Nitrous oxide (N20) is employed in dentistry for the primary purpose of reducing anxiety in the dental patient. It is estimated that 20 to 40 million adults in America avoid dental treatment because of fear.
The N20 gas was discovered by Joseph Priestly in 1772. By 1800, Sir Humphrey Davy had discovered its analgesic effect and recommended its use as an anesthetic. In 1844, Gardner Quincy Colton was publicly demonstrating the exhilarating effects of nitrous oxide as “laughing gas” while presenting popular science lectures. Dr. Horrace Wells, a dentist, observed one of these demonstrations and requested that Colton use it on him during dental treatment. Dr. Wells had a tooth extracted while under the influence of nitrous oxide and no pain was experienced! These two men unsuccessfully advocated use of this gas in dentistry from 1845 to 1863.
In 1868, Dr. Edmund Andrews, a Chicago surgeon, established the need to mix oxygen with nitrous oxide for use in operations of long duration. By the turn of the century (1903), Dr. Charles Teter, a Cleveland dentist, had applied this finding to invent the first nitrous oxide-oxygen machine.
After that time, periods of interest in nitrous oxide were followed by periods of little use. Research on the safe administration of nitrous oxide continued. In the 1950’s and 1960’s, nitrous oxide was becoming more frequently used in dentistry. The first “fail-safe” system was marketed in 1962.
These developments provided the basis for the system of nitrous oxide administration employed in dentistry today. Experiments continue on the physiologic actions and pharmacological effects of this gas. Much information is lacking; however, many questions have been answered during the research process.
Physiologic Effects of Nitrous Oxide
Two essential body systems are involved directly in the physiology of nitrous oxide. These systems include the nervous system and the respiratory system. A review of these systems and their relationship to the effects of nitrous oxide is essential prior to understanding the pharmacological effects of this gas.
The nervous system has two components: the central nervous system (CNS) and the autonomic nervous system (ANS). The CNS includes the brain and spinal cord. Three parts of the brain are
involved when nitrous oxide is administered: 1) the cerebrum, 2) the brain stem, and 3) the cerebellum. The cerebrum is responsible for conscious functions of the nervous system. The outer surface of the cerebrum is called the cerebralcortex. The cortex receives sensory information from the skin, eyes, ears, nose, mouth, etc. A person responds to sensations in these regions on the basis of past experience. For example, if a foreign object becomes lodged in the eye, the eye will water and the individual will close it immediately, based on previous experiences of relief when the eye is closed. An infant or young child may not respond as quickly if they had never experienced this sensation. When applying this information to dental pain and anxiety, it can be seen that the patient might react ot an oral injection by jerking or turning the head as the cortex receives this sensation from the oral cavity. The brainstem is located at the base of the brain continuous with the spinal cord. It is responsible for several functions which are applicable to the physiologic effects of nitrous oxide. These functions include:
the movement and sensation related to controlling the throat, neck and face;
the reflex activity involved in breathing;
the reflex activity involved in eye movement;
the control over the “wakefulness state” of the entire brain; and,
5. the major relay system and integration center for all senses except smell (called the thalamus).
Later in the module, effects of nitrous oxide on each of these functions will be discussed. The major point to consider, at this time, is that all pain sensations are relayed from the thalamus (a part of the brain stem) to the cortex. This is important because pain in the oral cavity will be received in the brain stem and relayed to the cortex for purposes of receiving that sensation. The patient then will react to pain based on the past experience.
If nitrous oxide is to slow pain reaction, or the patient’s response to pain, it must have a physiologic effect on these two parts of the brain (i.e., the cortex and the brain stem). The final segment of the brain, which is affected by nitrous oxide, is the cerebellum (see Figure 1 below). The cerebellum is responsible for a person’s orientation in space; therefore, light-headedness or a
F I G U R E 1
floating feeling may be related to effects on the cerebellum. Patients sometimes respond to nitrous oxide administration in this manner.
The second component of the nervous system that is involved in the physiology of nitrous oxide is the autonomic nervous system (ANS). It is responsible for innervating smooth muscle, viscera and glands which make-up many of the major internal body systems and/or organs. The innervation has a dual effect: increasing the activity of the tissue/organ and decreasing the activity of the tissue/organ. Some of these responses, which might be affected by the administration of nitrous oxide include:
dilation/constriction of the pupils,
acceleration/deceleration of the heart, and
Figure 1 includes a basic diagram of the brain and spinal cord. The major functions of each portion are outlined as a brief summary of the previously presented information relevant to physiology.
