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) escapes out the exhalation ports of the mask. As long as the O₂ input flow keeps the bag from collapsing more than about one-third during inhalation, CO₂ rebreathing is negligible.

Although it can provide a higher FiO₂ than a simple mask (see Table 38-3), a standard disposable partial rebreathing mask is subject to considerable air dilution. The result is delivery of a moderate but variable FiO₂ dependent on the same factors as with a simple mask.

A nonrebreathing mask prevents rebreathing with one-way valves (see Figure 38-11, B). An inspiratory valve sits on top of the bag, and expiratory valves cover the exhalation ports on the mask body. During inspiration, slight negative mask pressure closes the expiratory valves, preventing air dilution. At the same time, the inspiratory valve on top of the bag opens, providing O₂ to the patient. During exhalation, valve action reverses the direction of flow. Slight positive pressure closes the inspiratory valve, which prevents exhaled gas from entering the bag. Concurrently, the one-way expiratory valves open and divert exhaled gas out to the atmosphere.

Because it is a closed system, a leak-free nonrebreathing mask with competent valves and enough flow to prevent more than one-third bag collapse during inspiration can deliver 100% source gas. As indicated in Table 38-3, however, modern disposable nonrebreathing masks normally do not provide much more than approximately 70% O₂.²²

Large air leaks are the primary problem. Air leakage occurs both around the mask body and through the open (nonvalved) exhalation port. This open exhalation port is a common safety feature designed to allow air breathing if the O₂ source fails. The port also allows air dilution whenever inspiratory flow or volume is high. Although a disposable nonrebreathing mask can deliver moderate to high O₂ concentration, FiO₂ still varies with the amount of air leakage and the patient’s breathing pattern.

Nonrebreathing Reservoir Circuit

A nonrebreathing circuit operates with the same design principles as a nonrebreathing mask. Although the nonrebreathing circuit requires an elaborate combination of equipment and supplies, it can be more versatile than a nonrebreathing mask because it provides a full range of FiO₂ (21% to 100%) and can be used for both intubated and nonintubated patients.²² As shown in Figure 38-12, a typical nonrebreathing circuit incorporates a blending system to premix air and O₂. The gas mixture is warmed and humidified, ideally with a servo-controlled heated humidifier. Gas flows through large-bore tubing into an inspiratory volume reservoir, which includes a fail-safe inlet valve. The patient breathes through a closed airway appliance, in this case, a mask with one-way valves. A valved T tube also can be used in the care of a patient with an endotracheal or a tracheostomy tube.

High-Flow Systems

High-flow systems supply a given O₂ concentration at a flow equaling or exceeding the patient’s peak inspiratory flow. An air-entrainment or a blending system is used. As long as the delivered flow exceeds the patient’s flow, both systems can ensure a fixed FiO₂. The accompanying Rule of Thumb can help determine which devices truly qualify as high-flow systems.

Principles of Gas Mixing

All high-flow systems mix air and O₂ to achieve a given FiO₂. These gases are mixed with air-entrainment devices or blending systems. Computations involving mixtures of air and O₂ are based on a modified form of the dilution equation for solutions:

< ?xml:namespace prefix = "mml" />VFCF=V1C1+V2C2

In this equation, V₁ and V₂ are the volumes of the two gases being mixed; C₁ and C₂, the O₂ concentration in these two volumes; and V_F and C_F, the final volume and concentration of the resulting mixture.

Box 38-1 shows how to apply variations of this equation to compute (1) the final concentration of a mixture of air and O₂, (2) the air-to-O₂ ratio needed to obtain a given FiO₂, (3) the total output flow from an air-entrainment device, and (4) the amount of O₂ that must be added to a volume of air to obtain a given FiO₂. Clinical examples of these computations are provided in the accompanying Mini Clini boxes.

Box 38-1   Equations for Computing Oxygen Percentage, Ratio, and Flow*

1. To compute the O₂ percentage of a mixture of air and O₂:

%O2=(Air flow×21)+(O2flow×100)Total flow (Eq. 38-1)

(Eq. 38-1)

2. To compute the air-to-O₂ ratio needed to obtain a given O₂ percentage:

Liters airLiters O2=(100−%O2)(%O2−21) (Eq. 38-2)

(Eq. 38-2)

3. To compute the total output flow from an air-entrainment device (given the O₂ input):

a. Compute the air-to-O₂ ratio (see Equation 38-2).

b. Add the air-to-O₂ ratio parts.

c. Multiply the sum of the ratio parts by the O₂ input flow.

4. To compute the flow of O₂ and air needed to obtain a given O₂ percentage at a given total flow:

a. Compute the O₂ flow:

O2flow=Total flow×(O2%−21)79 (Eq. 38-3)

(Eq. 38-3)

b. Compute the air flow:

Air flow=Total flow−O2flow

---

^*For simplicity, in all equations, percentage concentration (0 to 100) is used instead of decimal-based FiO₂. To convert a computed percentage to the corresponding FiO₂, divide by 100.

Mini Clini

Conflicting Assessment Information

 Problem

A disoriented postoperative male patient breathing room air exhibits tachypnea, tachycardia, and mild cyanosis of the mucous membranes. Using a pulse oximeter, the RT measures the patient’s oxyhemoglobin saturation as 93%. What should the RT recommend to the patient’s surgeon?

Discussion

This is a classic example of how monitoring data and results of bedside assessment can conflict. Both the patient’s condition and the observed clinical signs indicate hypoxemia, but the pulse oximeter indicates adequate oxygenation. In situations such as this, it is always better to err on the side of the patient and recommend O₂ therapy—treat the patient, not the monitor. This concept is particularly important in the use of monitoring technologies known to have limited accuracy, such as pulse oximetry (see Chapter 18).

Mini Clini

Determining FiO₂ of an Air-Oxygen Mixture

 Problem

An air-entrainment device mixes at a fixed ratio of three volumes of air to each volume of O₂ (3 : 1 ratio). What is the resulting FiO₂?

Solution

Substituting air, O₂, and total (air + O₂) volumes into Equation 38-1:

%O2=(Air flow×21)+(O2flow×100)Total flow

%O2=(3×21)+(1×100)3+1

%O2=41

An air-entrainment device that mixes three volumes of air with one volume of O₂ provides a gas mixture with FiO₂ of approximately 0.40.

Mini Clini

Computing Total Flow Output of an Air-Entrainment Device

 Problem

A patient is receiving O₂ through an air-entrainment device set to deliver 50% O₂. The input O₂ flow is set to 15 L/min. What is the total output flow of this system?

