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All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2023. | This topic last updated: Nov 21, 2022.
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 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
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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).
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
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"Rapid sequence intubation for adults outside the operating room", section on 'Placement with
proof'.)
Capnography uses infrared (IR) radiation to make measurements. Molecules of CO2 absorb IR
radiation at a very specific wavelength (4.26 µm), with the amount of radiation absorbed having
a nearly exponential relation to the CO2 concentration present in the breath sample. Detecting
these changes in IR radiation levels, using appropriate photo-detectors sensitive in this spectral
region, allows for the calculation of the CO2 concentration in the gas sample.
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.
● 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
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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.
Following intubation, the presence of a waveform with all four phases ( figure 1) indicates the
ETT is through the vocal cords. A normal waveform can occur when the tube has been placed in
the right mainstem bronchus. In addition, a waveform resembling tracheal placement may be
present for a few breaths with an ETT placed in the hypopharynx just above the vocal cords, but
over time these waveforms are likely to become erratic due to movement of the ETT, suggesting
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that the ETT is not properly placed. A flatline waveform generally indicates esophageal
placement but can occur, albeit uncommonly, in several other situations, including:
● ETT obstruction
● Prolonged cardiac arrest with diffuse cellular death (in which no CO2 is produced because
of an absence of cellular respiration and CO2 exchange in the pulmonary bed is severely
compromised).
Nevertheless, a four phase capnogram may be present upon initial intubation in cardiac
arrest patients, indicating that the tube is correctly positioned in the trachea. In this
situation, tube placement should be verified if a flatline tracing subsequently develops
[19,20].
The accuracy of EtCO2 to confirm tracheal location of an ETT varies with the technology used
and the condition of the patient. For patients who are not in cardiac arrest, studies of qualitative
colorimetric EtCO2 and quantitative capnography have demonstrated 100 percent sensitivity
and 100 percent specificity for tracheal placement [21-26]. In contrast, clinical assessment using
physical signs is unreliable for determining ETT location. Fogging or condensation of the tube
occurs in 83 percent of esophageal intubations [27], and chest wall movement can be produced
by tracheal or esophageal tubes [28]. Anesthesiologists, under ideal operating room conditions,
using breath sounds as the sole means of verification, incorrectly identify ETT location in 16
percent of cases [29].
Although the accuracy of EtCO2 for verifying ETT placement in patients with spontaneous
circulation approaches 100 percent, sensitivities for tracheal placement vary greatly in cardiac
arrest patients, ranging from 62 to 100 percent, depending on the modality used and the
duration of the arrest [4,5,10,23,24,27-30]. In patients with low perfusion states and cadavers,
studies using quantitative modalities (ie, capnography) for determining tracheal location of the
ETT have shown 100 percent sensitivity [19,31-33]. Studies using qualitative (ie, colorimetric)
EtCO2 methods have shown variable sensitivity, because the exhaled CO2 concentration can fall
below the detection threshold [10,23,24,29].
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the small number of esophageal intubations in studies assessing the accuracy of capnography
for determining ETT placement in cardiac arrest patients limits the strength of these studies.
Capnography's true specificity for detecting esophageal intubation in cardiac arrest patients is
not certain.
When a capnogram is present in an intubated patient in cardiac arrest, the ETT can be assumed
to be within the trachea [33-35]. An absent (flatline) waveform may indicate esophageal or
placement above the trachea. Early in cardiac arrest, and when the patient is receiving effective
CPR, complete failure of CO2 exchange is unlikely, and the clinician should assume esophageal
intubation exists if a waveform is absent. In patients with prolonged cardiac arrest and an
absent waveform, the clinician should also assume an esophageal intubation exists. Physical
examination criteria, such as repeat laryngoscopy and auscultation of the lungs and
epigastrium, may be used, but the clinician must be aware of their limitations in discriminating
between esophageal and tracheal intubation. Algorithms for ETT verification are provided
( algorithm 1A-B). (See "Direct laryngoscopy and endotracheal intubation in adults", section
on 'Confirming proper tracheal tube placement'.)
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 [36] and is recommended as the most reliable method by
other national organizations [37-39].
A prospective, observational study of 153 prehospital intubations found a 23 percent UMI rate
among patients without continuous EtCO2 monitoring, while patients with continuously
monitored EtCO2 sustained the desired 0 percent UMI rate [18]. The attached figures depict one
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airway confirmation algorithm using colorimetric CO2 detectors and another using
capnography. They can be used for both prehospital and in-hospital intubated patients
( algorithm 1A-B).
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 [40]. During cardiac arrest, when alveolar ventilation and metabolism 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 [41] and ICU patients [40]. 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) [40,41]. 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 [42].
