Davies Veterinary Specialists, Manor Farm Business Park, Higham Gobion, Hertfordshire, UK
Introduction
The measurement of end-tidal carbon dioxide (ETCO2) allows the continuous monitoring of the adequacy of ventilation and circulation in the anaesthetised patient. It measures inspired and expired carbon dioxide (CO2) throughout the whole respiratory cycle using infrared spectroscopy. ETCO2 can be of value in the assessment of ventilation, metabolism and of a patient's circulatory status. In addition, it provides early detection of problems such as airway obstruction and disconnection from the anaesthetic breathing system.
Co2 Physiology
CO2 is a waste product of normal aerobic cellular metabolism. Oxygen (O2) is inhaled via the lungs where it diffuses across the alveolar-capillary membrane and enters the pulmonary circulation. The heart pumps the oxygenated blood to the cells where it is used for normal cellular metabolism. The waste product of this metabolism is CO2 which, like all other waste products, has to be removed from the body. Once the CO2 has been produced following metabolism it leaves the cells and is carried in the circulation to the heart, which in turn pumps the CO2 to the lungs where it is exhaled from the body during respiration. In order for CO2 to be effectively removed from the body, there must be adequate blood flow to the lungs, adequate gas change across the alveolar-capillary membrane, and adequate lung ventilation to remove the CO2 from the body. Therefore changes in expired CO2 may reflect alterations in metabolism, circulation and ventilation.
Normal Respiration
In conscious patients the CO2 and O2 levels in the blood are monitored by receptors called chemoreceptors that sit in the aorta, carotid artery and medulla. The chemoreceptors are responsible for maintaining normal levels of CO2 and O2 in the bloodstream. When an increase in CO2 is detected, the respiratory centres in the brain respond by increasing the rate and depth of respiration and subsequently more CO2 is expired from the body. Conversely, if CO2 levels are low the depth and rate of respiration is decreased and subsequently the CO2 levels are maintained within normal limits.
The chemoreceptors in the aorta and carotid artery also monitor the O2 content of the blood. If the O2 content falls the chemoreceptors and respiratory centres respond by increasing the rate and depth of respiration with the aim of maintaining tissue O2 delivery. Equally, if the O2 blood content increases, the chemoreceptors and respiratory centres will respond by decreasing the rate and depth of respiration.
Anaesthesia and Respiration
During anaesthesia many of the drugs we use, e.g., opioids (morphine) and inhalants (isoflurane), can result in depression of the body's 'normal' respiratory control mechanisms noted above. This can cause the patient to hypoventilate, which is characterised by slow and shallow respiration.
Respiratory depression during anaesthesia can also occur due to anaesthesia-induced muscle relaxation. The respiratory muscles, i.e., diaphragm, can become relaxed and subsequently less efficient. This can result in hypoventilation. In addition, positioning during anaesthesia, increased abdominal pressure, atelectasis and resistance from the endotracheal tube can exacerbate hypoventilation.
Once hypoventilation occurs, an excessive accumulation of CO2 can result. In the short term and in healthy patients a slight elevation in CO2 can probably be tolerated without adverse effects. However, if CO2 is severely increased or in cases of prolonged elevation, respiratory acidosis can occur. If severe this can cause cellular malfunction and can result in myocardial depression, cardiac arrhythmias and eventually narcosis. During anaesthesia it is important to monitor patient ventilation and ensure CO2 is removed from the body effectively. The best non-invasive way to monitor CO2 during anaesthesia is with capnography.
Capnograph Interpretation
Firstly check if a normal trace is present (Figure 1) and note the numerical value of the ETCO2. During capnograph interpretation, the contribution of metabolism, circulation and ventilation to the production of ETCO2 must be considered. For example, if metabolism and circulation are stable, then abnormal capnograph traces or ETCO2 levels are probably associated with ventilation. Conversely, if ventilation is stable, then abnormal capnograph traces or ETCO2 levels are probably associated with either metabolism or circulatory problems. In addition, the capnograph trace will also allow recognition of technical faults, airway patency and adequacy of fresh gas flow rates or soda lime efficiency (Figure 2).
