Part 2: Introduction to Capnography builds on the information presented in part one. It may be presented as part of the series or in as a separate independent class. This PowerPoint program is designed for initial training on capnography in EMS. It is strictly an introduction and all information be adapted to your local protocols. The program is not product specific and qualifies for continuing education credits through individual CE providers and/or the Center for Healthcare Education. Information on the Center for Healthcare Education and the CE process is contained on this CD. You may also contact the Center at 1-800-888-8700 or their website http://www.healthcareeducation.org All contents are under the copyright of Medtronic Physio-Control Corp.
Capnography provides objective information on your patient’s ventilation status similar to the heart rate and ECG waveform on the cardiac system. Part 2, Introduction to Capnography, relates this information to the phases of ventilation and introduces common waveform patterns.
The learning objectives in part two are that you will be able to: Differentiate between oxygenation and ventilation - and how to monitor each Define end-tidal CO 2 - and locate it on a waveform and monitor Identify phases of a normal capnogram Recognize patterns of hypoventilation, hyperventilation and bronchospasm
Although some healthcare providers interchange the terms oxygenation and ventilation, they are two totally different physiological processes. What is the difference?
Two completely different and separate functions: • Oxygenation is the transport of O 2 via the bloodstream to the cells - Oxygen is required for metabolism • Ventilation is the exhaling of CO 2 via the respiratory tract - Carbon dioxide is a byproduct of metabolism
This slide illustrates the differences between oxygenation and ventilation. Inhaled air contains around 21% oxygen and less than 0.03% carbon dioxide. The oxygen diffuses into the arterial bloodstream across the membrane of the the air sacs (alveoli) that terminate the respiratory tree. Hemoglobin molecules on red blood cells (RBC) carries the O 2 atoms to the cells throughout the body. Oxygen saturation of the RBCs is measured by pulse oximetry. At the cell site, oxygen diffuses across the membrane to be used in metabolism. The primary waste product of metabolism, carbon dioxide, is then diffused out of the cell into the venous blood and circulated back to the respiratory tree. Here, the CO 2 is diffused into the alveoli and exhaled out through the airway. This gas exchange and exhalation is the ventilation process and measured by capnography.
Oxygenation is measured noninvasively by pulse oximetry (SpO 2 ). • It detects the percentage of oxygen on red blood cells which is the percentage of oxygen-carrying hemoglobin (oxyhemoglobin) to the total hemoglobin available • Changes in ventilation take minutes to be detected by SpO 2 . Changes in ventilation become evident only when the circulating RBCs begin to become depleted - Pulse oximetry is affected by motion artifact, poor perfusion and some dysrhythmias
Here are common pulse oximeter sensors. It is placed on an extremity or ear lobe - quite a distance from the airway. This is the familiar pulse ox waveform with the pulsation pattern evident. Training note: Pulse oximetry is a very common measurement. Ask about students’ experiences such as, “has anyone had a situation where the pulse oximeter showed an “normal” oxygen saturation but your patient appeared to be in respiratory distress? This can happen because oxygenation is only half of the story.
Ventilation is the elimination of CO 2 from the body and can be measured by the end-tidal carbon dioxide. EtCO 2 is: • Expressed in the partial pressure (mm Hg) or percent volume (% vol) of CO 2 in the airway at the end of exhalation • Breath-to-breath measurement provides information within seconds • Not affected by motion artifact, poor perfusion or dysrhythmias
Capnography sensors are placed at the airway exit - the nose, mouth or ET tube hub. This is a normal capnography waveform - the “QRS” of ventilation monitoring.
Here’s a exercise to see the important difference in monitoring your patient’s airway with EtCO 2 instead of pulse oximetry alone: Monitor your own SpO 2 and EtCO 2 . On this monitor the SpO 2 waveform is in the second channel and the EtCO 2 waveform is in the third channel. Teaching note: This is a nice classroom demonstration with students on actual devices.
Now hold your breath. Note what happens to the two waveforms. How long did it take the EtCO 2 wave form to go flat line? How long did it take the SpO 2 to drop below 90%? Teaching Note: Have someone use a stop watch to clock the time differences. Ask class members about the impact that this time difference may have on the care of a patient in respiratory distress.
A quick summary of the two physiological processes. They require different monitoring modalities which are complimentary measures of your patient’s status.
Capnography has been used extensively in intubated patients to: • Verify and document ET tube placement • Immediately detect changes in ET tube position following correct placement • Assess effectiveness of chest compressions • Provide the earliest indication of ROSC • Determine the probability of success in a resuscitation • Optimally adjust manual ventilations in patients sensitive to changes in CO 2 Each of these applications will be discussed in detail in Part 3.
