Mastering sedation hinges on understanding the airway’s pivotal role. Professor James Roelofse, the father of sedation in South Africa, emphasized this crucial aspect. Reports show that inadequate oxygenation and ventilation lead to 31% of NORA claims. Protecting the airway is essential to ensure patient safety

The father of sedation in South Africa, Professor James Roelofse, noted, ‘Sedation is all about the airway’. This is confirmed by reports such as an ASA Closed Claim update stating that 31% of Non-Operating Room (NORA) claims were related to inadequate oxygenation and ventilation. The airway is often the first casualty of sedation.

Under normal circumstances, the patency of the upper airway is a balance between dilating and collapsing forces. During inspiration, the negative intra-thoracic pressure leads to negative intra-luminal pressure with a reduction in the cross-sectional area of the upper airway. This tends towards the collapse of the airway. However, if the antagonising forces are active, no collapse should occur.

The airway dilator muscles generate the antagonising forces, of which the genioglossus is the most important. If the collapsing forces are greater than the dilating forces, e.g., when extraluminal forces cause direct airway compression, complete collapse may occur. This may be a consideration in obese patients, where the compression forces are increased due to an increase in surrounding soft tissue.

Another factor that plays an important role in maintaining an open airway is consciousness. Consciousness influences the airway dilator muscle activity and therefore affects airway stability. During general anaesthesia and loss of consciousness, the airway is managed in a very specific way.

Therefore, airway management is one of the most important skills anaesthesia providers must master. In this aspect, sedation differs from general anaesthesia. For sedation to be successful, the patient should be able to maintain a native airway. The conundrum is that sedation tends to airway loss, with depression of consciousness, ventilation, and respiration, and so obtunds the same mechanisms which should keep the airway open. Therefore, one main goal during sedation is maintaining a native airway.

Drugs used in sedation:

The drugs used during sedation lead to direct depression of the central respiratory drive, with a decrease in respiratory rate and tidal volume. This may lead to a decrease in oxygen saturation (SpO2) and an increase in end-tidal CO2. There is also a reduction in oropharyngeal, head, neck, and respiratory muscle tone. The ventilatory response to these effects is also depressed.

Propofol:

Propofol is one of the drugs most often used for sedation. Several studies looked at the effect of propofol on the native airway.

Hillman et al. (Anesthesiology 2009, 111 (1) 63-710) looked at the effect on the airway of a slow stepwise increase in propofol effect-site concentration (Cet).

At lower propofol Cet, the upper airway was relatively well protected.

It was interesting to note that despite the stepwise increase in propofol Cet and the slow progression from hypnosis, sedation to loss of consciousness, the electromyogram (EMG) measurements in the genioglossus were disproportionate.

Upper airway collapse occurred in a narrow band of propofol Cet. Individuals more sensitive to propofol also showed the earliest depression of EMG.

There was also wide variation in the propofol Cet and loss of consciousness, and upper airway collapse. EMG of the genioglossus was preserved or even increased in some patients.

Beyond the maximum, the EMG decreased further as Cet increased and often suddenly to very low levels. The peak EMG occurred at or before a loss of consciousness. After the loss of consciousness, the EMG remained relatively low.

Also of interest is that loss of verbal response served as a guide to increased vulnerability to upper airway collapse.

The transition from conscious to unconscious was associated with a disproportionate increase in the risk of upper airway obstruction. Consciousness and airway preservation go hand in hand.

Remember that propofol does not have analgesic properties and should not be used as such. Furthermore, unlike benzodiazepines (BZD) and opioids, there is no reversal agent for propofol.

Benzodiazepines:

Benzodiazepines (BZD), especially the relatively short-acting BZD, midazolam, are often used in sedation, either alone or in combination with other drugs. An intravenous dose of 0.1mg/kg midazolam markedly increased upper airway resistance (Montravers et al. BJA 1992, 68 27-31). There were also increased periods of hypopnea and apnea.

Norton et al. (Anesthesiology, 2006; 104:1155–64) compared the tendency towards airway collapsibility between propofol and midazolam. Dynamic negative airway pressure was used to induce and measure airway collapsibility under propofol and midazolam sedation. They concluded that both drugs had the same propensity for upper airway collapse. They also found that loss of wakefulness, neuromuscular tone and airway drive caused by the drugs resulted in greater airway collapsibility of males than in females.

Opioids:

Opioids have the advantage that, at the dosages used for sedation, they do not induce unconsciousness. However, they do affect the respiratory muscles. There is a decrease in chest wall compliance and diaphragmatic muscle activity. There is an increase in the resistance of the airway dilator muscles because of the effects on the genioglossus, laryngeal muscles, and pharyngeal constrictors.

Muscle rigidity is a feared complication of opioids, which in awake patients may lead to anxiety due to laryngospasms and difficulty in breathing.

Dexmedetomidine:

Dexmedetomidine is often promoted as having minimal effects on the ventilatory drive. There is usually no tendency to upper airway obstruction. However, when Lodenius (Anesthesiology, 2019; 131: 962-73) and colleagues compared dexmedetomidine and propofol, they found that both drugs had similar collapsibility and reduction in ventilatory drive. They concluded that dexmedetomidine does not protect against upper airway obstruction.

