Oxygenate and Resuscitate Before You Intubate

Case #1

You are dispatched to a call for a 16-year-old female patient with a chief complaint of possible anaphylaxis. Upon arrival you find the patient lying supine in the front yard with a crowd of bystanders huddled around. The patient is not alert to even painful stimulus, and her breathing is shallow and labored at a rate of 34 a minute. Her skin is pale, and her lips appear cyanotic. Her initial oxygen saturation reads 75%.

You instruct your partner to bag-mask ventilate the patient as you quickly move her to the ambulance. As the engine crew obtains IV access and places the ECG electrodes, you attempt to obtain a history from bystanders, but it is sketchy at best. All they can tell you is they think the patient is allergic to pistachios and they were in her meal at dinner.

Her initial oxygen saturation only increases to 80%, and administration of IM epinephrine does little to improve things. The patient’s respirations are now becoming shallow and agonal, and her oxygen saturation continues to decrease. Your partner increases ventilations in an attempt to improve the oxygen saturation. You attempt to intubate, but just as you are about to place the endotracheal tube, the patient vomits and aspirates. What now?

Case #2

You are dispatched to a call to your local nursing home for a 64-year-old patient with altered mental status. Upon arrival you find the patient lying supine in bed with a nasal cannula placed in her nares, set at a flow rate of 2 lpm. The patient is responsive to painful stimulus, and her skin is pale and hot to the touch.

The staff informs you she has had a recent diagnosis of pneumonia and has become increasingly altered since this morning. They report her temperature is 102.3ºF and that she is normally alert and oriented to person, place and time. You quickly obtain a set of vital signs, which reveals the patient is tachycardic at a rate of 108 and tachypneic at a rate of 30. Her oxygen saturation is 82% on 2 lpm of oxygen, and her blood pressure reads 82/56. You place a nonrebreather on the patient at 15 lpm and obtain IV access as well as a 12-lead ECG. The 12-lead shows a sinus tachycardia, and the oxygen saturation does not improve at all. You remember reading somewhere about using a high-flow nasal cannula to improve oxygenation, so you turn up the patient’s cannula to 15 lpm, along with the nonrebreather. This only improves the saturation to 84%, so along with the patient’s mental status, you decide to intubate.

Your equipment is prepped and ready, and IV access has been obtained. You instruct your partner to bag-mask ventilate the patient to improve the saturation as you administer your induction agent followed quickly by your paralytic. The patient’s oxygen saturation begins to fall rapidly as you attempt intubation, but you secure the airway with the help of a gum elastic bougie. Intubation is confirmed via waveform capnography and bilateral breath sounds. Soon after intubation the patient goes into a bradyasystolic arrest and cannot be revived. What happened? How could this have been prevented?

Oxygenation and Ventilation

Proper airway management is a fundamental skill in which every emergency care practitioner must be proficient. The two cases illustrated above, while different, occur in both hospital and prehospital arenas every day. Whether you are a paramedic, EMT, nurse or physician, it is imperative to have a firm understanding of both basic and advanced airway management. Concepts such as delayed sequence intubation (DSI), apneic oxygenation and the use of supraglottic airways have broadened our medical armamentarium and helped improve patient outcomes. It is important to understand that not every airway case is the same, and there is no one treatment modality that works for every clinical situation. If we are to truly “do no harm” for our patients, we have to understand the pathophysiology of those treatments as well as the end goal of oxygenation and ventilation. Before exploring these common pitfalls sometimes associated with our interventions, we must first discuss the principles behind oxygenation and ventilation.

Oxygen is transported in the body in two ways. Approximately 97% of it is bound to hemoglobin, while the remaining 3% is dissolved in the blood plasma. Ventilation is the process by which we move oxygen from the environment into the body and the process of exhaling the byproducts of cellular respiration, mainly carbon dioxide. In the prehospital environment we can measure oxygenation status via pulse oximetry. An acceptable range on the patient breathing room air is 95% or greater. Keep in mind that pulse oximetry only measures the amount of oxygen bound to the hemoglobin molecule and not the actual percentage of hemoglobin in the body. Anemic patients can show an oxygen saturation well above 95% and yet still be clinically hypoxemic due to the lack of hemoglobin that can carry oxygen molecules.

