Capnography: A Versatile Life-Saving Tool

If a tool could tell us when we’d given enough albuterol to resolve a little eight-year-old girl’s asthmatic bronchospasm or that Mr. Smith’s cardiac output is steadily declining and he’s approaching cardiac arrest, I suspect we would all use it. Many EMS systems actually have this tool on their vehicles, but they may not have provided the necessary in-depth training to their paramedics and EMTs so they can fully use this incredibly versatile, life-saving piece of equipment. The tool is capnography, and its use is not limited to confirmation of a correctly placed endotracheal tube.

Capnography is simply an EKG for exhaled carbon dioxide (CO2); it plots the instantaneous concentration of CO2 against time during the patient’s respiratory cycle1,2 (Figure 1). Like an EKG, the resulting waveform produces unique shapes and rhythms that are meaningful in patient assessment and treatment. We can observe ST elevation by evaluating the shape of a waveform in a 12-lead EKG and suspect a heart attack, and it is the shape of the capnography waveform that alerts us that the eight-year-old girl needs a second nebulizer treatment because she is still in bronchospasm. And like the perilous EKG rhythm of a third-degree heart block, the rhythm of a capnogram-sometimes called trending-can signal decreasing cardiac output and impending arrest for Mr. Smith.


Figure 1. Normal Adult Capnograph
Illustrations by author.

 

CARBON DIOXIDE AND “NORMAL”

Understanding the mechanics of breathing and carbon dioxide is vital to using capnography fully. The brain’s respiratory center in the medulla oblongata controls breathing rate and volume. High CO2 concentrations cause the brain to increase respiratory effort; lower CO2 concentrations cause the brain to reduce respiratory effort.3 Through the controlling of breathing rate and volume, the brain attempts to narrowly maintain the concentration of CO2 in the blood at 40 mm Hg. (1.7) Maintaining the partial pressure of carbon dioxide (PaCO2) at 40 in the blood stream enables the removal of CO2 from the body, which is a passive process.


Figure 3. Decreasing PETCO2
From Hyperventilation

CO2 is a byproduct of energy production by mitochondria oxidizing glucose in a cell.4 This CO2 waste is removed from the body passively by moving it from the cell into the blood, from the blood into the alveoli, and then out of the body through breathing. This passive process occurs by getting the CO2 to move on its own from an area of high concentration to areas of lower concentration, resembling a river draining downstream. This process is called “diffusion.” The concentration of CO2 inside a cell is normally about 46 mm Hg. Since the cell membrane is permeable to carbon dioxide, CO2 (at 46 mm Hg inside the cell) diffuses across the membrane into the less concentrated bloodstream (40 mm Hg). This exact same process repeats itself in the lungs, where the concentration of carbon dioxide in the blood is higher than inside the alveolar air space, so CO2 moves out of the blood and into the lungs, where it is ultimately expelled from the body. (1, 10-12)


Figure 4. Decreasing PETCO2
From Hypoventilation

As you exhale, the first CO2 expelled comes from the passageways in the lungs (bronchi and bronchioles). The alveoli, which are the last to empty, are closest to the bloodstream and thus will have the highest concentration of expired CO2. As a result, the level of measured CO2 will steadily increase during the exhalation with the highest level of CO2 at the end of the breath. This is referred to as the “end tidal CO2 level” (PETCO2).5 A direct correlation between the partial pressure of carbon dioxide (PaCO2) actually in the blood (e.g., blood gas analysis) and the partial pressure of PETCO2 has been established: PETCO2 is 2-5 mm Hg lower than the actual blood PaCO2 in adults.6-13 (1,19)


Figure 5. Apnea

One of the most frequently asked questions about capnography is, “What are the normal values?” In a healthy adult, the PaCO2 is narrowly maintained near 40 mm Hg. Since PETCO2 is typically 2-5 mm Hg lower than PaCO2, a healthy adult “normal” capnometry (number) reading is 35-38 mm Hg of CO2 (Figure 2). While a capnometry reading of 34 or 39 mm Hg should not be a cause for concern, a reading of 28 or 52 mm Hg should be considered alarming until the underlying cause and its respective implications are identified and treated as appropriate.


