P: Posture

The approach described is for a patient who reports dizziness, lightheadedness, or feeling faint, among other signs of impending unconsciousness, namely, lying down with the feet raised 15–30°. If the patient does not recover consciousness after a few seconds with this maneuver, then we should suspect a more severe underlying condition (i.e. arrhythmia, myocardial infarction, cerebrovascular accident, hypoglycemia) (Greenwood 2008; Sambrook et al. 2011).

A: Airway

1. Remove any apparatus from the mouth, for example gauze, cotton rolls, removable dental prosthesis, removable orthodontics devices, rubber dam, clamps, etc.
2. Clear the airway of obstruction by soft tissue, mainly a closed tongue, which falls backwards. Leave the patient’s head in a horizontal position by removing the extra head supports before performing the following maneuvers:
   • Head tilt‐chin lift maneuver (standard maneuver) (Figure 23.2).
     • The dentist places him/herself to the side of the patient’s head and, with the palm of the hand on the forehead, pulls downward. With the index and middle finger of the other hand placed on the symphysis menti, the dentist pulls upward until the imaginary line that joins the earlobe with the chin is perpendicular to the floor. Thus, the head is turned backward and the neck extended.
     • During this maneuver, we should ensure that the patient’s mouth is not fully closed and that the full extension of the neck does not obstruct the airway.
   • Jaw‐thrust technique (Figure 23.3). Sometimes, the previous technique may not be sufficient to clear the upper airway. The head tilt‐chin lift maneuver may not be applicable if the patient has a limited range of motion, such as one acquired by having a cervical spinal fusion or cervical disc herniation. The jaw‐thrust technique allows manipulation of the airway without movement of the head or cervical spine. The technique is as follows:
     • The dentist places him/herself behind the patient’s head and places his/her index and middle fingers behind the posterior border of the mandibular ramus, with one hand on each side, and pulls the mandible upward.
     • The lower lip can be pulled back with the thumbs to help the patient exhale through the mouth and nose.
     • This maneuver is uncomfortable. However, any audible complaint from the patient is a positive sign because it shows that the degree of unconsciousness is not so deep.

B: Breathing

1. With the hands on the patient’s face to maintain the head tilt‐chin lift position, the dentist places his/her head with the ear approximately 2 cm from the patient’s nose and mouth and with the face looking toward the patient’s chest. This position enables the following (Figure 23.4):
   • The dentist can hear and feel air entering and leaving the patient’s nose and mouth (very reliable).
   • The dentist can see the movements of the patient’s chest. This is not as reliable since, while it shows that the patient is trying to breathe, it does not guarantee that gas exchange is taking place (as the diaphragm may be working against an obstructed upper airway). Sometimes, the patient’s clothing prevents the dentist from observing the movement of the chest.
2. A bubbling/gurgling noise indicates that the airway is partially obstructed by blood, saliva, water, secretions, or vomit and should be cleared. The approach to adopt is as follows:
   • The dentist positions the head downward and places the patient’s head turned to one side to facilitate expulsion and prevent the aspiration of liquids and debris.
   • The dentist opens the patient’s mouth with the index and middle finger and inserts an aspirator to suck out liquids and debris. The cannula can even be inserted – carefully – in the posterior part of the mouth and lower pharynx to remove any remaining debris. The cannular should be plastic (not metal) so as not to further damage soft and hard tissue.
3. If the patient is not breathing and there is no debris, the dentist should undertake artificial respiration maneuvers (not covered in this book). Please consult guidelines such as those of the European Resuscitation Council and the American Heart Association.

C: Circulation

At this point, the most important action is to palpate the carotid artery. With the patient in the low head tilt‐chin lift position, remove the hand from the chin and, as the patient has his/her neck stretched, palpate the thyroid cartilage (Adam’s apple). The carotid pulse is checked by placing the index and middle fingers between the thyroid cartilage and the sternocleidomastoid muscle.

If the pulse is weak but present, maintain the position until the patient recovers or until the emergency services arrive (see below) in the case of a patient whose condition remains unchanged or worsens.

If no pulse is felt for 10 seconds, start cardiopulmonary resuscitation. These maneuvers are beyond the scope of this book, although they are very well explained in other books and guidelines (Bennett and Rosenberg 2002; Malamed 2007; Monsieurs et al. 2015; Panchal et al. 2020; Topjian et al. 2020).

