Medical Gas Therapy



Medical Gas Therapy


Albert J. Heuer




Gas therapy is the most common mode of respiratory care. The origins of the field parallel the introduction of oxygen (O2) as a medical treatment. Since that time, understanding of the various medical gases and methods to deliver them has changed. Of particular importance is the acknowledgment that most medical gases are drugs. As with any drug, respiratory therapists (RTs) recommend and administer a dosage, monitor the response, alter therapy accordingly, and record these steps in relation to the care plan in the patient record. In this context, RTs must have more than technical knowledge of equipment. In consultation with the physician, a skilled clinician should be able to assess the patient’s need for therapy, determine the desired goals of therapy, select the mode of administration, monitor the patient’s response, and recommend and implement timely and appropriate changes.



Oxygen Therapy


Consensus exists among clinicians about the proper use of O2 therapy.1-4 As the primary member of the health care team responsible for O2 administration, the RT must be well versed in the goals and objectives of this therapy and its use in clinical practice.



General Goals and Clinical Objectives


The overall goal of O2 therapy is to maintain adequate tissue oxygenation, while minimizing cardiopulmonary work. Specific clinical objectives for O2 therapy are the following:






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



Clinical Practice Guideline


To guide practitioners in safe and effective patient care, the American Association for Respiratory Care (AARC) has developed and published clinical practice guidelines for O2 therapy. Excerpts from the AARC guideline on O2 therapy in acute care hospitals appear in Clinical Practice Guideline 38-1.2 Additional AARC guidelines for O2 therapy in the home or an extended care facility3 and for selection of O2 delivery devices for neonatal and pediatric patients4 are provided in Chapters 48 and 51.



38-1


Oxygen Therapy


AARC Clinical Practice Guideline (Excerpts)





Precautions and/or Possible Complications




• PaO2 greater than or equal to 60 mm Hg; ventilator depression may occur rarely in spontaneously breathing patients with elevated PaCO2


• With FiO2 greater than 0.5, absorption atelectasis, O2 toxicity, or depression of ciliary or leukocyte function may occur


• In premature infants, PaO2 greater than 80 mm Hg may contribute to retinopathy of prematurity


• In infants with certain congenital heart lesions such as hypoplastic left heart syndrome, high PaO2 can compromise the balance between pulmonary and systemic blood flow


• In infants, O2 flow directed at the face may stimulate an alteration in respiratory pattern


• Increased FiO2 can worsen lung injury in patients with paraquat poisoning or patients receiving bleomycin


• During laser bronchoscopy or tracheostomy, minimal FiO2 should be used to avoid intratracheal ignition


• Fire hazard increased in the presence of high FiO2


• Bacterial contamination can occur when nebulizers or humidifiers are used





Monitoring




For complete guidelines, see American Association for Respiratory Care: Clinical practice guideline: selection of an oxygen delivery device for neonatal and pediatric patients, Respir Care 47:707, 2002; and American Association for Respiratory Care: Clinical practice guideline: oxygen therapy for adults in the acute care facility, Respir Care 47:717, 2002.



Assessing the Need for Oxygen Therapy


There are three basic ways to determine whether a patient needs O2 therapy. The first is the use of laboratory measures to document hypoxemia. Second, a patient’s need for O2 therapy can be based on the specific clinical problem or condition. Third, hypoxemia has many manifestations, such as tachypnea, tachycardia, cyanosis, and distressed overall appearance. Astute bedside techniques of assessment for these and other symptoms can be used to determine the need for supplemental O2.