Return of spontaneous circulation — During cardiac arrest, EtCO2 is the earliest indicator of
the return of spontaneous circulation (ROSC) [40,41]. When the heart restarts, the dramatic
increase in cardiac output, and resulting increase in perfusion, leads to a rapid increase in EtCO2
as the CO2 that has accumulated during cardiac arrest is effectively transported to the lungs
and exhaled. This process manifests as a sudden rise in EtCO2. (See 'Effectiveness of CPR'
above.)
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
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compressions can safely be stopped while cardiac rhythm and blood pressure are assessed
[39,43].
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 occur [44]. Accordingly,
stopping compressions in response to a rhythm change in order to check for a pulse may result
in degradation of the rhythm, as coronary perfusion had not yet been restored. EtCO2 is a more
reliable harbinger of reperfusion than a pulse check. (See "Adult basic life support (BLS) for
health care providers".)
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 [45]. Subsequent retrospective studies support this general finding
[46,47]. 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 [46]. 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 [47].
Confounding factors in resuscitation — Drugs used in resuscitation may affect EtCO2 values.
EtCO2 often decreases rapidly moments after administration of epinephrine. Sodium
bicarbonate may produce a transient increase in EtCO2, but the rise in EtCO2 levels after ROSC is
greater and longer lasting than after a sodium bicarbonate bolus [48].
Prognosis in cardiac arrest — In several prospective, observational studies, EtCO2 levels of ≤10
mmHg measured 20 minutes after the initiation of advanced cardiac life support accurately
predicted death in adult patients with cardiac arrest [49-52]. The prognostic value of measuring
EtCO2 has been demonstrated in animal [53] and human studies [49-52,54].
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 [55,56]. 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,
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asthma, or drowning) had higher EtCO2 levels compared with patients in the ventricular
tachycardia/fibrillation group (initial rhythm of ventricular tachycardia/fibrillation associated
with acute myocardial infarction) [57]. These between group differences disappear within
minutes if return of spontaneous circulation has not occurred.
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 [58].
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 [66]. The presence of a normal waveform denotes a patent airway and
spontaneous breathing [67]. Normal EtCO2 levels (35 to 45 mmHg) signify adequate ventilation
and perfusion [40,68]. Capnography can be used to assess unresponsive patients ranging from
those who are actively seizing to victims of chemical terrorism ( table 1) [69]. Unlike pulse
oximetry, capnography does not misinterpret 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 [64,70].
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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 severe lower airway obstruction.
Respiratory depression caused by oversedation will manifest an abnormally high or low EtCO2
before pulse oximetry detects a falling oxyhemoglobin saturation, especially in patients
receiving supplemental oxygen. In one trial, the median time between the onset of respiratory
depression, as determined by EtCO2, and hypoxia was 60 seconds (range 5 to 240 seconds) [74].
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); assessment is summarized in the algorithm ( algorithm 2). 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.
● Increasing waveform height – This occurs with bradypneic hypoventilation and 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.
● Increasing waveform width – This occurs with hypoventilation and increasing expiratory
time.
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● 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 EtCO2) [81,82]. (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 [83,84]. 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) [85]. 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) [86]. (See
"Evaluation and management of suspected sepsis and septic shock in adults".)
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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.)
● 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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Following intubation, the presence of a waveform with all four phases ( figure 1) is a
highly accurate indication that the ETT is placed in the trachea, including upon initial
intubation in cardiac arrest patients. A flatline waveform generally indicates esophageal
placement but can occur with: ETT obstruction, complete airway obstruction distal to the
ETT (eg, foreign body), technical malfunction of the monitor or tubing, and prolonged
cardiac arrest. When the amplitude of the tracing is very small or CO2 is not detectable by
waveform or qualitative EtCO2 detection, clinicians should assume an esophageal
intubation exists ( algorithm 1A-B). (See 'Verification of ETT placement' above.)
● Assessing return of spontaneous circulation – EtCO2 is also the earliest indicator of the
return of spontaneous circulation. When the heart restarts, the dramatic increase in
cardiac output, and resulting increase in perfusion, leads to a rapid increase in EtCO2. (See
'Return of spontaneous circulation' above.)
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ACKNOWLEDGMENT
The editorial staff at UpToDate acknowledge Salvatore Silvestri, MD, now deceased, who
contributed to an earlier version of this topic review.
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Topic 273 Version 25.0
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GRAPHICS
C - D: Alveolar Plateau
D: End-tidal CO2
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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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Ricin
Earliest indicator of
respiratory compromise
Non-invasive identification of
metabolic acidosis
Rapid identification of
Lacrimators
bronchospasm
(Mace)
Earliest indicator of
Capsaicin respiratory compromise
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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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