Carbon dioxide (CO2) is a waste gas, so why do we care about it as long as we and our patients can get it out of the body? The reality is that blood levels of carbon dioxide are as critically important as blood oxygen levels. In fact, oxygen loading onto hemoglobin and transport to the tissues is highly dependent on the tight regulation of CO2. Furthermore, CO2 can act as a molecular signal affecting both nervous and smooth muscle tissues.
Origins and Mechanics
Long ago, Greek philosophers believed we had tiny internal combustion engines inside our bodies that produced “smoke” or capnos. It turns out the Greeks were essentially correct. Our internal combustion engines are really mitochondria, which are fueled by the sugar, fat and protein in our diet. After processing, the sugar enters the mitochondria, where it is “combusted” and carbon dioxide is “exhausted.” Once CO2 is transported to the lungs via the circulatory system, it can be exhaled with the alveolar air.
Exhaled air rich with CO2 can be captured continuously through devices intended to be used on either the intubated or non-intubated patient. The respiratory rate can be very accurately estimated and reported by measuring the tides between CO2 peaks. As captured air enters the capnography device, it passes between a light source and a detector, which measures how much light is being shone on it. As the concentration of CO2 increases, it absorbs more light, making less on the detector plate. This increased light absorption is a direct result of the CO2 and directly indicates how much CO2 is present. The monitor presents this information to the capnographer as both a number and a waveform.
Ventilation vs. Oxygenation
Ventilation and oxygenation are obviously interrelated, yet they are two distinct management issues. Oxygenation involves loading hemoglobin with oxygen for delivery to the tissues, while ventilation addresses clearing CO2 from the blood. Take, for example, the moderately sick asthma patient demonstrating “shark finning” with an elevated ETCO2 but 100% oxygen saturation. This patient is oxygenating well, but not ventilating well.
Capnography as a Clinical Tool
There are three physiological processes critical for capnography use and interpretation. They are metabolism, circulation and ventilation.
1. Metabolism: Your patient must be metabolizing. In other words, your patient must at least be alive. It is important to note, however, that several hours after cardiac arrest, some residual metabolism (liver, skeletal muscles, skin etc.) will continue to produce CO2. Some hypermetabolic states can also be identified using capnography.
2. Circulation: Blood must be moving in order to deliver CO2 from the tissues to the alveoli. Movement requires blood, a heartbeat and blood pressure (preload+afterload).
3. Ventilation: Air must move in and out of the alveoli and across the detector in order for the capnography monitor to measure CO2.
Continuous waveform capnography is recommended for EMS for verification of endotracheal tube (ETT) placement.1 The American Heart Association's 2010 ACLS guidelines have elevated the role of capnography to recommending continuous waveform capnographical monitoring during resuscitation.
Capnography is also capable of providing valuable cardiopulmonary information to assist paramedics in caring for non-intubated patients. Capnography is a powerful tool providing continuous real time objective data to quantify and qualify ventilatory status. It is the only technology able to display respiratory rate based upon the partial pressure of exhaled CO2 while providing the unique pattern recognition of CO2. Capnography can also quantify patient ventilation in terms of transporting CO2 from the pulmonary circulation across the alveoli for exhalation.
Capnography provides a graphic picture of the patient’s ventilatory status, gives early warning of changes in the patient's cardiopulmonary status, supplies indisputable documentation of the patient’s ventilatory status and detects the presence of pulmonary pathology. Abnormal capnography values can be traced to changes in ventilation, perfusion or metabolism.
Intubated Airway Management
Capnography provides an objective and reliable method to confirm endotracheal intubation. The presence of a waveform can easily demonstrate proper placement, even during CPR, which has been well documented over the past few years.1 Capnography can also be useful in detecting a change in position of the endotracheal tube. Given some of the untoward and noisy environments where cardiac arrest occurs, confirming ETT placement by lung sounds alone can be problematic and sometimes even deceiving, especially in smaller patients. A 2005 study compared prehospital intubations either with or without continuous capnography to confirm tube placement. The group using capnography achieved correct tube placement in 100% of their patients. The group practicing without the benefit of capnography had a misplaced tube (unrecognized esophageal or supraglottic) in 23% of their patients. An objective tool like capnography will allow paramedics to not only ensure the ETT is in the right place, but that ventilation support is adequate.
