Carbon Dioxide Monitoring (Capnography) - UpToDate
Carbon Dioxide Monitoring (Capnography) - UpToDate
All topics are updated as new evidence becomes available and our peer review process is complete.
INTRODUCTION
This topic review will discuss the basic physiology and interpretation of capnography and
its use in emergency settings.
The term capnography refers to the noninvasive measurement of the partial pressure of
carbon dioxide (CO2) in exhaled breath expressed as the CO2 concentration over time. The
relationship of CO2 concentration to time is graphically represented by the CO2 waveform,
or capnogram ( figure 1). Changes in the shape of the capnogram are diagnostic of
disease conditions, while changes in end-tidal CO2 (EtCO2), the maximum CO2
concentration at the end of each tidal breath, can be used to assess disease severity and
response to treatment. Capnography is also the most reliable indicator that an
endotracheal tube is placed in the trachea after intubation.
Oxygenation and ventilation are distinct physiologic functions that must be assessed in
both intubated and spontaneously breathing patients. Pulse oximetry provides
instantaneous feedback about oxygenation (see "Pulse oximetry"). Capnography provides
instantaneous information about ventilation (how effectively CO2 is being eliminated by
the pulmonary system), perfusion (how effectively CO2 is being transported through the
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vascular system), and metabolism (how effectively CO2 is being produced by cellular
metabolism).
Capnography became a routine part of anesthesia practice in Europe in the 1970s and in
the United States in the 1980s. It is now part of the standard of care for all patients
receiving general anesthesia and is part of routine monitoring in the pre-hospital and
acute care settings. (see "Basic patient monitoring during anesthesia", section on
'Capnography')
PRINCIPLES OF OPERATION
Carbon dioxide (CO2) monitors measure gas concentration, or partial pressure, using one
of two configurations: mainstream or sidestream. Mainstream devices measure
respiratory gas (in this case CO2) directly from the airway, with the sensor located on the
airway adapter at the hub of the endotracheal tube (ETT). Sidestream devices measure
respiratory gas via nasal or nasal-oral cannula by aspirating a small sample from the
exhaled breath through the cannula tubing to a sensor located inside the monitor (
picture 1).
Mainstream systems are configured for intubated patients. Sidestream systems are
configured for both intubated and nonintubated patients.
Sidestream systems are configured to use high flow rates (around 150 cc/min) or low flow
rates (around 50 cc/min). Flow rates vary according to the amount of CO2 needed in the
breath sample to obtain an accurate reading. Low-flow systems have a lower occlusion
rate (from moisture or patient secretions) and are accurate in patients with low tidal
volumes (eg, neonates, infants, and adult patients with hypoventilation and low tidal
volume breathing). Low-flow systems are also resistant to dilution from supplemental
oxygen. High-flow systems sampling at ≥100 cc/min have been shown to be inaccurate in
neonates, infants, young children, and in hypoventilating adult patients [1-3].
CO2 monitors are either quantitative or qualitative. Quantitative devices measure the
precise end-tidal CO2 (EtCO2) either as a number (capnometry) or a number and a
waveform (capnography). Qualitative devices (eg, colorimetric detectors) report the range
in which the EtCO2 falls (eg, 0 to 10 mmHg or >35 mmHg) as opposed to a precise value
(eg, 38 mmHg).
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The colorimetric EtCO2 detector, which consists of a piece of specially treated litmus paper
that changes color when exposed to CO2 (purple for EtCO2 <3 mmHg; tan for 3 to 15
mmHg; and yellow for >15 mmHg). Its primary use is for verification of ETT placement.
Exhalation of CO2 from an ETT placed in the trachea will change the color of the litmus
paper from purple to yellow. An improperly placed ETT in the esophagus will not conduct
CO2 and no change will occur in the color of the litmus paper, which will remain purple.
When evaluating studies of EtCO2, it is essential to distinguish those involving qualitative
measurements (colorimetric) from those describing quantitative methods with a graphic
waveform display (capnography). (See "Confirmation of correct endotracheal tube
placement in adults".)
CO2 WAVEFORM
● Phase 1 (dead space ventilation, A-B) represents the beginning of exhalation where
the dead space is cleared from the upper airway and the CO2 concentration
approaches zero.
