Correcting Hypoxemia

O₂ therapy corrects hypoxemia by increasing alveolar and blood levels of O₂. Correction of hypoxemia is the most tangible objective of O₂ therapy and the easiest to measure and document.

Decreasing Symptoms of Hypoxemia

In addition to relieving hypoxemia, O₂ therapy can help relieve the symptoms associated with certain lung disorders. Specifically, patients with chronic obstructive pulmonary disease (COPD) and some forms of interstitial lung disease report less dyspnea when receiving supplemental O₂.⁵ O₂ therapy also may improve mental function among patients with chronic hypoxemia.⁶

Minimizing Cardiopulmonary Workload

The cardiopulmonary system compensates for hypoxemia by increasing ventilation and cardiac output. In cases of acute hypoxemia, supplemental O₂ can decrease demands on both the heart and the lungs. Patients with hypoxemia breathing air can achieve acceptable arterial oxygenation only by increasing ventilation. Increased ventilatory demand increases the work of breathing. In these cases, O₂ therapy can reduce both the high ventilatory demand and the work of breathing.

Patients with arterial hypoxemia can maintain acceptable tissue oxygenation only by increasing cardiac output. Because O₂ therapy increases blood O₂ content, the heart does not have to pump as much blood per minute to meet tissue demands. This reduced workload is particularly important when the heart is already stressed by disease or injury, as in myocardial infarction, sepsis, or trauma.

Hypoxemia causes pulmonary vasoconstriction and pulmonary hypertension. Pulmonary vasoconstriction and hypertension increase workload on the right side of the heart. For patients with chronic hypoxemia, this increased workload over the long-term can lead to right ventricular failure (cor pulmonale). O₂ therapy can reverse pulmonary vasoconstriction and decrease right ventricular workload.⁷

Oxygen Toxicity

O₂ toxicity primarily affects the lungs and the central nervous system (CNS).9–11 Two primary factors determine the harmful effects of O₂: PO₂ and exposure time (Figure 38-1). The higher the PO₂ and the longer the exposure, the greater the likelihood of damage. Effects on the CNS, including tremors, twitching, and convulsions, tend to occur only when a patient is breathing O₂ at pressures greater than 1 atm (hyperbaric pressure). Pulmonary effects can also occur with enriched O₂ environments at normal atmospheric pressures.

Table 38-2 summarizes the physiologic response to breathing 100% O₂ at sea level. A patient exposed to a high PO₂ for a prolonged period has signs similar to bronchopneumonia. Patchy infiltrates appear on chest radiographs and usually are most prominent in the lower lung fields.

Underlying the gross clinical signs is major alveolar injury. Exposure to high PO₂ first damages the capillary endothelium. Interstitial edema follows and thickens the alveolar-capillary membrane. If the process continues, type I alveolar cells are destroyed, and type II cells proliferate. An exudative phase follows, resulting from alveolar fluid buildup, which leads to a low ventilation/perfusion ratio, physiologic shunting, and hypoxemia. In the end stages, hyaline membranes form in the alveolar region, and pulmonary fibrosis and hypertension develop.

As the lung injury worsens, blood oxygenation deteriorates. If this progressive hypoxemia is managed with additional O₂, the toxic effects worsen (Figure 38-2). However, if the patient can be kept alive while fractional inspired oxygen concentration (FiO₂) is decreased, the pulmonary damage sometimes resolves.

The toxicity of O₂ is caused by overproduction of O₂ free radicals. O₂ free radicals are by-products of cellular metabolism. If unchecked, these radicals can severely damage or kill cells.⁹ Normally, however, special enzymes such as superoxide dismutase inactivate the O₂ free radicals before they can do serious damage. Antioxidants such as vitamin E, vitamin C, and beta-carotene also can defend against O₂ free radicals.

These defenses normally are adequate to protect cells exposed to air. In the presence of high PO₂, however, free radicals can overwhelm the antioxidant system and cause cell damage. Cell damage provokes an immune response and causes tissue infiltration by neutrophils and macrophages. These scavenger cells release inflammatory mediators that worsen the initial injury. At the same time, local neutrophils and platelets may release more free radicals, which continue the process.