Capnography can be applied to non-intubated patients. Studies using capnography are underway to: • Objectively assess acute respiratory disorders including asthma, COPD and • Possibly gauge response to treatment These applications will be discussed in detail in Part 4.
Other new applications for capnography include: Gauging the severity of hypoventilation in: Drug and ETOH intoxication CHF Sedation and analgesia Stroke Head injury Some services use capnography in assessing a patient’s perfusion status and for noninvasive monitoring of patients in DKA.
Now that we have covered some of the basic uses for capnography, let’s look at the values, waveform, underlying physiology and interpretations.
This is a simplistic illustration of perfusion and diffusion in the pulmonary system. The pulmonary artery blood has a high concentration of CO 2 which diffuses across the alveolar membrane. Oxygen diffuses out of the alveolus into the pulmonary capillary. The process requires adequate blood flow and a healthy membrane.
Carbon dioxide is a byproduct of all metabolism and can be measured in Arterial blood - it is in a gaseous form called PaCO 2 – Normal range: 35-45mmHg Venous blood gas which is called PeCO 2 – Normal range: 46- 48mmHg Exhaled carbon dioxide and referred to as EtCO 2 – Normal range: 35-45mmHg
The amount of of carbon dioxide in a patient's arterial blood and airway may be slightly different. This difference is called the a-A gradient.
There is a difference between the CO 2 level in the exhaled airway and the arterial system in a patient with healthy lungs. • The normal range is up to 2-5mmHg known as the “a-A gradient” • Wider differences are found - In abnormal perfusion and ventilation conditions such as pulmonary embolus - Incomplete alveolar emptying as in emphysema - Poor sampling which may be seen with a misplaced cannula or a nasal cannula on a patient who is breathing primarily through their mouth Teaching Note: This is a key point. The EtCO 2 readings often differ from the arterial blood gas done in the ED. Some ED clinicians mistake this difference as a “wrong” number in the exhaled air. A 2-5mmHg is acceptable and a wider difference should be investigated for underlying pathology.
End-tidal CO 2 reflects changes in: • Ventilation - the movement of air in and out of the lungs • Diffusion - the exchange of gases between the air-filled alveoli and the pulmonary circulation • Perfusion - circulation of blood through the pulmonary capillaries
EtCO 2 can be used to detect and monitor many of the patient problems frequently seen in EMS such as: • Ventilation - anything that interferes with the flow of air such as asthma, COPD, airway edema, foreign body, stroke • Diffusion - pathology that interferes with the delicate exchange of carbon dioxide and oxygen across through the alveolar membrane including pulmonary edema, alveolar damage, CO poisoning, smoke inhalation • Perfusion - is affected by many of the cardiovascular events you frequently encounter such as shock, pulmonary embolus, cardiac arrest, severe dysrhythmias, CHF
This is the normal waveform of one respiratory cycle - the “QRS of ventilation”. Similar to the ECG waveforms: • The x axis, or height/amplitude, shows amount of CO 2 • The y axis, or length, depicts time or duration
It is important to note that there may be quite a difference in the duration of the waveform you see on the screen and the one on the printout. Capnography waveforms on the monitor screen are condensed to provide adequate information in the 4-second view. Teaching Note: A patient with a RR of 8 would have a respiratory cycle of one breath about every 7.5 seconds. If the waveform was not condensed, you would see one full screen of a flat line, then one end of the waveform, etc. Press the PRINT button anytime you need the accurate duration .
Although other gases are present in the airway, the capnograph detects only CO 2 from ventilation. There is usually no CO 2 present during inspiration so the baseline is normally on zero.
There is no carbon dioxide at the beginning of exhalation. The air is from the trachea, mouth and nose. This upper airway area is often called “dead space” because there is no gas exchanged in the upper airway. Teaching Note: An extension of the airway such as an ET tube, expands the “dead space”.
Phase one on the capnograph is the ending of inhalation and the beginning of exhalation. This baseline is normally at zero and shows the amount of carbon dioxide in the dead space.
In phase II, or the ascending phase, CO 2 from the alveoli begins to reach the upper airway and mix with the dead space air. This causes a rapid rise in the amount of CO 2 that is now detected in exhaled air.
Phase Two, shown here between B and C, shows the rapid assent from the CO 2 present in the bronchi.
In phase three, the carbon dioxide from the alveoli has reached the airway exit. The exhaled air is now rich in CO 2 . In normal ventilation of health lungs, the concentration of CO 2 in the air is uniform.
Phase three, the alveolar plateau, is flat with a slight upward tilt toward the end. This plateau illustrates the uniform concentration of carbon dioxide in the pulmonary system.
