Capnography is something I know very little about, but would definitely like to. I was told in PCP school that capnography was a necessary skill only when doing endotracheal intubation (something people who get paid more than me can do). This turns out to be not entirely true, and perhaps increasingly so. The new 2010 American Heart Association Guidelines now endorse wave form capnography as a Level I recommendation for ET tube verification, a Level IIa recommendation for detecting return of spontaneous circulation and a IIb for monitoring CPR quality.
Furthermore, on our units we have a neat little instrument called a CapnoLine Oral/Nasal sampling set. It has the option to provide patients oxygen via nasal cannula, while simultaneously taking a sample of exhaled breath and reporting it’s waveform and CO2 concentration on the monitor. Very cool, but doesn’t do me much good if I can’t read the data. The tool is relatively new to my service and we are just moving into a more avid use of it in non-tubed, non-CPR receiving, non-ROSCing patients in order to monitor their cardiopulmonary status more precisely.
My many years as a teacher and a student have entrenched in me that you truly learn best by teaching others. So (thanks to my resources) here goes…
Capnography works by capturing exhaled air and redirecting it into the capnography device. The air then passes between a light and a detector that measures how much light is shining on it. As the concentration of CO2 increases, more light is absorbed by the CO2 and less light is transmitted onto the detector plate. This increased light absorption directly correlates with the percentage of carbon dioxide. The monitor presents the CO2 concentration as both a number (capnometry) and a waveform (capnography). The respiratory rate can be very accurately estimated and reported by measuring the tides between CO2 peaks. The concentration of exhaled CO2 is also referred to as EtC02, or end tidal C02. (1)
Blood levels of carbon dioxide (PaC02) are as critically important as blood oxygen levels. Under normal circumstances our PaC02 (arterial carbon dioxide) levels are what determine our rate and depth of breathing.
Oxygenation is how we get oxygen to the tissue. Oxygen is inhaled into the lungs where gas exchange occurs at the capillary-alveolar membrane. Oxygen is loaded onto hemoglobin and transported to the tissues through the blood stream. Pulse oximetry (alligator thing on your finger) measures oxygenation.
At the cellular level, oxygen and glucose combine to produce energy. Carbon dioxide, a waste product of this process (The Krebs cycle), diffuses into the blood. Ventilation (the movement of air) is how we get rid of carbon dioxide. Carbon dioxide is carried back through the blood and exhaled by the lungs through the alveoli. Capnography measures ventilation. (2) Often changes are seen in EtCO2 prior to changes in pulse oximetry because of the body’s natural oxygen reserve.
Ventilation and oxygenation are interrelated, but represent distinct processes. Different diseases can affect the processes in different ways. Measuring exhaled CO2 can provide valuable insight into metabolism and circulation. Take, for example, the moderately sick asthma patient demonstrating a “shark fin” pattern with an elevated EtCO2 but 100% oxygen saturation. This patient is oxygenating well, but not ventilating effectively. (3)
In a healthy person, the amount of CO2 is tightly regulated by our body and brain between 35-45 mmHg. This would be reflected in EtCO2 values of 30-43 mmHg (capnometry). The difference between PaCO2 and EtCO2 is generally 2-5mmHg. However, the difference (also known as a-ADCO2) in diseased lungs can be much larger due to ventilation/perfusion mismatch.
Three Things That Keep Us Alive
1. Metabolism is the utilization of hydrocarbons to produce energy within the entire body. This process must be continuous for life to be sustained. It is important to note, that even several hours after cardiac arrest, some residual metabolism (liver, skeletal muscles, skin, etc.) will continue to produce CO2.
2. Circulation. Blood must be moving in order to deliver CO2 from the tissues to the alveoli. Circulation requires blood, an effective heartbeat, blood pressure, and a good container.
3. Ventilation. Air must move in and out of the alveoli effectively to get klj;k;lkjl;klkjl;kj;klj;kljlkjlkj;lkj;lkj;lkj;lkj;lkk;kj; rid of carbon dioxide and other waste products, and to inhale fresh lkoijoij oxygen. (5)
Why It Matters
Factors Effecting EtC02
|HypercapniaIncreased EtCO2||HypocapniaDecreased EtCO2|
EMS Hx Dx Tx
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. Waveform capnography is able to support those clinical assessment needs and can indicate the need to adjust ventilatory support. (6)
EtCO2 serves as a measure of the effectiveness of chest compressions, effective meaning keeping the EtCO2 number as high as possible. High quality compressions should result in EtCO2 of 10-20 mmHg. (7) In the cardiac arrest patient, EtCO2 directly correlates with cardiac output. If no carbon dioxide is measured in the patient’s exhaled air, it indicates either an improperly placed tube (during intubation) or no cardiac output. Systemic and pulmonary perfusion during cardiac compressions transports CO2 to the alveolar space. A “high” ETCO2 value represents good compressions, and good cellular perfusion- allowing cells to metabolize and circulation to deliver carbon dioxide to the lungs. (8)
A rapid rise in EtCO2 (at least 35-45 mmHg) during chest compressions can be the first indicator of return of spontaneous circulation (ROSC), possibly even before a pulse is detectable. This increase represents drastic improvement in blood flow (more CO2 being dumped in the lungs by the circulation) which indicates circulation. (9) 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 no pulses are 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. (10)
Clinical Death Confirmation
According to the New England Journal of Medicine, patients with an EtCO2 of less than 10 mmHg at the 20-minute interval of resucitation efforts have a 100% mortality rate. Their 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. (11)
Head Injury Patients
ITLS and the Brain Trauma Foundation have taken the lead in recommending capnography as the way to titrate CO2 ventilations in the patient with a closed head injury. If the patient has a GCS of less than 9 and they are posturing, have unequal pupils, or dropped two in front of you, then they should be selectively ventilated to an ETCO2 between 30-
35mm/hg. If the patient does not the signs (above) of deterioration, then ventilate the patient to levels, 35-45. Never ever bag them to lower than 25mm/hg. It causes cerebral vasoconstriction and creates an alkalosis not allowing O2 to dissociate from hemoglobin, making the brain injury worse. (12)
Generalized seizure, such as a tonic/clonic, can affects both hemispheres of the brain and the medulla. When the medulla is involved, the patient may not breath during seizure activity. Following the post-ictal state capnography can determine the need for further ventilation. (13)
Because CO2 is a by-product of metabolism, anything affecting the metabolic rate affects CO2 production and, consequently, corresponding end-tidal carbon dioxide (EtCO2) levels. Metabolic pathways must be supplied with essential nutrients, such as sugar, water and oxygen for a normal metabolic rate to occur. So if perfusion is compromised, so is the delivery of these components necessary for metabolism. The result is a decreased metabolic rate, resulting in decreased CO2 production. Or, if a patient is in metabolic acidosis (clinically defined as an acidotic pH with depleted bicarbonate), less CO2 will be created, resulting in lower EtCO2 levels.
