Health care providers should quickly determine if the patient demonstrates spontaneous breathing efforts.

Significant partial upper airway obstruction typically causes noisy airflow during inspiration (stridor or “crowing”) and cyanosis (late sign). Another sign of airway obstruction is use of accessory muscles, indicated by retractions of the suprasternal, supraclavicular, and intercostal spaces. Complete airway obstruction results in patient efforts at breathing against a closed airway this typically causes a rocking or “see-saw” motion of the chest and abdomen as the diaphragm moves into the abdomen, pushing the abdomen upward and the chest collapses in the absence of airflow to fill the lungs. If the patient is not making spontaneous breathing efforts, airway obstruction becomes more difficult to recognize and must be determined during attempts to provide positive-pressure ventilation. Occasionally, isolated bradycardia, secondary to occult hypoxemia, provides an early sign of airway obstruction. It is important to recognize the presence of airway obstruction caused by the tongue and epiglottis, as this is common in the unconscious patient due to loss of muscle tone.

The concentration of a substance in a fluid can be determined by its ability to transmit light. Oxygenated hemoglobin absorbs and reflects red and infrared light differently than nonoxygenated hemoglobin. Oxygenated hemoglobin primarily absorbs infrared light; reduced (nonoxygenated) hemoglobin primarily absorbs red light. In pulse oximetry, red and infrared light are passed through a pulsatile tissue bed, and a photodetector captures any nonabsorbed light on the other side of the tissue bed. A microprocessor calculates the relative absorption of red and infrared light that occurred as it passed through the tissue bed and can determine the percentage of oxygenated and nonoxygenated hemoglobin present in that tissue bed. In this way the pulse oximeters calculate the percent of hemoglobin that is saturated with oxygen (percent saturation, percent SO₂; percent SaO₂). In the absence of abnormal hemoglobins, such as carboxyhemoglobin or methemoglobin, if the arterial oxygen saturation is greater than 70%, there should be no more than 3% variance between pulse oximetry and the arterial oxyhemoglobin saturation measured by co-oximeter used in arterial blood gas determinations. Studies have shown pulse oximetry to be an accurate and useful guide for patient care in the in-hospital setting as well as in the prehospital EMS setting,^36,37,38,39 including transport by rotary-wing aircraft.⁴⁰

Analysis of arterial blood is an invasive procedure, and arterial blood gases are infrequently ordered, available, or clinically useful during cardiac arrest. Pulse oximetry was developed to provide a noninvasive, painless approximation of the percent of hemoglobin saturated with oxygen, usually designated as SpO₂ to distinguish it from the value measured by co-oximetry of an arterial blood sample (SaO₂). In cardiac arrest, the pulse oximeter will not function well because there must be pulsatile blood flow through the tissue where the light measurements are being made to obtain an accurate measurement although a reading may appear with adequate chest compressions. But pulse oximetry is commonly used for monitoring patients who are not in arrest, because it provides a simple, continuous method of tracking oxyhemoglobin saturation. There are three major determinants of adequate tissue oxygenation:

Arterial oxygen content is determined by the hemoglobin concentration and its saturation with oxygen. Normal pulse oximetry saturation, however, does not ensure adequate systemic oxygen delivery because it does not calculate the total
oxygen content (O₂ bound to hemoglobin + dissolved O₂) and adequacy of blood flow (cardiac output):

Arterial oxygen content (mL of oxygen per dL of blood)

= Hemoglobin concentration (g/dL)

× 1.34 (mL oxygen/g hemoglobin)

× Oxyhemoglobin saturation

+ (PaO₂ × 0.003)

(normal oxygen content = 18-20 ml/dL)

Measurement of the oxygen content is only part of the determination of effective oxygenation. The oxygen present must be delivered to the tissues for use. Peripheral cells must be able to uptake and use oxygen for cellular metabolism. Oxygen delivery is defined by how much oxygen is present and how much of it is delivered to the body. Oxygen delivery is defined by the following equation:

Oxygen delivery (mL of oxygen/min)

= arterial oxygen content (mL oxygen/dL blood)

× cardiac output (L/min)

(× 10 dL/L)

Pulse oximetry readings, even those that are accurate, do not necessarily correlate with cardiac output and oxygen delivery. In clinically evaluating a patient’s cardiac output and oxygen delivery, always assess systemic perfusion and be aware of the hemoglobin concentration. If cardiac output or hemoglobin concentration is low, oxygen delivery can be inadequate even if oxyhemoglobin saturation is normal.

The light absorption of carboxyhemoglobin (carbon monoxide) and of methemoglobin (nitrates or aromatic amines) differs from that of normal hemoglobin, so carboxyhemoglobin and methemoglobin are not recognized by pulse oximeters. If these altered forms of hemoglobin are present, the SaO₂ calculated by the pulse oximeters will be falsely high because most pulse oximeters calculate the percent of normal hemoglobin that is saturated with oxygen rather than the percent of total hemoglobin that is saturated with oxygen. When you suspect the presence of carbon monoxide poisoning or methemoglobin toxicity, you should measure the oxyhemoglobin saturation with a co-oximeter (this requires arterial blood sampling).

