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Capnography
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Marzeih Khezri
Qazvin University of Medical Sciences
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• Describe capnography
• Summarize normal respiratory physiology
• Review the differences between oxygenation and ventilation
• Identify basic capnography waveforms
• Applications of capnography
Introduction:
The primary goal of anesthesiologists is to prevent hypoxia, and capnography helps to identify
situations that can lead to hypoxia if uncorrected. Moreover, it also helps in the swift differential
diagnosis of hypoxia before hypoxia can lead to irreversible brain damage.
capnography constitutes an important non-invasive technique that can monitor C02 production,
pulmonary perfusion and alveolar ventilation as well as respiratory patterns. The measurement of
C02 in the expired air directly indicates changes in the elimination of C02 from the lungs.
Indirectly, it indicates changes in the production of C02 at the tissue level and in the delivery of
C02 to thhe lungs by th
he circulatorry system.
Capnograaphs usually y work on thee principle thhat CO2 absoorbs infra-reed radiation. A beam of
infra-red light is passsed across thhe gas samplle to fall on a sensor. Thee presence of
o CO2 in thee gas
leads to a reduction in
i the amounnt of light fallling on the sensor, whicch changes thhe voltage inn a
circuit. The
T analysis is rapid and accurate, buut the presennce of nitrouss oxide in thhe gas mix
changes the
t infra-red d absorption via the phennomenon of collision brooadening.1 Click
C here to shhow
Animaation
Applications of capnography:
Endotracheal intubation
When CO2 is absent as measured by above devices, it means either the endotracheal tube
is in a wrong position (esophageal) or there is an absent/ decreased presentation of CO2 to
the lungs as in a cardiac arrest. When cardiac output increases (e.g. After resuscitation),
PEtCO2 provides information about adequacy of ventilation and circulation. 2
patients.
Paramedics can attach the capnography filter to the ET tube prior to intubation and, in
cases where it is difficult to visualize the cords, use the monitor to assist placement. This
includes cases of nasal tracheal intubation.
Paramedics should document their use of continuous ETCO2 monitoring and attach wave
form strips to their PCRs. Print a strip on intubation, periodically during care and
transport, and then just prior to moving the patient from your stretcher to the hospital
table and then immediately after transfer. This will timestamp and document your tube as
good. Capnography can also be used for combitubes and LMAs.
Role in CPR:
White R.D. et al .3 used EtCO2 measurement in out-of hospital cardiac arrest. They concluded
that capnography can detect the presence of pulmonary blood flow even in the absence of major
pulses (pseudo-electromechanical dissociation- EMD) and also can rapidly indicate changes in
pulmonarry blood flow
w (cardiac output) causeed be alteratiions in cardiiac rhythm.
Studies in
i animals an nd humans demonstrated
d d that PEtCOO2 decreasess when a largge dose of
6
epinephrine was used d during CPR R. This deccrease in EtCCO2 has beenn attributed tot increase inn
shunt fraaction and alsso due to droop in cardiacc output secoondary to inccreased afterrload by
epinephrine .6 The du uration of deecrease in EttCO2 has nott been quantiified, but cliinically can be
b
7
useful for timing subbsequent epinnephrine dossing . PEtCO O2 can be ussed as a feeddback to optiimize
8
chest commpressions during
d CPR. Monitorinng PEtCO2 during d cardiaac arrest mayy detect
unrecognnized CPR prrovider fatiggue.
End Tid
dal CO2 As
A Predicttor of Resu
uscitation Outcome
End tidall CO2 monito oring can coonfirm the fuutility of resuuscitation as well as foreecast the
likelihood of resuscittation.
Caution: While a low initial ETCO2 makes resuscitation less likely than a higher initial
ETCO2, patients have been successfully resuscitated with an initial ETCO2 >10 mmHg
Other applications:
• ETCO2 waveform analysis can give information of leaks in breathing circuit, airway
obstruction (asthma, COPD).
• Diagnosis of Pulmonary embolism.
• Estimation of PaCO2 in mechanically ventilated patients: End-tidal PCO2 can be used to
estimate arterial PaCO2 in patients with healthy lungs.
• Indirectly measures metabolism and circulation
• Provides an immediate picture of patient condition of ventilation
• Perfusion Warning Sign
V/Q Mismatch
Time Caapnographs
The mostt commonly used type of capnograph plots PCO2 versus timee. The tracinng is traditionnally
divided into an inspirratory phasee and three (ssometimes foour) expiratoory phases:
Cllick here to sh
how animation
A terminal upswing at the end of phase 3, known as phase 4, can occur in pregnant subjects,
obese subjects and low compliance states.