Solution

Step 1: Compute the air-to-O₂ ratio by substituting 50 for the %O₂ in Equation 38-2:

Liters airLiters O2=(100−%O2)(%O2−21)

Liters airLiters O2=(100−50)(50−21)

Liters airLiters O2=5029

Liters airLiters O2≈1.71

Step 2: Add the air-to-O₂ ratio parts:

1.7+1=2.7

Step 3: Multiply the sum of the ratio parts times the O₂ input flow:

2.7×15L/min=41L/min

An air-entrainment device set to deliver 50% O₂ that has an input flow of 15 L/min provides a total output flow of approximately 41 L/min.

Air-Entrainment Systems

Air-entrainment systems direct a high-pressure O₂ source through a small nozzle or jet surrounded by air-entrainment ports (Figure 38-13). The amount of air entrained at these ports varies directly with the size of the port and the velocity of O₂ at the jet. The larger the intake ports and the higher the gas velocity at the jet, the more air is entrained.

Because they dilute source O₂ with air, entrainment devices always provide less than 100% O₂. The more air they entrain, the higher is the total output flow, but the delivered FiO₂ is lower. High flow is possible only when low O₂ concentration is delivered. For these reasons, air-entrainment devices function as true high-flow systems only at low FiO₂. If the flow output from an air-entrainment device decreases to less than a patient’s inspiratory flow, air dilution occurs, and FiO₂ becomes variable.

FiO₂ provided by air-entrainment devices depends on two key variables: the air-to-O₂ ratio and the amount of flow resistance downstream from the mixing site. Changing the input flow of an air-entrainment device alters the total output flow but has little effect on delivered FiO₂. Generally, FiO₂ remains within 1% to 2% of that specified by the manufacturer, regardless of input flow.²⁹

The size of the jet and entrainment ports of a device determines the air-to-O₂ ratio and the delivered FiO₂. The accompanying Mini Clini entiled Determing FiO₂ of an Air-Oxygen Mixture shows how to compute the FiO₂ provided by an air-entrainment system if the air-to-O₂ ratio is known.

A more common clinical problem arises when the total output flow from an air-entrainment system must be determined. As described in the previous Rule of Thumb, the total flow output of a system determines whether it truly performs as a high-flow device. The accompanying Mini Clini entitled Computing Total Flow Output of an Air-Entrainment Device shows how to determine the total output flow of an air-entrainment system.

Rather than using Equation 38-2 in Box 38-1 to compute air-to-O₂ ratio, many RTs derive quick estimates by using a simple mathematical aid called the magic box (Figure 38-14). To use the magic box, one draws a square and places 20 in the top left corner and 100 in the bottom left corner. One places the desired O₂ percentage in the center of the box (in this case, 70%). One subtracts diagonally from lower left to the upper right (disregard the sign). One subtracts diagonally again from upper left to lower right (disregard the sign). The resulting numerator (30) is the value for air, and the denominator (50) is the value for O₂.

By convention, the air-to-O₂ ratio is expressed with the denominator (liters of O₂) set to 1. An air-entrainment device with a 7 : 1 ratio mixes 7 L of air with 1 L of O₂. To reduce any ratio to a ratio of x:1, one divides both the numerator and the denominator by the denominator. In the magic box example (also see Figure 38-14):

3050=30/5050/50=0.611

The magic box can be used only for estimation of air-to-O₂ ratio. For absolute accuracy, Equation 38-2 always should be used. Based on Equation 38-2, Table 38-7 lists the approximate air-to-O₂ ratios for several common O₂ percentages.

TABLE 38-7

Approximate Air-to-Oxygen Ratios for Common Oxygen Concentrations*

Percentage O2	Approximate Air-to-O2 Ratio	Total Ratio Parts
100	0 : 1	1
80	0.3 : 1	1.3
70	0.6 : 1	1.6
60	1 : 1	2
50	1.7 : 1	2.7
45	2 : 1	3
40	3 : 1	4
35	5 : 1	6
30	8 : 1	9
29	10 : 1	11
24	25 : 1	26

^*Total output flow (air + O₂) in L/min can be calculated by multiplying the total ratio parts by the O₂ input flow (L/min).

The other major factor determining the O₂ concentration provided by an air-entrainment device is downstream flow resistance. In the presence of flow resistance distal to the jet, the volume of air entrained always decreases. With less air being entrained, total flow output decreases, and the delivered O₂ concentration increases.

Although the delivered O₂ concentration increases, the actual FiO₂ received by the patient may decrease, especially on devices set to deliver 30% to 50% O₂.²⁹ This phenomenon is caused mainly by the decrease in total output flow. As the total output flow decreases below the flow needed to meet the patient’s inspiratory needs, room air is inhaled. A similar event occurs if the air intake ports surrounding the jet are blocked. Under both conditions, these high-flow systems begin to behave as low-flow devices. The two most common O₂ delivery systems in which air entrainment is used are the air-entrainment mask (AEM) and the air-entrainment nebulizer.

Air-Entrainment (Venturi) Mask

The use of an O₂ mask for provision of controlled FiO₂ by means of air entrainment was first reported in 1941 by Barach and Eckman.³⁰ The system provided relatively high FiO₂ (>40%) through the use of adjustable air-entrainment ports that controlled the amount of air mixed with O₂. Almost 20 years later, Campbell³¹ developed an entrainment mask that provided controlled, low FiO₂ and called the device a Venturi mask or venti-mask.

As the name venti-mask suggests, the operating principle behind these devices has often been attributed to the Venturi principle (see Chapter 6). This assumption is incorrect.³² Rather than having an actual Venturi tube that entrains air, these devices have a simple restricted orifice or jet through which O₂ flows at high velocity. Air is entrained by shear forces at the boundary of jet flow, not by low lateral pressures. The smaller the orifice, the greater the velocity of O₂, and more air is entrained.

Figure 38-15 depicts a typical AEM, designed to deliver a range of low to moderate FiO₂ (0.24 to 0.40). The mask consists of a jet orifice or nozzle around which is an air-entrainment port (top drawing). The body of the mask has several large ports, which allow escape of both excess flow from the device and exhaled gas from the patient. In this design, FiO₂ is regulated by selection and changing of the jet adapter. The smallest jet provides the highest O₂ velocity, the most air entrainment, and the lowest FiO₂ (0.24). The largest jet provides the lowest O₂ velocity, the least air entrainment, and the highest FiO₂ (0.40). Other AEM designs may vary both jet and entrainment port size to provide an even broader range up to 50% FiO₂. The aerosol entrainment collar fits over the air-entrainment ports (see later).