Figure 2. Normal Capnogram

 

PULSE OXIMETRY VS. CAPNOGRAPHY

One of the most global misconceptions in EMS may be the notion that if a patient is receiving 100 percent oxygen and has a pulse oximetry saturation of 100 percent, he is “just fine.” This could not be further from the truth. Imagine a Chronic Obstructive Pulmonary Disease (COPD) patient in distress on 100-percent oxygen by nonrebreather mask with a pulse oximetry saturation that rises to 100 percent. Despite the patient’s still being in distress, some might be convinced the patient is fine and will improve in a “few minutes” because of the 100-percent oxygen saturation. However, by starting capnography, you might see a PETCO2 of 63 mm Hg. All the oxygen in the world isn’t going to matter if the patient’s CO2 levels are not reduced. Assisted ventilations with a BVM device are indicated, and cardiac irritability (and possibly multiple arrhythmias) should be anticipated. A patient’s CO2 levels can fall dramatically after only a few minutes of BVM-assisted ventilation, and the condition can be markedly improved.

Pulse oximetry is a great tool, but it gives us only half the picture. Pulse oximetry tells us the saturation of oxygen in the hemoglobin, but it doesn’t tell us anything about carbon dioxide or ventilatory effectiveness. High carbon dioxide levels in the bloodstream (hypercapnia) (Figure 6) can cause cardiovascular depression, cardiac arrhythmias (changes in pH and potassium shifts), increased cardiac demand, increased intracranial pressure, pulmonary vasoconstriction, and peripheral vasodilatation.14 PaCO2 levels greater than 75 mm Hg will eventually cause death.15 Pulse oximetry and capnography together can help us assess a patient’s ventilatory effectiveness, whether that ventilatory effort is spontaneous or artificial. We must ensure not only that a patient is receiving enough oxygen but also that the patient is getting rid of the carbon dioxide waste generated by cellular consumption of the oxygen.


Figure 6. Severely Damaged Alveoli

 

ASTHMA, BRONCHOSPASM, AND COPD

The capnography waveform shape resulting from asthma, bronchospasm, and COPD, fortunately, is one of the most characteristic and easy-to-spot capnography waveforms: It looks like a shark’s fin (Figure 7). A normal capnograph should rise quickly at the beginning of exhalation (nearly straight up), plateau (flat with a slight upward incline), and then rapidly fall off at the end of exhalation (straight down). When a patient experiences some type of partial airway obstruction or restriction, as in the case of asthma, bronchospasm, and COPD, the exhalation must be “forced” out under pressure. That “forcing” phenomenon causes the concentration of CO2 to slowly but continuously rise during the exhalation phase (the curved front of the shark’s fin) until the end of exhalation, when the CO2 level falls suddenly (the straight down back of the shark’s fin).


The visual depiction of bronchospasm in capnography provides EMS with a valuable and objective tool for assessing the seriousness of the patient’s condition. A bronchospastic capnograph obtained prior to treatment becomes an objective baseline that may be used to determine not only treatment effectiveness but also whether additional treatment is needed prior to arrival at a hospital or if the condition has been resolved enough to defer further treatment. Perhaps most importantly, continuous capnography monitoring can alert a paramedic to a patient’s worsening condition that appeared stable just a few moments ago.

CARDIAC OUTPUT AND CAPNOGRAPHY

Nothing in the body happens without being interrelated to something else, and the removal of carbon dioxide is no exception. Though the process of CO2 gas exchange is passive, it relies on the heart’s pumping action to move blood through the body and lungs so gas exchange can occur. If cardiac output falls, there is a decrease in pulmonary blood flow, gas exchange in the lungs is diminished, less CO2 makes it into the lungs, and a lower PETCO2 is observed via capnography (Figure 8). Conversely if cardiac output increases, pulmonary blood flow increases, gas exchange in the lungs increases, more CO2 makes it into the lungs, and a higher P ET CO2 is observed via capnography. (5) 16,17


A study of the partial pressure of end tidal carbon dioxide (PETCO2) and pulmonary blood flow during cardiac bypass quantified the correlation between PETCO2 and cardiac output. Normal cardiac output (the volume of blood pumped in a minute) in a resting adult is approximately 5 L/min.18 The study demonstrated that when PETCO2 was greater than 34 mm Hg, pulmonary blood flow was more than 5 L/min. When a PETCO2 greater than 30 mm Hg was observed, the cardiac output was more than 4 L/min.19 The capnography rhythm associated with decreasing cardiac output has the characteristic appearance of a row of stairsteps going down (Figure 9), whereas increasing cardiac output appears as stair steps going up. It is important to note two things. First, to correlate PETCO2 to cardiac output, the respiratory rate and volume (minute volume) must be relatively constant; otherwise it is impossible to know whether the PETCO2 changes are from cardiac output changes or respiratory rate and volume changes. Second, other conditions (e.g., pulmonary embolism, hypothermia, and other conditions) mimic the same stair-step appearance, so it should not be assumed the root cause is some type of heart failure or myocardial infarction. Nevertheless, it is critical for the patient.


