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17.01.2015
November 30, 2013 by Tim Leeuwenburg 4 Comments End-tidal CO2 is increasingly becoming used outside of the Operating Theatre and it is prudent for the rural doctor to have an appreciation of what it is, how to measure it, when to measure it and ita€™s utility in common scenarios. It is my belief that ETCO2 should be used not just in intubated patients, but as a valuable adjunct for procedural sedation, for monitoring patients a€?at riska€™ and to help guide resuscitation. Devices such as the Easy-Cap or Pedi-Cap are designed to confirm the presence or absence of expired CO2 – a pH detector (metacresol purple on filter paper) detects pH shifts and changes to the colour yellow in the presence of expired CO2. A sample line is placed as a sidestream to the breathing circuit (usually via the HME filter at intersection of endotracheal tube and breathing circuit). As an alternative to sampling expired gas directly from the anaesthetic circuit or HME filter attached to an endotracheal tube, it may be useful to monitor ETCO2 for spontaneously ventilating patients, whether on room air, nasal specs or oxygen mask. I use this routinely during endoscopy, colonoscopy in the operating theatre, as well as when performing procedural sedation in the ED. Remember that relying on SpO2 to confirm ventilation is inadequate – measured oxygen saturation may remain elevated for some time after cessation of breathing-A  and once a fall in SpO2 has been detected, your patient is already hurtling down the oxy-haemo-coaster.
End-tidal CO2 is classically considered as the standard of care when performing intubation.
End-tidal CO2 monitoring is mandatory not just for the intubated patient, but should be used whenever using a neurolept eg: sedation in ED, monitoring of psychiatric patient etc.
Even if you are not performing anaesthesia, know how to hook up ETCO2 monitoring for your spontaneously ventilating patients at risk of hypopnoea or apnoea.
Dedicated ETCO2 monitors exist, but most capnographs will hook up to existing monitors in OT, ED and ward defibs.
I am a Rural Doctor on Kangaroo Island, South Australia with interests in emergency medicine, anaesthetics & trauma. Areas of interest include difficult airway management outside of theatre (rural-ED-ICU), human factors, use of crisis checklists and "guerilla" sim training. What I want to understand more clearly is why the intubated patients waveform changes shape when mechanically ventilated vs spontaneously ventilating. You glance at the EMS monitor and note a slow narrow complex rhythm; chest compressions are continued, and his prehospital capnography tubing is connected to the ED monitor. Ventilation (the pulmonary exchange of carbon dioxide [CO2] and its subsequent expiration) is typically monitored in the ED by 2 modalities: colorimetric capnometry or continuous infrared spectroscopy. ETCO2 concentration (the concentration of CO2 at the end of exhalation) typically underestimates PaCO2 concentration in healthy individuals by 4 to 5 mm Hg.3 Regrettably, this gap precludes using ETCO2 as a noninvasive determination of PaCO2. The PaCO2-ETCO2 gradient will be increased in the acute scenario by any disorder that decreases pulmonary blood flow (thereby increasing alveolar dead space).
Lastly, any condition that decreases exhaled tidal volume, such as obstructive lung disease, increases the gradient. Thus, the determinants of the PaCO2-ETCO2 gradient are multifactorial, and the magnitude of their effect is often unpredictable. Perhaps the most useful application of continuous ETCO2 monitoring is to allow real-time confirmation of adequate ventilation through capnographic waveform analysis. Additionally, the use of continuous ETCO2 in confirming prehospital intubation during cardiac arrest has also been shown to be more effective than colorimetric capnometry and auscultation.
When performing procedural sedation, reliable monitoring of the patient’s ventilatory status is crucial.
Hyperventilation with hypocapnia may worsen outcome in brain-injured patients.18 Therefore, monitoring of ETCO2 is emerging as a fundamental component of TBI management not only in the hospital but also in the prehospital arena.