Exactly how much O₂ is safe is the subject of debate. Results of most studies indicate that adults can breathe up to 50% for extended periods without major lung damage.¹² Rather than applying strict cutoffs, one can weigh both FiO₂ and exposure time in assessing the risks of high PO₂ (see the accompanying Rule of Thumb).¹³ The goal always should be to use the lowest possible FiO₂ compatible with adequate tissue oxygenation.

Because the growing lung may be more sensitive to O₂, more caution is needed with infants. High PO₂ also is associated with retinopathy of prematurity (ROP) and bronchopulmonary dysplasia in infants.

Regardless of approach, supplemental O₂ never should be withheld from hypoxic patients. Although the toxic effects of high O₂ concentrations can be serious, it is not FiO₂ but rather PO₂ that results in such harmful effects. If a patient needs a high FiO₂ to maintain adequate tissue O₂, the patient should receive it.

Depression of Ventilation

When breathing moderate to high O₂ concentrations, a very small percentage of patients with COPD and chronic hypercapnia tend to ventilate less.¹⁴ Decreases in ventilation of nearly 20% have been observed in these patients with accompanying elevations in arterial partial pressure of carbon dioxide (PaCO₂) of 20 to 23 mm Hg.¹⁵ However, this hypoventilation is not typical of patients with COPD, and although these patients should always be carefully monitored, appropriate management of hypoxemia should never be avoided because of concern for O₂-induced hypoventilation.

The primary reason some patients with COPD hypoventilate when given O₂ is most likely suppression of the hypoxic drive. In these patients, the normal response to high partial pressure of carbon dioxide (PCO₂) is blunted, the primary stimulus to breathe being lack of O₂ as sensed by the peripheral chemoreceptors. The increase in the blood O₂ level in these patients suppresses peripheral chemoreceptors, depresses ventilatory drive, and elevates the PCO₂.16,17 High blood O₂ levels may disrupt the normal ventilation/perfusion balance and cause an increase in dead space-to-tidal volume ratio (V_D/V_T) and in PaCO₂.¹⁸

The fact that O₂ therapy can cause some patients to hypoventilate should never stop the RT from giving O₂ to a patient in need. Preventing hypoxia always is the first priority. Avoiding depression of ventilation is discussed in more detail later in this chapter.

Retinopathy of Prematurity

Retinopathy of prematurity (ROP), also called retrolental fibroplasia, is an abnormal eye condition that occurs in some premature or low-birth-weight infants who receive supplemental O₂. An excessive blood O₂ level causes retinal vasoconstriction, which leads to necrosis of the blood vessels. In response, new vessels form and increase in number. Hemorrhage of these delicate new vessels causes scarring behind the retina. Scarring often leads to retinal detachment and blindness.¹⁹ ROP most often affects neonates up to approximately 1 month of age, by which time the retinal arteries have sufficiently matured. Excessive O₂ is not the only factor associated with ROP; other factors associated with ROP include hypercapnia, hypocapnia, intraventricular hemorrhage, infection, lactic acidosis, anemia, hypocalcemia, and hypothermia.

Because premature infants often need supplemental O₂, the risk of ROP poses a serious management problem. The American Academy of Pediatrics recommends keeping arterial PO₂ in an infant less than 80 mm Hg as the best way to minimize the risk of ROP.⁸

Absorption Atelectasis

FiO₂ greater than 0.50 presents a significant risk of absorption atelectasis.²⁰ Nitrogen normally is the most plentiful gas in both the alveoli and the blood. Breathing high levels of O₂ quickly depletes body nitrogen levels. As blood nitrogen levels decrease, the total pressure of venous gases rapidly decreases. Under these conditions, gases that exist at atmospheric pressure within any body cavity rapidly diffuse into the venous blood. This principle is used for removing trapped air from body cavities. Giving patients high levels of O₂ can help clear trapped air from the abdomen or thorax.

