CAPNOGRAPHY – END-TIDAL CO2 MONITORING (References: “10 Things Every Paramedic Should Know About Capnography” website, UpToDate, Brady & Caroline Paramedic Textbooks, paramedicine.com, “Capnography for Paramedics” website, emsstaff.buncombecounty.org, AHA 2010 Guidelines, alibaba.com) Capnography is the measurement of carbon dioxide (CO2) in exhaled breath, often referred to as the “ventilation vital sign”. Capnography is an objective measurement of ventilation and hemodynamic status. The term “End Tidal CO2 (ETCO2), refers to the level of CO2 released at the end of exhalation, expressed as a percentage or in millimeters of mercury (mmHg). Normal values are 5-6% CO2, equivalent to 3545mmHg. CO2 reflects 4 metabolic processes: alveolar metabolism, cellular metabolism, cardiac output and pulmonary blood flow as gas is transported by the venous system to the right side of the heart then pumped to the lungs by the right ventricle. When CO2 diffuses out of the lungs into exhaled air, a “capnometer” measures the partial pressure or maximal CO2 concentration at the end of exhalation. There are 4 main physiologic CO2 components: 1. Production: CO2 is a metabolic byproduct of aerobic cell metabolism. As intracellular CO2 increases, CO2 diffuses into tissue capillaries and carried by venous circulation to the lungs, where it diffuses from pulmonary capillaries into the alveoli. Ventilation is one way the body rids itself of this toxic byproduct as CO2 carried through the blood to be lungs to be exhaled. 2. Transport: maintaining CO2 tension of arterial blood at 35-45mmHg. 3. Buffering: buffering action of hemoglobin and pulmonary blood flow maintains normal CO2 levels by eliminating excess CO2. CO2 either carried, dissolved or combined with water (H20) to form carbonic acid (H2CO3), which dissipate into hydrogen ions (H+) and bicarbonate (HCO3-) ions per the “Henderson Hesselbalch Equation”: (CO2 + H20 <=> H2CO3 <=> H+ + HCO3-). Hydrogen ions and bicarbonate ions buffered by hemoglobin account for 90% of CO2 transport. 4. Elimination: CO2 elimination by alveolar ventilation under control of the respiratory center. This process allows CO2 diffusion from blood to the alveoli where the partial alveolar pressure of CO 2 is lower than the tissue pressure. Any increased metabolic state increases CO2 production. Decreased cardiac output lowers CO2 delivery to the lungs decreasing ETCO2 levels. Any change in ETCO2 reflects changes in systemic and pulmonary blood flow and therefore is an objective tool to evaluate adequacy of ventilation and pulmonary blood flow during low cardiac output states, i.e. hemodynaminc instability, cardiac arrest, or to monitor effectiveness of compressions during CPR. MEASURING ETCO2 ETCO2 measured with a capnometer containing a source of infrared radiation, a chamber with a gas sample, and a photodetector. When expired CO2 passes between the beam of infrared light and photodetector, the absorbence proportional to the concentration of CO2 in the gas sample. The gas samples are analyzed by mainstream (in-line) or sidestream (diverting) techniques. ETCO2 attachments available are nasal w/O2 tubing, nasal w/o O2 tubing for use with a non-rebreather, and in-line for intubated patients. CAPNOGRAPHY VALUES AND WAVEFORM INTERPRETATION Normal capnography ranges between 35 to 45mmHg. ETCO2 <35mmHg means hyperventilation/hypocapnia; ETC02 >45mmHg means hypoventilation/hypercapnia. As the respiratory rate increases, the CO2 level decreases (and conversely). The ETCO2 wave form begins just prior to exhalation and ends with inspiration. A-B:post-inspiration/dead space exhalation B:start of alveolar exhalation B-C: exhalation upstroke where dead space gas mixes with lung gas C-D: plateau of exhalation D: end-tidal “peak” CO2 concentration D-E: inspiration washout Capnography provides a breath-to-breath trend of respirations and an early warning of respiratory distress. There are only a few abnormal waveform patterns to recognize: hyperventilation, hypoventilation, esophageal intubation and obstructive. A benefit of capnography over oximetry is that within a few breaths, capnography will change patterns, vs often over a minute for the PaO2 to change. Pay more attention to the ETCO 2 waveform trend than the actual number. A steadily