For controlled FiO₂ at flow high enough to prevent air dilution, the total output flow of an AEM must exceed the patient’s peak inspiratory flow.²⁹ With an entrainment ratio exceeding 5 : 1, an AEM set to deliver less than 35% O₂ has little trouble meeting or exceeding the 60 L/min high-flow criterion (see previous Rule of Thumb). At settings greater than 35%, total AEM flow decreases significantly, and FiO₂ becomes variable. For example, when set to deliver 50% O₂, some AEMs provide 0.39 FiO₂.^32–34

Air-Entrainment Nebulizer

Pneumatically powered air-entrainment nebulizers have most of the features of AEMs but have added capabilities, including additional humidification and temperature control. Humidification is achieved through production of aerosol at the nebulizer jet. Temperature control is provided by an optional heating element. In combination, these added features allow delivery of particulate water (in excess of needs for body temperature and pressure, saturated) to the airways. These devices are also widely known as jet nebulizers or large volume nebulizers.

Because of added humidification and heat control, air-entrainment nebulizers have been the traditional device of choice for delivering O₂ to patients with artificial tracheal airways. O₂ typically is delivered with a T tube or a tracheostomy mask. An alternative is to use an aerosol mask or a face tent to deliver an O₂ mixture via aerosol to patients with intact upper airways (Figure 38-16).³⁵

AEMs can vary both jet and entrainment port size to obtain a given FiO₂; however, gas-powered nebulizers have a fixed orifice. Air-to-O₂ ratios can be altered only by varying entrainment port size. Disposable nebulizers usually have a continuous range of settings from 28% to 100%. Less commonly used nondisposable nebulizers have fixed entrainment settings, such as 100%, 70%, and 40%.²²

Similar to AEMs, air-entrainment nebulizers perform as fixed-performance devices only when output flow meets or exceeds the patient’s inspiratory demand. In contrast to AEMs, air-entrainment nebulizers do not allow easy increases in nebulizer output flow by means of an increase in O₂ input. With most nebulizer systems, the extremely small size of the jet needed for aerosol production limits the maximum O₂ input flow to 12 to 15 L/min at 50 psig. For example, the total output flow of an air-entrainment nebulizer set to deliver 40% O₂ ranges from 48 to 60 L/min. Although this amount may be adequate for most patients, it is insufficient for patients with very high inspiratory flow or minute volume.³⁵

The actual FiO₂ received by patients may be affected by the choice of airway appliance. The FiO₂ delivered by face tent is consistently less than the set nebulizer concentration, especially at higher levels.³⁶

Air-entrainment nebulizers should be treated as fixed-performance devices only when set to deliver low O₂ concentration (≤35%).³³ When a nebulizer is used to deliver a higher concentration of O₂, the RT must determine whether the flow is sufficient to meet patient needs. There are two ways to assess whether the flow of an air-entrainment nebulizer meets the patient’s needs. The first method is simple visual inspection. With this approach (generally used only with a T tube), the RT sets up the device to deliver the highest possible flow at the prescribed FiO₂. After connecting the system to the patient, the RT observes the mist output at the expiratory side of the T tube. As long as mist can be seen escaping throughout inspiration, flow is adequate to meet the patient’s needs, and the delivered FiO₂ is ensured.

The second way to assess the adequacy of nebulizer flow is to compare it with the patient’s peak inspiratory flow. A patient’s peak inspiratory flow during tidal breathing is approximately three times minute volume. As long as the nebulizer flow exceeds this value, the delivered FiO₂ is ensured. If the patient’s peak flow exceeds that provided by the nebulizer, the device functions as a low-flow system with variable FiO₂ (see the accompanying Mini Clini for an example).³⁵

Mini Clini

Computing Minimum Flow Needs

 Problem

A physician orders 40% O₂ through an air-entrainment nebulizer to a patient with a tidal volume of 0.6 L and a respiratory rate of 33 breaths/min. If maximum nebulizer input flow is 12 L/min, will the patient receive 40% O₂? If not, what total flow is needed to meet this patient’s needs?

Solution

1. Estimate the patient’s inspiratory flow:

2. Compute the total flow of the nebulizer:

Sum of ratio parts (3:1)×Input flow (12L/min)=48L/min

3. Compare value 1 with value 2 (patient with nebulizer):

59.4L/min(patient)>48L/min(nebulizer)

Under these conditions, the patient does not receive 40% O₂. To deliver a stable 40% O₂ concentration, the total flow would have to be at least 59.4 L/min.

Troubleshooting Air-Entrainment Systems

The major problem with air-entrainment systems is ensuring that the set FiO₂ actually is delivered to the patient. Problems usually do not occur when the devices are used to deliver low FiO₂ (<0.35). However, the design of these devices makes it difficult to provide even moderate FiO₂ at the high flow needed to ensure a set O₂ concentration. The performance of all air-entrainment devices is affected by downstream resistance. The result can be inaccurate FiO₂ that makes delivery of a low O₂ concentration difficult with air-entrainment nebulizers.

Providing Moderate to High FiO₂ at High Flow

AEMs and air-entrainment nebulizers differ in ratio settings and input and output flow capabilities. Most AEMs can be set to deliver no more than 50% O₂. When set according to the manufacturer’s specifications to provide much more than 35% O₂, AEMs simply do not generate enough flow to ensure the set FiO₂. The solution is to boost the total output flow. With AEMs, total output flow can be boosted with a simple increase in input flow. For a 35% AEM (5 : 1 ratio) with an input flow of 8 L/min, the total output flow is 48 L/min. This flow is insufficient to ensure 35% O₂ delivery to all patients. Simply increasing the input flow to 12 L/min boosts the output flow of the AEM by 50%, to 72 L/min. The new high flow ensures delivery of the set O₂ concentration to essentially all patients.

This solution is impossible with most air-entrainment nebulizers. Because the small jets in many of these devices limit O₂ flow to 12 to 15 L/min, the input flow cannot be increased beyond these levels. A few nebulizer models, such as the Thera-Mist Barrel Nebulizer (Smiths Medical, London, England), supposedly can provide moderately high output flows of 54 L/min at FiO₂ 80%. However, most air-entrainment nebulizers cannot because of the total flow-to-FiO₂ tradeoff. The five alternatives for boosting the FiO₂ capabilities in these situations are presented in Box 38-2.