This same phenomenon can cause lung collapse, especially if the alveolar region becomes obstructed (Figure 38-3). Under these conditions, O₂ rapidly diffuses into the blood (see Figure 38-3, A). With no source for repletion, the total gas pressure in the alveolus progressively decreases until the alveolus collapses. Because collapsed alveoli are perfused but not ventilated, absorption atelectasis increases the physiologic shunt and worsens blood oxygenation.²⁰

The risk of absorption atelectasis is greatest in patients breathing at low tidal volumes as a result of sedation, surgical pain, or CNS dysfunction. In these cases, poorly ventilated alveoli may become unstable when they lose O₂ faster than it can be replaced. The result is a more gradual shrinking of the alveoli that may lead to complete collapse, even when the patient is not breathing supplemental O₂ (see Figure 38-3, B). For an alert patient, this is not a great risk because the natural sigh mechanism periodically hyperinflates the lung.

Fire Hazard

Despite numerous preventive measures, fires involving enriched O₂ environments continue to occur in health care facilities. Fires seem to pose the greatest risk in operating rooms and in association with selected respiratory procedures. During surgery and procedures such as tracheotomies, electronic scalpels and similar devices are often used while the patient is receiving supplemental O₂. To complicate matters, even higher O₂ concentrations may exist under surgical drapes.²¹ Other situations associated with increased fire risk involve home care patients smoking while receiving low-flow O₂ and the use of aluminum O₂ regulators. Additionally, hyperbaric oxygen (HBO) therapy or therapy at increased atmospheric pressures (discussed later in this chapter) often involves the administration of supplemental O₂ and greatly increases fire risk.

Some simple strategies can be used to reduce the fire risk in health care facilities. Effectively managing the fire triangle of O₂, heat, and fuel is key. An essential component is always using the lowest effective FiO₂ for a given clinical situation. In addition, using scavenging systems to minimize O₂ buildup beneath sterile drapes during surgery or while performing tracheostomies can help reduce fire risk. Avoiding the use of inappropriate or outdated equipment such as aluminum gas regulators and educating clinicians, patients and caregivers on safe O₂ use are also important measures. Additionally, fire prevention protocols for HBO therapy should be strictly followed.²¹

Low-Flow Systems

Typical low-flow systems provide supplemental O₂ directly to the airway at a flow of 8 L/min or less. Because the inspiratory flow of a healthy adult exceeds 8 L/min, the O₂ provided by a low-flow device is always diluted with air; the result is a low and variable FiO₂. Low-flow O₂ delivery systems include nasal cannula, nasal catheter, and transtracheal catheter.

Nasal Cannula

A nasal cannula is a disposable plastic device consisting of two tips or prongs approximately 1 cm long that are connected to several feet of small-bore O₂ supply tubing (Figure 38-5). The user inserts the prongs directly into the vestibule of the nose while attaching the supply tubing either directly to a flowmeter or to a bubble humidifier. In most cases, a humidifier is used only when the input flow is greater than 4 L/min.² Even with extra humidity, flow greater than 6 to 8 L/min can cause patient discomfort, including nasal dryness and bleeding.²² Cannulas should not be used in newborns and infants if their nasal passages are obstructed, and flows generally should be limited to 2 L/min unless a specialized high-flow cannula system is being used.² A high-flow nasal cannula, which is a variation of a standard nasal cannula, is discussed in more detail later in this chapter. Table 38-3 lists the FiO₂ range, FiO₂ stability, advantages, disadvantages, and best use of a nasal cannula.

Nasal Catheter

Although use is generally limited to short-term O₂ administration during specialized procedures such as a bronchoscopy, a nasal catheter is another low-flow O₂ delivery device. A nasal catheter is a soft plastic tube with several small holes at the tip that is inserted by gently advancing it along the floor of either nasal passage and visualizing it just behind and above the uvula (Figure 38-6). Once in position, the catheter is taped to the bridge of the nose. If direct visualization is impossible, the catheter may be blindly inserted to a depth equal to the distance from the nose to the earlobe.

