How to Read and Interpret End-Tidal Capnography Waveforms

Capnography is a great way to confirm airway device placement and monitor ventilation, but it can do so much more. Carbon dioxide (CO2) is a product of metabolism transported via perfusion and expelled through ventilation. End-tidal carbon dioxide (EtCO2) waveform monitoring allows you to measure all three simultaneously, making it the most important vital sign you use.1

To evaluate the metabolism, ventilation and perfusion of a patient through EtCO2 waveform monitoring you need to read the PQRST: proper, quantity, rate, shape and trend.

Proper means that you should know the normal readings for quantity, rate, shape and trending of EtCO2. In this case, normal means what we find in a healthy person with no metabolism, ventilation or perfusion problems. One of the great things about EtCO2 is that although ventilation rates vary based on age, normal readings for quantity, shape and trends are the same for men and women of all age groups, making them easy to remember.

Quantity; target EtCO2 value should be 35-45 mmHg.

Rate of ventilation should be 12-20 breaths per minute (bpm) for adults if the patient is breathing on their own and 10-12 bpm if you’re ventilating them. Children should be ventilated at a rate of 15-30 bpm; 25-50 bpm for infants. Ventilating too quickly won’t let enough CO2 build up in the alveoli, resulting in lower EtCO2 readings. Ventilating too slowly will allow extra CO2 to build up, resulting in higher readings.

Shape of the waveform should normally be a rectangle with rounded corners. Different waveform shapes can indicate different conditions.

Trending of the quantity, rate and shape of EtCO2 should be stable or improving.

Although reading EtCO2 waveforms can be easy, interpreting what you see requires understanding how the waveforms and numbers are produced.

An end-tidal capnography waveform measures and
displays the peak amount of CO2 at the end of exhalation.

Reading the Waves

When it comes to capnography, everyone knows the normal adult respiratory rate of 12-20 breaths per minute and most people know, or quickly learn, that the normal quantity of exhaled CO2 is 35-45 mmHg. What can be intimidating is the idea of reading the shape of the waveform, but in practice it’s not difficult at all.

An end-tidal capnography waveform is a simple graphic measurement of how much CO2 a person is exhaling. The normal end-tidal capnography wave form is basically a rounded rectangle.2 (See Figure 1, p. 48.) When a person is breathing out CO2, the graph goes up. When a person is breathing in, it goes back down.

Phase 1 is inhalation. This is the baseline. Since no CO2 is going out when a patient is breathing in, the baseline is usually zero.

Phase 2 is the beginning of exhalation. CO2 begins to travel from the alveoli through the anatomical dead space of the airway causing a rapid rise in the graph as the CO2.

Phase 2 measures the exhaled CO2 from the alveoli mixed with the gas that was in the dead space. This part of the graph goes up as the more concentrated CO2 gases from lower in the lungs rise up past the sensor.

Phase 3 is when the sensor is receiving the CO2-rich gas that was in the alveoli. Because this is a fairly stable amount, the graph levels off into a plateau. The measurement at the end of the tide of respiration, the peak measurement at the very end of phase 3, is the EtCO2 reading.

After the end of phase 3, the patient inhales again, bringing clear air past the sensor, dropping the graph back down to zero to start over again at phase 1.

Although it can be intimidating to try and memorize what each phase (and the angles between them) represents, you can think of it as follows: The left side shows how quickly and easily air is moving out of the lungs; the right side shows how quickly and easily air is going in; the top shows how easily the alveoli are emptying.

If all we wanted to read from capnography was ventilation, this would be enough, but to indirectly measure a patient’s perfusion and metabolic status we must understand how CO2 gets to the lungs to be exhaled.

Putting on the Pressure

Many factors affect how oxygen gets into the body and CO2 gets out; however, the biggest influence is the partial pressures of these gasses.

