Capnography in the Intubated Mechanically Ventilated Patient

Betina Santos Tomaz +

Sarah Gracielly Sena Sousa +

Marcelo Alcantara Holanda +

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By the end of this chapter, the reader should be able to:

1. Define capnography and capnometry;
2. Understand the relationship between exhaled CO₂, metabolism, ventilation, and pulmonary perfusion;
3. Interpret the normal capnogram and its integration with mechanical ventilation waveforms;
4. Recognize abnormal capnographic patterns and their implications across different clinical scenarios and conditions.

1. Capnography: Fundamental Concepts, Operating Principles, and Practical Relevance

Capnography is a non-invasive monitoring method that continuously measures the concentration or partial pressure of carbon dioxide (CO₂) in both inspired and expired gases throughout the respiratory cycle. The capnograph displays this information as a waveform plotted against time or expired volume. In addition to graphical tracing, capnography provides derived numerical values, the most used being the partial pressure of CO₂ at the end of tidal expiration, referred to as ETCO₂ (end-tidal carbon dioxide).

Capnometry, in contrast, refers exclusively to the numerical measurement of exhaled CO₂ without graphical representation. Thus, while capnometry provides only a single CO₂ value, capnography enables dynamic and integrated assessment by reflecting variations in ventilation, pulmonary perfusion, and cellular metabolism through analysis of capnogram morphology. ^{1, 2} Furthermore, changes in the capnogram waveform may precede alterations in absolute ETCO₂ values.²

Infrared absorption spectroscopy is the most widely used technique in capnography. CO₂ strongly absorbs infrared light at a wavelength of 4.3 μm. Based on this molecular property, capnographs emit infrared light that is transmitted through a gas sample toward a detector. As the CO₂ concentration increases, the intensity of light reaching the detector decreases, enabling measurement of the CO₂ fraction in the sample. At this wavelength, interference from other gases commonly present in the breathing mixture (such as water vapor, oxygen, and nitrous oxide), as well as inhaled anesthetic agents, is minimal, allowing reliable application across diverse clinical environments, including operating rooms, emergency departments, and intensive care units.^{3, 4}

Two principal capnograph technologies are available: mainstream and sidestream. Mainstream devices employ sensors positioned directly within the ventilator circuit, enabling real-time CO₂ measurement. Sidestream devices continuously aspirate a small gas sample from the respiratory circuit and transport it through a sampling line to an external analyzer, resulting in a short delay in response to changes in CO₂ concentration.⁵ Mainstream devices are particularly suitable for intubated patients receiving mechanical ventilation, ideally integrated with flow, volume, and pressure-time waveforms, as well as volumetric capnography. Sidestream devices, on the other hand, can be coupled to masks or nasal cannulas in non-intubated patients.

Despite the nearly universal use of capnography during anesthesia in high-income countries, its adoption in intensive care units has expanded more recently. In 2011, the Fourth National Audit Project conducted by the Royal College of Anaesthetists and the Difficult Airway Society in the United Kingdom identified an excessive number of airway-related deaths in ICUs, with approximately 80% associated with failure to use capnography or misinterpretation of its data. Publication of these findings led to increased routine capnography use in that setting.⁶

Currently, capnography is increasingly incorporated into modern mechanical ventilators, becoming part of routine monitoring during invasive ventilatory support. This integration has been associated with improved patient safety, earlier detection of critical airway events, and optimized ventilator settings.² In this chapter, the focus will be on time-based capnography integrated with invasive mechanical ventilation (MV), excluding volumetric capnography, which warrants dedicated discussion.

2. CO₂ Physiology and the Relationship Between PaCO₂ and ETCO₂: Integration of Metabolism, Ventilation, and Pulmonary Perfusion

CO₂ is the primary by-product of aerobic cellular metabolism, being continuously produced in peripheral tissues (V̇CO₂) and transported via venous blood to the lungs, where it diffuses into the alveoli and is subsequently eliminated into the atmosphere through alveolar ventilation. In the blood, CO₂ is predominantly transported as bicarbonate, with smaller fractions dissolved in plasma and bound to hemoglobin. Pulmonary CO₂ elimination depends on the interaction of three fundamental physiological components⁷:

Metabolism, determines the rate of CO₂ production;
Pulmonary perfusion, delivers CO₂ to the alveoli;
Alveolar ventilation, removes CO₂ from the alveolar space.

