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Emergency Medical Services


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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.

      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

Schematic illustration of 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 waveform analysis. Both chronic obstructive pulmonary disease (COPD) and asthma fall into this category, and the waveform produced will be similar. The classic description of this waveform is the “shark fin” morphology, consisting of a shallower upward sloping of the initial rise of the EtCO2 wave (Figure 6.2b). This represents a slower rate of exhalation. It may be considered analogous to the forced expiratory volume in one second measurement of the pulmonary function test. This slower exhalation is precipitated by collapse or partial occlusion of bronchioles in emphysema and chronic bronchitis and spasm in acute asthma attacks. As the condition improves following bronchodilation, the initial upward segment will become more vertical. However, in more severe cases, the numeric value or amount of EtCO2 will also rise, heralding respiratory insufficiency, and should lead the clinician to consider ventilatory support measures.

      Although less commonly employed, EtCO2 and waveform analysis may also be useful in assessment of metabolic derangements such as diabetic ketoacidosis and aspirin overdose. These conditions cause respiratory compensation of metabolic acidosis and will present with hyperventilation, typically with a decreasing level of EtCO2.

      While oxygenation and ventilation are distinct parameters, their assessment and management are often interdependent. Thus, we discuss them together.

      The initial and most basic treatment for inadequate oxygenation is the administration of supplemental oxygen to increase the relative amount, or fraction, of oxygen in inspired gases (i.e., FiO2). Oxygen should be provided to all patients with respiratory distress, with any clinical markers of respiratory compromise (e.g., altered mental status), or with measured inadequate oxygenation or ventilation. There is an increasing trend toward more selective application of oxygen with the growing recognition of oxygen toxicity. Most current guidelines and protocols endorse administering supplemental oxygen only if the oxygen saturation is less than 94%. Unnecessarily elevating the SpO2 above normal levels may in fact be harmful to patients experiencing neurological or cardiac insults associated with ischemic damage [7].

      Patients with underlying pulmonary disease, such as COPD and interstitial fibrosis, may have oxygen saturations below 94% on a chronic basis. A subset of these patients will also have chronically high PaCO2 levels (hypercapnia), which lead to dependence on a hypoxic drive for ventilatory control and stimulation. Providing supplemental oxygen, especially at high flow rates, may contribute to respiratory depression and potentially produce apnea [8]. EMS clinicians must carefully assess and monitor these patients, administer oxygen if needed, and be prepared to assist ventilation. Oxygen should not be withheld from a hypoxic patient because of concern for their dependency on a hypoxic drive for breathing.

Device name O2 flow rate (L/min) FiO2 (approximate %)
Nasal cannula