Box 38-2   Increasing FiO₂ Capabilities of Air-Entrainment Nebulizers

• Add open reservoir to expiratory side of T tube

• Provide inspiratory reservoir with one-way expiratory valve

• Connect two or more nebulizers together in parallel

• Set nebulizer to low concentration; bleed-in O₂; analyze and adjust

• Use a commercial dual-flow system

The simplest approach to achieving higher FiO₂ with these devices is to add a 50- to 150-ml aerosol tubing reservoir to the expiratory side of the T tube (Figure 38-17). Given its simplicity, adding an open volume reservoir to the expiratory side of T tubes is standard procedure in most clinical settings. This approach can be used only in the treatment of intubated patients. Even then, the small reservoir size limits the ability of this system to ensure stable FiO₂, especially greater than 40%, and larger reservoirs can cause rebreathing.

Rather than a simple open reservoir, a closed reservoir or nonrebreathing system similar to that shown in Figure 38-12 can be used. These systems combine an inspiratory volume reservoir (usually a compliant 3- to 5-L anesthesia bag) with a one-way expiratory valve. Whenever patient flow exceeds nebulizer flow, the expiratory valve closes, and the patient draws additional gas from the reservoir. Although they can ensure delivery of the set O₂ concentration, these systems pose considerable hazards. If source flow stops for any reason, the patient can suffocate. For this reason, these systems must be equipped with an emergency inlet valve that allows room air breathing in the event of source gas failure.

The third and most common approach to higher FiO₂ with air-entrainment nebulizers is to connect two or more devices together with a “wye” adapter (Figure 38-18).²² Although a single air-entrainment nebulizer set at 60% (1 : 1 ratio) with a maximum input flow of 15 L/min has a total output flow of only 30 L/min, connecting two of these devices together doubles the total output flow to 60 L/min (the minimum needed for a high-flow device). This approach works well only for delivery of a concentration of 60% or less to patients with a minute volume less than 10 L/min.^35,37

A fourth method for boosting FiO₂ provided by air-entrainment nebulizers is to set the device to a lower concentration than that prescribed (to generate high flow) while bleeding supplemental O₂ into the delivery tubing. This method increases both FiO₂ and total output flow. To achieve a specific FiO₂ in this type of system, the RT must analyze the delivered concentration and carefully adjust the supplemental O₂ input flow until the concentration is the desired value.

Commercial dual-flow systems entail a similar approach. One flow source powers the jet, while another flow source provides supplemental O₂. The Misty Ox (Vital Signs, Inc, Totowa, New Jersey) gas injection nebulizer is an example. This system is not an air-entrainment system because it does not depend on entrainment ports to increase total flow or O₂ concentration to the patient. Rather, it uses two flowmeters: one that operates the jet and one that feeds into the side of the jet manifold. The Misty Ox system can provide FiO₂ of 0.96 at a flow of 42 L/min and offers O₂ concentrations ranging from 0.21 to nearly 1.00.³⁵

If aerosol is not needed, a simple dual-flow device such as the Downs flow generator (Figure 38-19) can be used. This device is attached to a 50-psig O₂ source and provides O₂ concentrations of 30% to 100% at a flow up to 100 L/min.³⁸

Problems With Downstream Flow Resistance

Any increase in flow resistance downstream from (distal to) the point of air entrainment alters the performance of all air-entrainment systems. Increased downstream flow resistance causes back pressure. The back pressure decreases both the volume of entrained air and the total flow output of these devices. With less air entrained, the delivered O₂ concentration increases; however, because total flow output also decreases, the effect on FiO₂ varies. High downstream flow resistance usually turns air-entrainment systems from high-flow (fixed) O₂ delivery systems into low-flow (variable) O₂ delivery systems incapable of delivering a precise and constant FiO₂.²⁹

This problem explains why it is extremely difficult to deliver less than 28% to 30% O₂ with an air-entrainment nebulizer. The 5 to 6 ft (1.5 to 1.8 m) of aerosol tubing normally used with these devices produces enough flow resistance to decrease air entrainment and prevent a lower FiO₂.

A similar situation can occur when the entrainment ports of an air-entrainment device become obstructed (most common with AEMs). Delivered O₂ concentration increases, but total output flow decreases. The net effect usually is a variable FiO₂. The accompanying Mini Clini is an example of the effect of increased downstream flow resistance on the performance of an air-entrainment device.

Mini Clini

Effect of Downstream Flow Resistance on Performance of an Air-Entrainment Device

 Problem

A tracheostomy patient is receiving O₂ therapy through a T tube attached to an air-entrainment nebulizer set at 35% O₂ with an input flow of 10 L/min. Over the past 30 minutes, the patient’s SpO₂ has decreased from 93% to 88%. When assessing the patient, the RT finds that the large-bore delivery tubing of the nebulizer is partially obstructed with condensate and that aerosol mist at the T tube is not visible throughout inspiration. What is the likely problem, and what is the best solution?

Solution

The likely problem is a decrease in FiO₂ owing to the increased downstream resistance caused by the condensate. At 10 L/min input flow, the device was probably delivering approximately 60 L/min of 35% O₂ before the tubing became obstructed. Because aerosol mist is not visible at the T tube throughout inspiration, it is clear that the total output flow is no longer sufficient and that the patient is now diluting the delivered O₂ with room air. Draining the tubing restores the system flow and ensures delivery of the set FiO₂.

Blending Systems

When air-entrainment devices cannot provide a high enough O₂ concentration or flow, use of a gas blending system should be considered. With a blending system, separate pressurized air and O₂ sources are input, and the gases are mixed either manually or with a precision valve (blender). This system allows precise control over both FiO₂ and total flow output. Most blending systems can provide flow much greater than 60 L/min, qualifying them as true fixed-performance delivery devices. For adults, gas is delivered from the blender either through an open system, such as an aerosol mask or T tube, or with a closed nonrebreathing system. For many patients requiring high FiO₂ and breathing spontaneously, this is the ideal setup, provided that the gas is humidified. The use of high-flow blended systems with heated humidity as opposed to a heated aerosol are very well tolerated by most patients, including patients with tracheostomies.

Mixing Gases Manually

When gases are mixed manually, separate air and O₂ flowmeters must be adjusted for the desired FiO₂ and flow (see the accompanying Mini Clini). For adults, this approach requires calibrated high-flow flowmeters (at least 60 L/min) and monitoring of delivered FiO₂.

