Apnoeic Oxygenation

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Today we are going to look at the procedure of apnoeic oxygenation during emergency RSI. Essentially, this procedure delivers oxygen to the alveoli after neuromuscular blockade and the onset of paralysis. This increases the period of safe apnoea before oxygen saturations fall <90%.

In health and breathing room air, the body has enough oxygen to last about 60 seconds before desaturation (there’s about 450ml stored in the lungs, 850ml in the blood, and 250ml bound to myoglobin in the muscles). Within 2-3 minutes of apnoea our vital organs develop hypoxic injury leading ultimately to cardio-respiratory arrest and death. Not a good day in the office!

Critically ill patients may already demonstrate overt hypoxia, have a higher oxygen consumption and present with primary lung or cardiovascular pathology. These factors increase the likelihood of further desaturation and may necessitate emergency RSI. During this procedure they are at significant risk of further desaturation to potentially fatal levels.

In today’s episode we are going to look at how AO can lengthen the time to desaturation during RSI. If you haven’t seen our previous episode on sux vs roc in emergent RSI, take a look at it here and listen out for our future podcast on RSI checklists.

Whilst AO is an important procedure that may increase the period of safe apnoea, there are a number of other techniques that should be employed. In 2011, Weingart and Levitan published a definitive overview of the topic in Annals of Emergency Medicine. This is a key paper on all things to do with oxygenation in emergency airway management so if you haven’t already, check it out here.

What constitutes hypoxia?

Lets first define hypoxia, which is an arterial oxygen tension of <8.0kPa. The reason for this definition is somewhat arbitrary but can be better appreciated if we recall the oxyhaemoglobin dissociation curve, which relates Sa02 and blood oxygen tension (PaO2) and produces a sigmoid curve. This is important, because at the top of the curve there is a plateau where relatively large changes in arterial PaO2 result in a relatively modest change in Sa02. Since we use Sa02 to guide our measure of adequate blood oxygen tension we want this to be above 90%, which is around the 8kPa mark and the point where the curve starts to fall dramatically.

When performing an RSI in the ED there are two main goals:

  1. To increase oxygen saturation to 100%, or as near to 100% as possible
  2. To denitrogenate the lungs in place of oxygen, thus increasing the oxygen store prior to the onset of apnoea

If these two aims are achieved, the time to safe apnoea is increased and may exceed ten minutes in health, quite astonishing! In the critically unwell, this time may be significantly reduced due to increased metabolic rate and utilisation of oxygen. This is where apnoeic oxygenation may be useful!

So lets think about real life and when AO may be useful? Well, probably most situations where an RSI is being performed but especially in those who are critically unwell. I.e. our patients in ED! But what about conscious sedation? Seems reasonable. Particularly when the agents we use lead to apnoea or obtunded respiration.

How does apnoeic oxygenation work?

So how does AO work we hear you ask – it sounds like hocus pocus, surely?! Well the principle is quite straightforward. Arterial oxygenation relies on passive diffusion of oxygen down its concentration gradient from the alveoli into the blood stream. Carbon dioxide moves down its concentration gradient in the opposite direction. Since blood is continuously moving through the lungs the concentration gradient for diffusion is maintained. At the onset of apnoea ventilation ceases but the concentration gradient for oxygen movement is maintained and results in about 250ml/min of net oxygen movement. Carbon dioxide accumulates in the alveoli and quickly equilibrates with that of the blood, where it is buffered resulting in a net movement of only 10ml/min. Overall, there is a net removal of gas of 240ml/min from alveoli in the apnoeic patient. The pressure in the alveoli falls as a result and this negative pressure acts as a driving force for bulk flow of oxygen, a mechanism distinct from molecular diffusion.

At the onset of apnoea any oxygen that is delivered will accumulate in the pharynx – there is no entrainment of room air. This 100% oxygen forms a reservoir that can move under the action of bulk flow providing apneoic oxygenation.