When placed too deep, the catheter can provoke gagging or swallowing of gas, which increases the likelihood of aspiration. Nasal catheters also affect the production of secretions; for this reason, a nasal catheter should be replaced with a new one (placed in the opposite naris) at least every 8 hours. Nasal catheters should be avoided in most patients with maxillofacial trauma, basal skull fracture, nasal obstruction, and coagulation problems. It has also been determined that nasal catheters are inappropriate for neonatal patients. As a result of these notable limitations, nasal catheters are rarely used today.⁴

Transtracheal Catheter

A transtracheal O₂ catheter was first described by Heimlich in 1982.²⁴ A physician surgically inserts this thin polytetrafluoroethylene (Teflon) catheter with a guidewire directly into the trachea between the second and third tracheal rings (Figure 38-7). A custom-sized chain necklace secures the catheter in position. Standard tubing connected directly to a flowmeter provides the O₂ source flow.²⁵ Because flow is so low, no humidifier is needed.

Because the transtracheal catheter resides directly in the trachea, O₂ builds up both there and in the upper airway during expiration. This process effectively expands the anatomic reservoir and increases the FiO₂ at any given flow. Compared with a nasal cannula, a transtracheal catheter needs about half of the O₂ flow to achieve a given arterial partial pressure of oxygen (PaO₂).²⁵ Some patients need a flow of only 0.25 L/min to achieve adequate oxygenation. This reduced flow can be of great economic and practical benefit to patients needing continuous long-term O₂ therapy because it can greatly increase the duration of flow of portable O₂ systems. Transtracheal O₂ therapy can pose problems and risks, however, and these devices have not received widespread acceptance. Careful patient selection, rigorous patient education, and ongoing self-care with professional follow-up evaluation can help minimize these risks. Chapter 51 provides details on these aspects of transtracheal O₂ therapy. Table 38-3 lists the FiO₂ range, FiO₂ stability, advantages, disadvantages, and best use of a transtracheal catheter.

Performance Characteristics of Low-Flow Systems

Research studies on nasal low-flow systems show O₂ concentration ranging from 22% at 1 L/min to 60% at 15 L/min.2,3,22 The range of 22% to 45% cited in Table 38-3 is based on 8 L/min as the upper limit of comfortable flow. These wide FiO₂ ranges occur because the O₂ concentration delivered by a low-flow system varies with the amount of air dilution. The amount of air dilution depends on several patient and equipment variables. Table 38-4 summarizes these key variables and how they affect FiO₂ provided by low-flow systems.

Simple formulas exist for estimating FiO₂ provided by low-flow systems (see the accompanying Rule of Thumb). Given the large number of variables affecting FiO₂, however, the RT can never know precisely how much O₂ a patient is receiving with these systems. Even if it were possible to measure the exact FiO₂, this value could change from minute to minute and even from breath to breath with certain breathing patterns. Without knowing the patient’s exact FiO₂, the RT must rely on assessing the actual response to O₂ therapy.

Troubleshooting Low-Flow Systems

Common problems with low-flow O₂ delivery systems include inaccurate flow, system leaks and obstructions, device displacement, and skin irritation. The problem of inaccurate flow is greatest when low-flow flowmeters (≤3 L/min) are used. Given the trend toward assessment of outcome of O₂ therapy (with either blood gases or pulse oximetry), ensuring the absolute accuracy of O₂ input flow generally is not essential. Nonetheless, similar to all respiratory care equipment, flowmeters should be subjected to regular preventive maintenance and testing for accuracy. Equipment that fails preventive maintenance standards should be removed from service and repaired or replaced. Table 38-5 provides guidance on troubleshooting the most common clinical problems with nasal cannulas. Details on troubleshooting transtracheal catheters are provided in Chapter 51.

Reservoir Systems

Reservoir systems incorporate a mechanism for gathering and storing O₂ between patient breaths. Patients draw on this reserve supply whenever inspiratory flow exceeds O₂ flow into the device. Because air dilution is reduced, reservoir devices generally provide higher FiO₂ than low-flow systems. Reservoir devices can decrease O₂ use by providing FiO₂ comparable with nonreservoir systems but at lower flow. Reservoir systems in use at the present time include reservoir cannulas, masks, and nonrebreathing circuits. In principle, enclosure systems, such as tents and hoods, operate as reservoirs surrounding the head or body.