In several clinical situations, abnormal or inaccurate oximetry readings may occur. In a large review of pulse oximeter devices, the major sources of error were finger thickness, hemoglobin level, skin color, and peripheral temperature.

There are some safety precautions regarding use of the pulse oximetry equipment:

The body eliminates carbon dioxide through ventilation. When blood passes through the lungs, carbon dioxide moves from the blood, across the alveolar capillary membrane into the alveoli and then into the airways and is exhaled. Alveolar PCO₂ should be approximately equal to pulmonary venous, left atrial and arterial PCO₂. If there is a good match of ventilation and perfusion in the lungs and there is no airway obstruction, exhaled CO₂ should correlate well with arterial PCO₂, and exhaled carbon dioxide can be used to estimate arterial carbon dioxide tension. Carbon dioxide can be detected by either of two techniques:

A CO₂ concentration of >2% will react with the chemical reagent in a colorimetric CO₂ detector and change the color (Fig. 18-1). If the endotracheal tube is actually in the trachea, the CO₂ detector will turn a color determined by the manufacturer. In the absence of expired CO₂, the color of the colorimetric indicator will remain unchanged. Health care providers commonly use this color change with a disposable device as a quick check to provide one method of device confirmation of the success or failure of endotracheal intubation.⁴³

The product inserts for some commercially available semiqualitative colorimetric capnometers recommend that after intubation, six positive-pressure breaths be provided by hand or mechanical ventilation before attempting to identify exhaled CO₂. Six breaths will wash out any CO₂ that is present in the stomach or esophagus from bag-mask ventilation. Any CO₂ detected after six breaths can be presumed to be from the lungs.^44,45 There is no need to continue ventilation attempts if the endotracheal tube is clearly misplaced.

In patients who weigh >2 kg with a perfusing rhythm (not in cardiac arrest), the sensitivity and specificity of colorimetric capnometry methods approaches 100% if six ventilations have been provided following intubation. This means that if the endotracheal tube is in the trachea of a patient with a perfusing rhythm, the colorimetric device will change color with few exceptions (see “False-Positive Results,” below). If the tube is in the esophagus, there should be no CO₂ detected after six breaths, so a colorimetric CO₂ detector should remain unchanged.

Some capnography devices are infrared devices in which a light-emitting diode is used to measure the intensity of light transmitted across a short distance, usually the diameter of an endotracheal tube. The measured light absorption varies inversely with the concentration of CO₂ passing through the endotracheal tube. When attached to the end of an endotracheal tube, these infrared devices are called mainstream capnometers. These devices readily reveal low exhaled CO₂ indicative of esophageal intubation, and they can provide estimates of the adequacy of ventilation and the effectiveness of circulation during CPR. Conversely, sidestream capnometers draw a small sample of gas from the airway through a small tube to measure the CO₂ concentration in a device detached from the airway and the patient.

Capnography devices provide a continuous readout of the concentration of CO₂. They are used to monitor the quality of ventilation in nonarrest patients. Because of their high degree of sensitivity to expired CO₂, however, capnographs can often detect a sufficient quantity of CO₂ to indicate the presence of an endotracheal tube in the trachea even when cardiac arrest is present. Continuous capnography monitoring devices can identify and signal a fall in exhaled CO₂ consistent with endotracheal tube dislodgment. This may be very helpful when patients are being moved or during emergencies.

End-tidal CO₂ monitoring is a safe and effective noninvasive indicator of cardiac output during CPR capnography may be an early indicator of return of spontaneous circulation (ROSC) in intubated patients because an increase in exhaled CO₂ typically occurs when cardiac output increases and perfusion of the lungs improves. During cardiac arrest, CO₂ continues to be generated throughout the body; however, there is little pulmonary blood flow, and the level of CO₂ in exhaled gas may be too low to produce a color change or a graphic exhaled CO₂ waveform. In such situations, when a colorimetric device is attached to the distal end of a properly placed endotracheal tube, the color remains unchanged or the CO₂ level remains very low. Because the unchanged color and lack of exhaled CO₂ may also indicate that the tube has been placed in the esophagus, the health care provider must decide whether the lack of carbon dioxide indicates esophageal intubation or reflects the absence of blood flow to the lungs. The major determinant of CO₂ excretion is its rate of delivery from the peripheral production sites to the lungs. In the low-flow state during CPR, ventilation is relatively high compared with blood flow, so the end-tidal CO₂ concentration is low. If ventilation is reasonably constant, then changes in end-tidal CO₂ concentration reflect changes in cardiac output. Patients who are successfully resuscitated from cardiac arrest have significantly higher end-tidal CO₂ levels than those who cannot be resuscitated.