The end of phase three is also the end of exhalation. This termination of the breath cycle contains the highest concentration of CO 2 and is labeled the “end-tidal CO 2 ”. This is the number seen on your monitor. Normal EtCO 2 is 35-45mmHg.
End of phase III illustrates the end of exhalation which called the “end-tidal CO 2 ”.
Phase four shows the beginning of the next inhalation. Oxygen fills the airway and the carbon dioxide level quickly drops to the baseline.
When inspiration does begin again, the amount of measured CO 2 quickly drops to zero. The rapid descent to baseline is shown here between D and E. The return to the baseline is called Phase IV.
A quick review of the four phases of the normal capnography waveform:. Phase I Inspiration ends and exhalation begins, dead space air is eliminated first, no CO 2 is present. Phase II Alveolar air begins to mix with dead space air, a sharp upstroke is produced. Phase III Alveolar air predominates and the CO 2 level plateaus as the exhalation continues. • The EtCO 2 is noted at the end of exhalation • Normal range is 35-45mmHg (5% vol) Phase IV Inspiration occurs, CO 2 level quickly returns to baseline. Normal baseline is at zero. The pattern repeats with each breath. Teaching note: The capnography waveform seems to be the opposite of many providers’ intuitive thinking. A helpful class exercise is to have everyone exhale on one cycle. Then walk the class through a “breath-along” with this capnography waveform strip. Have them practice inspiration at baseline, then begin exhalation in Phase II, prolong the breath slightly to emphasize the EtCO 2 , inhale on phase IV. That’s the normal pattern, let’s see how it can change.
How would your capnogram change if you intentionally started to breathe at a rate of 30? • Frequency • Duration • Height • Shape Teaching note: Have the audience respond. Key changes are: 1) Rate: increased frequency of waveforms 2) Duration: the waveform cycle shortens 3) Amount: the peak or height of the plateau will lower as the CO 2 is blown off The shape of the waveform should remain in the normal box-like pattern.
In the normal metabolic state, hyperventilation is seen as the increase in respiratory rate leads to a depletion of CO 2 . When a respiratory rate is faster than the rate of needed to maintain homeostasis, the amount of carbon dioxide in the exhaled air will decline. Teaching note: Ask when would a rapid RR not show a decline in EtCO 2 ? Answers: Metabolic states in which there is a high production of carbon dioxide such as fever, running, DKA, etc.
How would your capnogram change if you intentionally slowed your breathing down to a rate of 8? • Frequency • Duration • Height • Shape Teaching note: Have the audience respond. Two key changes are: 1) Rate: decreased frequency of waveforms 2) Duration: the waveform cycle lengthens 3) Amount: the peak or height of the plateau will higher as the CO 2 in each breath increases to compensate for the slow rate
In the normal metabolic state, hyperventilation is seen as the increase in respiratory rate leads to a depletion of CO 2 . When a respiratory rate is faster than the rate of needed to maintain homeostasis, the amount of carbon dioxide in the exhaled air will decline. Teaching note: Ask when would a slow RR not show an increase in EtCO 2 ? Answers: Slow metabolic states in which there is a lower production of carbon dioxide such as severe hypothermia.
A comparison of three common waveforms: normal, hyperventilation and hypoventilation. Teaching Note: A review of the four phases, normal range and differences is helpful to some students.
How would the waveform shape change during an asthma attack?
Bronchospasm interferes with the normally smooth flow of air as the degree and timing of spasm varies throughout the pulmonary tree. Therefore, in an asthma attack, the alveoli are unevenly filled on inspiration and empty asynchronously during expiration. This uneven emptying dilutes the carbon dioxide which results in a slower rise in CO 2 concentration during exhalation. These spasmodic alterations in air flow affect phase II (ascending phase) and phase III (the plateau) of the capnography waveform and produce a characteristic pattern often referred to as the “shark fin”.
The waveform change due to bronchospasm is easy to see when compared to the normal waveform. Just as it is now easy to spot a ventricular beat on the the ECG monitor, these capnography waveforms become readily identifiable with practice.
In summary, oxygenation and ventilation: • Different and separate physiologic events • Require different monitors Pulse oximetry: • Measures O 2 saturation in blood • Slow to indicate change in oxygenation • Affected by motion artifact and poor perfusion Capnography: • Measures CO 2 in the the airway • Provides a breath-to-breath status of ventilation • Affected by motion artifact and poor perfusion
Capnographic waveform has four phases. The highest CO 2 concentration is at the end of Phase III. • End-tidal CO 2 • Normal EtCO 2 range is 35-45mmHg Several conditions can be immediately detected with capnography.
Quick review of common waveforms. Teaching note: Ask students to volunteer to “walk through” a waveform pattern and describe the changes .