Note: The assistant can place a stethoscope on the patient’s chest to evaluate the heart rate and take the patient’s blood pressure with a sphygmomanometer. If the situation persists, the patient should be assessed every 5 minutes (heart rate, blood pressure, and breathing rate).

Pathophysiology

The severe emotional reaction induced by anxiety leads to three types of reaction:

1. Severe hypotension. This is the main type of syncope. The emotional reaction and pain activate the parasympathetic nervous system in the brain (cholinergic), which acts via the vagus nerve (cranial nerve X), leading to the following:
   • Dilation of the vessels of the abdominal viscera (splanchnic circulation) (Bourne 1980).
   • Dilation of the vessels of the skeletal muscles in the absence of physical activity due to the lack of a fight or flight reaction (Harrison 1973; Edmondson et al. 1978; Bourne 1980).
   • Reduction in heart rate (bradycardia).

   These factors in turn lead to a severe reduction in blood pressure and therefore a reduction in blood flow to the brain. Curiously, the effect of this reaction can be triggered by stimulation of the autonomic nervous system (Taggart et al. 1976).

2. Hyperventilation syndrome. This syndrome does not always accompany vasovagal syncope, although when it does, the level of carbon dioxide (CO₂) falls, leading to a marked reduction in the concentration of this gas in blood (hypocapnia) and respiratory alkalosis caused by the increase in pH resulting from the reduction in carbonic acid. CO₂ is a key factor in the self‐regulation of cerebral blood flow, which is independent of arterial pressure, therefore the reduction in CO₂ causes cerebral vasoconstriction, reducing blood flow to this organ (Harrison 1973; Campbell et al. 1976; Noble 1977; Salins et al. 1992) and peripheral vasodilation (Noble 1977).
3. Hypoglycemia. The parasympathetic reaction leads to increased insulin levels, which in turn reduces the blood glucose level (hypoglycemia). This also deteriorates because the hyperglycemic effect of epinephrine is reduced in situations of respiratory alkalosis due to hyperventilation, as reported elsewhere (Salins et al. 1992). Interestingly, blood sugar levels tend to self‐regulate after the vasovagal syncope (Salins et al. 1992).

Predisposing Factors

As we have seen, anxiety, fear, and pain are the main triggers of vasovagal syncope, although other factors can favor its appearance. Here, we classify them as more important and less important:

• More important, main factors (Table 23.5):
  • Patient age. In general, patients aged under 30–35 years account for 80% of cases. However, in children aged <14 years, the frequency of this type of reaction is very low (one per 2000 = 0.05%) because children react to emotional tension differently than adults. They do not repress the fight or flight response, but rather scream, cry, and kick up a fuss. They resist the injection and therefore do not experience a vasovagal reaction (Kuster and Udin 1985). It is estimated that around one‐third of young adults are prone to this type of reaction (Yjipaavalniemi and Sane 1981).
  • Male sex. This is the main factor in 75% of cases. It is important to remember that males account for 40% of visits (Annex 1). The reason is that society teaches males not to show emotions such as fear or pain, therefore they repress the fight or flight reaction, thus leaving themselves open to vasovagal syncope.
  • Previous history. Patients with a history of fainting or syncope in other dental treatments or injections, blood donation, and vaccination. This is the case in almost half of all patients treated.
• Less important, additional factors (Table 23.5):
  • Lack of sleep.
  • Receiving dental treatment on an empty stomach.
  • Excess heat and humidity.

Clinical Manifestations

Vasovagal syncope occurs in 75% of cases during administration of the local anesthetic or shortly after during dental treatment (Table 23.6) and can progress through several phases:

1. Early phase, presyncope, or prodrome. This phase lasts several minutes and is characterized by the following:
   • The patient is ill at ease, dizzy, and weak, with facial flushing.
   • The first typical cutaneous signs appear, especially on the face, with pallor and cold sweat, sometimes accompanied by nausea (rarely vomiting) (McGimpsey 1977).
   • Occasionally, palpitations resulting from the increase in heart rate, as well as respiratory abnormalities with more frequent, superficial, or deep breathing (hyperventilation).
     