rising ETCO2 (i.e. as patient becomes sedated and hypoventilates) can help a provider anticipate when assisted ventilations or intubation may be necessary. Hyperventilation: When a person hyperventilates, their CO2 level drops (hypocarbia). Hyperventilation is caused by many factors including anxiety, bronchospasm, pulmonary embolus and diabetic ketoacidosis. Hypocarbia may also be present in low metabolic / low cardiac output states: cardiac arrest, hypotension, hypothermia, sepsis, pulmonary edema. Hypoventilation: When a person hypoventilates, their CO2 rises (hypercapnia). Hypoventilation can be caused by sedation states, including overdose, intoxication, post-ictal, head trauma, stroke, sepsis, and respiratory fatigue / failure. CO2 may be chronically high in smokers and with underlying lung disease (i.e. COPD). Obstructive: Bronchospasm produces a “shark fin” waveform created when the patient exhales against an “obstruction” producing the characteristic upstroke pattern. The sloping shape correlates to the level of bronchospasm / obstruction – patients with severe underlying COPD / asthma may have at baseline a small upstroke in their waveform pattern. With mild asthma, CO2 drops as the patient hyperventilates to compensate for their respiratory distress. As the asthma worsens, the C02 levels start elevating. When the bronchospasm becomes severe and patient tires and hypoventilates, they become hypercapnic. This is known as “CO2 Narcosis”, as high CO2 blood levels have a sedating effect. Successful bronchospasm treatment decreases the shark-fin slope returning the ETCO2 to a normal range. The waveform pattern in patients with CHF or pulmonary edema is more upright, and less “sloped” than in patients with COPD / asthma. This may help along with SAMPLE history and exam when differentiating between obstructive airway wheezing vs “cardiac wheezing” of CHF. Confirming, Maintaining , Assisting Intubation: Continuous ETCO2 monitoring can confirm a tracheal intubation or rapidly determine if an ETT becomes dislodged or is misplaced as a stable waveform ensures the ETT is in the trachea. One study evaluated prehospital intubations utilizing continuous waveform capnography to confirm ETI, demonstrating 0% unrecognized misplaced intubations in the waveform group versus 23% misplaced ETI in the group without waveform capnography (Silversti, 2005). An important caveat is in patients with cardiopulmonary arrest, good compressions are necessary to generate a waveform. In patients with a prolonged downtime, ETCO2 reading may be so low that the waveform looks “flat”, or appears to be consistent with an esophageal intubation. If the provider can ventilate without resistance with fog in the tube, bilateral lung sounds and no epigastric sounds, do not automatically pull the ETT; the patient may be “too dead” to produce anything but a scant amount of CO2, which looks flat or minimally elevated from baseline. Capnography cannot detect right main-stem intubations. Capnography can also be used for supraglottics, combitubes and LMAs. CARDIAC OUTPUT MEASUREMENT DURING CARDIOPULMONARY RESUSCITATION The 2010 AHA Guidelines endorse waveform capnography as a Level I recommendation for ETT verification, a Level IIa recommendation for detecting return of spontaneous circulation (ROSC) and a Level IIb for monitoring CPR quality. Colormetric ETCO 2 devices should only be used when waveform capnography not available (Class IIa), or for initial confirmation. Utilizing waveform ETCO2 during cardiopulmonary arrest with adequate compressions may show waveform oscillations immediately upon intubation, replaced by larger wave forms once ventilations initiated. The oscillations demonstrate that compressions alone produce some ventilation (further evidence behin AHA’s 2010 recommendations to not provide advanced airway management during the 1st 8 minutes of witnessed OOHCA). It has well documented that quality compressions are associated with elevated ETCO 2 levels (Gravenstein, Cambridge Press 2004). With the new AHA Guidelines calling for “hard, fast and deep” compressions, rescuers should switch places every two minutes. Set the monitor so providers can see the ETCO2 and cardiac monitors, with the goal of providing 100 compressions / minute and maintaining