The primary goal of airway management is to maintain tissue oxygenation so as to prevent patients from suffering hypoxic injury. While techniques exist which allow airway management without the occurrence of apnoea/airway obstruction, these may not always be successful or clinically appropriate. Additionally, these techniques are usually only implemented when a challenging airway is anticipated, and as such, have limited utility in the management of the unanticipated challenging airway. Thus the risk of an interruption to alveolar oxygen delivery and subsequent hypoxic harm, is inherently involved with the process of airway management in both the elective and emergency situation.
When apnoea/obstruction occurs, oxygen delivery to the alveoli must be restored before critical desaturation occurs in order to avoid the risk of hypoxic injury. Two complementary strategies are available to preserve tissue oxygenation and reduce the risk of patients suffering hypoxic injury:
Establishing alveolar oxygen delivery: is the definitive strategy to preserve tissue oxygenation. A sustained interruption to alveolar oxygen delivery will eventually inevitably lead to decreases in blood oxygen content (“blood oxygenation”) and delivery of oxygen to the tissues (“tissue oxygenation”). Interruptions to tissue oxygenation which are sufficiently prolonged or severe will result in hypoxic injury to the patient. Establishment of alveolar oxygen delivery is represented in the Vortex Approach by entry into the Green Zone.
Extending the safe apnoea time: is a supplementary strategy that can prolong the time until blood and tissue oxygenation decreases in the event that alveolar oxygen delivery by ventilation/insufflation is transiently interrupted (safe apnoea time). If alveolar oxygen delivery is not restored, however, the patient will still eventually falls in blood and tissue oxygenation to dangerous levels. Extending the safe apnoea time merely delays critical desaturation and provides time to implement the definitive strategy that will ultimately prevent/reverse desaturation. It is thus an adjunct, not an alternative, to restoring alveolar oxygen delivery.
Whilst other factors such as gas exchange, haemoglobin concentration and blood flow may also impact tissue oxygenation, these are not influenced by the interventions associated with airway management. Thus it is important to recognise that maintenance of normal oxygen saturations is not synonymous with entry into the Green Zone. Normal oxygen saturations may be maintained within the safe apnoea time despite the absence of ongoing alveolar oxygen delivery. Conversely factors influencing gas exchange or cardiac output may lead to compromise of oxygen saturations despite the presence of alveolar oxygen delivery. Note that the term "alveolar oxygenation" has been avoided due to ambiguity over whether it refers to delivery of fresh oxygen to the alveoli (alveolar oxygen delivery) or maintenance of high alveolar concentrations (which may occur due to effective preoxygenation despite airway obstruction and an interruption to alveolar oxygen delivery).
The concept of the oxygenation continuum provides a visual representation describing the relationship between techniques to establish alveolar oxygen delivery and techniques to prolong the safe apnoea time in minimising the risk of exposing patients to hypoxic injury.
Under routine circumstances the time taken to establish entry into the Green Zone is shorter than the time for critical desaturation, providing a margin of safety for airway management during which the oxygenation continuum is maintained, avoiding exposing the patient to critical hypoxia. The actual time available until critical desaturation occurs if alveolar oxygen delivery is interrupted is only known retrospectively but there are a number of patient factors which might influence it including:
Similarly the time taken to establish alveolar oxygen delivery is unknown prospectively but may be influenced by a number of patient, situational or clinician factors. These are outlined in relation to airway assessment.
If the safe apnoea time is shortened &/or the time to entry into the Green Zone prolonged, the margin of safety is reduced. If this occurs to a sufficient extent the oxygenation continuum may be interrupted, exposing the patient to critical hypoxia.
Minimising the risk of exposing the patient to prolonged hypoxia necessitates maximising the safe apnoea time and minimising the time to enter the Green Zone so as to optimise the margin of safety and decrease the chance of interruption to the oxygenation continuum.
