Capnography Explained

Capnography Explained
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Capnography Simplified
Capnography
by rjjaramillo
This is a repost from Jeremy Jaramillos Blog . Its a nice
resource. Do visit it at rjjaramillo.wordpress.com
Capnography (end-tidal CO2 monitoring) is a non-invasive measurement of
carbon dioxide in exhaled air to assess a patients ventilatory status. It may also
be referred to as partial pressure end tidal carbon dioxide monitoring (PETCO2).
The end-tidal CO2 (EtCO2) level is a reection of global CO2 production in the
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body. Cardiac function, pulmonary function, and metabolic rate all inuence the
amounts of CO2 produced. The end-tidal CO2 provides information on systemic
CO2 production (from exhaled alveolar gas), pathologic dead space, pulmonary
blood ow, and conrmation of endotracheal tube placement. Capnography
allows trending of CO2 levels using fewer arterial blood gas analyses, but does
not completely replace arterial blood gas analysis. Age, smoking, general
anesthesia, and systemic diseases can increase the dierence between the CO2
value obtained from non-invasive monitoring and arterial blood gas monitoring.
Note that capnography measures ventilation, not oxygenation.
Comparison of Capnography and Pulse
Oximetry
Capnography
Pulse Oximetry
Measures CO2
Measures oxygen saturation
Reects ventilation
Reects oxygenation
Hypoventilation / apnea detected

immediately
Changes lag with hypoventilation /

apnea
Should be used with pulse oximeter
Should be used with capnography
CLINICAL APPLICATION
Maintenance of a patients airway is always a primary patient care objective. If the
airway
patency is lost, no other treatment modalities can prevent death.
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Denitions:
1. Alveolar Dead Space: When gas exchange doesnt occur because air is
present, but no blood is available to exchange gas. Or there is blood but no
air. It could also be because the exchange surface is compromised by
pulmonary edema, pulmonary eusion, or swollen membranes
2. Alveolar volume (Va) Air that is available for gas exchange, which is
typically about 350 cc (Vt Vd = Va); Anything that aects the tidal volume
only aects the alveolar volume.
3. Anatomical Dead Space (Vd) Air not available for gas Exchange, which is
typically about 150 cc
4. Bradypnea slower than normal rate (<10 breaths/min), with normal depth
and regular rhythm. Associated with ICP, brain injury, and drug overdose.
5. Capnogram the wave form.
6. Capnography the measurement of carbon dioxide (CO2) in exhaled breath.
7. Capnometer the numeric measurement of CO2.
8. Dyspnea air hunger, dicult or labored breathing, shortness of breath
9. End Tidal CO2 (ETCO2 or PetCO2) the level of (partial pressure of) carbon
dioxide released at end of expiration. Normal values range between 35 and
45 mmHg
10. Hyperventilation Increased rate and depth of breathing that results in
decreased PaCO2 level. Fast breathing (tachypnea) doesnt necessarily
increase tidal volume, which can be caused by anxiety, head injuries,
diabetic emergencies, PE, AMI, and others
11. Hypoventilation Shallow, irregular breathing. Slow breathing (bradypnea)
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does not necessarily decrease tidal volume. Causes include CNS disorders,
narcotic use and others.
12. PACO2 Partial pressure of CO2 in the alveoli.
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13. PaCO2 Partial pressure of CO2 in arterial blood.
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14. PCO2 Partial pressure of CO2 in the blood