The second body system involved in the physiology of nitrous oxide is the respiratory system. Respiration is the transport of oxygen from the atmosphere to the cells and, in turn, transport of carbon dioxide from cells back to the atmosphere. When an individual breathes room air, oxygen is inhaled and carbon dioxide is exhaled.
The respiratory system can be divided into two segments: 1) those parts involved in transporting air from the atmosphere into the lungs and, 2) those parts involved in the exchange of gases from the lung into the blood stream and to the body’s cells. These portions of the respiratory system are called “external respiration” and “internal respiration,” respectively. External respiration involves the nose, pharynx, larynx, trachea, bronchi, and bronchioles. The final exchange of air from the lungs to the blood stream occurs in the alveolus. The alveolus is a pocket of air surrounded by a thin membrane that contains many capillaries (or small blood vessels). This thin wall is important for the rapid exchange of gases from the lung to the blood. There are 300 million alveoli (plural for alveolus) involved in respiration. Air is filtered, humidified and warmed as it travels to the lungs. It moves from the external environment through external respiration because of differences in pressure within the respiratory system. The inhaled air moves through the nose and throat, down the trachea to the lungs. Once the air reaches the lungs, it travels through the many smaller chambers until it reaches the smallest ones called the alveoli of the lungs. Here, gases are absorbed from the lungs into the blood stream. The blood stream carries oxygen to individual tissues and cells and the cells use it to complete their designated function. The cells undergo their own process of respiration and return carbon dioxide to the blood stream. The carbon dioxide is transported back to the lungs and exhaled into the atmosphere. Expired air has a higher concentration of carbon dioxide (4.0 %) than inspired air (0.4 %).
Normally, 97 percent of oxygen transported from lungs to tissue is carried by a chemical bond to hemoglobin. Hemoglobin is a pigment of the red blood cell. Oxygen uses this mechanism to attach to a red blood cell and be transported through the blood stream. In this way, hemoglobin buffers (i.e., reduces shock) oxygen to control air pressure in the tissues.
Sometimes breathing and respiration are not normal. A person may breath more or less rapidly than normal; or a person may breath normally, but respiration may not be completed properly due to some type of complication. The following terms are related to breathing and/or respiration and are defined here for clarity:
1. eupnea – normal breathing;
2. tachypnea – rapid breathing;
3. bradypnea – slow breathing;
4. hyperpnea – over respiration;
5. hypopnea – under respiration;
6. anoxia – total lack of oxygen;
7. hypoxia – decreased oxygen in tissue.
The effect of nitrous oxide on breathing and respiration will be discussed later in the module. At this time, the information relevant to physiology should be reviewed and understood prior to proceeding to the pharmacology of nitrous oxide.
Pharmacologic Effects and Properties of Nitrous Oxide Nitrous oxide is a nonirritating, colorless gas with a sweet taste and odor. It is dispensed a liquid under pressure in a container which is always marked BLUE for identification. The gas is stable at normal temperatures; it is non-flammable, but will burn readily if ignited. Nitrous oxide is soluble in water. It is a relatively safe gas; however, all gases should be handled with caution.
Nitrous oxide is a true general anesthetic and meets all of the properties of anesthetics. It is the least potent of all anesthetic gases. For example, halogen (an anesthetic gas used for surgical depth anesthesia in operating rooms) is 100% potent. Nitrous oxide is approximately 15% potent. The fact that N2O is a weak agent is beneficial for its use in dentistry because of its wide margin of safety.
The exact mechanism by which anesthetics act on the brain is unknown. Nitrous oxide travels through the respiratory system from the nose to the lungs in the same manner as oxygen. The gas is transferred into the blood stream through the alveoli in the lungs. The difference between respiration of nitrous oxide and respiration of oxygen is found in the transport of nitrous oxide through the blood stream. Rather than attaching to hemoglobin for transport (as oxygen does), nitrous oxide travels through the blood stream in a free gas state, without combining with any cell or portion of a cell. Nitrous oxide replaces nitrogen (N2) in the blood and because it is much more soluble that nitrous or oxygen, large volumes of N2O are absorbed. Total saturation in the blood occurs within 3 to 5 minutes of N2O-O2 administration. This fact is important because a patient may not react to initial administration within this time period. The clinician should be cautious about increasing the N2O concentration until maximal clinical effect has occurred.
