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The CO2 Conundrum

I dearly enjoy acronyms. Shorthand ways to say complex things, acronyms are ubiquitous in daily life. Emergency medicine and EMS are no different, and there are a host of useful acronyms in the world of prehospital care. Some of my favorites include TMCTL (Too Many Complaints to List), P3 (Pretty Poor Protoplasm) and the always useful OTD HTB (Out The Door, Hit The Bricks). I have a special soft spot in my heart for the double-edged WNL (Within Normal Limits or We Never Looked).

While many of my favorite acronyms are frankly unmentionable in a public discourse, such as this, I've recently become enamored with TMI ("too much information"). I am convinced that "TMI Syndrome" is a common scourge of society think of your worst first date and EMS is not immune to this disease. There are times that the very tools we use to extract clinical data give us information we don't really need.

Take end-tidal capnometry in the intubated patient. I think that five years in the future, capnometry will represent the seventh vital sign. (For those keeping score, the other six are pulse, respirations, blood pressure, temperature, pulse oximetry and Glasgow Coma Score). But like all vital signs, capnometry values must be interpreted within a clinical context. The paramedic must know which vital signs to address and which ones to ignore.

One of the goals of intubation is to promote the process of ventilation, or the expulsion of CO2 from the body. Intubation enhances ventilation by increasing tidal volumes and respiratory expansion. The expansion of the chest cavity enhances not only the volume of lung involved in the process of inhalation, but also promotes the elastic recoil of the chest. During the expiratory phase of respiration, the increased lung involvement and the increased force of chest-wall compression enhances CO2 excretion.

Enhancing CO2 excretion from the body helps us to avoid the perils of hypercarbia and respiratory acidosis, and one of our goals in ventilating the intubated patient is indeed to reduce pCO2 (the partial pressure of carbon dioxide in the blood) to acceptable levels. But without the use of end-tidal capnometry, we really can't know if we're doing an effective job in our efforts, whether we use a manual bag-valve device or a mechanical transport ventilator. Pulse oximetry, which evaluates the degree to which hemoglobin passing by the sensor is saturated with oxygen, is at best an indirect measure of oxygenation only. It does not reflect the results of ventilation, and cannot be used as a guide to the efficacy of our technique in reducing levels of CO2.

With capnometry, we now have the ability to monitor the effects of ventilation. In general, high values of end-tidal CO2 (the carbon dioxide content of expired air, or EtCO2) reflect hypoventilation. If high values are noted, we move to decrease the EtCO2. We can do this by either increasing the tidal volume of the respirations, increasing the rate of respirations or both. However, these are not benign procedures. Increasing the tidal volume of each breath means placing more volume into the closed spaces of the lung. If we've done it right, the lung has room to expand to encompass the extra volume. If lung capacity is limited, such as in cases of asthma, COPD or restrictive pulmonary disease, the extra volume will cause an untoward rise in airway pressures, risking rupture of fragile pulmonary tissues and possibly creating a tension pneumothorax.

Increasing the respiratory rate may produce a similar effect, as each breath is "stacked" upon residual volumes of air left over from the previous breath. In addition, it should be recognized that positive pressure ventilations decrease venous return to the heart (the "suction" effect of increasing negative intrathoracic pressure on blood flow through the vena cava back to the heart is a major determinant of cardiac output). Increasing the volume of respirations or the respiratory rate will further hamper central venous return. All of these effects are heightened in patients with asthma or COPD, where airway pressures are already high, and where bronchospasm or obstruction prevents full and rapid exhalation. These effects are common to any form of positive pressure ventilation, whether mechanical (transport ventilator), non-invasive (BiPAP or CPAP device) or manual (bag-valve-reservoir device).

A new ventilatory technique helps to avoid these problems. Known as "permissive hypercapnia," it turns the capnometry world upside down. By purposefully ignoring CO2 data, this technique offers a simple way to manage the ventilated patient.

The key to understanding the concept of permissive hypercapnia is to recognize that while patients with ventilatory failure do suffer from respiratory acidosis, the real danger in a buildup of CO2 is the lack of a respiratory drive. When CO2 becomes excessive, one simply stops breathing. But in the intubated patient, apnea from hypercarbia is a non-issue. The patient is intubated, so the airway is secured. If the patient stops breathing, we simply take over. Therefore, in the patient with an artificial airway in place, it's no big deal if the EtCO2 rises. We've already dealt with the major risk, and efforts to lower EtCO2 may cause further problems. Permissive hypercapnia does just that allows pCO2 its own way because the effects of a high pCO2 really don't matter.

Using this idea, the number we pay attention to in the field is pulse oximetry. As long as we can oxygenate the patient, we can use relatively high oxygen contents with small tidal volumes and avoid the risk of pneumothorax. As the patient's condition improves, we can gradually lower the inspired oxygen content and deliver larger and more frequent breaths to aid in the expulsion of built-up CO2.

There are a few caveats that go along with this novel idea. The technique of permissive hypercapnia is best applied to patients with readily reversible conditions, such as asthma and anaphylactic bronchospasm. As bronchospasm decreases with therapy, respiratory volumes may rise. While patients with COPD don't worry about a respiratory shutdown from excess levels of CO2 (their chronic respiratory acidosis has "shifted" their respiratory drive from being based on high CO2 content in the blood to a low oxygen level), the effect of this technique on minimizing respiratory volumes and pressures may benefit them as well. One might also surmise that this technique might be of value in patients with "stiff" lungs from pneumonia or restrictive lung disease (silicosis, fibrosis, etc).

The danger in permissive hypercapnia lies in the long-term use of this ventilatory mode. A prolonged and sustained rise in pCO2 may indeed lead to systemic acidosis (in solution within the blood and tissues of the body, CO2 functions as a weak acid). It stands to reason that patients with higher chronic levels of CO2, such as those with COPD, may be at some risk of an especially profound hypercapnia due to persistent saturation of the body's buffering systems. In the field, however, this may be of relatively small import. Because elevated levels of pCO2 may result in cerebral vasodilation and increased intracranial pressure, the technique should probably be avoided in cases of possible head trauma or stroke.

(It may have occurred to you that those medics who function without capnometry may have a better inherent grasp of this technique. It's because for years, they've been basing their ventilatory management on pulse oximetry alone. Now there's a physiologic reason why their technique works just as well as that of medics with bells and whistles. It's sort of like the great equalizer of respiratory care.)

While we've all heard the mantra "Treat the patient, not the numbers," it's admittedly hard to do. Monitors flash their data before us in ways that invariably get our attention. If you can make all the numbers match, good for you. If not, the concept of permissive hypercapnia allows you to better focus your efforts, and serves a means to let you use your data correctly or, sometimes, not at all.

Publisher's note: For another take on the prehospital use of capnography, review "Capnograpny in EMS: A Powerful Way to Objectively Monitor Ventilatory Status," January 2003 JEMS. In that article, Baruch Krauss, MD, EdM, FAAP (a researcher and educator in the field of capnography and procedural sedation and analgesia, an assistant professor of pediatrics at Harvard Medical School and a faculty member of the Division of Emergency Medicine at Children's Hospital in Boston), wrote: "This is an exciting time in prehospital care; the ability to use capnography in nonintubated patients opens many opportunities for research and enhancements in patient care. Capnography can provide important objective information in conditions where EMS professionals have previously had to rely on subjective assessment." The article reviews the terminology, technology, physiology and clinical applications for capnography, with an emphasis on using it as an objective assessment tool in the care of patients with bronchospastic disease and hypoventilation states.


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