Chapter 6 Vincent N. Mosesso and Angus M. Jameson Oxygenation and ventilation are critical life-sustaining functions, and their evaluation and management are primary components of out-of-hospital care. While these two parameters are related, they are distinct physiological functions that require independent assessment. The focus of this chapter will be on diagnostic aids and management, and EMS physicians and providers must develop and maintain expert physical examination skills for the proper assessment of these important processes. The astute provider will observe for demeanor, mentation, ability to speak, ease and volume of air exchange, work of breathing, upper or lower airway obstruction, pulmonary congestion, and central and peripheral cyanosis. These findings should be considered together with diagnostic test results to determine the status of oxygenation and ventilation in an individual patient, whether intervention is needed, and, if so, which treatment modalities are indicated. Adequate oxygen delivery to body tissues is a necessity for life, and is dependent on both the transfer of oxygen from the alveolar airspace to the blood and sufficient tissue perfusion with oxygenated blood. Oxygenation of the blood is dependent on a number of distinct factors, each of which can be impaired by various pathological processes (Table 6.1). Normal hemoglobin oxygen saturation in peripheral arterial blood is 96–99%. It is important to understand the relation between oxygen saturation and the partial pressure of oxygen. This is depicted by the oxyhemoglobin saturation curve (Figure 6.1). This curve demonstrates that above 90%, the saturation percentage is very insensitive to changes in partial pressure of oxygen between 750 and 760 mmHg. This means that, especially in patients on supplemental oxygen, severe impairment in oxygen transfer into the blood can occur without major changes in the saturation level. Considered another way, as long as the partial pressure of oxygen in blood is at least 60 mmHg, hemoglobin is able to transport oxygen efficiently to the periphery. Table 6.1 Conditions that impair oxygen transfer in the lungs Figure 6.1 Oxygen-hemoglobin dissociation curve. 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 blood samples (i.e. pO2). However, because of cost and the need to perform arterial 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. SpO2). This simple, non-invasive method reports the percentage of hemoglobin in arteriolar blood that is in a saturated state. It is critically important for prehospital clinicians to understand that standard pulse oximetry does not discriminate between hemoglobin saturated with oxygen and hemoglobin saturated with carbon monoxide (oxyhemoglobin versus carboxyhemoglobin). In cases of carbon monoxide exposure, pulse oximetry will be misleading to the unsuspecting clinician [1]. Fortunately, newer generation devices, cooximeters, are now available and can measure carboxyhemoglobin levels distinct from oxyhemoglobin [2]. Pulse oximetry may also 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 reflection of light waves, barriers such as fingernail polish or skin disease can interfere with accuracy. Measurement of tissue oxygenation (StO2) uses near-infrared light resorption to measure oxygen saturation of blood in the skin and underlying soft tissue. This allows assessment of oxygen delivery to local tissue rather than simply the amount of oxygen circulating in the arterial system. Initial studies are promising, but further research will be needed to determine the most appropriate clinical use of this modality [3]. Ventilation refers to the volume of air moved in and out of the lungs, and is measured as minute ventilation (volume of air exchanged per minute, which can be estimated by the equation tidal volume × respiratory rate). Normal ventilation ranges from 6 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. 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 (pCO2) 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 non-invasive modalities in the out-of-hospital setting, 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 semi-quantitative 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 about 5 mmHg lower than the actual pCO2 level in the blood due to alveolar dead space, but various clinical conditions can widen this gap. Continuous waveform capnography provides additional information on the frequency and flow rate of inhalation and exhalation by displaying a graphic depiction of measured expired CO2 versus time. Field providers 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 to EMS clinicians [4] (Box 6.2). As a monitor of respiratory function, capnography is superior to pulse oximetry because it changes nearly immediately with ventilation. On the other hand, hypoxia may be delayed by the body’s reserve and the shape of the hemoglobin oxygen dissociation curve 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. When EtCO2 values rise above normal ranges (35–40 mmHg), impaired ventilation is easily detected. 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 opiate analgesics, benzodiazepines, and other medications capable of producing respiratory depression (Figure 6.2). 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 shark fin waveform. (c) Hypoventilation. (d) Hyperventilation. Obstructive respiratory physiology is the most often described diagnosis made upon EtCO2
Oxygenation and ventilation
Introduction
Assessment of oxygenation
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
Assessment of ventilation
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