15. PETCO2 Partial pressure of CO2 at the end of expiration. ~ 38 mm Hg
(usually 1 6 mm Hg less than PaCO2)
16. (a-ET)PCO2 Arterial to end-tidal CO2 tension/pressure dierence or
gradient.
17. PvCO2 Partial pressure of CO2 in mixed venous blood.
18. Physiologic Dead Space is the alveolar gas that does not equilibrate fully
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with capillary blood. In normal subjects,
dead space
ventilationObstetric
(VD)
accounts for 20 to 30% of the total ventilation (VT), so VD/VT = 0.2 to 0.3
19. Respiration (or diusion) is measured by the amount of oxygen in the
blood.
20. Tachypnea rapid, shallow breathing (>24 breaths/min). Associated with
pneumonia, pulmonary edema, metabolic acidosis, septicemia, severe pain,
or rib fracture.
21. Tidal Volume (Vt) The amount of air moved in one breath, which is
typically around 500 cc in an adult at rest
22. Ventilation is measured by the amount of carbon dioxide in the blood.
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The Lungs
The lungs are cone-shaped organs that hold between 4 8 liters of volume. The
top portion is known as the apex, and the bottom is known as the base. The apex
of each lung rises above the clavicles a few centimeters and the base rests
against the diaphragm. The right lung has 3 lobes: upper, middle, and lower. The
left has two lobes: upper and lower.
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Aspiration pneumonias are often located in the right middle lobe due to the
shorter, straighter right mainstem bronchus.
The Diaphragm
The diaphragm is the major muscle of ventilation. It is a dome-shaped
musculobrous partition located between the thoracic and abdominal cavities. It
is composed of two muscles: the right and left hemidiaphragms. The diaphragm
allows the esophagus, the aorta, several nerves, and the inferior vena cava to exit
through it. The phrenic nerve exits the central nervous system between cervical
vertebrae 3 5 and extends down to innervate the diaphragm assisting in
controlling ventilation.
Patients with cervical spine injuries of C3, C4 and C5 are often dependent on
mechanical ventilation. This is due to interruption of nerve transmission to the
diaphragm and other ventilatory muscles.
Accessory muscles of ventilation
During vigorous exercise and the advanced stages of pulmonary disease
processes (e.g. COPD) the accessory muscles of inspiration and expiration are
activated to assist the diaphragm.
Muscles of Inspiration (I)
Muscles of Expiration (E)
Scalene muscles
Rectus abdominis muscles
Sternocleidomastoid muscles
External abdominal obliquus muscles
Pectoralis major muscles
Internal abdominis obliquus muscles
Trapezius muscles
Transversus abdominis muscles
External intercostal muscles
Internal intercostal muscles
PaCO2 Equation PaCO2 reects ratio of metabolic CO2 production to
alveolar ventilation
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The PCO2 equation puts into physiologic perspective one of the most common of
all clinical observations: a patients respiratory rate and breathing eort. The
equation states that alveolar PCO2 (PACO2) is directly proportional to the
amount of CO2 produced by metabolism and delivered to the lungs (VCO2) and
inversely proportional to the alveolar ventilation (VA). While the derivation of the
equation is for alveolar PCO2, its great clinical utility stems from the fact that
alveolar and arterial PCO2 can be assumed to be equal. Thus,
PaCO2
Condition in Blood
State of Alveolar Ventilation
> 45 mm Hg
Hypercapnia
Hypoventilation
35 45 mm Hg
Eucapnia
Normal ventilation
< 35 mm Hg
Hypocapnia
Hyperventilation
The constant 0.863 is necessary to equate dissimilar units for VCO2 (ml/min) and
VA (L/min) to PACO2 pressure units (mm Hg). Alveolar ventilation is the total
amount of air breathed per minute (VE; minute ventilation) minus that air which
goes to dead space per minute (VD). Dead space includes all airways larger than
alveoli plus air entering alveoli in excess of that which can take part in gas
exchange.
In the clinical setting we dont need to know the actual amount of CO2
production or alveolar ventilation. We just need to know if VA is adequate for
VCO2; if it is, then PaCO2 will be in the normal range (35-45 mm Hg). Conversely, a
normal PaCO2 means only that alveolar ventilation is adequate for the patients
level of CO2 production at the moment PaCO2 was measured. From the PCO2
equation it is evident that a level of alveolar ventilation inadequate for CO2
production will result in an elevated PaCO2 (> 45 mm Hg; hypercapnia). Thus
patients with hypercapnia are hypoventilating (the term hypoalveolar ventilating
would be more appropriate but hypoventilating is the conventional term).
Conversely, alveolar ventilation in excess of that needed for CO2 production will
result in a low PaCO2 (< 35 mm Hg; hypocapnia) and the patient will be
hyperventilating. (Confusion sometimes arises because the prex (hyper-, hypo-)
diers for the same condition depending on whether one is describing a blood
value or the state of alveolar ventilation.) For reasons that will be discussed
below, the terms hypo- and hyperventilation refer only to high or low PaCO2,
respectively, and should not be used to characterize any patients respiratory
rate, depth, or breathing eort.
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From the PCO2 equation it follows that the only physiologic reason for elevated
PaCO2 is a level of alveolar ventilation inadequate for the amount of CO2
produced and delivered to the lungs. Thus arterial hypercapnia can always be
explained by:
1. Not enough total ventilation (as may occur from central nervous system
depression or respiratory muscle weakness); or
2. Too much of the total ventilation ending up as dead space ventilation (as
may occur in severe chronic obstructive pulmonary disease, or from rapid,
shallow breathing); or
3. Some combination of 1) and 2).
Excess CO2 production is omitted as a specic cause of hypercapnia because it is
never a problem for the normal respiratory system unimpeded by a resistive load.
During submaximal exercise, for example, where CO2 production is increased,
PaCO2 stays in the normal range because VA rises proportional to the rise in
VCO2. With extremes of exercise (beyond anaerobic threshold) PaCO2 falls as
compensation for the developing lactic acidosis. In a healthy patient PaCO2 may
be reduced but is never elevated.
An important clinical corollary of the PaCO2 equation is that we cannot reliably
assess the adequacy of alveolar ventilation and hence PaCO2 at the bedside.
Although VE can be easily measured with a handheld spirometer (as tidal volume
times respiratory rate), there is no way to know the amount of VE going to dead
space or the patients rate of CO2 production. Other clinical factors include
respiratory eort, mental status, body habitus, temperature, etc.
A common mistake is to assume that because a patient is breathing fast, hard
and/or deep he or she must be hyperventilating. Not so, of course.
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PCO2 vs. Alveolar Ventilation