Laboratory measures for documenting hypoxemia include hemoglobin saturation and partial pressure of oxygen (PO2), as determined by either invasive or noninvasive means (see Chapter 18). Threshold criteria defining hypoxemia with these measures are described in the AARC clinical practice guideline (see Clinical Practice Guideline 38-1).2


O2 therapy is needed for patients with disorders associated with hypoxemia. Examples are postoperative patients; patients with carbon monoxide or cyanide poisoning, shock, trauma, or acute myocardial infarction, and some premature infants.1,2,8


Careful bedside physical assessment can disclose a patient’s need for O2 therapy. Table 38-1 summarizes the common respiratory, cardiovascular, and neurologic signs used in the detection of hypoxia. The RT combines this information with more quantitative measures such as arterial blood gas results to confirm inadequate oxygenation. The patient care team often relies on the RT to recommend administration of supplemental O2 based on quantitative and qualitative information.




Precautions and Hazards of Supplemental Oxygen


Excerpts from the relevant AARC clinical practice guidelines (see Clinical Practice Guideline 38-1) outline the major precautions and hazards associated with administration of supplemental O2.2 Five of these hazards are common enough to warrant additional discussion.



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 (VD/VT) 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



Oxygen Delivery Systems: Design and Performance


RTs can select from an array of systems for administering O2 and other therapeutic gases. Proper device selection requires in-depth knowledge of both the general performance characteristics of these systems and the individual capabilities.22 O2 delivery devices traditionally are categorized by design. Three basic designs exist: low-flow systems, reservoir systems, and high-flow systems. Enclosures, commonly identified as a fourth category, are reservoirs that surround the head or body. The design categories share functional characteristics, capabilities, and limitations.


Although design plays an important role in the selection of these devices, clinical performance ultimately determines how the device is used. The user judges the performance of an O2 delivery system by answering two key questions: (1) How much O2 can the system deliver (FiO2 or FiO2 range)? (2) Does the delivered FiO2 remain fixed or vary under changing patient demands?22


Regarding the FiO2 range, O2 systems can be broadly divided into systems designed to deliver a low (<35%), moderate (35% to 60%), or high (>60%) O2 concentration. Some designs can deliver O2 across the full range of concentrations (21% to 100%).


Whether a device delivers a fixed or variable FiO2 depends on how much of the patient’s inspired gas it supplies. If the system provides all of the patient’s inspired gas, FiO2 remains stable, even under changing demands. If the device provides only some of the inspired gas, the patient must draw the remainder from the surrounding air. In this case, the more the patient breathes, the more air dilutes the delivered O2, and FiO2 is lower. If the patient breathes less with this type of device, less air dilutes the O2, and FiO2 increases. A system that supplies only a portion of the inspired gas always provides a variable FiO2.23 FiO2 supplied with such systems can vary widely from minute to minute and even from breath to breath.


Figure 38-4 shows these concepts as applied to low-flow, reservoir, and high-flow systems. With the low-flow system (see Figure 38-4, A) the patient’s inspiratory flow often exceeds the flow delivered by the device; the result is air dilution (shaded areas). The greater the patient’s inspiratory flow, the more air is breathed, and FiO2 is lower. The high-flow system (see Figure 38-4, B) always exceeds the patient’s flow and provides a fixed FiO2. A fixed FiO2 can be achieved with a reservoir system (see Figure 38-4, C), which stores a reserve volume (flow × time) that equals or exceeds the patient’s tidal volume. For a reservoir system to provide a fixed FiO2, the reservoir volume must always exceed the patient’s tidal volume, and there cannot be any air leaks in the system. Table 38-3 outlines the general specifications for the common O2 therapy systems in current use.