Alternative Airway Devices
Recent studies have dulled the significance of endotracheal intubation and many prehospital providers are relying more often on alternative methods of securing the airway. Capnography is just as easily applied to alternative airways like the Combitube, King airway or the laryngeal mask airway (LMA). As with an endotracheal tube, with alternative airways it is imperative to ensure the device is providing sufficient protection of the airway to allow effective rescuer ventilation.
The capnography waveform assists in determining proper ventilation with any device that securely attaches to a bag-valve mask. No matter which device is in use, capnography can provide immediate indication of the loss of proper position or function. As with endotracheal intubation, when using alternative airways it is critical to continuously monitor the airway and assess ventilation status. Waveform capnography is able to support those clinical assessment needs and be used to adjust ventilation support.
Effective Chest Compressions
Capnography provides valuable information in the assessment of resuscitative efforts. In the cardiac arrest patient, ETCO2 correlates with cardiac output. Systemic and pulmonary perfusion during cardiac compressions transports CO2 to the alveolar space. Therefore, as long as the cardiac arrest victim has residual metabolic production of CO2, ETCO2 serves as a measure of CPR effectiveness. Studies as early as the 1980s discuss how ETCO2 can be used as a noninvasive measurement of cardiac output during cardiac arrest. During CPR, ETCO2 production by cellular metabolism remains constant; therefore, ETCO2 can assist in showing the effectiveness of chest compressions. The American Heart Association's Guidelines call for quality compressions ("push hard, push fast, push deep") and direct rescuers to switch places every two minutes to maintain effective CPR. By analyzing the ETCO2 waveform; a clinician can detect rescuer fatigue before the rescuer is aware of tiring.
Paramedics can set the monitor up so the compressors can view the ETCO2 readings as well as the ECG waveform generated by their compressions. It is important to encourage prehospital personnel to perform quality CPR to keep the ETCO2 number as high as possible.
Return of Spontaneous Circulation (ROSC)
A rapid rise in ETCO2 during chest compressions can be the first indicator of return of spontaneous circulation (ROSC), possibly even before a pulse is detectable. This rapid rise is likely due to the recruitment of circulation in tissues that were not being circulated due to the inefficiency of chest compressions (approximately 25%-30%), as compared to intrinsic cardiac contraction. A recent study found ETCO2 increased on average 13.5 mmHg with sudden ROSC before returning to a normal range.If paramedics encounter a sudden increase in ETCO2 during resuscitation, accompanied by a rhythm appearing capable of supporting perfusion, CPR should be briefly interrupted for a pulse check. If pulses are not yet present, CPR should be aggressively resumed, as ROSC may be near. It is important to note, however, that administration of sodium bicarbonate could also produce a “bump” in the ETCO2 as a result of bicarbonate ion conversion to CO2 during correction of acidosis.
While ETCO2 can be used to gauge the effectiveness of resuscitation, it can also be used as a determining factor in the decision to cease resuscitative efforts. In 1997, a study in the New England Journal of Medicine established that an end-tidal carbon dioxide level of 10 mmHg or less measured 20 minutes after initiation of advanced cardiac life support accurately predicts death in patients with cardiac arrest associated with electrical activity but no pulse. Patients with an ETCO2 of less than 10 mmHg at the 20 minute interval had 100% mortality. The study suggests that cardiopulmonary resuscitation may reasonably be terminated in such patients. Caution must be taken, however, that rescuers are not hyperventilating the patient if capnography is used as a determinant for termination of efforts.
With the advent of induced hypothermia in the treatment of cardiac arrest patients, new research is now needed to set guidelines for the use of ETCO2 in determining when to cease resuscitation efforts. In the induced hypothermia patient, the metabolic rate will be lowered, thus diminishing the production of cellular CO2. A guideline for CPR termination based on an ETCO2 of less than 10 mmHg for 20 minutes may not be adequately conservative for those patients receiving hypothermia treatment during CPR.