Figure 9. Characteristic “stair step” of falling cardiac output (trend mode displayed). Speed of decrease changes angle of decline.

 

AIRWAY CONFIRMATION

Of course, no discussion of capnography would be complete without addressing airway confirmation. The use of capnometry to confirm proper endotracheal tube placement is the standard of care.20 Two EMS-specific studies of unrecognized misplaced endotracheal tubes by paramedics have demonstrated the severity of the issue. While there were some questions surrounding the earlier study, the second study, conducted in 2005, was solid and demonstrated an inescapable conclusion: In the absence of capnography, paramedics fail to recognize misplaced endotracheal tubes. There has never been a more compelling argument for a piece of EMS equipment to be purchased and used. The rate of unrecognized misplaced intubations without the use of capnography was 23 percent! There were no unrecognized misplaced intubations when capnography was used.21,22

The bottom line is quite simple. When performing any type of airway management, use capnography (in conjunction with pulse oximetry) to assess and monitor ventilatory effectiveness. The PETCO2 of a patient after airway management should be near normal (35-38 mm Hg) with a normal-appearing capnographic waveform. If PETCO2 is significantly below normal, or if there is an abnormal waveform, something is wrong. Determine the underlying cause. Even in cardiac arrest, near normal (or slightly low) capnography levels can be observed when ventilation and CPR chest compressions are adequate. Figures 10-15 exhibit several abnormal capnograms that indicate a misplaced endotracheal intubation. If the capnometry reading is zero, something is wrong. Find it. Fix it.


null


null


Figure 12. Esophageal intubation. Alveolar gas can be forced into the stomach by BVM ventilation, causing some initial capnograms that will eventually go to zero.

null


Figure 13. Esophageal intubation. Carbonated beverages in the stomach can produce significant CO2 in expired gases during six breaths. Shape of the capnograms indicates esophageal intubation.

null


null


• • •

Capnography is a versatile tool that provides EMS with more information about a patient’s condition that can aid treatment decisionmaking. In addition to detecting misplaced endotracheal tubes, capnography can help paramedics and EMTs recognize asthma, bronchospasm, COPD, emphysema, decreasing cardiac output, and pulmonary embolism and objectively assess ventilatory effectiveness. Learning to interpret capnography is similar to learning how to read EKGs; proficiency cannot be obtained with an hour’s training. Although this article addresses some of the major areas of capnography, it is by no means a complete study. Additionally, this article does not address capnography in pregnancy or pediatrics. There is much more. Paramedics and EMTs are encouraged to continue reading and learning about capnography and its uses. Two Web sites that can enhance your knowledge on capnography are http://ww.capnography.com and http://emscapnography.blogspot.com, or test your knowledge by taking the “Capnography Challenge” at http://training.futurefd.com.

Endnotes

1. O’Flaherty, David. Capnography. (London: BMJ Publishing Group, 1994) 1.

2. Kodali, MD., Bhavani Shankar. “Definitions,” Capnography Edition 4 (2006): 1. Nov. 29, 2006 < http://www.capnography.com/Definitions/DefinitionsM.htm>.

3. The chemistry of the respiratory cycle and the brain is more complicated than this explanation. CO2 chemically affects the pH in cerebrospinal fluid, which in turn is sensed by chemoreceptor sites and causes the brain to react accordingly to stimulate or diminish respiratory effort.

4. Wikipedia. “Mitocondrion.” Wikipedia (2006): 1. Nov. 29, 2006 <http://en.wikipedia.org/wiki/Mitochondria >.

5 Kodali, MD, Bhavani Shankar. “(a-ET)CO2 difference and Alveolar dead space.” Capnography Edition 4 (2006): 1. Nov. 29, 2006 < http://www.capnography.com/Physiology/a-epd.htm>.

6. Kalenda Z. “Mastering infrared Capnography.” The Netherlands:Kerckebosch-Zeist, 1989.

7. Fletcher R. “The single breath test for carbon dioxide.” Thesis, Lund, 1980.

8. Bhavani-Shankar, AY Kumar, H Moseley, RA Hallsworth, “Terminology and the current limitations of time capnography,” J Clin Monit 1995;11:175-82.

9. Nunn JF, DW Hill. “Respiratory dead space and arterial to end-tidal CO2 tension difference in anesthetized man,” J Appl Physiol 1960;15:383-9.

