effectiveness is better evaluated by how well carbon dioxide (CO2) is being eliminated. Ventilation can be compromised by a number of conditions (Box 6.1), and its assessment is of equal importance to that of oxygenation.
Box 6.1 Conditions that impair ventilation
Airway obstruction:UpperLower (asthma, chronic obstructive pulmonary disease)
Muscle weakness (may be neurological)
Pleural effusion (large)
Pneumothorax
Sucking chest wound
Diaphragmatic malfunction (e.g., rupture, paralysis)
Pleuritic pain
Medications and recreational substances:OpioidsSedativesOxygen (in patients with hypoxic drive)
Ventilatory function can be determined directly by measuring the volume of air inhaled or exhaled per minute, or indirectly by measuring the CO2 level in blood or exhaled air. The partial pressure of carbon dioxide (PaCO2, may be measured in either arterial or venous blood samples using portable devices, as both provide similar results). However, just as oxygen content in the blood is usually assessed by noninvasive modalities in out‐of‐hospital settings, so too is CO2. Three types of devices are currently in use to detect and measure the presence and level of CO2 in exhaled air, which serves as a surrogate for the level of CO2 in blood. The simplest, but least useful, are semiquantitative colorimetric devices that use litmus paper to detect the acid generated by absorption of CO2 from exhaled air. These devices are compromised by prolonged exposure to air and by contamination from acidic gastric secretions. They may not be able to detect the extremely low levels of CO2 generated by patients in cardiac arrest. For these reasons, and due to the increasing availability of devices that can measure and continuously monitor exhaled CO2, colorimetric devices are being used less often than quantitative devices. Capnometry uses light absorption to measure the level of CO2 in exhaled air. Clinically, the level at the end of exhalation is the most useful value and is referred to as end‐tidal CO2 (EtCO2). This measurement reflects the CO2 content in alveolar gas and, therefore, in the pulmonary venous blood returning to the left heart.
The EtCO2 level is typically 32–42 mmHg. It is 3–5 mmHg lower than the PaCO2 level in arterial blood, due to physiological alveolar dead space. Various clinical conditions such as poor pulmonary perfusion, greater than normal dead space (i.e., shunting and V/Q mismatch), and cuff or sampling device leak can widen this gap to 10–20 mmHg [4]. EtCO2 cannot be higher than the PaCO2, but may be significantly lower, and this should be considered when modifying manual or mechanical ventilation. Whenever possible, in critical care transport scenarios, for example, baseline PaCO2 may be obtained and compared to the EtCO2 level at the time of blood sampling. Venous PaCO2 is typically about 4 mmHg higher than arterial PaCO2 (range +10 to –2) [5]. Continuous waveform capnography provides additional information on the frequency of respirations and the flow rate of inhalation and exhalation by displaying a graphic depiction of measured expired CO2 over time. Flow rate is affected by airway mechanics, including obstruction and bronchospasm, and is reflected in changes in the shape of the involved phase of ventilation. EMS clinicians should have a good understanding of the interpretation of EtCO2 values as well as waveform morphology, as they both are altered by a variety of clinical conditions and may provide diagnostic information (Box 6.2) [6].
As a monitor of respiratory function, capnography is superior to pulse oximetry because it changes nearly immediately with changes in ventilation. On the other hand, hypoxia may be delayed by the body’s reserve and the physiology of hemoglobin oxygen dissociation, as discussed above. When capnography waveform analysis is included, a near real‐time assessment is possible and EMS clinicians may identify inadequacy of ventilation or the presence of various respiratory disease states, and they may glean information about circulatory and metabolic function as well.
Impairment of ventilation is associated with rising EtCO2 values. When combined with waveform analysis, respiratory effort may also be monitored as to rate and depth of breathing. When respiratory rate or respiratory depth has become inadequate and EtCO2 values rise, clinicians can initiate or augment respiratory support prior to the development of hypoxia. In the prehospital environment, this application of waveform capnography is especially useful in monitoring respiratory status following the administration of opioid analgesics, benzodiazepines, and other medications capable of producing respiratory depression (Figure 6.2).
Box 6.2 Factors that affect EtCO2
True decrease in blood PaCO2:
Hyperventilation (primary or secondary)
Shock/cardiac arrest (with constant ventilation)
Hypothermia /decreased metabolism
True increase in blood PaCO2:
Hypoventilation
Return of circulation after cardiac arrest
Improved perfusion after severe shock
Tourniquet release
Administration of sodium bicarbonate
Fever/increased metabolism
Thyroid storm
Increased gap between blood PaCO2 and EtCO2:
Severe hypoventilation
Increased alveolar dead space
Decreased perfusion
Disconnected or clogged tubing
Figure 6.2 Capnography waveforms. (a) Normal waveform. Point A is beginning of expiration. A‐B is expiration of dead space air. B‐C shows rapid rise in level of CO2 as air from lungs is exhaled. C‐D is the plateau phase representing primarily alveolar air. D represents the value used for determination of EtCO2. D‐A represents inspiration. (b) Effect of bronchospasm. Note the slower rise in the CO2 level leading to the so‐called