At one time, it was thought that the anesthetic effect of N2O was caused by a decrease of oxygen (hypoxia) in the cells of the brain. It is now known that N2O can, even in the presence of adequate oxygen, cause an effect on the central nervous system (brain and spinal cord). Tissues with a greater blood flow—such as the brain, heart, liver, and kidneys—will receive greater amounts of N2O and absorb higher concentrations because the blood supply is saturated with the gas; thus, brain cells will react most readily to administration of nitrous oxide. The cerebrum, thalamus and midbrain functions discussed previously will be depressed when N2O inhalation anesthesia is delivered.
Because of the depressing action of N2O on the brain, signs and symptoms of nitrous oxide can be related to the CNS. Somnolence is the production of sleep. Since the brain stem is responsible for the “wakefulness state” of the brain, this symptom of N2O can be correlated with effects on the brain stem. Dissociation, or a distorted spatial orientation, can be related to the function of the cerebellum since it is responsible for orientation in space. Finally, decreased sensory perception, which reduces a person’s ability to perceive pain, can be correlated with effects on the thalamus and cortex. Remember, all pain sensations are relayed from the thalamus to the cortex. Almost all forms of sensation are depressed including not only pain but also sight, hearing, and touch. Memory also is dulled with degree of amnesia depending on concentration of N2O administration.
The uptake of nitrous oxide by other tissues with a lesser blood supply than the brain, like muscle and fat, absorb only a very small amount of N2O. For this reason, recovery from nitrous oxide after its administration is relatively fast. Only minute traces of nitrous oxide (1%) can be found in the blood several hours after administration.
As mentioned previously, the total circulation time for one breath of N2O is three to five minutes. This means that the gas is absorbed into the blood stream, transported through the body and returned to the lungs at a fairly rapid rate. Likewise, the diffusion of N2O from the blood stream after administration is terminated is quite rapid. If the patient is permitted to breath room air at this time, a phenomenon called “diffusion hypoxia” occurs. Diffusion hypoxia causes decreased oxygen and results in nausea, headache, and lethargy—or a “hangover” feeling. In order to prevent it, the clinician must always administer 100% oxygen to a patient for at least three to five minutes immediately following administration of N2O. Oxygen is administered until the patient regains normalcy; recovery is rapid and complete and negative side effects are prevented.
When administrated properly, N2O-O2 has little effect on other parts of the central nervous system, on the cardiovascular system, or on the respiratory system. The total circulation time for one breath of nitrous oxide/oxygen is three to five minutes. There are no changes in heart rate (pulse) or blood pressure. Changes in respiratory rate are related more to the relaxation of the patient than to the nitrous oxide itself; it is nonirritating to the lungs. With higher concentrations of nitrous oxide, greater than 70%, hypoxia can occur. Depression of heart rate, respiration, and brain functioning can occur. For this reason, it is imperative that appropriate levels of nitrous oxide and oxygen are administered. Side effects can be avoided with proper techniques and concentrations.
Pharmacologic effects of N2O-O2 will differ between patients. Average effects with various concentrations of N2O are:
100% will produce anoxia.
80% will produce hypoxia with hallucinations and bizarre dreams; may cause respiratory, cardiovascular, kidney, or liver damage.
65% can cause patients to enter the excitement stage.
35% usually provides maximum analgesia with maintenance and cooperation of the patient.
25% is claimed as analgesic as 10mg morphine sulfate.
Because the needs of individual patients will vary, the trituration method is recommended for administration of N2O-O2. In this method, the concentration of N2O is slowly increased until the patient has reached an acceptable level of analgesia. Concentrations over 50% should not be administered without special consideration.
Side Effects and Adverse Reactions As stated previously, side effects can be minimized or prevented with proper administration. Nausea is the most common side effect. Its incidence increases:
1. with prolonged administration or rapid induction,
2. with higher concentrations of N2O,
3. following a heavy meal,
4. following fasting (empty stomach),
5. in motion sickness sufferers or patients with pervious history of vomiting.
Nausea can be prevented by using the lowest effective concentration, administering oxygen every 45 minutes during prolonged procedures, suggesting that patients eat a light meal prior to the appointment, and avoiding use in patients with motion sickness or with a previous history of vomiting.