10. Fletcher R, B Jonson, “Dead space and the single breath test carbon dioxide during anesthesia and artificial ventilation,” Br J Anaesth 1984;56:109-19.

11. Bhavani-Shankar, H Moseley, Y Kumar, V Vemula, “Arterial to end-tidal carbon dioxide tension difference during Caesarean section anesthesia,” Anesthesia 1986;41:698-702.

12. Fletcher R, B Jonson, G Cumming, J Brew, “The concept of dead space with special reference to the single breath test for carbon dioxide,” Br J Anaesth 1981:53:77-88.

13. Bhavani-Shankar, H Mosely, AY Kumar, Y Delph, “Capnometry and anesthesia,“ Review article, Can J Anaesth 617-32.

14. Wikipedia. “Hypercapnia.” Wikipedia (2006): 1. Nov. 30, 2006. <http://en.wikipedia.org/wiki/Hypercapnia>.

15. Leigh MD, JC Jones, HL Motley, “The expired carbon dioxide as a continuous guide of the pulmonary and circulatory systems during anesthesia and surgery,” J Thoracic Cardiovascular Surg 1961;41:597-610.

16. Askrog V, “Changes in (a-A)CO2 difference and pulmonary artery pressure in anesthetized man,” J Appl Physiol 1966; 21:1299-1305.

17. Wikipedia. “Cardiac Output.” Wikipedia (2006): 1. Nov. 30, 2006 <http://en.wikipedia.org/wiki/Cardiac_output>.

18. Maslow A, G Stearns, A Bert, W Feng W, D Price, C Schwartz, S Mackinnon, F Rotenberg, R Hopkins, G Cooper, A Singh, SH Loring, “Monitoring end-tidal carbon dioxide during weaning from cardiopulmonary bypass in patients without significant lung disease,” Anesth Analg 2001;92:306-13.

19. Kodali, MD., Bhavani-Shankar, “ASA Standards of Care – Capnography.” Capnography Edition 4 (2006): 1. Dec. 2, 2006 < http://www.capnography.com/ASA/ASA.htm>.

20. Silvestri S, GA Ralls, B Krauss, J Thundiyil, SG Rothrock, A Senn, E Carter, J Falk, “The effectiveness of out-of-hospital use of continuous end-tidal carbon dioxide monitoring on the rate of unrecognized misplaced intubation within a regional emergency medical services system,” Ann Emerg Med. 2005 May; 45(5):497-503.

21. Katz SH, JL Falk, “Misplaced endotracheal tubes by paramedics in an urban emergency medical services system,” Ann Emerg Med. 2001 January.

22. Wikipedia. “Cardiac Output.” Wikipedia (2006): 1. Dec. 2, 2006 <http://en.wikipedia;org/wiki/Hypercapnia>.

William M. Godfrey, MBA, EMT-P, is a 23-year veteran of the fire service and chief consultant for FutureFD.com, a fire service and homeland security consulting firm. He is planning manager for US&R FL-TF4 and formerly was deputy chief of training and information technology for Orange County (FL) Fire Rescue. He is a paramedic and a fire instructor III. He has an MBA degree with additional degrees in public administration and EMS management. He specializes in simulation training and incident command.

Glossary

BVM. A bag valve mask airway management device.

Capnogram. CO2 waveforms, which can be of two types: FCO2 can be plotted against expired volume (SBTCO2 curve /volume capnogram/CO2 expirogram) or against time (time capnogram) during a respiratory cycle. (2)

Capnography. A graphic display of instantaneous CO2 concentration (FCO2) vs. time or expired volume during a respiratory cycle (CO2 waveform or capnogram). (2)

Capnometry. The measurement and display of carbon dioxide (CO2) on a digital or analogue monitor. Maximum inspiratory and expiratory CO2 concentrations during a respiratory cycle are displayed. (2)

Cardiac output. The volume of blood being pumped by the heart, in particular a ventricle, in a minute. It is equal to the heart rate multiplied by the stroke volume. (18)

CO2. Carbon dioxide.

Hypercapnia. A condition in which there is too much carbon dioxide (CO2) in the blood. 22

PaCO2. The partial pressure of CO2 in arterial blood. (2)

PETCO2. The partial pressure of CO2 at the end of expiration (end tidal). (2)

Trend Mode. A capnogram with a slower plot speed to display capnography over a longer time (e.g., 30 minutes). This longer-period view allows recognition of rhythms and longer-term patterns in a capnograph. The trend plot speed can vary among devices.