The relationship is shown for metabolic carbon dioxide production rates of 200
ml/min and 300 ml/min (curved lines). A xed decrease in alveolar ventilation (xaxis) in the hypercapnic patient will result in a greater rise in PaCO2 (y-axis) than
the same VA change when PaCO2 is low or normal.
This graph also shows that if alveolar ventilation is xed, an increase in carbon
dioxide production will result in an increase in PaCO2.
Eect of Increasing Arterial PCO2 or Reducing pH on Ventilation

Guyton & Hall, Textbook of Medical Physiology, 10th ed., 2000, Saunders p. 477.
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The eect of PCO2 on ventilation is primarily due to a region of the ventral

medulla referred to as the chemosensitive area. In this area, there are sensor
neurons that are excited by hydrogen ions. As arterial PCO2 rises, CO2 easily and
rapidly diuses through the blood brain barrier where it combines with water to
form carbonic acid which releases a hydrogen ion. So, the net eect of increased
arterial PCO2 is increased cerebrospinal uid (CSF) and brain interstitial acidity.
This strongly stimulates these sensor neurons which stimulate the respiratory
centers to increase ventilation (this will tend to reduce the arterial PCO2 back to
baseline).
Hydrogen ions themselves do not diuse as easily across the blood brain barrier
making the direct eect of pH less. The eect of PCO2 on ventilation is strongest
in the acute phase. If the person has a high PCO2 for a prolonged period (days or
longer, perhaps due to a lung or neurological problem), the pH of the CSF tends
to return toward normal because of adaptive eects related to bicarbonate. The
person becomes accustomed to the higher PCO2 and it causes less stimulus to
hyperventilate.
Ventilation Increases as PaO2 Decreases at Constant PaCO2
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Integrated Eects of PCO2, PO2 & pH on Alveolar Ventilation

Equipment
Currently, there are 2 basic types of CO2 detectors: quantitative and qualitative.
1. Qualitative CO2 detectors are colorimetric detectors that contain material
that reversibly reacts with CO2. This reaction causes the color to change,
most commonly, from purple to yellow. Qualitative capnography units can
be broken down into mainstream and sidestream congurations.
1. Mainstream units, or in-line units, are used for ventilated patients
who are intubated endotracheally. The sensor is placed directly on an
adapter attached to the endotracheal tube. From there, EtCO2 can be
directly measured.
2. Sidestream units have a sensor that is located on the main unit itself.
These systems aspirate the gas sample from the patients airway,
which then measures the EtCO2. In turn, sidestream units can be used
in awake or intubated patients.
2. Quantitative CO2 detectors give a measured value of EtCO2. This numeric
value is referred to as capnometry. Quantitative detectors can also be
displayed as a waveform called a capnogram. This waveform of
inspiratory/expiratory CO2 can be displayed over time or volume and is
referred to as a capnograph.
How medical equipment works Capnography
Levels or Phases
Information from Capnography can be broken down into levels, each with
increasing degrees of information
1. Level 1
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1. Breathing or not, i.e. apnoea monitor