Delaying desaturation by extending the safe apnoea time not only reduces the risk of exposing the patient to hypoxia while airway interventions are performed but also makes an important psychological contribution, decreasing clinician stress and thereby potentially improving both cognitive and motor function during airway management. These improvements act synergistically with the principles of the Vortex Approach to augment the quality of any interventions by improving both decision making and technical skills and thus the likelihood of success at establishing alveolar oxygen delivery by either the upper airway lifelines or CICO Rescue. Extending the safe apnoea time thus makes contributions to both technical and human factors considerations that can decrease the risk of patient hypoxia during airway management.
Preoxygenation is a safe, simple and effective technique to increase the safe apnoea time. Optimal preoxygenation requires attention to three key elements:
The first two elements increase the oxygen content in the FRC which can be used to sustain blood oxygenation in the event that alveolar oxygen delivery is interrupted. The third element improves uptake of alveolar oxygen into the blood and decreases shunt in order to maximise the blood oxygenation that can be achieved from these alveolar oxygen stores.
Effective preoxygenation with 100% oxygen increases the oxygen content of gas in the patient’s FRC from 21% towards 100% which should theoretically produce a proportionate increase in the safe apnoea time. Whilst in practice achieving alveolar oxygen concentrations of 100% is not possible, increasing the end-tidal oxygen concentration to levels of 80-90% is usually readily achievable. The requirements for maximising alveolar oxygen concentration are as follows:
1. High Oxygen Concentration Device: despite being connected to a wall outlet or cylinder which provides a source of 100% oxygen, not all oxygen delivery devices are able to supply this 100% oxygen to the patient undiluted.
This video explains the reasons for the variability in the oxygen concentration provided by an array of devices and demonstrates the FiO2 achieved with them under a variety of conditions. These results are summarised in the accompanying table.
2. Firm Seal: devices capable of delivering an FiO2 of 100% will only realise this potential if the face mask is correctly sized to fit the patient’s face and applied firmly so that there are no leaks which allow dilution of the inspired oxygen with room air. Prevention of leaks is dependent on mask design, operator technique and patient factors (e.g. more difficult with beard, edentulous). Even small leaks such as that depicted opposite can lead to a dramatic decrease in FiO2 due to entrainment of room air. In the demonstration depicted opposite this small leak resulted in end tidal oxygen concentrations of only 40% following 3 mins of preoxygenation with 100% oxygen supplied at 15L/min via an anaesthetic circle circuit. Thus preoxygenation holding the face mask above the patient’s face without any seal (as is sometimes observed in elective anaesthetic practice) allows entrainment of large volumes of room air and significantly decreases the effective inspired oxygen concentration, diminishing the effectiveness of pre- oxygenation and the safe apnoea time. This issue is exaggerated when pre-oxygenation is being performed via a bag-valve-mask device with a one way valve at the patient end to prevent rebreathing (see photo opposite), as limited oxygen will flow from the mask unless a pressure differential exists which opens the valve. This means that if the bag is held away from the patient’s face, such that a negative pressure cannot be generated by patient inspiration to open the valve, only low oxygen flows will be delivered and the patient will receive predominantly room air.
3. Adequate alveolar ventilation: washout of nitrogen and its replacement with high concentrations of oxygen being inspired during pre-oxygenation is a function of both the rate of alveolar ventilation and the duration of pre-oxygenation. Adequate pre-oxygenation is achieved with 3 mins of normal tidal ventilation. Similar degrees of pre-oxygenation can be achieved by 8 vital capacity breaths. The time to effective pre-oxygenation can be further reduced by encouraging cooperative patients to exhale to residual volume prior to commencing pre-oxygenation.
In addition to the above techniques to improve the oxygen concentration in the FRC, optimal preoxygenation should involve consideration of additional strategies to increase the volume of the FRC such as PEEP/CPAP and 20 degrees head up tilt. These strategies maximise the volume of the reservoir which can be filled with high concentration oxygen and is available in the event that an interruption to alveolar oxygen delivery occurs. By limiting atelectasis and shunting of pulmonary blood these techniques also improve gas exchange, maximising the impact of both preoxygenation, reoxygenation and apnoeic oxygenation techniques.