Capnography: A Versatile Life-Saving Tool

If a tool could tell us when we’d given enough albuterol to resolve a little eight-year-old girl’s asthmatic bronchospasm or that Mr. Smith’s cardiac output is steadily declining and he’s approaching cardiac arrest, I suspect we would all use it. Many EMS systems actually have this tool on their vehicles, but they may not have provided the necessary in-depth training to their paramedics and EMTs so they can fully use this incredibly versatile, life-saving piece of equipment. The tool is capnography, and its use is not limited to confirmation of a correctly placed endotracheal tube.

Capnography is simply an EKG for exhaled carbon dioxide (CO2); it plots the instantaneous concentration of CO2 against time during the patient’s respiratory cycle1,2 (Figure 1). Like an EKG, the resulting waveform produces unique shapes and rhythms that are meaningful in patient assessment and treatment. We can observe ST elevation by evaluating the shape of a waveform in a 12-lead EKG and suspect a heart attack, and it is the shape of the capnography waveform that alerts us that the eight-year-old girl needs a second nebulizer treatment because she is still in bronchospasm. And like the perilous EKG rhythm of a third-degree heart block, the rhythm of a capnogram-sometimes called trending-can signal decreasing cardiac output and impending arrest for Mr. Smith.


Figure 1. Normal Adult Capnograph
Illustrations by author.

 

CARBON DIOXIDE AND “NORMAL”

Understanding the mechanics of breathing and carbon dioxide is vital to using capnography fully. The brain’s respiratory center in the medulla oblongata controls breathing rate and volume. High CO2 concentrations cause the brain to increase respiratory effort; lower CO2 concentrations cause the brain to reduce respiratory effort.3 Through the controlling of breathing rate and volume, the brain attempts to narrowly maintain the concentration of CO2 in the blood at 40 mm Hg. (1.7) Maintaining the partial pressure of carbon dioxide (PaCO2) at 40 in the blood stream enables the removal of CO2 from the body, which is a passive process.


Figure 3. Decreasing PETCO2
From Hyperventilation

CO2 is a byproduct of energy production by mitochondria oxidizing glucose in a cell.4 This CO2 waste is removed from the body passively by moving it from the cell into the blood, from the blood into the alveoli, and then out of the body through breathing. This passive process occurs by getting the CO2 to move on its own from an area of high concentration to areas of lower concentration, resembling a river draining downstream. This process is called “diffusion.” The concentration of CO2 inside a cell is normally about 46 mm Hg. Since the cell membrane is permeable to carbon dioxide, CO2 (at 46 mm Hg inside the cell) diffuses across the membrane into the less concentrated bloodstream (40 mm Hg). This exact same process repeats itself in the lungs, where the concentration of carbon dioxide in the blood is higher than inside the alveolar air space, so CO2 moves out of the blood and into the lungs, where it is ultimately expelled from the body. (1, 10-12)


Figure 4. Decreasing PETCO2
From Hypoventilation

As you exhale, the first CO2 expelled comes from the passageways in the lungs (bronchi and bronchioles). The alveoli, which are the last to empty, are closest to the bloodstream and thus will have the highest concentration of expired CO2. As a result, the level of measured CO2 will steadily increase during the exhalation with the highest level of CO2 at the end of the breath. This is referred to as the “end tidal CO2 level” (PETCO2).5 A direct correlation between the partial pressure of carbon dioxide (PaCO2) actually in the blood (e.g., blood gas analysis) and the partial pressure of PETCO2 has been established: PETCO2 is 2-5 mm Hg lower than the actual blood PaCO2 in adults.6-13 (1,19)


Figure 5. Apnea

One of the most frequently asked questions about capnography is, “What are the normal values?” In a healthy adult, the PaCO2 is narrowly maintained near 40 mm Hg. Since PETCO2 is typically 2-5 mm Hg lower than PaCO2, a healthy adult “normal” capnometry (number) reading is 35-38 mm Hg of CO2 (Figure 2). While a capnometry reading of 34 or 39 mm Hg should not be a cause for concern, a reading of 28 or 52 mm Hg should be considered alarming until the underlying cause and its respective implications are identified and treated as appropriate.


