Like pulse oximetry before it alerting us to changes in oxygenation, end-tidal CO2 monitoring, or ETCO2, is rapidly becoming an additional vital sign. We routinely use ETCO2 to provide information on ventilation. But ETCO2 can also provide valuable information on the adequacy of cardiac perfusion. It can be an essential tool in ensuring optimal, high quality chest compressions during cardiac resuscitation.
Ventilation and oxygenation are different. Ventilation exchanges air between the lungs and the atmosphere so that oxygen can be absorbed and carbon dioxide can be eliminated. Oxygenation is simply the addition of oxygen to the body. Under normal circ*mstances, hyperventilation with room air will lower your arterial carbon dioxide content (PaCO2) significantly, but not change your oxygen levels much at all. On the other hand, if you breathe a high concentration of oxygen without changing your respiratory rate, your arterial oxygen content (PaO2) will greatly increase. However, your PaCO2 won’t change.
Oxygenation changes PaO2. Ventilation changes PaCO2.
When I started my anesthesia training in 1980, we monitored the patient with a manual blood pressure cuff, EKG, pulse, and temperature. Pulse oximetry and capnography were not yet in clinical use. If we wanted to determine PaO2, or PaCO2, we needed to draw a blood gas. Frequent blood gas determinations, or the need to monitor continuous perfusion pressures, often necessitated placement of an arterial line.
To provide an indirect indicator of perfusion, we used a precordial stethoscope attached to an earpiece to continuously listen to heart sounds. An attentive anesthesiologist could use changes in the loudness or crispness of the heart tones to alert him or her to changes in cardiac output. As the patient got lighter or if the blood pressure rose, heart tones got louder and sharper. Low blood pressure brought muffled, faint heart tones independent of heart rate. We were essentially using our ears in place of the plethysmograph waveform that pulse oximetry would eventually provide.
Pulse oximetry revolutionized anesthetic safety. Pulse oximetry was a non-invasive way of measuring oxygen saturation. Oxygen saturation is the percent of Hemoglobin (Hgb) binding sites in the blood that are carrying oxygen. Hemoglobin is a chemical molecule in the red blood cell (RBC) that carries oxygen on specific binding sites. Each Hgb molecule, if fully saturated, can bind four oxygen molecules. Depending on conditions, Hgb releases some percentage of the oxygen molecules to the tissues when the RBC passes through the capillaries. We can measure how many of these binding sites are combined, or saturated, with oxygen. This number, given as a percentage, is called the oxygen saturation or simply O2 Sat, commonly pronounced “Oh Two SAT”. it is also referred to as SPO2. When all the Hgb binding sites are filled, Hgb is 100% saturated.
Oxygen saturation and PaO2 are NOT equivalent, and they have significant clinical differences that you can read about here.
What’s The Difference Between Oxygen Saturation And PaO2?
However, with pulse oximetry we could now measure oxygen saturation. We could immediately see in real time if our patient was hypoxemic or hypoxic and, if so, diagnose the cause and treat it before harm was done.
Watching the quality of the waveform, along with the oxygen saturation, told us valuable information about perfusion. The higher the amplitude of the wave, the stronger the pulse was. The more damped out the waveform appeared, the weaker the pulse.
With this new tool, and with the OR environment becoming increasingly noisy, use of the precordial stethoscope has largely faded away. Pulse oximetry quickly spread to ICUs, on wards, and clinics to monitor patients at risk. Pulse oximetry has become a fifth vital sign.
I believe we are seeing the same transition with end-tidal CO2 monitoring.
What Is ETCO2?
Capnography refers to the process of measuring the partial pressure of end-tidal CO2 in each expired breath. Providers measure the value of ETCO2 in each exhaled breath with a very thin tube inserted into the breathing circuit or the patients oxygen mask or nasal prongs.
The waveform (capnogram) that you then see on the capnography monitor provides a real time recording of the patient’s respiratory rate, pattern and depth of breathing, and of course the value of CO2 exhaled. These measurements help the provider evaluate adequacy of ventilation.
The author looks at the capnography waveforms during an anesthetic to evaluate end-tidal CO2 (ETCO2) values and the adequacy of ventilation.
ETCO2 Helps Assess Adequacy of Ventilation
We routinely measure ETCO2 for every patient in the operating room. We use it increasingly for conscious sedation provided in treatment rooms and on the wards. ETCO2 and PaCO2 are not the same value. PaCO2 is the concentration of CO2 in arterial blood. ETCO2 is the concentration of CO2 in the exhaled breath, and is close to alveolar CO2. ETCO2 is usually about 5 mmHg below PaCO2. This makes sense. If the concentration of CO2 in the alveoli were higher than in the blood stream, CO2 could not enter the lungs and would not be exhaled.
ETCO2 offers a valuable trending tool to monitor and control ventilation. It alerts us immediately if the patient hyperventilates, hypoventilates, or becomes apneic.
- A normal trace appears as a series of rectangular waves in sequence, with a numeric reading (capnometry) that shows the value of exhaled CO2. “Normal” ETCO2 is in the range of 35 to 45 mmHg.
- In hyperventilation, the CO2 waveform becomes smaller and more frequent, and the numeric reading falls below the normal range.
- In hypoventilation), the waveform becomes taller and less frequent, and the numeric reading rises above the normal range.
- Fattening of the waveform indicates an airway obstruction.
- If the series of rectangular waves become a flat line, the patient is not breathing.
Use ETCO2 In The Perioperative Areas
I believe we should increase our use of ETCO2 in our perioperative areas and procedure rooms. Patients receiving conscious sedation on the ward or recovering from anesthesia are arguably at more risk of airway compromise than patients in the operation room. They are often under more intermittent observation. I encourage my recovery room nurses to use end-tidal CO2 monitoring when they are caring for patients at risk of hypovention or obstruction such as those:
- exhibiting prolonged sedation,
- with opioid induced respiratory depression,
- history of sleep apnea,
- any cardiovascular instability
- any time they are worried about a particular patient.