2. Respiratory rate
2. Level 2
1. Expired CO2 levels (4.5% or 35mmHg)
2. Inspired CO2 levels (0%)
3. From these parameters we can now begin to deduce the state of the
patient with regard to respiration i.e. normocapnic, hypocapnic or
hypercapnic
3. Level 3
1. Waveform prole
2. There are 4 recognised parts to a typical capnogram, each one having
characteristics that impart specic information
3. A typical capnogram obtained during controlled mechanical ventilation
showing:
1. i. Inspiratory baseline (A to B)
2. ii. Expiratory upstroke (B to C)
3. iii. Expiratory plateau (C to D)
4. iv. Inspiratory down stroke (D to E)
Advanced Emergency Nursing Journal Vol. 28, No. 4, pp. 301313
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Angles
1. (Alpha) angle Used to assess the Ventilation/ Perfusion (V/Q) status of
lung. During mismatches, the alpha angle is > ~ 90 degrees. The more
damaged and less uniform the alveoli, the larger the angle. Bronchospasm
(sharkn), COPD, etc.
2. (Beta) angle Used to assess rebreathing. During rebreathing, the beta
angle is > 90 degrees. May see in infants who are breathing faster than
capnograph can account for.
A normal capnogram look like the following.
Its analysis should include the following:

1. Verify presence of exhaled CO2
2.
3.
4.
5.
1. Is a waveform present?
Inspiratory baseline
1. Is there rebreathing?
Expiratory upstroke
1. Is it steep, sloping, or prolonged?
Expiratory plateau
1. Is it at, prolonged, notched, or sloping?
Inspiratory down stroke
1. Is it steep, sloping, or prolonged?
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6. Check PICO2 min and PECO2max

7. Estimate or measure PaCO2 PECO2 max
8. Search for causes of hypercapnia or hypocapnia, if either is present
Clinical Application Examples of Capnography
Slap the Cap The Role of Capnography in EMS
1. One of two sure signs of endotracheal intubation.
1. This is probably the most common use of capnography, yet limiting
oneself to this use only is a huge waste. In the beginning, color
change devices would detect CO2 levels. This is widely believed to be
able to accurately predict when the endotracheal tube is misplaced in
the esophagus. Theoretically, there should be no CO2 exhaled from
the esophagus, on the trachea. However, in low perfusion states, this
is not a very accurate reading and the manufacturer even suggests
using another conrming device besides this one. Therefore,
waveform capnography is the gold standard for endotracheal tube
conrmation. Tube conrmation is conrmed with a SQUARE
waveform. With a square waveform, the tube cannot be in the
esophagus, or the hypopharynx. It must be in the trachea, regardless
of the value of the return of CO2.
2. Right mainstem intubation. A square waveform can occur with a right