Alterations in any of these components directly affect CO₂ concentrations in arterial blood and exhaled gas.

Arterial CO₂ partial pressure (PaCO₂), measured by arterial blood gas analysis, serves as the reference standard for evaluating alveolar ventilation. The partial pressure of CO₂ at the end of expiration (ETCO₂), obtained noninvasively through capnography, reflects, under ideal conditions, alveolar CO₂ partial pressure (PACO₂).⁸

When metabolism, pulmonary perfusion, and alveolar ventilation remain relatively stable, PaCO₂ and ETCO₂ show a strong correlation, with typical reference values of approximately 40 mmHg and 38–35 mmHg, respectively. A small physiological pressure gradient is normally present due to the limited fraction of alveolar dead space, typically 2-5 mmHg, referred to as P(a–et)CO₂. Under these conditions, PetCO₂ can serve as a continuous, indirect marker of alveolar ventilation, enabling real-time bedside monitoring.^{7, 9, 10}

Dead space refers to the fraction of tidal volume that does not participate effectively in gas exchange and may be classified as anatomical, alveolar, or physiological. An increase in the dead space to tidal volume ratio (VD/VT) reduces CO₂ elimination efficiency and leads to widening of the P(a–et)CO₂ gradient.^{9, 10, 11}

Figure 1 presents the main indications and benefits of capnography in the invasively mechanically ventilated patient.

Figure 1. Indications and benefits of capnography integrated with mechanical ventilation waveforms in the intubated patient.

3. Interpretation of the Normal Capnogram and Its Integration with Mechanical Ventilation Waveforms

The normal capnogram displays a characteristic waveform composed of four phases:

Phase I: exhalation of anatomical dead space gas, with no detectable CO₂;
Phase II: transition between dead space gas and alveolar gas, characterized by a progressive rise in CO₂;
Phase III: alveolar plateau, representing predominantly alveolar gas;
Phase IV: Beginning of inspiration, marked by an abrupt decline in CO₂ toward the baseline.

The end of Phase III corresponds to ETCO₂, which under ideal physiological conditions approximates alveolar CO₂ partial pressure (PACO₂).^11-13

Figure 2 illustrates the normal capnogram and its relationship with the physiological and technical determinants involved in its acquisition in the invasively mechanically ventilated patient. Figure 3 presents capnography integrated with the conventional ICU mechanical ventilator waveforms.

Figure 2. Diagram illustrating mainstream capnography applied to the artificial airway of an intubated patient. Exhaled CO₂ partial pressure (PetCO₂) results from the interaction between CO₂ production (V̇CO₂), determined by cellular metabolism, pulmonary perfusion (the hemodynamic component), and alveolar ventilation (the ventilatory component). Continuous measurement of PeCO₂ throughout expiration yields a time-based capnogram composed of four phases. Phase I corresponds to exhalation of dead space volume, reflecting the dead space to tidal volume ratio (VD/VT), during which PeCO₂ equals zero. Phase II represents the transition as alveolar gas begins to empty, characterized by a rapid rise in PeCO₂. Phase III corresponds to the alveolar plateau at end-expiration, where the ETCO₂ (or PetCO₂) value is obtained. The gradient between arterial and end-tidal CO₂ partial pressures, P(a–et)CO₂, typically ranges from 2 to 5 mmHg and becomes smaller as ventilation–perfusion (V/Q) matching approaches ideal homogeneity.

Figure 3. Capnogram waveforms integrated with volume-time and flow-time curves of an ICU mechanical ventilator, demonstrating the four capnographic phases. Phase I corresponds to the exhalation of the dead space volume (VD), when PetCO₂ equals zero, and the potential quantification of VD from the tidal volume (VT) curve is possible. Phase II reflects the transition as alveolar gas is exhaled through the proximal airways, with a rapid increase in PetCO₂. Phase III represents the alveolar plateau extending to end-expiration, when expiratory flow returns to zero, and PetCO₂ is measured immediately before Phase IV, the onset of inspiration. ETCO₂ (PetCO₂) is shown with a normal physiological gradient of approximately 2–5 mmHg relative to PaCO₂, presented here for didactic purposes. Waveforms and data generated using the Xlung simulator.