Some clinicians have raised concerns that inspired oxygen concentrations of 100% may cause harm by causing absorption atelectasis and have advocated using an inspired oxygen concentrations of 80% or less for pre-oxygenation. Whilst preoxygenation with 100% vs 80% oxygen has been demonstrated to produce an increased degree of atelectasis on CT studies, no causal link has been demonstrated between this radiological finding and increased pulmonary complications. In any case any airway closure resulting from use of 100% oxygen for preoxygenation is readily reversed by use of a recruitment manoeuvre (>40cm H2O for >15 sec) once a definitive airway has been established. Conversely preoxygenation with 80% oxygen does result in a clinically significant decrease in the safe apnoea time. As such concerns regarding absorption atelectasis should not represent a deterrent and preoxygenation with 100% oxygen is advocated to maximise patient safety, particularly in situations where the possibility of a delay in restoring alveolar oxygen delivery &/or a more rapid desaturation with interruption to the oxygenation continuum, are anticipated.
Some clinicians are reluctant to perform preoxygenation due to concerns that a tight fitting mask will cause discomfort to patients. Most patients tolerate preoxygenation well but a small proportion do experience significant distress from application of a tight fitting mask. A number of techniques are available which still allow fulll preoxygenation in these patients without causing distress:
Using the above variations to the standard technique where necessary, it should be very rare that full preoxygenation is not possible due to patient discomfort.
Full preoxygenation may be difficult in patients who are uncooperative with having oxygen delivery devices applied for the required time. In these patients light sedation can be useful to assist with them tolerating a face mask. As patients who are acutely distressed and uncooperative also tend to unfasted, the risk of sedation and the attendant potential for impaired airway protection and pulmonary aspiration, must be weighed against the risk of interruption to the oxygenation continuum without preoxygenation. Small, titrated doses of ketamine tend to produce less risk of impairment of airway protective reflexes than other sedatives but ketamine sedation should not be considered to be without risk in this regard. The emergency medicine literature has formalised this process in terms of the technique of 'Delayed Sequence Intubation' (DSI). This technique conceptualises DSI as a form of procedural sedation in which the procedure is preoxygenation.
It is difficult to conceive of many circumstances in which there is inadequate time available to perform preoxygenation prior to advanced airway management, particularly when using the 8 vital capacity breaths technique. Time pressure should not generally be regarded as an impediment to performing preoxygenation which typically can be undertaken in parallel with other preparations for airway management.
Preoxygenation should ideally be performed with capnography attached. Whilst this is usual practice in an operating room setting using an anaesthetic machine, it may be overlooked in other settings such as the post-anaesthesia care unit (PACU), emergency department (ED) or intensive care unit (ICU) when a bag-valve-mask device or Mapleson circuit is being used. Preoxygenation with ETCO2 monitoring attached provides the following ancillary benefits:
Completion of effective pre oxygenation is typically determined one of the following criteria:
Note that oxygen saturations are not included amongst the list of criteria to assess the adequacy of preoxygenation. A static saturation reading is in fact irrelevant to determining whether a patient is adequately preoxgenated. Since most healthy individuals have an SpO2 close to 100% when breathing 21% oxygen, a high SpO2 cannot be used to infer that the FRC contains gas with an oxygen concentration approaching 100%. Similarly, very unwell patients may have poor gas exchange and thus poor oxygen saturations despite full preoxygenation. Only a dynamic SpO2 reading is relevant to determining whether the patient is adequately preoxygenated: if the SpO2 is continuing to rise during PreO2, then the oxygen content of the blood is rising and it is reasonable to assume that the alveolar oxygen concentration is also still rising, and to continue preoxygenation until the SaO2 plateaus, even if the 3 minute time period for PreO2 has already elapsed.
