Capnography: monitoring C[O.sub.2].
Using EtC[O.sub.2] to monitor respiratory function offers many benefits over pulse oximetry. It is important to understand the differences between these two monitoring methods, and why capnography is increasingly favoured in many situations. An understanding of the physiological processes involved in C[O.sub.2] excretion allows nurses to use capnography in a safe and meaningful way, while monitoring at-risk patients in acute care.
Monitoring C[O.sub.2] excreted by the Lungs (capnography) has been common in general anaesthesia since the late 1980s, where it has been used to detect airway management problems and provide early warning of cardiac and pulmonary dysfunction. (1) Since that time, use of end tidal C[O.sub.2] (EtC[O.sub.2]) monitoring in critical care has become increasingly common. While it is mainly used to check for correct placement of endotracheal tubes during intubation, continuous monitoring allows early detection of tube dislodgement or blockage and, in some cases, abnormal cardiac function. (2)
More recently, capnography has moved into the community. Emergency services are using EtC[O.sub.2] during cardiopulmonary resuscitation to check endotracheal tube placement and to monitor effectiveness of cardiac compressions.
Conscious sedation for minor procedures, such as endoscopy or in emergency departments, is increasingly recognised as a source of potential respiratory compromise. In the United States (US), sedation-related mortality during gastrointestinal endoscopy procedures is around eight per 100,000 cases, compared to anaesthesia-related mortality in operating theatres of an estimated 8.2 per million cases. (3) Guidelines recommend access to EtC[O.sub.2] monitoring, although some clinical areas have been slow to adopt this. (4,5,6) Monitoring of EtC[O.sub.2] via capnography is now entering general wards: opioid-induced respiratory depression is a major harm associated with analgesic therapy and capnography can be used to detect it early. In the US, post-operative respiratory failure was the third most-reported safety incident between 2006 and 2009.7 Studies show intermittent bradypnoea (respiratory rate of fewer than 10 breaths per minute) and desaturation are much more common in patients using opioids than are detected by intermittent monitoring and pulse oximetry: two per cent, versus 58 per cent detected via capnography. (8)
As with any new technology entering nursing practice, safe and proficient use requires a good understanding of the underlying principles of capnography: the physiological underpinnings of EtC[O.sub.2] and the function of devices used to measure it.
Atmospheric air contains negligible amounts of C0?, so fresh air moving into the lungs is considered to have no C[O.sub.2] in it. C[O.sub.2] exhaled from the lungs comes from the exchange of gasses in the alveoli, where the body excretes the C[O.sub.2] produced in its metabolic processes.
C[O.sub.2] is mainly produced during the breakdown of nutrients to form energy (ATP) in the cells. The amount of C[O.sub.2] produced depends on the rate of metabolism (exercise, fever, infection or trauma will increase production) and the relative amounts of carbohydrates, fats and proteins being converted to ATP.
Once formed, C[O.sub.2] diffuses from cells into the blood, where it is transported either attached to haemoglobin molecules or dissolved in the plasma as bicarbonate. C[O.sub.2] in the body performs several essential physiological roles, including buffering of pH and regulation of respiration.
Buffering role of C[O.sub.2]
When C[O.sub.2] enters the plasma, about 90 per cent of it is converted to bicarbonate ions through the equation:
C[O.sub.2] + [H.sub.2]O [left right arrow] [H.sub.2]C[O.sub.3] [left right arrow] HC[O.sub.3.sup.-] + [H.sup.+] carbon dioxide + water [left right arrow] carbonic acid [left right arrow] bicarbonate + hydrogen
This is a two-way equation. If more C[O.sub.2] is added to the plasma, the equation shifts to the right and acid is produced. The kidneys can buffer increasing amounts of bicarbonate in the blood, but this is a slow response.
If more acid ([H.sup.+]) is added to the plasma, the equation moves to the left and more C[O.sub.2] is produced. The lungs can rapidly excrete this extra C[O.sub.2] and pH is restored rapidly to normal physiological values. Impaired excretion of C[O.sub.2] from the lungs will quickly cause acidosis (a decrease in the body's pH level, making it too acidic).