Propofol vs Dexmedetomidine vs Ketamine:

Mishima et al. (Physiological reports 202 8 (10) e 14439) compared the upper airway pressure/flow relationship in awake patients versus patients under moderate sedation with propofol, dexmedetomidine or ketamine.

Ketamine maintained the passive upper airway patency better than dexmedetomidine or propofol. In addition, with ketamine, the compensatory response to acute upper airway obstruction remained intact. Ketamine showed a dose-dependent compensation for partial airway obstruction by an increase in the inspiratory duty cycle.

How to maintain a native airway:

Sedation is a continuum, ranging from minimal sedation to general anaesthesia, with moderate and deep sedation in between. Moderate and deep sedation levels are most often used for procedural sedation (PS). Patients can drift between levels since there are no clear-cut distinctions between the different levels.

The only way to distinguish between moderate and deep sedation is through verbal response. Once verbal response is lost, the patient is considered to be under deep sedation and may drift into general anaesthesia without the Sedation Practitioner (SP) being aware of this. The level of sedation directly relates to the impact on the native airway.

The deeper the sedation, the more likely is airway obstruction and the more likely it is that airway assistance may be needed. The level of sedation to aim for should be the level where the patient can maintain a native airway.

As mentioned above, most drugs used in PS negatively affect the native airway and ventilation. Sedation practitioners (SPs) should be aware of the different effects of different drugs. They should also realise that some patients may be more sensitive, having a bigger chance for detrimental effects. Elderly patients are especially sensitive to the effects of sedative drugs, and extra care should be taken when sedating this group of patients.

The anatomy of the patient’s airway will play an important role in the ability to maintain an open airway.

Careful examination of the patient’s airway before sedation is, therefore, an integral part of the pre-sedation patient evaluation. This may also impact whether the procedure should be performed outside the operating room. At his point, it may be good to refer the reader to the SASA Sedation Guidelines, which state that patients should receive the same level of care outside the theatre as inside the theatre (Ref).

To recognise possible respiratory problems, three questions should be answerd:

1. Does the patient have a potentially problematic airway?
2. Considering the drugs and dosages used, will the patient be able to maintain a native airway?
3. In the event of loss of the native airway, will the SP be able to rescue the airway

History:

A history of a previous event involving the airway, e.g., difficult intubation, should alert the SP to potential airway problems. Hoarseness or stridor may indicate underlying pathology involving the vocal cords, like polyps or nodules. These may be problematic during PS, where relaxation of the pharyngeal muscles occurs.

SPs should have a high index of suspicion for obstructive sleep apnea and specifically enquire about snoring or apnea episodes as noticed by bed partners. The Stop-Bang scoring system may be of value to evaluate for apnea/hypopnea syndrome (Anesthesiology: 2008; 108: 812-821). Male patients are more likely to experience upper airway collapse than their female counterparts. This has been attributed to the male upper body pattern of obesity compared to the female lower body. Smoking may negatively affect the way patients respond to the drugs used for PS. Extremes of age, under five years and older than 60, may indicate difficulties with maintaining a native airway.

Examination of the airway:

This should be done to recognise any potential airway problems. The following may raise suspicion of a problematic airway:

• a short, thick neck
• limited flexibility of the neck, e.g., after a cervical fusion
• a receding mandible
• limited mouth opening, e.g., in ankylosis of the temporomandibular joint o edentulous patients
• malocclusion with an overbite or prominent upper teeth
• large tongue, e.g., in trisomy 21
• a blocked nose
• enlarged lymphoid tissue, especially in children.
• Even though many of these may be obvious, there may be nothing striking about a patient’s features that points to a potentially difficult airway.

Rescue of the compromised airway:

SPs should be well-trained in rescuing the patient’s airway should the airway be lost. It is essential to check the level of sedation and whether the level of sedation is appropriate for the procedure.

If an infusion is used, the infusion should be turned down.

A chin lift and jaw thrust are the first manoeuvres to apply. These should resolve most airway problems.

Airway adjuncts, like an oral pharyngeal or nasal pharyngeal airway, may be needed to move the tongue away from the epiglottis.

Care should be taken not to use this in a conscious patient with an intact gag reflex, since this may cause more harm than good and even elicit laryngospasm. Ensure that a foreign body is not the cause of the obstruction, as the placement of an airway may push the foreign body further down the already compromised airway.

If the above-mentioned methods don’t resolve the obstruction, bag-mask ventilation should be started. In an already compromised airway, this may be problematic. Langeron et al. (Anesthesiology, 2000; 92:1229–36) identified five criteria that my predict difficult bag-mask ventilation. The five criteria are summarised in the mnemonic OBESE:

O = Obesity (BMI > 26kg/m2

B = Bearded

E = Elderly

S = Snorers

E = Edentulous

If there is any difficulty with airway management, the Difficult Airway Algorithm should be followed. Patients who are preoperatively identified as having difficult airways may be difficult to intubate, especially under emergency circumstances. Several methods and scores have been suggested to recognise potentially difficult intubation, like LEMON, Mallampati, Savva, Patel, and Didlikan. Unfortunately, no method serves as a foolproof predictive tool. Remember that intubation is not a goal in itself – oxygenation is.