Hedenstierna G. Oxygen and anaesthesia: what lung do we deliver to the post-operative ward? Acta Anaesthesiol Scand 2012; 56 675-685
Chrimes N. Not all bag-valve-mask devices are created equal: beware a possible lower FiO2 during spontaneous ventilation. Anaesth Intensive Care 2014; 42(2) 276
The opportunity to reoxygenate the patient arises any time the Green Zone is entered. Reoxygenation via positive pressure ventilation during airway management provides exactly the same benefits as those described using preoxygenation during spontaneous ventilation prior to airway management. Thus reoxygenation is not just an opportunity to return low oxygen saturations to normal levels but to replenish oxygen stores in the functional residual capacity (FRC) of the lung and restore the safe apnoea time in case there is a further interruption to alveolar oxygen delivery.
An ancillary benefit is that successful face mask ventilation following induction, while waiting for muscle relaxants to take effect, also provides the team with confirmation of being in the Green Zone which can decrease stress and allow airway subsequent airway management to be approached in a more controlled way. Conversely recognition of the inability to mask ventilate provides the opportunity to make the most efficient use of the safe apnoea time via early commencement of optimisation interventions according to the Vortex Approach and gives the team increased situational awareness of the significance of the inability to enter the Green Zone via other lifelines during subsequent attempts.
Even during a rapid sequence induction (RSI), gentle face mask ventilation with inspiratory pressures <15cmH2O whilst waiting for the onset of muscle paralysis is acceptable and should not cause gastric insufflation or increase the risk of regurgitation of gastric contents. Maintaining ventilation pressures below this limit is more reliably achieved in an operating theatre setting where circuits with soft bags (that provide good tactile feedback about airway pressures), adjustable pressure limiting valves and airway manometry provide some safeguards against excessive ventilation pressures. It may be reasonable to exercise greater caution during RSI in other environments where the lack of tactile feedback about ventilation pressures from the more rigid self inflating bag of a BVM device and the absence of airway manometry place clinicians at increased risk of causing gastric insufflation with the potential to provoke regurgitation and aspiration.
The process of apnoeic oxygenation (ApOx) relies on the discrepancy between the rate at which oxygen is normally removed from the alveoli compared with that at which carbon dioxide (CO2) is delivered to them. Predominantly due to differences in their respective solubilities in the blood, it is estimated that during apnoea CO2 enters the alveoli at a rate of only approximately 10ml/min whilst oxygen is removed at a rate of approximately 250ml/min. This 240ml/min net removal of gas volume from the alveoli during periods of apnoea results in a reduction in barometric pressure in the alveoli. The sub-atmospheric pressure which develops serves as the driving force for gas to move from the upper airway to the alveoli by the process of apnoeic mass movement, provided the airway is patent. The mechanism for apnoeic mass movement is thus bulk flow down a pressure gradient, not molecular diffusion yet is able to occur during periods of apnoea as it does not depend upon the generation of positive pressure in the upper airway nor on respiratory effort by the patient. This process has been recognised for over fifty years but has only recently started being used as a routine adjunctive technique to deliberately prolong the safe apnoea time in susceptible patients.
The requirements for effective apnoeic oxygenation are as thus as follows:
Oxygen source: insufflation of high flow oxygen into the upper airway via the nasal or buccal routes prevents entrainment of room air so that further high concentration oxygen is available to move down the trachea to the alveoli and replace that being consumed.
Patent Airway: oxygen delivered to the upper airway can only move towards the lungs in response to the subatmospheric alveolar pressure if the airway is patent. A nasopharyngeal airway may be useful to assist nasal oxygen passing from the nasopharynx into the hypopharynx.