C[O.sub.2] levels in the plasma and pH both affect the respiratory control centres in the brainstem. Hypercapnia, or acidosis, will trigger an increase in the depth and rate of ventilation to excrete more C[O.sub.2] and bring the pH back up to normal. It is the brainstem responses to hypercapnia that are particularly blunted by opioid drugs.
Acidosis is dangerous because it affects protein structures inside the cells and inhibits cellular metabolism. The impact of this on the brain and cardiovascular system can be life-threatening. Increased arterial C[O.sub.2] (hypercapnia) also has a direct impact on cerebral and cardiovascular function, causing vasodilation and raised intracranial pressure. C[O.sub.2] narcosis can lead to seizures, coma, respiratory arrest and death.
C[O.sub.2] is a highly soluble gas so normally functioning lungs can easily compensate for any increase in C[O.sub.2] production by the body. C[O.sub.2] builds up in the body where there is reduced ventilation or increased dead space. Increased C[O.sub.2] in the alveoli will eventually displace oxygen. This leads to low oxygen saturations and hypoxaemia, but the impact of this can be masked in people receiving supplementary oxygen.
In studying the role of capnography in assessing a patient's respiratory and metabolic states, it is important to understand the terminology associated with ventilation. Tidal volume is the amount of air moving in and out of the lungs during a single breath (inhalation and exhalation). The average 70kg male moves about 500-600ml of air during tidal breathing. The resting respiratory rate is between 12 and 16 breaths per minute in adults. These two figures can be combined to provide the minute volume--the amount of air exchanged between the lungs and the air each minute. This is normally around six to seven litres.
The airways can be divided into conducting and exchanging segments. The conducting portion (upper airways, trachea, bronchial tree) provides passage for air into and out of the exchanging portions. Air in these sections of the respiratory tract does not change its composition during the breathing cycle and is referred to as anatomical dead space air--it is not available for gas exchange.
During expiration, the first bit of air to exit the tract comes from the trachea and bronchi and has the same composition as atmospheric air --that is, minimal C[O.sub.2]. This accounts for phase one of the capnograph where, even though expiration has begun, there is no movement of the graph from baseline (see Figure 1, right).
When air enters the exchanging portions of the lungs, it mixes with, and replenishes, the residual air that stays in the lungs during normal quiet respiration. This air in the exchanging portion of the lungs (the terminal bronchioles and alveoli) has a gas content that has equilibrated with that of the blood in the pulmonary capillaries. When this alveolar air is exhaled, the C[O.sub.2] reading of the capnograph rises and eventually plateaus, reflecting the total amount of C[O.sub.2] in expired air (see Figure 1). The end tidal reading is the last of the air exhaled during normal (tidal) breathing and should have the greatest amount of C[O.sub.2].
Inspiration sees a sharp downward deflection of the capnograph as fresh atmospheric air, with negligible C[O.sub.2], is taken into the lungs.
Some regions of the lungs receive good airflow (ventilation--V) but not such good blood flow (perfusion--Q). This difference between ventilation and perfusion in certain areas of the lungs is called a V/Q mismatch. It happens naturally where gravity and blood pressure affect flow in the pulmonary capillaries and can also be caused where the airway or the capillaries are obstructed due to disease processes. Poor ventilation with adequate perfusion will cause an increase in EtC[O.sub.2], while poor perfusion causes decreased EtC[O.sub.2].
In the healthy lung, there is relatively little of this alveolar dead space. The combined alveolar and anatomical dead space is called the physiological dead space and consists of about one third of the volume of each breath in normal quiet breathing. Dead space is increased in the presence of any respiratory device that does not allow free gas exchange with the atmosphere, eg ventilator tubing.
There are two ways to monitor expired C[O.sub.2]--by detecting change in the pH of expired air, or by measuring the C[O.sub.2] concentration. A single check for C[O.sub.2] can be obtained by inserting a pH detector at the end of a tracheostomy or endotracheal tube. This will change colour in the presence of C[O.sub.2], thus confirming placement of the tube within the trachea (and also allowing detection of incorrect placement of gastrooesophageal tubes). These are single-use devices and cannot be used to monitor ongoing ventilation and C[O.sub.2] output.