● Phase 2 (ascending phase, B-C) represents the rapid rise in carbon dioxide (CO2)
concentration in the breath stream as the CO2 from the alveoli reaches the upper
airway.
● Phase 3 (alveolar plateau, C-D) represents the CO2 concentration reaching a uniform
level in the entire breath stream from alveolus to nose. Point D, occurring at the end
of the alveolar plateau, represents the maximum CO2 concentration at the end of the
tidal breath and is appropriately named the end-tidal CO2 (EtCO2). This is the number
that appears on the monitor display.
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● Phase 4 (D-E) represents the inspiratory cycle where the CO2 falls back to zero.
A normal capnogram (ie, a valid breath), for patients of all ages, is characterized by a
set of specific elements: the CO2 concentration starts at zero and returns to zero, a
maximum CO2 concentration is reached with each breath (ie, EtCO2), the amplitude is
a function of the EtCO2 concentration, the width is a function of the expiratory
time, and there is a characteristic shape with normal lung function.
● Patients with normal lung function have characteristic trapezoidal capnograms and
narrow gradients between their alveolar CO2 (ie, EtCO2) and arterial CO2
concentration (PaCO2) of 0 to 5 mmHg ( figure 1). Gas in the physiologic dead
space accounts for this normal gradient.
● Patients with obstructive lung disease have impaired expiratory flow and uneven
emptying of alveoli due to ventilation-perfusion mismatch, and demonstrate a more
rounded ascending phase and an upward slope in the alveolar plateau ( figure 2).
In patients with abnormal lung function and ventilation-perfusion mismatch, the
EtCO2-PaCO2 gradient widens depending on the severity of the lung disease [4,5].
The EtCO2 in patients with lung disease is only useful for assessing trends in
ventilatory status over time; isolated EtCO2 values may or may not correlate with the
PaCO2.
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figure 3A-B).
The accuracy of EtCO2 for confirming ETT location can help clinicians faced with difficult
airway management decisions. As an example, in a case involving one of the authors, a
patient resuscitated following a submersion injury became difficult to ventilate and
hypotensive following RSI, but the presence of a waveform reassured clinicians about ETT
placement, allowing them to consider other reasons for decompensation. Decompression
of the patient’s distended stomach with an orogastric tube resolved the difficulties with
ventilation and blood pressure.
Monitoring ETT location during transport — UMI has catastrophic consequences and
can occur when an ETT is dislodged during patient transport. Continuous monitoring of
ETT location during transport prevents UMI. EtCO2 confirmation of initial ETT placement
and continuous capnographic monitoring of ETT location is an accepted standard of care
by the American Society of Anesthesiologists [6] and is recommended as the most reliable
method by other national organizations [7-9].
Effectiveness of CPR — In the 1980s, studies using animal models showed that EtCO2
levels reflect cardiac output during cardiopulmonary resuscitation (CPR) and can be used
as a noninvasive measure of cardiac output. A landmark study in 1988 demonstrated this
principle in humans [11]. During cardiac arrest, when alveolar ventilation and metabolism
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are essentially constant, EtCO2 reflects pulmonary blood flow. Therefore, EtCO2 can be
used as a gauge of the effectiveness of cardiac compressions. As effective CPR leads to a
higher cardiac output, EtCO2 will rise, reflecting the increase in perfusion.
The measurement of EtCO2 varies directly with the cardiac output produced by chest
compression and has been described in both EMS [12] and ICU patients [11]. Both of these
prospective, observational studies found an EtCO2 level <3 mmHg immediately after
cardiac arrest, with a higher level generated during cardiac compressions and a mean
peak >7.5 mmHg just before return of spontaneous circulation (ROSC) [11,12]. This peak in
EtCO2 level is the earliest sign of ROSC and may occur before return of a palpable pulse or
blood pressure. Another observational study of data collected during human CPR found a
positive correlation between the depth of chest compressions and EtCO2 (10 mm increase
in compression depth increased EtCO2 by 1.4 mmHg), as well as ventilation rate and EtCO2
(increase of 10 breaths/minute decreased ETCO2 by 3 mmHg), and confirmed that higher
EtCO2 values during CPR correlate with increased ROSC and survival [13].