a stable and high ETCO2 waveform. A “spike” in ETCO2 during resuscitation is often the 1st sign of return of spontaneous circulation (ROSC). ETCO2 will elevate >35mmHg post ROSC due to CO2 tissue washout. Per AHA Guidelines, “ETCO2 monitoring during cardiac arrest is a safe and effective noninvasive indicator of cardiac output during CPR and may be an early indicator of ROSC in intubated patients.” Conversely, in a recently resuscitated or hemodynamically unstable patient, if the ETCO2 number dropping, immediately check pulses as this drop signals an acute loss of cardiac output, and compressions may be required. ETCO2 monitoring can confirm resuscitation futility in addition to predicting likelihood of resuscitation outcomes. Per Levine an ETCO2 <10 mmHg 20 minutes post initiation of resuscitation accurately predicts death in patients with PEA or VF arrest leading to the recommendation to terminate resuscitation ( NEJM, 1997). Multiple studies have noted that patients with a high initial ETCO2 level are more likely to be successfully resuscitated than those with lower initial ETCO2 levels. Levine’s study demonstrated that no patient with an initial ETCO2 <10mmHg survived while in patients with ROSC, ETCO 2 rose to at least 18 mmHg before any clinically detectable return of vital signs. Other studies have shown rare patients surviving resuscitation with an ETCO2 initially <10mmHg, especially in cold-water drowning. Like any vital sign or lab finding, the ETCO2 is one of many factors taken into consideration when terminating or continuing resuscitation efforts. MONITORING SEDATED PATIENTS Capnography should be used to monitor sedated patients for evidence of hypoventilation or apnea. ETCO2 monitoring flagged a problem before changes in oximetry or observed changes in respiratory rate. Capnography essential in intubated patients as small changes wave form indicates the patient is beginning to arouse from sedation or starting to breathe on their own. VENTILATING HEAD TRAUMA PATIENTS Capnography helps avoid hyperventilation in intubated head injured patients, avoiding secondary “insult” of excessive free radical formation cause by hyperoxygenation on the vulnerable ischemic brain “penumbra”. Hyperventilation decreases intracranial pressure by decreasing intracranial blood flow, resulting in cerebral ischemia emphasizing the importance of prehospital “appropriate” ventilation. One study showed patients with ETCO2 monitoring had a lower incidence of inadvertent hyperventilation (6%) than those without ETCO2 monitoring (13%). Patients in the hyperventilation group had a significantly higher mortality rate (56%) than those with “normal” ventilation (30%) (Davis, J Trauma 2004) OTHER CLINICAL SITUATIONS WHERE ETCO2 HELPFUL Patients with acidosis (i.e. diabetic ketoacidosis) hyperventilate to “blow off’ CO2. A pulmonary embolus increases pulmonary dead space decreasing alveoli available to offload CO2, causing a drop in ETCO2. Metabolism rises in fever & neuroleptic malignant syndrome, causing an elevation in ETCO2. A study of blunt trauma patients showed 5% with ETCO2 <26mmHg after 20 mins survived to discharge vs a median ETCO2 for survivors was 30mmHg (Deakin, J Trauma 2004). Capnography used as a triage tool to assess respiratory status in MCIs involving chemical attacks. ETCO2 provides warning to anaphylaxis reoccurrence after initial treatment, as the waveform starts sloping upwards before wheezing clinically noted or pulse oximetry drops. Capnography provides an accurate respiratory rate, as well as documents respiration trends. ETCO2 monitoring can provide an early warning sign of shock. A patient with a sudden drop in cardiac output will show a drop in ETCO2 numbers that may be regardless of any change in breathing. This has implications for trauma patients, cardiac patients – any patient at risk for shock. DOCUMENTATION Paramedics should document their use of continuous ETCO 2 monitoring and attach waveform strips to their PCRs for the following points of care: prior to intubation, immediately post-intubation, periodically during care and transport, and upon and after any patient transfer. This serves as both a timestamp and proof that your intubation was correctly placed.
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