. Halothane sensitizes the myocardium to catecholamines (caution serious tachyarrhythmias or ventricular fibrillation may accompany use of catecholamines as antihypotensives or toco-lytics). This effect is much less pronounced with enflurane and isoflurane. Unlike halothane, enflurane and isoflurane have a muscle-relaxant effect that is additive with that of nondepolarizing neuromuscular blockers. 

In addition to the medicines mentioned above, a number of opiate- and non-opiate-based analgesics, including COX-2 inhibitors, anaesthetics (e.g. propofol, desflurane, sevoflurane, ropivacaine, levobupivacaine and remifentanil), neuromuscular blockers (e.g. rocuronium bromid, zemuron, cisatracuiium, doxacurium. 

Nabazenil, 209 Naboctate, 209 Nafimidone, 90 Naflocort, 75 Nafoxidine, 65 Naftifme, 55 Nalmefene, 62 Naltrexone, 62 Napamezole, 87 Narcotic antagonist, 62 Nedocromil, 8 Nefazodone, 98 Neflumozide, 133 Netobimin, 36 Neuromuscular blocker, 69 Nifedipine, 106 Nilvadipine, 107 Nisoxetine, 30 Nitromifene, 65 Nizatidine, 95 Nomifensine, 146... 

---