Quantitative devices that use infrared light or lasers provide more extensive information about the patient's respiratory function. Infrared detection is the most commonly used and relies on passing a light beam through a sample of exhaled air. C[O.sub.2] absorbs a specific wavelength of the light and this is measured to calculate the amount of C[O.sub.2] in the sample. Calibration is required and the presence of other gases with wavelengths close to C[O.sub.2] can cause reading errors. Laser light that is precisely tuned to the wavelength of C[O.sub.2] is more accurate and allows analysis of smaller volumes of air. (6)
Sampling for capnographs can be either inline or sidestream. Inline capnography provides instant readings and also flow data, but adds weight and bulk to airway tubing and increases dead space in the ventilator circuit. Sidestream monitoring--where a sample of air is diverted from the tubing and used for analysis--has a slight delay and requires that a minimum volume of air be exhaled, which makes these unsuitable for infants and neonates. It is also subject to malfunction when water vapour accumulates in the sampling tubing. However, it is much less bulky and therefore able to be used with non-invasive oxygen delivery methods. (9) Capnography devices can give either numerical or waveform readings of EtC[O.sub.2]. There are now compact devices available that include pulse oximetry.
THE NORMAL CAPNOGRAM
Most commonly seen in clinical practice is the time-based capnogram (see Figure 1, above). This displays a steady increase in C[O.sub.2] after expiration commences, progressing to a slightly sloped plateau as the EtC[O.sub.2] is reached. EtC[O.sub.2] correlates to arterial C[O.sub.2] concentrations when ventilation and perfusion are normal, but is slightly lower due to dead space ventilation. The difference between arterial and EtC[O.sub.2] increases where there is increased physiological dead space (alveoli are ventilated but not perfused) or where there is poor perfusion of the lungs. (3,6)
Changes in waveform or height can indicate altered respiratory function or perfusion, or equipment malfunction. A steadily decreasing height can indicate increased ventilation (hyperventilation) or reducing lung perfusion. Increased height of the wave indicates hypoventilation. Failure to return to zero during inspiration indicates rebreathing of C[O.sub.2] and could indicate problems with ventilator circuits and settings.
When assessing a capnogram the following points should be noted: (6)
* Is the patient breathing? Is there evidence of apnoeic episodes? What is the respiratory rate?
* Is there evidence of slow and even expiration--a smooth, slanted upstroke and plateau?
* Is the down stroke steep (normal)? Is there slow inspiration or failure to return to the zero baseline?
* In mechanically ventilated patients, is there evidence of interrupted or spontaneous inspiratory efforts at the plateau?
Monitoring of EtC[O.sub.2] is commonplace in theatres, post-operative recovery rooms and intensive care and is becoming increasingly so in emergency care and for procedural sedation.
