Anesthetic action has three principal components: immobility, amnesia, and unconsciousness. Immobility Immobility is the easiest anesthetic end point to measure. Edmond Eger and colleagues introduced the concept of minimal alveolar concentration (MAC) to quantify the potency of an inhalational anesthetic. They defined 1.0 MAC as the partial pressure of an inhalational anesthetic in the alveoli of the lungs at which 50% of a population of nonrelaxed patients remained immobile at the time of surgical skin incision. Anesthetic immobility is mediated primar-ily by neural inhibition within the spinal cord but may also include inhibited nociceptive transmission to the brain. Amnesia The ablation of memory arises from several locations in the CNS, including the hippocampus, amygdala, prefrontal cortex, and regions of the sensory and motor cortices. Memory research-ers differentiate two types of memory: (1) explicit memory, ie, specific awareness or consciousness under anesthesia; and (2) implicit memory, the unconscious acquisition of information under adequate levels of anesthesia. Their studies have found that formation of both types of memory is reliably prevented at low MAC values (0.2–0.4 MAC). Prevention of explicit memory (awareness) has spurred the development of monitors such as the bispectral index, electroencephalogram (EEG), and entropy moni-tor of auditory evoked potentials to help recognize inadequate planes of anesthesia. Consciousness The ability of anesthetic drugs to abolish consciousness requires action at anatomic locations responsible for the formation of human consciousness. Leading neuroscientists study-ing consciousness identify three regions in the brain involved in generating personal awareness: the cerebral cortex, the thalamus, and the reticular activating system. Neural pathways emanating from these regions seem to interact as a cortical system to produce the mental state in which humans are awake, aware, and perceiving. Our current state of understanding supports the following framework: sensory stimuli conducted through the reticular for-mation of the brainstem into supratentorial signaling loops, con-necting the thalamus with various regions of the cortex, are the foundation of consciousness. These neural pathways involved in the development of consciousness are reversibly disrupted by anesthetic agents.
B. Cardiovascular Effects
Halothane, enflurane, isoflurane, desflurane, and sevoflurane all depress normal cardiac contractility (halothane and enflurane more so than isoflurane, desflurane, and sevoflurane). As a result, all volatile agents tend to decrease mean arterial pressure in direct proportion to their alveolar concentration. With halothane and enflurane, the reduced arterial pressure is caused primarily by myocardial depression (reduced cardiac output) and there is little change in systemic vascular resistance. In contrast, isoflurane, desflurane, and sevoflurane produce greater vasodilation with minimal effect on cardiac output. These differences may have important implications for patients with heart failure. Because isoflurane, desflurane, and sevoflurane better preserve cardiac output as well as reduce preload (ventricular filling) and afterload (systemic vascular resistance), these agents may be better choices for patients with impaired myocardial function.
Nitrous oxide also depresses myocardial function in a concentration-dependent manner. This depression may be significantly offset by a concomitant activation of the sympathetic nervous system resulting in preservation of cardiac output. Therefore, administration of nitrous oxide in combination with the more potent volatile anesthetics can minimize circulatory depressant effects by both anesthetic-sparing and sympathetic-activating actions.