Although hemoglobin, myoglobin and other body chemicals play a part in transporting gasses, it can be helpful to begin by just picturing the partial pressures pushing the gasses from one part of the body to the next.3

The normal partial pressure of oxygen in ambient air is approximately 104 mmHg. It gets humidified and absorbed by the body as it’s inhaled, bringing the partial pressure down to 100 mmHg by the time the oxygen reaches the alveoli. The partial pressure of oxygen in the alveoli is known as PaO2.

Oxygen is then pushed from the partial pressure of 100 mmHg in the alveoli to the lower partial pressure of 95 mmHg in the capillaries surrounding the alveoli. Oxygen gets carried through the circulatory system, getting absorbed along the way.

By the time the oxygen gets to the end of its journey, it has a partial pressure of approximately 40 mmHg, still high enough to allow it to move into muscles and organs that have a lower partial pressure of approximately 20 mmHg.4 (See Figure 2, p. 49.)

If the organs are functioning normally, the oxygen is metabolized, producing the CO2 that we’re ultimately going to measure. Although the journey back involves CO2 moving primarily through the body’s buffer system as bicarbonate (HCO3-) its movement is still largely governed by partial pressures.3

The partial pressure of carbon dioxide (PCO2) as it leaves the organs is approximately 46 mmHg, just high enough to push it into the capillaries which have a partial pressure of only 45 mmHg.4 CO2 travels through venous circulation largely untouched.

In the end it moves from 45 mmHg at the capillaries surrounding the alveoli into the alveoli themselves. From the alveoli to exhalation the CO2 is approximately 35-45 mmHg.4 At this level it will get exhaled and measured by the EtCO2 sensor, letting us know that the patient’s metabolism, perfusion and ventilation are all working properly taking up oxygen, converting it to CO2 and releasing it at a normal rate (or not).

If you were to know one more thing about oxygen and CO2 transport, it’s that high CO2 reduces the affinity of hemoglobin for oxygen. Referred to as the Bohr effect, during normal body function this is a good thing, (the high CO2 in muscles and organs help hemoglobin release needed oxygen). However, prolonged periods of high CO2 and associated acidosis make it hard for hemoglobin to pickup and transport oxygen. This can be seen as a shift of the oxyhemoglobin dissociation curve to the right.4,5 (See Figure 3, p. 50.)

Conversely, if the patient has low CO2, perhaps because of hyperventilation, it will cause an increased affinity for oxygen, allowing hemoglobin to pick oxygen up more easily. However, if the low CO2 is prolonged, the hemoglobin may not release the oxygen into the organs. This is referred to as the Haldane effect and is seen as a shift of the oxyhemoglobin dissociation curve to the left. In this case you may have a “normal” pulse oximetry reading even though organs aren’t getting the oxygen because hemoglobin is saturated with oxygen, but this oxygen remains “locked” to the hemoglobin.4,5 In this way your EtCO2 reading can help you better interpret the validity and meaning of other vital signs like pulse oximetry, blood pressure and more.


Now that we’ve peeked behind the curtain as to how CO2 is produced in metabolism and transported via perfusion, let’s use the PQRST (proper, quantity, rate, shape and trending) method to different types of emergency calls.

We read PQRST in order, asking, “What is proper?” Consider what your desired goal is for this patient. “What is the quantity?” “Is that because of the rate?” If so, attempt to correct the rate. “Is this affecting the shape?” If so, correct the condition causing the irregular shape. “Is there a trend?” Make sure the trend is stable where you want it, or improving. If not, consider changing your current treatment strategy.

Below are several examples.

Advanced Airway/Intubation

P: Ventilation. Confirm placement of the advanced airway device.6,7

Q: Goal is 35-45 mmHg.

R: 10-12 bpm, ventilated.