The intubated patient
A single reading of EtC[O.sub.2] is the gold standard for confirming placement of endotracheal tubing (ETT) following intubation. (2) Continuous monitoring of EtC[O.sub.2] for intubated and ventilated patients allows early detection of tube dislodgement (eg during repositioning or transportation), blockage, leakage or kinking. It contributes to assessment of the adequacy of gas flow, mechanical ventilation and reversal of neuromuscular blocking agents. (6) Lack of continuous capnography contributed to 82 per cent of airway incidents in intensive care causing death or severe neurological damage in a UK audit. (2) Use of capnography is universal in operating theatres worldwide, but very variable in intensive care units. In 2009, only 25 per cent of ICUs in the UK used capnography routinely, (1) while 64 per cent of Australian and New Zealand units use it continuously. (2)
Aside from checking for ETT placement, EtC[O.sub.2] monitoring has a valuable role during cardiopulmonary resuscitation. Monitoring of exhaled C[O.sub.2] can be used to assess adequacy of cardiac compressions. Increasing EtC[O.sub.2] indicates sufficient circulation to allow exchange of gases in the alveoli. It can be used as an early indicator of return of spontaneous circulation--increasing EtC[O.sub.2] will often precede palpable pulse or blood pressure. Prolonged low EtC[O.sub.2] in cardiac arrest has been associated with low survival. (6)
In emergency services and departments, EtC[O.sub.2] monitoring can be used to monitor breathlessness in acute asthma or exacerbations of chronic obstructive airway diseases. This non-invasive and effort-independent monitoring can detect responses to therapy and changes in the airway calibre. It also provides continuous monitoring of respiratory rate.j
Assessment of cardiovascular function
Aside from use during resuscitation, EtC[O.sub.2] can be an indirect measure of cardiac output and pulmonary circulation. In patients with normal ventilation and perfusion, the EtC[O.sub.2] closely correlates to the arterial concentration of C[O.sub.2]. Decreasing EtC[O.sub.2] in the presence of unchanged minute ventilation indicates less C[O.sub.2] being excreted in the alveoli. C[O.sub.2] is a highly soluble gas--if it is delivered to the lungs, it will exchange very readily. A decrease in EtC[O.sub.2] can indicate lack of pulmonary circulation due to either low cardiac output (eg hypotension or shock) or to a blockage in the pulmonary circulation--a pulmonary embolism. Measurement of arterial C[O.sub.2] would demonstrate increasing levels. (3)
Capnography for opioid analgesia
Fear of respiratory depression can lead to patients being under-medicated for pain--this can increase both their discomfort and length of stay in hospital. Insufficient pain relief can also reduce quality of living for those with cancer or chronic pain, and lead to poorer post-operative recovery. Opioid-induced respiratory depression risks permanent neurological damage or death, but identification of at-risk patients is problematic. (10) Furthermore, since most post-op patients are administered supplemental oxygen (at least in the initial 24 hours), pulse oximeters are inadequate to rapidly detect declining respiratory effort during initiation of opioid therapy.
Opioids inhibit chemoreceptor sensitivity to C[O.sub.2] and blunt chemoreceptor sensitivity to hypoxia. Also, they are believed to act directly on brainstem respiratory control centres to affect rate and rhythm of breathing. (11) As a result, respirations become slower and irregular. Opioids also cause central nervous system sedation (which always precedes respiratory depression). Sedation decreases the conscious drive to breath and limits feedback from sensations such as dyspnoea that would trigger this. The incidence of centrally mediated sleep apnoea episodes also increases. (11)
Opioids also decrease skeletal muscle tone in the upper airway, leading to mechanical obstruction of the airway similar to that experienced during obstructive sleep apnoea.
Risk of opioid-induced respiratory depression is increased with: (7, 17)
* Concurrent use of other respiratory depressant drugs, such as benzodiazepines, anaesthetic agents, antihistamines.
* Longer general anaesthetic time.
* Morbid obesity.
* Sleep apnoea or snoring.
* No previous exposure to opioids.
* Older age.
* Chest or upper abdominal surgery, or incision lines that impair chest movement.
* Cardiac, renal or respiratory disease.
* Surgery, within the first 24 hours.
* Continuous opioid infusions.
* Opioid dose escalation particularly within the first 24 hours.
Box 1. Monitoring respiratory rate (15,16) THE NORMAL respiratory rate (RR) for an adult is 12 to 20 breaths per minute (bpm). For infants and children it varies according to age: up to one year 25-60 bpm; ages one to four years 20-40 bpm; and ages five to 12 years 16-34 bpm. Abnormal respiratory rate is one of the best predictors of an impending adverse event such as clinical deterioration or cardiac arrest. An RR of 10 bpm or fewer is considered bradypnoea and indicative of respiratory depression. The RR should be counted in adults while palpating the patient's radial pulse so the patient is not aware of the measurement being taken (which will cause an alteration in their RR), but still understands that you cannot engage in conversation (which will also alter RR). Observation, or placing a hand on the patient's shoulder, may both be used for accurate counting. DO NOT tell the patient you are counting their RR! For infants, the RR should be measured using a stethoscope, since this is significantly more accurate than chest observation in this group. RR should be counted for a minimum of 30 seconds, and for a full minute in infants and young children, if the RR is outside normal values, or if the patient is severely unwell. Aside from RR, the nurse should observe for (and document) signs of increased respiratory effort such as nasal flaring, pursed lips, grunting in infants, use of accessory muscles, wheezing or coughing. Note should be made if breathing appears shallow or deeper than normal, or rhythm is irregular.