Mini Clini

Manually Mixing Air and Oxygen to Achieve Specified Concentration at a Given Flow

 Problem

To mix air and O₂ manually to provide a patient with 50% O₂ at a total flow of 60 L/min, what O₂ and air flow would the RT set?

Solution

1. Use Equation 38-3 to compute the O₂ flow:

O2flow=Total flow×(O2%−21)79

O2flow=60×(50−12)79

O2 flow=22L/min

2. Compute the air flow:

Air flow=Total flow−O2 flow

Air flow=60−22

Air flow=38L/min

To provide a patient with 50% O₂ at a total flow of 60 L/min, blend 22 L of O₂ with 38 L of air.

Oxygen Blenders

Rather than manually mixing air and O₂, the RT can use an O₂ blender. Figure 38-20 shows the major components of a typical O₂ blender. Air and O₂ enter the blender and pass through dual pressure regulators that exactly match the two pressures. Gas flows to a precision proportioning valve. Because the two gas pressures at this point are equal, varying the size of the air and O₂ inlets provides precise control over the relative concentration.

An alarm system gives an audible warning when either source gas fails or the pressure decreases below a specified value. The alarm system usually has a crossover or bypass feature whereby failure of one gas source causes the blender system to switch to the other. If the air source fails when delivering 60% O₂, the alarm sounds, and the blender switches over to delivery of 100% O₂.

Although they allow ideal control over both FiO₂ and flow, blenders are especially prone to inaccuracy and failure.39,40 To avoid these problems, the RT always should conduct an operational check of any blender before using it on a patient (Box 38-3). FiO₂ should be checked and confirmed with a calibrated O₂ analyzer at least once per shift.² As always, a device that does not perform according to expectations should be replaced immediately. When a blender is used in the care of a neonate, an O₂ analyzer should be kept in-line at all times. In the use of a nonrebreathing or closed delivery system, (1) all breathing valves should be inspected and tested before application to a patient, and (2) a fail-safe inspiratory valve should be included in the delivery system.

Box 38-3   Procedure for Confirming Operation of an Oxygen Blender

1. Confirm that inlet pressures of air and O₂ are within manufacturer’s specifications.

2. Test low air and O₂ alarms by disconnecting each source; also confirm safety bypass or crossover system.

3. Analyze O₂ concentration at 100%, 21%, and specified FiO₂.

Enclosures

The concept of enclosing a patient in a controlled-O₂ atmosphere is among the oldest approaches to O₂ therapy. Entire rooms once were used for this purpose. With today’s simpler airway devices, enclosures are generally used only in the care of infants and children. The primary types of O₂ enclosures used for infants and children are tents, incubators, and hoods.

Oxygen Tents

O₂ tents previously were the most common method of O₂ therapy in the treatment of both adults and children. Use of O₂ tents in both adults and children is rare at the present time. However, when they are used, it is common for tents to be air-conditioned or cooled with ice to provide a comfortable temperature within a plastic sheet canopy (Figure 38-21).

The main problem with tents is that frequent opening and closing of the canopy cause wide swings in O₂ concentration. Constant leakage makes a high FiO₂ impossible. In large tents, O₂ input flow of 12 to 15 L/min can provide only 40% to 50% O₂ levels. Comparable FiO₂ can be achieved in smaller pediatric or croup tents with flow of 8 to 10 L/min. Because of these limitations, tents are used primarily for pediatric aerosol therapy in the care of children with croup or cystic fibrosis.

Hoods

An O₂ hood, also known as an oxyhood, is often the best method for administration of controlled O₂ therapy to infants. As shown in Figure 38-22, an O₂ hood covers only the head, leaving the infant’s body free for nursing care. O₂ is delivered to the hood through either a heated air-entrainment nebulizer or a blending system with a heated humidifier. A minimum flow of 7 L/min should be set to prevent accumulation of CO₂.⁴¹ Depending on the size of the hood, flow of 10 to 15 L/min may be needed to maintain stable high O₂ concentration. Higher flow generally is not needed and may produce a harmful noise level and additional stress on neonatal patients.⁴²

In the care of premature infants, it is especially important to ensure that the gas mixture is properly warmed and humidified and not directed toward the patient’s face or head. Low temperatures or convection cooling produced by high flow over the head can cause heat loss and cold stress. In premature infants, cold stress can increase O₂ consumption and cause apnea.⁴³

The temperature of gases provided to an infant in an O₂ hood should be precisely set to maintain a neutral thermal environment (NTE). The NTE temperature varies according to an infant’s age and weight. The NTE temperature for newborns weighing less than 1200 g is 95° F (35° C). For older infants weighing 2500 g or more, the NTE is lower, approximately 86° F (30° C).⁴³ The importance of temperature regulation in infants is discussed in more detail in Chapter 48.

Incubators

Incubators, also known by the trade name Isolette (Dräger Medical AG & Co, Lübeck, Germany) are polymethyl methacrylate (Plexiglas) enclosures that combine servo-controlled convection heating with supplemental O₂ (Figure 38-23). In older models, humidification was provided with a blow-over water reservoir located under the patient platform. Because of the high infection risk associated with this design, these systems are no longer in common use. When it is needed, supplemental humidity usually is provided with an external heated humidifier or nebulizer.

Supplemental O₂ can be administered with a direct connection between the incubator and a flowmeter that has a heated humidifier. In some units, a filtered air-entrainment device limits the delivered concentration to approximately 0.40. However, leaks and frequent opening of the isolette dilute the O₂ levels to much less than 40%. Blockage of the inlet filter can cause less air entrainment and a higher O₂ concentration.⁴³

Given the highly variable O₂ concentration provided by these devices, the best way to control O₂ delivery to infants in an isolette is with an oxyhood. The oxyhood is placed over the infant’s head inside the isolette. The O₂ concentration and gas temperature within the oxyhood, not in the isolette, must be assessed. It is ideal to monitor isolette or oxyhood O₂ concentration continuously (see later).2,4

Because hoods allow better FiO₂ control, and because servo-controlled radiant heating warmers are generally more convenient, Plexiglas isolettes are not as popular as they used to be. However, these devices are still the best choice for providing O₂ to infants in stable condition with a NTE.⁴³

Other Oxygen Delivery Devices

Purpose

The general purpose or objective of all O₂ therapy is to increase FiO₂ sufficiently to correct arterial hypoxemia. Other objectives, including decreasing hypoxic symptoms and minimizing increased cardiopulmonary work, follow from this primary purpose.