mainstem intubation because the tube is still in the main
airway.Therefore, auscultation in the fth intercostal space
midaxillary, bilaterally, is necessary to rule out right mainstem
intubation.
2. Detection of untoward events e.g Disconnections or inadvertent
extubation.
3. Maintenance of normocapnia
4. Cardiopulmonary resuscitation
1. As an assessment tool during CPR, capnography is a direct
measurement of ventilation in the lungs, and it also indirectly
measures metabolism and circulation. For example, a decrease in
perfusion (cardiac output) will lower the delivery of carbon dioxide to
the lungs. This will cause a decrease in the ETCO2 (end-tidal CO2), and
this will be observable on the waveform as well as with the numerical
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measurement.
2. Two very practical uses of waveform capnography in CPR are: 1.)
evaluating the eectiveness of chest compressions; and 2.)
identication of ROSC. Evaluating eectiveness of chest
compressions is accomplished in the following manner: Measurement
of a low ETCO2 value (< 10 mmHg) during CPR in an intubated patient
would indicate that the quality of chest compressions needs
improvement.
3. An abrupt increase in PETCO2 may indicate return of spontaneous
circulation (ROSC), Increase in pulmonary circulation brings more CO2
into lungs for elimination. In most cases that have ROSC the ETCO2
goes into the 70-90s!
5. Weaning from mechanical ventilation
6. Monitoring the seizure patient
1. Generalized seizure, such as a tonic/clonic, can aects both
hemispheres of the brain and the medulla. When the medulla is
involved, the patient may not breath during seizure activity. Following
the post-ictal state capnography can determine the need for further
ventilation.
7. Metabolic Uses: DKA
1. Since CO2 is carried in the blood stream and bicarbonate Ion, it has a
direct clinical relationship to serum bicarb levels. Therefore, if the
patient
has a high Blood glucose, measure their ETCO2. If it is less than 29,
then
the patient has DKA. The blood gas bicarb will show a very low level
as
well, indication metabolic acidosis.
8. Pulmonary Embolism: This is easy. The combination of ETCO2 and an ABG
CO2 can easily call a V/Q mismatch. All you need then is a CT scan to gure
out where it is and
they are on their way. A high blood gas CO2 and a low ETCO2 tells us the
CO2 is not getting to the lungs to be exhaled.
9. Trauma?
1. In Tension Pneumothorax, pressure in the chest collapses a lung and
then
presses on the right side of the heart making it hard to ll with blood.
It
only takes about 7mm/hg pressure to stop the blood ow into the
right
atria. The rst and must reliable sign of a TENSION pneumothorax is
the
sudden drop in perfusion that is picked up immediately on a
capnogram.
By the same token, when the chest is successfully decompressed, it is
not
a rush of air but a sudden increase in ETCO2 that conrms
decompression
success. Furthermore, the capnogram can be used to keep watch in
case
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it develops again.
2. The same is true for Pericardial Tamponade and cardiocentesis. In
each
of these obstructive forms of hypoperfusion, the capnogram will
remain
square because it is a perfusion problem, not an airway problem, but
you
knew that, right?
10. Closed Head Injury. ITLS and the Brain Trauma Foundation have taken the
lead in recommending capnography as the way titrate CO2 ventilations in
the patient with a closed head injury. If the patient has a GCS of less than
9 and they are posturing, have unequal pupils, or dropped two in front of
you, then they should be selectively ventilated to an ETCO2 between 3035mm/hg. If the patient does not the signs (above) of deterioration, then
ventilate the patient to levels, 35-45. Never ever bag them to lower than
25mm/hg. It causes cerebral vasoconstriction and creates an alkalosis not
allowing O2 to dissociate from hemoglobin, make the brain injury worse.
11. Monitoring the non-intubated patient
1. Capnography helps conscious patients too
Specic Waveforms to Know
There are a few specic waveforms that you need to know.
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Capnography Outside the Operating Rooms