S: Near flat-line of apnea to normal rounded rectangle EtCO2 waveform. (See Figure 4a, p. 50.) If the top of the shape is irregular (e.g., like two different EtCO2 waves mashed together) it may indicate a problem with tube placement. (See Figure 4b, p. 50.) This shape can indicate a leaking cuff, supraglottic placement, or an endotracheal tube in the right mainstem bronchus. This shape is produced when one lung-often the right lung-ventilates first, followed by CO2 escaping from the left lung. If the waveform takes on a near-normal shape (see Figure 4c, p. 50) then the placement of the advanced airway was successful.8

T: Consistent Q, R and S with each breath. Watch for a sudden drop indicating displacement of the airway device and/or cardiac arrest. (See Figure 4d, p. 50.)

Cardiac Arrest

P: Ventilation and perfusion. Confirmation of effective CPR. Monitoring for return of spontaneous circulation (ROSC) or loss of spontaneous circulation.1,6,7,9

Q: Goal is > 10 mmHg during CPR. Expect it to be as high as 60 mmHg when ROSC is achieved. (See Figure 5, p. 50.)

R: 10-12 bpm, ventilated.

S: Rounded low rectangle EtCO2 waveform during CPR with a high spike on ROSC.

T: Consistent Q, R and S with each breath. Watch for a sudden spike indicating ROSC or a sudden drop indicating displacement of the airway device and/or re-occurrence of cardiac arrest.

Optimized Ventilation

P: Ventilation. May include hyperventilation situations such as anxiety as well as hypoventilation states such as opiate overdose, stroke, seizure, or head injury.1,6,7

Q: Goal is 35-45 mmHg. Control using rate of ventilation. If EtCO2 is low (i.e., being blown off too fast), begin by assisting the patient to breathe more slowly or by ventilating at 10-12 bpm. If EtCO2 is high (i.e., accumulating too much between breaths), begin by ventilating at a slightly faster rate.

R: Goal is 12-20 bpm for spontaneous respirations ; 10-12 bpm, for artificial ventilations.

S: Rounded low rectangle EtCO2 waveform. Faster ventilation will produce wave shapes that aren’t as wide or as tall since rapid exhalation doesn’t take as long and contains less CO2. (See Figure 6a, p. 51.) Slower ventilation produces wave shapes that are wider and taller as exhalation takes longer and more CO2 builds up between breaths. (See Figure 6b, p. 51.)

T: Consistent Q, R and S with each breath trending towards optimal ventilation.


P: Metabolism and perfusion. As perfusion decreases and organs go into shock-whether hypovolemic, cardiogenic, septic or another type-less CO2 is produced and delivered to the lungs, so EtCO2 will go down, even at normal ventilation rates. In the context of shock, EtCO2 can help differentiate between a patient who’s anxious and slightly confused and one who has altered mental status due to hypoperfusion. It can also indicate a patient whose metabolism is significantly reduced by hypothermia, whether or not it’s shock-related.1,7,10,11

Q: Goal is 35-45 mmHg. EtCO2 < 35 mmHg in the context of shock indicates significant cardiopulmonary distress and the need for aggressive treatment.

R: Goal is 12-20 bpm for spontaneous respirations; 10-12 bpm for artificial ventilations. Anxiety and distress can raise the patient’s respiratory rate. Likewise, it may cause a provider to ventilate too fast. Consider that faster rates will also lower EtCO2, and may also increase pulmonary venous pressure, decreasing blood return to the heart in a patient who’s already hypoperfusing.6

S: Rounded low rectangle EtCO2 waveform.

T: Quantity will continuously trend down in shock. The rate of ventilations will increase in early compensatory shock and then decrease in later non-compensated shock. The shape will not change significantly because of the shock itself. (See Figure 7, p. 51.)

Pulmonary Embolism

P: Ventilation and perfusion. Using EtCO2 along with other vital signs can help you identify a mismatch between ventilation and perfusion.

Q: Goal is 35-45 mmHg. EtCO2 < 35 mmHg in the presence of a normal respiratory rate and otherwise normal pulse and blood pressure may indicate that ventilation is occurring, but perfusion isn’t as the embolism is preventing the ventilation from connecting with the perfusion. This is a
ventilation/perfusion mismatch.12

R: Goal is 12-20 bpm for spontaneous respirations; 10-12 bpm for artificial ventilations.