Increasing our FiO₂ (fraction of inspired oxygen) typically is the fastest way to correct hypoxia. During procedures such as RSI, we preoxygenate our patient with 100% oxygen, ideally for three minutes, to increase the amount of oxygen in the lungs, thus building a reservoir. By filling every available functional alveoli in the lung with oxygen, we extend the time it takes before our patient becomes hypoxic.

As oxygen diffuses across the alveolar capillary membrane, it is bound to deoxygenated blood returning from the right side of the heart. This oxygen-rich blood can now be pumped out by the left side of the heart into the systemic circulation to diffuse into tissue cells and complete the process of cellular respiration.

One of the byproducts of cellular respiration is the production of carbon dioxide. Once again, blood returning to the right side of the heart is rich in carbon dioxide. This CO₂ now diffuses across the alveolar capillary membrane into the lungs, where it is exhaled to the external environment. Many factors, such as cardiac output, percentage of hemoglobin, and certain disease processes such as pneumonia and acute respiratory distress syndrome (ARDS), can influence this process of oxygenation and ventilation. It is beyond the scope of this article to discuss every possible factor that influences cellular respiration, but this simplified explanation given above lays a foundation as we further explore three pitfalls that providers sometimes make in regard to positive-pressure ventilation and how to correct them.

Three Pitfalls

Overzealous bag-mask ventilation—Bag-mask ventilation is a cornerstone of basic life support. It is often one of the first airway skills we learn as new EMTs. Proper mastery of this skill, as well as a thorough understanding of possible adverse events, can greatly influence the care we provide. Conversely, a lack of fundamentals in the skill’s proper use and lack of respect for the dangers imposed by it can have disastrous consequences, as evidenced in the cases above.

Often we lose sight of how fast we are ventilating our patients due to the high-stress environment of a resuscitation. As a result, the patient can inadvertently become hyperventilated.¹ One study published in the Journal of Critical Care Medicine showed that with increased ventilations, survival rates decreased.² The study design was a prospective clinical trial in adults intubated for out-of-hospital cardiac arrest, as well as a study using three groups of seven pigs with induced cardiac arrest. In the group of cardiac arrest patients being ventilated, the average ventilation rate was around 30 breaths a minute, with a range of 15 to 49! For the pig study group, ventilation rates were set at 12, 20 and 30 breaths/minute, and physiological parameters were then assessed. In the group of pigs ventilated with the 12 bpm, 6 of 7 survived. In the group of pigs that received 30 bpm, none survived.³ Another study, although small, demonstrated that even in emergency department environments, nurses and doctors were ventilating at rates of up to 41 times per minute!⁴

Hyperventilation is known to increase intrathoracic pressures, thus decreasing venous return and left ventricular filling pressures. This drop in preload and coronary filling pressures will also cause a resultant drop in cerebral perfusion pressures.⁵ This is exactly the opposite of what we want to do in a resuscitation! As illustrated in Case #2 above, the patient was hypotensive to begin with. Any further drop in preload can cause a precipitous drop in blood pressure, resulting in an undesirable outcome. Studies show that elderly patients are at an increased risk for adverse hypotensive events and cardiac arrest shortly after intubation and positive-pressure ventilation.⁶ The elderly are also on medications that can change their physiology and decrease preload. It is important to take this into consideration when attempting to intubate the hypotensive patient or the geriatric patient in general.

Another complication of overzealous bag-mask ventilation and positive-pressure ventilation is vomiting and aspiration. When a patient is hyperventilated prior to intubation, much of this ventilation is put into the stomach.⁷ This rapid insufflation of air distends the abdomen and pushes against the esophageal sphincter until the contents of the stomach are expelled upward. This is the exact place you did not want them to be! One reason we perform rapid sequence intubation in the field is to decrease the risk of vomiting in the patient who is not NPO. Paralytics will paralyze all the muscles of the body, including the lower esophageal sphincter, thus mitigating this risk.

Prior to administration of our paralytic, though, we must be cognizant of our ventilation rate and tidal volume. Pulmonary physiology studies have shown that on room air, it takes very few breaths to adequately ventilate our lungs.⁸ Adequate ventilation is defined as a PaO₂ (partial pressure of oxygen in the alveoli) around 100, taking into account any dead space. This is the amount of oxygen that is in the alveoli of the lungs and can be used to diffuse across the capillary membrane and dissolved into deoxygenated blood coming in from the right side of the heart.