Figure 2. Normal Capnogram

 

PULSE OXIMETRY VS. CAPNOGRAPHY

One of the most global misconceptions in EMS may be the notion that if a patient is receiving 100 percent oxygen and has a pulse oximetry saturation of 100 percent, he is “just fine.” This could not be further from the truth. Imagine a Chronic Obstructive Pulmonary Disease (COPD) patient in distress on 100-percent oxygen by nonrebreather mask with a pulse oximetry saturation that rises to 100 percent. Despite the patient’s still being in distress, some might be convinced the patient is fine and will improve in a “few minutes” because of the 100-percent oxygen saturation. However, by starting capnography, you might see a PETCO2 of 63 mm Hg. All the oxygen in the world isn’t going to matter if the patient’s CO2 levels are not reduced. Assisted ventilations with a BVM device are indicated, and cardiac irritability (and possibly multiple arrhythmias) should be anticipated. A patient’s CO2 levels can fall dramatically after only a few minutes of BVM-assisted ventilation, and the condition can be markedly improved.

Pulse oximetry is a great tool, but it gives us only half the picture. Pulse oximetry tells us the saturation of oxygen in the hemoglobin, but it doesn’t tell us anything about carbon dioxide or ventilatory effectiveness. High carbon dioxide levels in the bloodstream (hypercapnia) (Figure 6) can cause cardiovascular depression, cardiac arrhythmias (changes in pH and potassium shifts), increased cardiac demand, increased intracranial pressure, pulmonary vasoconstriction, and peripheral vasodilatation.14 PaCO2 levels greater than 75 mm Hg will eventually cause death.15 Pulse oximetry and capnography together can help us assess a patient’s ventilatory effectiveness, whether that ventilatory effort is spontaneous or artificial. We must ensure not only that a patient is receiving enough oxygen but also that the patient is getting rid of the carbon dioxide waste generated by cellular consumption of the oxygen.


Figure 6. Severely Damaged Alveoli

 

ASTHMA, BRONCHOSPASM, AND COPD

The capnography waveform shape resulting from asthma, bronchospasm, and COPD, fortunately, is one of the most characteristic and easy-to-spot capnography waveforms: It looks like a shark’s fin (Figure 7). A normal capnograph should rise quickly at the beginning of exhalation (nearly straight up), plateau (flat with a slight upward incline), and then rapidly fall off at the end of exhalation (straight down). When a patient experiences some type of partial airway obstruction or restriction, as in the case of asthma, bronchospasm, and COPD, the exhalation must be “forced” out under pressure. That “forcing” phenomenon causes the concentration of CO2 to slowly but continuously rise during the exhalation phase (the curved front of the shark’s fin) until the end of exhalation, when the CO2 level falls suddenly (the straight down back of the shark’s fin).


The visual depiction of bronchospasm in capnography provides EMS with a valuable and objective tool for assessing the seriousness of the patient’s condition. A bronchospastic capnograph obtained prior to treatment becomes an objective baseline that may be used to determine not only treatment effectiveness but also whether additional treatment is needed prior to arrival at a hospital or if the condition has been resolved enough to defer further treatment. Perhaps most importantly, continuous capnography monitoring can alert a paramedic to a patient’s worsening condition that appeared stable just a few moments ago.

CARDIAC OUTPUT AND CAPNOGRAPHY

Nothing in the body happens without being interrelated to something else, and the removal of carbon dioxide is no exception. Though the process of CO2 gas exchange is passive, it relies on the heart’s pumping action to move blood through the body and lungs so gas exchange can occur. If cardiac output falls, there is a decrease in pulmonary blood flow, gas exchange in the lungs is diminished, less CO2 makes it into the lungs, and a lower PETCO2 is observed via capnography (Figure 8). Conversely if cardiac output increases, pulmonary blood flow increases, gas exchange in the lungs increases, more CO2 makes it into the lungs, and a higher P ET CO2 is observed via capnography. (5) 16,17


A study of the partial pressure of end tidal carbon dioxide (PETCO2) and pulmonary blood flow during cardiac bypass quantified the correlation between PETCO2 and cardiac output. Normal cardiac output (the volume of blood pumped in a minute) in a resting adult is approximately 5 L/min.18 The study demonstrated that when PETCO2 was greater than 34 mm Hg, pulmonary blood flow was more than 5 L/min. When a PETCO2 greater than 30 mm Hg was observed, the cardiac output was more than 4 L/min.19 The capnography rhythm associated with decreasing cardiac output has the characteristic appearance of a row of stairsteps going down (Figure 9), whereas increasing cardiac output appears as stair steps going up. It is important to note two things. First, to correlate PETCO2 to cardiac output, the respiratory rate and volume (minute volume) must be relatively constant; otherwise it is impossible to know whether the PETCO2 changes are from cardiac output changes or respiratory rate and volume changes. Second, other conditions (e.g., pulmonary embolism, hypothermia, and other conditions) mimic the same stair-step appearance, so it should not be assumed the root cause is some type of heart failure or myocardial infarction. Nevertheless, it is critical for the patient.


