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The Pre-Oxygenation Period


Pre-oxygenation is the process of obtaining a desired oxygen saturation prior to intubation. In this article we will discuss the three different factors that will affect your ability to pre-oxygenate, and the variables that change the rate at which desaturation occurs. 

In a clean ventilation/perfusion ratio, the oxygen should be able to freely move through the airway, diffuse from the alveoli and into the pulmonary circulation. If either the ventilation side or the perfusion side is compromised, it will affect the efficiency of respiration. 

Diffusion Compromise

Water, bile, blood, and infiltrates can obstruct the alveolar territory in which gas exchange occurs. When you have blood moving from the right ventricle to the left ventricle without being properly oxygenated, it’s called shunting. Depending on the degree and surface area involved, shunting from pulmonary edema or infiltrates typically will not always be rectified by simply increasing the fraction of inspired oxygen (fi02). You will need to increase the respiratory surface area, and apply Henry’s law. This law states that the amount of gas that dissolved into a solution is proportional to the pressure present above the gas. The application of positive end expiratory pressure will increase the functional residual capacity, thus increasing surface area for gas exchange. In a spontaneous breathing patient, this can be accomplished by applying non invasive positive pressure ventilation (NIPPV). If a patient is apneic, manual manipulation of the airway will be needed to assure patent flow. NIPPV can be applied utilizing a BVM with a PEEP valve if a ventilatory function is desired. However, oxygen will only be delivered when the duckbill is in the open position. To maintain adequate inspiratory flow, a nasal cannula at >15LPM will need to be applied beneath the BVM mask.

Perfusion Compromise

Patent flow to the alveoli is only as good as the blood in which it greets. If perfusion is inadequate, or the systemic oxygen requirements increase, oxygenation will without doubt be affected. A hemoglobin molecule has four seats in which occupy oxygen molecules. When blood returns to the right atrium it usually has three of those four seats still saturated with oxygen. That means that our systemic oxygen demand is roughly 25%. This is why our normal central venous oxygen saturation (Scv02) is around 75%.  When metabolic demand increases, the Scv02 will drop due to the systemic oxygen demand. This is especially true during shock. 


The amount of air left in the lungs at the end of exhalation is called your functional residual capacity (FRC). This volume is essentially your apneic oxygenation reservoir. After a paralytic is pushed, the lungs will deflate to a resting phase. The oxygen left in the FRC will be part of what affects your rate of desaturation during intubation. The FRC is reduced exponentially when the patient is placed in the supine position. The diaphragm and abdomen will impede into the functional lung volume and decrease the apneic reservoir. This is why pre-oxygenation attempts should never be performed with the patient flat. And with knowing the importance of lining up your airway axis, intubating a patient flat is not a good practice.

Cooperative Binding

The oxyhemoglobin disassociation curve helps us understand the binding relationships between oxygen and hemoglobin. If oxygen just dissolved from the alveoli into the plasma, we would have no way of prioritizing where it is distributed. Because cells love oxygen, most of it would be absorbed early in circulation. This would render very poor concentrations for other organs of the body. That is the purpose of hemoglobin. It’s job is to prioritize where oxygen should be released. As hemoglobin travels throughout the body, it will loosen its binding with oxygen when high amounts of carbon dioxide and 2,3-DPG are encountered. This allows adequate delivery of oxygen to tissues working the hardest. 

As the partial pressure of oxygen(Pa02) increases in the plasma, two of the seats on the hemoglobin will be taken up immediately. However the concentration on a normal curve will need to increase to 60mmHg before oxygen saturation hits 90%. Our goal for pre-oxygenation is to reach an oxygen saturation of 94% for at least three minutes. This task can be difficult if a patient is not cooperating with your pre-ox attempts. It’s important to remember that a rushed intubation is a dangerous intubation. The concept of delayed sequence intubation (DSI) is essentially a procedural sedation, with that procedure being pre-oxygenation.


As you read this you are inhaling approximately 21% oxygen and 79% nitrogen. Nitrogen at physiological atmospheric pressures has low solubility and does not readily absorb into blood. Because of this, nitrogen will remain in the alveoli and keep them from collapsing. When you plan on intubating a patient, it is optimal to replace that nitrogen with oxygen. This allows a larger amount of your FRC to be filled with oxygen and thus prolong your safe apneic period.

Blocking the patient from breathing in nitrogen is harder than it sounds. You must overwhelm their inspiratory flow with purely oxygen. If at anytime their IFR overcomes the delivered oxygen, they will start to entrain nitrogen from the atmosphere. 