The type of procedure that is performed will influence the airway management:

Sharing the airway:

Procedures where the SP shares the airway and the proceduralist may compromise an open airway. These include procedures like gastroscopies and oral or dental procedures. Obstruction of the airway by instruments, soiling of the airway by water, blood or even pus may jeopardise the native airway. Laryngospasm is a feared complication.

Non-painful vs painful procedures:

During non-painful procedures, sedation is mainly used to keep the patient comfortable. Verbal contact with the patient is maintained, and this moderate level of sedation will have less detrimental effects on the airway.

Painful procedures, on the other hand, may need deep sedation, with an increased risk of airway obstruction. Local or regional analgesia should be considered as the first choice in pain control. If this is not possible, the sedation technique should be adapted to manage the painful stimuli. Inadequate sedation and analgesia may cause sympathetic stimulation with hypertensive extremes and tachycardia.

Patients under sedation whose pain is not managed efficiently may become uncooperative and can cause harm to themselves and those around them. Deepening the level of sedation may compromise the airway, while still not managing the pain.

Sedation for painful procedures should therefore be geared to manage the pain rather than relying on deep sedation alone.

Position of the patient:

The type of procedure will determine the position of the patient.

Changing from the upright to the supine position results in a decrease in the pharyngeal cross-sectional area. Therefore, special attention should be paid to the position of the head and neck during the procedure in the supine position. Traditionally the so-called ‘sniffing position’, with neck flexion and upper cervical extension, is considered the ideal position for opening the airway. Flexion of the neck with ensuing airway obstruction is a common occurrence as sedation deepens and breathing muscles relax. This can be prevented by simply extending the neck with a small pillow under the shoulders.

Procedures performed in the sitting position may lead to the same problems as in the prone position. As the muscles supporting the head relax and lose their tone, the head flexes, and the chin falls on the chest, resulting in airway obstruction. Reclining the chair and extending the neck will improve airway competence.

The tongue falls away from the posterior pharynx in the lateral position, ensuring a patent airway.

Managing airway problems during sedation:

Vigilant clinical monitoring of the patient’s airway throughout the procedure is paramount. In this way, airway compromise may be recognised before it becomes problematic, e.g., lifting the chin before airway obstruction occurs. The SP should watch for breathing movements, feel for airflow and listen for signs of obstruction like snoring. A stethoscope can be used if access to the airway is problematic. Be aware of the silent airway – a patient who stops snoring may have deteriorated from partial to complete obstruction.

When airway problems occur, it is important to look for the cause.

• Is it apnea or complete obstruction?
• Is it laryngospasm or bronchospasm?

Airway problems may also be caused by multiple factors rather than one single factor.

During apnea episodes, the patient should be stimulated, verbally or physically.

During moderate sedation, the patient should be able to respond to verbal commands or slight physical stimulation and follow instructions to take deep breaths. This may not be possible during deep sedation, and a painful stimulus, like a jaw thrust, may be needed to prompt the patient to start breathing.

This also indicates that the level of sedation is too deep and that the sedation should be adjusted. Reversal drugs, like naloxone and flumazenil, should be at hand to rescue the patient if a jaw thrust is unsuccessful.

Obstruction may be partial, as in snoring or stridor. During partial obstruction, the air flowing past the obstruction causes the surrounding tissue to vibrate – the reason for the snoring sound. Stridor occurs when there is an obstruction in the larynx, as happens during laryngospasm: There is a prolonged and intense glottic closure, causing high-pitched squeaky sounds. Forward displacement of the mandible with positive airway pressure may relieve the stridor. A small dose of muscle relaxant, like 5mg of Succinylcholine intravenously, may be needed to lift the spasm.

Loss of protective reflexes:

As sedation deepens and muscle relaxation takes place, there is the possibility of obtundation of the protective reflexes with the risk of aspiration. Patients often drift between different levels of sedation and as it is uncertain at what level of sedation these reflexes are lost, it is difficult to tell whether the patient’s reflexes are still intact.

Therefore, it is recommended that patients who undergo sedation should be starved, as is required for general anaesthesia

Even though some coughing during a procedure may be bothersome, it indicates that the patient’s reflexes are intact. For oral procedures where soiling of the oral cavity may occur, vigilant and adequate suctioning is mandatory.

In a nutshell:

To ensure a patent airway during sedation, special attention should be given to the following:

• Positioning of the head and neck
• The level of sedation – keeping the patient awake rather than asleep
• The drugs used – titrate to effects, rather than using large boluses
• Effective pain control
• Clinical as well as technical monitoring
• Vigilance
• Be prepared for the unforeseen
• Never leave the patient alone
• The golden rule to ensure a patent airway:

If general anaesthesia is about putting patients to sleep, sedation is about keeping patients awake.