Figure 9. Characteristic “stair step” of falling cardiac output (trend mode displayed). Speed of decrease changes angle of decline.

 

AIRWAY CONFIRMATION

Of course, no discussion of capnography would be complete without addressing airway confirmation. The use of capnometry to confirm proper endotracheal tube placement is the standard of care.20 Two EMS-specific studies of unrecognized misplaced endotracheal tubes by paramedics have demonstrated the severity of the issue. While there were some questions surrounding the earlier study, the second study, conducted in 2005, was solid and demonstrated an inescapable conclusion: In the absence of capnography, paramedics fail to recognize misplaced endotracheal tubes. There has never been a more compelling argument for a piece of EMS equipment to be purchased and used. The rate of unrecognized misplaced intubations without the use of capnography was 23 percent! There were no unrecognized misplaced intubations when capnography was used.21,22

The bottom line is quite simple. When performing any type of airway management, use capnography (in conjunction with pulse oximetry) to assess and monitor ventilatory effectiveness. The PETCO2 of a patient after airway management should be near normal (35-38 mm Hg) with a normal-appearing capnographic waveform. If PETCO2 is significantly below normal, or if there is an abnormal waveform, something is wrong. Determine the underlying cause. Even in cardiac arrest, near normal (or slightly low) capnography levels can be observed when ventilation and CPR chest compressions are adequate. Figures 10-15 exhibit several abnormal capnograms that indicate a misplaced endotracheal intubation. If the capnometry reading is zero, something is wrong. Find it. Fix it.


null


null


Figure 12. Esophageal intubation. Alveolar gas can be forced into the stomach by BVM ventilation, causing some initial capnograms that will eventually go to zero.

null


Figure 13. Esophageal intubation. Carbonated beverages in the stomach can produce significant CO2 in expired gases during six breaths. Shape of the capnograms indicates esophageal intubation.

null


null


• • •

Capnography is a versatile tool that provides EMS with more information about a patient’s condition that can aid treatment decisionmaking. In addition to detecting misplaced endotracheal tubes, capnography can help paramedics and EMTs recognize asthma, bronchospasm, COPD, emphysema, decreasing cardiac output, and pulmonary embolism and objectively assess ventilatory effectiveness. Learning to interpret capnography is similar to learning how to read EKGs; proficiency cannot be obtained with an hour’s training. Although this article addresses some of the major areas of capnography, it is by no means a complete study. Additionally, this article does not address capnography in pregnancy or pediatrics. There is much more. Paramedics and EMTs are encouraged to continue reading and learning about capnography and its uses. Two Web sites that can enhance your knowledge on capnography are http://ww.capnography.com and http://emscapnography.blogspot.com, or test your knowledge by taking the “Capnography Challenge” at http://training.futurefd.com.

Endnotes

1. O’Flaherty, David. Capnography. (London: BMJ Publishing Group, 1994) 1.

2. Kodali, MD., Bhavani Shankar. “Definitions,” Capnography Edition 4 (2006): 1. Nov. 29, 2006 < http://www.capnography.com/Definitions/DefinitionsM.htm>.

3. The chemistry of the respiratory cycle and the brain is more complicated than this explanation. CO2 chemically affects the pH in cerebrospinal fluid, which in turn is sensed by chemoreceptor sites and causes the brain to react accordingly to stimulate or diminish respiratory effort.

4. Wikipedia. “Mitocondrion.” Wikipedia (2006): 1. Nov. 29, 2006 <http://en.wikipedia.org/wiki/Mitochondria >.

5 Kodali, MD, Bhavani Shankar. “(a-ET)CO2 difference and Alveolar dead space.” Capnography Edition 4 (2006): 1. Nov. 29, 2006 < http://www.capnography.com/Physiology/a-epd.htm>.

6. Kalenda Z. “Mastering infrared Capnography.” The Netherlands:Kerckebosch-Zeist, 1989.

7. Fletcher R. “The single breath test for carbon dioxide.” Thesis, Lund, 1980.

8. Bhavani-Shankar, AY Kumar, H Moseley, RA Hallsworth, “Terminology and the current limitations of time capnography,” J Clin Monit 1995;11:175-82.

9. Nunn JF, DW Hill. “Respiratory dead space and arterial to end-tidal CO2 tension difference in anesthetized man,” J Appl Physiol 1960;15:383-9.

