You’re called to a residence for a 22-year-old male who’s having trouble breathing. On arrival you locate the patient, who appears to be in acute respiratory distress. He’s sitting in a chair and leaning forward in a tripod position. He has a hard time speaking and states he has a history of asthma and that this latest attack started about 25 minutes ago. He has used his inhaler twice without relief. He tells you he believes that his puffer is empty.
He’s speaking in short but complete sentences. His skin is pink, warm and dry. Your partner places a combination nasal/oral capnography filter line cannula with oxygen (O2) delivery capability on the patient and turns on the cardiac monitor with capnometer and pulse oximeter.
His initial capnogram shows a respiratory rate of 20 with a sloped leading edge to the waveform and an end-tidal carbon dioxide (EtCO2) of 48. The pulse ox reading is 92%. Realizing the severity of the condition, you hand the patient a small volume nebulizer with albuterol. After about three minutes of bronchodilator therapy, the patient appears less anxious. The capnogram shows a much different waveform this time because it has squared off, and the reading dropped to 40. The pulse ox increased to 94%. Auscultation of the chest reveals diffuse monophonic wheezes throughout the lateral vesicular fields.
After questioning the patient, he reveals that he’s not up to date on all his asthma medications because he can’t afford them. He’s transported to the hospital where his EtCO2 is trended and remains stable with a square waveform.
On arrival, you discuss the case with the attending physician noting the non-compliance with his asthma meds for financial reasons, as well as your assessment findings and the patient’s response to therapy. The physician auscultates the patient’s chest and, after noting that the patient still has some wheezing present, orders IV Solumedrol.
Discussion
Asthma is a common inflammatory disease that involves periodic episodes of severe but reversible bronchial obstruction. Frequent repeated attacks may lead to irreversible damage in the lungs and the development of chronic asthma.
Asthma affects millions of Americans and is responsible for thousands of deaths per year. It is more common in children and young adults, yet can occur any time in life.1
There are two basic types of asthma. The first one is called extrinsic asthma and involves acute episodes triggered by an allergic reaction to an inhaled irritant. Frequently, there’s a family history of allergies, such as hayfever. The onset usually occurs during childhood or in young adults. About 80% of the time, it occurs before age 10.2 Childhood asthma usually improves with age.
The second type of asthma is intrinsic asthma. In this disease, other types of stimuli initiate the acute attack. These stimuli include respiratory infection, exposure to cold air, exercise and exertion, stress, inhalation of irritants (e.g., cigarette smoke) and certain drugs, such as aspirin.
Many patients have a combination of the two types of asthma. Whatever the cause, it’s an airway problem, plain and simple. It interferes with respiratory gas exchange. We understand that it can be bad, but how do we really know? How can we judge the severity of the asthma attack? How do we know that what we’re doing is working?
Assessment Tools & Techniques
Traditional assessment of the patient with a respiratory complaint has been focused around subjective techniques, such as counting respiratory rates, estimating tidal and minute volumes by subjectively judging chest rise and fall to what “appear” adequate, along with the use of accessory muscles.
The accuracy of these rates can be debated forever, but in the end it must not be that important as respiratory rates are often estimated. And to think we’re comparing what we get to an arbitrary number that we’re tested over. The purpose of breathing is not to make the chest rise and fall; it’s to ventilate and to eliminate the waste product of metabolism, CO2.
I teach my students that noisy breathing is obstructed breathing, but not all obstructed breathing is noisy. Chest auscultation is another technique we’re taught. The classic wheezing is the sound most closely associated with asthma.
The wheezing sounds, heard on exhalation first, are a result of a narrowed airway. The narrowing of the airway can be caused by chronic inflammation or acute inflammation due to a disease process or other mechanical wheezing.
To reiterate, the noise is made by a narrowed airway. The inflammatory process causes inflammation that’s diffuse, so all airways are narrowed at the same width. The result is a single, toned wheeze called a monophonic wheeze. Imagine a group of flutes playing the same note.