The procedure of apnoeic oxygenation involves:

  • Preoxygenation with 100% oxygen via NRM with additional 15L/min of oxygen delivered via nasal cannulae – seems a bit much? There’s good evidence that this doesn’t cause trauma, so don’t worry! (Take a look at this paper)
  • RSI with IV induction agent and neuromuscular blocking agent
  • Continuous delivery of 15l/min of oxygen via nasal cannulae whilst maintaining the airway with simple maneuvers to ensure patency, adjuncts such as a NPA may be used
  • Intubation with ongoing apnoeic oxygenation via NC – the acronym NO DESAT stands for Nasal Oxygen During Efforts Securing a Tube

Is there evidence to support its use?

That’s all good and well but is there any evidence to support my practice you ask, quite rightly? Well yes as it happens there is and we’re going to take a look at a few papers now.

Dyett JF, Moser MS, Tobin AE. Prospective observational study of emergency airway management in the critical care environment of a tertiary hospital in Melbourne. Anaesthesia and intensive care. 43(5):577-86. 2015

This is a very recently published paper – we’ve only been able to review the abstract for the moment. It was designed as a prospective observational study of 129 patients (128 adult, one paediatric) receiving emergency airway management in the Emergency Department, ICU, and on the wards. I.e. outside of the operating theatre.

A variety of measures were observed including demographics, pre-oxygenation and apnoeic oxygenation data, drugs used, number of laryngoscopic attempts, adjuncts and airway manoeuvres used, and complications .

The most common indication for intubation was respiratory failure (n=38). In those without respiratory failure, nasal cannulae apnoeic oxygenation (NCAO) resulted in a significant reduction in incidence of hypoxaemia (n=0/31 [0.0%]) compared to those not receiving NCAO (n=10/60; p=0.0016) with an absolute risk reduction of 16.7% and a NNT of six.

It’s not possible to say from the abstract alone what the study methodology was or whether NCAO was beneficial in those with respiratory failure (the most common indication for intubation). It does provide credence to support formal RCTs in this area, however.

Wimalasena Y, Burns B, Reid C, Ware S, Habig K. Apneic oxygenation was associated with decreased desaturation rates during rapid sequence intubation by an Australian helicopter emergency medicine service. Ann Emerg Med. 2015 Apr;65(4):371-6.

This is fantastic article from the Sydney HEMS team who introduced apnoeic oxygenation with NC to all emergency RSI’s in 2011.

By design, this was a retrospective study looking at airway registry data collected in a prospective manner with each RSI. The data collection was undertaken over nearly four years between 2009-2013, spanning the introduction of AO. A total of 728 cases were included for analysis with 310 in the RSI group and 418 in the RSI + AO group.

They found that AO resulted in a 6.1% reduction in desaturation compared to RSI without AO (16.5% versus 22.6%, respectively, 95%CI 0.2-11.2%).

The great thing about this study is that it looks at a patient cohort that is similar to those requiring RSI in the ED.

Yong Mao, Zong-He Qin. Association of apneic oxygenation with decreased desaturation rates during rapid sequence intubation by a Chinese emergency medicine service. Int J Clin Exp Med 2015;8(7):11428-11434

It looked at both pre-hospital and in-hospital RSI performed by ICU doctors in a large Chinese hospital and was retrospective in design. Data was reviewed over a 22-month period and controls (RSI only) compared against intervention (RSI+AO).

A total of 667 RSI’s were performed in critically unwell patients. AO reduced the incidence of desaturation to <93% from 50% to 12.6% compared to control. Most RSI’s were performed in the pre-hospital environment in the context of trauma. The mean time to desaturation in those receiving AO was 169 seconds compared for 94 seconds amongst controls.

This large retrospective study demonstrates that in the context of critically unwell patients, primarily in those with trauma, AO significantly decreased the likelihood of desaturation and almost doubled the time it took to do so.

Taha SK, Siddik-Sayyid SM, El-Khatib MF, Dagher CM, Hakki MA, Baraka AS. Nasopharyngeal oxygen insufflation following pre-oxygenation using the four deep breath technique. Anaesthesia. 61(5):427-30. 2006.