     Factor	Harrington‐Kiff (1969) (%)	McGimpsey (1977) (%)	Edmondson et al. (1978) (%)	Salins et al. (1992) (%)	Rounded average (%)
     Main factors
     Younger age	82	81	83	—	80
     Male sex	76	81	70	—	75
     Previous history	50	28	48	—	45
     Additional factors
     Lack of sleep	—	—	0, 7	12	5
     Empty stomach	28	80	8	19	35
     Heat	24	—	23	—	25

     Data expressed as percentages for main and additional factors.

     Reference	Sample size	During anesthesia (%)	During extraction (%)	Total: anesthesia and extraction (%)
     Hannington‐Kiff (1969)	50	—	—	84
     McGimpsey (1977)	100	31	47	78
     Edmondson et al. (1978)	139	45	22	67
     			Mean	75

   • Less frequently, ringing in the ears (tinnitus), blurred vision, and mouth opening, such as when yawning.
   • Examination of cardiovascular parameters at the onset of this phase reveals increased blood pressure and heart rate due to anxiety (Campbell et al. 1976), although this all changes radically during the next phase.

2. Late phase or syncope (faint). The main characteristic of this phase is loss of consciousness (syncope or fainting) due to severe hypotension and bradycardia. It is important to point out that this does not occur in all patients who experience vasovagal syncope: if the patient realizes what is happening and starts treatment during the first phase, it can be avoided relatively easily. In older studies on extractions, 30% of patients fainted (Hannington‐Kiff 1969; McGimpsey 1977), although today, and with the patient lying down, this percentage is much lower. Thus, we can observe the following:
   • Loss of consciousness (fainting or syncope). If timely measures are taken, as we will see, the fainting episode lasts less than 1 minute and rarely more than 2 minutes (Hannington‐Kiff 1969; McGimpsey 1977).
   • The faint may be accompanied by dilation of the pupils (mydriasis).
   • Trembling or shaking is relatively common.
   • The cardiovascular examination reveals the biphasic response. Low blood pressure, which may fall to lower than 50–60 mmHg (systolic) and at which point the patient faints (Harrison 1973; Campbell et al. 1976; Kuster and Udin 1985), and bradycardia (under 50–60 beats per minute).
3. Recovery phase, which is characterized by recovery of consciousness, accompanied by confusion, disorientation, weakness, and, occasionally, headache.

Management by the Dentist

When the patient is conscious, it is essential to apply the initial measures we saw in the section on basic management of complications, as follows:

1. Place the patient lying down (supine decubitus) with the head at the same height as the heart so that the blood can reach the brain and raise the legs 15–30° to facilitate venous return.
2. Unfasten tight clothing, belts, ties, and shirt collars so as not to interfere with blood flow.

   Note: Some professionals tend to place the patient in a seated position with the head between the legs at the level of the heart to help blood reach the head. This posture is not recommended because it prevents us from monitoring the patient’s breathing and consciousness and from raising the patient’s legs to favor venous return (McCarthy 1982).

   Most patients recover with these measures and therefore do not reach the next phase:

   • When the patient is already unconscious, we apply the basic PABC or PCAB management protocol. However, it is important to implement the following:
     1. Maintain the posture: patient lying down with the legs raised.
     2. Provide 100% oxygen through a mask (Hannington‐Kiff 1969; Verrill 1975; McCarthy 1982; Milan et al. 1986).
     3. Initiate support measures:
        • Inhalation of ammonia salts arousal and consciousness (McCarthy 1982; Kuster and Udin 1985).
        • Placement of cold towels on the patient’s head and forehead (McCarthy 1982; Kuster and Udin 1985).
        • If the patient is cold, cover him/her with a blanket (McCarthy 1982; Kuster and Udin 1985).
        • If possible, check blood glucose.

          If the patient does not recover within 30–60 seconds of applying these measures, call the emergency services: the patient may have a more severe underlying problem (i.e. myocardial infarction, cardiac arrhythmia, cerebrovascular accident, hypoglycemia) (Greenwood 2008; Sambrook et al. 2011).

   • When the patient has recovered:
     1. Do not allow him/her to stand up until total resolution of symptoms.
     2. Provide a sugary drink to raise the low sugar levels resulting from the vasovagal syncope (Edmondson et al. 1978; Salins et al. 1992). Hypoglycemia may also be a contributing factor to the syncopal episode, which often occurs as patients may skip a meal and come to the dental appointment.
     3. Decide whether the patient should continue with the treatment. We suggest the following:
        • If the loss of consciousness lasts less than 10–15 seconds, the total recovery time takes less than 15 minutes, and the patient is less than 35 years old, treatment can be continued if the patient agrees.
        • If the loss of consciousness lasts more than 1 minute, the total recovery time takes more than 30 minutes, and the patient is older than 40 years of age, suspend treatment, recommend the patient to see a doctor and not to drive, and ask a relative or friend to take the patient home.
        • If in doubt, suspend treatment.