Several studies have demonstrated the incidence of induced hypocapnia during the field management of TBI patients. As discussed previously, pulmonary CO2 exchange is affected by multiple factors at the level of the alveoli. An ECG of the patient after regaining his pulse revealed ST elevations in the lateral precordial leads.
Capnography allows for the continuous verification of ETT placement, which is essential in the unstable prehospital and ED environment in which patients are frequently moved; achieving adequate sedation can be difficult, and accidental extubation is an ongoing risk. Continuous capnography by spectroscopy may be superior to qualitative CO2 detectors in detecting correct ETT placement during cardiac arrest. An ETCO2 less than 10 mm Hg following 20 minutes of CPR is predictive of death and indicates that continued attempts at resuscitation are likely futile.
A rapid increase in ETCO2 concentration during CPR often represents ROSC and can be a useful guide in determining timing of rhythm and pulse checks.
Continuous noninvasive ETCO2 monitoring can be useful in the monitoring of patients with tenuous respiratory status, such as those with severe reactive airway disease or congestive heart failure. While a low ETCO2 concentration is difficult to interpret, an ETCO2 concentration greater than 40 mm Hg will almost always indicate hypercapnia. All content on this website, including dictionary, thesaurus, literature, geography, and other reference data is for informational purposes only. Exhaled gas is sampled by a dedicated analyser (anaesthetic monitor or some defibrillators). The ones I worry about most are the absent or rapidly disappearing ETCO2 rtace seen in inadvertent oesophageal intubation…and the falling ETCO2 waveform with loss of cardiac output. Most ETCO2 sampling equipment is dedicated to sit in-line as either an adaptor between ETT and circuit, or as a filter line to attach to HME filter.
Either colorimetric or waveform capnography can be used to confirm the presence of exhaled CO2 and hence confirm desired tracheal vs inadvertent oesophageal intubation. Also why does the inspiratory slope decrease with inspiratory valve malfunction, but only the baseline increases with expiratory valve malfunction. Per the paramedic crew, the patient is a 62-year-old man initially complaining of chest tightness who became unresponsive and apneic during transport approximately 3 minutes prior to arrival. The characteristic waveform reassures you of proper ETT placement, and the ETCO2 is 14 mm Hg.
Colorimetric capnometers display a threshold concentration of CO2 qualitatively or semiquantitatively by color change, providing the clinician with confirmation of ETT placement. Such conditions include pulmonary embolism, cardiogenic shock, cardiac arrest, or hypovolemia. Continuous ETCO2 monitoring is a valuable tool for preventing misplacement of the ETT, either through continuous verification of placement following intubation or for airway management during CPR or transport. The presence of ETCO2 greater than 5 mm Hg after 6 breaths was found to be 100% sensitive and 100% specific for correct placement of the ETT, while qualitative capnometry was 100% specific but only 80% sensitive in cardiac arrest.
After TBI, there may be a period of prolonged hypoperfusion with cerebral blood flow (CBF) reduced by as much as two-thirds of normal. In a retrospective study from San Diego, 59 adult severe TBI patients who were unable to be intubated without rapid sequence intubation (RSI) were matched to 177 historical nonintubated controls. In contrast to this, at extremely low flow states, ETCO2 is determined almost entirely by pulmonary flow secondary to a logarithmic relationship between cardiac output and ETCO2 that exists during cardiac arrest.33 This relationship between pulmonary flow and ETCO2 during arrest makes capnometry an important prognostic marker during CPR in the ED.


The patient was taken to the cardiac catheterization lab for revascularization on hospital day 1 He was extubated on hospital 1day 2 and optimized on antiplatelet drugs, beta-blockers, and lipid-lowering agents prior to discharge. Tell a friend about us, add a link to this page, or visit the webmaster's page for free fun content.
All sources I have found simply state that “this is how the waveform changes in this instance” but does not explain why?? The rhythm was noted initially to be ventricular fibrillation; after a single biphasic countershock, his rhythm became organized, but he remained pulseless. Therefore, while a low ETCO2 value may provide little information regarding a patient’s ventilatory status, a high ETCO2 value almost always correlates with an equal or higher PaCO2 value. This is especially true when one considers the fallibility of traditional physical examination techniques.
The results of this randomized controlled study showed that patients monitored by capnography had significantly fewer hypoxic episodes compared to those where the treating physician was blinded to the capnography data.
Hyperventilation can further decrease CBF, potentially to the point of cerebral ischemia or by converting ischemic areas into infarction. The study utilized ETCO2 monitoring and found an association between hypocapnia and mortality and a statistically significant association between ventilatory rate and ETCO2. He was intubated en route and is now being wheeled into your critical care area receiving active chest compressions. At the following rhythm check, you note ventricular fibrillation; he receives another shock, and chest compressions continue. This concept may prove particularly beneficial during the continuous monitoring of patients at risk for tiring out, such as those patients with status asthmaticus or decompensated congestive heart failure. Rather, this vertical height of the wave portrays the amount of CO2 being exhaled through the intra-nasal cannula.30 While ETCO2 monitoring for sedation is considered standard of care in the United States in operating suites, its necessity during sedation in the ED is still controversial. Both the lowest and final ETCO2 readings were associated with increased mortality versus matched controls.
You now note an ETCO2 of 36 mm Hg, a central pulse is appreciated, and his plethysmographic waveform becomes clearly defined.
Likewise, in situations in which targeted PaCO2 levels may be of value (such as in patients with evidence of increased intracranial pressure and acute brain herniation), a high ETCO2 value may signal the need for adjustments in the patient’s mechanical ventilatory parameters or, at the minimum, the need to check a blood gas.
ETCO2 monitoring was used in 144 patients to assess whether closer monitoring would result in a lower rate of inadvertent severe hyperventilation (defined as an ETCO2 less than 25) after RSI.
In these cases, the continuation of normal oxygen saturation on the pulse oximeter readout can fail to indicate hypoventilation or apnea; this makes ETCO2 monitoring a superior real-time monitoring solution to identify oversedation or apnea in these patients. Patients with ETCO2 monitoring had a significantly lower incidence of severe hyperventilation.
For those patients who were severely hyperventilated, there was a statistically significant increase in mortality (56% vs 30%).18 However, as previously discussed, the PaCO2-ETCO2 gradient in traumatically injured patients is unreliable, specifically in regards to low ETCO2 concentrations.
A recent study by Lee et al examined 77 patients and showed a poor concordance between ETCO2 and PaCO2 in multitrauma patients.32 Therefore, the reliance on ETCO2 as an indicator of hypocapnia must be further evaluated in the emergency setting before it is used to guide ventilatory management of traumatically brain injured patients in the ED.



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