For clinical examples of how ETCO2 can change during clinical care and how we can use ETCO2 to guide our treatment, read more here.
How Does Hypoventilation Cause Hypoxemia?
Anatomic Dead Space Affects Hypoventilation
Don’t Withhold Oxygen From That CO2 Retainer
ETCO2 Helps Verify Intubation
Esophageal intubation or accidental extubation are always risks. Monitoring ETCO2 increases safety. The continued presence of CO2 in the exhaled breath can only mean placement of the tube in the trachea. Loss of the ETCO2 trace indicates extubation or disconnection from the circuit the ETCO2.
The shape of the capnography waveform can also indicate the severity of problems such as bronchospasm or other cause of increased resistance to breathing or exhalation.
ETCO2 Is An Early Sign Of Poor Perfusion or Cardiac Arrest
Oxygen delivery and carbon dioxide removal depend on three systems: lungs, blood and circulation. It’s important to remember that adequate oxygen absorption and delivery depends on the interaction between lung function and circulation. As soon as cardiac output starts to fall, blood perfusion through the lungs falls. CO2 now has more difficulty being carried to the lungs for exhalation. This leads to a rise in PaCO2 in the blood stream and a fall in ETCO2.
Oxygen delivery and CO2 removal from the lungs depend on lung function, blood hemoglobin concentration, and circulation. Disturbance in any of these risks respiratory distress or failure. If lung function and Hgb are stable, then changes in ETCO2 imply changes in perfusion.
In the operating room, I often see a drop in ETCO2 even before blood pressure itself starts to fall. As long as there is some circulation, there will be some ETCO2 present, even if you can’t feel a weakened peripheral pulse. ETCO2 can therefore be an early warning of developing shock, or pulmonary embolus.
If ETCO2 drops to zero, then the heart has stopped. This is true even for patients who are continuing to receive manual ventilation, because although air is moving into and out of the lungs, there is no CO2 being delivered to exhale. Loss of ETCO2 can also be the first sign of cardiac arrest. A patient may still have an EKG trace in pulseless electrical activity, but not have circulation and therefore will not have a measurable ETCO2.
Here is a simplified flow chart for using ETCO2 to alert you to perfusion or ventilation problems.
ETCO2 is a valuable tool for early recognition of poor perfusion and cardiac arrest.
Adequacy Of Chest Compressions
Good quality CPR depends on high quality chest compressions. When I practice with my staff during Critical Event Training, failure to perform adequate chest compressions is common, a fact that reinforces the need to routinely practice.
During one particular exercise, one diminutive RN was having trouble making her compressions meet the 2-2.5 inch depth, 100 compressions per minuteon the manikin (as measured by our test device). The rest of the team encouraged her until she got it correct. The following weekend her Dad suffered a cardiac arrest in her living room. She went into action delivering chest compressions while the family dialed 911. Her father made a full recovery, and she gave credit to the training she had just received.
Good quality compressions can save lives. ETCO2 is one valuable tool we have to tell us that good quality compressions are being delivered. The higher the ETCO2 measured during compressions, the better the perfusion being supplied by CPR. The goal should be to maintain ETCO2 no lower than 10-20 mmHg. An ETCO2 below 10 mmHg is associated with poor outcome.
Good quality chest compressions will also generate a waveform on the ETCO2 capnograph that allows you to estimate the rate of compressions.
Return of Spontaneous Circulation
Return Of Spontaneous Circulation (ROSC) is accompanied by a sharp rise in ETCO2, usually within a range higher of 35-45 mmHg or higher as CO2 is now delivered to the lungs and then exhaled. This is often accompanied by a palpable pulse and a rising blood pressure.
Good news. However, the next 10 minutes are a very dangerous time for your patient. The heart is still stunned and cardiac output may still be poor.Current consensus guidelines for cardiopulmonary resuscitation (CPR) recommend that chest compressions resume immediately after defibrillation attempts and that rhythm and pulse checks be deferred until completion of 5 compression:ventilation cycles or minimally for 2min.
One study showed that perfusion remained poor for greater than 2 minutes in 25% of patients successfully defibrillated [1].Continue to monitor that ETCO2! This is now your powerful tool to see if perfusion is adequate and being maintained. Assuming ventilation is consistent, a drop in ETCO2 during this period can indicate failing circulation. A loss in ETCO2 can mean re-arrest.
Check to make sure your endotracheal tube is still properly positioned, check a pulse, and decide your appropriate actions.
Prognosis During CPR Efforts
ETCO2 below 10 mmHg can be caused by poor compression technique. It can also be caused by low perfusion and metabolism from prolonged shock despite good compressions — in other words the cardiac pump is damaged and failing. If high quality compressions are being delivered, and an advanced airway is in place allowing accurate ETCO2 measurements, then an ETCO2 persistently below 10mmHg after 20 minute of resuscitation is a poor prognostic sign. It can be used as an indication to consider terminating resuscitation efforts.
On the other hand if ETCO2 is above 15mmHg, or it continues to rise, that is one indication that resuscitation efforts should continue, as the brain and heart are being perfused. There are case reports of patients surviving prolonged CPR with higher ETCO2 readings.
We’ve come a long way since I had to depend on a precordial stethoscope, skin color and finger on the pulse to supplement blood pressure and EKG to assess perfusion in my patients. Capnography and pulse oximetry are powerful tools. However, don’t forget that in the absence of either, you can still look at your patient and be vigilant. Without vigilance, all the tools in the world will not protect your patient.
