The Nose Knows

It’s dinner time at the station and you are just about to sit down and enjoy a hot meal when the tones go off. You are dispatched to the local nursing home for a 62-year-old female with a chief complaint of difficulty breathing.

When you arrive, you find the patient sitting upright in bed and responsive to painful stimulus only. You quickly instruct your paramedic partner to obtain a set of vital signs while you begin your initial assessment. Her skin is pale and diaphoretic and her pulse is weak and rapid at a rate of 100 bpm. She is breathing at a rate of 40 per minute and once your partner has placed the pulse oximetry probe you see her oxygen saturation is only 74% on room air.

You tell your partner to place a non-rebreather mask on the patient at a flow rate of 15 lpm and one of the engine crew members begins to obtain IV access for you. You know you need to protect the patient’s airway, but after placing the non-rebreather mask the patient’s oxygen saturation only improves to 80%. A properly sized nasal trumpet is placed and a BVM is applied using a two-person technique, improving oxygen saturation to 92%. You make the decision to protect the patient’s airway with an endotracheal tube using a rapid sequence intubation, but you know the patient is at risk for rapid desaturation and possibly hypoxic arrest if you encounter any difficulties. What do you do?

Introduction

This article discusses a concept called apneic diffusion oxygenation, or simply apneic oxygenation. This powerful technique for oxygenating your patient has received quite a bit of notoriety in emergency medicine literature and has started to trickle into the prehospital realm as well.¹ This article explores the clinical significance, history and pathophysiology behind apneic oxygenation, and how the reader can use it to improve the quality of care their patients receive, building upon traditional airway management techniques while giving readers another “tool” to use as part of their airway management strategy.

Apneic Oxygenation

Apneic oxygenation is usually achieved by the placement of a simple nasal cannula into the patient’s nares. The oxygen is then applied at a flow rate of 12–15 liters per minute to facilitate preoxygenation in the patient who qualifies for a rapid sequence intubation.¹ Most of us were taught the maximal flow rate for a nasal cannula is six liters per minute. Six liters per minute would be all you would want to administer in a consciously breathing, awake patient, but as we will explore further apneic oxygenation is for the purpose of RSI and the anticipated difficult airway.

The gold standard of emergency airway management is oxygenation, and ventilation and rapid sequence intubation is one way to provide this. Studies show it carries a high success rate when in the hands of a properly trained provider.² While it’s considered best practice to preoxygenate all patients requiring intubation, it is especially important for those who require RSI. The rationale behind preoxygenating your patient is to extend their duration of safe apnea. Relatively speaking, there is no absolute “safe” time for apnea, but what this means is the time it takes for your patient’s oxygen saturation to go from 100% to 93% on the oxygen hemoglobin dissociation curve. After 93%, a person’s oxygen saturation will drop precipitously, putting the patient at risk for hypoxic brain damage, cardiac arrhythmias and possibly cardiac arrest.

Healthy patients undergoing elective intubation who have been adequately preoxygenated have been shown to tolerate apnea for up to 8 minutes.³ Unfortunately EMS providers do not typically intubate healthy patients. Patients intubated during prehospital or ED care typically present with poor lung pathology from conditions such as pneumonia, COPD, asthma and CHF. These patients’ oxygen saturations may never start out at 100% and can drop faster than a healthy patient with good lung function. Obese, pediatric and pregnant patients are also known to desaturate more quickly during RSI.⁴

Traditionally, the practice of preoxygenation is achieved with the placement of a 100% non-rebreather mask. This is actually a misnomer, as the NRB mask only really delivers 60%–75% FiO₂ due to the rebreathing of CO₂ and the mask being bent and misshaped, which causes entrainment of room air and dilution of pure oxygen.³ The use of a BVM is usually reserved for the patient with an oxygen saturation of less than 93% or who has no spontaneous ventilations. If positive pressure ventilations are provided to aggressively, this can lead to insufflation of air into the stomach, and increase the risk of vomiting and aspiration, all of which we want to avoid. Poor mask technique also allows air leaks and entrainment of room air and negates the value of BVM ventilation. This typically can be remedied with a two-person BVM technique.⁵ Once the patient is rendered apneic it becomes a race against time to place the endotracheal tube.

The placement of a high-flow nasal cannula can fix these issues. The nose is a direct conduit for oxygen to passively flow into the oropharynx. A 2012 study demonstrates the validity of this powerful technique.¹ A simple nasal cannula is placed on your patient at 5–6 lpm with a NRB at 15 lpm placed over the nasal cannula. You allow your patient to receive preoxygenation ideally for a period of 3 minutes. The purpose is too maximally oxygenate your patient and bring the oxygen saturation as close to 100% as possible. Ideally your goal should be 95% or better.

After administration of an induction agent, the oxygen on the nasal cannula is turned up to 15 lpm and you then administer your paralytic agent. You want to use the highest oxygen setting you can to maximize your FiO₂ and typically 15 is as high as we can go in the prehospital setting. Some might argue this concentration of oxygen may dry the patient’s nares out or cause pain to the patient. We must remember, though, that the patient is undergoing intubation and has been given an induction agent and paralytic, so this will be of little consequence. Also, the duration of time we will have them on the nasal cannula is minimal so this will not cause any adverse effects. The NRB is then removed from the patient but the nasal cannula is left in place to continue to oxygenate the patient passively during your intubation attempt. Oftentimes, but not always, you will actually see your patient’s oxygen sats go up during your intubation attempt.

