A wide range of drugs are available for inducing anesthesia and providing neuromuscular blockade. All intravenous anesthetics and sedatives (except etomidate and ketamine) have the potential for causing cardiovascular collapse by either myocardial depression or vasodilatation (direct or by histamine release). This likelihood is reduced by ensuring adequate cardiovascular resuscitation, using as small a dose as is feasible, and being aware of the possibility of a slow circulation time in the critically ill and therefore a slow onset of anesthesia.
Sedatives can be used as an adjunct to intubation under local anesthesia. However, even small doses in the very ill can lead to unconsciousness, a compromised airway, or hypotension. If used as the sole agent for inducing anesthesia, the onset of action is slower than the general anesthetic agents. Midazolam (dose range 0.1-0.35 mg/kg) acts appreciably faster than diazepam (dose range 0.1-0.6 mg/kg).
Any of the natural or synthetic opioids can be used, but the newer synthetic derivatives such as fentanyl and alfentanil have a more rapid onset and shorter duration of action, together with negligible cardiovascular effects. Therefore, if used in conjunction with an intravenous anesthetic agent, they allow a reduction in dose of that agent and hence greater cardiovascular stability. Morphine can cause hypotension due to histamine release and meperidine in high doses causes myocardial depression, but fentanyl and alfentanil in high doses have minimal effects on the heart and vasculature.
Opiates in high doses can be used as sole agents for anesthetic induction, but the onset is slower than when they are combined with an intravenous anesthetic agent. A good combination is to use a moderate dose of opioid prior to giving an anesthetic agent. This will achieve both a rapid onset of anesthesia and obtund the hypertensive response to laryngoscopy and intubation, if this is undesirable in a particular patient.
Opiate dose ranges are shown in Table3.
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Table 3 Opiate doses
All anesthetic induction agents have the potential to produce cardiovascular collapse in the critically ill, particularly if the dose and speed of injection are not modified to take account of the severity of illness. A slow circulation time means that further incremental doses may be given before observing the effect of a dose that has already been administered. Thus there may be an unnecessary accumulation of both dose and adverse effects.
Ketamine (by sympathetic nervous system stimulation) and etomidate (by lack of depressant effect) are least likely to cause hypotension, but the onset of effect of intravenous ketamine is slightly slower than that of the other agents. The neuropsychiatric side-effects may be minimized by the concurrent administration of a benzodiazepine such as diazepam 0.1 to 0.2 mg/kg intravenously. Ketamine may also be given by the intramuscular route, although this takes several minutes to be effective. However, it has the additional advantages of providing analgesia and retaining some degree of muscle tone, thereby aiding maintenance of a patent airway in the unconscious patient. Ketamine and etomidate may also be preferred in the patient with bronchospasm as neither cause histamine release. Etomidate causes pain on injection and myoclonia, while ketamine should not be used where there is pulmonary hypertension or when any increase in systemic vascular resistance is contraindicated.
Thiopental (thiopentone) and propofol can both lead to potentially severe hypotension in the critically ill patient by direct myocardial depression or vasodilatation. Again, this risk is minimized by slow injection, the use of the smallest dose feasible, and the use of adjuncts such as opiates and sedatives. Propofol causes pain on injection and should not be used if there is a history of convulsions. Thiopental is an effective anticonvulsant but is contraindicated in porphyria.
Dose ranges of anesthetic inuction agents are shown in T§bJe,„.,4. team« ¡qjfyJVori|bK)M|ftlt
Table 4 Anesthetic induction agent doses
Succinylcholine (suxamethonium) is the only agent currently available which provides good intubating conditions in less than a minute. At a dose of 1 mg/kg it causes initial neuromuscular excitation exhibited as muscle fasciculation, followed by flaccid neuromuscular blockade within one arm-brain circulation time. Structurally, it has two acetylcholine molecules linked through the acetate and methyl groups. Succinylcholine has important cholinergic side-effects such as bradycardia. There is the possibility of prolonged paralysis in those with a deficiency in plasma cholinesterase which normally rapidly metabolizes succinylcholine; variants of this deficiency occur in up to 4 per cent of the population. Patients with liver disease may also be deficient in this enzyme. Malignant hyperpyrexia is another important adverse effect. Its effect may last for 3 to 4 min and repeat doses may be used if necessary, although cholinergic effects are more likely and atropine 0.3 to 0.6 mg should be given concurrently.
Once intubation is performed, longer-duration neuromuscular blockade can be achieved with a variety of non-depolarizing agents (e.g. atracurium, vecuronium, mivacurium, pancuronium). The choice depends on concurrent disease (e.g. delayed metabolism and excretion of vecuronium and pancuronium in hepatic and renal disease) and histamine release leading to bronchospasm and hypotension (atracurium and, less so, mivacurium). Important drug interactions, such as prolonged blockade with the aminoglycoside antibiotics, some antiarrhythmic drugs, and local anesthetics, may occur in the intensive care setting.
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