4. Capnographic Interpretation Based on Pathophysiological Mechanisms in Common Clinical Conditions

4.1. Alterations in Metabolic CO₂ Production

Conditions such as fever, sepsis, seizures, increased muscular activity, and hypercaloric nutritional support elevate metabolic CO₂ production, resulting in increased ETCO₂ while preserving the P(a–et)CO₂ gradient, provided that ventilation and pulmonary perfusion remain stable. The opposite pattern is observed in conditions associated with reduced cellular metabolism, including hypothermia, hypothyroidism, deep sedation, and low caloric intake. Figure 4 illustrates the effects of increased cellular metabolism and its consequences on capnography.¹⁴

Figure 4. Capnography in intubated patients receiving mechanical ventilation under conditions of increased metabolism and CO₂ production.

Fever, sepsis, and other hypermetabolic states increase CO₂ production (V̇CO₂), resulting in higher mixed expired CO₂ values (PECO₂). When ventilation–perfusion matching is preserved, both PaCO₂ and ETCO₂ rise proportionally, maintaining a normal P(a–et)CO₂ gradient. For example, an increase in body temperature (36 °C vs. 40 °C) alters capnographic values if the alveolar ventilation does not change. It elevates CO₂ levels without changes in the expiratory flow pattern, indicating that alveolar hypoventilation, the primary differential diagnosis, is not responsible for the observed changes. Waveforms and data generated using the Xlung simulator.

4.2. Alveolar Hypoventilation

A reduction in alveolar ventilation, whether due to decreased respiratory rate or reduced tidal volume, leads to CO₂ retention, with proportional increases in both PaCO₂ and ETCO₂. In such cases, the P(a–et)CO₂ gradient typically remains within normal limits. Figure 5 presents capnographic findings integrated with the volume-time waveform.^14-16

Figure 5. Capnography in intubated patients receiving mechanical ventilation during alveolar hypoventilation secondary to tidal volume reduction. A decrease in tidal volume reduces alveolar ventilation and results in CO₂ retention, producing proportional increases in PaCO₂ and exhaled CO₂ partial pressure (PetCO₂). In the presence of preserved ventilation–perfusion matching, the P(a–et)CO₂ gradient remains within the physiological range. Integration of physiologically normal-shaped capnograms with volume-time curves demonstrating a reduction in exhaled tidal volume from 500 mL to 250 mL supports hypoventilation as the mechanism responsible for increased PaCO₂ and ETCO₂. Waveforms and data generated using the Xlung simulator.

4.3. Reduced Pulmonary Perfusion or Circulatory Shock

A reduction in cardiac output or pulmonary perfusion impairs CO₂ delivery to the alveoli, leading to a decrease in alveolar CO₂ partial pressure (PACO₂) and consequently a reduction in ETCO₂. This condition is frequently associated with widening of the P(a–et)CO₂ gradient and an increase in the VD/VT ratio due to expansion of alveolar dead space.^{12, 14} Capnographic monitoring may assist in evaluating the response to fluid resuscitation in patients with shock or in evaluating the response to treatment in conditions such as severe pulmonary embolism.

Figure 6 illustrates the effects of reduced pulmonary perfusion on capnography and CO₂ values.

Figure 6. A decrease in cardiac output results in impaired pulmonary perfusion and reduced CO₂ delivery to the alveoli, leading to lower exhaled CO₂ (ETCO₂) despite preserved or elevated arterial CO₂ (PaCO₂). This condition is associated with increased physiological dead space (VD/VT) and widening of the P(a–et)CO₂ gradient. Capnograms obtained under conditions of normal (6 L/min) and reduced (2 L/min) cardiac output demonstrate a marked reduction in ETCO₂ with unchanged mechanical ventilation, highlighting the predominantly hemodynamic contribution to the observed capnographic alterations. Waveforms and data generated using the Xlung simulator.

