Oxygenation Is the Priority

The priorities in the airway game are 1) oxygenation and 2) avoidance of vomit and management of fluids. Avoidance of vomit and management of fluids are directly related to priority number one. On rare occasions, when patients have severe metabolic acidosis with a compensatory respiratory alkalosis, ventilation becomes critical. For almost all patients, however, it is hypoxia that kills quickly, and the frequent co-conspirator is fluid in the airway.

Taking an abstract overview of airway management, all airway emergencies are directly or indirectly oxygenation emergencies—immediate evidence of hypoxia or threatening of hypoxia.

The patients present upright, with their head forward relative to chest, straightening cervical and thoracic trachea, and breathing through their nose and out their mouth. All of this is to improve upper airway patency and also expand the area of gas absorption in the alveoli (ie, open the lower airway). In addition to positioning, breathing faster is the body’s main way to increase oxygen absorption. Pursed lips can add a small amount of native positive end-expiratory pressure (PEEP).

As clinicians, we should realize that our therapies should align with the patient’s effort. They want to live! We can instantly help by boosting FiO2, but we must be mindful that the route of oxygenation is via the nose and that the negative inspiratory flow in their trachea far exceeds the 15 lpm given by a non-rebreather mask. This is why they rip off their mask—it is not meeting inspiratory needs and forces them to rebreathe their exhaled CO2—actually lowering their FiO2.

The patient who is driving you crazy—pulling off their mask and holding it above their nose, uncovering their mouth—is actually delivering a higher FiO2 than they would achieve by having a non-rebreather over their face.

A standard nasal cannula opened up to “jet speed” (a loud audible hiss)—setting the manometer valve to flush—will blow nearly 70 lpm in most hospitals in the United States and Canada (not quite as high elsewhere around the world). End-tidal CO2 cannulas will not permit this flow (they pop off at 6 lpm due to their small aperture). Warm humidified special-purpose high-flow systems (Fisher & Paykel and Vapotherm) are great but often not immediately ready at the bedside. If pulse oximetry is not improving with high-flow nasal oxygen, we need to consider the need for PEEP and ventilatory assistance (noninvasive ventilation, or intubation).

All While Addressing the Underlying Problem

While immediately initiating oxygen administration and optimizing conditions for oxygen absorption (positioning, suctioning), we also face the simultaneous task of determining the cause of the patient’s respiratory distress or airway emergency.

Emergency airways are, in fact, a minute-by-minute round-and-round of rapid assessment, oxygenation and optimization, and interventions. The very definition of “emergency” involves the component of time.

Experienced clinicians “thin-slice” the basics of patient presentation through sight, sound, and feel. We visually assess a patient’s breathing, respiratory rate, depth, body habitus, work of breathing, flaring of nostrils, patency of oropharynx and mouth opening, chest wall integrity, chest rise, diaphragmatic movement, swelling of the legs, diaphoresis, color, and appearance of the nail beds. We listen with our ears for stridor, upper airway noises, and grossly audible airway noise as well as with a stethoscope over the lungs, neck, and heart. We feel for crepitus, edema, and temperature.

Even prior to basic imaging and labs, we frequently instantly recognize the patterns and patient appearance of chronic obstructive pulmonary disease (COPD), asthma, congestive heart failure (CHF), pneumonia, pneumothorax, pulmonary embolus, and other common presentations.

After our immediate assessment, a relatively small group of imaging studies can be used to dial in our patient’s diagnosis. Ultrasound, stat portable X-rays, and endoscopy are the quickest to utilize at the bedside. CT scans take significantly longer and require patient transport but give us the best look at the lungs and upper airway (Ludwig’s angina, masses, hematomas, postoperative swelling, trauma, and the full array of pulmonary pathology). Unfortunately, patients who are severely compromised, either from poor pulmonary function or upper airway problems, do not tolerate the flat positioning that CT requires. Sometimes, the necessity for CT imaging triggers the decision point to manage the airway (ie, intubate the patient).

Airway interventions involve therapies that treat the underlying cause of the airway problem or involve plastic being placed into the mouth, neck, or chest. Pharmacological therapy includes things I consider “airway magic.” They work fast: naloxone for opioid overdose, epinephrine for anaphylaxis, nitroglycerin for CHF, nebulizers for COPD and asthma, and racemic epinephrine for stridor. While bradykinin and kallikrein inhibitors have revolutionized treating angioedema, they do not work instantly. Steroids and antibiotics are important and commonly used therapeutic interventions, but they take longer to work.

Let’s think about equipment. The fastest and simplest are supraglottic airways. Unfortunately, they work poorly when fluids are emerging from below. The chest can be rapidly decompressed (finger thoracostomy, chest tubes). Intubation requires more preparation, especially in unstable patients who should have intubation sequenced to their resuscitation (eg, those with high shock index, severe hypoxia, etc.). Intravenous fluids, blood, and pressors sometimes need to be initiated before the patient can safely undergo induction and positive pressure ventilation. Critically hypoxic patients should have preprocedural oxygenation maximized before intubation.