10. Fletcher R, B Jonson, “Dead space and the single breath test carbon dioxide during anesthesia and artificial ventilation,” Br J Anaesth 1984;56:109-19.

11. Bhavani-Shankar, H Moseley, Y Kumar, V Vemula, “Arterial to end-tidal carbon dioxide tension difference during Caesarean section anesthesia,” Anesthesia 1986;41:698-702.

12. Fletcher R, B Jonson, G Cumming, J Brew, “The concept of dead space with special reference to the single breath test for carbon dioxide,” Br J Anaesth 1981:53:77-88.

13. Bhavani-Shankar, H Mosely, AY Kumar, Y Delph, “Capnometry and anesthesia,“ Review article, Can J Anaesth 617-32.

14. Wikipedia. “Hypercapnia.” Wikipedia (2006): 1. Nov. 30, 2006. <http://en.wikipedia.org/wiki/Hypercapnia>.

15. Leigh MD, JC Jones, HL Motley, “The expired carbon dioxide as a continuous guide of the pulmonary and circulatory systems during anesthesia and surgery,” J Thoracic Cardiovascular Surg 1961;41:597-610.

16. Askrog V, “Changes in (a-A)CO2 difference and pulmonary artery pressure in anesthetized man,” J Appl Physiol 1966; 21:1299-1305.

17. Wikipedia. “Cardiac Output.” Wikipedia (2006): 1. Nov. 30, 2006 <http://en.wikipedia.org/wiki/Cardiac_output>.

18. Maslow A, G Stearns, A Bert, W Feng W, D Price, C Schwartz, S Mackinnon, F Rotenberg, R Hopkins, G Cooper, A Singh, SH Loring, “Monitoring end-tidal carbon dioxide during weaning from cardiopulmonary bypass in patients without significant lung disease,” Anesth Analg 2001;92:306-13.

19. Kodali, MD., Bhavani-Shankar, “ASA Standards of Care – Capnography.” Capnography Edition 4 (2006): 1. Dec. 2, 2006 < http://www.capnography.com/ASA/ASA.htm>.

20. Silvestri S, GA Ralls, B Krauss, J Thundiyil, SG Rothrock, A Senn, E Carter, J Falk, “The effectiveness of out-of-hospital use of continuous end-tidal carbon dioxide monitoring on the rate of unrecognized misplaced intubation within a regional emergency medical services system,” Ann Emerg Med. 2005 May; 45(5):497-503.

21. Katz SH, JL Falk, “Misplaced endotracheal tubes by paramedics in an urban emergency medical services system,” Ann Emerg Med. 2001 January.

22. Wikipedia. “Cardiac Output.” Wikipedia (2006): 1. Dec. 2, 2006 <http://en.wikipedia;org/wiki/Hypercapnia>.

William M. Godfrey, MBA, EMT-P, is a 23-year veteran of the fire service and chief consultant for FutureFD.com, a fire service and homeland security consulting firm. He is planning manager for US&R FL-TF4 and formerly was deputy chief of training and information technology for Orange County (FL) Fire Rescue. He is a paramedic and a fire instructor III. He has an MBA degree with additional degrees in public administration and EMS management. He specializes in simulation training and incident command.

Glossary

BVM. A bag valve mask airway management device.

Capnogram. CO2 waveforms, which can be of two types: FCO2 can be plotted against expired volume (SBTCO2 curve /volume capnogram/CO2 expirogram) or against time (time capnogram) during a respiratory cycle. (2)

Capnography. A graphic display of instantaneous CO2 concentration (FCO2) vs. time or expired volume during a respiratory cycle (CO2 waveform or capnogram). (2)

Capnometry. The measurement and display of carbon dioxide (CO2) on a digital or analogue monitor. Maximum inspiratory and expiratory CO2 concentrations during a respiratory cycle are displayed. (2)

Cardiac output. The volume of blood being pumped by the heart, in particular a ventricle, in a minute. It is equal to the heart rate multiplied by the stroke volume. (18)

CO2. Carbon dioxide.

Hypercapnia. A condition in which there is too much carbon dioxide (CO2) in the blood. 22

PaCO2. The partial pressure of CO2 in arterial blood. (2)

PETCO2. The partial pressure of CO2 at the end of expiration (end tidal). (2)

Trend Mode. A capnogram with a slower plot speed to display capnography over a longer time (e.g., 30 minutes). This longer-period view allows recognition of rhythms and longer-term patterns in a capnograph. The trend plot speed can vary among devices.