Prevention

Although vasovagal syncope is easily controlled in healthy patients, in ASA III patients with cardiovascular abnormalities, who tolerate anxiety and pain poorly, the situation may become life‐threatening:

1. Position during treatment

   Ever since the contour dental chair was introduced in the 1960s, we have been working with the patient lying back, the dentist seated (Golden 1959; Anderson 1960), and a high aspiration rate (Thompson 1967). Not only does this form of working improve precision dental work, but with the patient lying back, cerebral blood flow is better. In addition, the risk of vasovagal syncope is higher with the patient seated and the dentist standing (Bourne 1957, 1970).

   Table 23.4 shows that the frequency of vasovagal syncope in the pre‐1980, when patients were seated while the dentist stood, was higher than when dental work was carried out with the patient lying down and the dentist seated (1.5% vs. 0.5%).

2. Control of anxiety

   Patients with high levels of anxiety should be offered techniques to reduce anxiety and approaches that are beyond the scope of this book (conscious sedation, intravenous sedation). To determine the level of anxiety, we propose two key questions in the health questionnaire (Chapter 8):

   1. How frightened/anxious are you about dental treatment?

      Not at all □ A little □ Some □ Quite a lot □ A lot □

      If the patient selects the last two options (quite a lot or a lot), and especially the last, we should obtain more detailed information.

   2. Have you ever had an abnormal reaction, felt dizzy, or fainted at the dentist’s or doctor’s office when receiving a local anesthetic or vaccination or giving blood?

      Yes □ No □

      An answer in the affirmative should lead us to question the patient, given that a previous history is a major predisposing factor (see above) (Table 23.5).

Pathophysiology

The main cause of the syndrome is the patient’s emotional status (anxiety, fear, hysteria, phobia), which increases the respiratory rate, thus reducing the level of carbon dioxide in blood and leading to hypocapnia, also known as hypocarbia. CO₂ is a basic factor in the self‐regulation of cerebral blood flow that is independent of arterial blood pressure, with the result that the constriction of the cerebral vessels reduces the quantity of blood in the brain (Campbell et al. 1976; Noble 1977; Chapman 1984; Milan et al. 1986; Salins et al. 1992; Gardner 2000) and leads to peripheral vasodilation (Noble 1977).

The reduction in the pressure of CO₂ in blood reduces carbonic acid levels, therefore blood pH increases (respiratory alkalosis) from 7.4 (normal) to 7.55, leading to two phenomena:

• The Bohr effect, which describes the effect of changes in blood pH on the avidity with which hemoglobin binds oxygen. In acidic conditions, the hemoglobin binds oxygen with less affinity and makes it more available to the tissues. In alkaline conditions, such as with hypocarbia, the hemoglobin binds oxygen with more affinity, thus making it more difficult to release and worsening oxygenation of the brain (Chapman 1984).
• Reduction in ionized calcium, leading to musculoskeletal irritation, which manifests as cramps, shaking, and tetany (muscle spasms) (Harrison 1973; Chapman 1984).

Anxiety also leads to increased activity of the sympathetic nervous system and release of epinephrine and norepinephrine, which in turn produces cardiovascular manifestations in the form of increased arterial pressure and heart rate (tachycardia) (Harrison 1973; Chapman 1984; Milan et al. 1986). Finally, a vicious cycle is created: anxiety leads to hyperventilation, which in turn increases anxiety (Compernolle et al. 1979).