Patient

Key patient considerations in selecting O₂ therapy equipment for use in acute care are summarized in Box 38-4. Knowledge of these factors helps guide the RT in selecting the appropriate equipment. For example, a simple mask at 5 to 6 L/min is probably more suitable than a nasal cannula at 4 L/min for a mouth breathing, mildly hypoxemic patient. An infant with moderate hypoxia and a normal airway usually needs an O₂ enclosure (hood or enclosed incubator).

Performance

O₂ systems vary according to actual FiO₂ delivered and stability of FiO₂ under changing patient demands. Generally, the more critically ill the patient, the greater the need for a stable, high FiO₂. Less acutely ill patients generally need a lower, less exact FiO₂. Table 38-8 lists guidelines for selecting an O₂ delivery system on the basis of the level and stability of the FiO₂ needed.

General Goals and Patient Categories

On the basis of overall consideration of the three Ps, general goals can be set for several patient categories. In emergencies in which tissue hypoxia is suspected, patients should be given the highest FiO₂ possible—ideally 100%. This level can be achieved with a true high-flow or a closed reservoir system. The goal is the highest possible blood O₂ content. Clinical examples include respiratory or cardiac arrest, severe trauma, shock, carbon monoxide poisoning, and cyanide poisoning. Carbon monoxide and cyanide poisoning may necessitate HBO therapy (see later).

A critically ill adult patient with moderate to severe hypoxemia needs either a reservoir or a high-flow system capable of at least 60% O₂. Thereafter, changes in FiO₂ (and device) should be based on results of assessment of physiologic values. The goal is a PaO₂ greater than 60 mm Hg or oxyhemoglobin saturation greater than 90%.

In the care of adult patients in more stable condition but who are acutely ill with mild to moderate hypoxemia, a system capable of low to moderate O₂ concentration can be used. In these cases, stability of FiO₂ is not critical. Applicable devices include a nasal cannula at moderate flow or a simple mask. Common examples include patients in the immediately postoperative phase and patients recovering from acute myocardial infarction.

Adult patients with chronic lung disease and accompanying acute-on-chronic hypoxemia present a special case. In the care of these patients, the goal is to ensure adequate arterial oxygenation without depressing ventilation. Adequate oxygenation of these patients generally means SaO₂ of 85% to 92% with PaO₂ of 50 to 70 mm Hg.31,44 These values usually are achieved with either low-flow nasal O₂ or a low-concentration (24% to 28%) AEM. The less stable the patient’s condition, the greater the need for a high-flow AEM.²²

Because of size, discomfort, and appearance, AEMs are less well tolerated than nasal cannulas for long-term therapy. In contrast to a cannula, an AEM must be removed for eating and drinking. Because even a short break in O₂ therapy can cause a rapid decrease in PaO₂ in some patients, these patients should be taught to switch to a nasal cannula whenever they must remove the mask.²²

Lastly, it is sometimes necessary to modify O₂ delivery systems to facilitate patient transport. An example is a spontaneously breathing patient with a tracheostomy tube receiving a moderate FiO₂ via a blended system or an air-entrainment nebulizer connected to a tracheostomy mask. Given the impracticalities of transporting a patient on an air-entrainment nebulizer, it may be more suitable to connect a Venturi adapter temporarily to provide the appropriate FiO₂ to the tracheostomy mask during the transport. It is important to remember to reconnect patients back to the original set-up immediately after the transport to avoid exposing them to dry gases for long time periods.

Air Embolism

Air embolism is a complication that can occur with certain cardiovascular procedures, lung biopsy, hemodialysis, and central line placement. Air bubbles that reach the cerebral or cardiac circulation can cause severe neurologic symptoms or sudden death. HBO decreases the volume of air bubbles and helps oxygenate local tissues. Typical therapy for air embolism involves immediate pressurization in air to 6 ATA for 15 to 30 minutes. This step is followed by decompression to 2.8 ATA with prolonged O₂ treatment.47–49

Carbon Monoxide Poisoning

Carbon monoxide poisoning accounts for about half of all poisoning deaths in the United States. The condition of a patient with carbon monoxide poisoning improves quickly with HBO treatment because this treatment is the fastest way to remove carbon monoxide from the blood.⁵² If a patient breathes air, it takes more than 5 hours to remove only one half of the carboxyhemoglobin in the blood. Breathing 100% O₂ reduces this “half-life” to 80 minutes. The half-life of carboxyhemoglobin under HBO at 3 ATA is only 23 minutes. Box 38-7 lists the major criteria for selecting patients with acute carbon monoxide poisoning for treatment with HBO.⁵²

Indications

After several years of clinical testing, inhaled NO was approved in December 1999 by the U.S. Food and Drug Administration (FDA) for treating selected neonates. Specifically, NO, in conjunction with such therapies as ventilatory support, has been approved for the treatment of term and near-term (>34 weeks) neonates with hypoxic (type I) respiratory failure with associated pulmonary hypertension. As a result of the clinical benefits of reduced pulmonary vascular resistance, improved oxygenation, and less need for a highly invasive method for increasing tissue oxygenation known as extracorporeal membrane oxygenation, inhaled NO is emerging as the standard of care for near-term neonates with this type of respiratory failure.⁵⁴

In adults, studies have shown that inhaled NO has been effective in treating pulmonary hypertension associated with acute respiratory distress syndrome (ARDS). However, these benefits seem to be short-lived, and no significant improvement in clinical outcomes, including mortality, has been shown to date. As a result of these findings and lower cost alternative drug therapies, including inhaled epoprostenol sodium (Flolan) and similar medications (discussed in Chapter 32), the use of inhaled NO in adults has neither been approved by the FDA nor gained widespread acceptance, However, potential indications and various delivery methods for inhaled NO continue to be examined. Potential indications for inhaled NO are listed in Box 38-9.^54,55

Dosing

The amount of NO needed to improve oxygenation or decrease pulmonary vascular pressure in neonates is relatively low. The therapeutic range of NO is 2 to 20 ppm, and an initial dose of 20 ppm is commonly used. Treatment should be continued until underlying oxygenation desaturation has resolved. For many patients, dosages often can be reduced to less than 20 ppm at the end of 4 hours of initial treatment, as tolerated. At these levels, NO has minimal toxicity.⁵⁴ In clinical trials, higher doses were not shown to be more effective and placed the patient at a higher risk of complications.^53–55