S: Low, rounded rectangle EtCO2 waveform.

T: As with shock, the quantity will continuously trend down as the patient’s hypoperfusion worsens.


P: Ventilation. Although the classic “shark’s fin” shape is indicative of obstructive diseases like asthma, EtCO2 can provide additional information about your patient.7,8

Q: Goal is 35-45 mmHg. The trend of quantity and rate together can help indicate if the disease is in an early or late and
severe stage.

R: Goal is 12-20 bpm for spontaneous respirations; 10-12 bpm for artificial ventilations.

S: Slow and uneven emptying of alveoli
will cause the shape to slowly curve up (phase 3) resembling a shark’s fin (if the shark is swimming left) instead of the normal rectangle. (See Figure 8, p. 51.)

T: Early on the trend is likely to be a shark’s fin shape with an increasing rate and lowering quantity. As hypoxia becomes severe and the patient begins to get exhausted, the shark’s fin shape will continue, but the rate will slow and the quantity will rise as CO2 builds up.

Mechanical Obstruction

P: Ventilation. The “shark’s fin” low-expiratory shape is present but is “bent” indicating obstructed and slowed inhalation as well.8

Q: Goal is 35-45 mmHg.

R: Goal is 12-20 bpm for spontaneous respirations; 10-12 bpm for artificial ventilations.

S: Again, slow and uneven emptying of alveoli mixed with air from the anatomical “dead space” will cause the shape to slowly curve up resembling a shark’s fin looking left instead of a rectangle. In this case, phase 4 inhalation is blocked (e.g., by mucous, a tumor or foreign body airway obstruction) causing the righthand side of the rectangle to lean left, like the shark is trying to swim left even faster. (See Figure 9.)

T: Again, as hypoxia becomes severe and the patient begins to get exhausted, the shark’s fin shape will continue, but the rate will slow and the quantity will rise as CO2 builds up.

Emphysema & Pneumothorax

P: Ventilation. Patients with emphysema may have so much damage to their lung tissue that the shape of their waveform may “lean in the wrong direction.” In a similar way, patients with a pneumothorax won’t be able to maintain the plateau of phase 3 of the EtCO2 wave. The shape will start high and then trail off as air leaks from the lung, producing a similar, high on the left, lower on the right shape.8,13

Q: Goal is 35-45 mmHg.

R: Goal is 12-20 bpm for spontaneous respirations; 10-12 bpm for artificial ventilations.

S: An indication of very poor surface area for emphysema or leaking alveoli in pneumothorax is that the top of rectangle slopes down from left to right instead of sloping gradually up. (See Figure 10.)

T: Consistent Q, R and S with each breath as always is our goal. You should watch for and correct deviations.

Patient with Diabetes

P: Ventilation and perfusion. EtCO2 can aid in differentiation between hypoglycemia and diabetic ketoacidosis. Sometimes the difference is obvious, but in other situations, every diagnostic tool can help.

Q: Goal is 35-45 mmHg.

R: Goal is 12-20 bpm for spontaneous respirations. A hypoglycemic patient is likely to have a relatively normal rate of respiration. A patient who’s experiencing diabetic ketoacidosis will have increased respirations, lowering the quantity of CO2. In addition, CO2 in the form of bicarbonate in the blood will be used up by the body trying to buffer the diabetic ketoacidosis. In this way, low EtCO2 can help indicate the presence of significant ketoacidosis.1,8,14

S: Rounded rectangle EtCO2 waveform.

T: Consistent Q, R and S with each breath for hypoglycemia. A fast rate of respirations and low quantity for DKA.

Pregnant Patients & Poor Lung Compliance

P: Ventilation. In addition to using EtCO2 in the ways described above, patients with poor lung compliance, obese patients and pregnant patients may also exhibit a particular wave shape that may indicate that they’re highly sensitive on adequate ventilation.8

Q: Goal is 35-45 mmHg.