Although apnoeic oxygenation has been shown to prolong the safe apnoea time significantly this is not guaranteed and some patients may still rapidly desaturate despite these techniques. Apart from airway obstruction another factor limiting the efficacy of apnoeic oxygenation is alveolar collapse. Rather than draw further gas into the alveolus, the negative pressure generated there can potentially lead to loss of volume and ultimately collapse of the alveolus (aborption atelectasis). This can result in a pulmonary shunt and depression of the oxygen saturations. Patients with pre-existing shunt physiology and those pre-disposed to developing it during periods of apnoea are therefore less likely to benefit from apnoeic oxygenation techniques. The likelihood of developing absorption atelectasis in depends in part on the balance of expansive and retractive forces acting on the alveoli and the resistance to gas flow in the respiratory tree. Unfortunately morbidly obese patients in whom prolongation of the safe apnoea time might be most desirable are are more susceptible to developing shunt physiology during apnoea and may have the least benefit. Still, prolonged periods of sustained blood oxygenation have been demonstrated in obese patients using apnoeic oxygenation. Even obese patients, who desaturate more rapidly due to shunt, may still be demonstrating significant prolongation of their safe apnoea time relative to what it might have been in the absence of apnoeic oxygenation. This is supported by animal models where even though a higher shunt fraction has been associated with a more precipitous initial fall in SpO2 at the onset of apnoea (even with use of apnoeic oxygenation), the value at which the falling SpO2 has plateaued has been higher when apnoeic oxygenation has been implemented suggesting that a benefit is still being derived. Once shunt becomes sufficiently severe, however, the plateau SpO2 level will not longer be sufficiently high to qualify as 'safe'. A high shunt may be responsible for the inability to demonstrate a benefit from apnoeic oxygenation during airway management in critically ill patients.
Minimising atelectasis via application of CPAP and head up tilt should reduce shunt and maximise the impact of apnoeic oxygenation techniques.
The important point is to be aware that apnoeic oxygenation is a important adjunctive tool to extend the safe apnoea time but that it cannot be relied upon or used as an alternative to the definitive strategy of restoring alveolar oxygen delivery via one of the upper airway lifelines or CICO Rescue. Apnoeic oxygenation should be used to extend the time available to efficiently make attempts to restore alveolar oxygen delivery by these techniques without desaturation occurring but the maintenance of high saturations it provides should not influence decision making about the need to move on to alternative strategies where best efforts at one or more of the upper airway lifelines have not secured entry into the Green Zone.
Effective decision making during airway management requires the ability to rapidly confirm whether alveolar oxygen delivery has been achieved by a particular strategy. This allows an immediate judgement to be made about the need to perform optimisation manoeuvres or move on to an alternate technique. The inability to promptly identify that a technique to achieve alveolar oxygen delivery has been unsuccessful wastes valuable ‘safe apnoea time’ during which rescue strategies could have be implemented and increases the risk of exposing the patient to sustained hypoxia. Apnoeic oxygenation techniques do do not allow a prospective assessment to be made of whether they are achieving alveolar oxygen delivery or how long existing oxygen saturations are likely to be maintained before desaturation occurs. Since apnoeic methods for oxygen delivery do not typically produce a rise in existing oxygen saturations, their success or failure can only be identified in hindsight by observing when oxygen saturations begin to decline. Thus from a practical perspective, apnoeic mechanisms to deliver oxygen to the alveoli do not provide the information required to make timely decisions about whether this goal is being achieved and the need to optimise or move on to an alternate technique during airway management. As such the Vortex Approach restricts the meaning of the term "alveolar oxygen delivery" to refer only to the concept of confirmed alveolar oxygen delivery. Since alveolar oxygen delivery cannot be directly measured, real-time assessment of whether it is occurring must be inferred from other clearly definable endpoints. Real-time confirmation of alveolar oxygen delivery can thus only be achieved by confirming ventilation with oxygen or direct tracheal insufflation of oxygen via a neck airway. In most circumstances this involves obtaining a capnography trace and/or evidence of an upward trend in oxygen saturations (as opposed to sustained high saturations). The ability to confirm alveolar oxygen delivery is thus restricted to those techniques which involve cyclical inflation/deflation of the lungs as the mechanism to deliver oxygen – ventilation via the upper airway lifelines or ventilation/intermittent insufflation via neck airways. Techniques involving apnoeic mechanisms for delivering oxygen (“unconfirmed” alveolar oxygen delivery) are better considered as techniques to prolong the safe apnoea time.