Toxicity and Adverse Effects

The toxicity of NO is caused by its own direct action and its chemical by-products. In high concentrations (5000 to 20,000 ppm), NO causes acute pulmonary edema that can be fatal. Inhalation of a lower concentration has been associated with direct cellular damage and impaired surfactant production.55,56

Most of the toxic effects of NO are caused by its chemical by-products, especially NO₂. NO₂ is produced spontaneously whenever NO is exposed to O₂. NO₂ is more toxic than NO. Levels greater than 10 ppm can cause cell damage, hemorrhage, pulmonary edema, and death. The U.S. Occupational Safety and Health Administration has set the safety limit for NO₂ exposure at 5 ppm. The clinical goal is to keep NO₂ exposure less than 2 ppm during administration of NO.⁵⁶

Other harmful chemical by-products produced in reaction with NO include methemoglobin and peroxynitrite (produced when NO reacts with superoxide). Although it can occur with NO administration, methemoglobinemia probably is not a large problem considering the doses commonly used and the required monitoring systems discussed later in this section. Peroxynitrite is a potent oxidant that can cause severe cell damage; however, there is no hard evidence supporting its toxic effects during NO administration.

Potential adverse effects associated with NO therapy are listed in Box 38-10.⁵⁶ A poor or paradoxical response to NO has been observed in some patients. Of patients with ARDS, 40% do not have initial improvement in oxygenation with NO therapy, and some patients have experienced more severe hypoxemia (probably because of a worsening ventilation/perfusion imbalance when no shunt was present). NO inhibits platelet agglutination, and the result is an antithrombotic effect. However, no significant increase in bleeding time has been reported in NO trials with human subjects. Because it can quickly reduce right ventricular afterload, NO may increase left ventricular filling pressure in some patients. In the presence of congestive heart failure, this effect could cause or worsen pulmonary edema. Concerns involving increased left heart pressures also account for inhaled NO being contraindicated for neonates with certain cardiac and vascular anomalies such as coarctation of the aorta.⁵⁴ In certain patients, the withdrawal of NO has resulted in development of hypoxemia and pulmonary hypertension, perhaps worse than they were before therapy was started. This phenomenon is known as a rebound effect. This rebound effect occurs because the administration of nitric oxide depresses the body’s normal production of NO. NO after use for more than a few hours should always be slowly weaned over hours. When NO is finally discontinued, FiO₂ frequently needs to be initially increased then slowly reduced to baseline over 1 or 2 hours.⁵³

Although NO has been used safely with other drugs and treatments such as dopamine, steroids, surfactant, and high-frequency ventilation, the interaction of NO with other medications is still being studied. One investigational area may involve the study of patients receiving both inhaled NO and other NO-related compounds such as nitroglycerin and the possible development of methemoglobinemia or systemic hypotension. Likewise, the carcinogenic, mutagenic, and other adverse effects of NO are still under investigation.⁵⁵

Methods of Administration

Before inhaled NO administration, the patient ideally should be stabilized as much as possible. To stabilize the patient, thought must be given to clinical considerations such as FiO₂, blood pH, sedation, and possibly muscle relaxation. After the patient is prepared, NO is administered to mechanically ventilated patients through a system with the capability for operator-determined concentration of NO in the breathing gas, a constant concentration throughout the breathing cycle, and a concentration that does not cause generation of excessive inhaled NO₂. Features of an ideal NO delivery system are listed in Box 38-11.

The INOmax DS (Delivery System) (Ikaria, Clinton, New Jersey) shown in Figure 38-26 provides these features.^55,57 The INOmax DS delivers INOmax (NO for inhalation) into the inspiratory limb of the patient’s breathing circuit in a manner that provides a constant concentration of NO, as preset by the clinician, throughout inspiration. Through a dual-channel design, the first channel uses a delivery mechanism, flow controller, and injector module to ensure precise delivery of NO. The highly specialized injector module allows tracking of the ventilator flow waveforms and the delivery of synchronized and proportional dose of NO. The second channel uses a separate monitoring mechanism, electrochemical gas sensors, and a graphically enhanced user interface to monitor O₂, NO₂, and NO continuously. The INOmax DS uses several alarm systems to alert clinicians when problems arise, including alarms for high and low NO, high NO₂, and high and low O₂. Other alarms can be set to notify clinicians of a significant decrease in source gas pressure, if the electrochemical cells fail, and when calibration is required.⁵⁸

These systems entail use of cylinder mixtures of NO containing up to 800 ppm of NO in nitrogen. This high concentration of NO is diluted with nitrogen, air, or O₂ before delivery to the patient. Because adding NO to the circuit decreases the FiO₂, O₂ concentration must be continuously monitored downstream from the titration site.

The INOmax DS can also be interfaced with specialty ventilators including high-frequency oscillators and jet ventilators and anesthesia machines. Inhaled NO has also been used with noninvasive ventilation, but rebreathing inherent in this mode of ventilation can cause NO₂ levels to increase beyond acceptable levels. Other special considerations apply, and resources such as ventilator procedure manuals and department policy and procedures should be reviewed to help ensure proper setup and patient safety.⁵⁷

The administration of inhaled NO to spontaneously breathing patients is also possible. This use and some other uses are described in the research literature but have not yet officially been approved by the FDA and are regarded as off-label use. INOmax DS can be used with a nasal cannula and a face mask. The maximum delivered NO via cannula is generally 20 ppm. When titrating NO via cannula, it is recommended that the concentration not be increased by more than 5 ppm in a 5-minute period, and the clinician should be aware that excessive flow can cause back pressure leading to monitoring failure alarms. Inhaled NO delivery via face mask is similar to a cannula setup except that it is important to use a tight-fitting mask and a flow sufficient to prevent entrainment of air into the mask.⁵⁷

Withdrawing Therapy

Care must be taken when NO therapy is withdrawn to prevent the rebound effect. First, the NO level should be reduced to the lowest effective dose (ideally ≤5 ppm). Second, the patient’s condition should be hemodynamically stable, and the patient should be able to maintain adequate oxygenation while breathing a moderate FiO₂ (≤0.4) on low levels of positive end-expiratory pressure. Third, the patient should be hyperoxygenated (FiO₂ 0.6 to 0.7) just before discontinuation of NO inhalation. Preparation should also be made to provide hemodynamic support in the event the patient needs it. Close monitoring of patients and use of these measures usually avoid any untoward effect of NO withdrawal.⁵⁴

Guidelines for Use

Because it is inert and unable to support life, helium always must be mixed with at least 20% O₂. The most common combination is 80% helium and 20% O₂. From the standpoint of its ability to oxygenate, this mixture is comparable to air, but helium is used in place of nitrogen. Although air has a density of 1.293 g/L, the density of an 80% helium mixture is 0.429 g/L. For a comparable flow through constricted large airways, this low-density mixture can dramatically decrease the work of breathing.