Capnography can help paramedics optimize ventilation in intubated patients with suspected increased intracranial pressure (ICP). Avoiding hypo- and hyperventilation in these patients is absolutely critical and difficult. Increased ICP may be caused by a head injury, intracerebral hemorrhage, a tumor or mass, or infection. Hyperventilation of patients with increased ICP has been associated with increased mortality. Hyperventilation decreases intracranial pressure by decreasing intracranial blood flow, thereby increasing the risk of cerebral ischemia. In a recent study of head-injured patients, those with ETCO2 monitoring had a lower incidence of hyperventilation. While a target ETCO2 recommendation is outside the scope of this article and should be protocol driven, ventilation should be tightly controlled in this patient population.
Capnography is equally relevant in nonintubated patients. Capnography can be used to differentiate between the varying causes of respiratory distress often seen in the field, such as asthma, COPD exacerbation and CHF. It can provide paramedics with early warning signs of hypoventilation, apnea, airway obstruction and hypercarbia before compensatory changes are seen in heart rate and/or blood pressure.
Ventilation: Asthma, CHF and COPD
Patients with acute obstructive disease processes of the lung (asthma, COPD, bronchitis), all of whom may experience bronchospasm in the lungs, may be identified by a unique characteristic change seen in the ETCO2 waveform. Bronchospasm will produce a “shark fin”-appearing capnography waveform as a result of regional obstruction that causes a turbulent mixing of dead space air with alveolar air. This mixing softens the rapid rise in CO2 concentration of exhaled air. It is important to note that the shark fin appearance of the capnograph has a direct physiological cause and is characteristic of bronchospasm. In other words, shark-finning cannot be faked.
By analyzing the CO2 waveform over time, medics can monitor the severity of asthma or COPD and the effectiveness of therapy provided. Capnogram analysis may be used to indicate airwayobstruction in these patients, but further work is required to correlatecurve indices to the degree of airway obstruction.
ETCO2 values in asthma attacks will change depending on severity of the disease. Early in an acute asthma attack, hyperventilation may occur, lowering ETCO2 levels with a slightly abnormal waveform. As the attack progresses, the ETCO2 may read in the normal range with a more prominent looking shark fin waveform on the monitor. Finally, as the attack becomes severe, the ETCO2 rises and the wave becomes indistinguishable in its shark fin form. Once treatment is decided upon and bronchoconstriction decreases, the ETCO2 number may increase initially as gas exchange improves. Recognize that the waveform will appear to be normalizing. The return of a normal waveform indicates resolution of the bronchoconstriction.
The same concepts will apply with a COPD patient; however, the initial numbers may be high due to retaining CO2 in their disease process. In contrast, CHF with respiratory distress does not typically result in bronchoconstriction, so the waveforms will not necessarily have a shark fin appearance unless the patient has a pulmonary co-morbidity. Capnography can alert to early recognition in CHF even before the onset of pulmonary edema is apparent. It is important to note that a patient with significant pulmonary edema may have a significant disparity (due to the relative solubility of O2 vs. CO2) between oxygenation and ventilation.
Paramedics are frequently required to administer medications that have a depressant effect on the central nervous system (CNS), which may include narcotic analgesics (morphine sulfate, fentanyl), benzodiazapines (Valium, midazolam, lorazepam), or other sedative agents (etomidate, ketamine). With any medication that depresses the CNS, there is a risk of hypoventilation. Capnography should be routinely used to monitor patients receiving pain management or sedation for evidence of hypoventilation and/or apnea.
Paramedics may also encounter patients who are “self-medicated” with CNS depressants, including alcohol, GHB, Oxycontin, Xanax and many of the prescription compounds listed above. Overdose of alcohol and/or CNS depressants put the patient at risk for hypoventilation. Capnography is invaluable and proven to be the earliest indicator of respiratory compromise due to medications with pain or sedative association. The ETCO2 waveform dampens prior to a change in pulse oximetry due to the oxygen reserve in human anatomy.Capnography can be utilized in any patient who has ingested a significant quantity of CNS depressant, particularly those who are somnolent.