As such while apnoeic oxygenation, when successful, does technically achieve "alveolar oxygen delivery" the Vortex Approach emphasises the need to achieve ‘confirmed’ alveolar oxygen delivery and uses the term "alveolar oxygen delivery" in this way.
NO DESAT (Nasal Oxygen During Efforts Securing A Tube)
While, if the airway is patent, apnoeic oxygenation occurs in any preoxygenated patient while a face mask is applied, the NO DESAT technique allows the benefits of apnoeic oxygenation to be yielded even during attempts at laryngoscopy. This enables apnoeic oxygenation to be achieved even in many patients in whom airway patency cannot be established via the three lifelines of face mask, supraglottic airway and endotracheal tube. This is possible because even when a patent airway cannot be achieved via one of the three lifelines, in the absence of laryngeal pathology or a foreign body, it is likely that during attempts at laryngoscopy the upper airway will still be patent and able to allow delivery of oxygen to the alveoli via apnoeic mass movement – even though a view of the larynx may not be able to be achieved or an endotracheal tube passed. Thus whilst the patent airway achieved with a laryngoscope in place does not allow for positive pressure ventilation, if a reservoir of high concentration oxygen can be created in the nasopharynx it can be drawn towards the alveoli by apnoeic mass movement.
Nasal cannulae alone provide only low inspired oxygen concentrations in spontaneously ventilating patients. This occurs because even during quiet breathing the inspiratory flow rate (in contrast to the minute ventilation which is the averaged flow rate over time derived from intermittent inspiration/expiration) of gas in and out of the lung is much higher (upto 30Lt/min) than the oxygen flow rate delivered by the cannulae. The result is that significant volumes of room air must also be entrained during inspiration to make up this difference. This low oxygen concentration gas mixes with the 100% oxygen entering the nasopharynx via the nasal prongs (as well as with low oxygen concentration gas present in the anatomical dead space at the end of the previous expiration), diluting the concentration of oxygen in the gas that is drawn into the alveoli with inspiration down to around only 30% .
The effect of oxygen delivery via nasal cannulae in the apnoeic patient is quite different, however. In the absence of ventilation, no room air or expired gas with a low oxygen concentration enters the nasopharynx to dilute the 100% oxygen insufflated by the nasal prongs. The result is that if nasal cannulae are applied with flows of 15Lt/min during preoxygenation, then once apnoea occurs they provide a reservoir of near 100% oxygen in the nasopharynx which is available to be drawn down the trachea into the alveoli by apnoeic mass movement. A second oxygen oxygen source, in addition to that being used to supply the mask being used, is required to provide oxygen flow for the nasal cannula.
Using nasal cannulae at 15L/min, apnoeic oxygenation has been demonstrated to extend the duration of apnoea without desaturation to beyond 10mins in some cases.
THRIVE (Transnasal Humidified Rapid Insufflation Ventilatory Exchange)
THRIVE employs very high flow (upto 70L/min) humidified nasal oxygen and has resulted in extension of the safe apnoea time by a mean of 14 mins and upto an hour in some patients. In addition to apnoeic oxygenation, THRIVE has the following benefits:
The equipment for nasal oxygen delivery during THRIVE involves bulky corrugated tubing which prevents being able to achieve a seal with a face mask while it is in place. As such THRIVE must be removed and replaced before and after each attempt at face mask ventilation.
Buccal Oxygen Delivery
This technique provides supplementary oxygen flow via the oral route using an adapted RAE endotracheal tube secured in the left buccal space. Like NODESAT this technique allows the benefits of ApOx to be obtained during attempts at laryngoscopy and does not interfere with the ability to face mask ventilate between these attempts (unlike THRIVE - see above).
