The expired CO2 waveform can identify a variety of pulmonary and airway pathology:
- Oesophageal intubation
- Endobronchial intubation
- Mechanical airway obstruction
- Reversal of alveolar slope in emphysema
- Cardiac oscillations
- The "Curare Cleft"
- Recirculated CO2 due to a saturated CO2 absorber
- A low end-tidal CO2 in hypothermia
- A high peak of the alveolar phase in poorly compliant lungs
Congratulations, you're in the oesophagus. Though initially there is some CO2 returning though the tube, one finds with subsequent breaths the end tidal graph is lower and lower, and the patient is getting more and more hypoxic.
Other reasons for a flat trace include the following:
- Ventilator disconnection
- Airway obstruction (eg. patient suddenly bit down on the tube)
- ETT perforation (the end-tidal gas is escaping via the hole before it gets to the capnograph)
- Capnograph disconnection or obstruction
- Water droplet contamination of capnography module
- Apnoea test in a brain dead patient
- Cardiac/respiratory arrest
It would probably be important to qualify that last point with a caveat. The end-tidal CO2 waveform in cardiac arrest would only be completely flat if the heart has stopped and you're not doing anything about it. Under normal circumstances, the patient would be having CPR, which means there would be some (decreased) cardiac output from the cardiac compressions, and the waveform would not be perfectly flat. In other words, if you're doing CPR and the EtCO2 trace has flatlined after intubation, the only rational explanation is that the endotracheal tube is in the wrong position. This issue is held to be sufficiently important to merit a public health campaign, complete with a catchy mnemonic slogan. Specifically, the UK Royal College of Anaesthetists (RCoA) and the Difficult Airway Society
(DAS) have collaborated to create the video resource Capnography: No Trace = Wrong Place to raise awareness of this issue.
This bifid waveform represents the differential ventilation of two lungs. basically, as the ETT is positioned mainly in the right main bronchus, the airflow through the right lung is the best, and right-sided gas forms the first (brisk and steep) part of the waveform. Afterwards, one notices that there is a secondary transitional phase, which is the gas from the left lung escaping slowly up into the ETT. Of course, if the left lung was completely isolated (i.e. you have the cuff inflated in such a way as to block it totally) you would not see this waveform.
This is the classical sawtooth slope of the asthmatic patient. As the airway obstruction in the bronchi worsens, so the slope of the transitional phase becomes more gradual. Note that there is no distinct alpha angle; this means that the bronchial constriction is so severe that the dead space has not finished emptying by the time the next inspiration comes along. Thus, as bronchospasm is relieved, the alpha angle will again appear.
In the case of airway obstruction by some sort of fixed mechanical obstacle (eg. big gross tumour) the inspiratory flow will also be affected. Thus, both the transitional phase and the inspiratory phase will be affected, and most strikingly the inspiratory phase slope will become less steep, indicating that the obstruction cannot be overcome even by the powerful ventilator turbine.
This pattern can be generated without any pathology by the intensivist who sets the inspiratory rise time to be prolonged for whatever reason.
In emphysema, the alveolar slope will be reversed. The gas exchange surface is so poor, and the compliance of the lungs so abnormally increased, that the alveolar gas exchanges very rapidly. Thus, the part of the curve which represents arterial CO2 is the early peak, not the end-tidal value.
Thereafter, gas in the ventilator tubing diffuses backwards into the patient. There is an equilibration between the higher CO2 inside the patient and the lower CO2 in the ventilator circuit, with a resulting gradual drop of the total CO2 concentration in the capnograph-adjacent tubing.
This pattern can be seen in anaesthetic machines with rapid gas flow, where the ventilator contributes fresh gas to the tubing next to the capnometer. An alternative explanation is a pneumothorax with massive air leak - the air leak sucks CO2-rich air out of the capnometer, attracking fresh gas back through it.
This waveform represents the pulsation of an extra-large heart, transmitted to the lung parenchyma. The resulting changes in lung volume are enough to move a small amount of gas back and forth, creating "ventilation" of a sort. In some circumstances, this may be a feature of cardiomegaly.
The "curare cleft" seen in the alveolar plateau is actually a patient making an attempt to breathe. With their feeble inspiratory effort, some fresh gas sucked from the ventilator tubing and past the capnometer, generating this pattern. It is most frequently seen in anaesthetic machines where there is a constant flow of fresh gas across the circuit.
Another feature unique to anaesthesia. If the CO2 absorbing lime bucket is saturated, the circuit becomes inundated with expired CO2 and the baseline gradually increases. In the ICU, such a thing is unknown, and it would be very surprising to see a rising CO2 baseline.
In hypothermia, the total body CO2 production is greatly decreased (as the metabolic rate is decreased by 6% for every degree below 36°). The end-tidal CO2 in these people will be unnaturally low.
This can be seen in a number of other conditions. For instance, a low-cardiac-output state generates a low end-tidal CO2 because there is simply not enough flow across the pulmonary circulation. Or, alternatively, deep anaesthesia and muscle paralysis will result in a similar picture.
This pattern is called a "pigtail" capnogram. It is typically seen in poor lung compliance, but it can also occur in pregnant women and obese patients. Essentially, the sudden peak of pre-inspiratory expired CO2 is due to sudden airway closure. It occurs when a poorly compliant lung (or a huge fat chest wall, or a big pregnant belly) crushes the last few milliliters of CO2-rich gas from the alveoli before the collapse of the lung parenchyma also occludes the small bronchi and puts an end to the escape of gas.