An asthma attack occurs when bronchospasms occur, causing the airflow to be reduced from the alveoli at different diameters. This causes several different “pitched” wheezes to occur–polyphonic wheezes.
Imagine several different sizes of horns playing different notes. Sounds simple, right? The problem is the lack of sensitivity in auscultation due to inexperience of the clinician or misidentifying of the sounds.3 Perhaps another reason is not being able to hear anything anyway because of ambient noise. It could be that the patient isn’t taking deep enough breaths to make an audible wheeze. Also, stethoscope training widely varies with little consistency on how to do it correctly.4 With practice and proper training, however, stethoscopy skills can be a valuable asset.5
Capnography’s Role
I refer to capnography as a clinical upgrade. In my opinion, it’s the most important clinical upgrade I’ve seen in the more than 30 years I’ve provided care. Because it’s the only noninvasive measure of a fundamental life process, it can be used as a triage tool for the patient with a wide variety of complaints. In fact, capnography can give you your airway, breathing and circulation assessment in as little as three breaths.
EMS providers have questioned the accuracy of these non-invasive CO2 monitors, specifically regarding their concordance with blood gas and partial pressure CO2 (PaCO2). In patients with severe asthma attacks, however, a study showed that the concordance of the EtCO2 and the blood gas CO2 was high.6
The meaning for EMS is clear. Capnography gives a good indication of the arterial blood gas level, thus providing EMS providers with an objective, reliable and accurate tool for assessing the severity of an asthma attack.
Using the EtCO2 values to triage and to trend response to therapy is a leading reason for the use of capnography in the emergency setting. Patients early on in an asthma attack will tend to hyperventilate due to catacholamine release. This will lead to hypocapnia (low EtCO2 reading below normal range, which is less than 35mmHg). These are considered to be mild asthma attacks. As the patient begins to tire, EtCO2 may return to normal (35—45 mmHg). This patient is experiencing a moderate asthma attack.
The patient in the case mentioned earlier fell into this category. Finally, if the EtCO2 rises above normal range (hypercapnia), then the patient is in ventilatory failure and hypoventilation. Aggressive therapy is warranted.5
Again, the value measures the adequacy of ventilation and to another extent, oxygenation. In recalling the Fick Principle of O2 transport, one of the conditions of perfusion is that red blood cells must be able to offload their O2 molecule into the blood stream to be used by the cells for metabolism. In a state of hyperventilation, it causes a left shift of the oxyhemoglobin curve. In English, that means it makes the O2 bind more tightly to the red blood cells.
The result is hypoxic tissues with a pulse ox reading of 100%. Conversely, if the patient is exhibiting hypercapnia (hypoventilation), that will cause a right shift of the curve with acidosis and then the hemoglobin can’t bind well. So the O2 may not get to the cells.
Rapid descent of the saturation of peripheral oxygen (SPO2) is evident in cases in which there’s hypercapnia. So pulse oximetry and capnography both have a role in assessing the respiratory patient. An SPO2 of 90 is the same as a PaO2 of 60. A PaO2 less than 60 would be considered hypoxemia. Therefore, the combination of hypoxemia and hypercapnia can instantly triage a patient to the ominous category of respiratory failure.
In trending the EtCO2 through continuous monitoring, you can observe patient improvement or the direction you’re headed. If the EtCO2 trends upward (above 50), the patient is getting worse; if it trends downward (below 50), then the patient is improving. If the EtCO2 remains the same, then the patient is remaining stable.
The patient is also triaged before and after therapy to see if they’re improving. The value, however, can tell you their breathing adequacy. The actual waveform is used to assess the airway status.
Technical Aspects
The waveform on the screen usually doesn’t look like the printout because most cardiac monitors’ screens scroll at a rate of 25mm per second and typically display about three seconds of activity at a time. This works well for heart rates. But when a patient takes 12 breaths per minute, you wouldn’t see a waveform on the scope.
The screen section chosen to display the waveform is sped up about 10 times so the waveform is visible. But when the waveform is printed, it’s printed real time on the paper and will be a lot wider than what you see on the scope.