It is therefore not surprising that studies under anesthesia have found the PETCO2-PaCO2 gradient
to be slightly elevated at 5 to 10 mm Hg.13 An extreme example of acutely increased alveolar
dead space is pulmonary embolism. Thus, an abruptly decreased PETCO2 with ventilation held
constant is often indicative of a sudden decrease in cardiac output or pulmonary embolism. Other
common causes of a widened gradient include obstructive lung disease, smoking, and advanced
age. High mixed venous CO2 tension and malignant hyperthermia have also been reported to
cause a negative PaCO2-PETCO2 gradient.14 In such cases, PETCO2 is clearly not an accurate
estimate of PaCO2, and the average alveolar PCO2 obtained from a volume capnograph may be
more indicative of PaCO2.15
volume capnograph
A volume capnograph is obtained by plotting expired PCO2 versus exhaled gas volume, usually
obtained with a spirometer or pneumotachometer. There is no inspiratory phase in a volume
capnograph, and the curve is divided into three expiratory phases.
Capnography has been used to titrate positive end-expiratory pressure (PEEP) settings inasmuch
as narrowing of the PaCO2-PETCO2 gradient suggests reduced alveolar dead space and shunt
fraction as a result of alveolar recruitment and improved V/Q matching. These changes are
often subtle or absent on a time capnograph and may be detectable only with volume
capnography.16 It has been suggested that an incompetent inspiratory valve and rebreathing
during mechanical ventilation may require volume capnography to be detected reliably.17 The
technique may also be better than time capnography for the diagnosis of pulmonary embolism.18
Volume capnograph: single-breath CO2 (SBCO2) curve. The horizontal axis of the graph represents expiratory/inspiratory tidal
volume and is generally divided into three areas: I, the anatomic dead space volume (VDSanat): II, the transitional phase II volume;
and III, the phase III alveolar volume. The sum of these values is the tidal volume. The vertical axis represents the concentration
of CO2. PCO2, partial pressure of carbon dioxide. (From Pilbeam SP, Cairo JM: Mechanical Ventilation: Physiological and
Clinical Applications, 4th ed. St. Louis, Elsevier, 2006.)
Volume capnograph: graph of the percentage of carbon dioxide (%CO2) (y axis) and volume (x axis). A horizontal line drawn at
the top of the curve represents %CO2 in arterial blood. Three distinct regions are established. Area X represents the actual CO2
exhaled in one breath (assuming that no CO2 is rebreathed), area Y is the amount of CO2 that is not eliminated because of
alveolar dead space, and area Z is the amount of CO2 not eliminated because of anatomic dead space. The ratios of these areas are
the same as in the relationship seen in the Bohr equation: (PaCO2 - PECO2)/PaCO2 = (Y + Z)/(X + Y + Z). PECO2, mixed expired
PCO2; VA, alveolar volume; VDS, dead space volume.
ETCO2 35-45 mm Hg is the normal value for capnography. However, some experts say
30 mm HG - 43 mm Hg can be considered normal.
Hyperventilation
When a person hyperventilates, their CO2 goes down.Hyperventilation can be caused by
many factors from anxiety to bronchospasm to pulmonary embolus. Other reasons C02
may be low: cardiac arrest, decreased cardiac output, hypotension, cold, severe
pulmonary edema.
Hypoventilation
When a person hypoventilates, their CO2 goes up.Hypoventilation can be caused by
altered mental status such as overdose, sedation, intoxication, postictal states, head
trauma, or stroke, or by a tiring CHF patient. Other reasons CO2 may be high: Increased
cardiac output with increased breathing, fever, sepsis, pain, severe difficulty breathing,
depressed respirations, chronic hypercapnia.
Multiple studies have confirmed the sloping shape correlates to bronchospasm and
obstructive lung disease.
Successful treatment will lessen or eliminate the shark fin shape and return the ETCO2 to
normal range.
Hypoxic Drive
Capnography will show the hypoxic drive in COPD "retainers." ETCO2 readings will steadily
rise, alerting you to cut back on the oxygen before the patient becomes obtunded. Since it has
been estimated that only 5% of COPDers have a hypoxic drive, monitoring capnography will
also allow you to maintain sufficient oxygen levels in the majority of tachypneic COPDers
without worry that they will hypoventilate.
It has been suggested that in wheezing patients with CHF (because the alveoli are still, for the
most part, emptying equally), the wave form should be upright. This can help assist your clinical
judgement when attempting to differentiate between obstructive airway wheezing such as COPD
and the "cardiac asthma" of CHF.
Capnography can help paramedics avoid hyperventilation in intubated head injured patients.
In a study of 291 intubated head injured patients, 144 had ETCO2 monitoring. Patients with
ETCO2 monitoring had lower incidence of inadvertant severe hyperventilation (5.6%) than those
without ETCO2 monitoring (13.4%). Patients in both groups with severe hyperventilation had
significantly higher mortality (56%) than those without (30%). 20A target value of 35 mmHg is
recommended.
End tidal CO2 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.
In the study cited below, 5 pigs had hemorrhagic shock induced by bleeding, 5 pigs had septic
shock induced by infusion of e-coli, and 6 pigs had cardiogenic shock induced by repeated
episodes of v-fib. The pigs' cardiac output was continuously measured as well as their PETCO2.
