Several tools have been developed that can reliably measure oxygenation of blood in the prehospital environment. Portable devices are available that can measure oxygen content in arterial and venous blood samples (i.e., PaO2). However, because of cost and the need to perform vascular puncture, these devices are typically only used at selected special event venues and by critical care teams. Most commonly, oxygen levels in the field are determined by pulse oximetry (i.e., oxygen saturation, SpO2). This simple, noninvasive method reports the percentage of hemoglobin in arteriolar blood that is in a saturated state. It is important for prehospital clinicians to understand that standard pulse oximetry does not discriminate between hemoglobin saturated with oxygen and hemoglobin saturated with carbon monoxide (i.e., oxyhemoglobin versus carboxyhemoglobin). In cases of carbon monoxide exposure, pulse oximetry will be misleading to the unsuspecting clinician [1]. Newer‐generation devices are available that can measure carboxyhemoglobin levels distinct from oxyhemoglobin [2].
Pulse oximetry may be unreliable in states of low tissue perfusion, such as with shock or local vasoconstriction due to cold temperature. Additionally, as this technology relies on transmission and absorption of light waves, barriers such as fingernail polish or skin disease can interfere with accuracy.
Measurement of tissue oxygenation saturation (StO2) uses near‐infrared light resorption to measure oxygen saturation of blood in the skin and underlying soft tissue. This enables assessment of oxygen delivery and consumption in local tissue rather than simply the amount of oxygen circulating in the arterial system, which is measured by pulse oximetry. While there are increasing reports of the utility of this technology, it is not yet in widespread clinical use due to cost, technical limitations, and lack of large clinical studies [3].
Table 6.1 Conditions that impair oxygen transfer in the lungs
| Physiological process | Pathological conditions |
| Partial pressure of oxygen in inhaled air | Displacement by other gases |
| Minute ventilation (volume of air inhaled per minute) | External compression of chest |
| Muscle weakness (chest wall and/or diaphragm) | |
| Central nervous system control malfunction | |
| Decreased lung compliance | |
| Pneumothorax | |
| Hemothorax and pleural effusion | |
| Diffusion of oxygen across the alveolar membrane | Pneumonitis |
| Alveolar and/or interstitial edema | |
| Perfusion of the alveoli | Decreased cardiac output |
| Hypotension | |
| Shunting |
Figure 6.1 Oxygen‐hemoglobin dissociation curve
Assessment of Ventilation
Ventilation refers to the movement of air into and out of the lungs. It is measured as minute ventilation (volume of air exchanged per minute), which can be calculated by the equation, minute ventilation = tidal volume × respiratory rate. Normal ventilation ranges from 6 L/minute to 7 L/minute. Although hypoventilation can lead to decreased oxygenation and hemoglobin oxygen saturation, ventilatory 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