TABLE 38-3


Overview of Oxygen Therapy Systems





















































































































































Category Device Flow FiO2 Range FiO2 Stability Advantages Disadvantages Best Use
Low flow Nasal cannula image-8 L/min (adults) ≤2 L/min (infants) 22%-40% Variable Use on adults, children, infants; easy to use; disposable; low cost; well tolerated Unstable, easily dislodged; high flow uncomfortable; can cause dryness, bleeding; polyps; deviated septum and mouth breathing may reduce FiO2 Patient in stable condition who needs low FiO2; home care patient who needs long-term therapy, low to moderate FiO2 while eating
  Nasal catheter image-8 L/min 22%-45% Variable Use on adults, children, infants; good stability; disposable; low cost Difficult to insert; high flow increases back pressure; needs regular changing; polyps, deviated septum may block insertion; may provoke gagging, air swallowing, aspiration Procedures in which cannula is difficult to use (bronchoscopy); long-term care of infants
  Transtracheal catheter image-4 L/min 22%-35% Variable Lower O2 use and cost; eliminates nasal and skin irritation; improved compliance; increased exercise tolerance; increased mobility; enhanced image High cost; surgical complications; infection; mucous plugging; lost tract Home care or ambulatory patients who need increased mobility or do not accept nasal O2
  Reservoir cannula image-4 L/min 22%-35% Variable Lower O2 use and cost; increased mobility; less discomfort because of lower flow Unattractive, cumbersome; poor compliance; must be regularly replaced; breathing pattern affects performance Home care or ambulatory patients who need increased mobility
  Simple mask 5-10 L/min 35%-50% Variable Use on adults, children, infants; quick, easy to apply; disposable; inexpensive Uncomfortable; must be removed for eating; prevents radiant heat loss; blocks vomitus in unconscious patients Emergencies; short-term therapy requiring moderate FiO2; mouth breathing patients requiring moderate FiO2
  Partial rebreathing mask Minimum of 10 L/min (prevent bag collapse on inspiration) 40%-70% Variable Same as simple mask; moderate to high FiO2 Same as simple mask; potential suffocation hazard Emergencies; short-term therapy requiring moderate to high FiO2
  Nonrebreathing mask Minimum of 10 L/min (prevent bag collapse on inspiration) 60%-80% Variable Same as simple mask; high FiO2 Same as simple mask; potential suffocation hazard Emergencies; short-term therapy requiring high FiO2
  Nonrebreathing circuit (closed) 3 × VE (prevent bag collapse on inspiration) 21%-100% Fixed Full range of FiO2 Potential suffocation hazard; requires 50 psi air/O2; blender failure common Patients who need precise FiO2 at any level (21%-100%)
High flow AEM Varies; should provide output flow >60 L/min 24%-50% Fixed Easy to apply; disposable, inexpensive; stable, precise FiO2 Limited to adult use; uncomfortable, noisy; must be removed for eating; FiO2 >0.40 not ensured; FiO2 varies with back pressure Patients in unstable condition who need precise low FiO2
  Air-entrainment nebulizer 10-15 L/min input; should provide output flow of at least 60 L/min 28%-100% Fixed Provides temperature control and extra humidification FiO2 < 0.28 or >0.40 not ensured; FiO2 varies with back pressure; high infection risk Patients with artificial airways who need low to moderate FiO2
  Blending system (open) Should provide output flow of at least 60 L/min 21%-100% Fixed Full range of FiO2 Requires 50 psi air/O2; blender failure or inaccuracy common Patients with high Ve who need high FiO2
  High-flow nasal cannula system Up to 40 L/min (depending on system) 35%-90% Variable or fixed depending on system and input flow Wide range of FiO2 and relative/absolute humidity; use on adults, children, infants FiO2 not ensured depending on input flow and patient breathing pattern; infection risk Patients of all ages with high or variable Ve who need supplemental O2, positive pressure, or humidity
Enclosure Oxyhood ≥7 L/min 21%-100% Fixed Full range of FiO2 Difficult to clean, disinfect Infants who need supplemental O2
  Isolette 8-15 L/min 40%-50% Variable Provides temperature control Expensive, cumbersome, unstable FiO2 (leaks); difficult to clean, disinfect; limits patient mobility; fire hazard Infants who need supplemental O2 and precise thermal regulation
  Tent 12-15 L/min 40%-50% Variable Provides concurrent aerosol therapy Expensive, cumbersome, unstable FiO2 (leaks); requires cooling; difficult to clean, disinfect; limits patient mobility; fire hazard Toddlers or small children who need low to moderate FiO2 and aerosol


image


image


Ve, Minute volume.




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.


image
FIGURE 38-5 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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