4.4. Airflow Limitation and Auto-PEEP

Obstructive airway diseases, characterized by increased airway resistance, promote expiratory flow limitation, air trapping, and the development of auto-PEEP. The capnogram typically exhibits a progressive upward slope in Phases II and, most prominently, Phase III, producing the classic “shark-fin” appearance. This pattern is frequently associated with reduced ETCO₂ and increased physiological dead space, as well as widening of the P(a–et)CO₂ gradient. This phenomenon is further exacerbated when expiratory time is insufficient, particularly in patients with severe COPD during acute exacerbations, due to marked ventilatory heterogeneity, excessive airway resistance, reduced elastic recoil in the presence of emphysema, and a substantial increase in the expiratory time constant.^{2, 12}

In this context, PetCO₂ does not reliably reflect PaCO₂ and therefore cannot replace arterial blood gas analysis for accurate evaluation of alveolar ventilation. Conversely, optimization of ventilator settings and/or improvement of the underlying pulmonary condition, resulting in reduced air trapping, decreased auto-PEEP, and in more complete lung emptying during expiration, generally leads to a reduction in P(a–et)CO₂ toward the normal range. The opposite pattern is observed with clinical deterioration.

Figure 7 illustrates the effects of increased airway resistance, pulmonary hyperinflation, and auto-PEEP on capnogram morphology and CO₂ measurements.

Figure 7. Capnography in an intubated patient receiving mechanical ventilation with airflow limitation, increased airway resistance, and the development of auto-PEEP. Increased airway resistance (Raw) promotes expiratory flow limitation, impairing complete lung emptying. This condition results in dynamic air trapping and the generation of auto-PEEP, evidenced by the inability of expiratory flow to return to zero before the onset of the next inspiratory cycle. Consequently, effective alveolar ventilation is reduced, leading to an increase in the dead space-to-tidal volume ratio (VD/VT). Capnography typically demonstrates reduced ETCO₂ values despite a concomitant rise in PaCO₂, reflecting alveolar hypoventilation associated with widening of the P(a–et)CO₂ gradient. The capnogram exhibits a progressive upward slope of Phases II and III, characteristic of the classic shark-fin pattern seen in airflow obstruction. At the same time, the flow-time waveform confirms the presence of auto-PEEP. Waveforms and data generated using the Xlung simulator.

4.5. Recovery of Respiratory Effort and Patient–Ventilator Asynchrony

During recovery of spontaneous respiratory effort following neuromuscular blockade, ineffective inspiratory efforts that fail to trigger the ventilator may occur. These events can be detected on ventilator waveforms, particularly the flow-time curve, as well as on the capnogram, where they appear as characteristic “curare clefts.” Such events may alter CO₂ partial pressure throughout expiration and transiently affect ETCO₂ values, potentially producing intermittent variations in the measured ETCO₂ and the P(a–et)CO₂ gradient. Figure 8 illustrates the capnographic effects of ineffective inspiratory efforts.

Figure 8. Diagram illustrating ineffective inspiratory efforts, visible on the flow waveform, and their corresponding effects on the capnogram. In this example, waveforms were generated by simulating reduced inspiratory muscle effort, as may occur during partial recovery from neuromuscular blockade (curare cleft). These events may occur near end-expiration, producing transient entrainment of CO₂-free gas, thereby altering PetCO₂ and potentially affecting ETCO₂ measurements. Consequently, variations in the P(a–et)CO₂ gradient may also be observed. NMB: neuromuscular blockade. Waveforms and data generated using the Xlung simulator.

4.6. Progression to Cardiorespiratory Arrest

During progression to cardiorespiratory arrest (CRA), a rapid and progressive decline in ETCO₂ toward values near zero is observed, despite preservation of the ventilatory pattern. This finding reflects the abrupt interruption of pulmonary perfusion. Within the appropriate clinical context, this pattern should be considered strongly suggestive of CRA. The abrupt reduction in ETCO₂ reflects the cessation of CO₂ transport from tissues to the lungs and represents an early, highly sensitive marker of circulatory collapse. The capnogram demonstrates progressive loss of Phase III and collapse of the alveolar plateau, ultimately resulting in a nearly flat or absent tracing, while the ventilator continues to cycle, indicating absence of effective circulation.^{12, 15, 16}

Figure 9 illustrates the characteristic capnographic findings associated with this critical condition.

