In all cases of dental sedation patients should remain awake. If the patient tends to fall asleep, they should be awakened. It is very difficult if not impossible to tell a patient who has just dozed off from one who is under general anesthesia. General anesthesia, if a person is well trained, has been described as great amounts of boredom occasionally dispersed with moments of stark terror. I cannot recommend too strongly that unless you are well equipped, well trained, certified (in some states) and have extra insurance coverage to cover deep sedation/general anesthesia, you do not want patients to be unconscious and it is not possible to tell physiologic sleep from general anesthesia without trying to wake the person up. If the patient awakes, keep them awake. If they do not awaken, you have a case of general anesthesia and all the risks associated with anesthesia. Your biggest problem and concern will be to assure that adequate respiration continues and that cardiovascular parameters remain constant.

If patients do not easily awaken in response to one's voice, one should evaluate their level of sedation to determine whether they may, in fact, be under general anesthesia or have some medical problem. With some drugs, our concern must be that we have depressed the respiration to the point that an adequate exchange of gas is not taking place. It is not the scope of this discussion to describe the treatment of respiratory depression or arrest. However, the presence of an open airway should be established, evaluation of the level of respiration assessed and vital signs should be taken. It should be noted that several studies have shown that watching the chest and/or reservoir bag move is not adequate to assure an adequate minute volume. Skin color has been relied on in the past as a way of assuring adequate tissue profusion. However, the arterial oxygen level can be dangerously low before we see the blue tinge of cyanosis. Anyway, cyanosis is no longer considered to be an adequate monitor of arterial oxygen levels. In this case a pulse oximeter and/or capnograph is invaluable in assessing the adequacy of ventilation.

To properly appreciate the importance of monitoring respiration as well as the advantages of the benzodiazepine drugs, it would be wise to review a topic we all learned in dental school but in all likelihood have not had reason to refer to in our practices. It is with that thought in mind that I offer the following section. This is not intended to be a complete discussion. It should be used as the minimal level of knowledge one can possess and still have some appreciation of what we are doing with the drugs we use.

Physiological basis of ventilation

Ventilation is the movement or circulation of air through the respiratory tract and is the principal component of respiration influenced by depressant drugs. We can control our ventilation by conscious effort, however, our bodies have an exquisite system of sensors, reflexes, and feedback loops to control ventilation involuntarily. The involuntary control originates in the chemosensitive area of the respiratory center located in the ventral portion of the medulla. Metabolic processes of our body produce carbon dioxide (CO2) which is carried dissolved in our blood. When CO2 combines with the water in our plasma, it forms carbonic acid which disassociates into hydrogen ions and bicarbonate ions. The negative logarithm of our hydrogen ion concentration determines the pH of our blood. It is this pH which stimulates the chemosensitive region of the respiratory center.

Carotid and Aortic Bodies

The carotid and aortic bodies are closely associated with major arteries of the neck. These harbor other chemosensitive formations sensitive to the low arterial oxygen levels of the blood. Their greatest influence occurs at tension below 60 torr. Because normal levels are well above this value 95-99 torr, these serve as a back-up to the central CO2 sensitive chemoreceptors. Exceptions occur when the central chemosensitive area is depressed by sedative drugs or is tolerant to elevated CO2 tensions that accompany chronic obstructive pulmonary disease (COPD). Ascending impulses from this area travel via the IX and X cranial nerves to the respiratory center.

Respiratory Center Once the respiratory center is stimulated, impulses travel a short distance to the more dorsally located inspiratory area. This area produces descending neural impulses that lead to the inspiratory musculature causing a contraction of these muscles and inflation of the lung. Once the lung is inflated, stretch receptors ascend to depress the inspiratory area, allowing the inspiratory musculature to relax. This in turn allows the lungs to deflate. Although the involuntary respiratory control is most important during sleep and drug induced sedation or unconsciousness, it is also important in our minute-to-minute functioning while awake. It should be remembered that this system can be overridden by voluntary control. This is important as it allows us to talk. One should not forget that while the patient is conscious ventilation can be controlled voluntarily. Simply stated, a conscious but sedated patient can be told to breathe, should hypoventilation occur.

CNS depressants can depress ventilation by a number of methods. The opioid drugs -- those which stimulate the mu receptors - depress the sensitivity this system has for pH changes. This leads to a situation where the volume of air moved is less for any given concentration of CO2, but as the level of CO2 rises the increase in respiration to this increase is much less than normal (the response curve is "shifted to the right" but the slope of the curve is also depressed). This can lead to high CO2 levels. If the CO2 exceeds concentrations of 10%, it too is a respiratory depressant. The mu antagonists have also been found to depress peripheral hypoxic drive.

Benzodiazepines, in contrast to the opioids, tend to depress the slope of the CO2 response curve but do not appear to shift it to the right. It is fairly difficult to cause serious problems to respiration with benzodiazepines, with the possible exception of midazolam.

One further drug deserves mention. Subanesthetic doses of nitrous oxide (30% to 60%), such as used for sedation in dental practice, have little if any influence on the CO2 response but have produced a 65% reduction in the hypoxic drive. This could present serious problems if a deeply sedated patient has had CO2 mechanism depressed by opioid drugs or is a COPD patient.

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