Heliox combinations can be prepared at the bedside, or commercially available cylinders of premixed gases can be used. The premixed cylinders are commonly available in an 80 : 20 or a 70 : 30 combination. The 70% helium and 30% O₂ mixture has a density of 0.554 g/L and can provide additional O₂ for the management of the hypoxemia that can occur with large airway obstruction. Other combinations such as 60 : 40 and 65 : 35 mixtures are being examined and show promising results.62,66

Several methods have been used to mix heliox at the bedside, although many are improvised setups. One method involves running a nebulizer connected to an O₂ flowmeter at 10 L/min or more, bleeding in 100% helium via a small-bore connection, and titrating the flow to achieve the desired FiO₂. An O₂ analyzer with active alarms should always be used to measure continuously the FiO₂ of the heliox mixture output flowing to the patient. Continued use of improvised setups or setups that are not approved by the FDA for heliox administration can place the patient, clinician, and hospital at risk. Devices cleared by the FDA for use with heliox should be integrated into clinical practice.62,67

The low-density benefit of heliox is the same attribute that presents challenges in selecting a delivery device. Because helium is highly diffusible, administration through low-flow systems such as a nasal cannula tends not to deliver sufficient concentrations to treat obstructive disorders in adults. However, heliox administered via cannulas with an adequate seal at the nares has shown to be effective in some infants.⁶⁸ Generally, however, heliox should be delivered to most spontaneously breathing patients via a tight-fitting nonrebreathing mask with a fully functional valved exhalation port. The delivery system should be high flow, sufficient to meet or exceed the patient’s minute ventilation and peak inspiratory flow requirements. Closed systems with demand valves and reservoirs or the use of demand regulators has proved to be suitable for delivering heliox to patients with artificial airways.⁶⁷

Helium mixtures can be given through a cuffed tracheal airway with a positive-pressure ventilator. However, the performance of ventilators in delivering heliox tends to vary significantly by model, and only some of them have received FDA clearance for such use. Consequently, RTs should ensure that an appropriate ventilator is being used to administer heliox, determine if a conversion factor is needed to adjust settings, and ensure that the patient is monitored closely while such an approach is being used.⁶⁹

Other methods of heliox administration have been examined, including the use of large-volume enclosures, such as hoods. These devices have generally proven to be unsatisfactory because helium tends to concentrate at the top of the devices, and the much higher thermal conductivity of helium can cause excessive heat loss and hypothermia. Blenders have also been used to administer heliox, When a blender is used, the 80 : 20 heliox is generally attached to the air inlet, and an O₂ analyzer is placed downstream. However, because the accuracy of blenders tends to vary, the system’s FiO₂ readings should first be tested, and the difference between the set and actual FiO₂ should be known.

Heliox has also been combined with bronchodilator therapy to treat acute obstructive disorders such as status asthmaticus. Heliox improves aerosol deposition mainly because of a reduction in turbulence and less impaction and medication loss. When administering such a therapeutic combination, the RT should be mindful that only certain nebulizers have been approved for such use and that output may vary because of the characteristics of heliox.

When a helium-O₂ mixture is given alone or as part of nebulization, the RT should realize that a typical hospital O₂ flowmeter is inaccurate because of the lower density of helium. Flowmeters calibrated for helium should be used to ensure accurate delivery. However, correction factors are available for O₂ flowmeters. The correction for an 80 : 20 helium-O₂ mixture is 1.8; this means that for every 10 L/min indicated flow, 10 × 1.8, or 18 L/min, of the 80 : 20 mixture actually leaves the flowmeter. For delivery of a specific flow from an 80 : 20 helium-O₂ source, the RT sets the flowmeter to the desired flow divided by 1.8. If a flow of 9 L/min of an 80 : 20 helium-O₂ mixture is needed, the RT sets the flowmeter to 9/1.8, or 5 L/min. Factors for any other mixture can be calculated if needed. The factor for a 70 : 30 helium-O₂ mixture is 1.6.

In addition to special flow considerations, the RT should use an O₂ analyzer to monitor heliox (actually O₂) concentrations continuously between the source of the mixture and the patient. The basis for this recommendation is that the gas is either helium or O₂, and if the FiO₂ is known, assuming there are no leaks, the remaining gas is helium. This monitoring helps ensure that the patient is receiving the therapeutic benefits of a less dense gas while maintaining the appropriate FiO₂.

Troubleshooting and Hazards

The low density of helium mixtures makes them poor vehicles for aerosol transport. High-density bland water aerosols are difficult to deliver with helium mixtures. The low density of helium mixtures also makes coughing less effective. An expulsive cough depends in part on the development of turbulent flow in the large airways. Because helium promotes laminar flow, clearance of secretions by coughing is impaired. If the patient can develop an effective cough, this problem can be rectified by means of washing out the helium before coughing.

The most common side effect of helium is a benign one. When a patient is breathing a helium mixture, the spoken word is badly distorted at a pitch so high as to make it almost unintelligible. This effect is caused by the passage of a low-density gas through the vocal cords on exhalation. The effect is important only to conscious, nonintubated patients, who should be warned of the effect and reassured that it disappears immediately after therapy is stopped.

A more serious problem is hypoxemia associated with breathing helium mixtures.67,70 Although this problem may have been caused by using too low an O₂ concentration (20%), there is another possibility. Very rarely, some commercial helium-O₂ cylinders stored for long periods of time have been found to contain these gases in an unmixed, or separated, state. The only way to avoid this potential hazard is to analyze the O₂ concentration coming from the cylinder before administering the gas.

As clinical applications for heliox have expanded, other hazards have emerged. One potential problem is volume-induced lung injury when heliox is administered via a mechanical ventilator. This risk can be addressed by using only ventilators approved by the FDA for heliox administration. The use of heliox for bronchodilator nebulization may present another possible hazard. The lower density of helium-O₂ mixtures may result in greater variability in medication delivery to the airways. Careful patient monitoring during such therapy can help minimize this concern. Another rare but possible problem is hypothermia to infants receiving heliox via an oxyhood. This risk results from the high thermal conductivity of helium and can be avoided by warming and humidifying the heliox gas.⁶⁷