Figure 9. Capnography in an intubated patient receiving mechanical ventilation during progression to cardiorespiratory arrest (CRA). As severe and rapidly progressive hemodynamic deterioration occurs, with abrupt reduction in cardiac output, pulmonary perfusion collapses, leading to a marked reduction in CO₂ delivery to the alveoli. Consequently, ETCO₂ rapidly declines toward near-zero values despite preservation of the ventilatory pattern, as evidenced by the maintained flow-time waveform.

4.7. Capnography During Cardiopulmonary Resuscitation and Return of Spontaneous Circulation

During cardiopulmonary resuscitation (CPR), ETCO₂ directly reflects pulmonary blood flow generated by chest compressions and serves as an indirect marker of chest compression quality. Return of spontaneous circulation (ROSC) is characterized by a sudden and sustained increase in ETCO₂, representing recovery of cardiac output and pulmonary perfusion. This parameter is particularly valuable for guiding and monitoring resuscitation efforts. Effective chest compressions are typically associated with ETCO₂ values between 10 and 20 mmHg, with higher values within this range generally indicating better perfusion.^{12, 14} Capnography is increasingly recognized as an essential tool for assessing CPR effectiveness and early identification of ROSC. Figure 10 presents capnographic waveforms before, during varying compression effectiveness, and following ROSC.

Figure 10. Capnography in an intubated patient receiving mechanical ventilation during cardiopulmonary resuscitation, from cardiorespiratory arrest (CRA) through initiation of chest compressions to return of spontaneous circulation (ROSC). During CRA, ETCO₂ values directly reflect pulmonary blood flow generated by chest compressions, functioning as an indirect marker of chest compressions quality. Ineffective compressions are associated with low ETCO₂ values, whereas more effective compressions produce progressive increases in ETCO₂ within the target range. A sustained and abrupt rise in ETCO₂ represents the classic indicator of ROSC. Flow-time waveforms demonstrate maintenance of ventilatory pattern throughout resuscitation, with oscillations related to chest compressions. At the same time, the capnogram shows the transition from low exhaled CO₂ levels during CPR to higher, more stable values after ROSC. Waveforms and data generated using the Xlung simulator.

4.8. Capnography During PEEP Titration in Patients with Acute Respiratory Distress Syndrome (ARDS)

Pioneering studies have evaluated the effects of PEEP titration in ARDS on physiological parameters, including cardiac output and respiratory mechanics. The optimal PEEP for a given patient with ARDS should not be defined solely by improvements in oxygenation, but rather by the level that achieves the best balance between alveolar recruitment and hemodynamic stability, ensuring adequate oxygen delivery to tissues and organs without causing alveolar overdistension. Excessively high PEEP levels tend to increase alveolar dead space due to parenchymal overdistension and/or reduced capillary perfusion. In contrast, insufficient PEEP levels favor alveolar collapse, recurrent expiratory atelectasis, and increased pulmonary shunt. PEEP levels associated with global improvement in respiratory system compliance may approximate the best compromise, minimizing overdistension in normally aerated or hyperaerated lung regions while maintaining alveolar patency in dependent lung zones. This strategy contributes to reducing the risk of ventilator-induced lung injury (VILI – Ventilator-Induced Lung Injury).^17-19

Figure 11 illustrates the effects of PEEP titration on driving pressure, a variable reflecting the relationship between tidal volume and respiratory system compliance, and on the P(a–et)CO₂ gradient, which reflects alveolar dead space. Both variables may provide complementary physiological information during bedside optimization of mechanical ventilation in ARDS, contributing to a lung-protective strategy.