Anaerobic metabolism increases during poor perfusion states, which increases acidic byproducts. However, simply increasing acid in the system doesn’t equate to an increase in CO2 production. In the human body, bicarbonate levels are strictly regulated by the kidneys and are slow to respond to pH changes. Thus, you can have all the acid you want building up in the system, but without a proportional increase in bicarbonate available for buffering, you won’t see the increase in CO2 production that may seem intuitive. (14)
For example, in a DKA (diabetic ketoacidocis) patient: the more acidotic the patient, the lower the HCO3 and the higher the respiratory rate and lower the EtCO2. (15)
In Tension Pneumothorax, pressure in the chest collapses a lung and then presses on the right side of the heart making it hard to fill with blood. It only takes about 7mm/hg pressure to stop the blood flow into the right atria. The first and must reliable sign of a TENSION pneumothorax is the sudden drop in perfusion that is picked up immediately on a capnogram. By the same token, when the chest is successfully decompressed, it is not a rush of air but a sudden increase in ETCO2 that confirms decompression success. Furthermore, the capnogram can be used to keep watch in case it develops again.
The same is true for Pericardial Tamponade and cardiocentesis. In each of these obstructive forms of hypoperfusion, the capnogram will remain square because it is a perfusion problem, not an airway problem. (16)
Capnography can be used to differentiate between the varying causes of respiratory distress often seen by paramedics in the field, such as asthma, COPD exacerbation and CHF. It can also 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.
Bronchospasm will produce a “shark fin” capnography waveform due to difficulty emptying alveoli. The characteristic shark fin appearance is a result of regional obstruction, which 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”.
The chart below represents normal waveform breathing, to the development of severe bronchoconstriction, leading to respiratory arrest. A similar development is seen in airway obstruction.
Carbon dioxide values in asthma will change depending on severity of the disease. Hyperventilation may occur early in an acute asthma attack, 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 the bronchoconstriction decreases, the EtCO2 number may increase initially as gas exchange improves. Recognize that the waveform will appear to be normalizing. (17)
You’re probably thinking, “What if they’re a CO2 retainer?” as in advance COPD patients. Good question. A CO2 level of 50–60 could be normal for them because their medulla is accustomed to high levels over a long period of time. Generally, in healthy individuals, a rate of PaCO2 above 50 is considered ventilatory failure. However in end stage COPD patients, their hypoxic drive (lack of oxygen) stimulates them to breath as opposed to increased levels of CO2. How can you tell? Well, if they’re indeed a hypoxic breather, giving them oxygen could depress their stimulus, causing the CO2 to go up. (18) However, this usually takes at least 20 minutes to manifest.
Congestive heart failure (CHF) patients have circulatory compromise, which results in changes in carbon dioxide delivery. This means that as the disease worsens, or as the patient approaches decomposition, EtCO2 will continue to decline as alveolar perfusion decreases. Respiratory distress due to CHF does not typically result in bronchoconstriction, so the waveforms will not necessarily have a shark fin appearance unless the patient has a pulmonary comorbidity. 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. (19)
Paramedics frequently are required to administer medications that have a depressant effect on the central nervous system (CNS). This may include narcotic analgesics (morphine sulfate, fentanyl), benzodiazepines (Valium, midazolam, lorazepam) or other sedative agents (etomidate, ketamine). With any medication that depresses the CNS, there is a risk of hypoventilation.
At times, paramedics 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 puts 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. (20)
ETCO2 is being used on an ambulatory basis to teach patients with anxiety disorders as well as asthmatics how to better control their breathing. Try (it may not always be possible) to get your anxious patient to focus on the monitor, telling them that as they slow their breathing, their ETCO2 number will rise, their respiratory rate number will fall and they will feel better. (21)
Some patients who suffer anaphylactic reactions to food they have ingested (nuts, seafood, etc.) may experience a second attack after initial treatment because the allergens remain in their stomach. Monitoring ETCO2 may provide early warning to a reoccurrence. The wave form may start to slope before wheezing is noticed. (22)
GETTING TO KNOW THE WAVES
Good luck with that!
(1, 3, 5, 10, 17, 19, 20)http://www.emsworld.com/article/10287447/capnography-as-a-clinical-tool
(2, 5, 6, 8, 11, 21, 22) http://emscapnography.blogspot.ca/