Adverse reactions associated with N2O are infrequent. When concentrations below 50% are used and nitrous oxide is administered by the trituration method, the record of patient safety is excellent. Clinicians must be careful not to become complacent, however, assuming that N2O is harmless. The potential for adverse reactions increases with improper administration and with higher concentrations.
The following are known adverse reactions which can be prevented:
1. Hypoxia: most obvious and immediately lethal effect. Always administer enough oxygen. Check analgesia machine regularly, and especially after refilling tanks, to be sure fail safe system is operating correctly. Also, be sure to fully oxygenate patients upon completion of administration in order to prevent diffusion hypoxia.
2. Bone Marrow Depression: nitrous oxide may have some cytotoxic effect in humans, especially with increased frequency of use. This hazard may not be relevant to dental inhalation unless a patient receives frequent and prolonged exposures to N2O. But, dental personnel who frequently use N2O should be concerned.
3. Pressure/Volume Effect: N2O diffusion into any air-containing body cavity temporarily increases either the volume or the pressure in the air space. These changes can affect the middle ear and auditory acuity, intestinal gas volume leading to gastrointestinal distension, or air emboli in the blood stream.
4. Psychologic Reactions: particularly hallucinations or claustrophobia. Patients with a history of psychiatric disorders should not receive N2O without special consideration and medical consultation. Also, since dreams and hallucinations associated with N2O are sometimes sexually oriented, the operator should not be alone while administering it.
5. Fire: N2O is combustible. Be particularly careful when using electrocautery. Also, never allow grease to contact valves of N2O tanks.
6. Protective Reflexes: present knowledge is incomplete. It seems that normal protective reflexes remain intact, yet reactive gag reflexes of anxious patients are reduced. Methods for prevention of airway complications are recommended.
REMEMBER: The safety of any pain control technique depends upon the health status of the patient, the inherent toxicity of the drug used, and the competence of the practitioner.
ANESTHESIA AND ANALGESIA As stated previously, nitrous oxide is classified as an anesthetic; however, many dental practitioners refer to it as an analgesic. The terms anesthesia and analgesia need to be understood prior to discussing the administration of this drug.
Anesthesia produces a lack of all sensation. When an injection is given for local anesthesia, the nerve is blocked and the patient does not feel pain in that particular area. Surgery is often performed under a general anesthetic and the patient is unconscious, thereby producing a total lack of sensation. Analgesia creates a decreased ability or inability to perceive pain. Total analgesia completely eliminates a patient’s reaction to pain. Relative analgesia, which is accomplished in dentistry through the use of nitrous oxide, decreases a patient’s pain reaction; but, the patient is able to cooperate. Sedation is the calming of a nervous apprehensive patient without loss of consciousness.
General anesthetics can be employed to various levels to produce analgesic results or anesthetic results depending upon desired effects. There are four stages of anesthesia. An explanation of each stage follows.
Stages of Anesthesia I. Analgesia:the patient is conscious, comfortable, and cooperative. Pain reaction is decreased.
II. Delirium: this is the excitement stage. The patient becomes extremely stimulated, raged and possibly angry. Loss of consciousness begins in Stage II. Delirium is an undesirable effect; therefore, it should be avoided.
III. Surgical: at this point, the patient is unconscious and life support is required. There is a total lack of sensation.
IV. Respiratory Paralysis: death occurs in this stage.
When a general anesthetic is administered for surgery, the patient is brought through the first two stages rapidly and maintained in stage three. Any of the general anesthetics, however, can be utilized to maintain a patient in stage one: analgesia. Nitrous oxide is particularly good at this level because it is a relatively weak general anesthetic. In dentistry, nitrous oxide most commonly is utilized at analgesic levels. This is why many practitioners refer to nitrous oxide as an analgesic even though it is classified as an anesthetic.
The stage of analgesia has been divided further into three planes. Each plane has a variety of possible signs and reactions; although, all of them probably will not be seen in one particular administration. A list of clinical manifestations for each plane of analgesia follows.
Planes of Analgesia: Clinical Effects 1. Plane 1
a. Patient appears normal, relaxed, awake.
b. Patient may feel slight tingling in toes, fingers, tongue, or lips.
c. Patient may giggle.
d. There are no definite clinical manifestations.
e. Vital signs remain normal.