A–B: Exhalation of CO2 free gas contained in dead space (endotracheal tube, breathing circuit tubing) at the beginning of expiration
B–C: Expiratory phase, representing the emptying of connecting airways and the beginning of emptying of the alveoli. Note the sudden rise in CO2 as it is expired
C–D: Expiratory plateau, representing emptying of alveoli
D: ETCO2
D–E: Inspiratory phase, as the patient begins to inhale fresh gas
E–A: Continuing inspiration, where CO2 remains at zero
Normocapnia 35–45 mmHg
Hypocapnia < 35 mmHg
Hypercapnia > 45 mmHg
For abnormal capnograph traces - www.capnography.com. This internet site contains capnographs for human traces. Not all are applicable to veterinary patients.
| Figure 1. Normal capnograph trace. | 
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Figure 2. Changes in ETCO2 during anaesthesia.
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ETCO2 level
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Cause of change
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CO2 production/
metabolism
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Pulmonary
perfusion
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Alveolar
ventilation
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Technical errors/
machine faults
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Hypercapnia
(Increased ETCO2)
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Early sepsis/fever causes increased metabolism
Hypermetabolic states - malignant hyperthermia
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Increased cardiac output - increased pulmonary blood flow
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Hypoventilation:
- Deep anaesthesia
Opioids
- Anaesthesia-induced atelectasis
- Increased abdominal pressure (ascites/pregnancy)
- Partial airway obstruction - kinked endotracheal tube
- Pneumothorax / haemothorax etc.
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Rebreathing CO2
Exhausted CO2 soda lime absorber
Inadequate fresh gas flow
Faulty/sticking breathing system valves
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Hypocapnia
(Decreased ETCO2)
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Hypothermia resulting in reduced metabolism
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Reduced cardiac output - reduced pulmonary blood flow
Imminent cardiac arrest
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Hyperventilation:
- Light anaesthesia
- Invasive surgical stimulation
- Pain
- Excessive assisted ventilation
- Hypoxia
- Pyrexia
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Leak around endotracheal tube cuff
Excessively high fresh gas flow causing dilution of ETCO2 sample
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Absent ETCO2
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Cardiac arrest
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Oesophageal intubation
Apnoea
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Breathing circuit disconnection
Capnograph calibration/zeroing
Accidental extubation
Pressure build-up in anaesthetic breathing circuit, e.g., closed scavenge valve
Complete endotracheal tube occlusion
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Cardiopulmonary Cerebral Resuscitation (CPCR) and Capnography
The delivery of CO2 to the lungs requires blood flow. One of the earliest signs of cardiovascular collapse or cardiac arrest is an abrupt decrease in ETCO2.
Capnography can be a valuable tool during CPCR. Studies have shown that the closer to normal the ETCO2 levels are the more effective cardiac output is during resuscitation. Lower ETCO2 levels observed during resuscitation may signal a need for change in CPCR techniques.
ETCO2 levels during CPCR have prognostic value for successful resuscitation. Patients with an ETCO2 > 14 mmHg are more likely to have a positive outcome following CPCR.
References
1. Bryant S. Anesthesia for Veterinary Technicians. Oxford: Wiley-Backwell. 2010.
2. Kolar M, Križmaric M, et al. Partial pressure of end-tidal carbon dioxide predict successful cardiopulmonary resuscitation - a prospective observational study. Critical Care 2008:12(5).
3. Seymour C, Duke-Novakovski K. BSAVA Manual of Canine and Feline Anaesthesia and Analgesia. 2nd ed. Quedgeley: British Small Animal Veterinary Association. 2007.
4. Welsh L. Anaesthesia for Veterinary Nurses. 2nd ed. Oxford: Wiley-Backwell. 2009.
5. www.capnography.com