The assessment of respiratory rate is a core clinical assessment for monitoring of respiratory depression but it is not always performed correctly (see Box 1, above). Respiratory rate should ideally be counted for a whole minute, which is often perceived as difficult in a busy ward. Perhaps this accounts for research showing nurses recording respiratory rates fewer than 30 per cent of the required times before the introduction of early warning scoring systems. (12) Furthermore, in a recent study it was found that up to 35 per cent of patients who experienced hypoxaemia while undergoing procedural sedation for endoscopy had normal ventilation. Even in a one-on-one monitoring situation, simple observation missed 25 per cent of apnoea episodes (longer than 20 seconds) in one study. (3) C[O.sub.2] levels in the blood can increase even where there is an apparently adequate respiratory rate, if the amount of gas reaching the alveoli is not sufficient for gas exchange to occur with the blood. This phenomenon is known as hypopnoeic hypoventilation decreased tidal volume without a change in respiratory rate that causes an overall reduction in minute volume.
Nurses cannot rely on pulse oximeters to replace respiratory rate monitoring, nor can they rely solely on counting respirations to monitor for respiratory sedation. But capnography has been shown to detect declining respiratory effort or function up to two hours earlier than oxygen saturation monitoring in patients receiving opioids via patient-controlled analgesia (PCA). (13) A study of children undergoing procedural sedation with ketamine discovered that 72 per cent of episodes of hypoxia were preceded, on average by three to four minutes, by an increase in EtC[O.sub.2], when gaseous exchange reduced in the child's alveoli. (14)
The amount of C[O.sub.2] exhaled from the lungs is determined by metabolism (C[O.sub.2] production), perfusion (C[O.sub.2] transport and delivery to the alveoli) and alveolar ventilation. Monitoring of EtC[O.sub.2] can provide insights into all three of these processes but is most useful from a nursing perspective in monitoring the rate at which C[O.sub.2] is being removed from the lungs. This provides accurate and continuous information about minute ventilation and the patient's respiratory status. Hypercapnia, rather than hypoxia is the issue here--failure to exhale C[O.sub.2] means it is accumulating in the blood. Hypercapnia causes C[O.sub.2] narcosis and may occur in the absence of hypoxia (oxygen saturation less than 90 per cent). Raised EtC[O.sub.2] can occur minutes earlier than desaturation in patients receiving oxygen therapy, providing an early warning of impending respiratory compromise.
More common use of capnography in the clinical arena could help to prevent harm from drugs that cause respiratory depression.
Georgina Casey, RN, BSc, PGDipSci, MPhil (nursing), is the director of CPD4nurses.co.nz. She has an extensive background in nursing education and clinical experience in a wide variety of practice settings.
After reading this article, and completing the accompanying online learning activities, you should be able to:
* Outline the production, transport, excretion and roles of C[O.sub.2] in the body.
* Describe the significance of increased and decreased EtC[O.sub.2] levels.
* Discuss the methods used to measure EtC[O.sub.2], and their advantages and disadvantages.
* Compare the information provided by EtC[O.sub.2] monitoring with that from pulse oximetry.
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(1) Whitaker, D. (2011) Editorial: Time for capnography--everywhere. Anaesthesia; 66, pp544-549.
(2) Husain, T., Gatward, J.J., Hambidge, O.R., Asogan, M. & Southwood, T.J. (2012) Strategies to prevent airway complications: a survey of adult intensive care units in Australian and New Zealand. British Journal of Anaesthesia; 108: 5, pp800-806. doi:10.1093/bja/aes030.
(3) Restrepo, R.D., Nuccio, P., Spratt, G. & Waugh, J. (2014) Current applications of capnography in nonintubated patients. Expert Review of Respiratory Medicine; 8: 5, pp629-639.