Reservoir Cannula

Reservoir cannulas are designed to conserve O₂ and are an alternative to the pulse-dose or demand-flow O₂ systems described in Chapter 51. There are two types of reservoir cannula: nasal reservoir and pendant reservoir. Table 38-3 lists the FiO₂ range, FiO₂ stability, advantages, disadvantages, and best use of a reservoir cannula.

A nasal reservoir cannula operates by storing approximately 20 ml of O₂ in a small membrane reservoir during exhalation (Figure 38-8). The patient draws on this stored O₂ during early inspiration. The amount of O₂ available increases with each breath and decreases the flow needed for a given FiO₂. Although the device is comfortable to wear, many patients object to its appearance and may not always comply with prescribed therapy.

The pendant reservoir system helps overcome esthetic concerns by hiding the reservoir under the patient’s clothing on the anterior chest wall (Figure 38-9). Although the device is less visible, the extra weight of the pendant can cause ear and facial discomfort.

At low flow, reservoir cannulas can reduce O₂ use 50% to 75%. A patient at rest who needs 2 L/min through a standard cannula to achieve an arterial oxygen saturation (SaO₂) greater than 90% may need only 0.5 L/min through a reservoir cannula to achieve the same blood oxygenation. During exercise, reservoir cannulas can reduce flow needs approximately 66%; the savings is approximately 50% at high flow.²⁶

Although flow savings is predictable, factors such as nasal anatomy and breathing pattern can affect the performance of the device. For these devices to function properly at low flow, patients must exhale through the nose (this reopens or resets the reservoir membrane). In addition, exhalation through pursed lips may impair performance, especially during exercise. For these reasons, prescribed flow settings should be individually determined by means of clinical assessment, including SaO₂ monitoring, during rest and exercise.²⁶

The low flow at which the reservoir cannula operates makes humidification unnecessary. Excess moisture can hinder proper action of the reservoir membrane.²⁶ Even regular use can cause membrane wear. For this reason, patients should replace the reservoir cannula approximately every 3 weeks. Replacement needs partially offset the O₂ cost savings afforded by these devices.

Reservoir Masks

Masks are the most commonly used reservoir systems. There are three types of reservoir masks: (1) simple mask, (2) partial rebreathing mask, and (3) nonrebreathing mask. Table 38-3 lists the FiO₂ range, FiO₂ stability, advantages, disadvantages, and best use of each of these devices.

A simple mask is a disposable plastic unit designed to cover both the mouth and the nose (Figure 38-10). The body of the mask itself gathers and stores O₂ between patient breaths. The patient exhales directly through open holes or ports in the mask body. If O₂ input flow ceases, the patient can draw in air through these holes and around the mask edge.

The input flow range for an adult simple mask is 5 to 10 L/min. Generally, if flow greater than 10 L/min is needed for satisfactory oxygenation, use of a device capable of a higher FiO₂ should be considered. At a flow less than 5 L/min, the mask volume acts as dead space and causes carbon dioxide (CO₂) rebreathing.²⁷

Because air dilution easily occurs during inspiration through its ports and around its body, a simple mask provides a variable FiO₂. How much FiO₂ varies depends on the O₂ input flow, the mask volume, the extent of air leakage, and the patient’s breathing pattern.²⁸

As shown in Figure 38-11, a partial rebreathing mask and a nonrebreathing mask have a similar design. Each has a 1-L flexible reservoir bag attached to the O₂ inlet. Because the bag increases the reservoir volume, both masks provide higher FiO₂ capabilities than a simple mask. The key difference between these designs is the use of valves. A partial rebreathing mask has no valves (see Figure 38-11, A). During inspiration, source O₂ flows into the mask and passes directly to the patient. During exhalation, source O₂ enters the bag. However, because no valves separate the mask and the bag, some of the patient’s exhaled gas also enters the bag (approximately the first third). Because it comes from the anatomic dead space, the early portion of exhaled gas contains mostly O₂ and little CO₂. As the bag fills with both O₂ and dead space gas, the last two-thirds of exhalation (high in CO₂

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