At room air, which is 21% oxygen, it only takes around 3 lpm to reach a PaO₂ of 100. Assuming you are ventilating with a tidal volume of 500 ml, that would be around six breaths. If you were ventilating at a tidal volume of 700 ml, this would be around 4–5 breaths. At increased FiO₂ (fraction of inspired oxygen), the number of breaths needed to maintain an acceptable PaO₂ is decreased further (see Figure 1). While many other factors can influence oxygenation and cellular respiration, such as acid-base balance, physiological and anatomical shunts, and cardiac output, the take-home point is that faster ventilations are not necessarily better. In the next few paragraphs, we will explore simple maneuvers, such as proper mask seal in conjunction with an adequate rate and tidal volume, that can improve the oxygenation status of our patients before intubation and help to prevent adverse events.

Improper mask seal—The inability to obtain a proper mask seal can be the difference between oxygenating your patient or not. Prehospital and emergency care providers are typically taught a variety of methods for obtaining a mask seal, including the E-C technique. Much of what we learn in terms of airway management comes from techniques used in the operating room. The difference between us and providers in the OR is that they perform this procedure many times daily over many years and develop mastery of it. We may go many shifts before we are called upon to mask-ventilate someone, causing skill retention to erode. For the typical street paramedic or nurse in the ED, any break in the mask seal will negate any benefits to oxygenation due to entrainment of room air and a loss of high-flow oxygen. The addition of a high-flow nasal cannula under the mask can provide a continuous source of oxygen, even when the bag is not being squeezed.⁹

While there are many factors that can influence the oxygenation of your patient, collapsed and inefficient alveoli are one culprit when the administration of high-flow oxygen does not work. Positive-pressure ventilation can help achieve this, but only with a good mask seal.

An alternative way for obtaining a proper mask seal is called the thenar eminence technique or, more simply, the “two thumbs down” technique.¹⁰ This is done by placing your two thumbs down against the edge of the mask and performing a jaw thrust to lift the face into the mask (see Figure 2). A first provider is designated to squeeze the mask, while the second holds the seal. This works well because it incorporates the strongest parts of your hands to hold the seal while allowing you to detect the slightest mask leak and adjust accordingly.

Focus on intubation before resuscitation—Another possible pitfall that emergency providers can make is becoming fixated on securing an airway as fast as possible, while ignoring the physiological derangements the patient is showing.¹¹ We should always take a step back and view the patient’s entire clinical picture before rushing in to place an endotracheal tube. The acutely decompensating patient with shock, whether from a hemorrhagic or cardiac etiology, may need to be stabilized first. Hypotension due to volume depletion or a failing pump only increases our possible adverse events from intubation. As discussed before, intubation and positive-pressure ventilation increase intrathoracic pressures and will decrease preload. With decreased preload comes decreased left ventricular filling pressures. All of this sets the patient up for hypotension and possible cardiac arrest.

Many medications used in the practice of RSI can also decrease preload and cause respiratory depression, further increasing our risk of an untoward event. BLS maneuvers such as the administration of high-flow oxygen and proper bag-mask ventilation should always be performed prior to intubation. Use slow, easy breaths, as discussed above, and administer a fluid bolus to increase volume status and stave off intubation-related hypotension. The administration of fluids will increase intravascular volume, thus increasing right ventricular preload to the heart. If the patient is in cardiogenic shock, vasopressors such as norepinephrine or dobutamine can be started and the patient further stabilized before proceeding with your RSI.

If it is imperative to intubate immediately and if your medical direction allows it, push-dose pressors may be an option.¹² Push-dose pressors are a relatively new treatment modality in the prehospital realm but have been used in the operating room for years. Their use consists of drawing up a small dose of a vasopressor such as epinephrine and administering small aliquots to increase blood pressure. One advantage of push-dose pressors is that they can be faster to administer then a drip, especially in time-sensitive settings such as with a hypotensive patient who is about to arrest.