Clinical Manifestations

Clinical manifestations can be classified as follows:

1. Manifestations due to anxiety.
   • 80% with dizziness, disorientation, weakness that rarely progresses to loss of consciousness (syncope/fainting) (Compernolle et al. 1979; Chapman 1984); in 60% accompanied by anxiety, nervousness, and agitation (Compernolle et al. 1979).
   • 60% with palpitations owing to the increased heart rate (Compernolle et al. 1979).
   • 60% with pallor and excessive sweating (diaphoresis) (Compernolle et al. 1979; Chapman 1984).
   • Other manifestations are headache, blurred vision, ringing in the ears (tinnitus), nausea, and, more rarely, vomiting (Harrison 1973; Compernolle et al. 1979).
   • During the examination, the state of agitation reveals an increase in heart rate (tachycardia) and arterial blood pressure.
   • Sometimes the patient feels a sensation of chest tightness (distress) that may be made worse by breathing, although it is neither serious nor irradiated (Harrison 1973; Chapman 1984). The sensation is caused by irritation of the intercostal muscles and diaphragm due to increased respiratory effort (Chapman 1984).
2. Respiratory manifestations.
   • Increased respiratory rate (tachypnea) in 75% of cases, which reaches 25–30 breaths per minute instead of the normal rate (9–16). The breaths are deep or superficial. This is a basic sign (Harrison 1973; Noble 1977; Chapman 1984; Milan et al. 1986).
   • Sensation of asphyxia and difficulty breathing (dyspnea), occasionally with a “lump in one’s throat” (globus sensation) in 50% of cases (Compernolle et al. 1979).
   • Frequent movements to open the mouth and dry mouth sensation caused by anxiety and continuous breathing with the mouth open.
3. Musculoskeletal manifestations (caused by reduced ionized calcium levels). Typical findings for this manifestation include the following:
   • Feeling of numbness, tingling, and dullness (paresthesia) in the fingers and hands in 80% of cases, feet in 50% of cases, and face (tongue and lips) in 40% of cases, with muscle cramps and pain that can lead to muscle stiffness.
   • Tetany (50% of cases), which is characterized by muscle spasms in the hands and feet (carpopedal spasm) involving the following:
     • Stiffness of the hands (fingers and wrists) in flexion or extension, which is often painful (Geffner and Murgatroyd 1980).
     • Feet (less common), with stiffness of the toes and ankles in flexion.

Differential Diagnosis

• Vasovagal syncope. Hyperventilation syndrome does not involve loss of consciousness or reduced heart rate/arterial blood pressure; in addition, it does not improve with the patient lying down.
• Asthma or allergic respiratory manifestations (Gardner 2000). Hyperventilation syndrome does not involve breath sounds (wheezing) because there is no constriction of the bronchioles. In addition, it improves with treatment.
• Heart attack (angina pectoris or myocardial infarction). The chest pain is not severe and does not irradiate to the arms or shoulders. Furthermore, it improves with treatment.

Management by the Dentist

We apply the basic measures (initial measures) seen above, although here we place emphasis on the patient’s position. As the patient experiences difficulty breathing, he/she should be seated, not lying horizontally (in contrast with the approach to a vasovagal syncope) (Harrison 1973; Chapman 1984). Furthermore, specific measures for these cases are presented in increasing order of importance, as follows:

1. Explain to the patient what is happening to reassure him/her and ask him/her to breathe more slowly (six to eight breaths per minute) and thus reduce the respiratory rate (Harrison 1973; Chapman 1984). This measure is usually successful.
2. Breathe into a paper or plastic bag. This approach should only be applied when the previous measure has failed. The patient is asked to place a paper bag over his/her nose and mouth and breathe into the bag (a plastic bag is also suitable, although as it is softer, it collapses easily over the nose and mouth). Thus, by breathing his/her own air, CO₂ re‐enters the patient’s lungs and the signs and symptoms tend to improve (Harrison 1973; Compernolle et al. 1979; McCarthy 1982; Chapman 1984).

   Today, paper bag rebreathing should never recommended unless myocardial ischemia can be ruled out and the patient’s oxygenation has been directly measured by arterial blood gases or pulse oximetry: since these conditions are impossible to achieve outside the hospital this method is not recommended (Callaham 1989).

3. Medication. If the previous measure fails because the patient is very nervous, then this last alternative must be applied. This situation is very unusual because the previous measures are usually successful. In this case, intramuscular midazolam 5 ml (5 mg) is injected, and in 5–15 minutes the patient relaxes and recovers. Midazolam can also be given orally, although its effect takes more than 30 minutes.

   A classic alternative is to inject diazepam (Valium^®) 2 ml (10 mg) intramuscularly, although as it is not water‐soluble, this is more painful (Chapman 1984).

Patients who experience hyperventilation syndrome generally recover very well, do not lose consciousness, and can continue with their dental treatment.