A smaller study from 2006 involving 30 patients. This study was looking at the time to desaturation (<96%) from the onset of apnoea in patients receiving AO vial nasopharyngeal oxygen at 5l/min (n=15) versus those not receiving AO (n=15). All patients were either ASA I or II and admitted for elective surgery – i.e. they were generally healthy and anaesthesia was planned.

A couple of key points – 1. Preoxygenation prior to induction of anaesthesia was undertaken for 30 seconds during which time patients were asked to take four full inspirations and expirations (i.e. at vital capacity breaths). This is far less than the three minutes we are taught to give prior to RSI. Whether this approach is applicable to RSI and in particular RSI in the critically unwell requires some thought! 2. AO was delivered using 5l/min of oxygen, which isn’t a particularly high flow rate.

Interestingly, they found that AO after pre-oxygenation using the four deep breath technique significantly reduced the incidence of desaturation. In the control group, mean time to desaturation <96% was 3.65 minutes whilst in the study group, no patients desaturated during the pre-determined six minutes observation period (at which point patients were ventilated regardless of saturation).

So what does this small paper tell us? Well, potentially we may be able to achieve AO with lower flow rates and after shorter periods of preoxygenation using deep breathing. Sure, the study wasn’t in critically unwell patients but it is certainly interesting.

Ramachandran SK, Cosnowski A, Shanks A, Turner CR. Apneic oxygenation during prolonged laryngoscopy in obese patients: a randomized, controlled trial of nasal oxygen administration. Journal of clinical anesthesia. 22(3):164-8. 2010.

We’ve included this study because obese patients share some of the features of critically unwell patient: 1) they have a higher metabolic demand and oxygen consumption per minute (i.e. >250ml/min) resulting in increased desaturation during RSI, 2) lung compliance is reduced making ventilation more difficult, 3) increased incidence of difficult airways during RSI resulting in longer times to intubation.

Again, this was a small study of 30 obese men undergoing GA with total-intravenous anaesthesia (TIVA). The single study centre was designed as an RCT.

Patients were preoxygenated along standard lines and duration of SpO2 >95% was measured in both groups (AO vS no AO) up to a maximum of six minutes.

Nasal O2 administration was associated with significant prolongation of SpO2 ≥95% time (5.29 ± 1.02 vs. 3.49 ± 1.33 min, mean ± SD), a significant increase in patients with SpO2≥95% apnea at 6 minutes (8 vs. one pt), and significantly higher minimum SpO2 (94.3 ± 4.4% vs. 87.7 ± 9.3%). Resaturation times were no different between the groups.

So, AO seems to buy us more time in patients with higher oxygen demand and longer times to successful intubation – nice work!

So, what next?

These studies provide good evidence to support the use of AO in the critically unwell patient undergoing RSI. Specifically, it reduces the likelihood of desaturation and if it is going to happen, it takes longer to occur. These factors are clearly advantageous in any situation but in particular those with increased metabolic demand, poor cardio-respiratory reserve and potentially abnormal airway anatomy.

AO is easy to deliver with relatively few risks to the patient. So next time you’re faced with a patient requiring RSI don’t forget to attach the nasal cannulae and deliver some apneic oxygenation.

Ps…….

So since recording this podcast a paper from the American Journal of Respiratory and Critical Care Medicine has been published looking at apneic oxygenation, during intubation of patients on ITU, the FELLOW study. It was a randomized control trial of patients receiving endotracheal intubation with apneic O2 via nasal specs or standard pre oxygenation. They looked for the maximum desaturation from placement of the tube to 2 minutes after. Effectively they found no significant difference between the 2 groups in the 150 patients studied. There is a superb blog post over at St Emlyns which goes into this in further depth.

But does this change our practice? Probably not.

It does suggest that the evidence may not be so conclusive but until a stronger trial is developed and published with such a simple intervention of low cost and potentially high benefit we’ll keep on using apnoeic oxygenation.

 

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