2. Plane 2 a. Patient may have dreamy look.
b. Reactions of patient are slowed.
c. Partial amnesia may occur.
d. Voice will sound “throaty.”
e. Patient will feel warm and drowsy.
f. Patient may drift in and out of environment.
g. Patient may hear pleasant ringing in ears.
h. Vital signs may remain normal.
i. Pain is reduced or eliminated but touch and pressure is still perceived.
j. Patient is less aware of surroundings; sounds and smells are dulled.
3. Plane 3
a. Patient becomes angry with hard stare.
b. Patient’s mouth tends to close frequently.
c. Patient no longer cooperates.
d. Patient is totally unaware of surroundings.
e. Patient may hallucinate.
f. Patient’s chest may feel heavy.
g. Sensation of flying or falling or uncontrolled spinning.
h. Pupils may dilate.
It is essential that clinicians who administer nitrous oxide become totally familiar with the signs and symptoms of each plane in order to maintain a patient at the desired level. In most cases, plane two will be ideal. The patient will be comfortable, pain reaction will be decreased or eliminated, and the patient will be able to cooperate. Plane three is undesirable because, at this point, the patient is approaching stage two of anesthesia (delirium). If the patient is in deep plane two, approaching plane three, he/she will not hear you or the mouth will tend to close. The patient also may not be able to follow instructions. At this point, the concentration of nitrous oxide should be reduced so that the patient is maintained in plane two. These symptoms might occur before plane three; but pain will still be perceived. Tables 1-3 describe clinical manifestations in each plane of analgesia. Each clinician involved in the monitoring or administration of nitrous oxide must be able to recognize clinical manifestations in each plane of analgesia in order to monitor the patient’s response. Be sure to study the information presented in this section and in these tables prior to proceeding to the next segment of the module.
T A B L E 1 The Planes of Analgesia: Plane 1
Normal and regular
Pupils normal and contract normally to light; conjuntiva sensitive
Patient maintains an open mouth without mouth props
A feeling of relaxation; may experience tingling in fingers, toes, lips and tongue
NOTE: Some patients prefer Plane 1, especially if they are apprehensive about N2O effects, or unfamiliar with feelings of sedation
T A B L E 2 The Planes of Analgesia: Plane 2
Normal, but breathing may be slower due to relaxation
Normal, but relaxed
Pupils normal; rate of winking reduced; a relaxed dreamy, far-away look
Patient maintains an open mouth without mouth props
Patient follows directions
Yes, but more slowly
Degree of Amnesia
Moderate to complete
Effect on Pain
Pain reaction markedly reduced or eliminated
Effect on Fear
Appearance of Patient
Relaxed; euphoric; less aware of immediate surroundings and less concerned with activity around him/her
May feel a warm wave suffuse entire body; humming, droning, or vibratory sensation; a feeling of headiness, lethargy or drowsiness; voice becomes “throaty”; a feeling of euphoria, safety; thoughts may wander beyond treatment room; less idea of lapse of time
NOTE: Plane 2 is considered ideal for many apprehensive, anxious or fearful dental patients.
T A B L E 3 The Planes of Analgesia: Plane 3
May be normal, irregular, superficial or prolonged
Usually normal; sometimes rigid mandible or rigid body
Very hard stare; angry or very sleepy look; eyes may close; eyeball may become eccentric; pupils may be dilated
Normal; may be accelerated
Patient maintains an open mouth without mouth props
No—mouth tends to close. May open if operator presses on lower lip, but immediately closes again
Patient follows directions
Degree of Amnesia
Effect on Pain
Pain reaction eliminated
Effect on Fear
A short exposure (1-2 minutes) to this plane is useful for controlling extreme fear; longer exposure brings many patients into a state of fear, and then excitement
Appearance of Patient
Begins to assume appearance of unconsciousness, totally unaware of surroundings; jaw may become rigid; body may stiffen
NITROUS OXIDE-OXYGEN INHALATION SEDATION The primary reason for administration of N2O-O2 to dental patients is to reduce fear and anxiety. Even non-threatening dental procedures can be traumatic for patients who experience dental fear. Dental office personnel have the responsibility of selecting appropriate cases for administration of nitrous oxide. An updated, thorough personal and health history must be completed for each patient prior to administration. Indications (reasons why N2O-O2 should be given) and contraindications (when N2O-O2 should be avoided) are discussed in this section.