So I recommend that the paper capnogram be used to evaluate for airway issues, not the scrolling part on the screen. The scrolling part on the screen can be used to look at a square capnogram (for tube placement confirmation) or apnea (flat line). Everything else should be evaluated on the printout. It’s the easiest and most accurate way to study the capnograph.
Capnography measures CO2 flow and draws a picture of CO2 flow over time. CO2 comes from the alveoli. So if the capnogram is a square, then there’s no obstruction preventing the CO2 from moving in and out of the airway. Inflammatory process can cause a narrowing of the airway, but the alveoli still empty at the same rate and will display a square waveform.
Even though the patient may have wheezes, they don’t have a bronchospasm because the waveform is square. What does this mean? Bronchodilators may not be necessary and probably wouldn’t work on inflammation. On the other hand, patients who have a bronchospasm (e.g., patients with reactive airway disease), have uneven alveolar emptying. This means some alveoli rapidly purge their CO2; others may be more constricted, so it takes longer. This is what produces the severe angle to the upstroke and plateau on the waveform.
Bronchospasm responds well to bronchodilator therapy, such as albuterol. In this case, the patient had a bronchospasm. That rapid triage with capnography gave the EMS provider objective, reliable and measurable evidence of what the problem was, how severe it was and what to do about it. The most severe bronchospasm will produce a waveform that truly looks like a “shark’s fin.” In other words, the leading edge of the capnogram curves or bends over and angles up until the inhalation phase. When this happens, the waveform loses the “plateau,” or flat part. This is troubling and means that the EtCO2 is much higher than it reads, and the patient can’t empty the alveoli due to air trapping. It also means the patient’s airway is so bad that they’re at risk for dynamic hyperinflation syndrome. Another word for this is “auto peep.”
Although this can occur in the spontaneous breathing patient, it also can easily occur with assisted ventilation, positive pressure ventilation and with continuous positive airway pressure when the patient is breathing too much. This occurs when the respiratory rate and depth doesn’t allow enough time to fully exhale. As a consequence, the alveoli can’t completely empty; with each breath, the alveoli trap more air. This can result in increased work of breathing to inhale and exhale, and even apnea. This condition will show a waveform without an alveolar plateau–a true shark’s fin.
Conclusion
In the patient with an asthma attack, if the patient responds to bronchodilator therapy, the resulting objective waveform will show the bronchospasm has been relieved–with the waveform now being square. If it doesn’t change, then it may be time for another medication. In the patient with acute asthma attack, capnography is a valuable tool for triage of the severity of their condition. It also objectively trends the effectiveness of your treatment. Having the ability to provide reliable, objective and accurate assessment of the asthma patient is an important clinical upgrade that’s ready for prime time.
Disclosure: The author has reported receiving no honoraria and/or research support, either directly or indirectly, from the sponsor of this supplement.
References
1. American Lung Association Epidemiology and Statistics Unit Research and Program Services Division. November 2007. Trends in Asthma Morbidity and Mortality. In American Lung Association. Retrieved Oct. 19, 2011, from www.lungusa.org/finding-cures/our-research/trend-reports/asthma-trend-report.pdf.
2. Singulair. N.d. Title TK. In Singulair. Retrieved Oct. 19, 2011, from http://singulair.com/montelukast_sodium/consumer/asthma/asthma-medication/index.jsp.
3. Murphy RL. Auscultation of the lung: Past lessons, future possibilities. Thorax. 1981;36(2):99—107.
4. Welsby PD, Parry G, Smith D. The stethoscope: Some preliminary investigations. Postgrad Med J. 2003;79(938):695—698.
3. Page B. Lung sound assessment: The lost art of using a stethoscope. JEMS. 2011; 36(8):26—28.
5. Delerme S, Freund Y, Renault R, et al. Concordance between capnography and capnia in adults admitted for acute dyspnea in an ED. Am J Emerg Med. 2010;28(6):711—714.
6. Corbo J, Bijur P, Lahn M, et al. Concordance between capnography and arterial blood gas measurements of carbon dioxide in acute asthma. Ann Emerg Med. 2005;46(4):323—327.