(4) ANZCA (Australian and New Zealand College of Anaesthetists). (2014) Guidelines on sedation and/or analgesia for diagnostic and interventional medical, dental or surgical procedures, www.anzca.edu.au/resources/professional-documents/pdfs/ps09-2014-guidelines-on-sedation-and-or-analgesia-for -diagnosticand-interventional-medical-dental-or-surgical-procedures.pdf. Retrieved 12/09/15.
(5) Royal College of Anaesthetists and the College of Emergency Medicine. (2012) Safe sedation of adults in the emergency room. www.rcwm.ac.uk/code/document.asp?ID=6691. Retrieved 12/09/15.
(6) Spiegel, 3. (2013) End-tidal carbon dioxide: the most vital of vital signs. Anesthesiology News; October, pp21-27.
(7) Carlisle, H. (2014) The case for capnography monitoring in patients receiving opioids. American Nurse Today; 9: 9, pp22-27.
(8) Overdyk, F.J., Carter, R., Maddox, R.R., Callura, 3., Herrin, A.E. & Henriquez, C. (2007) Continuous oximetry/capnometry monitoring reveals frequent desaturation and bradypnea during patient-controlled analgesia. Anesthesia & Analgesia; 105: 2, pp412-418.
(9) Bauman, M. & Cosgrove, C. (2012) Understanding end-tidal C0? monitoring. American Nurse Today; 7: 11, pp12-17.
(10) McCarter, T., Shaik, Z., Scarfo, K. & Thompson, L.J. (2008) Capnography monitoring enhances safety of post-operative patient-controlled analgesia. American Health & Drug Benefits; 1: 5, pp28-35.
(11) Pattinson, K. (2008) Opioids and the control of respiration. British Journal of Anaesthesia; 100: 6, pp747-758.
(12) McBride, J., Knight, D., Piper, J. & Smith, G.B. (2005) Long-term effect of introducing an early warning score on respiratory rate charting on general wards. Resuscitation; 65:1, pp41-44.
(13) Maddox, R. & Williams, C. (2012) Clinical experience with capnography monitoring for PCA patients. Newsletter--the Official Journal of the Anesthesia Patient Safety Foundation; Winter 2012. www.apsf.org/ newsletters/html/2012/winter/05_capMonitor.htm. Retrieved 12/09/15.
(14) Langhan, M., Chen, L. & Marshall, C. (2011) Detection of hypoventilation by capnography and its association with hypoxia in children undergoing sedation with ketamine. Pediatric Emergency Care; 27: 5, pp394-397.
(15) Elliott, M. & Coventry, A. (2012) Critical care: the eight vital signs of patient monitoring. British Journal of Nursing; 21: 10, pp621-625.
(16) The Royal Children's Hospital Melbourne. (2014) Clinical Practice Guidelines: Normal Ranges for Physiological Values. www.rch.org.au/clinicalguide/guideline_index/Normal_Ranges_for_Physiological_Variables/. Retrieved 12/09/15.
(17) Jarzyna, D., Jungquist, C.R., Pasero, C., Willens, J.S., Nisbet, A., Oakes, L., Dempsey, S.J., Santangelo, D. & Polomano, R.C. (2011) American Society for Pain Management Nursing guidelines on monitoring for opioid-induced sedation and respiratory depression. Pain Management Nursing; 12: 3, pp118-145.
Table 1. Comparing capnography with pulse oximetry Capnography Pulse oximetry Measures End tidal carbon Oxygen saturation of dioxide haemoglobin Effect of supplemental oxygen Not affected Increases Also can provide data on Respiratory rate Heart rate Useful for Immediate indication Indication of changing of hypoventilation, oxygen content in the apnoea, airway blood. obstruction Indirect assessment of ventilation. Cannot provide Oxygenation status Ventilation in the data on presence of supplemental oxygen. Actual delivery of oxygen to the tissues. Real-time changes in oxygenation or ventilation.
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|Publication:||Kai Tiaki: Nursing New Zealand|
|Date:||Oct 1, 2015|
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