Kodali, Bhavani Shankar Anesthesiology. 118(1):192-201, January 2013. doi:
10.1097/ALN.0b013e318278c8b6
A, Prolonged phase II, increased angle, and steeper phase III suggest
bronchospasm or airway obstruction.
B, Expiratory valve malfunction resulting in elevation of the baseline, and the
angle between the alveolar plateau and the downstroke of inspiration is
increased from 90. This is due to rebreathing of expiratory gases from the
expiratory limb during inspiration.
C, Inspiratory valve malfunction resulting in rebreathing of expired gases from
inspiratory limb during inspiration (reference 5 for details).
D, Capnogram with normal phase II but with increased slope of phase III. This
capnogram is observed in pregnant subjects under general anesthesia (normal
physiologic variant and details in reference 9).
E, Curare cleft: Patient is attempting to breathe during partial muscle paralysis.
Surgical movements on the chest and abdomen can also result in the curare cleft.
(You have maybe 3 minutes to sedate the patient before they begin to waken or
start to ght the tube.)
F, Baseline is elevated as a result of carbon dioxide rebreathing.
G, Esophageal intubation resulting in the gastric washout of residual carbon
dioxide and subsequent carbon dioxide will be zero.
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H, Spontaneously breathing carbon dioxide waveforms where phase III is not well
delineated.
I, Dual capnogram in one lung transplantation patient. The rst peak in phase III is
from the transplanted normal lung, whereas the second peak is from the native
disease lung. A variation of dual capnogram (steeple sign capnogram dotted
line) is seen if there is a leak around the sidestream sensor port at the monitor.
This is because of the dilution of expired PCO2 with atmospheric air.
J, Malignant hyperpyrexia where carbon dioxide is raising gradually with zero
baseline suggesting increased carbon dioxide production with carbon dioxide
absorption by the soda lime.
K, Classic ripple eect during the expiratory pause showing cardiogenic
oscillations. These occur as a result of to-and-for movement of expired gases at
the sensor due to motion of the heartbeat during expiratory pause when
respiratory frequency of mechanical ventilation is low. Ripple eect like wave
forms also occur when forward ow of fresh gases from a source during
expiratory pause intermingles with expiratory gases at the sensor.
L, Sudden raise of baseline and the end-tidal PCO2 (PETCO2) due to
contamination of the sensor with secretions or water vapor. Gradual rise of
baseline and PETCO2 occurs when soda lime is exhausted.
M, Intermittent mechanical ventilation (IMV) breaths in the midst of
spontaneously breathing patient. A comparison of the height of spontaneous
breaths compared to the mechanical breaths is useful to assess spontaneous
ventilation during weaning process.
N, Cardiopulmonary resuscitation: capnogram showing positive waveforms
during each compression suggesting eective cardiac compression generating
pulmonary blood.
O, Capnogram showing rebreathing during inspiration. This is normal in
rebreathing circuits such as Mapleson D or Bain circuit.
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Resources
1. AHRQ Guideline Capnography/capnometry during mechanical ventilation:
2011
2. BCEMS
1. Capnography Part I
2. Capnography Part II
3. Capnography
4. Capnography Outside the Operating Rooms
5. Capnography/Capnometry During Mechanical Ventilation: 2011 (pdf)
6. Cecil medicine Chapter 104 Respiratory Monitoring in Critical Care
7. Council of the Intensive Care Society Capnography Guidelines
8. Dicult Airway Society Capnography the Future
9. Emergency Nurses Association Wave Form Capnography The 12 Lead of
the Lungs!
10. Interpreting your capnogram
11. Life in the Fast Lane
1. Capnography
2. Respiratory Monitoring in the ED
12. NIAA National Audit Project 4
13. Noninvasive Monitoring of End-Tidal Carbon Dioxide in the Emergency
Department
14. Phillips Clinical Measurements A Quick Guide to Capnography
15. Physiology of Oxygenation and Ventilation
16. Slap the Cap The Role of Capnography in EMS
17. Rapid Results Capnography: A Key Patient Assessment Tool
18. Riding the Waves (pdf)
19. The Alveolar Gas Equation (pdf)
this is a repost from this website Its a wonderful resource. Do check it.
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Capnography Explained

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Capnography Explained

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Capnography Explained

ISA KAKINADA Education Portal Home

Home / PG students / General Anesthesia / Capnography Simplied

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Measures oxygen saturation

Hypoventilation / apnea detected

Changes lag with hypoventilation /

Should be used with pulse oximeter

Should be used with capnography

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May 20th, 2014

13. PaCO2 Partial pressure of CO2 in arterial blood.

14. PCO2 Partial pressure of CO2 in the blood

May 10th, 2014

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State of Alveolar Ventilation

PCO2 vs. Alveolar Ventilation

Eect of Increasing Arterial PCO2 or Reducing pH on Ventilation

The eect of PCO2 on ventilation is primarily due to a region of the ventral

Integrated Eects of PCO2, PO2 & pH on Alveolar Ventilation

1. Breathing or not, i.e. apnoea monitor

Advanced Emergency Nursing Journal Vol. 28, No. 4, pp. 301313

Its analysis should include the following:

6. Check PICO2 min and PECO2max

2. Right mainstem intubation. A square waveform can occur with a right

Capnography Outside the Operating Rooms

By subodhchaturvedi | January 28th, 2016 | Categories: General Anesthesia, PG students | Tags:

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