Figure 11. Capnography in an intubated patient with Acute Respiratory Distress Syndrome (ARDS) receiving mechanical ventilation in volume-controlled ventilation (VCV) mode with tidal volume set at 6 mL/kg predicted body weight during decremental PEEP titration (15 → 10 → 5 cmH₂O). A PEEP level of 10 cmH₂O resulted in the lowest driving pressure and the smallest P(a–et)CO₂ gradient, findings consistent with reduced pulmonary overdistension and greater alveolar aeration and improved ventilation–perfusion (V/Q) matching compared with the other tested PEEP levels. Waveforms and data generated using the Xlung simulator.

4.9. Additional Clinical Conditions Commonly Identifiable by Capnography

Capnography enables rapid identification of various clinically relevant conditions and technical problems in intubated patients receiving mechanical ventilation. Abrupt and marked changes in ETCO₂ values, baseline shifts, or capnogram morphology can function as early warning signs of potentially serious events, often preceding overt clinical manifestations.

Integrated analysis of the capnogram alongside mechanical ventilator waveforms allows detection of endotracheal tube malposition, circuit disconnections, artificial airway migration, leaks, and malfunction of inspiratory or expiratory valve mechanisms within the ventilator circuit.¹² Figures 12 and 13 illustrate representative examples of ventilatory delivery abnormalities, circuit-related disturbances, and airway positioning errors. Such scenarios represent high-risk adverse events that can lead to catastrophic outcomes if not promptly recognized and corrected.

Figure 12. Capnography in intubated patients receiving mechanical ventilation with abnormalities in the control of inspiratory and expiratory gas flow within the ventilator circuit. In A) CO₂ rebreathing caused by expiratory valve malfunction results in partial return of exhaled gas at the onset of inspiration (Phases IV and I of the capnogram). An increase in inspired CO₂ partial pressure is observed (PiCO₂ > 0), proportional to the severity of rebreathing. In the absence of compensatory hyperventilation, PetCO₂ may also increase. In B) the presence of a circuit leak causes early reduction of PetCO₂, preventing formation of the alveolar plateau and generating a characteristic capnogram morphology.

Figure 13. In A) esophageal intubation is characterized by extremely low or absent PetCO₂ values, sometimes displaying small transient waveforms due to residual CO₂ within the upper gastrointestinal tract immediately after intubation, followed by a flat tracing. The expression “no trace, wrong place” has been proposed to emphasize the urgency of immediate corrective action. In B) migration of the distal end of the endotracheal tube into the right main bronchus produces asymmetric lung emptying, resulting in a biphasic capnogram morphology. This pattern is typically corrected following appropriate repositioning of the distal extremity of the tube within the trachea.

5. Summary and Conclusions

Figure 14 presents an illustrated summary of the main clinical conditions and corresponding capnographic findings discussed throughout this chapter.

Figure 14. Summary table.

Capnography has become firmly established as an essential monitoring modality in intubated patients receiving mechanical ventilation, with expanding applications across diverse clinical scenarios. Scientific evidence supports its value in integrated assessment of ventilation and perfusion, while also facilitating early detection of technical problems with the artificial airway, which may represent high-risk, potentially fatal events if not promptly recognized and corrected. Awareness of its physiological and technical limitations, along with appropriate clinician training, is fundamental for its safe and effective use.

There is growing recognition that capnography education remains insufficient in medical training and across other health professions. In this context, incorporating capnography into the virtual simulators on the Xlung platform is a valuable educational resource that supports the teaching of applied respiratory physiology and mechanical ventilation.²⁰

Ongoing technological advances are expected to expand the integration of capnography into mechanical ventilation systems, making this monitoring tool increasingly accessible, reliable, and clinically relevant.

6. Xlung Trainer Exercises

Access simulation exercises involving capnography application in intubated patients:

7. References

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18. Amato MBP, Meade MO, Slutsky AS, et al. Driving pressure and survival in ARDS. N Engl J Med. 2015.
19. Sarah Gracielly Sena Sousa. Desenvolvimento de simulador capnométrico à plataforma de simulação Xlung. Início: 2024. Dissertação (Mestrado profissional em Programa de Pós-graduação (PPG) Tecnologia Minimamente Invasiva e Simulação) - Centro Universitário Unichristus.