While breathing room air, oxygen saturation drops precipitously to below 90% within about a minute of the start of apnea in the average healthy adult. One of the most important safety measures we use in anesthesia is to preoxygenate our patients prior to induction of anesthesia and in preparation for intubation. This is especially true if we are planning a rapid sequence induction. Adequate preoxygenation can more than double the time to hypoxia during apnea, allowing more time for intubation to occur.
Preoxygenation increases the margin for safety. It treats any pre-existing hypoxemia in the critically ill patient. It also postpones the onset of hypoxia while the patient is apneic during the intubation attempt. This becomes especially important if the intubation attempt becomes difficult and prolonged.
Speed of onset of hypoxia with apnea depends on metabolic rate and on the actual amount of oxygen available in the patient’s functional residual capacity. To see how preoxygenation can effect this let’s review some physiology.
A Quick Review of Oxygen Saturation
We’re all familiar with the oxygen-hemoglobin desaturation curve. As the partial pressure of oxygen rises, there are more and more oxygen molecules available to bind with Hgb. As each of the four binding sites on an Hgb molecule binds to an oxygen molecule, its attraction to the next oxygen molecule increases and continues to increase as successive molecules of oxygen bind. The more oxygen is bound, the easier it is for the next oxygen molecule to bind, so the speed of binding increases and the oxygen saturation percentage rises. You can see this in the graph as the curve shows more and more oxygen saturation occurring as the arterial oxygen levels go up.
An O2 sat of 90% corresponds to a PaO2 of 60 mmHg. This is the minimum oxygen concentration providing enough oxygen to prevent ischemia in tissues. Once the O2 sat falls below 90%, the PaO2 drops quickly into the dangerously hypoxic range as fewer and fewer oxygen molecules are bound to Hgb. That’s why we want to try to keep O2 saturation above 90%.
You can divide the curve into areas of risk. That 85-95 PaO2 range is an area of high risk because that represents the portion of the curve where desaturation can occur within seconds. It’s also important to remember that there can be a lag time in critically ill patients of about a minute for most pulse oximeter readings — meaning your warning alarm may come later than the onset of the hypoxia.
How Does Metabolic Rate Affect Oxygen Drop?
A nonfebrile adult at rest uses roughly 3 ml/kg of oxygen per minute. A child can use 6 ml/kg/min. Fever, seizure, increased activity raise that oxygen consumption significantly When we inhale room air with a concentration of 21%, we usually exhale gas containing a concentration of about 15% oxygen.. In between, the average 80kg adult removes about 240 ml (3 ml/kg X 80kg) of oxygen from his lungs. It metabolic rate goes up, then oxygen will be removed from the lungs at a much faster rate.
Functional Residual Capacity: It Matters How Much Oxygen Is In The “Tank”
Functional Residual Capacity (FRC) is the amount of air left in the lung after a normal exhalation. FRC is an important concept. It represents the combined gas volumes providing most of the normal functional lung oxygen exchange. Think of it as the patient’s oxygen tank. The larger the FRC, the bigger the “tank”. A small child, who has a smaller FRC than an adult, can’t hold his breath as long without getting hypoxic because he has a smaller “tank”.
Position can change FRC. An awake adult who lies supine loses about a liter of FRC as the abdominal contents push the diaphragms upward by about 4 cm. The patient with marginal respiratory reserve or morbid obesity may feel short of breath in the supine position because he can’t compensate for the decreased FRC as well: too much weight pushing up from below the diaphragm.
Induction of anesthesia, and presumably unconsciousness, causes the diaphragm to move still higher, further decreasing FRC by approximately 0.4 liters. If the patient is breathing spontaneously, hypoventilation can occur.
FRC is important to the concept of preoxygenation because when the patient becomes apneic, oxygen will continue to be absorbed from this volume until it’s depleted. The more oxygen in this “tank” before apnea, the longer the patient can hold his or her breath until they start to be come hypoxic.
How Fast Can Oxygen Saturation Drop?
Let’s look at some simple math to see why the average person starts to get hypoxic after about a minute of apnea.
You can estimate the PaO2 of a patient with normal lungs to be roughly equal to about 5 times the inspired oxygen concentration. Breathing room air, 5 X 21% inspired oxygen equals an expected PaO2 of 105, and that corresponds to an oxygen saturation of 100%
For an 80 kg adult with a total lung volume of 3000 ml filled with room air, there would be about 640 ml of oxygen available (21% oxygen X 3,000 ml). After 1 minute, assuming we’ve removed 240 ml of oxygen (3ml/kg/min X 80kg), there is now 640-240 ml of oxygen left in 3,000 ml or 13%.