R: Goal is 12-20 bpm for spontaneous respirations; 10-12 bpm for artificial ventilations.

S: Rounded low rectangle EtCO2 waveform, but with a sharp increase in the angle of phase 3 that looks like a small uptick or “pig tail” on the righthand side of the rectangle, sometimes referred to as phase 4 of the waveform. This is CO2 being squeezed out of the alveoli by the poorly compliant lung tissue, obese chest wall, or pregnant belly, before the same weight closes off the small bronchi. These patients are progress quickly from respiratory distress to respiratory failure.

T: Consistent Q, R and S with each breath.


The PQRST method is designed to be a simple and practical way to expand the use of EtCO2 as a diagnostic tool, but it’s by no means the end of the story.

When used with patients who have been administered paralytics or who are on ventilators, other waveforms can help providers finetune their critical care by identifying medication problems such as inadequate sedation or malignant hyperthermia, mechanical problems such as air leaks and ventilator rebreathing, and physiological issues such as ventilation/perfusion mismatch conditions.3,12

Although no single vital sign is definitive, as a simultaneous measure of metabolism, ventilation and perfusion, end-tidal waveform capnography is one of the most important diagnostic tools available to EMS providers.

Acknowledgment: Special thanks to Patrick Holland, LP, and David Bunting, RRT, AEMT, MS, for their assistance with this article.


1. Rieves A, Bleess B. (2017.) Be all end-tidal: The expanding role of capnography in prehospital care. National Association of EMS Physicians. Retrieved May 19, 2017, from

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3. American Academy of Orthopaedic Surgeons. Nancy Caroline’s emergency care in the streets. Jones & Bartlett Learning: Burlington, Mass., 2017.

4. OpenStax. (March 6, 2013.) Anatomy and physiology. Retrived May 20, 2017, from

5. Desai R. (2017.) Bohr effect vs. Haldane effect. Khan Academy. Retrieved May 20, 2017, from

6. Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult advanced cardiovascular life support: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2015;132(18 Suppl 2):S444-464.

7. DiCorpo JE, Schwester D, Dudley LS, et al. A wave as a window. Using waveform capnography to achieve a bigger physiological patient picture. JEMS. 2015;40(11):32-35.

8. Yartsev A. (Sep. 15, 2015.) Abnormal capnography waveforms and their interpretation. Deranged Physiology. Retrieved May 20, 2017, from

9. Murphy RA, Bobrow BJ, Spaite DW, et al. Association between prehospital cpr quality and end-tidal carbon dioxide levels in out-of-hospital cardiac arrest. Prehosp Emerg Care. 2016;20(3):369-377.

10. Guerra WF, Mayfield TR, Meyers MS, et al. Early detection and treatment of patients with severe sepsis by prehospital personnel. J Emerg Med. 2013;44(6):1116-1125.

11. Hunter CL, Silvestri S, Ralls G, et al. A prehospital screening tool utilizing end-tidal carbon dioxide predicts sepsis and severe sepsis. Am J Emerg Med. 2016;34(5):813-819.

12. Gravenstein JS, Jaffe MB, Gravenstein N, et al., editors. Capnography. Cambridge University Press: Cambridge, UK, 2011.

13. Thompson JE, Jaffe MB. Capnographic waveforms in the mechanically ventilated patient. Respir Care. 2005;50(1):100-108; discussion 108-109.

14. Bou Chebl R, Madden B, Belsky J, et al. Diagnostic value of end tidal capnography in patients with hyperglycemia in the emergency department. BMC Emerg Med. 2016;16:7.


  • Rommie L. Duckworth, LP, is a dedicated emergency responder and award-winning educator with more than 25 years of experience working in career and volunteer fire departments, hospital healthcare systems, and public and private EMS. He's a member of the JEMS editorial board, a career fire captain and paramedic EMS coordinator, founder and director of the New England Center for Rescue and Emergency Medicine and an emergency services advocate, author and speaker at conferences around the world.

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