Waveform capnography is a direct measure of the changes in elimination of CO2 from the lung and indirectly indicates changes in the production of CO2 at the cellular level. It reflects the delivery of CO2 to the lungs by the circulatory system. With no pulmonary or circulatory disorders, ETCO2 may indicate patient anxiety or a metabolic disorder. In diabetic ketoacidosis (DKA), Kussmaul’s respirations result in hyperventilation as a means for the patient to lessen their ketone load and attempt to correct metabolic acidosis. The increased rate of breathing causes the ETCO2 to decrease. End-tidal carbon dioxide is linearly related to bicarbonate (HCO3) in healthy subjects, and has been found to be significantly and chronically lower in children with DKA. Although more research is needed, in conjunction with clinical assessment, capnography may help discriminate between patients with hyperosmolar, hyperglycemic nonketotic conditions and DKA.
Monitoring ETCO2 can provide an early warning sign of shock. A patient with a sudden drop in cardiac output will show a diminished CO2 waveform and a drop in the ETCO2 number that may occur regardless of any change in breathing rate. Capnography should be used on all trauma and cardiac patients and any patient at risk for shock. Cardiac output and end-tidal partial pressure of carbon dioxide (PETCO2) were highly related in diverse experimental models of circulatory shock in which cardiac output was reduced by >40% of baseline values. The measurement of PETCO2 is a noninvasive alternative for continuous assessment of cardiac output during low-flow circulatory shock states. A patient with low cardiac output from a shock state does not deliver as much CO2 per minute back to the lungs to be exhaled, which will result in a decreased ETCO2. It doesn’t necessarily mean the patient is hyperventilating or has reduced arterial CO2 level. Reduced perfusion to the lungs and/or tissues alone can be the sole cause.
It is important to note the effect on ventilation/perfusion (V/Q) mismatch while using ETCO2. V/Q mismatch occurs when there is an injury or disease process that affects normal blood circulation and/or lung function. For example, V/Q mismatch is often seen in pulmonary embolism in which the alveolar tissue is capable of gas exchange. However, a vascular blockage prevents blood flow to areas of the lungs, so the ETCO2 decreases because there is essentially fresh air being exhaled from the non-perfused portion of the lung. This V/Q mismatch results in increased CO2 in the systemic circulation, with decreased exhaled CO2.
Some seizure patients breathe during a seizure. Capnography can be a powerful tool to determine the aggressiveness of seizure management. If capnography reveals ventilatory failure, this will require aggressive airway and pharmacologic intervention. If a seizure patient has moderate elevations in ETCO2 with an unalarming respiratory rate, perhaps less aggressive ventilatory support with or without medications would be indicated until the seizure approaches the end of its “cycle.” If capnography indicates that a patient’s ventilatory status is sufficient, then only supportive measures are required.
Putting It All Together
In order to properly assess ventilation, it is important to understand what determines respiration and ventilation in the human body. Factors such as metabolic rate, acid-base status, central CO2 respiratory drive, physiologic deadspace and lung mechanics all play a role. There are factors that increase ventilatory demand, such as arterial hypoxemia, increased metabolic rate, increased physiologic deadspace, metabolic acidosis, pulmonary edema, increased work of breathing, confusion and central nervous system stimulation. Changes in any of the latter factors affect ETCO2. Waveform capnography provides further insight in caring for your patient in many clinical states and is a tool paramedics should not be without. Table 1 lists some of the causes of both increased and decreased CO2.
Capnography has a clinical utility in EMS with many types of disease states, including not only respiratory compromise, but factors also affecting perfusion and metabolism. The capnography waveform is a key vital sign when determining treatment for patients in the field. Capnography sampling devices are useful in all types of airways, whether or not the patient is intubated.
1. The American Heart Association. Highlights of the 2010 AHA Guidelines for CPR and ECC. http://static.heart.org/eccguidelines/pdf/90-1043_ECC_2010_Guidelines_Highlights_noRecycle.pdf
David Wampler, PhD, LP, University of Texas Health Science Center San Antonio, Department of Emergency Health Sciences, Office of the Medical Director.