An alveolar oxygen concentration of 13% corresponds to a PaO2 of about 65 (5 X 13) — corresponding to an oxygen saturation of about 90%. Within a minute, oxygen saturation falls to the steep part of the curve and starts to drop quickly. If the patient is febrile, excited, or with a premorbid condition such as obesity, COPD, or sepsis, oxygen saturation will actually drop faster than this.
That’s the main reason we try to limit intubation attempts to less than a minute before we ventilate the patient. Since the pulse oximeter warning can lag behind the actual drop in saturation, it’s best not to delay until the alarm sounds.
The speed of onset of hypoxia and hypercarbia depend on several things.
- The starting values for PaO2 and PCO2
- The age of the patient (children have higher metabolic rate)
- The medical condition of the patient
- comorbidities such as obesity, COPD which impair lung oxygenation
- anemia which decreases oxygen carrying capacity
- fever, sepsis, excitement which increase oxygen consumption
- Are you providing apneic oxygenation?
Preoxygenation Delays Onset of Hypoxia
By fully preoxygenating an adult patient, the time to desaturation can be increased to potentially as much as 8 minutes during apnea, although typically it is shorter than this. Full preoxygenation is achieved by:
- Bringing the oxygen saturation as close to 100% as possible
- Fully removing all of the nitrogen from the alveoli (denitrogenate) to maximize the amount of oxygen in the lungs
- Maximizing PaO2 or the actual amount of oxygen in the bloodstream— remember oxygen saturation and PaO2 are different. You can be 100% saturated yet not have maximum oxygen content in the blood stream (see my prior blog entry)
Let’s look at our patient with the FRC of 3,000 again. With full preoxygenation that patient now has an effective oxygen tank of 3,000 ml of oxygen. Removing it at 240 ml per minute means it theoretically would take about 10.5 minutes to get down to our oxygen saturation of 85-90%. (3,000 – 10.5 x 240 ml = 360 ml.) Now of course this assumes that nothing changes to stimulate the patient, release adrenalin and increase metabolic rate. it also ignores the fact that carbon dioxide is rising during this period of apnea and CO2 also takes of room in the alveoli. You are unlikely to get this much time. But clearly good and full preoxygenation gives you a large margin of safety during intubation.
How do you know if your patent is fully preoxygenated? If you have a mass spectrometer in your circuit, as most modern anesthesia machines have, you can simply wait while you watch the expired concentrations. Over several minutes you will see the levels of nitrogen drop and expired oxygen concentration rise. However, in the absence of this, two common ways used to preoxygenate a patient are:
- Allowing the patient to breathe through a tight fitting non-rebreather mask at 15L/min for 4 minutes. (It must be tight fitting to avoid entraining room air around the mask)
- Having the alert patient take 8 full tidal volumes of oxygen with a tight mask (these must be deep maximal breaths)
Depending on the clinical circumstances, it may not be possible to fully preoxygenate or hyperventilate your patient prior to laryngoscopy, thereby increasing the risks of significant hypoxia or hypercarbia. Despite preoxygenation, the patient may still be at risk of rapid desaturation if the patient’s metabolic rate is increased (fever, seizure, sepsis) or their PaO2 cannot be raised because of shunting. Even if you have preoxygenated, you must always be prepared to ventilate the patient if the intubation attempt becomes prolonged. Remember, it’s lack of oxygen that will harm your patient, not lack of n endotracheal tube.
What About Carbon Dioxide during Apnea?
While preoxygenation increases the time to hypoxia, it does not change the rate of rise in carbon dioxide. Compared to 250 ml/min of oxygen moving out of the alveoli to the bloodstream, only eight to 20 ml/minute of carbon dioxide moves into the alveoli during apnea, with the remainder being buffered in the bloodstream. This typically causes a rise of 8-16 mmHg carbon dioxide during the first minute and then 3-4 mmHg carbon dioxide per minute thereafter. A rising PCO2 will progressively drop pH.
You can increase the time to significant hypercarbia by:
· Asking your patient to hyperventilate for a minute or so prior to induction
· Hyperventilating your patient manually with bag-valve-mask after induction of unconsciousness
Can Anything Else Be Done To Delay Hypoxia With Apnea?
Yes: Apneic oxygenation which is the provision of oxygen into the oropharynx of your apneic patient during the intubation attempt itself. The next post will discuss the procedure of apneic oxygenation, which is an easy way to potentially delay the onset of hypoxia. It’s a technique you can use if you expect a difficult intubation or have a patient who will tolerate apnea poorly.