American Heart Association (AHA) guidelines for cardiac resuscitation emphasize the
importance of continuing chest compressions without interruption until a perfusing
rhythm is reestablished. Experimental evidence indicates that interruptions in chest
compressions are followed by sustained periods of reduced blood flow, which only
gradually return to pre-interruption levels. Capnogram monitoring virtually eliminates the
need to stop chest compressions to check for pulses. Reestablishment of a perfusing
rhythm is accompanied immediately by a dramatic increase in EtCO2. Once this rise in
EtCO2 is noted, chest compressions can safely be stopped while cardiac rhythm and blood
pressure are assessed [9,14].
According to an observational study of 145 patients with out of hospital cardiac arrest
(OHCA), several seconds may be required after electrical conversion to a potentially
perfusing rhythm before effective mechanical contractions and a subsequent rise in EtCO2
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Specific EtCO2 levels have been shown to correlate with ROSC. In a systematic review of 17
observational studies including over 6100 adults with cardiac arrest, which included
metaanalyses of data from five studies, EtCO2 ≥10 to 20 mmHg during CPR was strongly
associated with ROSC while persistent EtCO2 below 10 mmHg after 20 minutes of CPR had
a 0.5 percent likelihood of ROSC [16]. Subsequent retrospective studies support this
general finding [17,18]. A retrospective, observational study of 526 OHCA patients with a
nonshockable rhythm found that the first ETCO2 measured after placement of an airway
device predicted ROSC and survival after hospital admission [17]. Specifically, patients with
an ETCO2 >45 mmHg had an increased probability of sustained ROSC and 30-day survival.
A retrospective study of 324 OHCA patients found that higher EtCO2 levels were associated
with higher rates of successful defibrillation [18].
Cause of cardiac arrest — EtCO2 may also be helpful in determining the etiology of
cardiac arrest. Two animal studies reported higher EtCO2 levels at the onset of cardiac
arrest caused by primary asphyxia than arrest caused by ventricular fibrillation [27,28].
Researchers found results consistent with these animal experiments in a prospective,
observational study of prehospital victims of cardiac arrest. Patients in the asphyxia group
(initial rhythm of asystole or pulseless electrical activity associated with conditions such as
airway foreign body, aspiration, asthma, or drowning) had higher EtCO2 levels compared
with patients in the ventricular tachycardia/fibrillation group (initial rhythm of ventricular
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Increased ICP and trauma prognosis — EtCO2 monitoring can help clinicians avoid
inadvertent hyperventilation of patients with traumatic brain injury and suspected
increased intracranial pressure (ICP). It may also help determine the prognosis of trauma
victims.
Arterial CO2 tension affects blood flow to the brain. High CO2 levels result in cerebral
vasodilation, while low CO2 levels result in cerebral vasoconstriction. Sustained
hypoventilation (defined as PaCO2 levels ≥50 mmHg) results in increased cerebral blood
flow and increased ICP, which can harm head-injured patients. Sustained hyperventilation
(defined as PaCO2 ≤30 mmHg) is also detrimental and is associated with worse neurologic
outcome in severely brain-injured patients. Consequently, ventilation rates to achieve
eucapnia are recommended by the brain trauma foundation [30].
Studies have found that a low EtCO2 in trauma patients is associated with mortality and
hemorrhagic shock:
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Assessing airway, breathing, and circulation — The airway, breathing, and circulation
(ABCs) of patients can be rapidly assessed using the capnography waveform and end-tidal
carbon dioxide (EtCO2) values [38]. The presence of a normal waveform denotes a patent
airway and spontaneous breathing [39]. Normal EtCO2 levels (35 to 45 mmHg) signify
adequate ventilation and perfusion [11,40]. Capnography can be used to assess
unresponsive patients ranging from those who are actively seizing to victims of chemical
terrorism ( table 1) [41]. Unlike pulse oximetry, capnography does not misinterpret
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motion artifact and provides reliable readings in low perfusion states. Studies have found
that an EtCO2 ≤29.5 mmHg was independently predictive of the need for massive
transfusion [36,42].