For example, one popular option is to take a 10-ml saline syringe and expel 1 ml out. Then draw up 1 ml of cardiac-dose epi and mix by shaking (see Figure 3). This will give you a concentration of 100 mcg of epi in 10 ml of saline. You can now administer 5–10 mcg every 2–5 minutes as needed to increase blood pressure before or after intubation. Always make sure to follow your local protocols and discuss these treatment options with your medical director.

Conclusion

Now we can apply what we’ve learned to the cases above. In Case #1 you recognize that your partner is ventilating too fast. You instruct him to slow down and squeeze the bag with slow, easy breaths. You also have an engine crew member assist your partner using a two-person BVM technique. The addition of a high-flow nasal cannula under the mask helps to improve oxygenation as well.

With the patient’s oxygenation status corrected, you can now proceed safely with intubation. As you intubate, you notice substantial swelling of the oropharynx, but intubation is successful with the aid of a bougie. En route, you continue to monitor the airway and start the patient on an epinephrine drip. Upon arrival at the hospital, it is determined the patient had a life-threatening anaphylactic reaction, and she is further stabilized.

In Case #2 you realize the patient may be septic and her hypotension needs to be further stabilized before proceeding with intubation. You administer a 500-ml fluid bolus as you maximally oxygenate the patient with high-flow nasal cannula and a nonrebreather. As a precaution you draw up a push-dose pressor of epi in cause the patient’s blood pressure does not respond to the saline bolus.

Her saturation does not respond to high-flow oxygen, so you decide to quickly move to assisted ventilations with a BVM and a two-person mask seal. A nasopharyngeal airway and jaw thrust is also added to maintain airway patency. The patient’s blood pressure improves after administration of the fluid bolus and with the oxygen saturation. With the patient’s hypotension and oxygenation status corrected, you can now safely intubate. Intubation is successful, and the patient is transported to the emergency department, where a diagnosis of bilateral pneumonia and sepsis is confirmed. The patient spends several days in the ICU and is eventually extubated and discharged.

In conclusion, it is important to understand our patients’ physiological state and how it relates to the procedures we perform. We must first realize that oxygenation and ventilation are our main goals, not necessarily placing an endotracheal tube. We should understand that basic airway maneuvers such as bag-mask ventilation can sometimes be just as dangerous as advanced airway maneuvers and have a methodical plan in place to deal with these situations.

So remember, the next time you are faced with an airway emergency, think resuscitate and oxygenate before you intubate!

References

1. Aufderheide TP, Lurie KG. Death by hyperventilation: a common and life-threatening problem during cardiopulmonary resuscitation. Crit Care Med, 2004 Sep; 32(9 Suppl): S345–51.

2. Ibid.

3. Ibid.

4. O’Neill JF, Deakin CD. Do we hyperventilate cardiac arrest patients? Resuscitation, 2007 Apr; 73(1): 82–5.

5. Manthous CA. Avoiding circulatory complications during endotracheal intubation and initiation of positive pressure ventilation. J Emerg Med, 2010 Jun; 38(5): 622–31.

6. Hasegawa K, Hagiwara Y, Imamura T, et al. Increased incidence of hypotension in elderly patients who underwent emergency airway management: an analysis of a multi-centre prospective observational study. Int J Emerg Med, 2013 Apr 24; 6: 12.

7. Weiler N, Heinrichs W, Dick W. Assessment of pulmonary mechanics and gastric inflation pressure during mask ventilation. Prehosp Disaster Med, 1995 Apr–Jun; 10(2): 101–5.

8. Calder I, Pearce A, eds. Core Topics in Airway Management. Cambridge University Press, 2005.

9. Weingart SD, Levitan RM. Preoxygenation and prevention of desaturation during emergency airway management. Ann Emerg Med, 2012 Mar; 59(3): 165–75.

10. Jin Y, Lee BN, Park JR, Kim YM. Comparison of two mask holding techniques for two person bag-valve-mask ventilation: A cross-over simulation study. Resuscitation, 2010 Dec; 81(2).

11. Dunford JV, Davis DP, Ochs M, Doney M, Hoyt DB. Incidence of transient hypoxia and pulse rate reactivity during paramedic rapid sequence intubation. Ann Emerg Med, 2003 Dec; 42(6): 721–8.

12. Weingart S. Push-dose pressors for immediate blood pressure control. Clin Exp Emerg Med, 2015; 2(2): 131–2.

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.