Nasal Cannula + Non Rebreather

One commonly accepted method for this task is to place a nasal cannula at 15LPM  on the patient. The nasal cannula alone will obviously not prevent the patient from breathing in room air. However, applying the nasal cannula underneath a non re-breather will hopefully provide enough inspiratory flow rate, and prevent the patient from exceeding the flow at which the NRB provides. It is important to fully understand the anatomy of the NRB and assure a snug fit. If you note the patient is not partially deflating the reservoir bag, re-evaluate the fit and ensure the patient is not pulling in peripheral flow from poor mask seal.

The NRB has two unidirectional valves which set on each of the mask. This allows gases to exit but prevents entrainment of room air. Many hospital systems buy NRB’s with only one of these valves in place. The other side of the mask will just have a few small holes to prevent asphyxiation in the event of oxygen delivery failure. If your mask does not have both of these unidirectional valves, it will pull in room air and prevent true de-nitrogenation. 

 If at anytime the patients IFR exceeds the liters per minute provided by both devices, the patient will entrain room air from around the mask. During delayed sequence intubation this is usually not an issue because the patient is disassociated with Ketamine. Trying to efficiently prep a combative patient for intubation is impossible. 

The pre-oxygenation period is crucial to a safe and effective elective intubation. A strong understanding of oxygen physiology is crucial for any clinician who manages airways. 

Tyler Christifulli CCP-C, NRP, FP-C

Peer Review by Eric Bauer

Tyler brings up the vast physiology involved with our ability as providers to oxygenate our patients during the pre-oxygenation phase.  These many variables constitute the sum of all moving parts that ultimately dictate being successful in this process. Obviously, our patients are far from normal, with physiology that often hinders us through one or many of the physiological areas needed to deliver oxygen to our Hgb. There are few processes in this chain reaction that I’d like to add to Tyler’s in-depth overview.

  1. Henry’s Law: This gas law is essential in our ability to deliver oxygen through the alveolar membrane, with the resulting diffusion into the capillaries. We often discuss Henry’s Law as the primary means for diffusion. However, Henry’s law is just a small part of this process. As Tyler stated, Henry’s Law is about a gases solubility in a solution.  Meaning that each gas has a different diffusion rate based on its molecular weight, thus causing a different diffusion potential.  Henry’s Law demonstrates how a gas diffuses into the solution based on the pressure exerted above the gas in a solution.  With that being said, there are two other gas laws that we need to apply in this process.
  2. Dalton’s Law: Dalton’s Law is the gas law of partial pressure. This means that our ability to utilize the gas (O2) is dependent on the overall partial pressure of that gas. This means that our altitude (elevation) directly dictates our partial pressure of oxygen. At a lower altitude, we can utilize the gas much better in comparison to higher altitudes.  As Tyler discussed, by increasing the gas concentration, we then increase the partial pressure.  A great quick calculation you can use in transport is to multiple your FiO2 concentration by 5 (FI02 x 5). This will give you a calculated partial pressure of alveolar dissolved oxygen (PAO2). Example: If applying 0.50 (50%) FiO2, your calculated PAO2 would be 250 (0.50 x 5 = 250).
  3. Fick’s Law:  Fick’s law is often forgotten, but plays such an important role in our ability to have gases diffuse across the alveolar capillary membrane. Fick’s laws states that diffusion through a tissue membrane is proportional to the driving pressure, molecular weight and membrane thickness. As you can see, we often use Henry’s law to demonstrate many of these attributes. However, Fick’s Law actually plays the biggest role in a gas molecules ability to diffuse across the alveolar-capillary membrane.
  4. Lastly, the denitrogenation process is our attempt at raising the PaO2 as high as possible.  As Tyler clearly stated, raising the total amount of dissolved oxygen in arterial blood is our ultimate goal.  However, one part of physiology is altered when we do this. The concept of absorptive atelectasis needs to be considered. We know that atmospheric air is made of primarily Nitrogen at 78%. Nitrogen is a dense gas that doesn’t diffuse easily. Its main role is to aid in maintaining our intrinsic alveolar PEEP during normal homeostasis. This is said to be between 3-5 cmH20. However, when we apply high concentrations of oxygen, we drive out the Nitrogen that remains in the alveolar.  This can cause alveolar collapse (atelectasis) and alveolar injury.  With that being said, this can and will hinder our ability to have proper functional residual capacity.

As you can see by Tyler’s article, there are a multitude of intermixing processes in play that all intertwine to bring dissolved oxygen to the blood stream, where tissue oxygenation can happen. By having one part of this process broken, we are faced with identifying the problem and attempting to fix the broken part of the chain.


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