Seizure — Capnography is the only monitoring modality that is accurate and reliable in
actively seizing patients because the capnogram is determined entirely by respiratory
activity and is not confounded by muscle activity or movement artifact. Capnographic data
(respiratory rate, EtCO2, and capnogram) can be used to distinguish among:
● Seizing patients with apnea (flatline waveform, no EtCO2 reading, and no chest wall
movement)
● Seizing patients with ineffective ventilation (small waveforms, low EtCO2 values), and
● Seizing patients with effective ventilation (normal CO2 waveform, normal EtCO2
values). (See "Convulsive status epilepticus in adults: Classification, clinical features,
and diagnosis" and "Convulsive status epilepticus in adults: Management".)
By measuring EtCO2 and respiratory rate with each breath, capnography provides
instantaneous feedback on the clinical status of the patient. Respiratory rate is measured
directly from the airway (nose and mouth) with oral or nasal cannula, providing a more
reliable reading than impedance respiratory monitoring. In upper airway obstruction and
laryngospasm, impedance monitoring detects chest wall movement, interprets this as a
valid breath, and displays a respiratory rate, even though the patient is not ventilating. In
contrast, capnography detects no ventilation and shows a flatline waveform.
Clinicians can rapidly assess EtCO2 trends. A patient with a respiratory rate of 30 will
generate 150 EtCO2 readings in five minutes. This provides sufficient information to
determine whether the patient's ventilation is worsening despite treatment (increasing
EtCO2), stabilizing (stable EtCO2), or improving (decreasing EtCO2). As an example,
increasing EtCO2 would reflect the worsening ventilation of an acutely tachypneic patient
with obstructive lung disease who is developing respiratory muscle fatigue or a more
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Common capnographic findings during PSA include the following and are summarized in
the figures ( figure 3A and figure 3B):
● Flatline waveform – This can occur from monitor calibration (will indicate
"calibrating" on the monitor), cannula occlusion (will indicate "occlusion" on the
monitor), or apnea (central or obstructive). The combination of absent chest wall
movement and a flatline waveform differentiates central apnea from obstructive
apnea (upper airway obstruction or laryngospasm), which manifests chest wall
movement. Response to airway alignment maneuvers (eg, chin lift, jaw thrust) can
distinguish upper airway obstruction from laryngospasm.
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reflects increasing EtCO2. An EtCO2 >70 mmHg in a patient without COPD indicates
respiratory failure.
● Decreasing waveform height – This occurs with hypopneic hypoventilation (ie, low
tidal volume breathing) and reflects decreasing EtCO2.
● Waveform does not return to zero – An off-baseline waveform can occur with
rebreathing.
By increasing minute ventilation, these patients are able to lower arterial CO2 tension to
help correct their underlying acidemia. The more acidotic the patient, the lower the HCO3,
the higher the respiratory rate, and the lower the EtCO2. Capnography can be used as an
indicator of metabolic acidosis in these patients. In addition, EtCO2 can be used to
distinguish diabetics in ketoacidosis (metabolic acidosis, compensatory tachypnea, and
low EtCO2) from those who are not (nonacidotic, normal respiratory rate, and normal
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EtCO2) [53,54]. (See "Approach to the adult with metabolic acidosis" and "Approach to the
child with metabolic acidosis".)
Prognosis in sepsis — There is an inverse relationship between EtCO2 and lactate levels in
sepsis, severe sepsis, and septic shock. EtCO2 performs similarly to lactate as a predictor
for mortality in patients with suspected sepsis [55,56]. In a prospective study of 183
patients performed in the prehospital setting, patients with suspected sepsis and an
EtCO2 value ≤25 mmHg were more frequently diagnosed with sepsis (78 versus 43
percent) and severe sepsis (47 versus 7 percent), and had higher mortality (11 versus 5
percent) [57]. The use of EtCO2 to predict mortality, sepsis, and severe sepsis in
prehospital patients outperformed another well-accepted screening tool, the quick
sequential organ failure assessment score (qSOFA) [58]. Patients with severely
compromised respiratory reserve who cannot appropriately compensate for the lactic
acidosis resulting from severe sepsis or septic shock have the worst prognosis despite
ETCO2 values that are not low. (See "Evaluation and management of suspected sepsis and
septic shock in adults".)