Primary Indications 1. Fear and Anxiety Fearful or anxious patients will present patient management problems. They also are more prone to medical emergencies because stress can initiate an exacerbation of their medical problems. Patients who have a history of upsetting or painful experiences in the dental office may be more anxious. Nitrous oxide-oxygen sedation can serve to safely relax most fearful or anxious dental patients. Some persons, however, are not comfortable with the effects of N2O and others will not achieve adequate sedation at safe concentrations. When adequate sedation cannot be achieved within safe limits, another form of sedative should be selected for that patient.
2. Patient who refuses or is allergic to local anesthesia Although N2O-O2 is not a true substitute for local anesthesia, it can be used to reduce pain sensation when local anesthesia is contraindicated.
3. Prominent gag reflex Gagging is a potential problem during many dental procedures. Administration of
N2O-O2 will reduce or eliminate severe gagging without jeopardizing protective cough reflexes. Seating the patient in an upright position might also be helpful.
4. Patient gets impatient at long appointments Patients who are nervous or stressed sometimes become impatient at long appointments. Because nitrous oxide reduced the patient’s awareness of the lapse of time, it can be beneficial in these cases. A clinician should, however, administer pure oxygen every 45 minutes to reduce the potential for adverse reactions associated with prolonged administration.
Indications with Special Consideration In the recent past, N2O-O2 sedation has become increasingly important in management of medically comprised patients. It is particularly indicated when these patients are stressed or anxious because stress can result in an oxygen deficit or cause an acute exacerbation of an underlying medical problem. Nitrous oxide should only be administered to these patients with special consideration given to each case. It is critical to determine whether the medical condition is under treatment and control. If not, administration of N2O is not recommended. A physician consultation is recommended prior to administering N2O-O2 sedation. As long as the following conditions are not severe, nitrous oxide is the sedative of choice because of its margin of safety and its adjunctive use of oxygen during administration.
1. Cardiovascular disease N2O-O2 inhalation sedation can minimize the risk of myocardial infarction (heart attack) or angina pectoris (chest pain) resulting from stress during a dental appointment. It is the most appropriate technique for sedating patients with a history of cardiovascular disease. It is not recommended, however, within 6 to 9 months following a heart attack or when there is cardiac dysfunction.
2. Cerebrovascular disease The patient who has cerebrovascular disease, or a history of a stroke, can receive N2O-O2 for stress/anxiety reduction. Levels beyond 50% are not recommended due to the threat of hypoxia.
3. Respiratory disease: asthma
Patients with bronchial asthma can receive nitrous oxide because it is nonirritating to the bronchial and pulmonary tissues. Increased stress can lead to an asthmatic attack; therefore, N2O-O2 sedation can be helpful. Refer to contraindications for respiratory disease that prohibit the use of nitrous oxide.
4. Hepatic disease
of drugs because the agent is biotransformed in the liver. Since N2O-O2 is not biotransformed anywhere in the body, it can be used in patients with hepatic disease.
5. Epilepsy and other seizure disorders
Again, because stress might trigger the onset of a seizure, the use of N2O-O2 can be useful in these patients. It is important to avoid hypoxia; therefore, higher concentrations of N2O must be avoided.
6. Patients taking tranquilizers, analgesics, antidepressants, or hypnotics
Many of these drugs cause depression of the central nervous system; therefore, it is difficult to predict and control the pharmacological effects of nitrous oxide. All drugs taken by patients who are to receive nitrous oxide should be evaluated for effects on the CNS, or for contraindications with anesthetics. Some examples include tranquilizers (diazepam), analgesics (morphine, percodan, meperidine), and hypnotics (barbiturates). Nitrous oxide should not be used in conjunction with these drugs unless absolutely necessary. If used, N2O should be administered in low concentration.
7. Patients using alcohol Nitrous oxide is not recommended for patients who are chronic alcohol abusers or for patients who may have had a social drink immediately prior to the dental appointment.
8. Allergies There are no known allergies to nitrous oxide
9. Thyroid disease Hyperthyroidism or hypothyroidism routinely causes the dental professional to be more cautious in the administration of certain drug groups (e.g. Vasopressers, CNS depressants). In most instances, however, the patient will have a normal level of thyroid activity because of drug therapy or surgical intervention to control hyperthyroidism or hypothyroidism. A physician consultation to determine current status is indicated.