A 1959 study looked at the effects of this phenomenon, known as apneic diffusion oxygenation.⁶ The study took eight patients undergoing various elective surgical procedures and sedated and paralyzed them using a combination of Thiopental and Succinylcholine. They then intubated them and allowed them to passively receive oxygen without ventilations. The duration of apnea lasted anywhere from 30–55 minutes. The patient’s oxygen saturation, pH and arterial CO₂ levels were monitored throughout the duration of apnea. All the subjects’ oxygen sats stayed between 98% and 100%. The only complications indicated were that some patients experienced PVCs. The PaCO₂ values for the patients ranged from 130–250. Obviously, you would expect high PaCO₂ values if your patient is not being ventilated to exhale the buildup of CO₂. More recent studies include one by Babinski and others showing up to 30 minutes of apnea with no significant oxygen desaturations using endobronchial oxygen catheters.⁷ While these studies were conducted in an operating room setting, as opposed to the prehospital environment, they do illustrate the power and utility of apneic oxygenation as a means to provide optimal care for patients.

How Gases Diffuse

To better understand apneic oxygenation we have to look at the basic laws of physics and how gases diffuse.

Gases will always move from an area of higher pressure to an area of lower pressure. This is the basis of how humans breathe.

When our intercostal muscles and diaphragm contract our lungs expand, creating a negative pressure inside our chest cavity. This pressure created inside our thoracic cavity is lower than atmospheric pressure, which causes a net flow of gases to move from the atmosphere through our mouth and trachea and into our lungs.

Once these inhaled gases reach our lungs they enter the alveoli where the exchange of oxygen and CO₂ takes place. The pressure of oxygen in the alveoli is higher than the pressure of CO₂. The reverse is true in the arterial pulmonary arteries where the pressure of oxygen is lower and CO₂ is higher. This creates a pressure differential that pulls oxygen from the alveoli and exchanges it for CO₂.

This same process of gases diffusing from a higher pressure to a lower pressure is evident at the tissue level as well.The concentration of CO₂ is higher in the tissues then in the arterial circulation causing CO₂ to diffuse back into the circulation.The pressure of arterial oxygen is higher than in the tissues causing oxygen to diffuse into the tissues and the process starts all over again.

When a patient undergoes RSI and a paralytic medication is administered, all the muscles of the body are paralyzed, but the alveoli in the lungs are still exchanging oxygen and carbon dioxide. When a person is apneic, the alveoli will continue to diffuse oxygen across the alveolar capillary membrane and carbon dioxide will continue to diffuse from the pulmonary artery into the alveoli until the oxygen reservoirs are depleted.

By using a high-flow nasal cannula you essentially create an oxygen reservoir in the back of the pharynx with which to pull gases from. The high partial pressure of oxygen in the pharynx vs. the now low partial pressure of oxygen in the alveoli creates a sub-atmospheric pressure, which will pull gases from the back of the pharynx. This process of using a high-flow nasal cannula serves to both hyper-oxygenate your patient and buy you time during your intubation attempt.

Case Scenario

Returning to the scenario presented at the start of the article, you decide this patient needs to be intubated using a rapid sequence technique. While your partner obtains an IV, you place a nasal cannula in the patient’s nares and place a non-rebreather mask on the patient. You turn the oxygen up to 15 lpm for both devices and sit the patient up to facilitate preoxygenation. Your patient’s oxygen saturation is now at 96%. You draw up 28 mg of Etomidate and 84 mg of Rocuronium. After 3 minutes of preoxygenation you push the Etomidate and Rocuronium and take the non-rebreather off of the patient, but leave the nasal cannula in place. The oxygen saturation continues to go up and is now at 98% as you intubate. You initially have trouble with placing the tube, but after repositioning the patient and the aid of a bougie you are successful. This is confirmed by waveform capnography and the presence of bilateral breath sounds. You transport the patient code 3 to the hospital where it’s confirmed by chest X-ray that she has a multi-lobar pneumonia. She spends four days in the ICU, after which she is extubated and makes a full recovery.

Conclusion

Using a high-flow nasal cannula to facilitate apneic oxygenation will greatly aid us in our oxygenation and airway management strategy. While there is ongoing controversy as to the validity of paramedic drug-assisted intubation, it is imperative we continue to stay abreast of new techniques and methodologies to improve the care of our patients. So, the next time you’re faced with an airway emergency, just remember—the nose knows!

References

1. Weingart SD, Levitan RM. Preoxygenation and prevention of desaturation during emergency airway management. Annals of Emergency Medicine, 2012; 59(3): 165–175.
2. Dufour DG, Larose DL, Clement SC. Rapid sequence intubation in the emergency department. The Journal of Emergency Medicine, 1995; 13(5): 705–710.
3. Walls RM. Rapid sequence intubation. Manual of Emergency Airway Management, 4th ed. Philadelphia: Lippincott Williams and Wilkins, 2012, pp. 47, 220–32.
4. Tanoubi I. Oxygenation before anesthesia (preoxygenation) in adults. Anesthesiology Rounds, 2006; 5(3): 1–6.
5. Otten D, et al. Comparison of bag-valve-mask hand-sealing techniques in a simulated model. Annals of Emergency Medicine, 2014; 63(1): 6–12.
6. Frumin MJ, Epstein RM, Cohen G. Apneic oxygenation in man. Anesthesiology, 1959; 20(6): 789–798.
7. Babinski MF, et al. Clinical application of continuous flow apneic ventilation. Acta Anaesthesiologica Scandinavica, 1985; 29(7): 750–52.

Russ Brown, NREMT-P, is a firefighter/paramedic and EMS field training officer for Southlake Fire Department in Southlake, TX. He has worked for a variety of services including fire, private and hospital-based EMS systems. He has a particular interest in airway management and cardiac resuscitation science. Contact him at Rbrown@ci.southlake.tx.us.