LIMITATIONS
In high-flow CO2 systems, when the tidal volume of the patient drops below the flow rate
of the system, the monitor will entrain room air to compensate, falsely diluting the EtCO2
reading and slurring the ascending phase of the waveform. For this and other reasons,
low flow systems are preferred. (See 'Principles of operation' above.)
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● CO2 waveform – The capnogram consists of four phases: dead space ventilation,
ascending phase, alveolar plateau, and descending inspiratory phase, which are
depicted in the figure ( figure 1). (See 'CO2 Waveform' above.)
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EtCO2 reflects pulmonary blood flow and can be used as a gauge of the effectiveness
of cardiac compressions. As effective CPR leads to a higher cardiac output, EtCO2 will
rise. (See 'Effectiveness of CPR' above.)
ACKNOWLEDGMENT
The editorial staff at UpToDate acknowledge Salvatore Silvestri, MD, who contributed to an
earlier version of this topic review.
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42. Stone ME Jr, Kalata S, Liveris A, et al. End-tidal CO2 on admission is associated with
hemorrhagic shock and predicts the need for massive transfusion as defined by the
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GRAPHICS
Reproduced with permission from: Krauss B, Deykin A, Lam A, et al. Capnogram shape in obstructive lung disease. Anesth
Analg 2005; 100:884. Copyright © 2005 Lippincott Williams & Wilkins.
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The photo shows a child being monitored with capnography: 29 is the end tidal CO2. The
capnographic waveform appears in the screen adjacent to the number. The nasal prongs and the
bladder that extends from the front of the mouth detect exhaled CO2.
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Examples of capnograms collected over one respiratory cycle from a normal subject, a COPD
patient, and a CHF patient. The evident variations in morphology suggest that the waveforms can
be used for diagnostic purposes.
CO2: carbon dioxide; PetCO2: end tidal carbon dioxide; COPD: chronic obstructive pulmonary
disease; CHF: congestive heart failure.
Reprinted with permission from: Abid A, Mieloszyk RJ, Verghese GC, et al. Model-Based Estimation of Respiratory
Parameters from Capnography, With Application to Diagnosing Obstructive Lung Disease. IEEE Trans Biomed Eng 2017;
64:2957. Copyright © 2017 IEEE.
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Reproduced with permission from: Krauss, B, Hess, DR. Capnography for Procedural Sedation and Analgesia in the
Emergency Department. Annals of Emergency Medicine 2007; 50:172. Copyright © 2007 The American College of
Emergency Physicians.
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Reproduced with permission from: Krauss, B, Hess, DR. Capnography for Procedural Sedation and Analgesia in the
Emergency Department. Annals of Emergency Medicine 2007; 50:172. Copyright © 2007 The American College of
Emergency Physicians.
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VX Direct measure of
ventilatory status
Ricin
Earliest indicator of
respiratory compromise
Non-invasive
identification of metabolic
acidosis
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(Mace) bronchospasm
Reproduced with permission from: Krauss B. Capnography as a rapid assessment and triage tool for chemical
terrorism. Pediatr Emerg Care 2005; 21:493. Copyright © 2005 Lippincott Williams & Wilkins.
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Contributor Disclosures
Baruch Krauss, MD, EdM, FAAP No relevant financial relationship(s) with ineligible companies to
disclose. Jay L Falk, MD No relevant financial relationship(s) with ineligible companies to
disclose. Jay G Ladde, MD, FACEP, FAAEM No relevant financial relationship(s) with ineligible
companies to disclose. Ron M Walls, MD, FRCPC, FAAEM Other Financial Interest: Airway
Management Education Center [Health care provider education and resources]; First Airway [Health
care provider education and resources]. All of the relevant financial relationships listed have been
mitigated. Susan B Torrey, MD No relevant financial relationship(s) with ineligible companies to
disclose. Michael Ganetsky, MD No relevant financial relationship(s) with ineligible companies to
disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found,
these are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.
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