“Cardiac output and PEtCO2 were highly related in diverse experimental models of circulatory
shock in which cardiac output was reduced by >40 % of baseline values. Measurement of PEtC02
is a noninvasive alternative for continuous assessment of cardiac output during low flow
circulatory shock states of diverse causes.21
A patient with low cardiac output caused by cardiogenic shock or hypovolemia resulting from
hemorrhage won’t carry as much CO2 per minute back to the lungs to be exhaled. This patient’s
ETC02 will be reduced. It doesn’t necessarily mean the patient is hyperventilating or that their
arterial CO2 level will be reduced. Reduced perfusion to the lungs alone causes this phenomenon.
The patient’s lung function may be perfectly normal.22
9. Other Issues:
Diabetic Ketoacidosis
Patients with DKA hyperventilate to lessen their acidosis. The hyperventilation causes their
PaC02 to go down.
“End-tidal C02 is linearly related to HC03 and is significantly lower in children with DKA. If
confirmed by larger trials, cut-points of 29 torr and 36 torr, in conjunction with clinical
assessment, may help discriminate between patients with and without DKA, respectively. 23
Pulmonary Embolus
Pulmonary embolus will cause an increase in the dead space in the lungs decreasing the alveoli
available to offload carbon dioxide. The ETCO2 will go down.
Hyperthermia
Metabolism is on overdrive in fever, which may cause ETCO2 to rise. Observing this
phenomena can be live-saving in patients with malignant hyperthermia, a rare side effect of RSI
(Rapid Sequence Induction).
Trauma
A 2004 study of blunt trauma patients requiring RSI showed that only 5 percent of patients with
ETCO2 below 26.25 mm Hg after 20 minutes survived to discharge. The median ETCO2 for
survivors was 30.75.24
“Capnography can serve as an effective, rapid assessment and triage tool for critically injured
patients and victims of chemical exposure. It provides the ABCs in less than 15 seconds and
identifies the common complications of chemical terrorism. 25
Anxiety
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.
Anaphylaxis
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.
Unrecognized exhaustion of CO2 absorber resulted in substantial rebreathing and rising ETCO2
values. The closed circuit without functioning absorber mimicked Mapleson D circuit
Contamination of capnometer results in the sudden elevation of base line as well as ETCO2
values
Curare cleft(when a neuromuscular blockade wears off, The patients tackes small spontaneous
respirations in the paralyzed patient).
Resembling curare cleft due to an artifact created by surgeon leaning on the chest, or pushing
against the diaphragm during expiration. Partial disconnect of main stream capnometer.
Dilution of expiratory gases by the forward flow of fresh gases during the later part of expiration
when expiratory flow rate decreases below the forward gas flow rate
Elevation of base line- A classic representation of rebreathing.
Occasionally, there can be a reverse phase 3 slope seen in patients with emphysema. Most like
this may be due to destruction of alveolar capillary system in emphysematous lungs resulting in
the delivery of carbon dioxide to expired gases.
Endobronchial intubation may not result in a characteristic waveform. However, occasionally, it
may be like the one seen in COPD or the above.
A gradual decrease in end tidal carbon dioxide can occur during reduced metabolism,
hypothermia, hyperventilation, small tidal volume ventilation due to inadequate alveolar
sampling, and leaks in the sampling system, decrease in cardiac output .
Sampling problems such air or oxygen dilution during nasal or mask sampling of carbon dioxide
in spontaneously breathing patients.
Expiratory valve malfunction can result in prolonged abnormal phase 2 and phase 0.
References:
1.Daniel B. Raemer and Ignatius Calalang (1991), Journal of Clinical Monitoring and
Computing Volume 7, Number 2, 195-208.
14. Kwetny I, Finucane BT: Negative arterial to end-tidal carbon dioxide gradient: An
additional sign of malignant hyperthermia during desflurane anesthesia. Anesth
Analg 2006; 102:815-817.
15. Breen PH, Mazumdar B, Skinner SC: Comparison of end-tidal Pco2 and average
alveolar expired Pco2 during positive end-expiratory pressure. Anesth
Analg 1996; 82:368-373.
16. Rich GF, Sconzo JM: Continuous end-tidal CO2 sampling within the proximal
endotracheal tube estimates arterial CO2 tension in infants. Can J
Anaesth 1991; 38:201-203.
18. Sanders AB: Capnometry in emergency medicine. Ann Emerg Med 1989; 18:1287-
1290.
20. Davis, The Use of Quantitative End-Tidal Capnometry to Avoid Inadvertant Severe
Hyperventilation in Patients with Head Injury After Paramedic Rapid Sequence
Intubation, Journal of Trauma, April 2004
21. Xiahua, End-tidal carbon dioxide as a noninvasive indicator of cardiac index during
circulatory shock, Critical Care Medicine, 2000, Vol 28, No 7.
23. Fearon. End-tidal carbon dioxide predicts the presence and severity of acidosis in
children with diabetes, Academic Emergency Medicine, December 2002.
24. Deakin CD, Sado DM, Coats TJ, Davies G. Prehospital end-tidal carbon dioxide
concentration and outcome in major trauma.” Journal of Trauma. 2004; 57:65-68.
25. Krauss, Heightman. 15 Second Triage Tool, JEMS, September 2006.