It has been postulated that buccal oxygen delivery may be superior to NODESAT and THRIVE because it offers additional protection from the theoretical risk of pulmonary or gastric barotrauma with these techniques (see below), since the position of the oxygen source in the oral cavity ensures that any rise in pharyngeal pressure will be vented via the mouth. In contrast it is theoretically possible for airway pressures to rise during NODESAT if the oral cavity becomes obstructed by the tongue/soft palate. Additionally it has been suggested that the efficacy of NODESAT may be limited by the occurrence of retropalatal obstruction when obese patients are induced for airway management. Supplementary oral oxygen is not impacted by obstruction of passage between the naso- & oropharynx by the soft palate, and effective ApOx using this technique requires only that airway patency between the oro- & laryngopharyx is able to be maintained by performance of sustained laryngoscopy. Buccal oxygen supplementation is also advantageous when performing ApOx in patients in whom nasal instrumentation is contraindicated.
In obese patients, ApOx using a buccal oxygen source at 10L/min has been demonstrated to significantly reduce the risk of desaturation during apnoeic episodes in excess of 12 minutes. This flow rate (which is less than that used with NODESAT) provides a high pharyngeal oxygen concentration during apnoea, allowing ApOx to occur, but probably provides negligible CPAP and does not produce the apnoeic ventilation phenomenon of THRIVE.
Interference with Face Mask Seal: one concern with use of the NODESAT technique is the possibility that the nasal cannula oxygen tubing might interfere with getting a good seal for face mask ventilation – though in practice this is not usually an issue, and nasal cannulae could be easily removed if this were the case. The large diameter corrugated tubing used for THRIVE does prevent a face mask seal but the THRIVE nasal cannulae can be easily removed to allow face mask ventilation and replaced again during attempts at laryngoscopy. This does provide an extra task during management of a challenging airway and it is forseeable that replacing the THRIVE cannula during laryngoscopy could be overlooked resulting in a termination of apnoeic oxygenation.
Barotrauma: the pressure generated from insufflation of gas into the upper airway is a function of the rate of gas flow and the resistance flow of this gas back to the atmosphere via the upper airway. If none of the insufflated gas were able to be vented to the atmosphere it would rapidly accumulate in the stomach or lungs leading to a rise in volume/pressure and the potential for serious complications. Gastric rupture has been reported with insufflation of relatively low flows (4L/min) of oxygen via long nasal/nasopharyngeal catheters during procedural sedation but remains a only theoretical concern with use of NO DESAT & THRIVE which utilise shorter intranasal cannulae but at much higher flow rates. THRIVE has been shown to produce elevation of pulmonary pressures equivalent to only 5cmH2O but this limit is dependent on the upper airway remaining unobstructed to allow venting of insufflated gas. Supplementary oxygen via the buccal route has been postulated to be safer a safer technique for ApOx by providing a reliable, low resistance route for egress of insufflated oxygen and avoiding this theoretical risk.
In addition to allowing apnoeic oxygenation there are a number of potential ancillary benefits from using nasal insufflation of oxygen during preoxygenation and airway management.
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Techniques which decrease oxygen consumption allow more effective use to be made of the oxygen reserves during periods of apnoea thereby conserving oxygenation. In particular, skeletal muscle fasciculations caused by suxamethonium have been shown to result in an increase in oxygen consumption of nearly 10% in animal models. Minimising or avoiding these fasciculations can prolong the time to critical desaturation. This can be achieved by the following techniques:
Tang L, Li S, Huang S, Ma H, Wang Z. Desaturation following rapid sequence induction using succinylholine vs. rocuronium in overweight patients. Acta Anaesthesiol Scand 2011; 55: 203-208
Taha SK, El-Kathib MF, Baraka AS, Haidar YA, Abdallah FW, Zbeidy RA, Siddik-Sayyid SM. Effect of suxamethonium vs rocuronium on onset of oxygen desaturation during apnoea following rapid sequence induction. Anaesthesia 2010; 65: 358-361